First published in Great Britain in 1999 by the Royal College of Surgeons of England

Second edition 2003

Third edition 2010
This fourth edition published in 2017 by
The Royal College of Surgeons of England
35-43 Lincoln’s Inn Fields,
London, WC2A 3PE


www.rcseng.ac.uk

©2017 The Royal College of Surgeons of England

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 2

Assessment of the critically

ill surgical patient

18
 Chapter 2  Assessment of the critically ill surgical patient

Learning outcomes 
This chapter will help you to:

n recognise the critically ill patient who must undergo simultaneous examination
and resuscitation when first seen;

n assess and manage critically ill patients systematically;

n recognise that examination and resuscitation must be performed in a

systematic manner;

n understand why abnormal physiology needs to be treated irrespective of the

cause;

n recognise the importance of finding an underlying explanation for

deterioration in a patient’s condition;

n formulate management plans for patients irrespective of physiological

stability.

Introduction
All patients in hospital should have a management plan. This plan will differ depending
on the underlying problem and degree of physiological instability of the patient.

The CCrISP three-stage assessment process will help you to define the acuity of
your patients, what the underlying problems are, what interventions are needed and
how frequently the patients should be reviewed. Most UK hospitals now use ‘track
and trigger’ systems, such as the National Early Warning Score (NEWS), to aid the
recognition of the deteriorating patient. The role of the CCrISP course and three-stage
assessment process is to allow you to assess these patients properly when called to
see them and to plan their subsequent care.

Most often, surgical patients who end up requiring critical care will either have
been admitted acutely unwell or will have suffered an acute deterioration on the
ward following admission or elective or emergency surgery. These patients require
simultaneous resuscitation and diagnosis, followed by definitive treatment, and
CCrISP helps you to do this in an organised manner.

19
Care of the Critically Ill Surgical Patient®

Other patients will be relatively more stable but remain at risk of deterioration, either
on the ward or in an HDU setting. These patients need to be re-evaluated, and
their management plan updated, at least twice daily. The aim is to ensure that the
patient is getting better. It is better to prevent morbidity by detecting problems as
early as possible; failure to progress is an important sign that an incipient problem
is present. If you fail to diagnose and treat that problem until it has resulted in a
major deterioration in the patient’s condition, then the patient’s chance of survival
is dramatically reduced. Case reviews of patients who have apparently undergone
an acute deterioration often reveal evidence of subtle signs of impending problems
that were not dealt with promptly and correctly. This is our challenge as surgeons:
to minimise the risk of adverse events and to give each patient the best chance of
experiencing a good outcome.

The CCrISP system of assessment is shown in Figure 2.1. It is the system that many
experienced doctors use. The same system is used for all patients to help determine
whether they are stable or unstable. In this context, it needs to be recognised that
stability is a relative term and often a patient will be stable but ill and needs to be
treated with great attention to detail, something which the three-stage assessment
process will guide.

The CCrISP ethos therefore is to apply the three-stage assessment process to all
patients both during scheduled ward rounds and in the event of deterioration.
The CCrISP system of assessment
®

Immediate management
Investigations
Airway | Breathing | Circulation | Dysfunction of CNS | Exposure
Blood | X-ray

Specialist opinion
Full patient assessment
Nutrition
Chart review | History and systematic examination | Available results
Requirement | Route

Fluid balance prescription

Decide and plan
Oral intake
Unstable/unsure Stable

Drugs and analgesia

Treat condition | Prophylaxis | Comorbid disease

Diagnosis required
Daily management plan Physiotherapy
Chest | Mobility

Drains and tubes removal

Move to a lower level of care

Medical | Surgical | Radiological

FigureCCrISP
2.1 4thThe
edition CCrISP system
© Royal College of Surgeons of assessment.
of England 2017 All rights reserved Registered Charity No. 212808 www.rcseng.ac.uk 4th edition

20
 Chapter 2  Assessment of the critically ill surgical patient

Immediate assessment and treatment of the acutely ill

patient
When assessing a patient, your goal is to determine whether the patient is acutely
unwell and, if so, what is making the patient ill and, having identified any life-
threatening problem, to treat it immediately. Life-threatening illnesses kill in a
predictable and reproducible pattern. When viewed in isolation, a disease process
that produces an obstructed airway will kill more quickly than a problem in the lungs,
which, in turn, kills more quickly than isolated haemorrhage. Many critically ill surgical
patients have abnormalities of more than one system and it is important therefore that
you are not distracted by obvious, and potentially minor, factors but assess and treat
patients systematically.

Immediate management
A Airway assessment and treatment.

B Breathing assessment and treatment.

C Circulation assessment and treatment.

D Dysfunction of the CNS and treatment.

E Exposure of the patient sufficient for full assessment and treatment.

This process prioritises the order in which assessment and treatment is carried out;
although represented as a sequence, such information can often be obtained virtually
simultaneously. For example, the patient’s response to the question ‘How are you?’
can be very revealing. A patient who is able to reply in a coherent manner has, at
least at that moment, sufficient airway control to allow an adequate intake of breath,
adequate respiratory function to produce oxygen transfer, adequate circulatory
function to perfuse the brain and adequate CNS function to formulate a reply.
While this is encouraging, it does not relieve you of the need to perform a detailed
assessment of each of the ABCDE components of the immediate assessment;
detailed examination picks up the subtle abnormalities that are not always obvious
unless specifically sought out.

21
Care of the Critically Ill Surgical Patient®

Practice point 
Do not be falsely reassured by patients who look well from the end of the bed.

A: Airway
Recognition that airway obstruction is present is based on a simple ‘Look, Listen and
Feel’ clinical assessment, with immediate treatment if there is airway compromise.

n LOOK for the presence of central cyanosis, an obstructed ‘see-saw’ pattern of

respiration or abdominal breathing, the use of accessory muscles of respiration,
tracheal tug, alteration of level of consciousness and any obvious obstruction by
foreign body or vomitus.

n LISTEN for abnormal sounds such as grunting, snoring, gurgling, hoarseness or

stridor.

n FEEL for air flow on inspiration and expiration.

n TREAT. If objective signs of airway obstruction are present, the immediate

goals are to obtain and secure the airway to provide for adequate oxygenation
and prevent hypoxic brain damage. Administer high-flow oxygen (12–15 L/min,
preferably humidified, via a reservoir bag).

Often, only simple methods are required to obtain an airway, such as chin lift or jaw
thrust to open the airway, suction to remove secretions and the insertion of either an
oral Guedel airway (if tolerated) or a soft nasopharyngeal airway (if the gag reflex is
present). Problems with the airway are covered in Chapter 3. If you cannot maintain
the airway by the simple measures outlined as above, you need to call for help.

Remember that patients can be maintained with an airway, plus bag and mask
ventilation as required while waiting for the anaesthetist – this is often a better option
for the non-expert, particularly in a hospital, where skilled help is usually rapidly
available.

Patients who are not fully conscious may be unable to protect their airway with the
result that it is patent only intermittently. These patients may tolerate and benefit
from airway manoeuvres while the cause of their reduced consciousness level is
addressed.

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 Chapter 2  Assessment of the critically ill surgical patient

Although unusual in the non-trauma situation, if there is a risk of coexisting pathology

of the cervical spine, all airway manoeuvres should be performed while maintaining
manual in-line immobilisation of the cervical spine.

Practice point 
Get help from an anaesthetist early to secure a compromised airway.

B: Breathing
Objective evidence of respiratory distress or inadequate ventilation can also
be determined using the clinical ‘Look, Listen and Feel’ technique, followed by
immediate treatment of life-threatening conditions:

n LOOK for central cyanosis, use of accessory muscles of respiration, respiratory

rate, equality and depth of respiration, sweating, raised jugular venous pressure
(JVP), patency of any chest drains and the presence of any paradoxical abdominal
movement. Note the inspired oxygen concentration (FiO2) and saturation. Pulse
oximetry should be in use but remember that pulse oximetry does not detect
hypercarbia.

n LISTEN for noisy breathing, clearance of secretions by coughing, the ability of the
patient to talk in complete sentences (evidence of confusion or decreased level
of consciousness may indicate hypoxia or hypercarbia, respectively) or change
in percussion note and auscultate for abnormal breath sounds, heart sounds and
rhythm.

n FEEL for equality of chest movement, the position of the trachea, the presence of
surgical emphysema or crepitus, paradoxical respiration and tactile vocal fremitus
if indicated. Percuss the chest superiorly and laterally. Abdominal distension may
limit diaphragmatic movement and should be looked for as part of respiratory
assessment.

n TREAT. The precise resuscitative treatment will be determined by the cause of

the respiratory embarrassment and will be discussed later in the chapter on
respiratory failure (Chapter 4). During the immediate assessment, you should
specifically look for signs of the immediately life-threatening conditions: tension

23
Care of the Critically Ill Surgical Patient®

pneumothorax, massive haemothorax, open pneumothorax, flail chest and cardiac

tamponade should be identified and treated without delay. Consider the diagnoses
of bronchial obstruction, bronchoconstriction, pulmonary embolism (PE), cardiac
failure (see C: Circulation) and unconsciousness (see D: Dysfunction of the
nervous system). Simple manoeuvres such as sitting the patient up can help.
However, if the patient is tiring to the point of incipient respiratory arrest, assisting
ventilation by bag/mask is obligatory, in conjunction with whatever airway
manoeuvres have been necessary, until help arrives.

C: Circulation
Hypovolaemia should always be considered to be the primary cause of circulatory
dysfunction in the surgical patient until proven otherwise. Haemorrhage (overt or
covert) must be rapidly excluded. Furthermore, unless there are obvious signs of
cardiogenic shock (particularly raised JVP), you should regard any patient who is
cool and tachycardic to have hypovolaemic shock, so establish and secure adequate
venous access with at least one large (16G) cannula, send off blood for cross-
matching and other routine tests, and initiate appropriate fluid replacement.

Start with a rapid fluid challenge of 10 ml/kg warmed crystalloid in the normotensive
patient or 20 ml/kg if the patient is hypotensive. You should be more tentative in
patients with known cardiac dysfunction, starting with an initial bolus of 5 ml/kg.
Closer monitoring may be needed in these patients.

Having identified and treated airway and breathing abnormalities that can compromise
the circulation, life-threatening circulatory dysfunction is recognised by looking for:

n reduced peripheral perfusion (prolonged capillary refill time, pallor, coolness,

collapsed or underfilled veins – remember that blood pressure can be normal in
the shocked patient);

n obvious external haemorrhage from either wounds or drains;

n evidence of concealed haemorrhage: (i) thoracic or abdominal, even when an

empty drain is present; (ii) into the gut or from pelvic or femoral fractures.

Initially, you should assess perfusion and the simplest way of doing this is to measure
capillary refill time. Institute management with a fluid bolus based on your findings.
Check the blood pressure at an early point; it can often be preserved in a patient with

24
 Chapter 2  Assessment of the critically ill surgical patient

significant circulatory problems. Marked hypotension can be a late sign in a young, fit
person and needs rapid correction.

Feel for pulses, both peripheral and central, assessing for rate, quality, regularity and
equality. Treatment and monitoring are covered in detail in Chapters 6 and 7 and
should be directed towards haemorrhage control and restoration of tissue perfusion.

No amount of fluid replacement will be of use in the face of on-going severe

haemorrhage. Immediate surgery to control haemorrhage may be required at this
stage as the only effective form of resuscitation. More frequently, urgent but non-
immediate surgery will be needed to stop lesser degrees of continued haemorrhage.

Shocked patients fall into three categories and fluid challenges can be both
diagnostic and therapeutic, helping you to determine into which category the patient
falls:

n In obviously exsanguinating patients, immediate definitive treatment (usually

surgery) is required to save the patient’s life.

n Unstable patients need rapid resuscitation and repeated reassessment over a

short period while the cause is identified and treatment planned. Such patients
may appear to respond transiently to aggressive fluid resuscitation. Urgent
definitive treatment is essential.

n Patients with a relatively minor problem will respond rapidly and adequately to a
fluid challenge and remain stable on reassessment.

Reassessment (which should be performed after each intervention) determines

whether or not a patient is responding to treatment. If there is no response (or only a
transient or inadequate response), different treatment is needed immediately. Patients
requiring large and on-going volumes of fluid are not stable, even if reasonable vital
signs are maintained.

Occasionally is it necessary to give uncross-matched blood as type-specific blood

is relatively safe and can be obtained within 20 minutes. Blood is presently the best
resuscitation fluid for the bleeding patient who has cardiovascular instability and who
requires, as a guide, more than 1500–2000 ml of resuscitation fluid.

Avoid ‘blindly’ continuing to transfuse the patient who, in reality, needs surgery.
Bleeding patients who need immediate surgery are encountered on the ward as well
as in the emergency room – patients with postoperative bleeding or recurrent bleeding

25
Care of the Critically Ill Surgical Patient®

from a peptic ulcer who are pale and shocked are typical examples. Once you have
determined that a patient is not responding to resuscitation, you should call for senior
help, cross-match 6 units of blood and alert theatre, the anaesthetist and the porters.
Shocked or hypotensive patients who are not bleeding are also seen regularly – do
not continue to ‘blindly’ fill up a patient with litres of fluid without a clear diagnosis, a
clear plan or senior review. The message is to use the assessment process, come to a
sensible conclusion, carry out an intervention, review the patient and seek help if the
patient is not responding as expected.

Most surgeons have failed to respond adequately to continuing haemorrhage at some

point during their career – so reassess and reconsider and do not leave a patient with
inadequate perfusion without further adequate treatment.

Practice points 
• Most unwell surgical patients benefit from administration of oxygen and fluids
while further assessment is undertaken.
• Reassess as resuscitation proceeds – it often takes more than one assessment
to decide on all aspects of the problem.

D: Dysfunction of the CNS

In the initial assessment, a rapid determination of neurological status is performed by
examining the pupils and by using the AVPU system:

n A – Alert.

n V – responds to Verbal stimulus.

n P – responds only to Pain.

n U – Unresponsive to any stimulus. Remember that in surgical patients alteration

of consciousness level can be due to causes other than a primary brain injury.
Hypoxia and cerebral underperfusion due to shock should have already been
detected.

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 Chapter 2  Assessment of the critically ill surgical patient

Recent administration of sedatives, analgesics or anaesthetic drugs may be

responsible. Hypoglycaemia is a common (and sometimes overlooked) cause that you
should look for and treat. If you have thought of all these and the patient is still not
fully conscious, reassess and review the ABCs: you might have missed something.

E: Exposure
In order to make accurate diagnoses and allow access to the patient for therapeutic
manoeuvres, it is essential that the patient is adequately exposed. However, be aware
that the patient may become cold and preserve the patient’s dignity at all times.

End of immediate management

By the end of the phase of immediate assessment and management, the patient will
hopefully be showing signs of improvement and progressing out of immediate danger;
if not, you need help. You may have called for help and the patient may have been to
theatre or moved to intensive care before this point is reached.

By this stage, the patient should be receiving oxygen and IV fluids. If not done already,
establish monitoring by attaching a pulse oximeter, check the blood pressure and
confirm that oxygen saturation (SaO2) is above 94% and determine the frequency of
on-going observations. Arrange pressing investigations that you know have not been
done recently and that are targeted and integral to the immediate assessment
(perhaps arterial blood gases (ABGs), chest X-ray or ECG), insert a urinary catheter (if
appropriate) and, if necessary, alert senior colleagues (if you have not already done
so). Before you start the next phase, quickly reassess the ABCs.

Practice point 
If, at any time during the immediate assessment, the patient’s condition
deteriorates, you must reassess the ABCs.

Having started resuscitative manoeuvres, it will often take a few minutes for their
effects to become apparent. Vital signs may not yet be normal but, provided the
patient’s condition is not deteriorating, you should use the time to continue with the

27
Care of the Critically Ill Surgical Patient®

next stage of assessment in order to determine the underlying cause of deterioration.

However, if the patient is deteriorating, then quickly reassess, get help and arrange for
further immediate treatment as appropriate.

Assessment of the ‘stable’ surgical patient

In many surgical patients, particularly during ward rounds, the vital signs will be
normal. Often this can be determined simply by looking at the patient, by asking how
they are, asking the nurse how the patient is doing, and reviewing the observation
charts and recent results. If any abnormality is spotted, a detailed immediate
assessment should be performed, which with practice can be done very quickly.
Using the system in this way can avoid simple errors, particularly when you are tired
or stressed.

Full patient assessment

Now that the immediate management phase has been completed, the aim is to gather
all available information from a variety of sources, which will lead to a diagnosis of
current or potential problems and, hence, to a plan of action. The full assessment
incorporates a review of the charts and available results plus a full history and
examination.

Chart reviews
Inspection of the observation and fluid charts, preferably at the end of the bed,
together with discussion with nursing and other junior medical staff, may bring to light
any recent or outstanding problems. It also allows a more focused clinical assessment
to be carried out. Charts, particularly those in HDU or ICU, may appear to carry
an overwhelming amount of information, but this too can be handled by breaking
the chart into sections and systematically noting both absolute values and trends
(Box 2.1), together with the degree of intervention needed to maintain physiological
stability.

It is not possible to give a comprehensive account of management for every potential

scenario, but you should consider both general and specific aspects of care.
For example, general care includes cardiorespiratory function and fluid balance;

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 Chapter 2  Assessment of the critically ill surgical patient

Box 2.1  Logical approach to charts

Respiratory

Respiratory rate

Inspired oxygen concentration (FiO2)

Oxygen saturation (SaO2)

Circulation

Heart rate and rhythm

Blood pressure

Urinary output

Fluid balance

Intravenous lines

Cardiac output measurements

Surgical

Special requirements of this operation

Temperature

Drainages (nature and volume)

alternatively, following liver surgery, one might look specifically for production or
drainage of bile, liver function tests, albumin, glucose and clotting factor levels.

Check the drug chart to see what new drugs have been given, and which of the
patient’s usual drugs might have been forgotten: either may be influencing the
current clinical findings. Also consider whether drugs given prophylactically and any
prescribed antibiotics are still needed.

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Care of the Critically Ill Surgical Patient®

History and systematic examination

The history of the patient’s present illness and subsequent treatment is just as
important in critical illness as in the rest of clinical practice. However, the impact of
comorbid conditions is almost as great and these are overlooked or underestimated
at considerable peril. The patient, the case note and nursing and junior medical
staff are the main sources of these types of information and the appropriate source
will vary from case to case, depending on your prior knowledge of the patient. On
occasion, family and other professional staff can also supply useful information.

The patient is then examined fully, paying particular attention to vital systems, the
systems or regions involved by surgery or underlying disease and to potential
problems already highlighted. This should follow the standard format, beginning with
the hands, and include neck, chest, abdomen and limbs. Wounds or stomas may also
require examination. The importance of clinical examination is often underestimated
by inexperienced staff, particularly when it comes to diagnosing incipient problems in
silent areas; for example, early signs of atelectasis are much more likely to be
detected clinically than radiologically (case scenario 2.1).

Case scenario 2.1 

You are on the orthopaedic ward at 3am with a trauma case when you are asked
to see a 48-year-old male patient who is tachycardic (HR 110), 12 hours after he
underwent fixation of shaft of femur following a motorcycle accident. The main
ward lights are not on, the patient is distressed and in pain and the foundation
year doctor has just started a 500 ml bolus fluid challenge and prescribed more
analgesia. The patient’s blood pressure is 105/75 mmHg. His capillary refill time
before the fluid challenge was 3 seconds and you are not unduly concerned.
You have a cup of coffee and then review the patient again. You realise that,
despite 500 ml of saline, his perfusion is worse, he is oliguric and he has a tender,
slightly distended abdomen. It is now clear to you that the patient may well have
continuing bleeding from an occult abdominal injury and that more intensive
resuscitation and consideration of urgent operation or imaging is required.

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 Chapter 2  Assessment of the critically ill surgical patient

Review of available results

Available investigation results should now be reviewed (Box 2.2). With emergencies, a
great deal of useful data may be available from reviewing any previous routine blood
results, microbiology samples or imaging requests, so do not overlook this important
source of information.

Box 2.2  Review available results

• Biochemistry profile
– ABGs
– Glucose level

• Haematology
– Blood count
– Clotting
– Cross-matched blood available

• Microbiology
• Radiology
– Review reports or examine films

• ECG
• Other tests, eg echocardiography
• Return to charts and review any necessary points

Ensuring that all results are reviewed on routine ward rounds is also very important,
and not doing so is a classic source of error. Most hospitals now have electronic
systems. It is also important to check what has been requested so that you can chase
results and avoid repeating tests unnecessarily.

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Care of the Critically Ill Surgical Patient®

Decide and plan – stable or unstable?

Once you have assessed the patient and the available information, you need to make
a decision – is the patient stable or unstable? Patients about whom you are unsure
should be managed as if they were unstable. Also, you should be very cautious
about being too quick to assign patients who were previously unstable but who have
responded to treatment to the stable group. Instability is a relative term, but training
yourself to make this decision is important as it will focus your mind on one of two
very different subsequent approaches.

Stable patients – daily plan

Stable patients have normal signs and are progressing as expected. No major
interventions will be required to maintain normal physiological parameters and they
will not have experienced any recent untoward events. This will apply to most patients
seen on the daily ward round and so the immediate management phase of the three-
stage assessment process can be completed quickly. Once the charts and results
have been reviewed to confirm that there are no significant abnormalities, the patient
can be considered to be stable. It is then your duty to formulate a management
plan. On the ward this will be daily (Box 2.3); however, in the HDU, 12-hourly or more
frequent assessment and planning will be needed.

In particular:

1 Ensure that necessary therapeutic drugs, including analgesia, are prescribed

(modify these as the patient recovers).

2 Check that appropriate prophylaxis, particularly against venous thromboembolism,

is prescribed.

3 Check that any antibiotic prescriptions are still required and the drug prescribed is
appropriate to the sensitivities of the organism in question.

4 Verify that routine medications are being given (if necessary by an alternative
route).

5 Consider what implications comorbid conditions or treatment might have for

present management or prognosis.

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 Chapter 2  Assessment of the critically ill surgical patient

Speak to patients, to encourage and reassure them, to ensure that they know what is
happening, when they can expect to go home and what they need to achieve to be
able to be discharged. Sum up your plan with clear instructions for your nursing
colleagues and junior staff and make (or supervise) an entry in the notes so that this is
clear to someone reading the notes who has no knowledge of the patient.

Practice point 
Plan and sum up, communicate and document.

Box 2.3  Daily plan

• Investigations
– Blood tests and imaging, specialist opinions

• Removal of drains/tubes
• Oral intake
• Fluid balance and prescription
• Nutrition
– Requirement
– Route
– Is it being given?

• Physiotherapy
– Chest and mobility

• Drugs and analgesia

– Therapeutic (eg antibiotics, analgesia)
– Preventative (eg subcutaneous heparin)
– Routine (eg cardiac)

• Consider level of care

33
Care of the Critically Ill Surgical Patient®

Unstable patients
If progress is not satisfactory, further investigation or definitive treatment will be
needed. If a cause is already evident from your evaluation, treatment can be planned
directly. Inform your senior and consider whether a higher level of care is needed.

Specific targeted investigations

These are carried out as necessary to find out why the patient is unstable and to let
you or others do something about it subsequently.

These range from the simple to the very complex. Usually, simple blood tests will have
already been sent off during the immediate management phase but now is the time to
check. Likewise, chest radiographs, ECGs and cultures may have already been done
or may be needed now.

The safest way to accomplish more complex and specific investigations will differ
between patients depending on the test required, the degree of urgency and how sick
the patient is. Remember that the radiology department is an unsafe place for sick
patients unless they have adequate support from medical and nursing staff.

The ideal test may have to be forgone in some circumstances, or it may be better
to transfer the patient to critical care for full support before a planned transfer to
the radiology department. Specialist opinions (eg cardiology, anaesthesia, intensive
care) may be required. If you reach an impasse (either a diagnostic or organisational),
involve your senior colleagues. If you are unsure at this stage how to make things
happen, ask for help. However, do not give up on a necessary investigation or
treatment just because it is difficult to arrange or beyond your expertise, or the timing
is not convenient (case scenario 2.2).

Be careful to maintain momentum; on busy wards, multiple small delays at each stage
can add up to a lengthy delay in treating the underlying cause, which can result in
your previous resuscitation being in vain. Making things happen is an important skill.

Investigations may take time, during which you must ask yourself repeatedly:

n Is the present level of physiological support optimal?

n Are we reaching a diagnosis and a definite plan of action?

n Are we doing so quickly enough?

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 Chapter 2  Assessment of the critically ill surgical patient

If not, a change of plan is needed.

Case scenario 2.2 

An elderly patient with known mild heart failure underwent endoscopy and
diathermy of a bleeding duodenal ulcer at 8pm. He became steadily oliguric from
11pm and received two cautious fluid challenges from the junior ward doctor. You
are asked to see him at 3.35am and note that he is not well perfused and mildly
dyspnoeic. You give a further 350 ml of saline over 15 minutes without any change
in his condition. You are unsure what fluids are required and feel that more
invasive monitoring and assessment may be needed. You are aware that the
patient needs to be reviewed by the critical care team, but they are already busy
and you do not explain the full extent of your concerns. You elect to continue
with maintenance fluids until the 8am ward round and do not arrange any further
review. By then, the patient is anuric and has evidence of acute kidney injury.

Learning points 
• Unstable patients require diagnosis and definitive treatment without undue
delay.
• Involve senior staff if you think patients do not appear to be receiving the care
you feel they require.

When you have attended a patient, you must record the event in the case notes (Box 2.4).
This serves several functions: writing your assessment helps clarify your thoughts, your note
tells other staff what happened and lets them gauge the response, you can define clear
criteria for further interventions and the note can be of medicolegal importance.

It should be clear from the note who saw the patient and when, why they were seeing them
(routine review or called to see), what information was gathered, how that information was
interpreted, what the decision was, what the plan was, who was to carry it out and when the
patient is to be reviewed. Depending on the situation, it may also be prudent to record what
was said to the patient and any concerns they have.

35
Care of the Critically Ill Surgical Patient®

Box 2.4  Writing your notes

• Name in capitals, date and time, contact details
• Assessment and findings
• Brief summary of past and present events
– Present clinical features
– Interventions performed
– Response to any treatment already given

• Summary of current abnormalities

• Differential diagnosis if relevant
• Plan
– Further investigations
– Other specialist opinions
– Treatment

• Communications to relatives, staff, seniors, etc.

• Review
– By you
– By others

• Parameters for change

Definitive treatment
The underlying aim of critical care practice is to begin definitive treatment of life-
threatening pathology or complications as quickly as possible. Steps taken in the
immediate management phase keep the patient alive: however, unless you treat the
underlying problem adequately, the patient will deteriorate again and may die. Once
the need for intervention is clear to all, the situation may be irretrievable, so speed is
of the essence.

Treatment may be medical, surgical or radiological or all three, so coordination is

important. When the patient has a surgical problem, you will need to play a leading

36
 Chapter 2  Assessment of the critically ill surgical patient

role in coordinating efforts. Consider where non-operative treatment should best be

carried out, by whom, and what support will be necessary. If the patient is transferred,
especially to an area unfamiliar with surgical patients (eg the coronary care unit),
detailed instructions will need to be written in the case notes and frequent review will
be necessary to ensure that other surgical aspects of care continue to be delivered
even though the staff members are unfamiliar with them.

Reassessment
Finally, once any treatment has been instituted, whether simple fluid therapy or a
complex surgical operation, you must reassess the patient to ensure that he or she
has responded to the treatment. The necessary time frame for doing this will depend
on the urgency of the case.

If the patient has not responded adequately, then you need to look all the harder for
a different cause to treat. Reassessment is the final step – and, if necessary, the first
step in repeating the whole process.

Summary
The CCrISP system encourages you to assess all your patients in a similar way to
determine whether they are stable or unstable and to guide appropriate interventions.
It is the system that many senior surgeons and intensivists use instinctively. With
practice, the use of a system will allow you to assess patients without overlooking
simple and potentially disastrous abnormalities and it will serve as a framework
whereby you can apply your theoretical knowledge to clinical problems.

The CCrISP course encourages you to:

n use a structured system to assess patients and reduce serious omissions;

n identify those in need of immediate life-saving resuscitation – assess and treat

them simultaneously;

n reach a diagnosis that accounts for clinical deterioration;

n formulate and institute a plan of definitive treatment;

n plan investigations to be selective and carried out in a safe environment;

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Care of the Critically Ill Surgical Patient®

n utilise repeated clinical assessment as the cornerstone of good practice – it

identifies things missed first time around and tells you whether the patient is
getting better in response to your interventions;

n inform and involve your senior colleagues as appropriate;

n consider the level of care necessary at each stage of the process;

n communicate and document clearly.

38
 3

Airway management

40
 Chapter 3  Airway management

Learning outcomes 
This chapter will help you to:

n describe the principles behind airway management;

n outline the indications for tracheostomy in critically ill patients;

n outline the key elements of tracheostomy care;

n model how to deal with common tracheostomy emergencies.

The most common reason for admission to a critical care unit is the provision of
airway management and ventilatory care to critically ill patients.

The early recognition and treatment of an airway or ventilatory problem will often
prevent further patient deterioration and is the basis of effective resuscitation. Many
patients on surgical wards exhibit signs of respiratory compromise and their effective
management in the ward environment is an important part of surgical critical care.

As outlined in Chapter 2, you should exclude an airway problem when assessing

every patient. Often the patient will respond to you verbally but, if not, suspect airway
compromise.

Alteration in the level of consciousness for any reason can result in loss of airway
control. The decreased protective gag and laryngeal reflexes that accompany
significant reductions in consciousness level also increase the risk of aspiration of
gastric contents into the lungs.

Whilst significant airway problems are not particularly common on a general surgical
ward, they are more commonly encountered in other surgical specialties and are
generally quite intimidating for surgical trainees. Applying basic principles is vital.

It is important to remember that the ‘ABCDE’ approach of the CCrISP algorithm also
applies in cases of apparent airway problems. The signs of an obstructed airway are
noisy breathing including inspiratory stridor. Remember that complete obstruction will
be silent. Other signs include seesaw breathing and indrawing of the suprasternal,
supraclaviclar and intercostal spaces on attempted inspiration.

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Care of the Critically Ill Surgical Patient®

The signs of breathing difficulties include:

n dyspnoea, tachypnoea or apnoea

n inability to speak in complete sentences

n wheezing

n use of accessory muscles of respiration

n central cyanosis

n sweating and tachycardia

n showing a decreased level of consciousness or becoming agitated and difficult to

control.

There are two golden rules to airway management:

n Always give oxygen in the highest concentration possible.

n Use simple methods of airway management first.

Techniques of airway control

If the patient is breathing spontaneously, administer the highest flow rate of oxygen
possible using a mask with a reservoir bag (Figure 3.1). This increases the available
inspired oxygen concentration during inspiration by filling the reservoir with oxygen
during expiration.

During resuscitation, you should not worry about the possibility of depressing
ventilation by giving high concentrations of oxygen. Although some patients may have
a hypoxic drive to control respiratory rate in the face of chronic hypercapnia, hypoxia
kills people quicker than loss of respiratory drive and the condition is relatively rare
in surgical patients. Apply a pulse oximeter to allow you to assess that oxygen
administration is improving the patient’s oxygen saturation level. Once the patient
has stabilised, the oxygen concentration can be decreased to maintain adequate
saturations (> 94% unless there is clear evidence of a hypoxic drive, in which case the
British Thoracic Society recommends a target saturation range of 88–92%).

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 Chapter 3  Airway management

Figure 3.1  Facemask with reservoir bag.

Remember that pulse oximetry does not give an indication of hypercapnia or the
effectiveness of ventilatory effort. Be very wary of any signs that the patient may be
tiring.

Escalating airway support

In increasing measure, airway support can be achieved by using:

n chin lift/jaw thrust

n suction

n airway adjuncts such oropharyngeal (Guedel) or nasopharyngeal airways

n a laryngeal mask or endotracheal tube

n a surgical airway.

Basic manoeuvres without airway adjuncts are often sufficient to improve gas
exchange through a compromised airway. If not, an oral Guedel airway should be
inserted (Figure 3.2). If the patient tolerates a Guedel airway, you need someone with
advanced airway skills to attend the patient immediately.

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Care of the Critically Ill Surgical Patient®

Figure 3.2  Oropharyngeal (Guedel) airways.

Neither technique should be attempted by the inexperienced or untrained practitioner.

The Guedel airway is sized from the tragus of the ear to the angle of the mouth and in
adults is inserted upside down and rotated into place over the tongue.

Ensure that suction is present. If the patient has a gag reflex, it may be easier to insert
a nasopharyngeal airway, but this carries a risk of epistaxis. Never force insertion of
an oropharyngeal or nasopharyngeal airway.

In situations of airway compromise, call for help early. Seek anaesthetic/critical care
help at any point if you are unable to cope or think you may reach the limits of your
competence.

If the patient is apnoeic or has very shallow respiration, then ventilation using a bag/
valve/mask system is necessary (Figure 3.3). This will usually maintain sufficient
oxygenation until an anaesthetist arrives. Take every opportunity you can to practise
your basic airway skills. One way is to ask the anaesthetist if you can practise manual
ventilation under supervision in the anaesthetic room prior to elective surgery.

Patients who are semiconscious and unable to tolerate an oral airway will not tolerate
endotracheal intubation or laryngeal mask insertion without additional sedation and
so you must seek additional help to secure the airway.

With appropriate training, attempting to insert a laryngeal mask airway can often be
simpler, quicker and easier than attempting intubation.

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 Chapter 3  Airway management

Figure 3.3  Bag/valve/mask.

If you try to intubate the patient and fail, or if you are unable to ventilate the patient
manually or with a laryngeal mask airway, then you are committed to performing
a surgical airway by surgical cricothyroidotomy in order to ensure life-saving
oxygenation and ventilation. Emergency front of neck access is beyond the scope of
the CCrISP course but should be practised in simulation.

Tracheostomy
A tracheostomy is a hole in the trachea through which a person can breathe or be
ventilated and can be required for various reasons (Box 3.1). There are two distinct
types of tracheostomy.

1 Upper airway absent. Tracheostomy after laryngectomy: this is an end stoma

formed when a patient has had a laryngeal resection. There is no upper airway
connection to the lungs.

2 Upper airway present:

a Surgical tracheostomy: this is performed under direct vision and involves

making a surgical cut in the trachea.
b Percutaneous dilational tracheostomy: this is performed using a Seldinger
technique to dilate a needled hole in the trachea.

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Care of the Critically Ill Surgical Patient®

It is important to identify which type of tracheostomy a patient has as it affects the

management of tracheostomy difficulties.

Practice point 
The most important difference is between a laryngectomy stoma, in which case
there is no remaining upper airway, and those forms of tracheostomy that allow
management of the upper airway if problems arise.

Box 3.1  Reasons for a tracheostomy

• Upper airway obstruction
• Post laryngectomy/upper airway surgery
• Musculoskeletal disorders affecting ventilation (eg muscular dystrophy, spinal
cord injury, motor neurone disease, post-traumatic brain injury)
• To assist weaning from ventilation on critical care
– Reduced airway resistance
– Improved airway toilet
– Allows reduction in sedation as better tolerated than an oral tube

• Incompetent swallow/impaired upper airway reflexes

Tracheostomy is often performed on long-stay ICU patients, and in some hospitals

patients with tracheostomies are managed on non-ENT wards following discharge
from critical care. It is therefore important for surgeons to have knowledge of, and be
able to deal with, common complications of tracheostomies.

Tracheostomy tubes come in a variety of types and sizes, and in the practical
sessions of the CCrISP course you will have the opportunity to examine a number of
them. The type of tube inserted, and its size, should be documented in the patient’s
notes. To facilitate this, specific documentation is being developed (eg the Trachi-
pass), and an example of this will be shown on the course. Many hospitals are now
developing local guidelines for managing patients with a tracheostomy tube, and a

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 Chapter 3  Airway management

National Tracheostomy Safety Project initiative is also on-going (www.tracheostomy.

org.uk).

Other features of tracheostomy tubes are listed in Box 3.2 and different types are
shown in Figure 3.4.

Box 3.2  Types of tracheostomy tubes

Tracheostomy tubes are available in a number of sizes and types. The choice of
tracheostomy tube depends on the needs of the patient and the clinical situation.

Inner tubes are usually recommended, to facilitate cleaning, unless the tube will
be required for only a very short time.

• Cuffed: used if an airway seal is required (eg for intermittent ventilation in

critical care)
• Uncuffed: primarily used in patients requiring a tracheostomy long term as they
are less likely to cause trauma, which is usually due to cuff pressure
• Unfenestrated: usually used in association with a cuffed tracheostomy tube
when intermittent ventilation is required, eg in surgical patients
• Fenestrated: allow upper airway flow for phonation, designed for medium- to
long-term use

Information on tube size should be located on the flange. There is no uniformity of

tracheostomy tube size with regard to length and dimensions so this needs to be
checked for each type of tube. Most females will accommodate an internal diameter
tube of 7–8 mm and males usually 8–9 mm. Selecting a tube of the appropriate size is
important to maximise the internal tube dimensions and reduce the work of breathing
through the tube. However, an oversized tube can cause pressure necrosis and
damage the tracheal mucosa. If the tracheostomy tube is too small, the cuff will need
to be overinflated to prevent accidental displacement of the tube or leakage during
positive-pressure ventilation. Cuffed tracheostomy tubes available in critical care have
an aspiration port above the cuff that is used to keep this area clear of secretions,
thus reducing the risk of ventilator-acquired pneumonia.

Management of tracheostomies on the ward is usually straightforward, provided

simple principles are followed.

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Care of the Critically Ill Surgical Patient®

Figure 3.4  Types of tracheostomy tube.

General management
n Humidification and regular suction are essential: blockage of the tracheostomy
tube is often due to failure to carry out basic toileting of the airway.

n Tubes should not be changed within 3 days of a surgical procedure, and ideally
not within 7–10 days of a percutaneous procedure, to ensure that the tract has
formed properly.

n On the wards, single lumen tubes are generally undesirable because of the risk of
blockage. These should be replaced with a tracheostomy tube with a removable
inner tube to facilitate cleaning as soon as it is safe to do so. Use the CCrISP
algorithm to determine whether the tracheostomy tube is still required.

Practice point 
Tracheostomy tubes should be changed only by staff who have the necessary
skills. If you have not had training you should not plan to undertake the
procedure unsupervised.

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 Chapter 3  Airway management

Problems with tracheostomies

The commonest problems with tracheostomies are:

n displacement

n obstruction

n haemorrhage.

These can easily be remembered with the mnemonic: DOH!

Critical incidents
n Apply the CCrISP algorithm when asked to deal with a tracheostomy problem.

n Determine when the procedure was performed and what type of tracheostomy
tube the patient received. Specifically, check if the patient has an existing upper
airway.

n The National Tracheostomy Safety Project (www.tracheostomy.org.uk) publishes

algorithms to deal with tracheostomy critical incidents.

n The management of tracheostomy problems is logical once a general

understanding has been achieved. Think clearly and do not panic.

Desaturation with a tracheostomy with an existing airway: follow the

CCrISP algorithm

This is generally due to displacement or obstruction.

n Call for help.

n Recognise that the patient has a patent upper airway.

n Recognise that the patient is breathing but that this is suboptimal.

n Administer 100% oxygen via facemask and tracheostomy tube.

n Assess tracheostomy patency assessing for improving ventilation after each step:

• remove inner cannula

• apply suction
• deflate cuff

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Care of the Critically Ill Surgical Patient®

• remove tracheostomy tube

• manage upper airway with bag and mask ventilation plus airway adjuncts
(remembering to temporarily cover the tracheostomy hole with a dressing)
• attempt bag and mask ventilation at tracheostomy stoma site (this can be
difficult)
• perform upper airway intubation (this should only be done by a clinician
skilled in the technique).

Haemorrhage from a tracheostomy tube: follow the CCrISP algorithm

n Bleeding from a tracheostomy is generally due to erosion into blood vessels at

or under the tracheostomy site. It can be life-threatening, particularly if there is
significant haemorrhage into the airway. Most tracheostomy bleeds are minor and
can be managed conservatively.

n Erosion into the innominate artery or vein at the superior end of the sternum,
whilst rare, can be catastrophic and will need specialist assistance if the patient is
to survive.

n Call for help: anaesthetic and surgical airway specialists may be needed.

n Follow the CCrISP algorithm; apply 100% oxygen to tracheostomy and face. Gain
large-bore IV access.

n Inspect the stoma site without dislodging the tracheostomy and apply manual
pressure to any obvious bleeding sites.

n Infiltration of dilute adrenaline (1:80,000 to 1:200,000 with or without local

anaesthetic) can be attempted if there is diffuse bleeding. Application of
adrenaline-soaked swabs may also be effective.

• If the bleeding is significant, gentle pressure to the sternal notch and

hyperinflation of the tracheostomy cuff may alleviate the situation temporarily
until specialist help arrives.
• Do not deflate the cuff or remove the tube.
• A blood sample should be taken for full blood count (FBC), ABG analysis
and cross-matching, but this should not be prioritised over securing the
airway.

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 Chapter 3  Airway management

Removal of a tracheostomy tube

Daily assessment of the continuing need for a temporary tracheostomy should always
form part of a patient’s management plan. Removal of a tracheostomy tube is usually
called decannulation. This should be done only by someone with the relevant skills
and should involve assessment of:

n neurological status

n ventilation and oxygenation needs

n quality of upper airway (including cord function and assessment of upper airway
oedema)

• ability to cough and clear secretions

• confirmation that the original indication for tracheostomy has been
successfully treated
• confirmation that the patient is generally stable

Most dilational percutaneous tracheostomies require only an occlusive stoma site

dressing after removal. Surgical tracheostomies may require formal operative closure.

After decannulation, a period of close monitoring and observation is necessary.

Failure to successfully decannulate may present as rapid airway failure and it is
therefore vital that specialist airway equipment and expertise are available.

Many patients require formal speech and language therapy and swallowing
assessments prior to commencing oral diet.

Summary
n Airway management should always follow two simple rules:

• Always administer the highest oxygen concentration possible.

• Use the simplest methods of airway control first.

n Seek specialist airway help early.

n Tracheostomy complications are usually due to displacement, obstruction or

haemorrhage (DOH).

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Care of the Critically Ill Surgical Patient®

Further reading
National Tracheostomy Safety Project (www.tracheostomy.org.uk).

Resuscitation Council UK. Advanced life support (ALS) guidelines and guidance 2015
(www.resus.org.uk/resuscitation-guidelines/).

52
 4

Respiratory compromise in
the surgical patient

54
 Chapter 4  Respiratory compromise in the surgical patient

Learning outcomes 
This chapter will help you to:

n understand the importance of respiratory failure and its prevention for good
surgical outcomes;

n recognise the patient with respiratory failure and provide a management

approach to respiratory failure;

n be familiar with common methods of providing respiratory support;

n understand the basic concepts of mechanical ventilation.

Introduction
Respiratory failure occurs when there is inadequate pulmonary gas exchange such
that blood oxygen and carbon dioxide cannot be maintained at normal levels. A PaO2
of 8 kPa is the point on the oxygen dissociation curve when rapid desaturation occurs
if there is any further fall in PaO2 (Figure 4.1).

Respiratory failure is the commonest cause of a decreased level of consciousness in

general surgical patients and is classified in accordance with the CO2 level:

n Type 1 failure. Failure of oxygen uptake leads to hypoxia (PaO2 of less than 8 kPa:
normal range 10.6–13.3 kPa) but normal or reduced PaCO2 (normal range 4.7–
6.0 kPa).

n Type 2 failure. Failure of oxygen uptake and of carbon dioxide removal leads to
hypoxia and hypercarbia (PaCO2 of greater than 6.7 kPa).

Type 2 failure may be acute or may have a chronic element. This is determined by
looking at the bicarbonate level and also from the patient’s history. Bicarbonate levels
are high in patients with a chronic degree of type 2 respiratory failure, eg those with
chronic obstructive pulmonary disease (COPD).

Respiratory failure is more likely where surgery is prolonged and painful. Inadequate
analgesia is an important contributor to respiratory failure; however, opiates also
increase that risk.

55
Care of the Critically Ill Surgical Patient®

100
90
80
70
60
SaO2 (%)

50
40
30
20
10
0
0 1 2 3 4 5 6 7 8 9 10 11 12 13
PaO2 (kPa)
Figure 4.1  The oxygen–haemoglobin dissociation curve. Below a PaO2 of 8 kPa the slope drops
away steeply. Keep the saturation > 94% to ensure that the PaO2 is above 8 kPa.

There are a number of common causes of respiratory failure in the surgical patient,
which can be classified into three broad groups:

1 Acute fall in functional residual capacity (FRC) without pulmonary vascular

dysfunction:

• failure of chest mechanics after trauma or other processes that render the
lungs stiff and non-compliant;
• acute postoperative atelectasis, sputum retention, pneumonia or depression
of respiration caused by analgesic, sedative or neuromuscular blocking
drugs.

Frailty and malnutrition contribute.

2 Acute fall in FRC with pulmonary vascular dysfunction. This includes left
ventricular failure, fluid overload, pulmonary hypertension, PE, neurogenic
pulmonary oedema or adult respiratory distress syndrome (ARDS).

3 Airflow obstruction – including increased lung volume states such as COPD,

asthma or other airflow obstruction.

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 Chapter 4  Respiratory compromise in the surgical patient

Factors that increase the risk of respiratory problems include:

n a history of pre-existing respiratory disease, such as asthma, COPD and

obstructive sleep apnoea

n obesity

n smoking

n thoracic surgery

n upper abdominal surgery

n older age.

Immediate assessment and management

Although ABG analysis is often the first point at which respiratory failure is diagnosed,
the initial assessment and management of the patient with respiratory problems
should follow the systematic approach of the CCrISP algorithm.

Remember the ABCDEs. An unconscious patient with no airway must be resuscitated

quickly to prevent hypoxic brain damage. Review airway management in Chapters 2
and 3.

Patients with respiratory failure may be easily recognised if they are:

n dyspnoeic, tachypnoeic or apnoeic;

n unable to speak in complete sentences;

n using accessory muscles of respiration;

n centrally cyanosed;

n sweating and tachycardic;

n exhibiting a decreased level of consciousness.

All patients should be given high-flow oxygen via a reservoir bag in the first instance
if still spontaneously breathing. During resuscitation, you should not worry about
the possibility of depressing ventilation by giving high concentrations of oxygen to a
patient with chronic pulmonary disease whose breathing is normally regulated by a
hypoxic drive. Hypoxia kills more quickly than hypercarbia.

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Care of the Critically Ill Surgical Patient®

Apply a pulse oximeter and once the patient has stabilised, the rule is to give the
minimum added oxygen to achieve the best oxygenation.

Pulse oximetry
Pulse oximetry has become a central tool in the monitoring of critically ill surgical
patients. It is a method of continuously monitoring oxygen saturations, not absolute
oxygen levels or ventilation.

Understanding its working will make you aware of the limitations. Pulse oximetry
works by combining two principles based on light transmission and reception
through tissue. First, the probe detects pulsatile flow plethysmographically. Second,
it differentiates between oxygenated and reduced haemoglobin by their differing light
absorption. Signal processing produces a display of heart rate and arterial oxygen
saturation (SaO2).

Saturation does not equate to the partial pressure of oxygen (which is responsible for
gas exchange). The oxygen dissociation curve in Figure 4.1 links these parameters.
Note that SaO2 of 94% often equates to a PaO2 of about 8 kPa so it is advisable to
keep the SaO2 above 94% and to set the alarms accordingly. There is a delay of
around 20 seconds between actual and displayed values.

If a patient is chronically hypercapnic (identified by a high bicarbonate on ABG

analysis) then a target SaO2 of 88–92% is usually appropriate when the patient is
stable. The pulse oximeter does not detect hypercarbia or acidosis – only blood gas
analysis can do this. Carboxyhaemoglobin can cause a pulse oximeter to give an
erroneously high reading. Other factors that can impede accurate pulse oximetry
include:

n movement: shivering, rigors, tremor, agitation;

n peripheral vasoconstriction – shock, hypothermia;

n cardiac arrhythmias;

n profound anaemia (rarely seen in UK practice);

n SaO2 below 70% (the device is not accurately calibrated below 75%);

n diathermy;

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 Chapter 4  Respiratory compromise in the surgical patient

n bright lights;

n dirty skin, pigmentation including jaundice, or the use of nail varnish (most modern
pulse oximeters will work with nail varnish present).

Full patient assessment

Chart review
Chart examination may reveal changes in respiratory rate, temperature, pulse rate,
blood pressure, level of consciousness, a fall in oxygen saturation or deterioration in
ABGs if previously recorded. Fluid balance charts should be assessed and the patient
examined for signs of fluid overload. Ask the patient about any changes in the colour
or amount of sputum. A deteriorating trend in any of these physiological variables
is an essential diagnostic tool and the importance of accurate charting cannot be
overemphasised.

History and systematic examination

You should quickly review the patient’s history in an effort to determine any likely
source of respiratory difficulty. The patient may be known to suffer from asthma
or chronic bronchitis or may recently have received a large dose of opiates. The
examination should initially be clinical, based on simple ‘Look, Listen and Feel’
techniques described in the assessment chapter (Chapter 2) and aimed at detecting
the physiological changes of developing respiratory failure.

Available results
Full blood count

Correction of anaemia will help to improve oxygen delivery to the tissues if the
haemoglobin is less than 80 g/L. An elevated white cell count may indicate concurrent
infection that may be pneumonic in origin.

Urea and electrolytes

The levels of urea and electrolytes in the blood may give some indication of the
patient’s fluid and renal status.

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Care of the Critically Ill Surgical Patient®

ABG analysis

This is the most useful blood test in cases of respiratory failure. You should be familiar
with the practical skill of blood sampling and the interpretation of the results. The
interpretation of ABGs is outlined in Chapter 5. Treat the patient as a whole and do
not act only on the blood gases in isolation from the clinical findings.

ECG

An ECG will provide information regarding the presence or absence of myocardial

ischaemia and rhythm and rate abnormalities that could be responsible for the onset
or worsening of respiratory failure. Cardiac and respiratory physiological variables are
inseparable when it comes to assessment and treatment of respiratory failure. Further
investigation of cardiac function, such as echocardiography or estimations of cardiac
output or cardiac index, may be appropriate if the patient is receiving a higher level of
care.

Chest X-ray

Plain chest X-ray remains a valuable diagnostic tool. Radiographic changes often
lag behind the clinical changes and it is important to treat the patient, not the X-ray.
Interpretation of chest X-rays must follow a systematic approach, as described in
Box 4.1. For the acutely deteriorating patient, a portable chest X-ray machine may be
helpful.

Lung function tests

Preoperative lung function tests (peak expiratory flow rate, vital capacity and forced
expiratory volume in 1 second (FEV1)) are useful in predicting the patient at risk,
although a patient’s ability to climb a flight of stairs in one go or to conduct everyday
tasks also provides valuable information. Hand-held spirometers are simple and easy
to use, and spirometry should be conducted preoperatively in any patient who gives a
history of respiratory disease. It is increasingly common for patients undergoing major
surgery to undergo formal cardiopulmonary exercise testing (CPET) to determine the
dynamic functioning of the lungs and heart as a unit, i.e. measurement of anaerobic
threshold. Looking in the notes for this preoperative information may give a valuable
clue as to the cause of any current deterioration.

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 Chapter 4  Respiratory compromise in the surgical patient

Chest ultrasound is frequently used clinically in critically ill patients to determine

the presence of a pleural effusion, and to guide its drainage. CTPA (CT pulmonary
angiography) should be used when a patient is hypoxic and there is no clear cause
for the deterioration. An alternative investigation in the unstable patient may be to
arrange Doppler scanning of the legs and bedside echocardiography to look for
evidence of right heart strain. Infection is the most common cause of respiratory
failure, and samples of blood for culture should be obtained before commencing
antibiotic therapy. Positive blood cultures have been reported in up to 40% of patients
with hospital-acquired pneumonia. Sputum samples should be collected at the
first opportunity but this should not delay administration of antibiotics. Additional
microbiological samples may also be required if there is no clear cause for the
respiratory deterioration. Seek advice about further samples, for example the need for
flu swabs in a patient recently admitted from home.

Stable patients – daily management plan

Frequent assessment of all surgical patients, but especially those at high risk, is
important.

Routinely assess respiratory rate, SaO2 (along with oxygen requirements), cyanosis,
ability to cough and deep breathe and adequacy of analgesia, looking for signs of
respiratory distress, sweatiness and tachycardia. Formal examination of the chest
should also be carried our regularly. If there any concerns, consider the investigations
outlined above.

Prescribe humidified oxygen therapy by mask at an appropriate concentration.

Monitor clinical signs (especially respiratory rate), oxygen saturation and ABGs. For
patients with lower oxygen requirements, nasal cannulae may be used, but remember
that oxygen should be administered to patients to keep their SaO2 above 94%.
Communicate with nursing staff and ensure that they are aware of the frequency of
observations required and triggers for escalation.

If patients require oxygen by mask for > 24 hours, or are likely to have a high sputum
load, ensure that appropriate humidification is used. Physiotherapy review should
be sought for all patients at risk of, or developing, respiratory problems. Early
mobilisation and sitting up are the best ways of preventing later respiratory problems.
However, other aspects to be considered are patient positioning, exercises to
encourage deep breathing, suction of respiratory secretions using nasopharyngeal

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Care of the Critically Ill Surgical Patient®

airways, techniques such as percussion and use of devices such as incentive

spirometry and cough incentive machines.

Ensure that patients' routine prescriptions for any respiratory disease are continued
and consider changing inhalers to nebulisers if appropriate. Consider use of nebulised
saline to loosen secretions. If a patient develops a wheeze (which can occur in
the absence of previous respiratory disease), prescribe nebulised salbutamol and
ipratropium. Some patients use home non-invasive ventilation (NIV) or continuous
positive airway pressure (CPAP) devices. Ensure that any patient who uses these
brings them into hospital and that staff who will be looking after the patients are
familiar with their use. Keep interruptions to patients’ usual CPAP/NIV regimes to a
minimum. Adequate analgesia is important to enable patients to cough and deep
breathe. Conversely, overuse of opiates leads to narcotisation and airway and
respiratory compromise (see Chapter 14 for advice on analgesia). For most surgical
patients, 4-hourly observations are appropriate but, if you are concerned, increase
the frequency to hourly. Monitoring consistent with NEWS charts standards is the
minimum. Abnormalities in observations should be escalated in accordance with your
hospital policy.

Case scenario 4.1 

A 45-year-old man had a laparoscopic gastric bypass 2 days ago. His body mass
index (BMI) is 45 kg/m2 and he has a history of obstructive sleep apnoea but
has refused home CPAP. He has a history of chronic back pain problems and
normally takes regular paracetamol and oral morphine as required. You are called
to see him because his saturations are 90% and he is complaining of pain.

He is maintaining an airway, and immediate assessment reveals a temperature

of 37.3°C, respiratory rate of 24 and SaO2 of 90% on room air. He has not been
out of bed since the operation. He also has non-insulin-dependent diabetes
mellitus (NIDDM) and hypertension. He is cyanosed but well perfused. You
review him in detail and find that he has not been receiving his normal analgesia,
oxygen therapy has not been given for 6 hours and that he has not seen the
physiotherapist today. He has poor air entry bilaterally, particularly at the right
base. Blood gases now show a mild respiratory acidosis and a PaCO2 just
above the upper limit of normal. You prescribe humidified oxygen to maintain his

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 Chapter 4  Respiratory compromise in the surgical patient

oxygen saturation above 95% and start regular nebulised salbutamol as he uses
salbutamol as necessary at home. A CXR is requested, which reveals atelectasis
at both bases. You arrange for immediate review by the on-call physiotherapist
and by the pain team. The physiotherapist obtains a sputum sample for culture
but, as this looks clear and the white cell count is normal, you elect not to start
antibiotics at present. You review him 1 hour later, confirm that his improved
analgesia has allowed him to increase his air entry and clearance of secretions
and, thereby, oxygenation. The blood gases have improved. You discuss the
case with the nurse and agree the necessary frequency of observations and
parameters of saturation, respiratory rate and pain score that would necessitate
further urgent medical review. You plan to review in any event at 8am to discuss
with (and feed back to) the patient’s own team.

Learning points 
• Predict the patient at risk and establish the correct level of care from the
outset.
• Ensure early mobilisation – provide good analgesia with regular physiotherapy
input.
• Regular nursing observations and medical review vary – once-daily medical
review is not enough in some cases.
• Use preventative techniques including chest physiotherapy, nebulised saline,
monitored humidified oxygen, adequate analgesia and sputum culture.

Practice point 
The frequency with which early chest problems are encountered cannot be
overemphasised, nor can the importance of examining the chest routinely and
adopting simple preventative measures.

Preventing respiratory deterioration following surgery

• Identify those at risk.

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Care of the Critically Ill Surgical Patient®

• Examine and assess.

• Encourage early mobilisation.
• Provide adequate analgesia.
• Arrange for chest physiotherapy.
• Administer nebulised saline.
• Administer humidified oxygen at a titrated dose.
• Take sputum for culture.
• Reassess regularly.

Practical skill: interpreting chest radiographs

Objectives

At the end of this section, participants should:

n be able to view a system for examining chest radiographs in the critically ill;

n be aware of the complementary information provided by clinical and

radiographic examination.

The chest radiograph is one of the most frequently ordered investigations in the
management of the critically ill. In many cases, abnormal signs will be picked up
earlier on clinical examination as radiographic appearances tend to lag behind
the clinical findings. The chest X-ray (Figure 4.2) offers valuable confirmatory and
complementary diagnostic evidence (or reassurance). The aim here is not to list
exhaustively the clinical scenarios and diagnoses in which it may be of help, but
rather to revise a system for reviewing chest images.

Always use a system for looking at chest X-rays: you may miss pathology if you don't.

The most useful chest view for assessing the heart is a straight, erect posteroanterior
(PA) film, taken at full inspiration. This type of radiograph is more likely to give a true

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indication of heart size than the portable anteroposterior (AP) film, which may suggest
cardiomegaly. Be aware of which type you are looking at and remember to check
name, date and time. Compare with previous films.

Your routine should be:

n note overall shape of the chest and obvious abnormalities

n use a system to assess the CXR fully (Box 4.1).

Box 4.1  Example system for assessment of CXR

• Soft tissues. Look for air (surgical emphysema), foreign bodies or disruption of
contours.
• Bony structures. Use the mnemonic RCS’s (ribs, clavicles, scapulae, sternum).
• Lung markings. Do they extend to the chest wall? Is there pneumothorax or
haemothorax? Trace around the edge to avoid missing a small pneumothorax.
Is the volume of parenchyma increased (chronic obstructive airways disease
(COAD), lots of ribs visible) or reduced (poor respiratory effort, abdominal
distension)?
• Examine the lung fields for opacities.
• Double check the costophrenic angles for fluid (erect film?).
• Is there air beneath the diaphragm (erect film?) or any obvious intra-abdominal
abnormality to investigate specifically, such as distended bowel?
• Note the position of the trachea and heart size. Trace round the mediastinum
and check the location of any tubes or lines. The width of the mediastinum
should be noted but may be unreliable.

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Care of the Critically Ill Surgical Patient®

(a)

(b) Trachea

Superior vena cava

Aortic arch

Left hilium
Right hilium Pulmonary artery
and right branches fan out
main bronchus
Left atrium
Right atrium
Lung peripheries

Cardo-phrenic Left ventricle

angle

Costophrenic angle

Figure 4.2  Chest X-ray (a) and diagrammatic representation of a chest X-ray (b).

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Air bronchogram
A bronchus is not normally visible if surrounded by aerated lung since both are
equally radio-translucent. Anything that causes the normal lung tissue to lose its
aerated property will produce a difference in opacity and the bronchus, provided it still
contains air, will be visible. The presence of an air bronchogram suggests oedema,
infection or other infiltrates in the surrounding lung tissue.

Kerley B lines
These are horizontal lines that meet the pleural surface at right angles. They tend to
be about 1–2 cm long and 1–2 mm thick. They are caused by increased fluid or tissue
within the intralobular septa.

Bronchitis and emphysema

Bronchitis and emphysema can be present even if there are few or no chest X-ray
abnormalities. What may be present is increased lucency of the lung and regional or
general loss of vascularity in the peripheral lung fields. The lung fields are increased in
size.

Pleural effusion
A small effusion may produce only a blunting of the costophrenic angle. A large
effusion will produce evidence of lung compression and is usually associated with
clinically apparent respiratory problems. The mediastinum may be displaced to the
opposite side and the diaphragm flattened on that side. It is important to be aware
that, with an X-ray taken with the patient supine, an effusion may show only as a faint
diffuse opacity spread over the lung field. This is because the fluid is spread thinly
over a wide area.

Repeat the X-ray after the patient has been sitting up for 15 minutes or obtain an
ultrasound scan. An effusion due to a cardiac disorder tends to be bilateral.

Consolidation
Consolidation will not produce a mediastinal shift unless there is significant collapse,
in which case the mediastinum will be drawn over to the side of the lesion.

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Pericardial effusion
There are many reasons for an enlarged cardiac silhouette. The most common
pathological reasons include ventricular hypertrophy, pericardial effusion and
ventricular aneurysm. An effusion may produce an outline that is globular in
appearance, but hypertrophy of the left ventricle can do the same. Left atrial
enlargement can produce a straightening of the left cardiac border. A significant
pericardial effusion is likely to produce evidence of tamponade with poor cardiac
function and raised central venous pressure. If in doubt, echocardiography will
confirm the diagnosis.

Cardiac failure may give rise to a variety of signs including upper lobe blood diversion,
cardiomegaly, pleural effusions, Kerley B lines and parenchymal shadowing (diffuse or
hilar ‘bat’s-wing’ shadowing).

Management of respiratory failure and compromise

The treatment plan for managing respiratory failure follows a stepwise increase/
decrease in support depending on its severity (Figure 4.3).

During initiation of treatment, start at the left of the scale and progress to the right as
determined by your assessment of the patient’s response.

Adjunctive therapies

PEEP and recruitment

Intubation and ventilation

NIV

Mask/tracheal CPAP

Mask oxygen therapy

Increasing severity of respiratory failure

Figure 4.3  Treatment plan for managing respiratory failure.

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 Chapter 4  Respiratory compromise in the surgical patient

Only conventional mask oxygen therapy is possible on the majority of surgical wards.
Fixed-delivery oxygen masks are available up to an inspired oxygen concentration of
60%, ie an FiO2 of 0.6.

All oxygen delivery systems should be humidified. Otherwise the dry, cold gas
may contribute towards thickening of the patient’s secretions and promote sputum
retention. Nebulised 0.9% saline (with bronchodilators if indicated) and regular
treatment from a respiratory physiotherapist may prevent worsening of incipient
respiratory failure if they are used early.

Devices such as high-flow nasal oxygen therapy (Figure 4.4) are becoming available
on the wards although they are not yet in widespread use. They provide higher
flows and concentrations of oxygen than conventional facemasks along with gas
humidification and are often well tolerated by patients.

The response of the patient is assessed according to the improvement of clinical

status, oxygen saturation and ABG analyses. If the patient’s condition does not
improve with increased inspired oxygen concentration up to 60%, then you have a

Figure 4.4  High-flow oxygen device.

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Care of the Critically Ill Surgical Patient®

very unstable patient and further diagnosis and definitive treatment are required. This
will require expert help and the safe transfer of the patient to a higher level of care.

Even if the patient responds to supplemental oxygen therapy and the ABGs improve,
you must remember that oxygen is only one aspect of treatment – you must treat the
underlying cause of the respiratory failure.

Treat the cause of respiratory failure

Supportive and definitive treatments are needed. Use appropriate antibiotics,
physiotherapy, diuretics, bronchodilators and cardiac or other drugs as necessary.
Basal signs may indicate continuing abdominal pathology (eg subphrenic abscess).
Systemic factors influence respiratory function (eg mobility, nutrition) – it is important
to treat these too.

Review the patient’s requirement for and response to analgesia; either too little or too
much can be a factor in preventing adequate clearance of secretions by inhibiting
coughing and by limiting the patient’s tolerance of physiotherapy.

Where sputum clearance is the primary problem, a nasopharyngeal airway may be

considered, or discuss the use of a cough assist machine with the physiotherapists.

Do not assume that confusion or a depressed level of consciousness is due to the

effects of opiate analgesia. Hypoxia may cause an acute confusional state and
hypercarbia may lead to obtundation.

Reassess
Detect failure of improvement or further patient deterioration: persisting or worsening
signs and symptoms of respiratory failure require further immediate management and
transfer to a higher level of care.

Detecting respiratory failure

It is essential to be alert to this situation as it is common, can be rapidly fatal and
requires a prompt change in management.

Failure of mask oxygen therapy at high FiO2 may be indicated by:

n increasing respiratory rate;

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n increasing distress, dyspnoea, exhaustion, sweating and confusion;

n oxygen saturation 80% or less (this may be a late sign);

n PaO2 less than 8 kPa;

n PaCO2 greater than 7 kPa.

Case scenario 4.2 

A 62-year-old woman with chronic bronchitis who underwent right abdominal
nephrectomy 4 days ago is now tachypnoeic and pyrexial. Air entry is reduced
and examination reveals bronchial breathing and dullness to percussion at the
right lung base. Her FiO2 was increased to 0.8 in order to maintain SaO2 above
97%. The physiotherapist obtained a sample of yellow sputum for culture and
antibiotics were prescribed for hospital-acquired pneumonia. A CXR showed
typical localised changes at the right base. It is now 7pm and the HDU nurse
has called you because the patient is again tachypnoeic and hypoxic despite the
therapy above. The patient’s chest signs are unchanged but she is noticeably
sweaty and starting to look tired. She is not in pain and, on detailed review, there
does not seem to be anything else you can do to improve matters. Recent blood
gases show that the PaCO2 has risen from 4 kPa to 7.3 kPa over the last 10 hours.
The HDU nurse is experienced and worried that the patient might suddenly tire
and arrest. You accept her advice and ask for an urgent ICU review. The ICU
consultant is pleased that you called at this stage. The patient is hypercarbic and
it is decided to take her to ICU for intubation and ventilation.

Learning points 
• Use your routine ward rounds to monitor progress systematically but reassess
and hand over patients who are not right at the end of the routine day.
• Detect patients who are failing to respond or deteriorating despite reasonable
therapy and refer promptly.
• Clinical signs (eg tiredness and sweating) are also important in detecting the
patient at risk of respiratory failure and arrest.

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The clinical signs and blood gas analysis are the most important factors. Tachypnoeic
patients suddenly tire and arrest. You must intervene before this stage by acting on
early symptoms and signs, particularly tachypnoea. Transfer the patient to a higher
level of care for further therapy to improve gas exchange. An arterial line will probably
be inserted if frequent blood gas analysis is to be performed. Anticipate problems in
patients with severe chronic lung disease (eg vital capacity less than 15 ml/kg or FEV1
less than 10 ml/kg) and monitor them closely.

Continuous positive airway pressure

If the primary problem is type 1 respiratory failure, CPAP may help.

A high-flow source of oxygen-enriched air is supplied through a tight-fitting facemask

with a range of expiratory valves (Figure 4.5). These valves maintain a set airway
pressure, which can range from 2.5 to 10 cmH2O. During ventilation, airway pressure
cannot drop below the pressure indicated on the valve. This leads to recruitment of
underventilated alveolae, increases FRC, decreases intrapulmonary shunt and the
work of breathing and may improve oxygenation.

The masks vary from full face to nasal and may cause nasal pressure sores. If air
swallowing occurs, it may result in gastric dilatation and regurgitation. Some patients
are unable to tolerate a full-face mask but may tolerate a nasal mask. They must

Figure 4.5  Diagrammatic representation of patient receiving CPAP therapy.

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keep their mouth closed to prevent loss of pressure. Hood devices are also available;
these are noisy and can be claustrophobic to wear, but do not require any patient
coordination. After some forms of surgery, eg upper GI surgery, there may be some
concerns regarding the effect of CPAP on any high anastomosis.

The CPAP device may also be connected directly via a T-piece to a pre-existing
tracheostomy tube. The patient must have a reasonable respiratory rate and tidal
volume, be in control of his or her own airway and able to cooperate. Patients who fail
to tolerate CPAP are recognised by refractory hypoxaemia, increasing respiratory rate
and progressively smaller tidal volumes with subsequent CO2 retention. More obvious
clinical signs include intolerance of the CPAP device and agitation or, conversely,
obtundation.

Patient selection is key to the success of CPAP. Frequent monitoring of the patient is
required, including regular ABGs, within an HDU environment. A plan should be made
of how frequently CPAP is to be given, and for what length of time. Generally, to be
beneficial, a minimum of 2 hours of continuous CPAP is required. CPAP may also be
used as part of the weaning process from formal ventilation or, alternatively, used after
major surgery to reduce the risk of respiratory complications, eg following aneurysm
surgery.

Non-invasive ventilation by mask

If type 2 respiratory failure (CO2 retention) develops, NIV support by mask should
be considered. Essentially, two different pressures are applied to the patient via a
facemask – a higher one during inspiration (around 20 cmH2O) and a lower one in
expiration (5 cmH2O). This may be termed bilevel positive airway pressure mask
ventilation (BIPAP). The pressure difference generates gas flow into the lungs during
inspiration.

The BIPAP machine detects the initial drop in airway pressure that occurs during
inspiration. It then automatically raises the pressure to that set on the machine for
inspiration and then changes back to the lower level on expiration. The tidal volume
delivered is determined by the lung compliance, duration of inspiration and the driving
pressure. This method of respiratory support may pre-empt the need for intubation
and ventilation but requires critical care support. It is not effective in all patients and,
as with CPAP, careful selection of patients is required. It is not appropriate for patients
who are cardiovascularly unstable or those with a decreased level of consciousness,

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severe metabolic acidosis or a poor respiratory rate. Patients must be in control of

their own airway and able to cooperate and a nasogastric tube is usually required to
reduce gastric distension. Patients who fail to tolerate mask ventilation are recognised
by refractory hypoxaemia, increasing respiratory rate and progressively smaller tidal
volumes with worsening CO2 retention. In general terms, if the patient’s CO2 has not
improved within 30 minutes, mask ventilation is unlikely to succeed. NIV can be used
post extubation in patients in whom the risk of reintubation is thought to be high.

Ventilation
Intubation and ventilation allows administration of oxygen at concentrations of up to
100% and enables the volume of each breath (tidal volume, VT ) and respiratory rate or
frequency (f ) to be adjusted to suit the patient’s needs. The minute volume (MV = VT × f )
may be varied by altering the frequency or tidal volume. The greater the MV, the
greater the removal of carbon dioxide, but if the tidal volume is too high lung damage
may result. Use of a low tidal volume approach improves outcome for ICU patients.
Target VT should be 6 ml per kilogram of predicted body weight. Controlling VT may
improve outcome in patients undergoing intrabdominal procedures. Use of sedatives,
paralytic agents and permissive hypercapnia may enable these targets to be
achieved.

High-flow nasal oxygen

High flow nasal oxygen can deliver up to 100% O2 with high flows and high
humidity. This benefits patients with a high sputum load or those who cannot
clear secretions. As the flow is so high, a pressure equivalent to CPAP 5 cmH2O
is delivered to the patient, and can help improve the work of breathing. High-
flow nasal oxygen is generally well tolerated by patients and, importantly, allows
communication and oral nutrition without interruption. However, as with all these
methods of respiratory support it is important to ensure that treatment is targeted
at the cause of hypoxaemia, and that the patient’s response is observed carefully.
Unless patients improve rapidly, intubation may be required. The main use of
high-flow nasal oxygen in the surgical patient is in treatment of type 1 respiratory
failure.

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A form of synchronised intermittent mandatory ventilation (SIMV) is used to try and

preserve some of the patient’s respiratory muscle activity by synchronising ventilation
around the patient’s own respiratory effort. ‘Controlled mandatory ventilation’ requires
the patient to be fully sedated to tolerate the presence of the tracheal tube and the
compulsory positive-pressure breaths from the ventilator. This mode of ventilation
allows the patient to play no part in breathing and is rarely used.

Ventilators are increasingly sophisticated and offer different forms of ventilation,

which may be used in combination (Figure 4.6). With modern modes of ventilation,
such as combining SIMV with pressure-controlled ventilation (PCV), pressure support
ventilation (PSV) and positive end-expiratory pressure (PEEP), there is much less need
for heavy sedation and paralysis.

PSV, alongside PEEP, may be used once the patient has achieved a good respiratory
rate and pattern. Generally, paralysis is necessary only in the most difficult to ventilate
patients, and then only for short periods until control is achieved.

With PEEP, pressure is administered during expiration to prevent airway collapse

and recruit underventilated alveoli (just like CPAP). Normally 5 cmH2O PEEP is used;
however, in very hypoxic patients high PEEP can improve oxygenation rapidly by
recruiting alveoli. Once oxygenation is improved, PEEP pressure should generally
be brought down. Lung compliance, tidal volume and how fast the tidal volume is
‘pushed’ into the patient determine the pressure reached within the airways at the end
of each breath from the ventilator.

Escalation of respiratory PCIRV and

support via a ventilator high PEEP
PCV and
moderate PEEP

PSV and PEEP 5

CPAP or PEEP
only via ventilator
T-piece or TC

Increasing severity of respiratory failure

Figure 4.6  There are numerous modes of ventilatory support. A balance needs to be reached
between adequate gas exchange and prevention of complications associated with artificial
ventilation.

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A high peak airway pressure can have adverse consequences. The intrathoracic
pressure is always positive on inspiration during ventilation. This causes decreased
venous return and a fall in cardiac output, which may be very severe if the
patient is hypovolaemic. PEEP can exacerbate this problem. High values of peak
airway pressure and PEEP predispose to barotrauma, which can result in tension
pneumothorax.

High pressures plus high oxygen concentrations may also promote the toxic effects
of oxygen; consequently, concentrations of oxygen greater than 80% are rarely used,
and then only for the shortest time possible.

The process of volutrauma promotes alveolar and vascular damage, resulting in

fluid leak and worsening of lung compliance. This, in turn, predisposes to even
higher airway pressures. Pressure control modes of ventilation allow a breath to be
administered to a set pressure, kept below 26 cmH2O; the tidal volume then depends
on the patient’s lung compliance. By preventing high peak pressures, the risk of
barotrauma is reduced. With pressure support, the ventilator senses that the patient
has taken an inspiration and administers pressure to provide a higher tidal volume.
The aim is not to achieve a normal ABG but to provide adequate ventilation without
causing barotrauma. Usual tidal volume is 10–12 ml/kg, but much lower volumes
(6 ml/kg predicted body weight) are used during mechanical ventilation. This leads
to a higher PaCO2, termed permissive hypercapnia. The CO2 is allowed to rise as
long as the pH is above 7.2. This reduces ‘ventilator-induced lung injury’ and is
associated with improved survival (termed ‘lung-protective ventilatory strategy’). If
lung compliance is very poor, the CO2 may rise too high.

Lung recruitment strategies such as PEEP must be combined with regular

physiotherapy, suction and turning the patient to prevent alveolar collapse. CXR,
ultrasonography or fibre-optic bronchoscopy should be used to identify any lung
collapse amenable to bronchoscopic reinflation, pleural effusions or undiagnosed
pneumothoraces.

Normally, the ventilator is set to provide less time for inspiration than for expiration. If
the lungs are very poorly compliant and ‘stiff’, the inspiratory time may be increased
to be equal to or even longer than the expiratory time. This process is known as
adjusting the inspiratory to expiratory (I/E) ratio. The I/E ratio may thus be normal
(1:2 or 1:3), equal (1:1) or inverse (2:1). Applying a limited pressure for a prolonged
period of time aims to improve gas exchange by opening the poorly compliant alveoli,

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holding them open for as long as possible to maximise gas exchange at pressures
that will not cause barotrauma or volutrauma or decrease cardiac output.

A patient receiving pressure-controlled inverse ratio ventilation (PCIRV), a high FiO2

of > 0.8, PEEP > 10 cm H2O and with permissive hypercarbia who fails to achieve
oxygen saturation of greater than 85% is at high risk of death. Death will occur
from multiple organ failure as tissue oxygen delivery fails to meet demand. At this
point, the use of an FiO2 of 1.0 is justified and other adjuncts to ventilation can be
considered. The most commonly used is to turn the patient from the supine to prone
position. Redistribution of blood flow to the less consolidated or collapsed, more
easily ventilated, anterior portions of the lung may result in improved oxygenation
and outcome. Finally, extracorporal life support with veno-venous cardiopulmonary
bypass could be considered although this is available in only a few centres.

Survival depends on treating the underlying cause of respiratory failure, but all these
techniques allow time for interventions such as antibiotics and pleural drainage to
work.

Weaning from ventilatory support

Whatever the method of mechanical ventilatory support used, if treatment of the
underlying cause of respiratory failure has been successful, then the patient must
be ‘weaned’ from the ventilator (ie returned to spontaneous respiration in a safe,
controlled manner). As soon as patients are able to participate in ventilation, they
should be encouraged to do so as prolonged ventilation will lead to atrophy of the
respiratory muscles. Various modes of ventilation can be used to allow a gradual
reduction in the amount of work performed by the ventilator and an increase in the
respiratory effort of the patient.

In general, it is unwise to attempt weaning until:

n The original cause of respiratory failure has been treated successfully.

n Sedative drugs have been reduced to a level at which they will not depress
respiration. Daily sedation holds alongside spontaneous breathing trials have been
shown to improve survival.

n A low inspired oxygen concentration (40%) maintains a normal PaO2.

n CO2 elimination is no longer a problem.

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n Sputum production is minimal.

n Nutritional status, minerals, trace elements are normal.

n Neuromuscular function of the diaphragm and intercostals is adequate.

n The patient is reasonably cooperative.

However, not all of these goals may be achievable, and baseline function must
be considered. The most commonly used ‘step-down’ ventilation modes are
SIMV, assisted spontaneous breathing (ASB) and PSV, again often in combination.
Alternatively, a simple T-piece, requiring the patient to do all the work of breathing,
may be used for periods of time, with mechanical ventilation being resumed when
the patient shows objective signs of diminished respiratory effort. The ventilator
can be set to simply compensate for the presence of the tube (tube compensation).
The periods of time spent breathing spontaneously are increased until extubation is
possible. In the majority of critical care units, a combined approach is used with
PCV → SIMV → ASB/PSV → CPAP and T-piece followed by extubation. Patients may
fail to tolerate extubation as a result of poor airway control, laryngeal oedema, poor
cough, sputum retention or simple fatigue. If patients require reintubation or have a
decreased consciousness level (eg after head injury) then a tracheostomy may be
used as part of the weaning process.

Discharge from ICU

The period following ICU discharge is critical. When transfer occurs to a general
ward without a period in HDU, the patient has to adapt to reduced levels of nursing
care, physiotherapy and monitoring. A discharge summary and suggested treatment
plan will usually accompany patients as they leave ICU, but it is important that this is
understood by the ward staff and is implemented immediately. This does not happen
automatically. This period of care exemplifies the importance of good personal
communication and organisation – communication between ICU and surgical staff,
and between surgical and ward staff, of clear written instructions and repeated
assessment of the patient. Apart from clinical reassessment, ensure that medications
have been changed to ward format and started, arrange out-of-hours physiotherapy
as needed, check the oxygen concentration needed and ensure that any monitoring
(such as pulse oximetry) is available on the ward. ITU follow-up by critical care
outreach teams should improve communication, and allow monitoring by critical care.

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Speak to the on-call team and ask for formal review of the patient. If the patient does
deteriorate, contact critical care staff at an early stage; usually, attention to the details
of care and ensuring they actually happen will prevent this.

Common surgical respiratory problems

Atelectasis
Atelectasis is defined as an absence of gas from all or part of the lung. It is commonly
seen in surgical patients, particularly following abdominal and thoracic procedures.
Reduced lung expansion from pain and splinting leads to retention of secretions and
distal airway collapse. This is exacerbated in the elderly, the overweight, smokers and
those with pre-existing lung disease.

It should be anticipated in these patient groups and prevented by preoperative

breathing exercises to improve expansion, intraoperative care with humidification,
ensuring good tidal volumes and avoiding unnecessarily high FiO2. If unrecognised, it
can rapidly deteriorate to respiratory failure.

The symptoms of atelectasis are cough, chest pain or breathing difficulty, low oxygen
saturations, pleural effusion (transudate) and cyanosis (late sign) or tachycardia.
Diagnosis is by CXR. Generally, the white cell count (WCC) and C-reactive protein
(CRP) levels remain in the normal range, though they may be increased if there is
superimposed pneumonia. The mainstay of treatment is physiotherapy, focusing
on deep breathing, encouraging coughing, and effective analgesia. An incentive
spirometer is often used as part of the breathing exercises. Mobilisation should also
be encouraged to improve lung inflation. There may be benefit in early use of high-
flow nasal oxygen therapy if available.

Pneumonia
Pneumonia causes parenchymal or alveolar inflammation and abnormal filling of the
alveoli with fluid (consolidation and exudation). In surgical patients, pneumonia is
usually bacterial or chemical secondary to aspiration. Large-volume aspiration leading
to pneumonia is associated with a high mortality rate but can be prevented in patients
with gastric dilatation or vomiting by insertion of a large-bore nasogastric tube.
Symptoms of pneumonia include cough, chest pain, fever and difficulty in breathing.

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Physical examination of the lungs may be normal but often shows decreased
expansion of the chest on the affected side, bronchial breathing or crackles.
Percussion may be dulled over the affected lung. CXR, WCC, CRP and sputum and
blood cultures all help in diagnosis.

Hospital-acquired pneumonia is more likely to be due to resistant bacteria such as

methicillin-resistant Staphylococcus aureus (MRSA), Pseudomonas spp., Enterobacter
spp. and Serratia spp. Ventilator-associated pneumonia is a subset of hospital-
acquired pneumonia and occurs after 48 hours of mechanical ventilation.

Aspiration pneumonia is caused by aspirating oral or gastric contents and can

occur at any time. Material aspirated may contain anaerobic bacteria, leading to a
secondary infective pneumonia. Treatment depends on the clinical classification of
pneumonia and also the known bacterial resistances within each hospital. Antibiotic
guidelines should be consulted, and if unsure microbiological advice should be
sought.

Patients with pneumonia have a high risk of developing respiratory failure and
may trigger ARDS, which results from a combination of infection and inflammatory
response. The lungs quickly fill with fluid and become very stiff. This stiffness,
combined with severe difficulties extracting oxygen due to the alveolar fluid, creates a
requirement for mechanical ventilation.

The CURB 65 score, developed for assessment of community-acquired pneumonia,

is frequently used when looking at severity of pneumonia: Confusion; Urea
> 7 mmol/L; Respiratory rate > 30 per minute; Blood pressure (SBP < 90 mmHg or DBP
< 60 mmHg); age > 65 years. Although not designed for surgical patients and patients
with hospital-acquired pneumonia, it can be a useful tool in flagging up the severity of
the condition and likely need for additional critical care support.

Pulmonary embolism
PE comprises embolic obstruction of a vascular branch beyond the right ventricular
outflow tract, usually from an associated deep vein thrombosis (DVT). PEs are still
relatively common in surgical practice, though thromboprophylactic measures reduce
the risk substantially.

Common symptoms include dyspnoea, pleuritic chest pain, cough, haemoptysis and
palpitations, while signs include hypoxia, tachypnoea and tachycardia. Diagnosis

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Figure 4.7  CT pulmonary angiogram showing a saddle embolus and substantial thrombus burden
in the lobar branches of both main pulmonary arteries.

is based on these clinical findings in combination with laboratory tests and imaging
studies. CT pulmonary angiography is commonly used to make the diagnosis
(Figure 4.7).

CXR may be helpful in excluding other causes of deterioration. ABG analysis may
show hypoxia and hypocarbia. The most common ECG change, apart from sinus
tachycardia, is T-wave inversion in the anterior leads and echocardiography may be
very useful in the unstable patient to look for right heart dysfunction.

Treatment
In most cases, anticoagulant therapy is the mainstay of treatment. Usually, low-
molecular-weight heparin (LMWH) is administered initially, prior to administration
of warfarin or other novel oral anticoagulants (NOACs). In the perioperative patient,
treatment is complicated by the risk of bleeding. If the risk of bleeding is moderate,

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unfractionated heparin by infusion may be used with close monitoring of the activated
partial thromboplastin time (APTT).

If there is a concern regarding bleeding, stopping heparin will result in reversal of

its effect within 3 hours. Alternatively, it can be reversed with protamine if a more
immediate effect is required. The effect of LMWH cannot be fully reversed.

On some occasions it may still be appropriate, in a very high-risk patient, to insert an

inferior vena caval filter.

Decisions regarding anticoagulation for PE and DVT in perioperative patients can

be complex and should involve discussion with the responsible surgeon and the
haematology and critical care departments as required.

Practical skill: chest drains

Chest drains are inserted either for pneumothorax or for drainage of pleural fluid.
There are two main types of drain in common use. Seldinger-type chest drains are
mostly used for drainage of pleural effusions and small pneumothoraces, while more
traditional drains are inserted for larger pneumothoraces (Figure 4.8). The size of the
chest drain used depends on the indication: a large-bore tube (28–30F) should be
used for haemothorax, large and/or tension pneumothorax and a smaller calibre tube
(10–14F) for pleural effusions. Maintenance of patency of chest drains is important for

Figure 4.8  Chest X-ray showing chest drain in area of partially resolved right-sided pneumothorax.

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 Chapter 4  Respiratory compromise in the surgical patient

safety; frequently, larger tubes are inserted if there is any doubt. However, larger chest
drains are associated with increased pain.

The technique of chest drain insertion is not taught on the CCrISP course, however,
surgical trainees should be able to state the indications, methods and complications
associated with chest drainage.

All chest drains should be monitored for swinging, draining and bubbling and should
have an underwater seal. Chest drains should be removed as soon as they are
no longer required, ie a pleural effusion drained to dryness (remember that about
100–150 ml of pleural fluid is normally produced per day) or the pneumothorax is
fully inflated. Caution must be used when patients are ventilated (including CPAP
and NIV) as recurrence of pneumothorax is common and these may well be tension
pneumothoraces. If a patient has a pneumothorax, generally any central line required
should be put in that side to prevent the occurrence of bilateral pneumothorax.

Summary
n Assess respiratory function in all ward patients who have undergone major surgery
and use simple measures to prevent major respiratory compromise.

n Routine assessment is predominantly clinical and aims to identify the patient who
is deteriorating.

n Use the CCrISP system of assessment to identify those patients with respiratory
failure.

n Instigate the level of treatment appropriate to the severity of failure.

n Treat the cause of the failure as well as hypoxia/hypercarbia.

n Reassess clinical signs, oximetry and, most importantly, ABGs.

n Arrange transfer to higher level of care for those who do not respond.

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 5

Arterial blood gases and

acid–base balance

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 Chapter 5  Arterial blood gases and acid–base balance

Learning outcomes 
This chapter will help you to:

n describe the rationale for blood gas analysis;

n evaluate blood gas analysis in the surgical patient;

n describe how to manage acid–base disturbance using the CCrISP system of

assessment.

Introduction
Blood gas measurements are very useful in the assessment and management of
critically ill surgical patients and are probably underused in routine practice. Arterial
blood gases (ABGs) can provide a guide to acid–base status, ventilation and
global tissue perfusion, as well as showing how well compensatory mechanisms
are working. Acid–base status affects blood pH, ventilation (through the partial
pressures of oxygen and carbon dioxide) and tissue perfusion through base excess/
base deficit and lactate level. Examining the trends in these values in the critically ill
allows clinicians to analyse the severity of patient deterioration and the effectiveness
of management plans. Abnormalities in ABGs may arise before a patient becomes
obviously unwell and provide clinicians with the opportunity for early intervention: the
importance of this in the assessment of the severity of sepsis is reinforced in Chapter
12. Blood gas analysers give rapid results and also provide considerable useful
additional information, eg lactate, Hb, K+, Na+, Ca2+ and glucose levels. A venous
sample may be taken either initially, when taking blood for other tests, or if an arterial
sample cannot be obtained, but the results need to be interpreted with caution. A
normal venous lactate may be reassuring but an elevated value may or may not
indicate significant physiological disturbance and an arterial sample should then be
obtained. It is important to ensure that venous blood is not taken from an arm where
an IV infusion is running as this may lead to erroneous results.

ABG samples are obtained either by arterial puncture (usually the radial artery) or from
an arterial line (a-line; see Chapter 8). The complication rates of such a procedure
are low but include bleeding and haematoma formation (particularly in coagulopathic
patients), distal ischaemia and pseudo-aneurysm formation (the last usually as a
consequence of infected in-dwelling catheters).

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The arterial partial pressure of oxygen (PaO2) is a reflection of the amount of oxygen
dissolved in the blood. Its relationship with the oxygen saturation of haemoglobin
(SaO2) is affected by factors such as temperature, partial pressure of carbon dioxide
(PaCO2) and pH, which is reflected by the oxygen dissociation curve (Figure 5.1). The
PaO2 can be used as an indicator of the pressure gradient that has the potential to
drive oxygen into the tissues. A normal (or supranormal) value does not necessarily
ensure effective oxygen utilisation by the tissue but it does reflect adequate
management of oxygen delivery by the respiratory and cardiovascular systems.

Regardless of what other ABG values show, hypoxia should be treated with oxygen
therapy. A small group of patients with severe COPD rely on hypoxaemia to drive their
ventilation, and high inspired oxygen concentrations (FiO2) may suppress ventilation
and cause hypercapnia. However, in the acute phase of critical illness, oxygenation is
imperative and patients should not be denied oxygen for fear of loss of their
respiratory drive. Clinical progress and serial ABG measurement can assist in the
management of these patients; trainees should always seek appropriate advice and
help if unsure about the potential for causing hypercapnia.

Practice point 
While hypercapnia can kill slowly, hypoxaemia will kill quickly. When
interpreting the PaO2, any ventilatory support used and the FiO2 should be noted
and clinicians should be aware of relative hypoxaemia, ie an absolute PaO2 may
be within ‘normal limits’ (10–14 kPa) but the amount of supplementary oxygen
and ventilatory support may be high. A more effective means of assessing for
relative hypoxaemia is the PaO2/FiO2 ratio, with a ratio of < 40 kPa deemed
hypoxic. Remember that, as the FiO2 increases towards 1.0 (100% oxygen),
the PaO2 should increase. An oxygen saturation of 100% and PaO2 of 13 kPa
indicates good oxygenation for an individual breathing air (FiO2 0.21, PaO2/FiO2
ratio 61.9 kPa) but not necessarily for a patient on supplemental oxygen (ratio 13
if the inspired oxygen is 100%). Note also that pulse oximetry does not measure
CO2 so reflects effective oxygenation rather than effective ventilation. ABGs
provide a better overall picture of the ventilatory process (see below).

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 Chapter 5  Arterial blood gases and acid–base balance

100
90
80
70
SaO2 (%) 60
50
40
30
20
10
0
0 1 2 3 4 5 6 7 8 9 10 11 12 13
PaO2 (kPa)

Figure 5.1  The oxygen dissociation curve.

Metabolic activity in body tissue produces energy (heat), carbon dioxide and acid,
which reduces the affinity of oxygen for haemoglobin; thus, for a given PaO2, oxygen
is less tightly bound to haemoglobin enhancing its off-loading into cells. As this
occurs, 2,3-diphosphoglycerate (2,3-DPG) present in red blood cells further loosens
the bonds between haemoglobin and oxygen. The reverse is the case in the lungs,
resulting in increased binding between haemoglobin and oxygen.

Interpreting arterial blood gas values

A simple sequential approach to interpreting ABGs can allow you to detect
abnormalities, basic pathophysiological processes (metabolic versus respiratory)
and compensatory mechanisms of any acid–base disturbance. Approximate normal
ranges for ABG components are outlined overleaf.

Acid–base balance
The concentration of hydrogen ions within the body is normally tightly controlled at
40 nmol/L, which is 7.42 pH units (pH = –log10[H+]).

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Normal ranges for ABG components

pH. Normal range 7.35–7.45. Shows whether a pathophysiological process has
resulted in acidaemia or alkalaemia.

PaCO2. Normal range 4.5–6.0 kPa. This provides information about the absolute
ventilatory state of a patient and possible respiratory compensatory mechanisms.

HCO3–. Normal range 24–28 mmol/L. Bicarbonate is the main plasma buffer;

a low value suggests consumption, often due to increased acid load (usually
lactic acid in surgical patients), and a high value suggests retention of base to
compensate for hypoventilation causing an acidaemia (see below).

Base deficit/base excess. Normal range +2 to –2 mmol/L. This describes

whether the body’s buffers are being consumed (deficit) or retained (excess).

PaO2. Normal range 10–14 kPa. Outlines the level of oxygenation (taking into
account the FiO2).

Serum lactate. Normal range < 1.2 mmol/L. This is primarily a reflection of the

extent of anaerobic metabolism occurring within the body and secondarily a
reflection of the liver’s ability to metabolise lactate and regenerate bicarbonate
anions.

Anion gap. Normal range 10–15 mmol/L. Plasma exists in electrochemical

neutrality, ie the numbers of cations and anions balance; however, the majority
of laboratory assays measure approximately 95% of cations and 85% of anions,
creating a differential described as the anion gap or AG.

AG = ([Na+] + [K+]) – ([Cl–] + [HCO–])

The majority of ‘unmeasured anions’ are plasma proteins but also small
concentrations of phosphate, sulphate and organic acids. An acidaemia with
an increase in the anion gap indicates an increase in the concentration of these
unmeasured anions (eg lactate and ketones). An acidaemia with a normal anion
gap equates to the total concentration of measured anions being unchanged
usually as a consequence of hyperchloraemic acidaemia. This is most frequently
seen following vigorous resuscitation with 0.9% saline but is also associated with
bladder surgery and ileal conduit formation.

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Over 1000 mmol of hydrogen ion is produced per day, primarily as a result of the
production of carbon dioxide. This is excreted by the lung and is dependent upon
the minute ventilation as controlled by chemoreceptors in the medulla. A smaller
quantity of hydrogen ion is also produced as non-volatile acid products of metabolism
of non-carbohydrate substrate, such as phosphates and sulphates. This amounts to
approximately 1 mmol H+/kg/day and must be excreted by the distal nephron. There
are, therefore, two control mechanisms maintaining hydrogen ion homeostasis –
respiratory and renal.

The respiratory mechanism is a rapid response system that requires normal CNS
function (central pH chemoreceptors) and lung function to allow carbon dioxide to be
transferred from pulmonary venous blood to alveolar gas and excreted in expired gas.
Any dysfunction of the mechanics or control of respiration will cause retention of CO2
and a rise in hydrogen ion concentration ([H+]) (respiratory acidosis) or overexcretion
and a fall in hydrogen ion concentration (respiratory alkalosis).

The renal mechanism is a slower responding system that depends upon the excretion
of hydrogen ions in the urine by the distal nephron. Conditions that impair renal
function and, in particular, distal nephron function (eg obstructive uropathy, circulating
volume depletion) will prevent non-volatile hydrogen ion excretion resulting in a
metabolic acidosis.

The body’s homeostatic mechanisms with regard to the maintenance of acid–base

balance are powerful, and a patient can have a normal pH in the face of marked
physiological disturbance.

The pH scale is a log-based scale, so small changes in pH represent major

physiological disturbances. Proteins are the primary buffer of retained hydrogen ion;
however, because of the importance of the carbon dioxide/bicarbonate system in the
elimination of hydrogen ions, the acid–base status of the body is best reflected by
the measurement of carbon dioxide tension and bicarbonate level in the blood. This
measures both the volatile and non-volatile arms of the system.

(H+) + HCO3– ⇌ H2CO3 → H2O + CO2

Non-volatile Volatile
(Renal) (Respiratory)

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Respiratory acidosis
The retention of carbon dioxide will cause a rise in [H+] by driving the acid–base
equation to the left. The kidney will respond slowly over approximately 48 hours to
compensate by increasing H+ excretion in the distal nephron, thus returning [H+]
towards normal, although complete normality will not be achieved.

Metabolic acidosis
The inability of the kidney to excrete non-volatile hydrogen ion or a sudden increase
in non-volatile acid load (such as in sepsis) will drive the equation to the right and
respiratory function will rapidly respond by increasing minute volume, reducing CO2
and cause [H+] to return towards normal.

Respiratory alkalosis
Respiratory alkalosis results when the minute ventilation is higher than that required to
maintain the PaCO2 appropriate for a [H+] of 40 nmol/L. The PaCO2 is driven down and
the [H+] falls (pH rises). This is usually caused by an increased central respiratory drive
commonly caused by fever, hepatic disease, aspirin toxicity or CNS dysfunction.

Metabolic alkalosis
Metabolic alkalosis occurs when the level of bicarbonate in the blood is increased due
to either abnormal retention or administration of bicarbonate or the loss of non-volatile
acid from the body (gastric outlet obstruction or chronic nasogastric aspiration).
Abnormal retention of bicarbonate can occur in association with chloride depletion
due to loop diuretics and is also seen in chronic hypokalaemia.

Knowing the [H+]/pH, PaCO2 and bicarbonate allows the patient’s acid–base status to
be determined, and thus the type of abnormality and degree of compensation to be
estimated.

The most useful bicarbonate measure is the standardised value, which corrects
the measured bicarbonate to the value that would be present if the PaCO2 was
normal (40 mmHg or 5.4 kPa). The non-volatile acid–base state is also summarised
by the calculated base excess, which gives a value of the difference between the

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 Chapter 5  Arterial blood gases and acid–base balance

standardised bicarbonate and the normal value. This is otherwise considered as the
amount of acid or alkali needed to return blood in vivo to normal pH under standard
conditions.

Management of acid–base disturbance

The first step is to manage the patient in accordance with CCrISP principles and then
investigate the nature of the disturbance using ABG samples and other investigations
relevant to the patient’s history. The importance of determining the underlying primary
disturbance is that it can point you towards definitive treatment of an underlying
problem. While this is achieved, measures may be required for temporary correction
of the pH by other means.

Aetiology of common acid–base disturbances

Metabolic acidosis

n Impaired tissue perfusion – deal with the cause, improve circulation/perfusion.

n Renal failure – deal with the cause; possible treatments include bicarbonate, renal
replacement therapy.

n Hepatic failure – ?suitable for transplant.

Respiratory acidosis

n Head or spinal injury – ventilation.

n Drug overdose – specific antidote (eg naloxone) and/or ventilation if indicated.

n Chest wall deformity or injury – ventilation if indicated, surgery for flail chest/
multiple rib fractures.

n Myopathy or peripheral neuropathy – ventilation if indicated.

n Pulmonary disease – treat the disease, respiratory support and ventilation if

indicated.

n Massive pulmonary embolus – re-establish perfusion of ventilated lung.

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Quick guide to interpreting blood gases

Look at the pH. Is the patient acidotic or alkalotic or is the pH normal?

Then, bearing the pH in mind, look at the PaCO2. If the PaCO2 is high,
there is a respiratory acidosis; if it is low, there is a respiratory alkalosis or a
compensated(ing) metabolic acidosis.

Then look at the standard HCO3. If the HCO3 is low, there is a metabolic acidosis
or a compensated(ing) respiratory alkalosis; if the HCO3 is high, there is a
metabolic alkalosis or a compensated(ing) respiratory acidosis.

The primary abnormality is often indicated by the direction of H+ change. The

nature of the primary abnormality is determined by considering the clinical
context.

Look at the lactate: the higher the lactate, the greater your concern should be.

Look at other variables such as K+, Ca2+ and Hb.

Examples of acid–base disturbance in clinical practice

Case 1 
A 54-year-old man, 14 hours after a laparoscopic hemicolectomy, is receiving
oxygen at 4 L/min via a facemask and using a morphine PCA. His respiratory rate
is 8/min and his ABGs are as follows:

pH 7.24

PaCO2 9.8 kPa

PaO2 15.1 kPa

HCO3– 24.2 mmol/L

Lactate 0.9 mmol/L

BE +0.2 mmol/L

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What is the nature of the blood gas abnormality and how should you
manage the situation?

The patient has an uncompensated respiratory acidosis, most probably caused

by hypoventilation as a result of excess opiate. Oxygenation remains good;
however, in time, the patient will become hypoxaemic without intervention.
Assess using the CCrISP system with early administration of supplemental
oxygen. The diagnosis may be suspected in ‘B’ with the slow respiratory rate and
in the assessment of ‘D’ as there may be pinpoint pupils, or at the point of full
patient assessment when the observation and drug charts are assessed.

Treatment should include removal of his PCA initially. Analgesia should be

ensured by maximising non-opioid analgesia. If the patient has a decreased
consciousness level, naloxone should be given. A 400-µg ampoule should be
diluted to 10 ml with normal saline and then given in 2-ml aliquots. It is important
to remember that giving naloxone rapidly can lead to poor analgesia, and also
that naloxone is a short-acting drug in comparison with morphine, so the patient
may become drowsy again. Ensure that they are monitored regularly.

Case 2 
An 85-year-old man who has undergone a Hartmann’s procedure is shocked and
hypotensive with a respiratory rate of 24/min. His ABGs on air are:

pH 7.29

PaCO2 2.2 kPa

PaO2 10.6 kPa

HCO3– 10.5 mmol/L

BE –18 mmol/L

Hb 55 g/L

Na+ 140 mmol/L

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K+ 6.0 mmol/L

Cl– 111 mmol/L

Ca2+ 1.2 mmol/L

Glucose 7.8 mmol/L

Lactate 12.5 mmol/L

What is the nature of the abnormality and how should you manage
the situation?

This patient has a partially compensated metabolic acidosis and is hypoxic. He is

likely to have either intra-abdominal blood loss or sepsis with increased acid load
secondary to organ hypoperfusion, and this has led to a high serum lactate.

The tachypnoea is a consequence of an attempted compensation for the acidosis

and also the likely consequence of pain, which in turn can cause diaphragmatic
splinting, atelectasis and hypoxia. If ineffectively managed, this will eventually
lead to hypercapnia and a mixed metabolic and respiratory acidosis. This
patient needs aggressive volume resuscitation, blood transfusion and adequate
analgesia. The underlying problem needs to be brought under control. The high
K+ may be secondary to inadequate renal perfusion and should come down with
aggressive fluid resuscitation.

Practice point 
Be aware that blood gases give other vital information, such as Hb level, which
can aid early treatment.

Case 3 
A 48-year-old man presents with Crohn’s disease, an ileostomy and large stoma
losses. He is tachypnoeic and breathing room air. His ABGs are as follows:

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 Chapter 5  Arterial blood gases and acid–base balance

pH 7.25

PaCO2 3.2 kPa

PaO2 17.1 kPa

HCO3– 14.2 mmol/L

BE –9.9 mmol/L

Lactate 1.0 mmol/L

What is the nature of the blood gas abnormality and how should you
manage the situation?

The patient has a metabolic acidosis with attempts at compensation, but these
are not effective enough to prevent a low pH. There is likely to have been large
losses of bicarbonate from the stoma. In addition to CCrISP assessment,
investigation and treatment of the cause, fluid replacement with a crystalloid such
as Hartmann’s solution is appropriate to replace many of the electrolytes being
lost. If the patient’s liver function is normal, the lactate anions can be utilised to
generate bicarbonate, help replace losses and correct the acidosis.

Case 4 
A 78-year-old man presents to surgical admissions with abdominal distension
and pain, nausea, vomiting and diarrhoea. He has received opiate analgesia. An
ABG analysis on air is performed:

pH 7.51

PaCO2 8.0 kPa

PaO2 8.0 kPa

HCO3– 45.5 mmol/L

BE +21 mmol/L

Hb 91 g/L

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Na+ 150 mmol/L

K+ 1.8 mmol/L

Glucose 4.5 mmol/L

Lactate 1.3 mmol/L

What is the nature of the blood gas abnormality?

The patient has a partially compensated metabolic alkalosis; his PaCO2 is further
raised secondary to excessive opiate administration as hypoventilation as a
compensatory mechanism is limited. Important extra information is the presence
of hypokalaemia and hypernatraemia. Fluid resuscitation is necessary, as is
replacement of K+ losses. As the patient’s K+ level is so low, this will most likely
need to take place in a critical care unit via a central venous catheter. Careful
monitoring will be required.

Summary
The interpretation of blood gases is an essential part of caring for surgical patients.

n pH indicates whether there is acidosis or alkalosis.

n Base excess indicates whether acidosis is metabolic (negative base excess) or

respiratory.

n Low PaO2 indicates the presence of hypoxia and should be interpreted with the
FiO2.

n High PaCO2 and acidosis (plus high HCO3– and positive base excess) indicates
respiratory acidosis.

n Further information, such as the concentrations of lactate, Hb, Na+, K+ and

glucose, may be helpful in emergencies.

n Initial management of any acid–base disturbance begins with the CCrISP

algorithm.

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 6

Cardiovascular disorders,
diagnosis and management

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 Chapter 6  Cardiovascular disorders, diagnosis and management

Learning outcomes 
This chapter will help you to:

n assess if a patient’s cardiovascular system is functioning adequately;

n determine if a patient is unwell because of a cardiovascular problem;

n decide where and how the patient should be appropriately treated;

n initiate safe and appropriate management of common cardiac

pathophysiologies;

n involve and communicate effectively with other specialists as required.

This chapter and the next two chapters deal with aspects of cardiovascular disorders,
shock (Chapter 7) and monitoring (Chapter 8) and should be considered together.
This chapter will focus on clinical assessment and the diagnosis and management
of cardiac disorders. This first section will introduce a basic pattern of thinking that
should enable the early detection of an impending or actual cardiovascular problem.
Preventative measures, simple treatments or referral to a specialist unit can then be
initiated appropriately.

Disorders of the cardiovascular system (CVS) are very common in the unwell surgical
patient with pre-existing comorbidities or may appear as a new disorder following
surgery. Despite the presence of an intact airway and adequate ventilation, any
problem causing decreased efficiency of the CVS can result in delivery of oxygen
to the tissues being inadequate for the patient’s metabolic needs. This will initiate
a cascade of adverse events that will lead to the development of organ failure. The
range of pathologies that cause CVS disturbance is broad, and includes inadequate
circulating volume (eg haemorrhage), primary ‘pump’ problems (eg myocardial
ischaemia or arrhythmias) and increased or reduced afterload (eg sepsis). Detecting
problems before the development of overt organ failures can be difficult: early signs
may be subtle and gradual, i.e. slightly deranged pulse rate and blood pressure. Early
recognition of an impending problem and initiation of treatment will increase your
patient’s chances of survival and help to prevent further complications. Prediction
and prevention are vital, hence the role of National Early Warning Scores (NEWS) as

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a means of detecting these derangements and prompting a trigger for medical review
and/or planning of subsequent patient care.

The approach to the examination of the CVS must be systematic, accurately

documented and repeated frequently. The effect of any intervention, such as fluid
administration, must be reassessed to ensure its efficacy and durability. It is also vital
to consider a patient’s concurrent cardiac medications and other organ pathologies as
managing these can be complex in the perioperative period. It is important to decide
what medications to continue and the route of administration should the patient be nil
by mouth following surgery.

Patient assessment and management

Immediate assessment and resuscitation

Establish that the patient does not need immediate cardiopulmonary resuscitation
by making your immediate ‘ABCDE’ assessment, then progress using the CCrISP
algorithm. Keep an open mind and do not try and make the findings fit any
preconceived diagnosis, whilst giving immediate and appropriate resuscitation
during the assessment. Potential causes of cardiac disturbance are numerous and
include hypovolaemia due to haemorrhage or unreplaced fluid losses, sepsis, cardiac
dysfunction or PE. Jumping to conclusions can be catastrophic for the patient as the
treatments required vary considerably between these conditions.

The presence of dyspnoea increases the likelihood of a cardiac and/or respiratory

problem. Respiratory and cardiovascular function are inextricably linked; a disorder
of the respiratory system (eg tension pneumothorax) may produce CVS signs and,
similarly, a CVS disorder (eg left ventricular failure) may produce respiratory signs.
All other organ systems are dependent on the effectiveness of the circulation. This
is particularly true of the renal and the central nervous systems, and the integrity
of these end organs can give valuable information about the function of the CVS.
If the patient is obtunded or too confused to respond coherently, then cerebral
hypoperfusion or hypoxia is likely and prompt action will be needed.

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 Chapter 6  Cardiovascular disorders, diagnosis and management

Life-threatening CVS disorders are recognisable if you examine the patient

appropriately:

n Look for pallor, signs of poor peripheral perfusion, underfilled or overfilled central
veins, obvious blood loss from wounds, drains or stomas, swelling of soft tissues
or other evidence of concealed haemorrhage into the chest, abdomen or pelvis.

n Listen to the patient: confusion might be due to poor cerebral perfusion; if the
patient complains of feeling faint on sitting up or is thirsty, consider hypovolaemia.
A complaint of breathlessness on lying flat may point to pulmonary oedema.
Complaints of chest pain and feeling feverish or cold are all helpful in indicating
potentially serious underlying pathology and should not be ignored. New-onset
pain in the operated cavity may suggest a surgical complication that may need
investigation. Listen to the chest and heart and compare what you hear now with
what has been recorded previously.

Practice point 
Listen to the heart – are there normal heart sounds or a gallop rhythm? Is there a
new murmur?

n Feel for carotid and femoral pulses if peripheral radial pulses are not present.
Assess rate, quality (weak/thready/strong), regularity and equality. Examine the
patient for swelling, distension or painful areas that may indicate internal bleeding
or ischaemia.

n Feel for changes in skin temperature and always assess capillary refill time.

Practice point 
Unwell surgical patients will benefit from 15 L/min oxygen and consideration of a
fluid challenge whilst you are performing your assessment.

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Full patient assessment

Chart review
The notes and charts contain a lot of data; a systematic approach minimises the
chance of missing important facts. It can be useful to complete your note and chart
review before speaking in detail to the ward nurses and doctors. This provides you
with a factual base for discussing the patient in more detail. The notes will provide
basic clinical information on the patient’s premorbid status, comorbidities and any
procedures performed. On the charts, look at both the absolute values and the trends.
Absolute values need to be considered, but trends and, if possible, a comparison
with the patient’s known observations when well, eg in preassessment clinic, are
also important. The charts should indicate the progress of the patient and important
parameters include:

n respiratory rate, administered oxygen and measured saturation

n heart rate and rhythm

n blood pressure – systolic/diastolic

n CVP (if measured)

n temperature

n urinary output

n IV lines – position and date of insertion

n fluid therapy – prescribed versus given

n drainage of all types.

Review drug chart for drugs with cardiovascular effects (are they being given or
omitted) and the most recent blood results including near-patient testing.

Respiratory rate

This is the most sensitive marker of the ‘ill’ patient and often the first parameter
to change as the patient deteriorates. Accurate observation and recording is
essential. Low rates may be due to opiate/sedative overdose or other causes of CNS
depression, including low cardiac output states, whereas a high respiratory rate is an

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early sign of many kinds of shock, as well as respiratory disease or cardiac failure. An
increased respiratory rate may also be found as part of the response to hypoxia and/
or metabolic acidosis. If a full patient assessment fails to reveal an obvious cause of
a high respiratory rate, check the blood gases to establish if acidosis is a contributory
factor.

Heart rate and rhythm

n Heart rates rise as the body attempts to maintain cardiac output and delivery
of oxygen to the tissues. This is supply attempting to match demand. Not all
patients will be able to mount a response to an increasing demand, eg if they
are on β-blockers or are in receipt of mechanical pacing. The cause may also be
autonomically driven; pain, anxiety and pyrexia can all increase heart rate. How
a patient responds to a circulatory insult depends on his or her cardiovascular
reserve and reactivity. Patients with little reserve will show obvious signs of
dysfunction in response to a relatively small insult whilst fitter patients will tolerate
a larger insult for longer but will eventually collapse dramatically. These patients
will show signs of cardiovascular stress if carefully assessed, eg prolonged
capillary refill time. It is important to understand this interpatient variability to
successfully manage an unstable patient.

n Tachycardia along with increased respiratory rate and altered mental state can
be an early sign of shock, and acute dysrhythmia can be an important sign of
biochemical derangement, sepsis or myocardial failure/ischaemia. The rhythm
may also change as the heart attempts to maintain supply. This can indicate
myocardial ischaemia or biochemical abnormalities that should be investigated
further. Myocardial perfusion occurs in ventricular diastole and tachycardia or
tachyarrhythmia may precipitate an ischaemic cardiac event that may not be
symptomatic.

Blood pressure

Changes in both systolic and diastolic pressure are often late signs but, when present,
should flag up the severity of the underlying problem. It is more useful to think of
organ perfusion rather than blood pressure: a high or normal blood pressure with
poor perfusion is of little benefit to the patient. Look at the blood pressure and the
urine output together. Is there a blood pressure that is associated with a better urine

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output? Urine output responds less quickly than capillary refill time when cardiac
output is improved.

In the elderly, hypertensive patient who usually has a blood pressure of

180/100 mmHg, a pressure of 110/70 mmHg represents significant hypotension and
potentially impaired organ perfusion.

Learning point 
• Clinical signs may be unreliable; normal values do not exclude significant
abnormality. Abnormal values should be assessed and acted upon.

Jugular venous pressure/central venous pressure

It is unusual for CVP to be monitored in a ward environment, and a more practical

and clinically useful assessment of filling can be made by measuring the capillary refill
time. Capillary refill time is the time in seconds it takes for perfusion to return and is
measured by pressing on a distal nail bed or over the sternum for 5 seconds until
blanching occur.

Jugular venous distension is measured with the patient inclined at 45° and will give a
clinical indication of the CVP. Collapsed neck veins with the patient at 45° indicates
a likely low CVP. An internal jugular vein that is not visible with the patient lying flat is
always abnormal.

The response to a fluid bolus is a better guide to fluid status than absolute values. A
change in capillary refill time is a very valuable tool in assessing on-going fluid status
and response to a fluid challenge.

Formal CVP monitoring may be needed to manage patients where further fluid
management is becoming problematic eg the patient whose blood pressure is not
responding to several fluid challenges and who is not bleeding. However, if you are
considering the need for a CVP line you should probably be asking for expert advice
and assistance from critical care.

Abnormalities relating to capillary refill time are detailed in Box 6.1.

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Box 6.1  Abnormalities of capillary refill time and central venous

pressure
• A prolonged capillary refill time may be:
– due to inadequate fluid therapy
– an indication of continued bleeding
– due to vasodilatation in response to sepsis
– associated with a low cardiac output state, eg cardiogenic shock.
A prolonged capillary refill time must not be tolerated if the patient is
hypotensive.

• A high CVP may be:

– temporary following a rapid fluid bolus
– a result of fluid overload
– due to right ventricular failure as a result of MI or PE
– due to cardiac failure
– due to chronic respiratory disease
– caused by pericardial effusion with tamponade.

If in any doubt as to the cause or treatment required, seek expert help.

Temperature

Low-grade pyrexia may occur after an MI, in bacterial endocarditis (look out for a
cardiac murmur and anaemia) or with diurnal variation in a warm environment (highest
in the early evening).

Fluid balance

Assess the losses (urine, drains, stomas and nasogastric aspirates) against the inputs
(nasogastric feed, oral fluids, IV fluids and IV nutrition). Urine output is frequently used
as a surrogate marker of cardiac output and tissue perfusion as it is relatively easy to
monitor on the ward. However it is not an immediate and acute measurement of organ
perfusion. Look out for a steady decline in hourly urine output to indicate a problem
rather than sudden complete anuria, which is more often due to a blocked catheter.

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It is the trend that is most useful and comparing what the other charted vital signs
were just before the urine output trended down can provide a timeline for the patient’s
deterioration.

Intravenous lines, intracavitary drains and tubes

Large-bore IV access is required to deliver an appropriate rapid fluid bolus and you
should aim to insert the largest cannula that will fit into the vein. Tissued lines cause
morbidity both locally owing to the effect of extravasated fluids and drugs and
systemically as a result of the failure of the fluid and drugs to reach the circulation.

Careful aseptic insertion and management of IV lines is essential, as cannula site

cellulitis and sepsis is a significant cause of hospital-acquired morbidity.

Look for the drain that is no longer draining; blocked chest drains (the fluid in the tube
should ‘swing’ and the drain may bubble if there is an on-going air leak) can cause a
tension pneumothorax while blocked abdominal drains can conceal blood loss and
pus, both of which may result in cardiovascular instability. Examine the colour and
possibly the smell of drain contents. Brown or green fluid in an abdominal drain may
represent a significant complication. It is much more common for unwell surgical
patients to be hypovolaemic than to be fluid overloaded. Pulmonary oedema may
be iatrogenic, particularly in the elderly patient who develops a new pathology, eg
perioperative MI with associated heart failure. In these patients, fluid should be given
in small repeated boluses to correct hypovolaemia and invasive monitoring in an
HDU/ICU environment may be necessary. All patients are different and not everyone
responds in the same way to apparently similar fluid regimens.

Assess the type and quantity of fluids given, review the fluid balance for the current
24 hours and for the preceding days and link this to the rest of the full patient
assessment.

Drug chart review

Omission of regular cardiac medication while the patient was ‘nil by mouth’
contributes to perioperative morbidity, eg hypertension and dysrhythmia. Alternatively,
the patient may have been given drugs that have produced adverse cardiovascular
effects as a result of overdosage, accumulation or interaction with other medication,

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especially in the presence of renal dysfunction (eg digoxin can accumulate if the
patient develops a new acute kidney injury).

Case notes

History

Taking a careful and detailed history from the patient and from the notes will help to
identify cardiac problems. Remember that nursing colleagues and relatives can be
useful additional sources of information. Specific points worth remembering include:

n speed of onset and duration of any symptoms;

n pain, its nature, severity, site and radiation;

n presence of dyspnoea;

n functional exercise tolerance.

The preadmission cardiac status, functional capacity and medication should be

identified from the notes when making an assessment of the patient’s CVS, both
when complications are occurring and when the daily management plan is being
formulated.

Examination

Use all the available clinical information and think about perfusion. Concentrate on the
CVS as part of the full patient assessment (Box 6.2).

Look

• Overview – is the patient alert now that oxygen has been administered? A
reduced level of consciousness is often a clear sign of reduced cardiac output.
• Colour – look for peripheral or central cyanosis or obvious pallor.
• Peripheries – assess for peripheral perfusion and the presence of oedema.
• Neck veins – can you see them?

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Listen

Breath sounds

• Assess for the presence of basal crepitations, which may be indicative of left-
sided heart failure.
• In early, left-sided heart failure, bronchial wheeze (cardiac asthma) may be
caused by small airway narrowing as a result of interstitial pulmonary oedema.

Heart sounds

• Assess for the presence of added sounds or murmurs (?new).

• Time the murmur with the carotid pulse: remember that a diastolic murmur is
never ‘physiological’.

Feel

• Assess limb temperature. The skin may feel clammy and capillary refill time
may be poor in patients with cardiogenic shock. Alternatively, the skin may feel
warm and capillary refill may be good in patients with sepsis.
• Liver – assess for presence of hepatomegaly or ascites, which may be an
indication of right heart failure. Heart failure can cause abdominal pain as a
result of acute distension of the liver capsule.

Box 6.2  Indicators of a low cardiac output

• Cool, clammy skin with poor capillary refill time
• Rapid, thready pulse
• Peripheral cyanosis
• Oliguria or anuria
• Confusion
• Metabolic acidaemia

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Available results

Include the available results and previous investigations in your assessment.

Remember that ward care is different to HDU/ICU care and it is unlikely that the
complete range of cardiovascular tests will have been performed. Be realistic; look at
what is available and use the findings of your clinical examination and note and chart
review to determine if any further specific tests are required. Demanding unnecessary
tests is time-consuming and costly and inflicts further discomfort on the patient.

As a minimum to aid your assessment, look at the most recent results of

haemoglobin, white cell count, platelet count and electrolytes (potassium and
magnesium especially) and compare them with those taken when the patient was
well. If no contemporary results are available since the patient’s deterioration, these
will need to be ordered. Additional tests will be necessary if you suspect particular
problems (eg cardiac enzymes for MI).

Haemoglobin

Anaemia may well precipitate heart failure in patients with critical ischaemia.
Transfusions should be used to maintain a haemoglobin level around 80 g/L in the
stable patient as this reduces the number of units a patient is exposed to without
increasing cardiac morbidity. If the patient is actively bleeding, or has new acute
cardiac pathology, a higher haemoglobin and further blood transfusion will be
required.

Electrolytes

Potassium and magnesium are particularly important for cardiac function (see
Chapter 11). If infarction/ischaemia is suspected, serial troponin levels should be
measured from 6 hours after the onset of symptoms, bearing in mind the problems
of measurement in the perioperative period. Troponin levels (either troponin I or
troponin T) are the most frequent measure of cardiac ischaemia. An absolute level 6
hours after an index event or a change in the level from baseline is often considered
diagnostic; however, troponin levels can be raised in patients with sepsis or other
cardiorespiratory pathologies, eg acute heart failure or pneumonia, and levels may
be raised several days after an event if the patient has other organ dysfunctions, eg
chronic renal failure (CRF). Interpretation can be difficult without integrating the results
with the rest of the full patient assessment.

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Brain natriuretic peptide (BNP) levels (if available) may help in assessing heart failure.

Chest radiography

This can help differentiate respiratory conditions from cardiovascular and aids in the
positive identification of heart failure. Check previous films and decide if the current
clinical picture suggests something different. Refer to the system for looking at
radiographs in Chapter 4.

Departmental chest X-rays take time and should not delay treatment. Unwell patients
should not be sent to the radiology department unless they can be monitored and
receive the appropriate level of care. Portable films are frequently preferable in unwell
patients.

Electrocardiography

As with other investigations, ECGs should never be looked at in isolation but should
be interpreted in light of the clinical findings and compared with any previous ECGs.
An ECG may show nothing significantly new, even in the failing heart, but it is
important to be able to recognise common patterns. Most bedside monitors do not
show a trace adequate for accurate diagnosis so a formal 12-lead ECG is essential.

Interpreting the ECG

Work to a routine when looking at an ECG (Table 6.1). Check the patient name/date/
time and compare with previous ECGs.

Table 6.1  The routine for looking at an ECG

Axis Use deflection in bipolar leads
Rhythm Use the R wave (lead II) ?Regular
Rate Use the R wave ?Normal
P wave Presence and morphology ?Sinus rhythm
PR interval Short or Long Pre-excitation (eg Wolff–Parkinson–White syndrome, heart
block)
QRS complex Height, width, presence Q waves ?MI, ?bundle branch block
ST segment Depressed or elevated ?MI, ?ischaemia, ?digitalis toxicity
T wave Height, shape ?Ischaemia, ?biochemical abnormalities
U wave Presence ?Hypokalaemia

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Rotation of the heart and morphology of the precordial QRS

complexes
The rotation of the heart determines the appearance of the QRS complexes in the
different leads (Figure 6.1). The size of the R wave increases progressively from
V1 to V6 because the underlying myocardium becomes progressively thicker over
the left ventricle. This reflects myocardial thickness as depolarisation spreads from
endocardium to epicardium. Occasionally, the R wave in V6 may be smaller than that
in V5 and that in V5 may be smaller than that in V4 – this can occur if the electrodes in
these leads are further away from the myocardium.

The size of the S wave (the first negative deflection after the R wave) tends to
decrease towards V6.

The direction of the first part of the QRS complex is upwards, ie positive, in V1 to
V3 (an R wave) but becomes negative as it progresses to V6 (Q wave). This is not
pathological and is due to rotation of the heart about a near-vertical axis (left hip
to right shoulder), thus producing a variation in the relative positions of the two
ventricles. This rotation causing the variations in QRS complexes is not clinically
significant and is dependent on the individual.

Since the height of the R wave and depth of the S wave are influenced by the
thickness of the underlying myocardium, these deflections will be abnormally large in
conditions producing hypertrophy, for example left ventricular hypertrophy secondary
to hypertension or aortic valve disease. However, in thin patients the R wave may be
‘abnormally’ high over V4 to V6.

The electrical axis of the heart

The spread of depolarisation across the myocardium produces ‘vector loops’ of
electrical activity. When the depolarisation wave moves towards an electrode, an
upwards or positive deflection will be recorded. Conversely, moving away from an
electrode will produce a downwards or negative deflection. The angle at which this
electrical wave moves in relationship to a particular electrode will determine the
degree of upward or downward deflection recorded by it. Each lead of the ECG
‘looks’ at the heart from a different aspect, or angle. These ‘angles’ can be displayed
using the hexaxial reference system.

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V1 V2 V3
V4
(a)
V5

V6

Cl o
(b)

ck
V1 V2 V3

wi
se
V4

A´
V5

B´

V6

A´´
(c)
V1 V2 V3

V4
i se
ck w
i cl o
A nt

V5

V6

B´´

Figure 6.1  Rotation of the heart and morphology of the precordial QRS complexes. The cross-
section through the thorax is viewed from below. (a) Intermediate position; (b) clockwise rotation;
(c) anticlockwise rotation.

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a)

R L L I

I
−90˚ II F
−120˚ −60˚

−150˚ −30˚ III R

R L III II
F
−180˚ I
0˚
+180˚
b)

+150˚ III II +30˚ R L

F
+120˚ +60˚
+90˚ I L I

II F

III R
III II
F

Figure 6.2  Electrical axes of the heart.

Figure 6.2 shows the ‘angle’ at which each bipolar lead ‘sees’ the heart. By
comparing the relative heights of the R wave and depth of the S wave, the electrical
axis or sum of the depolarisation vectors can be determined. Basically, the more the
electrical axis points towards an electrode, the greater the deflection produced by that
electrode. See leads II and F in Figure 6.2a and leads L and I in Figure 6.2b.

This description is simplified and is only intended to give you an outline of the subject.

Look at the example provided in Figure 6.3. Using the theory above, can you
determine the electrical axis?

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II

II

−90˚
−120˚ −60˚

(aVR)−150˚ −30˚ (aVL)

R L
aVR

−180˚ I
0˚(I)
+180˚

+150˚ III II +30˚

F
aVL
+120˚ +60˚
(III) +90˚ (II)
(aVF)

aVF

Figure 6.3  Example to demonstrate determining the electrical axis of the heart.

Normal ranges in ECG interpretation

The normal ranges in ECG interpretation are shown in Table 6.2 and in Figures 6.4 and
6.5.

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Table 6.2  Normal ECG ranges

At 25 mm/s Large square = 0.2 seconds, small square = 0.04 seconds
QRS width Normal < 0.12 seconds, wide > 0.12 seconds
Tachycardia Is a ventricular rate > 100 bpm
Bradycardia Is a ventricular rate < 60 bpm
Electrical axis +90° to –30°
Vertical +60° to +90° (tall individuals)
Intermediate +30° to +60°
Horizontal +30° to –30° (stocky, squat individuals)
Axis shifts towards the left in the elderly
T wave Normally upright, except in aVR lead. Inversion can also occur in leads III, V1 and V2
P wave Normally upright
Inversion can occur in retrograde P waves in atrioventricular nodal rhythm
Tall, peaked waves in pulmonary hypertension (‘pulmonary P’)
Biphasic in mitral valve disease (‘mitral P’)
PR interval Measured from the start of the P wave to the first deflection of the QRS complex, whether it
is upright or inverted
Range = 0.12–0.2 seconds
QT interval Variable, depends on rate
Q wave The first downward (negative) deflection after the P wave
Normal in lead III and aVR and sometimes in V4, V5, V6
Width no more than 0.04 seconds’ duration
Depth no more than one-quarter the height of the following R wave
U wave Normal when T wave is normal, but in hypokalaemia it may become more prominent as the
T wave flattens

(mV) R Time

T
P

Q
S

Wave P QRS T

Segment PQ ST

0.12-0.2s c. 0.35s
Interval PQ QT
(frequency dependent)

Figure 6.4  Normal annotated PQRST.

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I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Figure 6.5  Normal ECG trace.

Decide, plan and treat

The clinical assessment and investigations described above should lead to a
diagnosis that explains the patient’s deterioration. The next task is to reach a decision
based on the findings and, if needs be, arrange further appropriate investigations
or specialist opinions. Make a management plan to treat the problem and prevent
recurrence.

Conditions that do not rapidly resolve with relatively simple measures will require
expert help and a higher level of care. After any intervention you will need to reassess
and modify the management plan.

Remember the CVS has considerable reserve and, by the time dysfunction is evident,
the problems are marked. Do not leave patients with obviously compromised
cardiovascular systems.

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Specific management problems

Diagnosis and management of hypotension

Hypotension is the commonest cardiovascular problem seen in unwell surgical
patients.

Diagnosis and management of tachyarrythmias

A frequent trigger for NEWS scoring and need for review is the patient with a
tachycardia (Table 6.3). A patient with unstable vital signs needs prompt assessment
and treatment. At the other end of the spectrum, long-standing, asymptomatic
AF is common in the elderly and might simply need attention to fluid balance and
electrolytes and reinstitution of routine digoxin treatment. Usually, some action will be
required. If any doubt exists, ask for senior help.

n Rule out/correct hypovolaemia, hypoxia, hypokalaemia, hypomagnesaemia.

n Check routine medications have been given.

Table 6.3  Causes of tachycardia (the type of tachycardia will only be evident from the ECG)

Trauma Hypovolaemia, anaemia, contused myocardium

Inflammatory Pyrexia, pericarditis, sepsis
Metabolic Acidosis
Haematological Anaemia
Circulatory Shock, from any cause
Arrhythmias, PE, MI
Endocrine Thyrotoxicosis
Drugs Aminophylline, digitalis toxicity, beta-agonists
Anxiety and pain

Autonomic manoeuvres

Valsalva manoeuvres may correct a supraventricular tachycardia as described below,

but this is unlikely to be permanent.

Drugs

Care must be taken with all drugs, particularly in patients with poor ventricular
function or hypotension. Only use/prescribe a drug if you are familiar with its actions

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and its side effects: if there is any doubt about a drug, it should not be given and
advice should be sought.

In the longer term, if atrial fibrillation or atrial flutter persists, anticoagulation may be
necessary in order to prevent emboli, but it is rarely required in the acute phase and
may have significant risks for the acutely unwell surgical patient. It is not the role of
the surgical trainee to decide on long-term anticoagulation for a surgical patient.

DC cardioversion

Cardioversion can be considered when there is a very rapid rate or evidence of

compromise, particularly in the case of ventricular tachyarrythmias. It is less effective
in cases of long-standing atrial arrhythmias. Help from the critical care team and/or
cardiology must be sought at an early stage.

Pacing and surgical ablation

The use of these treatments is beyond the scope of this course. They should be used
under the guidance of a cardiologist.

Ventricular tachyarrythmias

Ventricular tachycardias
Safe and effective management of even the most common arrythmias (Box 6.3) may
require cardiology input. Ventricular tachycardias (VTs) are potentially very serious and
require prompt specialist referral. They should be distinguished from supraventricular
tachycardia (SVT) by the appearance of the ECG (Figures 6.6 and 6.7 and Table 6.4).
Cardioversion is often required for VT and is particularly urgent if the patient has
evidence of compromised cardiac output. SVT may respond, although sometimes
only temporarily, to intense vagal stimulation, eg a Valsalva manoeuvre. Alternatively,
adenosine can be administered (6 mg bolus first dose, 12 mg bolus second dose
if given via a peripheral cannula). Adenosine has a powerful blocking effect on the
atrioventricular (AV) node, thus slowing ventricular rate if the dysrhythmia is atrial in
origin. It acts for only 15–20 s and is relatively safe in inexperienced hands. Its use
should be avoided in the asthmatic patient and in the presence of dipyridamole, which
greatly prolongs its action.

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Case scenario 6.1 

A 73-year-old man with hypertension who usually takes amlodipine underwent
anterior resection for carcinoma of the rectum this morning. You review him at
8 pm on the HDU on the evening of surgery and find him to be in AF with a rate
of 90 bpm. This developed about 30 minutes previously. On your immediate
assessment you find that he appears quite well and he tells you that he feels
comfortable (he has an epidural infusion in progress). His respiratory rate is 18
breaths/min and his oxygen saturation is 97% with facemask oxygen at 40%. You
examine him and find that his peripheries are well perfused. His blood pressure is
unchanged from preoperatively at 150/80 mmHg. Your initial assessment reveals
no other findings. You review his charts and notes and find that his urine output
has only been 40 ml over the last 2 hours. His CVP has been gradually decreasing
since return from theatre and is now reading 2 mmHg. He was prescribed two
units of blood to run over 3 hours each, followed by 1000 ml of saline 8-hourly.
The first litre of saline has just been started. You ask the nurse to give him the
500 ml of saline over 20 minutes, and check a full blood count and his urea and
electrolytes. His haemoglobin is satisfactory at 110 g/L. His serum potassium is
3.2 mmol/L. All other electrolytes, including magnesium, are within normal limits.
You prescribe 20 mmol of potassium to be given in 100 ml of saline via the central
line over the next hour and arrange with the ward nurse in charge of HDU to
review him in an hour. When you review him, he is in sinus rhythm with a rate of
75 bpm, his CVP has risen to 6 mmHg and he has passed 30 ml of urine over the
past 30 minutes. You change the fluid prescription to 1000 ml saline with 20 mmol
KCl at 100 ml/h and arrange to review the patient again later that evening.

Learning points 
• Use the CCrISP system of assessment to review all patients.
• Regular review of patients at risk will lead to early detection of potential
problems.
• Correction of hypovolaemia, hypoxia and electrolyte disturbances is simple
but is often very effective.

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Box 6.3  Common causes of arrhythmia

• Ischaemic heart disease
• Oxygen, fluid and electrolyte disturbances
• Drugs
• Rheumatic heart disease
• Cardiomyopathy
• Thyrotoxicosis

Figure 6.6  Supraventricular tachycardia.

Fusion beats

Figure 6.7  Ventricular tachycardia.

Table 6.4  Differentiating SVT and VT

Supraventricular (SVT) Ventricular (VT)
QRS narrow complex Often broad complex
Often no P waves P waves dissociated rhythm
Usually regular May be irregular
QRS right way up QRS inverted
Slowed with adenosine No response to adenosine

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Ventricular ectopics
Ventricular ectopics (VEs) may be unifocal (each ectopic will have the same shape) or
multifocal (different shapes). The pulse will be irregular.

ECG is the only certain way to distinguish VEs from other causes of an irregular pulse.
The danger lies in the fact that an ectopic arising on the apex of a T wave (R on T
phenomenon) may produce ventricular fibrillation. Clearly, the more ectopics there are,
the greater is the probability of this happening. Treatment should be considered if the
ratio of VE to normal QRS is greater than 1:6 or if VEs are multifocal.

Development of new VEs may also indicate another significant underlying problem:
sepsis. Although VEs can occur in healthy people without evidence of any disease,
they can also occur after MI and in patients with electrolyte disturbance (eg
hypokalaemia and hypomagnesaemia), valvular heart disease, cardiomyopathies,
hypoxia or digitalis toxicity.

Common types of atrial tachycardia

Sinus tachycardia (Figure 6.8)

n The heart is regular: up to 160 bpm or so in young patients.

n The maximum rate is lower in older patients.

n The P wave and morphology are normal.

n Onset is gradual.

n Treat the cause – hypovolaemia, anaemia, PE, sepsis, etc.

P wave P wave

150/minute 180/minute

Figure 6.8  Sinus tachycardia.

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Paroxysmal supraventricular tachycardia (Figure 6.9)

n This term describes any tachycardia originating in the AV node, atria or sinoatrial
(SA) node.

n P waves can be of abnormal shape and may or may not be seen.

n QRS width is usually normal but may be wide if there is associated bundle branch
block (BBB).

n Paroxysmal SVT may be associated with ST depression, suggesting ischaemia.

n The heart rate is regular: 150–250 bpm.

n Paroxysmal SVT can be abolished/slowed by adenosine.

n Treat with verapamil, digoxin or beta-blockade (avoid β-blockers in conjunction

with verapamil).

Atrial fibrillation (Figure 6.10)

n The heart rate is irregularly irregular and ventricular rate variable, but often 100–180
bpm.

n AF is very common postoperatively in surgical patients.

n It is
Figure associated
6.9  Paroxysmalwith
SVT. hypovolaemia, hypoxia and electrolyte disorders.

n AF is also associated with cardiopulmonary disease (eg ischaemic or rheumatic heart

disease).

The management of AF depends on the cause and effects. Many new cases occur
after surgery, caused by hypovolaemia, hypoxia or electrolyte imbalance, particularly
hypokalaemia and hypomagnesaemia. These episodes can be rapidly treated by correcting
the causal factors alone. Identify and treat any underlying problems that would cause these
predisposing factors to recur.

When new AF causes serious adverse signs (particularly hypotension, shock, chest pain,
heart failure, decreased conscious level or marked tachycardia > 140 bpm), urgent treatment

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Figure 6.10  Atrial fibrillation.

is needed with either DC cardioversion or intravenous amiodarone. Seek expert help

immediately.

New AF that does not cause serious adverse signs and which does not respond to the
correction of the factors listed above is usually treated with digoxin or amiodarone.
Again, if problems persist or recur, or you are unsure, get expert help.

Long-standing AF can worsen after surgery if a patient’s usual drugs have been
omitted.

Atrial flutter (Figure 6.11)

n There are regular flutter P waves at 300/min.

n The QRS is normal with variable AV block.

n Atrial flutter is usually associated with cardiac disease.

n It may respond to adenosine or the adenosine may reveal flutter waves.

n Atrial flutter and fibrillation may be present in the same patient.

n Treatment is cardioversion, digoxin or verapamil.

Left ventricular hypertrophy (Figure 6.12)

A hypertrophied left ventricle has a greater influence on the electrical axis of the heart
and causes left-axis deviation. This gives the picture of tall R waves in I and aVL with
S waves in III and aVF. Most noticeably, the increase in the left ventricular muscle
mass also produces tall R waves in leads over the left ventricle (V4 to V6), and deep S
waves in leads over the right ventricle (V1 to V3).

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Flutter waves ORS complexes

Figure 6.11  Atrial flutter.

Learning point 
• In all the above cases, investigate the underlying cause.

Clinical associations
Left ventricular hypertrophy is associated with conditions causing an increase in
afterload or work on the left ventricle, for example aortic valve disease and systemic
hypertension.

Right ventricular hypertrophy (Figure 6.13)

When the electrical activity of the hypertrophied right ventricle predominates over
the left, there is right-axis deviation (leads I, II, III) with a tall R wave in V1 and deep S
wave in V6. A tall pulmonary P wave suggests right atrial hypertrophy.

Clinical associations
Right ventricular hypertrophy is associated with conditions causing increased right
ventricular afterload, for example pulmonary hypertension, cor pulmonale and
pulmonary stenosis.

Left bundle branch block (Figure 6.14)

Electrical activity in the left ventricle is delayed because conduction to it must take
place via the right ventricle. The resultant delay in left ventricular depolarisation
produces the ‘M’-shaped QRS wave, typically in V5, V6, I and aVL, and a ‘W’-shaped
QRS in some of the reciprocal leads, typically leads III and aVF.

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I aVR V1 V4 I aVR V1 V4

II aVL V2 V5 II aVL V2 V5

III aVF V3 V6 III aVF V3 V6

Figure 6.12  Left ventricular hypertrophy. Figure 6.13  Right ventricular hypertrophy.

Right bundle branch block (Figure 6.15)

Conversely, in right BBB, right ventricular depolarisation occurs via the left ventricle.

In right BBB the ‘M’-shaped QRS would typically be in leads V1, V2 and V3. Right
BBB with left axis deviation suggests bifascicular block.

This condition will often necessitate pacing – seek help early.

Clinical associations
Right BBB is associated with coronary artery disease, valvular heart disease,
ventricular hypertrophy and fibrosis, and cardiomyopathies.

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I aVR V1 V4 I aVR V1 V4

II aVL V2 V5 II aVL V2 V5

III aVF V3 V6 III aVF V3 V6

Figure 6.14  Left bundle branch block. Figure 6.15  Right bundle branch block.

Bradyarrythmias
Slow heart rates are problematic if associated with hypoperfusion or hypotension
(Box 6.4). They are common in the elderly and should not be taken as evidence that
the patient is ‘fit’.

Practice point 
The treatment options for a tachyarrhythmia or bradyarrhythmias will be found
within your hospital’s advanced life support protocols.

Patients likely to develop troublesome heart block (eg those with bifascicular block) should
be detected preoperatively and considered for elective pacing and referred for cardiology
opinion. In patients with symptomatic bradycardia, atropine (0.6–1.2 mg) may help but

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Box 6.4 Conditions associated with bradycardia

Autonomic

• Pain, especially visceral (may also be associated with tachycardia)

• Raised intracranial pressure
• Drugs: β-blockers
• Epidural

Non-autonomic

• Myocardial infarction (particularly inferior MI)

• Sepsis
• Hypoxia
• Drugs – digitalis toxicity
• Hypothyroidism
• Hypothermia

pacing may be needed. Isoprenaline infusion may be used under guidance of an intensivist
or cardiologist.

Myocardial infarction
Pre-existing ischaemic heart disease is very common and often occult in patients
with poor exercise tolerance for other reasons. This is particularly true of elderly
patients or patients with peripheral or cerebrovascular disease or diabetes mellitus.
Perioperative MI is associated with a higher mortality rate than MI occurring unrelated
to surgery. A recent MI (within the previous 6 months) significantly increases the risk
of morbidity resulting from surgery and is a valid reason to delay elective surgery if
possible, since the incidence of perioperative MI is higher during this period in this
group. Cardiac drugs should be continued up to and including the day of operation
and recommenced at the earliest opportunity postoperatively, although care and
planning may be needed, and antiplatelet medication may need to be instituted,

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especially if the patient has had a coronary vessel stent inserted. Patients on the
newer antiplatelet drugs with stents require complex multidisciplinary planning
and discussion between surgeon, anaesthetist, cardiologist and possibly also the
haematologist.

Perioperative MI is often silent, but may present with shortness of breath,

hypotension, evidence of decreased organ function (including confusion) secondary
to cardiogenic shock, acute dysrhythmias, sudden pulmonary oedema or cardiac
arrest. It should also enter the differential diagnosis of acute upper abdominal pain. A
high index of suspicion is required, particularly in high-risk groups.

The ECG may show typical changes of anterior, anterolateral or inferior MI with
ST-segment elevation of > 1 mm in the relevant leads overlying the infarct (primary
changes) and inversion in the leads opposite to it (reciprocal changes). T waves flatten
and invert within hours to days of MI and Q waves develop over 1–2 days. Changes
may be masked by a pre-existing left BBB and new BBB should make you suspicious.

The ECG may be normal after an MI, certainly for the first hour or so. A normal ECG
does therefore not exclude MI. If an MI is a potential diagnosis then the ECG should
be repeated.

Early treatment influences the outcome significantly and many patients are given
percutaneous coronary interventions in the acute phase (see below). If you suspect
the presence of an MI, then seek urgent advice from a cardiologist, who will be best

Practice point 
Recognition of patterns of ECG changes in MI:

• anterior infarct – primary changes V1, V2, V3, V4;

• inferior infarct – primary changes II, III, aVF;
• posterior infarct – isolated ST depression V1, V2.

Treatment:

• oxygen, analgesia – refer and transfer to high-care area;

• involvement of cardiologist and senior staff for consideration and planning of
percutaneous coronary interventions.

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placed to arrange the appropriate pathway of treatment for this patient: percutaneous
coronary intervention or clot thrombolysis. Inform your surgical seniors as a decision
may need to be made regarding the type of intervention required in a patient who has
recently undergone surgery, as will decisions regarding on-going anticoagulant or
antiplatelet therapy.

In the meantime:

n Check and correct the ABCDEs.

n Make the patient comfortable with a suitable opiate analgesic. Morphine (or
diamorphine) is best, titrated to response intravenously (1–2 mg boluses every
2 minutes). Ondansetron 4 mg or cyclizine 50 mg intravenously can be used to
prevent or treat nausea.

n Give high-flow oxygen to reduce hypoxia (monitor SaO2).

n Give glyceryl trinitrate (sublingual or spray) to reduce coronary artery spasm.

Nitrates also have a synergistic effect with thrombolysis.

n Consider aspirin 300 mg, orally or rectally.

n Commence treating conditions that can exaccerbate myocardial hypoperfusion:

anaemia, fluid overload, extreme hypertension.

n Arrange appropriate investigations: (i) ECG (serial ECGs are required); and (ii)
blood tests to exclude anaemia and electrolyte disturbances, and for troponin
levels.

ECG changes of MI are localised to ischaemic or infarcted areas whereas generalised

changes are seen in, for example, hyperkalaemia (peaked T waves) or pericarditis (ST
elevation). The timing of changes is shown in Table 6.5.

Anterior myocardial infarction

ECG shows raised ST segments in V1–V4 (Figure 6.16).

Inferior myocardial infarction

Raised ST segments and Q waves can be seen in leads II, III and aVF (with reciprocal
ST depression in leads I, aVL and V2–V4). Non-pathological Q waves can be present

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Table 6.5 Timing of ECG changes after MI

Change Onset/duration
Peaked T waves Seconds
ST changes (usually elevation) Hours
Q waves Hours to days
T-wave inversion Hours to days

in leads II and III (Figure 6.17). Compare this with the example of the anterior infarction
above.

I aVR V1 V4 I aVR V1 V4

II aVL V2 V5 II aVL V2 V5

III aVF V3 V6 III aVF V3 V6

Figure 6.16  Anterior MI. Figure 6.17  Inferior MI.

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Acute treatment of proven myocardial infarction with ST segment elevation

This should be determined by the cardiology team and will depend on local resources but
will require close liaison with the surgical team: there will need to be discussion regarding
risks of bleeding versus the benefits of intervention, anticoagulation and anti-platelet
treatment. Always inform your seniors if intervention is planned.

Acute treatment (NICE Guideline CG167) involves (i) aspirin; (ii) primary percutaneous
intervention followed by anticoagulation with heparin or low-molecular-weight
heparin or thrombolysis depending on local arrangements; (iii) glycoprotein IIb/3a
inhibitors; (iv) glycaemic control, particularly in diabetic patients (blood glucose
< 11 mmol/L); and (v) β-blockers (providing there is no evidence of cardiac failure,
bradycardia or hypotension, β-blockers have been shown to improve survival).
If primary percutaneous intervention is not available, fibrinolytics, eg alteplase (a
recombinant tissue plasminogen activator, rTPA) can be used, particularly if there
is persistent chest pain and gross ECG changes, though not in the immediate (< 2
weeks) postoperative period because of the risk of bleeding. Other contraindications
to fibrinolytics include:

n active peptic ulcer;

n previous haemorrhagic stroke;

n recent head injury, however minor;

n prolonged traumatic cardiopulmonary resuscitation (CPR).

NICE Guideline CG167 discusses the management of acute myocardial infarction.

Secondary therapy with an angiotensin-converting enzyme (ACE) inhibitor and a statin
should also be considered as soon as the patient is haemodynamically stable.

Acute coronary syndromes

‘Acute coronary syndrome’ is an all-encompassing term that refers to a variety of
myocardial conditions and includes acute MI (both Q wave and non-Q wave) and
unstable angina. The full range of conditions included is listed in Box 6.5.

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Box 6.5  The acute coronary syndromes

Acute myocardial infarction

• Transmural myocardial infarction

• Q-wave myocardial infarction
• ST elevation myocardial infarction (STEMI)

Non-Q-wave myocardial infarction

• Sub-endocardial infarction
• Non-ST elevation myocardial infarction (non-STEMI)

Unstable angina

In most of these patients, the development of an acute coronary syndrome is due to rupture
or erosion of an atherosclerotic plaque within the walls of a coronary artery, leading to
thrombus formation. This is then followed by platelet aggregation and vasoconstriction of
the associated vessels. Less commonly, an acute coronary syndrome is the result of emboli or
coronary spasm. It is often impossible to distinguish between the different causes clinically.

Treatment strategies
Again, this will need to be instituted by the cardiology team following surgical
discussion regarding risk of bleeding versus benefit of anticoagulation and anti-
platelet treatment.

Measure serial troponin levels.

Consider

n aspirin;

n other antiplatelets, eg clopidogrel;

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n anticoagulation;

n glycaemic control (blood glucose < 11 mmol/L);

n β-blockade.

It is likely that patients with acute coronary syndromes will require further cardiology
review and investigation prior to discharge.

Cardiac failure
Cardiac failure varies in severity from mild dyspnoea, which is easily treated, to
cardiogenic shock. Demands on the heart are increased by surgical illness and this
may unmask or worsen cardiac failure. Signs of heart failure prior to surgery are a
significant risk factor for increased morbidity and mortality.

Cardiac function depends on preload, intrinsic myocardial function and afterload. This
concept can be simplified in the following way. If the heart is thought of as a simple
pump, the preload is analogous to the priming of the pump; it will work well only if
it has something (and not too much) to pump. Ensuring adequate cardiac filling is
essential. Any condition that disturbs ‘pump filling’ will affect preload and, therefore,
cardiac function (Box 6.6a).

Intrinsic myocardial function is analogous to the function of the pump itself; if the
pump fails in any way, it will not be able to cope with the demands made on it. Any
condition that directly affects the function of cardiac muscle will affect intrinsic
myocardial function (Box 6.6b). Afterload can be thought of as the work that is
demanded of the pump to overcome the resistance to forward flow. If the resistance
to flow is low, less work will be required of the pump; if it is high, the pump will
have to work harder to produce the same output. Conditions that alter circulatory
resistance (systemic or pulmonary vascular resistance) or cause an obstruction
to flow will affect afterload (Box 6.6c). Increases in afterload raise the cardiac
oxygen demand, yet there is decreased supply to the subendocardial areas as the
contracting muscle squeezes the subendocardial capillaries. If there is a simultaneous
tachycardia, the diastolic time interval is reduced and the coronary artery blood flow is
reduced, decreasing myocardial oxygen delivery even further.

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Box 6.6  Causes of cardiac failure in surgical critical care

(a) Conditions affecting preload

• Hypovolaemia (bleeding, inadequate volume replacement, etc)

• Fluid overload
• Pneumothorax/cardiac tamponade (see (b) and (c))

(b) Conditions affecting intrinsic myocardial function

• Ischaemia
• Infarction
• Dysrhythmias
• Chronic heart failure + ‘operative stress’
• Hypocalcaemia and other electrolyte disturbances
• Myocardial depressant factors (eg in sepsis)
• Pneumothorax/cardiac tamponade (see (a) and (c))

(c) Conditions affecting afterload

• Aortic/pulmonary valvular stenosis

• PE
• Pneumothorax/cardiac tamponade (see (a) and (b))
• Aortic dissection

After surgery, a patient may develop heart failure as a result of any of the conditions
listed in Box 6.6. Sometimes, multiple factors apply in a single patient and the
range of specific disease processes that may produce these problems is wide.
Most commonly, it is a result of fluid overload. The cause of fluid overload may be
obvious (eg giving blood or parenteral nutrition simultaneously with maintenance
fluids to a patient with borderline cardiac function). Fluid balance can also become
positive insidiously – perhaps as a result of several days of giving slightly too much

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maintenance fluid to a small, elderly patient, who may also have had routine diuretics
omitted or developed AF.

The pathophysiology of heart failure is such that patients enter a downward spiral
of increasingly inefficient cardiac function. The physiological response to the failing
heart (as it is to surgical pathology) is to increase catecholamine release in an attempt
to stimulate cardiac output. Unfortunately, the failing heart has a ‘flat Frank–Starling
curve’: one shifted down and to the right compared with the curve in Figure 6.18. It
is unable to respond and maintain cardiac output by increasing its stroke volume and
tends to rely on an increase in rate. This is inefficient in that diastole is short, which
reduces the time available for diastolic filling (affecting preload) and for perfusion of
the coronary arteries, leading to development of relative or absolute ischaemia (and
further affecting intrinsic myocardial function).

Cardiogenic pulmonary oedema occurs with acute left ventricular failure or during an
exacerbation of congestive cardiac failure. Such patients usually have hypertension
and ischaemic heart disease and are often elderly. They may develop symptoms as a
result of MI or acute ischaemia precipitated by pain from non-cardiac sources.
Sudden withdrawal of epidural analgesia may cause acute afterload increases in
susceptible patients while increasing preload as the sympathetic block wears off. The

Decreasing afterload
Increasing contractility
150
Stroke volume (ml)

100

50

0
0 10 20 30

Ventricular filling pressure (mmHg)

Figure 6.18  Cardiac function: Frank–Starling curve.

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commonest causes are iatrogenic fluid overload, dysrhythmia and MI. Patients
become acutely dyspnoeic, orthopnoeic and tachypnoeic. They are tachycardic,
sweaty and often hypertensive, and a gallop rhythm may be present with a high
jugular venous pressure. They become hypoxic with increased work of breathing,
which further aggravates myocardial ischaemia. Chest auscultation reveals
crepitations basally, possibly with some wheeze (cardiac asthma) and, if oedema is
very severe, pink, frothy sputum may be produced. The CXR may show fluid in the
horizontal fissure, peribronchial cuffing, upper lobe diversion, a perihilar ‘bat’s-wing’
appearance and, rarely, Kerley B lines.

Practice point 
Treatment follows ABCDE principles:

• Administer oxygen: sit the patient up, and administer CPAP if practicable.
• Administer diuretics and small doses of opiate intravenously to aid
vasodilation.
• Reduce afterload as well as decreasing anxiety and dyspnoea, with drugs if
necessary.
• If intravenous vasodilators/inotropes are being considered, transfer to a high-
care area.

Case scenario 6.2 

A 65-year-old woman with long-standing ischaemic heart disease had a right
mastectomy 2 days ago. You are asked to see her on the third postoperative
day because she has become acutely short of breath following an episode of
severe central chest pain that lasted about 10 minutes but has since settled.
When you arrive on the ward, the patient is obviously dyspnoeic and is unable to
speak in complete sentences. She looks very unwell, and her skin feels cool and
clammy. The staff nurse who is with her reports that her pulse is 110 bpm and her
blood pressure is 170/95 mmHg. You ask the nurse to give the patient high-flow
oxygen, using a mask with a reservoir bag. You examine the patient’s chest and
find that she has a respiratory rate of 28 breaths/min and fine crepitations up to

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the mid-zones on both sides. It is difficult to hear her heart easily but you do not
think you can hear any murmurs, although you think she has a gallop rhythm. Her
blood pressure is now 140/90 mmHg. You ask the nurse to help you sit the patient
up and establish intravenous access. An examination of the patient’s ward charts
shows that she was progressing well until this episode. The case notes reveal
that she is hypertensive, has occasional angina (about one attack every 2 weeks
associated with exercise or cold weather) and usually takes bendroflumethiazide
2.5 mg and atenolol 50 mg each morning. From the prescription, it seems that she
has not had these since her operation as she has felt nauseous as a result of the
morphine PCA she has been using until recently.

Although she seems slightly better with the oxygen and repositioning, you decide
to give her 40 mg of furosemide IV. You ask for an ECG to be carried out and
order a CXR. The ECG shows a sinus tachycardia of 100 bpm but is otherwise
unchanged from the one obtained preoperatively. The CXR confirms pulmonary
oedema. You arrange for the patient to be transferred to the HDU, where she
can have continuous ECG, oxygen saturation and blood pressure monitoring
and be considered for CPAP as well as review from the cardiology team. In the
meantime, you arrange for routine blood tests and cardiac enzymes to be sent.

Learning points 
• Treat the ABCDEs first.
• Give high-flow oxygen to all patients during initial assessment.
• Transfer patients to a higher level of care if closer monitoring is required.
• Seek expert help early.

The acute management of heart failure is as follows:

n Assess and treat ABCDEs.

n Give oxygen and monitor SaO2.

n Stop IV infusions (may be only a temporary measure).

n Drugs: consider diuretics (eg furosemide 80 mg IV), nitrates (patch, sublingual,
buccal or IV), diamorphine 2.5–5 mg IV.

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n Carry out 12-lead ECG.

n Treat any underlying cause such as dysrhythmia, pulmonary embolus or

tamponade.

n Consider CPAP if the patient is not improving.

n Montor CVP.

n Consider early specialist referral.

Cardiogenic shock is defined as severe impairment of cardiac function with

hypotension of less than 90 mmHg or 30 mmHg less than the patient’s ‘normal’
systolic pressure. The patient may be tachycardic or bradycardic. Among the causes,
the commonest is severe myocardial ischaemia or infarction. The cardiac output falls,
systemic hypotension occurs and there is a progressive fall in organ perfusion.

Left ventricular end-diastolic pressure rises and pulmonary venous pressure

increases, which leads to pulmonary oedema formation. The patient becomes
dyspnoeic and hypoxic and a downward spiral develops as low SaO2 and low
diastolic pressure further compromises myocardial perfusion.

The acutely failing heart is very sensitive to too much or too little fluid. The patient
normally has pulmonary oedema so increasing preload with IV fluid is often
detrimental. Occasionally, the failing heart can have a high preload requirement and
reducing preload by diuresis may worsen cardiac output. If the afterload is high,
reducing it by using vasodilators may be beneficial, but subsequent worsening
hypotension may be detrimental to myocardial perfusion.

Accurate individualised treatment requires the measurement of cardiac output,

preload and afterload so invasive cardiac monitoring is required to optimise fluid
loading, inotropic support and/or vasodilator therapy. Senior critical care input and
monitoring are urgently needed.

Risks of surgery
It is very important to be aware of the risks of surgery in the patient with ischaemic
heart disease with recent myocardial infarction and, particularly, of the risk of
reinfarction (Table 6.6). It should be clear that delaying surgery, if at all possible, will
have a marked effect on the outcome.

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Table 6.6  Risk of cardiac disease in non-cardiac surgery

Higher Lower
Recent MI MI > 6 months
Unstable angina Stable angina
Severe aortic stenosis Abnormal ECG
Decompensated heart failure Compensated heart failure
Severe hypertension Compensated valvular lesions
Cardiac arrhythmias Cardiomegaly

The risk of perioperative MI is greater with abdominal and thoracic surgery and is
related to the duration of operation. The chance of re-infarction has been estimated
as:

n 60% if within 3 weeks of MI

n 27% if MI within 3 months of procedure

n 11% if MI within 3–6 months of procedure.

The presence of cardiac failure pre-operatively indicates a significant anaesthetic risk.

Measurement of cardiorespiratory function and reserve, eg by means of

echocardiography and cardiopulmonary exercise testing can help quantify this.

Hypertension
In patients with chronic hypertension, avoid stopping long-term antihypertensive
medication suddenly unless the patient is hypotensive. Remember to review the
prescription chart of patients on cardiac drugs on a daily basis. As with almost all
cardiac medication, antihypertensive drugs (with the exception of ACE inhibitors and
angiotensin receptor antagonists) should be given on the morning of surgery and
reinstituted as quickly as possible afterwards. Many antihypertensive drugs have
side-effects including hypokalaemia (diuretics), hyperkalaemia (ACE inhibitors) and
impaired responses to hypovolaemia (vasodilators and β-blockers).

Acute, life-threatening hypertension is rare. If the blood pressure remains at

220/120 mmHg or above with signs of organ dysfunction, involve cardiology
immediately.

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Pacemakers
Patients who have pacemakers frequently require surgery. Pacemakers can vary
between the simple fixed-rate type (rarely used) to the complex demand type with or
without internal defibrillators. They can be bipolar or unipolar, the casing acting as
the return earth in the latter. It is vital to be aware that your patient has a pacemaker
because the use of diathermy can inhibit the demand type, though this is less likely to
cause problems with a standard fixed-rate type. The important points are:

n Any patient who has a pacemaker and requires surgery should have had a recent
cardiology review to ensure that the pacemaker is functioning optimally. This may
mean switching off the internal defibrillator function on the day of surgery.

n The diathermy earthing pad should be placed as far from the pacemaker as
possible (eg on the thigh or under the buttocks). Never place the pad on the back
of the patient behind the pacemaker.

n Use short bursts of diathermy rather than long bursts.

n Bipolar diathermy is safer than unipolar.

n Avoid using diathermy near the pacemaker if possible.

n Always monitor the ECG during any procedure. Pacemaker types are classified
using a three- or four-letter code. Classification is based on which chambers are
paced, the response of the pacemaker to a sensed beat and programmability.
Recognition of the codes and details of pacemaker function are beyond the scope
of this manual and the CCrISP course. If you have any doubts or worries consult a
cardiologist.

Summary
n The detection and treatment of early clinical signs can prevent major deterioration.

n Abnormal signs must be acted on quickly – patients deteriorate rapidly from

cardiovascular problems and abnormalities need to be corrected as quickly as
possible.

n Normal clinical findings do not always exclude significant abnormality – further

investigations and monitoring can help.

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n New and long-standing cardiac disorders occur frequently in surgical patients – be

aware of common management strategies.

n Impaired perfusion, hypotension, end-organ dysfunction and poor response to

treatment suggest severe problems.

n Patients with acute abnormalities of cardiovascular function should have a clear

management plan including appropriate treatment and a timely reassessment

n Higher levels of care are often required – either pre-emptively if the patient has
long-standing problems preoperatively, or in response to acute events.

n Seek specialist help (anaesthetic/cardiology/critical care) as appropriate at an

early stage.

Further reading
National Institute for Health and Care Excellence (NICE) produce the following
guidelines:

n Acute Coronary Syndromes (QS68);

n MI with ST Segment Elevation (CG167);

n Acute Heart Failure (CG187);

n Atrial Fibrillation (CG180).

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Shock and haemorrhage

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Learning outcomes 
This chapter will help you to:

n define shock;

n understand the various aetiologies of shock;

n recognise the clinical features of a patient with shock;

n initiate early treatment of the shocked patient;

n Decide on an appropriate level of care based on the history, clinical condition

and response to treatment.

Definition
Shock is acute circulatory failure, with inadequate tissue perfusion causing
cellular hypoxia.

Regardless of the underlying cause, shock is characterised by an acute alteration of

the circulation in which inadequate perfusion leads to cellular damage, dysfunction
and failure of major organ systems.

The clinical features of shock are so variable that they cannot be used to define the
shocked state. Although the terms ‘hypotension’ and ‘shock’ are often considered
synonymous, cellular perfusion may be inadequate despite a normal blood pressure.
Perfusion includes blood flow but also the supply of substrates (including glucose and
oxygen) and the removal of waste products. Use of phrases such as ‘inadequate
tissue perfusion’ rather than ‘reduced perfusion’ is important since blood flow and
substrate supply may be increased in hypercatabolic states (eg trauma and sepsis)
and yet inadequate for the demands of the tissues due to increased metabolism and
failure to extract substrates from the circulation. In the shocked state, the distribution
of blood flow is also important. While some organs preserve flow through
autoregulation (eg brain, heart, kidney), others cannot (eg gut, skin) and may be
hypoperfused preferentially to maintain the integrity of perfusion of the other organs.
Intestinal hypoperfusion may occur in the face of a normal blood pressure and pulse

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and, following a brief hypotensive episode, a prolonged period of intestinal hypoxia

may occur, with generation of cytokines. This mechanism is the commonest pathway
for the initiation of a mediator response that results in the onset of systemic
inflammation. Systemic inflammatory mediators can, in turn, lead to further
deterioration in organ function and begin the decline to multiple organ dysfunctions
and refractory shock. This is why it is so important to detect the early more subtle
signs of shock and initiate treatment straightaway: predict and prevent.

Learning point 
• Patients may be in shock despite a normal systolic blood pressure.

Aetiology of shock
Failure of end organ perfusion can occur through several mechanisms (Table 7.1),
which can be grouped into four principal categories:

n hypovolaemic

n cardiogenic

n obstructive

n vasodilatory or (apparent hypovolaemia).

It is helpful within this classification to consider the underlying problem as one of

either reduced preload, pump failure (including obstructive causes) or reduction in
afterload (Figure 7.1).

Rapid assessment of the patient may give an early indication of the cause of
shock, but the classification system is helpful to avoid the risk of a given diagnosis
being overlooked. This is especially the case when more than one factor may be
contributing to the shocked state, eg when a patient presents with shock secondary
to abdominal sepsis, in which case the primary problem is vasodilatation but
hypovolaemia due to ileus also contributes.

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Table 7.1  Common mechanisms of shock

Type of Shock Aetiology
Hypovolaemia Haemorrhage
Fluid loss
Dehydration
Cardiogenic MI
Heart failure
Arrhythmia
Obstructive PE
Cardiac tamponade
Pneumothorax
Vasodilatory Sepsis
Neurogenic
Anaphylaxis
Adrenal insufficiency

Preload Heart Afterload

Cardiogenic Vasodilatory
Hypovolaemia MI, CCF, arrhythmia Sepsis
Haemorrhage
Fluid loss Obstructive Neurogenic
PE, tamponade, Anaphylactic
Dehydration
pneumothorax Adrenal insufficiency

Figure 7.1  Classification of shock in relation to the effect on the circulation.

Hypovolaemic shock
Stroke volume dictates cardiac output, and is directly linked to ventricular filling
pressure by the Frank–Starling curve (Figure 7.2). The curve can be shifted up and to
the left (ie improved cardiac contractility for the same degree of filling) by the use of
inotropic drugs and sympathetic stimulation. It is important to consider the Starling
curve when thinking about the clinical manifestation of shock, but also the rationale
for and response to treatment.

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Decreasing afterload
Increasing contractility
150

Stroke volume (ml)

100

50

0
0 10 20 30

Ventricular filling pressure (mmHg)

Figure 7.2  Frank–Starling curve plotting ventricular filling pressure (venous return) against stroke
volume (cardiac output). The curve is shifted up and to the left by sympathetic stimulation or
inotropic agents.

Hypovolaemia is the commonest cause of shock in a surgical patient. The low cardiac
output is a direct reflection of reduced venous return (preload). It may result from any
of the following causes:

n Haemorrhage is a common cause of hypovolaemia. Its effects vary with the

duration and severity of blood loss, the patient’s age and myocardial condition,
and the speed and adequacy of resuscitation. It has been classified, according to
the degree of blood loss, into four stages: stage 1, < 750 ml; stage 2, 750–1500 ml;
stage 3, 1500–2000 ml; and stage 4, > 2000 ml. In practice this classification
serves little useful purpose as the clinical signs of haemorrhagic shock are not
directly correlated with the degree of shock and the physiological response to a
given amount of volume loss in an individual patient is determined by the patient’s
cardiovascular responsiveness, physiological reserve and any concurrent cardiac
medication.

n Loss of gastrointestinal fluid may be due to vomiting and diarrhoea, fistulae or

sequestration of fluid in the bowel lumen in intestinal obstruction.

n Trauma and infection increase capillary permeability with local sequestration of

fluid and oedema. In addition to causing hypovolaemia, trauma and infection may
lead to sepsis.

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n Burns lead to direct loss of fluid from the burned surface and tissue fluid
sequestration.

n Renal loss of water and electrolytes (eg in sodium-losing chronic nephritis,

diabetic ketoacidosis or Addisonian crisis) is an occasional cause of shock.

n Iatrogenic surgical factors often contribute to hypovolaemia (eg poor fluid

prescription, slow or tissued intravenous infusion, inappropriate use of diuretics,
mechanical bowel preparation, fasting prior to anaesthesia, and insensible fluid
losses during prolonged operations and on-going fluid loss from dissected areas
for some hours after surgery).

Cardiogenic shock
Primary impairment of cardiac function may result from myocardial infarction or
ischaemia, acute arrhythmias, acute cardiomyopathy, acute valvular lesions (caused
by aortic dissection or trauma) or myocardial contusion.

Obstructive shock
Secondary impairment to cardiac function can result from obstruction to cardiac
output. Causes include cardiac tamponade producing constriction of the heart,
pressure on the heart from a tension pneumothorax or major PE with obstruction to
right ventricular outflow.

In all shock states, myocardial performance is affected adversely by reduced

coronary arterial perfusion and, in some cases, by circulating myocardial depressant
substances (particularly in septic shock).

Vasodilatory or distributive shock

Neurogenic factors

True neurogenic shock follows spinal transection or brainstem injury with loss of
sympathetic outflow beneath the level of injury and consequent vasodilation. The
rapid increase in size of the vascular bed, including venous capacitance vessels,
leads to reduced venous return and reduced cardiac output. There is often a relative
bradycardia. An analogous condition may be seen during epidural analgesia,

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although, in this case, the block is seldom high enough to cause a bradycardia unless
it involves the higher thoracic segments.

Anaphylaxis

Anaphylactic reactions are mediated by IgE antibodies, which results in massive

degranulation of mast cells in sensitised individuals. Activation of mast cells
releases histamine and serotonin and, with systemic kinin activation, this leads to
rapid vasodilation, a fall in systemic vascular resistance (SVR), hypotension, severe
bronchospasm with hypoxia and hypercarbia. In contrast to sepsis, the fall in SVR
is so sudden and profound that blood pressure falls markedly. Prompt treatment
with oxygen, fluids, adrenaline, hydrocortisone and an antihistamine is required, plus
removal and subsequent avoidance of the trigger substance.

Endocrine factors

Although adrenal failure is in itself a potent cause of shock due to the sudden
withdrawal of circulating cortisol and aldosterone, the role of the adrenal cortex in the
production of shock by other causes is debatable. Acute adrenal failure may occur
in severe sepsis (Waterhouse-Friderichsen syndrome), usually meningoccal in origin.
Adrenal insufficiency (often subacute) is also seen in patients in whom necessary
perioperative steroid cover has been omitted or in cases of severe sepsis requiring
high levels of pressor and inotropic support. In these cases, patients may need
additional doses of steroids, eg 50 mg hydrocortisone QDS.

Septic shock
Sepsis and septic shock are complex and are covered in more detail elsewhere. In
septic shock, the patient becomes hypotensive and the tissues are inadequately
perfused as a result of organisms, toxins or inflammatory mediators. Common
sources include the abdomen, chest, soft tissues, wounds, urine and intravascular
lines (central or peripheral) or other medical implants.

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Case scenario 7.1 

You receive a trauma team call to the emergency department – the paramedics
have advised that they will be arriving in 4 minutes with a 34-year-old patient
who has a BP of 80 mmHg systolic and a stab wound to the back between the
shoulder blades.

What form of shock might this patient be suffering from?

Haemorrhagic shock? ‘Pump failure’ due to pericardial tamponade? ‘Pump

failure’ due to tension pneumothorax? Neurogenic shock due to spinal cord
transection? All are possible.

What action may be necessary?

This depends on the cause, but immediate attention to an ABCDE assessment

with administration of oxygen and consideration of a fluid challenge, along with
diagnosis and definitive treatment, are the mainstays of treatment.

Clinical features of shock

Assessment
The early signs of shock can be subtle and the CCrISP system of assessment
allows a logical approach to assessment and management with simultaneous
resuscitation where appropriate in the initial assessment stage. Provided that there
is some response to these manoeuvres it is important to proceed with a full patient
assessment, including chart review, history, examination, review of the notes and
gathering the results of available recent investigations. The whole picture will then
inform the decision regarding the patient’s progress. A shocked patient is generally
unstable and may require special investigations. It is important to discuss the patient
with the consultant in charge, to obtain the opinions of other specialists and consider
an intervention or an operation. This will all require careful planning and coordination.

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Case scenario 7.2 

The nurses ask you to see a 75-year-old patient 5 days following a right
hemiarthroplasty for a subcapital fracture of the head of femur sustained when
tripping over a carpet at home 24 hours before the operation. She has become
agitated and uncooperative. Her response to your initial questions is in short
phrases but the words are confused. The respiratory rate is 18 breaths/minute,
the trachea is central and chest expansion equal with a resonant percussion
note and basal crepitations. You ask for an oxygen saturation probe, which
records 90%, and arrange for supplementary oxygen at 15 L/min via a non-
rebreathe mask (which she repeatedly tries to take off). Her peripheries feel cold,
the capillary refill is 4–5 seconds and her pulse is 90 bpm with dropped beats
and BP 130/95 mmHg. You place a wide-bore cannula, taking bloods for FBC,
chemistry profile and serum to be stored in the blood bank: the blood glucose
level is 4.8 mmol/L. A bolus of 500 ml of compound Ringer’s lactate is started
through the cannula (the patient’s body weight is 60 kg). The pupils are equal
and react to light normally and her Glasgow Coma Scale (GCS) score is 14.
On exposure, the chest findings are the same, the abdomen mildly distended
and non-tender with bowel sounds present and there are faecal rocks in the
rectum (bowels have not been open since the operation). Her hip wound is mildly
bruised, but with no obvious collection or leakage. There is no drain in place.

Charts show that the pulse has been around 75 bpm and BP 140/90 mmHg for
the last few days. Over the same time period, her temperature has been < 37°C,
but was 37.3°C this morning. Oral intake has been poor and the last recorded
urine output was early the previous evening: her 24-hour urine output over
the preceding 3 days has been 550 ml, 610 ml and 590 ml. Her GCS score has
not been formally recorded for the past 3 days, but the nurses report that she
was progressing well and being cooperative with her early mobilisation. The
drug chart reveals daily administration of prophylactic subcutaneous (SC) low
molecular weight heparin (LMWH), a single shot of antibiotic at the time of her
surgery, bendroflumethiazide and amlodipine daily, glyceryl trinitrate (GTN) spray,
Gaviscon and oral analgesia all prescribed prn, none of which has been required.
The notes reveal a trip over the edge of a carpet at home (where she normally
lives alone, independently), sustaining the fracture. She has treated hypertension,
hiatus hernia with oesophagitis and underwent laparoscopic cholecystectomy

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5 years ago, when she was a current smoker of 20 cigarettes per day and
developed a DVT. Recent investigations (on the third postoperative day) show
a Hb level 90 g/L, WCC 10.1 × 109/L, platelets 150 × 109/L , Na+ 131 mmol/L,
K+ 3.1 mmol/L, HCO3− 20 mmol/L, urea 9.9 mmol/L, creatinine 129 µmol/L
(compared to admission values of Hb 115 g/L, WCC 8.8 × 109/L, platelets
120 × 109/L, Na+ 138 mmol/L, K+ 4.0 mmol/L, HCO3− 25 mmol/L, urea 7.0 mmol/L,
creatinine 99 µmol/L). A preoperative ECG showed sinus rhythm with T-wave
inversion in the lateral chest leads. A postoperative hip X-ray shows a right
hemiarthroplasty prosthesis in good position.

This patient has evidence of shock and a problem which requires further
management. Initially it is good practice to reassess the patient and her response
to your initial treatment and then consider the possible diagnoses so that
your investigations may be targeted to defining the problem. This patient has
deteriorated postoperatively and is showing subtle signs of shock associated with
hypoxia, which may be due to cardiac disease, PE, infection or hypovolaemia.

Important features to note

• Is there an obvious cause that requires immediate treatment?
• Does the age or previous history of a patient suggest a possible myocardial
component?
• Has the patient recently received medication that may have an effect on the
cardiovascular or respiratory systems?
• Does the fluid balance chart of the patient show a gradually deteriorating
urine output or likelihood of a significantly abnormal fluid balance? Remember
that trends in the charted observations may be more important than absolute
values and that patients with hypovolaemic shock may still have a normal
systolic blood pressure.
• Does the patient have a temperature, high WCC or a history of an operative
procedure that may make sepsis a more likely diagnosis?

Most patients with shock have a low cardiac output; an exception is septic shock,
in which the cardiac output may be increased. The classic appearance of a patient
with low-output shock is that seen after haemorrhage. The features are partly due

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to loss of circulating volume and tissue perfusion and partly to intense sympathetic
stimulation. Early diagnosis of shock depends on recognition of the signs of
decreased tissue perfusion, particularly of the skin, kidneys and brain.

Signs of decreased tissue perfusion are summarised in Box 7.1. These are
accompanied by varying degrees of tachycardia, hypotension and tachypnoea.

Increased respiratory rate is frequently seen before any significant tachycardia, but
marked tachypnoea is an important sign of impending deterioration. Confusion may
be an early sign of marked cerebral hypoperfusion whilst coma is often a late sign.

In haemorrhagic shock, decreased venous return to the heart results in a low right
atrial pressure, low right ventricular end-diastolic volume and reduced right heart
output. This usually reduces the left atrial and ventricular end-diastolic volumes and
stroke volume (SV) falls. Since cardiac output (CO) = heart rate (HR) × stroke volume
(SV), for a fixed SV, an increase in HR is the first compensatory measure available. The
only way the body has to increase the SV acutely is to decrease the amount of blood
contained in the resistance and capacitance vessels by vasoconstriction, squeezing
the periphery to return more blood to the heart. This gives the appearance of cold,
shut-down peripheries. The heart rate response to hypovolaemia may be modified
in the elderly, in patients with ischaemic heart disease, in patients on β-blockers, in
trained athletes and in young adults.

Box 7.1  Signs of decreased tissue perfusion

• Cool peripheries
• Poor filling of peripheral veins
• Increased respiratory rate
• Increased core–peripheral temperature gradient
• Capillary refill time prolonged (> 2 seconds)
• Poor signal on pulse oximeter
• Poor urine output (< 0.5 ml/kg body weight/h)
• Anxiety and restlessness
• Decreased consciousness level
• Metabolic acidosis or raised serum lactate levels

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The effect of haemorrhage on blood pressure is particularly variable. It depends on

the duration and magnitude of blood loss, the patient’s age and cardiovascular status,
and the speed and adequacy of resuscitation. Initially, the systemic blood pressure
is maintained, and may actually increase, particularly in young patients. The pulse
pressure may drop (difference between systolic and diastolic pressure) as a result of
peripheral vasoconstriction, but this is a subtle sign. It is possible for up to 25% (or
even 30%) of circulating volume to be lost without affecting systolic pressure because
of the intense vasoconstriction and, to a lesser extent, the shift of fluid from the
interstitial to intravascular space.

A small further volume loss can lead to serious cardiovascular collapse, perhaps with
bradycardia rather than the expected tachycardia.

Practice point 
Systolic blood pressure may be normal in the presence of significant loss of
circulating volume.

Specific features of cardiogenic shock

Cardiogenic shock is inadequate tissue perfusion resulting directly from myocardial
dysfunction. Common causes in surgical patients include myocardial infarction, acute
arrhythmias, post-cardiac surgery myocardial ‘stunning’ and cardiac contusions due
to trauma. The clinical features are similar to those of hypovolaemic shock. Although
there is no primary loss of circulating volume, cardiac output falls and catecholamine-
induced vasoconstriction produces cool clammy peripheries, reduced capillary return,
reduced urine output and reduced level of consciousness. The picture is modified,
however, by elevation of cardiac filling pressure leading to elevation of the CVP or JVP
and pulmonary oedema, but low arterial pressure.

A careful history and examination of the chest, heart sounds (there may be a gallop
rhythm or associated murmur) and neck veins, together with assessment of a chest
radiograph and ECG, should prevent the possibility of cardiogenic shock being
overlooked in a surgical patient. Urgent echocardiography may be valuable in making
the diagnosis and should be attempted if the diagnosis is unclear.

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Specific features of obstructive shock

Cardiac tamponade, tension pneumothorax and PE are the principal causes of
obstructive shock. Through a variety of mechanisms, each restricts the work of the
heart, leading to a drop in the cardiac output. Typically, the JVP can be elevated
in each and assessment of the JVP should be routine. Tamponade and tension
pneumothorax need prompt intervention to relieve the pressure on the heart, but all
can respond temporarily to intravenous fluids and oxygen pending arrival of expert
assistance.

Specific features of septic shock

Sepsis is dealt with and defined elsewhere in this book and further comments here
are limited to establishing a diagnosis only. Clearly, haemodynamic instability and
pyrexia 5–7 days after a colonic resection with primary anastomosis should raise
considerations of anastomotic leak or chest infection as a source of sepsis but, in
general, the early features of sepsis (Table 7.2) are subtle. Diagnosis is difficult and a
high index of suspicion is essential. The patient may look remarkably well, largely
because of the pink, well-perfused extremities. As already stressed, clues may be
obtained from the history or the patient’s charts; in postoperative patients, blood gas
measurements can aid early diagnosis if you are suspicious and are part of the early
assessment and response to patient with suspected sepsis (see Chapter 12).

Practice point 
• A serious error for inexperienced staff is to treat restlessness (due to hypoxia
and hypovolaemia) with sedation rather than appropriate patient assessment
and resuscitation.

In septic shock, an early effect of the mediators is to cause a fall in SVR due to
vasodilation. The decrease in SVR reduces the afterload on the heart and leads to a
reflex increase in cardiac output, provided the patient has a healthy myocardium and
adequate volume state. In early sepsis, blood pressure may be well maintained, and
often the patient is pink with flushed peripheries and possibly a low diastolic pressure.
This is in contrast to cardiogenic or pure hypovolaemic shock, in which the SVR rises
in response to the drop in cardiac output.

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Table 7.2  Clinical features of sepsis

Early Late
Restlessness and slight confusion Decreased consciousness level
Tachypnoea Tachypnoea
Tachycardia Tachycardia
Vasodilation
High cardiac output Low cardiac output
Systolic BP normal or slightly decreased Systolic BP less than 80 mmHg
Oliguria Oliguria
Metabolic acidosis, elevated blood lactate Metabolic acidosis, elevated blood lactate
Warm, dry, suffused extremities Cold extremities

In the later stages, or if the patient is already hypovolaemic, the heart may be unable
to maintain an adequate output in the face of a falling SVR, so that blood pressure
falls (BP = CO × SVR). The patient may then become almost indistinguishable from
someone suffering from hypovolaemic shock. Hence, the patient may be hypothermic
or hyperthermic depending on the phase. As the septic process progresses, fluid loss
due to increased capillary permeability may also contribute to hypotension and, in
addition, myocardial depressant factors reduce cardiac function directly. Initially, the
patient requires oxygen and fluids but it is vital that cultures are taken and the source
is identified and treated.

Principles of monitoring and management

Restoration of adequate perfusion at the cellular level is the essential aim of
treatment. In practice, the initial resuscitation of patients with any form of shock is
influenced more by the nature of the associated physiological disturbances than by
the specific underlying cause. On the other hand, the ultimate success of treatment
depends largely on detection and elimination of the underlying cause (such as arrest
of bleeding or drainage of a source of sepsis).

The mainstays of early treatment are infusion of fluid and oxygen administration
with the aim of improving cardiac output and oxygen transport. If cardiogenic
and obstructive forms of shock are not suspected from the details of the clinical
presentation, all patients with shock can be initially treated with fluid administration
(initial bolus 10 ml/kg body weight of crystalloid if normotensive, 20 ml/kg body weight
if hypotensive). Oxygen should initially be given in high flow (12–15 L/min via a non-
rebreathe bag) until blood gas analysis or saturation measurements are available.

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Practice point 
In monitoring and management, the essential principles are:

• resuscitate
• diagnose
• treat the underlying cause.

You may encounter a patient with major haemorrhage who requires operative
resuscitation, eg because of leaking abdominal aortic aneurysm. You will find it very
difficult to fully resuscitate a patient with major haemorrhage; prolonged attempts are
futile and merely lead to coagulopathy, hypothermia and death.

Exsanguinating patients need immediate definitive treatment – usually by surgery or

interventional radiology.

It is the indices of tissue perfusion which are most useful in the early management of
hypovolaemia. Do not be misled into thinking that a patient is well perfused simply
because the blood pressure and heart rate are normal, a lucid patient with rapid
capillary refill, warm dry skin and a good urine output is unlikely to have significant
hypovolaemia.

Monitoring and instrumentation

Successful clinical monitoring depends on the frequent measurement of simple
haemodynamic indices and assessment of tissue perfusion. The following guidelines
apply to all forms of shock.

Venous access

Reliable venous access must be obtained early by inserting at least one large-
bore (16G) peripheral cannula in a reliable vein. Access is normally obtained in the
antecubital fossa or via the cephalic vein at the wrist. If vasoconstriction makes it
difficult to gain access, a ‘cut-down’ can be performed in the antecubital fossa or
on the long saphenous vein in front of the medial malleolus. In profoundly shocked
patients, it may be necessary to obtain the initial access by cannulating the femoral

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vein percutaneously in the groin. Draw blood for urgent cross-matching, haematology
and biochemistry.

Bladder catheterisation

A bladder catheter is inserted transurethrally unless there is a possibility of urethral

injury (as in severe pelvic fractures), or when dealing with young children. Under these
circumstances, a suprapubic catheter is inserted under ultrasound control once the
bladder has filled. Urine output must be measured hourly.

ECG monitoring

ECG monitoring will detect arrhythmias and myocardial ischaemia. It is indicated

particularly in primary cardiogenic shock, myocardial dysfunction secondary to
ischaemia, direct thoracic injury and sepsis. Arrhythmias are more likely when there is
electrolyte or acid–base disturbance. In many hospitals this may require transfer from
a general surgical ward to a level 2 area.

Pulse oximetry

A pulse oximeter attached to a finger or ear lobe allows transcutaneous estimation of

oxygen saturation of haemoglobin. The accuracy of such peripheral probes depends
on good peripheral perfusion. In poorly perfused patients, good equipment gives a
visual or audible warning of a poor signal, giving a useful index of tissue perfusion.

Central venous catheterisation

A catheter can be inserted percutaneously via the internal jugular or subclavian

veins so that it lies in the superior vena cava, thus allowing measurement of the CVP.
An aseptic technique is important for this procedure and accurate insertion is now
commonly aided by the use of B-mode ultrasound guidance. It is important to obtain
a chest X-ray to ensure correct positioning and exclude serious complications such
as pneumothorax or haemothorax, which are potentially fatal. The length and bore
of central venous catheters makes them less suitable for rapid fluid administration
than large-bore short peripheral catheters and the latter should preferably be used
in an overtly hypovolaemic patient. However, following initial administration of fluid
and oxygen, measurement of CVP can be useful for monitoring the response to
shock over time, measuring central venous oxygen saturation or when there is clinical

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uncertainty as to volume status and cardiovascular function. Patients will generally

be in high dependency or intensive care situations when this monitoring is being
employed.

In a shocked patient, a low (< 5 mmHg) or even negative CVP indicates the need for
more fluid. At the other extreme, a very high CVP (> 20 mmHg) may indicate right
ventricular or biventricular failure and the need for diuretics, vasodilators or inotropic
agents, or an obstructive cause. In practice, static measurement of CVP can be
misleading. For example, a young patient may have an apparently normal CVP (say
10 mmHg) as a result of vasoconstriction. A ‘fluid challenge’ can resolve doubt. This is
performed by measuring CVP before and after the administration of a small fluid bolus
(100–200 ml). If the CVP does not rise and remain elevated after 15 minutes, further
fluid can be given safely; a significant rise in CVP to a small fluid challenge suggests
myocardial failure or dysfunction and avoids inadvertent fluid overloading (Figure 7.3).

Core and peripheral temperature measurement

Using your hand to assess skin temperature is useful in shocked patients. If
thermistors are used to measure core and peripheral temperatures, the core–

16

14

12

10
CVP (cmH2O)

0
0 1 2 time (ml) 4 5 6
200ml fluid bolus
well-filled
redistributing
hypovolaemic

Figure 7.3  CVP response to a 200-ml bolus in different clinical situations.

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peripheral gradient provides a useful index of skin perfusion. Core temperature

measurement also detects hypothermia, as in injured patients who have been
exposed to a cold environment (eg water immersion) or following prolonged open
abdominal and chest surgery.

Fluid administration
In most cases, the type of fluid lost in shock has little influence on the choice of fluid
for initial replacement. Successful initial resuscitation depends more on the rapidity
and adequacy of fluid replacement. Initial fluid management consists of boluses
of warmed crystalloid ( up to 20 ml/kg body weight). Subsequent administration
depends on monitoring the response to treatment, and all shocked patients need
careful and repeated assessments (Box 7.2).

Box 7.2  Continuing assessment of the shocked patient

Monitor clinical appearance, noting respiratory rate, state of the peripheral
circulation and restlessness or confusion (cerebral hypoxia).

Monitor pulse rate, capillary refill time, systemic blood pressure, hourly urine
output and CVP (if appropriate).

Gain valuable additional information by monitoring or periodically checking:

• blood urea and electrolyte concentrations;

• haemoglobin concentration, white cell count and haematocrit;
• ABGs including lactate level;
• pulse oximetry;
• core and peripheral temperature.
Remember to send appropriate samples (eg blood, urine, sputum, drain fluids)
for bacteriological examination when sepsis is suspected, and institute cardiac
monitoring and perform serial ECG in cases of cardiogenic shock.

Most importantly, diagnose and treat the underlying cause.

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For those patients with major blood loss or on going haemorrhage, there are
strategies to replace the losses early with red cell concentrate, platelet and
fresh-frozen plasma transfusion, and most hospitals have major blood loss and
transfusion protocols. This will include early intervention to stop bleeding, either
surgically or using interventional radiology, and to provide best haemostasis, prevent
coagulopathy, increase organ perfusion and reduce the risk of multiple end-organ
dysfunction. Selective use of other blood fractions or synthetic clotting analogues to
replace deficient clotting factors will need to be performed with expert haematological
advice.

Considerable degrees of coagulopathy can be simply observed and monitored in

the absence of active bleeding, but clotting factors are required early if the patient is
bleeding or surgery is likely. Hypothermia also contributes to a bleeding diathesis by
causing platelet dysfunction and so strategies are required to reduce the risk of this,
including warming of resuscitation fluids, particularly when massive transfusion is
needed.

Colloid or crystalloid?

Fluid resuscitation in shock has been subject to extensive research. Normal saline
and Ringer’s lactate solution are the most commonly used crystalloids. Currently,
Ringer’s lactate is preferred because it can buffer metabolic acidosis and avoids the
hyperchloraemic acidosis associated with large-volume normal saline infusions. In
most circumstances either fluid can be used initially but there is a theoretical risk of
hyperkalaemia when using Ringer’s in patients with an acute kidney injury or chronic
kidney disease.

Colloid infusions are theoretically retained in the intravascular space more than
crystalloids. In spite of this quality, studies do not show any benefit over crystalloid
use in clinical outcomes and there are concerns about the safety of colloid use in
patients with sepsis. In a mixed ICU population, colloid administration was associated
with a poorer outcome. Colloid infusions, both albumin and those based on synthetic
starch polymers, carry risks of anaphylaxis, coagulopathy and acute kidney injury.

Important points:

n In most situations, both colloid and crystalloid are able to replenish blood volume
if given in sufficient quantity.

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n To replace a given amount of blood loss, the volume of crystalloid required is

approximately three times that of colloid.

n When crystalloid resuscitation is used, there is a greater weight gain and probably
more tissue oedema than when colloid is used.

n There is no fixed relationship between serum albumin concentration and colloid

osmotic pressure until serum albumin falls very low (below 15 g/L).

n In septic shock with increased capillary permeability, both colloids and crystalloids
pass through the vascular basement membrane.

n Many experienced practitioners would limit the volume of crystalloid used during
resuscitation to < 50% of non-blood fluid infusion.

The principal changes in practice that occur with experience are the early
identification and rapid treatment of hypovolaemic states, prompt use of blood
when haemorrhage is occurring and, most importantly, the surgical treatment of any
underlying cause, particularly haemorrhage.

Assessment of response
One of the most important steps in the management of the shocked patient is the
assessment of the response to treatment. For every exsanguination, you will meet
many more patients who become critically ill with shock in a less dramatic, but no
less important, manner. During resuscitation, and at least every 30 minutes or so, you
should reassess the patient’s progress. If the patient’s signs are not improving, you
need to change your plan of action (Box 7.3). The aim is to detect those patients you
have initially misjudged or those who are temporary responders. These patients are
common and it can be difficult to assess the need for surgery. Involve senior help if
you are in doubt.

Case scenario 7.3 

You are called to see a 68-year-old man on the surgical ward. Five days ago
he underwent a difficult anterior resection for a colonic tumour. He weighs
125 kg and has NIDDM, and a history of hypertension. He has been spiking a
temperature for the last 48 hours but has remained reasonably well until now. It is

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8pm, and the nurses on the ward are concerned because he has become cold,
clammy and restless. You follow the CCrISP algorithm and establish that the
airway is clear. His SaO2 is 92%, respiratory rate 28 per minute, pulse 110 and the
urine output has been 20 ml over the last hour. He is restless but cooperative.

What form of shock might this man have and what would you do?

Hypovolaemic/haemorrhagic shock? Cardiogenic shock? Septic shock?

Obstructive shock? All are possible and there may be more than one pathology
here. He has been spiking a temperature, so sepsis is possible. This might also
have led to a secondary haemorrhage. He has risk factors for cardiac disease,
and myocardial infarction or acute arrhythmia, possibly related to sepsis, is
possible. He may also have had a PE causing obstructive shock. Following the
CCrISP protocol, you should be able to tell which type of shock is most likely.
You institute high-flow oxygen, gain intravenous access and send blood samples
including cross-match and cultures. The patient’s BP is 115/60 mmHg, which, you
note from chart review, is lower than before. His urine output has also tailed off.
Abdominal examination is difficult but feels tense. There is no acute change on
ECG.

How would you further manage this situation?

This man is clearly shocked and needs simultaneous assessment and

resuscitation. The response to a fluid challenge while you wait for available results
will give you a much better idea of the problem. You give a fluid challenge of 20
ml/kg body weight and reassess. His BP initially rises to 140/80 mmHg, but then
drops again and he remains restless and tachycardic. On a blood gas, his Hb is
70 g/L, and he has a metabolic acidosis with lactate of 5 mmol/L.

What action may be necessary?

The most likely cause here is secondary haemorrhage, possibly secondary to

intra-abdominal sepsis. He has responded temporarily to fluid challenge but
further intervention (probably surgery) is necessary to deal with the cause. You
must seek senior help at this stage as you have treated the patient appropriately
but he remains unstable. As a bare minimum, he needs a higher level of care,
with invasive monitoring and further aggressive resuscitation.

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Learning points 
• There may be more than one cause of shock – the CCrISP system will help
you to decide the correct cause in any particular case.
• Shock may not be amenable to resuscitation alone – surgery may be required
to stop the bleeding or deal with the cause.
• Some surgical patients are difficult to assess – if you are not sure, or the
patient fails to respond to simple resuscitative measures, get help early.

Box 7.3  Responses to treatment of shock

• No response, eg exsanguination
• Temporary response, eg continuing slow but steady postoperative
haemorrhage
• Full response, eg simple sepsis caused by repeat urinary catheterisation which
responds to fluid resuscitation and early administration of antibiotics

Refractory shock
If hypovolaemic shock proves refractory to fluid replacement and oxygen
administration, the factors shown in Box 7.4 may be responsible.

Box 7.4  Refractory shock

• Underestimation of the degree of hypovolaemia
• Failure to arrest haemorrhage
• Presence of cardiac tamponade or tension pneumothorax
• Underlying sepsis with inadequate source control
• Secondary cardiovascular effects due to delay in instituting treatment
Further action is necessary.

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Algorithm of cardiovascular monitoring/support

An algorithm of cardiovascular monitoring/support is given in Box 7.5. Many surgical

patients become hypovolaemic and present with oliguria, hypotension, tachycardia,
hypoxia or acidosis in isolation or almost any combination. Many do not develop
a full picture of shock but require prompt treatment just the same. Most are simply
treated with conventional measures including adequate fluid replacement (and other
necessary treatments). You need to have a method of management clear in your mind.
You should review them later to ensure that normal function has been re-established.
Patients who need anything more than simple correction of minor to modest fluid
deficit should be managed in a high-dependency environment.

Treat any underlying pathology, particularly haemorrhage (which often needs surgery),
in addition to giving intravenous fluids and oxygen.

Box 7.5  Algorithm of cardiovascular monitoring/support

Establish and maintain normovolaemia

• Assess with CCrISP system

• Give reasonable intravenous fluid challenge (10–20 ml/kg crystalloid initially;
see text)
• Treat any underlying cause (blood loss, sepsis, etc)
• Determine recent fluid balance

Assess response

• Clinically (skin perfusion, BP, urine output, JVP, pulse)

• By simple investigations (repeat FBC, pulse oximetry, pH, BE, lactate)
• Improving: adjust fluid regimen, treat underlying cause, plan to review shortly
• Deteriorating: resuscitate and involve expert help directly
• No progress, reassess: if different diagnosis, treat and seek help; if still
hypovolaemic, continue fluids and find/treat cause
• Not sure if normovolaemic: measure CVP and seek higher level of care

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CVP

• Inadequate: establish normovolaemia

• Adequate: (> 8 cmH2O), but inadequate circulation: reassess cause (and treat
as necessary); consider inotrope in higher level of care; no/poor response,
seek help directly
• High: (> 15 cmH2O), and patient exhibits signs of cardiac failure: simple LVF,
treat; suspect cardiogenic shock, call for help

Invasive monitoring and inotrope treatment

• Transfer to HDU/ICU

Patients who have incipient failure of more than one system need the help of an
intensivist directly and you should have a very low threshold for involving help and
informing your consultant. All these patients should be receiving monitored oxygen
therapy.

Young and fit patients tolerate rapid infusion well and CVP line insertion is indicated
when there is doubt about progress, adequacy of filling or likely tolerance of the
administered fluid.

Patients who continue with inadequate cardiovascular function and whose good
cardiovascular filling has been confirmed by CVP measurement may require inotropic
support. In these cases senior help is mandatory and patients should be treated in a
critical care environment.

Metabolic monitoring in refractory shock

Urea and electrolyte levels are required to establish a baseline and monitor
progress. Arterial pH and blood gas measurements are essential to assess hypoxia,
hypercapnia and acid–base balance. Blood lactate levels are a good index of cellular
hypoxia and hepatic function.

Metabolic acidosis associated with inadequate perfusion should correct once cardiac
output is improved; its disappearance is a marker of adequate resuscitation. It is
rarely necessary to give bicarbonate in a ward setting to treat acidosis, but it may be

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considered in a higher care area if the patient’s pH is very low (< 7.1) and myocardial
depression from acidosis may be contributing to the shock.

Respiratory acidosis with an increase in arterial PaCO2 usually indicates the need for
endotracheal intubation and assisted ventilation.

Higher levels of care

Shock is an immediate life-threatening condition and should be treated as such.

The ability of the cardiovascular system to compensate has been discussed and
shock reflects the state that is reached once decompensation is occurring. Although
uncomplicated hypovolaemia can often be managed satisfactorily without intensive
care facilities, patients with severe trauma, sepsis, cardiogenic shock or shock
complicated by secondary myocardial dysfunction will all benefit from the monitoring
and support available in a critical care environment.

Consideration should be given to early critical care referral for patients with significant
comorbidity. Patients who fail to respond quickly and completely should be discussed
with the critical care team and a surgical consultant. Assessment and monitoring of
the cardiovascular system is detailed elsewhere (Chapter 8). The basis of critical care
is the same as outlined previously, with attention to fluid administration, oxygenation
and definitive treatment.

Based on the underlying cause of shock and measurement of cardiovascular

parameters (particularly the confirmation of an adequate circulatory volume), some
patients require inotropic support. The selection of an inotropic agent is based on
the cardiovascular effects of the drug and the underlying pathophysiology. The
cardiovascular effects of many agents can be predicted from a knowledge of their
particular effect on adrenergic receptors (see Chapter 8).

Summary

Definition
n Shock is inadequate tissue perfusion causing cellular hypoxia.

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Diagnosis
n Assess the patient and determine the degree of organ perfusion and not simply
blood pressure.

n Identify the different common patterns of presentation of shock.

Treatment
n Restore perfusion as a matter of urgency.

n A common initial approach is treatment with oxygen and fluid bolus administration.

n Find and treat the underlying cause.

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Cardiovascular monitoring
and support

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Learning outcomes 
This chapter will help you to:

n understand the indications for cardiovascular monitoring and support;

n be familiar with the methods used to assess cardiovascular function in a

critically unwell or perioperative patient;

n understand how drug and fluid therapies may be used to manipulate

cardiovascular function.

Introduction
Maintaining adequate tissue perfusion and hence oxygen delivery to the cells is one
of the primary goals in the management of the critically ill surgical patient.

The main determinant of oxygen delivery is cardiac output; therefore, the monitoring
and therapeutic manipulation of cardiac output are essential components of critical
care practice. Cardiac output is, in turn, determined by preload, cardiac function
and compliance, and afterload (Figure 8.1), all of which can be monitored and
manipulated.

In most patients a full clinical assessment, eg RR, HR, BP, capillary refill time and
urine output, provides a suitable first step bedside evaluation of cardiovascular
functioning. The efficacy of oxygen and nutrient delivery to the tissues, and removal
of carbon dioxide and other products of tissue metabolism, depends upon a cardiac
output sufficient to meet the demands of tissue metabolism. This is highly variable
depending on how ill a patient is. Furthermore, the cardiac output must be regionally
matched to the metabolic needs of individual organs.

Preload Heart Afterload

Figure 8.1  The determinants of cardiac output.

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In the early stages of deterioration, deviation from the normal ranges of any of
these components of cardiac output can occur unexpectedly, rapidly and with only
subtle clinical changes. Therefore, reliance on clinical assessment alone may well be
inadequate and the accuracy of estimation of volume status compared with more
intensive monitoring techniques may be as low as 30%. Objective measurements
showing change should be detected as early as possible to allow rapid corrective
therapy before vital organ damage occurs. At this stage arterial blood gas
measurement can provide additional useful information on the adequacy of tissue
metabolism, which is especially helpful in determining whether the patient might need
additional monitoring and a higher level of care. Monitoring equipment can provide
rapid, accurate and reproducible measurements of cardiovascular performance and
the effects of treatment.

Organs vary in their ability to maintain their own perfusion usually through
autoregulation. Certain organs, notably the gut, are prone to cellular hypoxia as they
cannot autoregulate and hypoxia may continue to drive the inflammatory process
(including multiple organ failure) even once the initial causal factors have been dealt
with. One approach to overcome this was to try and ensure that the critically ill patient
with multiple organ failures has a circulation that provides an oxygen delivery which is,
if anything, greater than normal, minimising the chance of occult cellular hypoxia. This
is less commonly attempted nowadays but a related approach is to monitor plasma
lactate level and/or negative base excess (BE) and central venous oxygen saturations
on the grounds that elevated values of these suggest that tissue hypoxia may be
present.

An alternative strategy has been to try and measure specific visceral perfusion
(eg that of the intestine, brain) by techniques such as tonometry or microdialysis
catheters.

There is much to be said for pursuing similar objectives, at an appropriate level, in

all unwell patients and particularly in the pre-operative preparation of the critically ill
surgical patient.

Indications for intensive monitoring of the cardiovascular system are:

n failure to restore and maintain cardiovascular homeostasis with simple techniques

(IV fluids, oxygen, surgery, non-invasive blood pressure, pulse oximetry);

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n procedures that may give rise to rapid or profound changes in preload or afterload,
eg emergency abdominal aortic repair;

n treatment with vasoactive drugs that influence preload, afterload or myocardial

function, to monitor response to treatment and guide management strategies;

n any patient who has, or is at risk of developing, a low perfusion state from any
cause, eg the high-risk patient with poor cardiac function.

The parameters that can be monitored include:

n blood pressure

n CVP

n cardiac output or cardiac index (CI).

Measurement of blood pressure

Non-invasive intermittent measurements of arterial blood pressure can be performed
using an automated sphygmomanometer. Non-invasive readings can be erroneous
if cuff size or positioning is incorrect. Automated devices are useful to demonstrate
trends in blood pressure and are reliable in most stable patients as well as easy to use
in a ward setting.

In unstable patients, better accuracy is achieved using invasive techniques. A line

can be inserted into an artery and the mechanical energy of blood pressure changes
converted to electrical energy using a transducer, allowing continuous monitoring
on a screen as well as frequent blood sampling. CVP monitoring utilises the same
principles and has the same potential pitfalls as arterial pressure monitoring.

Transducers
The physical principles of how these individual measurements are made are beyond
the scope of this course; however, certain basic scientific principles apply. Changes in
any parameter to be measured must be detected accurately with sufficient sensitivity,
over the range required, at a suitable frequency response, often from inaccessible
sites, and converted by a transducer so that the signals vary in proportion to the
changes in the parameters under study. A transducer converts the mechanical energy
of pressure changes to electrical energy so that the electrical output of the transducer

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varies directly with the change in pressure. An example of this kind of system is
shown in Figure 8.2.

A pressure wave is transmitted from the vessel (in this case an artery) to the
transducer through rigid tubing. The transducer converts the mechanical signal to
an electronic one, displayed on the monitor. The three-way tap on the transducer
allows zeroing to atmospheric pressure and sampling of arterial blood. Patency of the
cannula is maintained by a slow constant flush of saline (up to 3 ml/h) under pressure
and most systems incorporate a button for bolus flushing to clear any debris and
improve the signal.

The electrical signals must be displayed and processed so that derived results may
be calculated. The measurement system must be zeroed and calibrated. If pressure
is measured, it should be done with the transducer level relative to the point within
the patient at which the pressure is to be measured, eg midaxillary line for the
measurement of arterial and central venous pressures in a supine patient, external
auditory meatus for intracranial pressure measurement. Care should be taken to
minimise the interference and damping of the measurement signal to ensure optimal
signal-to-noise ratio. Failure to zero or calibrate will produce erroneous results. This
can also happen when the cannula or catheter is kinked, abuts the vessel wall or is
partly occluded by clot.

Pressure bag

Monitor

Flush device
Transducer

Arterial cannula

Figure 8.2  Signal transduction from an arterial cannula.

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Safeguards
Certain standards are common to all procedures used during invasive monitoring
methods:

n The operator should have a sound knowledge of relevant practical anatomy.

n The operator should be competent in the technique of insertion of the line.

n The procedure should be explained to the patient.

n All procedures must be performed using an aseptic technique.

n Contraindications and complications of the procedure and monitoring technique

must be known.

n The benefit accrued must exceed the risks of the procedure.

n The patient must be looked after by staff who know how to manage the lines, all of
which must be Luer-locked to prevent disconnection.

n All lines should be clearly labelled and injections into or sampling from lines
performed only at designated sites by people trained to do so.

n Attendants should be familiar with the monitors to ensure that the data derived
from them are accurate.

n Lines must be dressed aseptically and other equipment, eg line transducer sets
changed at appropriate intervals.

Arterial pressure monitoring

A peripheral artery can be cannulated either to allow continuous measurement of
arterial blood pressure by connecting the cannula to a transducer or to allow for
repeated sampling of arterial blood for analysis. The radial artery is the anatomical site
most frequently used, followed by the dorsalis pedis artery, and a 20G or 22G cannula
is used. The brachial and femoral arteries should be avoided if possible because of
lack of collaterals and, in the case of the femoral site, the risk of sepsis.

When using the radial artery, check for ulnar flow supply to the palmar arch using
Allen’s test prior to cannulation (Figure 8.3). Local sepsis and coagulopathy are the
main contraindications, while complications include haematoma, thrombosis, distal

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ischaemia, intimal damage, false aneurysm formation, disconnection and injection

of irritant drugs. Samples from arterial cannulae should be taken aseptically and the
line flushed and re-sealed afterwards. After cannulation of the artery, the cannula
should be connected to a continuous-flush device containing saline under pressure,
which maintains patency and allows blood pressure changes to be conducted without
letting blood flow out of the artery into the line.

Pressure on
arteries and
elevation to
blanch hand

Th

Little finger

Release
pressure

Figure 8.3  Allen’s test. Blanch the hand by clenching the fist then simultaneously occlude the
radial and ulnar arteries at the wrist. An adequate pink flush of the hand on release of the ulnar
pressure confirms an adequate ulnar supply to the palmar arterial arches.

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Technique for radial arterial puncture/cannulation (Figure 8.4)

Position and palpate

• Position the hand and yourself comfortably, with adequate light and
assistance.
• Palpate the artery with two fingers.
• Feel and imagine its course above and below the point of entry.
• Insert at 45°, avoiding the superficial vein which often overlies.

Puncture

• Advance needle tip in a linear fashion – do not wiggle it around.

• If you miss, repalpate and search in a systematic fashion with further straight
insertions.
• Let syringe fill and withdraw.
• Pressure haemostasis – 5 minutes.

Cannulation: the Seldinger technique

This requires strict asepsis:

• Puncture as above.
• Advance guidewire through hollow needle.
• Remove needle.
• Railroad cannula over guidewire.
• Check backflow and secure cannula.
• Connect transducer and flushing set-up.

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If the arterial cannula is to be used for pressure monitoring, it is connected via a short
length of rigid tubing to a three-way tap, flush device and transducer. Check that the
transducer is zeroed and calibrated at the correct level, and that the line does not
contain air bubbles, which would cause damping of the signal. The arterial waveform
gives real-time information about the blood pressure and heart rate, but can also
transform pressure changes into variations in stroke volume or cardiac output using
commercial devices, i.e. LIDCO™.

Flexor carpi
Abductor radialis tendon
pollicis longus
Radial artery
tendon

Radial
styloid

Puncture Advance guidewire

Railroad cannulation Connect and secure

Figure 8.4  Technique for radial arterial puncture/cannulation.

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mmHg
( a) ( b) ( c)
100 100
100

0 0 0

Figure 8.5  Arterial waveforms showing influence of damping. (a) Adequately damped;
(b) underdamped; (c) overdamped.

Some devices, such as LIDCO™, need to be calibrated by an independent

mechanism in order to compensate for the different levels of vascular compliance
seen between and within patients. The shape of the individual waveform can give
information about the systemic vascular resistance and cardiac contractility in both
normal and pathological conditions. In particular, a sharp peaked up-swing and
down-swing with a low dicrotic notch can reflect significant hypovolaemia, but it is
dangerous to draw such conclusions unless the system is adequately damped (Figure
8.5).

Changes in the arterial pressure trace with the fluctuations in intrathoracic pressure
during artificial mechanical ventilation can be used to determine which patients will
respond to a fluid challenge by increasing their stroke volume.

These changes can be characterised by the systolic pressure variation, the pulse
pressure variation or when combined with a cardiac output monitor, the stroke volume
variation.

Central venous pressure measurement

CVP measurement is one of the most commonly used monitoring tools in critical
care, indicating preloading of the pulmonary circulation and a rough guide to systemic
preload given a number of provisos. The CVP is the pressure within the superior vena
cava as it enters the right atrium, and reflects the ability of the right heart to accept
and deliver circulating volume. The CVP is influenced by various factors, including
venous return, right heart compliance, intrathoracic pressure and patient position.

While absolute measurements of CVP are useful (with the normal range 0–8 mmHg or
0–10 cmH2O), often the trend in CVP, and response to fluid challenge or therapeutic
manoeuvres is more important. This is particularly useful when trying to find and treat
the cause of shock (see Chapter 7).

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Central vein cannulation

Infraclavicular subclavian route

This technique is rarely used blindly by experienced operators and access is

more likely to be achieved using ultrasound guidance.

• Tilt the patient 20° head down, arms by the side and head turned away from
the side of entry.
• Make a skin nick and insert the cannula 1–2 cm below the midpoint of the
clavicle.
• Advance horizontally towards the suprasternal notch – remember to advance
needle tip in a linear fashion – do not wiggle it around.
• Try to visualise the anatomy beneath as you do it – think where your needle
tip is, particularly in relation to the clavicle and pleura, and the narrow gap
between clavicle and first rib, where the subclavian artery and vein run.
• If you miss, search in a systematic fashion with further straight insertions,
trying to picture where the vein is most likely to be.
• When venous blood is aspirated freely, remove syringe and insert the
guidewire.
• Leave enough guidewire outside to let you railroad the catheter over it without
losing the wire inside the patient.
• Advance the catheter to a previously measured point, so the tip lies in the
distal superior vena cava (SVC).
• Secure the catheter and check its position by chest X-ray.

Ultrasound image of the jugular vein and carotid artery

• Using ultrasound, the vein is located at the medial border of sternomastoid, at

the level of the thyroid cartilage and anterolateral to the carotid artery.
• Displace the artery medially and, under ultrasound guidance, advance the
needle through a skin nick.

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• Advance inferiorly at 30° to the skin, parallel to the artery but lateral: this is
often towards the ipsilateral nipple.
• Puncture and proceed as above.

CVP access
The route for access to the central venous circulation depends on the skill and
experience of the operator and the presence of site-specific contraindications such
as local sepsis, coagulopathy, abnormal anatomy, operative site and previous vein
usage. While the techniques are illustrated in Figure 8.6a, the UK National Institute
for Health and Care Excellence (NICE) recommends that ultrasound imaging should
be used to guide placement of central venous catheters into the internal jugular vein
in elective situations. NICE also recommends that those involved in placing central
venous catheters should undertake training to achieve competence in the use of
ultrasound for this purpose. Ultrasound should also be used in emergency cases,
although the anatomical landmark method may still be used for the subclavian route
due to poor ultrasonic visualisation of the subclavian vein behind the clavicle.

(a) (b)

Figure 8.6  (a) Infraclavicular subclavian vein cannulation using the Seldinger technique. (b)
Ultrasound image of the jugular vein and carotid artery.

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The internal jugular site is better in terms of a lower rate of complications, but access
at this site is uncomfortable and difficult to dress. The subclavian route has a higher
risk profile, in particular the risk of pneumothorax and intrathoracic bleeding, which
can be difficult to control.

Practice point 
Central venous catheterisation should only be done by an experienced person.

CVP measurement
The best zero reference point, which represents the level of the SVC, is the midaxillary
line at the fourth intercostal space, with the patient supine. The alternative, the
second intercostal space at the sternal edge, represents a point about 5 cm above the
atrium. For readings to be comparable at separate times, they should always be taken
from the same point (Figure 8.7).

The electronic transducer produces an electronic signal, analysis of which allows

the mean pressure to be displayed in mm of mercury. The set up of the transducer is
identical to that for arterial pressure measurement.

Giving set

Manometer
Position of the three-way
top for recording

Zero to sternal edge

b
b=a–5
5
a

To central line

Figure 8.7  Liquid manometer for CVP.

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A
C

V
X
Y

Figure 8.8  The CVP waveform. A wave, atrial contraction; C wave, bulging of the tricuspid valve
into the right atrium; X descent, atrial relaxation; V wave; rise in atrial pressure prior to tricuspid
valve opening; and Y descent, atrial emptying.

CVP waveform
The CVP waveform has a characteristic pattern that reflects changes in atrial pressure
during the cardiac cycle, as shown in Figure 8.8.

Indications for CVP measurement

CVP measurement is indicated in the following situations:

n administration of fluid replacement therapy for hypovolaemia when conventional

access is not possible, when concern exists about overtransfusion or when there
is uncertainty about fluid volume status;

n central vein cannulation is not advocated as a primary route of access because

of the risk of complications and low flow rates achievable (remember Poiseuille’s
law);

n to measure the effect of vasoactive drugs on venous capacitance, particularly

vasodilators;

n to aid diagnosis of right ventricular failure, when a high pressure will be seen in the
presence of poor cardiac output;

n administration of potent drugs, eg inotropes;

n administration of parenteral nutrition, which must be done using a dedicated clean

lumen.

Practice point 
CVP as a value does not ‘equal’ intravascular volume and is not an indicator of
left ventricular function.

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Pitfalls in practice
n Inaccurate readings can result from failure of zeroing or calibration, placement of
the cannula tip in the right ventricle, tricuspid regurgitation and incompetence, AV
dissociation and nodal rhythms.

n Variations in intravascular volume, sympathetic tone, cardiac output and

intrathoracic pressure (particularly during positive pressure ventilation) may lead to
a false impression of a much higher right ventricular filling pressure than is actually
present (Figure 8.9).

n Before using the line and acting on measurements made, always check for easy
aspiration of blood and pressure fluctuation with respiration and confirm the
position of the line by X-ray.

n Complications of central line insertion are numerous and relate to damage to

either the veins themselves or adjacent structures. They include rupture of vessel
and haemorrhage with local haematoma or haemothorax, tension pneumothorax
(particularly if the patient is on positive-pressure ventilation), air embolism,
extravascular catheter placement, knotting of catheters, catheter breakage,
catheter misplacement, neurapraxia, arterial puncture, lymphatic puncture,
tracheobronchial puncture and sepsis. Do not underestimate the potential severity
of central line sepsis.

General
anaesthetic

a b c d e

Figure 8.9  CVP and intravascular volume: pitfalls in the shocked surgical patient. (a) Normal.
(b) Shocked but compensating (by peripheral vasoconstriction) with low CVP. (c) Rapid refill
and (temporarily) high CVP. (d) Redistribution and falling CVP as degree of compensatory
vasoconstriction lessens. (e) General anaesthesia with vasodilatation, loss of compensation and
very low CVP.

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Staff involved in the care of patients with central venous access should ensure
compliance with care bundles for central venous catheter care to prevent catheter-
associated infections. The care bundle approach considers aspects of line insertion,
including aseptic techniques, skin preparation and hand hygiene and on-going care of
the line, including regular inspection, aseptic techniques and regular replacement of
administration sets.

Measurements of cardiac output/cardiac index

In shock states, the delivery of oxygen to the tissues is at least as important as the
level of systemic arterial pressure. Global oxygen delivery is a product of cardiac
output and arterial oxygen content. Cardiac output is a pivotal variable in the
management of the critically ill surgical patient.

The understanding of the relationship between cardiac output and other parameters
allows an estimate of systemic vascular resistance, using the following equation:

Cardiac output = driving pressure (mean arterial pressure (MAP) – CVP)/systemic

vascular resistance

With a measurement of cardiac output, MAP and CVP, an estimate of SVR can be
calculated and the combination of variables used to guide rational decisions about
volume resuscitation and vasoactive therapies.

The pulmonary artery catheter (PAC or Swan–Ganz catheter) was the gold standard
for advanced haemodynamic monitoring. Its use is now limited to cardiac and
some vascular surgery. Pulmonary artery pressure and pulmonary artery occlusion
(or ‘wedge’) pressure can be used to monitor right heart function and preload of
the systemic circulation. This is achieved using thermodilution techniques and a
thermistor on the PAC. The technique is highly invasive and is associated with a
significant risk of serious complications. This, combined with ready availability of less
invasive cardiac output monitors, has led to reduced use of PAC in general critical
care units and in theatre. Cardiac indexing corrects any variable for patient size
(Box 8.1).

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Box 8.1 Variables derived from cardiac output measurements

Systemic vascular resistance (SVR)

• If too high (vasoconstriction), tissue hypoperfusion is likely

• If too low, maintenance of an adequate mean blood pressure will be difficult

Stroke volume (SV), stroke index (SI)

• A major determinant of cardiac output and governable by preload

Left ventricular stroke work index (LVSWI)

• An index of the function of the systemic side of the heart

Oxygen delivery (DO2)

• An index of the oxygen delivered to all tissues

Oxygen uptake (VO2)

• Index of oxygen consumption

Non-invasive measurement of cardiac function

There are several less invasive techniques, including trans-oesophageal Doppler
(TOD), echocardiography, pulse contour cardiac output with indicator dilution (PiCCO)
and the LiDCO™ (lithium dilution cardiac output) system.

Trans-oesophageal Doppler

TOD uses the Doppler shift principle to make measurements of blood velocity
in the descending aorta. A disposable Doppler probe contained at the tip of a
90 cm × 5.5 mm probe is passed down the oesophagus to lie at the level of the
descending aorta (around 35–45 cm) and rotated until the arterial waveform is
displayed. This appears as a triangular waveform since the shift signal is displayed
as a velocity–time plot. The shape of the waveform provides information on preload,

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a
c
b d

Time
Figure 8.10  Stylised TOD waveforms for vascular abnormality. (a) Best waveform, normal
configuration. (b) Failing left ventricle – decreased waveform height and low peak velocity. Giving
inotropes increases waveform height and restores velocity. (c) Hypovolaemia – narrow waveform
base with decreased FTc (giving volume lengthens flow time and widens waveform base). (d) High
systemic vascular resistance/afterload – reduced waveform height and narrow base.

stoke volume and afterload (Figure 8.10). The area under the curve represents the
stroke volume flowing through the descending aorta and applying a factor determined
from the patient’s age, height and weight allows the stroke volume to be calculated.
The corrected flow time (FTc) is calculated: it is low in hypovolaemia and may be used
to derive SVR. The disadvantage of TOD is that the patient must be anaesthetised
and intubated to tolerate the probe. The technique is very position and therefore
operator dependent. It cannot be used in patients who have coarctation of the
aorta or who are on intra-aortic balloon pumps, or in those undergoing surgery to
the oesophagus or in whom insertion of the probe into the oesophagus would carry
additional risks, eg patients with known bleeding from oesophageal varices and/or
oral surgery patients.

Trans-thoracic and trans-oesophageal echocardiography

Bedside echocardiography is becoming increasingly available and training in

echocardiography image acquisition and interpretation at a basic level is becoming
widespread. Its main role in critically unwell patients is the assessment of preload
and cardiac contractility before and after an intervention, and the diagnosis of major
cardiac structural abnormalities (pericardial tamponade, severe valvular and regional
wall motion abnormalities). Some image windows, eg transhepatic views, allow
assessment of inferior vena cava size and therefore patient filling. It can be difficult
to get good views in ventilated patients or those who have recently undergone
abdominal surgery.

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Indicator dilution and pulse contour analysis

Instead of measuring cardiac output by means of temperature changes in the

pulmonary artery, which requires a PAC, a thermistor can be placed in the systemic
arterial circulation. PiCCO calculates cardiac output from a peripheral arterial cannula
providing beat-to-beat information to a computer, which in turn follows the heart
rate and pressure waveform and integrates the area under the curve. The accuracy
of the method is improved as the cannula contains a sensitive thermistor, allowing
thermodilutional calibration. The small drop in the temperature of arterial blood that
follows the injection of a bolus of ice-cold saline into a central vein is proportional to
cardiac output. The thermodilution measurement is used to calibrate the continuous
cardiac output monitoring software, which calculates changes in cardiac output by
analysing the pulse contour of the arterial waveform. PiCCO requires recalibration at
regular intervals and becomes unreliable when the arterial waveform is suboptimal,
for example with a kinked line, air or blood clots in the system or any other cause of a
damped trace.

Other indicators can be used to replace thermodilution techniques. For example,

lithium chloride can be injected into a central vein and the lithium concentration
analysed with an ion-sensitive electrode (LiDCO™). In this case, the blood can
be sampled from a normal peripheral arterial line. Several drugs interfere with the
lithium analysis, notably some muscle relaxants, eg atracurium, and lithium is
contraindicated in some patients, eg pregnant women. As with thermodilution, lithium
dilution is combined with continuous pulse contour analysis and similar recalibration
requirements and issues with damped arterial traces apply. Some devices provide
information on the pulse waveform without calibration; these use the arterial
waveform to compute cardiac output continuously by multiplying heart rate by a
calculated stroke volume. Although easy to use and providing continuous data, the
lack of calibration may make these devices inaccurate, particularly when large cardiac
output changes occur, eg during haemodynamic instability due to haemorrhage or
sepsis.

Cardiovascular support using vasoactive drugs

In the normal heart, cardiac output is determined by preload, afterload, heart rate,
rhythm, contractility and balance of oxygen demand and supply. If the heart is

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damaged, for a given preload or afterload, cardiac output will decrease. This can
be represented graphically either by pressure–volume loops or by the more familiar
Frank–Starling curve (see Figure 7.2).

If the cardiac output remains low after correcting any hypovolaemia with a fluid
challenge, inotropic or other vasoactive drugs are used to optimise myocardial
contractility by balancing myocardial oxygen supply and demand. Measurements of
derived variables can predict the best therapeutic regimens (Table 8.1).

Inotropes are drugs that increase cardiac output and ejection fraction. Ideally, in
addition to these properties, they should reduce afterload and preload, resulting in
decreased transventricular wall tension, promoting coronary blood flow, increasing
myocardial oxygen delivery and reducing oxygen consumption. Regrettably, the
ideal inotrope does not exist, but the most commonly used are adrenaline and
dobutamine. They all act by providing an upward and left shift in the Frank–Starling
curve, as shown in Figure 7.2. Noradrenaline has a specific use in septic shock as a
vasopressor: it is used to increase and maintain SVR within the normal range.

Table 8.1  Action of inotropic agents

Receptor Effect Clinical use
Noradrenaline α-Adrenoreceptor agonist Arteriolar vasoconstriction Septic shock with low
SVR
Adrenaline α- and β-adrenoreceptor Positive inotropic and chronotropic. Widespread in conditions
agonist, predominantly Vascoconstricts at high doses of low cardiac output;
β1-adrenoreceptor useful in emergency
agonist at low doses situations
Dopamine α- and β-adrenoreceptors. Low dose: splanchnic vasodilation, Used less frequently
Dopamine (DA) 1 and 2 increased renal and hepatic
receptors blood flow (DA1). High dose:
vasoconstriction
Dopexamine DA1, DA2 and Increases splanchnic blood flow Controversial – in
β-adrenoreceptor agonist perioperative optimisation
Dobutamine Similar to dopexamine Reduces SVR and increases Cardiogenic shock
cardiac output
Milrinone Prevents breakdown Inotropic action by increasing Heart failure, cardiogenic
of cAMP by intracellular calcium shock
phosphodiesterase

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Vasodilators such as sodium nitroprusside or nitrates are of use when pulmonary

oedema occurs in heart failure, although they can produce a reflex tachycardia if
the blood pressure falls. Occasionally, both inotropes and vasodilators are used
in combination (eg adrenaline and nitroglycerine in severe LVF) or inotropes and
vasoconstrictors are used in combination (eg dobutamine and noradrenaline in severe
sepsis).

Inotropes and vasodilators can only be used safely where a full range of monitoring
is available. They should never be used on ordinary surgical wards and never in the
presence of hypovolaemia. Their dose ranges, modes of delivery, etc, are outside the
scope of this course, although there should be opportunity to discuss these more
during the workshops. Your task as a surgical trainee caring for ward-level patients is
to recognise the clinical conditions that mandate their use and refer the patient for the
appropriate level of monitoring and care.

Summary
n Adequate cardiovascular function is a prerequisite for survival.

n To determine cardiovascular function accurately, invasive monitoring is necessary

when ward based assessment and therapy is failing to produce a response.

n All techniques of advanced CVS monitoring have complications and limitations to

their use.

n The method of monitoring chosen should be appropriate to the specific patient

and problems.

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Renal failure, prevention

and management

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Learning outcomes 
This chapter will help you to:

n understand the functions of the kidney;

n anticipate and predict patients at risk of developing acute kidney injury (AKI);

n outline the initial management of a patient with AKI and associated life-
threatening emergencies;

n state the common causes of AKI in the critically ill surgical patient;

n be aware of the implications for management of chronic kidney disease in the

surgical patient.

Abnormal renal function is not infrequent in surgical patients and poor urine output
is one of the most common reasons why you and your team may be called to
see a patient. The kidneys have a wide range of functions and play a vital role in
homeostasis. In the context of the critically ill patient, they can also be thought of as
‘bilateral retroperitoneal indicators of cardiovascular stability’. Abnormal renal function
is frequent in surgical patients, and poor urine output is one of the most common
reasons for you and your team being called to see a patient. The kidneys have a wide
range of functions and play a vital role in homeostasis.

Acute kidney injury (AKI) in critically ill patients is associated with increased mortality
and is often preventable, particularly by careful fluid balance management in the
perioperative period. It is the responsibility of the surgical team to anticipate and
prevent AKI where possible. When it occurs, treatment is essentially supportive,
but you must be aware of the associated life-threatening complications of AKI
(hyperkalaemia, pulmonary oedema) and know how and when to refer for renal
replacement therapy.

Functions of the kidney

The primary functions of the kidney are:

n elimination of water-soluble waste products of metabolism other than carbon

dioxide;

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n elimination of water-soluble drugs;

n fluid and electrolyte homeostasis;

n acid–base balance;

n blood pressure control: renin–angiotensin system;

n endocrine function: erythropoietin and vitamin D production.

Physiology of renal function

The kidney regulates fluid and electrolytes by filtration, secretion and reabsorption.
Renal blood flow is approximately 20% of cardiac output (1000 ml/min in an adult) and
renal plasma flow (RPF) is approximately 600 ml/min. The glomerulus filters 125 ml/min
of renal plasma. This glomerular filtration rate (GFR) is a more accurate marker of renal
function than plasma creatinine and can be estimated from the serum creatinine, BMI
and gender. Most filtered fluid is reabsorbed, with only 1% passed as urine (0.5–1 ml/
kg/h).

Renal blood flow is autoregulated and relatively constant over a wide range of mean
arterial pressure (MAP). At low MAP, RPF and GFR become supply dependent and
urine output decreases – this is the kidney protecting itself from further reduction
in perfusion pressure (Figure 9.1). It is reversible in the short term but the kidney
becomes more vulnerable to other insults, particularly the tubular cells deep in the
medulla, which is more poorly perfused than the cortex.

The plasma creatinine level and GFR are inversely related. If the plasma creatinine
level drifts outside the normal laboratory range, the GFR may already be 50% of
normal values. It is important to recognise that a borderline creatinine may pose an
increased risk of AKI, particularly in the elderly, as the GFR decreases with age (Figure
9.2).

Practice points 
• Normal adult urine output is 0.5–2.0 ml/kg/h.
• Oliguria is < 0.5 ml/kg/h.
• Anuria is < 100 ml/day (approximately 0.1 ml/kg/h).

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Autoregulation

0 20 40 60 80 100 120 140 160 180 200 220

Main Arterial Pressure

Renal Plasma Flow (RPF)

Glomerular Filtration Rate (GFR)
Urinary Output

Figure 9.1  Autoregulation maintains a steady GFR through a wide range of renal perfusion
pressures.

140

120

100
GFR (ml/min)

80

60

40

20

0
0 1 00 200 300 400 500 600 700 800 900 1000
Serum creatinine (µmol/l)

20-year-old 90 kg male
80-year-old 50 kg female

Figure 9.2  The GFR steadily decreases with age, but this is not evident in raised creatinine until a
relatively low level is reached.

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Acute kidney injury

There are five points to consider in the development of AKI in the surgical patient:

n The kidneys cannot function without adequate perfusion.

n Renal perfusion is dependent on adequate blood pressure.

n A surgical patient with poor urine output usually requires more fluid.

n Absolute anuria is usually due to urinary tract obstruction.

n Poor urine output in a surgical patient is not initially treated with diuretics.

Case scenario 9.1 

Eight hours following an expedited open abdominal aortic aneurysm repair for
leak, a 68-year-old man develops oliguria despite receiving 100 ml/h Hartmann’s
solution with no major change in pulse rate or blood pressure. He is ventilated
and there are no signs of major haemorrhage or excess loss from the nasogastric
tube. His CVP is 16 mmHg but the critical care nurse feels that the trace is
unreliable and ‘positional’, and suggests that the patient is suboptimally perfused.
The patient’s Hb is 111 g/L. The junior trainee recommends a dose of furosemide
(80 mg IV) to improve the urine output. This improves the urine output to 100 ml
for 2 hours, after which it falls again to 20 ml/h. The on-call senior trainee
prescribes a further dose of furosemide (40 mg IV) by telephone. This has no
effect and the ICU consultant is contacted. She re-sites the CVP line and CVP
is found to be very low (2 mmHg). Establishment of cardiac output monitoring
(pulse pressure variation) also confirms a low stroke volume and intra-abdominal
pressure is measured with no evidence of abdominal compartment syndrome.
Immediate circulatory volume expansion does not restore urinary output despite
improved stroke volume and a small increase in CVP. By the next day, the plasma
creatinine and urea levels have risen rapidly and renal replacement therapy is
required. The patient has a long and complicated course and dies of multiple
organ failure 3 weeks later.

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Learning points 
• Adequate renal perfusion is the critical factor – this is achieved with careful
attention to fluid balance and cautious fluid challenges.
• Insensible and tissue fluid losses continue after surgery – postoperative
hypovolaemia is common and is not necessarily caused by acute
postoperative haemorrhage.
• CVP readings may complement clinical assessment but are influenced by
multiple factors, particularly in the context of positive pressure ventilation.
• Consider advice from experienced nursing staff and always perform a three-
stage CCrISP assessment of the patient.
• Furosemide will not salvage renal function in a hypovolaemic patient.
• The five points to consider in AKI would have helped in planning management
of this patient.

Definition of AKI
Acute kidney injury is a biochemical diagnosis associated with an acute increase in
serum creatinine resulting from injury or an inability to excrete the nitrogenous and
other waste products of metabolism.

There have been over 20 different classifications of acute renal failure. The system
currently in use is that of Acute Kidney Injury Network (AKIN). The term AKI is
preferred to renal failure as the pathophysiology may be reversible. AKI is compatible
with the multiple insult hypothesis that a kidney exposed to multiple insults is more
likely to be damaged, and so attention should be paid to ensuring other insults are
dealt with or prevented. AKI is recognised as one of three clinical scenarios:

n an abrupt (within 48 hours) reduction in kidney function defined as an absolute

increase in serum creatinine level of > 26.4 μmol/L (0.3 mg/dl); or

n a percentage increase in serum creatinine level of > 50% (1.5-fold from baseline);

or

n a reduction in urine output (documented oliguria of < 0.5 ml/kg/h for > 6 hours.

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These criteria should be applied in the context of the clinical presentation, following
adequate fluid resuscitation and the exclusion of urinary tract obstruction.

There are three stages of AKI based on GFR and urine output, detailed in Table 9.1.

Epidemiology
The incidence of AKI depends on the population being studied, from 5% of general
acute hospital admissions, to 10% of unplanned surgical admissions to ICU and 50%
of those with septic shock.

Aetiology
There are diverse aetiologies to AKI, usually classified as prerenal, intrinsic renal
and post-renal (Box 9.1). In surgical patients, prerenal failure is the most common
aetiology (75%), followed by intrinsic renal and post-renal (20% and 5%, respectively).

In prerenal aetiologies, the kidney is structurally and functionally intact but blood flow,
and GFR is reduced. This is a reversible state if treated urgently, but it can progress to
acute tubular necrosis (ATN) in hours.

The renal vasculature, glomerular and tubulo-interstitium may all be affected in

intrinsic renal damage. ATN also results from a combination of ischaemic and
nephrotoxic injury. Post-renal failure results from obstruction and back-pressure,
which disturbs tubular function. Relief of obstruction enables urine to flow, but tubular
function may be disturbed during the recovery period.

In some people with certain genotypes, normal renal function may be restored more
rapidly because some cells aestivate, ie they effectively shut down with hypoperfusion
but maintain their microanatomical architecture throughout the period of AKI.

Table 9.1  Acute kidney injury classification: the AKIN criteria

Stage GFR criteria Urine output criteria
1 Increase in creatinine > 26.4 μmol/L or 1.5- to 2.0-fold from baseline < 0.5 ml/kg/h over 6 hours
2 Increase in creatinine 2- to 3-fold from baseline < 0.5 ml/kg/h over 12
hours
3 Increase in creatinine 3-fold from baseline or serum creatinine < 0.3 ml/kg/h over 24
> 354 μmol/L hours

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Box 9.1  Common causes of AKI

Prerenal

• Hypovolaemia
• Sepsis
• Low cardiac output

Intrinsic renal

• Acute tubular necrosis

• Ischaemic injury – hypoxia, hypoperfusion
• Nephrotoxic injury – endotoxins, drugs, contrast, pigments
• Abdominal compartment syndrome
• Hepatorenal syndrome

Post-renal

• Bladder outflow obstruction

• Bilateral ureteric obstruction

Management of renal dysfunction

In surgical patients, there are four common scenarios regarding renal dysfunction:

n an elective patient at risk of AKI (with or without pre-operative chronic renal

impairment);

n AKI in a critically ill patient;

n a patient with established AKI;

n a patient with chronic kidney disease (CKD).

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Preoperative management and prevention of renal dysfunction:

predict and protect
It is essential to identify patients at risk of developing perioperative renal dysfunction,
particularly those with pre-existing renal impairment. Common causes of CKD include
hypertension, diabetes, renal artery stenosis, glomerulonephritis and long-term use of
drugs, eg diuretics, ACE inhibitors, non-steroidal anti-inflammatory drug (NSAIDs or
aminoglycoside).

In the case of patients scheduled to undergo elective procedures, it is sometimes

prudent to delay surgery, investigate the cause of pre-existing renal impairment
and look at measures to protect renal function, including a review of drug therapy
and considering the effect of nephrotoxins such as contrast media. Relevant
investigations may include urinalysis, renal ultrasound and more detailed tests of split
renal function, such as a MAG3 scan, although this is usually reserved for patients
in whom nephrectomy is being contemplated. It is worth seeking the opinion of a
renal physician at an early stage. Ensure optimum perioperative fluid balance and
optimise the patient’s cardiovascular status, especially in terms of volume, avoiding
hypotension and hypovolaemia. Diabetes should also be closely monitored and
controlled.

In the emergency setting, strict attention to fluid balance and maintenance of

optimum cardiac output is essential, as is further avoidance of renal insults,
including nephrotoxic drugs, and aggressive management of any sepsis. It is often
a combination of factors that tip a patient into renal dysfunction, in particular the
combination of hypovolaemia, nephrotoxic drugs and sepsis, rather than one specific
insult. In both the elective and emergency setting, patients at risk should be reviewed
regularly.

Management of acute kidney injury

Management involves the three-stage CCrISP assessment protocol, with particular
attention to:

n recognition and correction of respiratory and circulatory problems;

n immediate identification and management of any life-threatening consequences of

renal impairment;

n exclusion of urinary tract obstruction if anuric;

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n careful search for, and correction of, the underlying cause;

n help early from appropriate specialists.

Case scenario 9.2 

A 45-year-old previously healthy woman presents with jaundice and cholangitis.
She has a pyrexia (38.4°C) and a tachycardia (115 bpm) but is normotensive. She
is treated with intravenous antibiotics and fluids and her condition improves.
An urgent ultrasound scan suggests stones in the common bile duct. She is
scheduled to undergo ERCP later in the week.

ERCP proves difficult and adequate drainage of the common bile duct is not
achieved. External biliary drainage (EBD) is scheduled for the following day but,
12 hours after ERCP, the patient becomes hypotensive and pyrexial. The serum
amylase and radiography are normal. Treatment is started with oxygen, and
intravenous fluid challenges and intravenous antibiotics are continued. She is
transferred to the HDU and a CVP line inserted (> 10 mmHg). The blood pressure
is restored but the urine output remains poor and by the following morning
the urea is 25.7 mmol/L and creatinine 229 µmol/L. The patient is not on any
nephrotoxic drugs.

It is clear that definitive treatment in the form of biliary drainage is needed

urgently. Emergency EBD is arranged for later the same day. The EBD is
performed by a consultant radiologist with an anaesthetist and an HDU nurse
in attendance and with appropriate monitoring. Successful biliary drainage is
achieved but the patient requires several days of haemofiltration. She eventually
makes a slow, but full, recovery, followed by successful ERCP and, subsequently,
elective laparoscopic cholecystectomy.

Learning points 
• Multiple factors often contribute to AKI in surgical critical care – biliary
obstruction, sepsis and hypovolaemia are a potent combination.
• Patients with obstructive jaundice tend to be hypovolaemic and need
adequate fluid therapy and clinical monitoring.

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• Procedures such as ERCP and EBD can exacerbate hypovolaemia or sepsis

in a number of ways and adequate periprocedural antibiotics and intravenous
fluids are needed in such cases – they are easily overlooked.
• Timely, definitive treatment of the underlying cause is usually the key to
success.

Practice point 
Complete anuria means lower urinary tract/catheter obstruction until proven
otherwise.

Patient assessment
An accurate history is essential, supplemented by information available from relatives,
the patient’s GP and the case notes. A note should be made of any factors that
predispose the patient to increased risk of renal failure.

Frequently, there are no specific symptoms associated directly with AKI. Uraemic
symptoms, commonly seen in CRF (such as anorexia, nausea, vomiting and itching),
are rare. Signs caused by the uraemic state, particularly fluid overload and pulmonary
oedema, may be attributed to other clinical problems, especially in the patient with
multi-organ failure. A thorough systematic examination is essential to identify any
subtle signs of underlying disease, such as skin lesions in vasculitis, enlarged prostate
and/or bladder and polycystic kidneys.

A thorough and repeated assessment of intravascular volume should be performed.

This can be difficult in the critically ill patient, who may have adequate or excessive
fluid but in the wrong compartment. The signs of hypovolaemia should be revised,
but note that hypovolaemia can exist in the presence of normotension and significant
extravascular oedema. Fluid overload may lead to an elevated blood pressure and
a raised JVP/CVP. Extravascular fluid overload may manifest as peripheral and
pulmonary oedema, ascites and effusions.

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Investigations in acute kidney injury

Dipstick urinalysis is mandatory in renal dysfunction. Marked proteinuria or
microscopic haematuria with casts suggests a primary renal insult. Urine biochemistry
and microbiology should also be considered, with biochemistry sometimes helping to
distinguish between prerenal and intrinsic renal failure (see below). A renal ultrasound
scan is also mandatory in any anuric patient. This should be performed immediately
in an anuric patient, if an obvious urinary tract obstruction is not detected clinically.
Ultrasound will also provide information regarding renal size and blood flow.

Plain abdominal X-ray is rarely useful, but plain chest X-ray can reveal pulmonary
oedema. Further radiological investigation should be ordered only after discussion
with your seniors, as it will often entail a contrast load and further renal insult for the
patient. CT is the most useful investigation, along with radionucleotide studies, in
identifying problems with renal blood flow, renal function and obstruction.

Blood tests should be considered to complement routine biochemistry depending on

the clinical scenario (Box 9.2).

Box 9.2  Blood tests to complement routine biochemical

analysis
• FBC: to detect anaemia, infection
• Routine biochemistry: urea, creatinine; check potassium
• LFT: to recognise hepatorenal syndrome
• Calcium phosphate: if associated malignancy, rhabdomyolysis or tumour lysis
suspected
• Creatine kinase: to detect rhabdomyolysis
• C-reactive protein: as a measure of infection and/or inflammation
• ABG and lactate: to assess hypoxia, acidosis and tissue/organ ischaemia

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Treatment
Look for a reversible cause and act urgently to:

n restore and maintain renal perfusion;

n relieve any obstruction;

n oxygenate the tubules;

n remove/avoid toxins;

n identify and treat any underlying cause.

Checklist

Is it prerenal?

Consider the clinical scenario. Surgical patients often become hypovolaemic, for a
variety of reasons. Often, oliguria can be corrected by restoring volume.

Distinguish prerenal from intrinsic renal problems due to ATN

Classically, with prerenal pathology, the concentrating ability of the tubular system
is retained, producing urine with high osmolarity, high urea and creatinine and low
sodium concentration. ATN results in a low osmolar urine with high sodium and low
urea/creatinine is produced (Table 9.2). Note there are many confounding variables
and, in clinical practice, the full biochemical analysis is rarely performed as a routine.

Table 9.2  Urine values in prerenal and intrinsic renal failure

Investigation Prerenal Intrinsic renal
Urinary specific gravity > 1.020 < 1.010
Urinary sodium (mmol/L) 10–20 > 20
Urinary osmolality (mosmol/L) > 500 < 350
Urine/plasma osmolality ratio > 2 < 1.1
Urine/plasma urea ratio > 20 < 10
Urine/plasma creatinine ratio > 40 < 20
Fractional sodium excretion < 1% > 1%
Renal failure index < 1 > 1
Note that: fractional sodium excretion = (urine/plasma sodium ratio)/(urine/plasma creatinine ratio) × 100, and
renal failure index = (urine sodium)/(urine/plasma creatinine ratio).

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Restore renal perfusion with volume

Aim to restore euvolaemia (using balanced salt solutions) and ensure regular
monitoring of cardiovascular parameters, including urine output. Once the patient
is euvolaemic, give maintenance fluid to match urine output and any on-going
hourly losses. If circulating volume is not rapidly restored, invasive cardiovascular
monitoring may be required. This may include central venous access and inotropic/
vasoconstrictor support.

There is no significant evidence to support the use of diuretics or ‘low-dose’

dopamine in the prevention or treatment of renal impairment.

Exclude post-renal obstruction

Exclude post-renal obstruction with ultrasonography and treat accordingly.

Distinguish between acute and chronic renal problems

Ultrasound may reveal small kidneys (< 9 cm) with echo-bright parenchyma,

suggesting chronic damage. The acutely injured but normal kidney will be echo bright
due to oedema, but will be of normal size and is more likely to recover. Acute on
chronic renal failure is much less likely to recover.

Oxygenate the tubules

Give oxygen and maintain a saturation of greater than 94%. Also ensure that the Hb
level is greater than 70 g/L.

Exclude toxins

Review the drug chart and avoid nephrotoxins, including contrast medium. Common
examples are aminoglycosides, NSAIDs, ACE inhibitors and β-blockers (because
of their hypotensive effect). When renal function is impaired, the dose of any drug
excreted by the kidney, eg opioids, must be altered to prevent toxic side-effects. This
is often overlooked on surgical wards. If in doubt, ask a pharmacist. Test for pigments
such as myoglobinuria and haemoglobinuria where appropriate.

Rhabdomyolysis is the breakdown of damaged muscle with release of myoglobin into

the circulation. This commonly occurs following crush injuries or acute limb ischaemia
and is also recognised after prolonged surgery or immobility. Myoglobinuria manifests

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as dark-brown urine that tests positive for myoglobin on urinalysis. Treatment includes
aggressive volume expansion and sodium bicarbonate to alkalinise the urine, creating
a diuresis and limiting the negative effect of acid breakdown products of myoglobin
on renal tubules. This is successful only if the condition is recognised early and
treated immediately.

Management of established AKI

Indications for dialysis

If acute kidney injury fails to respond to the above measures, renal replacement
therapy (RRT) will be required. The indications for RRT are summarised in Box 9.3.

Box 9.3  Indications for renal replacement therapy

Absolute

• Refractory hyperkalaemia (> 6 mmol/L)

• Refractory pulmonary oedema and fluid overload
• Uraemic encephalopathy

Relative

• Acidosis (pH < 7.2)

• Uraemia
• Pericarditis
• Toxin removal

Haemodialysis
Haemodialysis is a process by which low-molecular-weight solute equilibrates
between a blood compartment and a dialysate compartment separated by a
semipermeable membrane. Solute waste moves across the membrane down a
concentration gradient (Figure 9.3a). The dialysate contains normal solutes, including

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sodium, calcium, magnesium and chloride, in the appropriate concentration to

maintain normal levels. Dialysis can be intermittent or continuous. Intermittent dialysis
creates rapid changes in plasma osmolality and volume, making continuous methods
preferable in critically ill patients.

Haemofiltration
In haemofiltration, there is a continuous convection of molecules across a permeable
membrane (Figure 9.3b). The fluid that is removed is replaced with a buffered
physiological solution. This is more effective in removing large quantities of fluid,
but not as effective as dialysis at clearing smaller molecules. Filtration is usually
performed using a continuous veno-venous method (ie continuous veno-venous
haemofiltration, CVVH). This method provides the least risk of significant intravascular
fluid shifts and haemodynamic instability and is therefore frequently the method of
choice for providing renal support to patients in ICU.

(a)
Blood
flow

Dialysate
flow

(b) Replacement
fluid
Blood
flow

Filtrate

Semipermeable membrane
Concentration of solute

Figure 9.3  (a) Dialysis. (b) Haemofiltration.

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The threshold for RRT in uraemia is controversial and relates to the rapidity of rise
as well as the absolute level of urea and the presence of symptoms. A rise above
35 mmol/L unresponsive to other therapies is usually an absolute indication. RRT can
be performed by dialysis or haemofiltration, depending on the clinical circumstances.

Management of life-threatening complications

Hyperkalaemia
Acute hyperkalaemia (K+ above 6.5 mmol/L) requires immediate treatment to prevent
life-threatening cardiac dysrhythmia and VF/asystolic arrest. Rate of rise is also
important: a rapid rise to 6 mmol/L is equally a cause for concern. There are usually
no symptoms specific to a rise in potassium and clinical suspicion in the vulnerable
patient is crucial.

Any underlying contributory cause should be identified and stopped, including

blood transfusions, drugs that reduce renal potassium excretion (potassium sparing
diuretics, ACE inhibitors, etc) or intravenous fluid containing potassium and potassium
supplements.

An ECG should be performed. Hyperkalaemia may cause peaked T waves, absent P

waves, widened QRS and ventricular arrhythmias. In the presence of ECG changes
and a potassium above 6mmol/L, emergency measures should be instituted to reduce
K+ levels temporarily, though this will only shift the potassium into the intracellular
space. Immediate measures include (also see Table 9.3):

Table 9.3  Emergency therapy for hyperkalaemia

Drug Mechanism of action Pros and cons
Calcium gluconate IV (10–30 ml of 10% Membrane stabilisation Rapid effect but transient action
solution)
Insulin/dextrose [insulin (10–20 U of Drives potassium into cells Rapid effect, intermediate action but
Actrapid) in 100 ml of 20% dextrose IV may cause hypoglycaemia
over 30 minutes]
Sodium bicarbonate (50 mmol IV over Transfer of potassium Rapid effect – intermediate action,
5–10 minutes followed by IV infusion of into cells by exchange for best with metabolic acidosis; beware
1.26% or 1.4% solution at 100 ml/h) hydrogen across membrane sodium overload
Salbutamol (5–10 µg/min by IV infusion, Transfer of potassium into Rapid effect, short action; risk of
or nebulised) cells tachycardia, vasodilator effect,
frequent use can raise serum lactate

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n commencing continuous cardiac monitoring;

n insulin (10–20 units of Actrapid) in 100 ml 20% dextrose intravenously over 30

minutes;

n sodium bicarbonate 50 mmol intravenously over 5–10 minutes;

n 10% calcium gluconate intravenously (10–30 ml);

n β2-agonist, eg nebulised or IV salbutamol.

If, after emergency treatment, renal function is not improving, treatment should
be introduced to reduce total body potassium. This can be achieved by (i) renal
replacement therapy (particularly if combined with fluid overload); or (ii) ion exchange
resin (in the form of calcium resonium, 15 g 6- to 8-hourly or 30 g rectally (this binds
potassium within the gut but is very unpleasant to take and is of limited benefit).

Pulmonary oedema
Pulmonary oedema presents as acute shortness of breath, associated with anxiety,
tachycardia, tachypnoea, cool peripheries, and widespread crepitations/wheeze. If
pulmonary oedema is suspected, a chest X-ray should be performed immediately (if
safe to do so). Sit the patient upright, stop all intravenous infusions, give high-flow
oxygen and monitor saturations with a view to achieve SaO2 of greater than 94%.
Further treatment options include:

n intravenous diamorphine 2.5 mg for vasodilatory and anxiolytic effects;

n intravenous GTN infusion, if systolic BP is greater than 100 mmHg: commence

infusion at 2 mg/h and titrate upwards every 15 minutes;

n intravenous furosemide, 250 mg in 50 ml saline over 1 hour;

n review regularly;

n discuss higher level of support, particularly in the presence of oligo/anuria,

continued tachypnoea (> 30/min), signs of fatigue, respiratory failure (PaO2 < 8 kPa,
PaCO2 > 7 kPa), acidosis (pH < 7.2).

CPAP can also be helpful in treating pulmonary oedema.

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Checklist when making a nephrology referral

Expect to answer the following:

n Clinical scenario – what do you think is going on?

n What is the patient’s premorbid state?

n What are the most recent creatinine, serum potassium and ABG results?

n What is the patient’s volume and cardiovascular status?

n What volumes of urine is the patient passing?

n What was the ‘pre-insult’ renal function?

n What does the ultrasonography show?

n What drugs is the patient on (in particular have they received any nephrotoxins)?

Prognosis and recovery

As individual nephrons recover, the kidney behaves as in CRF. Because only a
proportion of the nephron mass has recovered, each nephron has a much higher
solute load to excrete. There is, therefore, a major limitation in the kidneys’ ability to
conserve sodium, potassium, bicarbonate and water. With modern management of
renal dysfunction, it is unusual to see major problems with large fluid and electrolyte
losses. The major exception is in postobstructive diuresis, when losses need to be
measured and replaced as appropriate. It is important that the recovering kidney is
not exposed to further hypotensive or nephrotoxic insults. By 6 months, the kidney
will normally have recovered 85–90% of premorbid function, though some 10% of
patients may progress to CRF requiring permanent RRT or transplantation.

Prognosis is often determined by the severity of the underlying incident that caused
the injury. However, in-hospital AKI due to ATN carries 20–30% mortality, most
commonly due to infection or cardiovascular complications.

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Case scenario 9.3 

You are asked to see a 75-year-old hypertensive diabetic woman on the ward
who had a reversal of Hartmann’s procedure 2 days ago. Her observations reveal
a BP of 110/70, pulse 100 bpm, temperature 37.8°C, O2 saturations 89% (on air)
and urine output of 20 ml for the past 3 hours. Her blood tests this morning are
available: Hb 101 g/L, urea 8 mmol/L, creatinine 123 μmol/L, Na+ 130 mmol/L,
K+ 5.0 mmol/L.

What are your priorities and what other information do you want to
know?

• Follow the CCrISP three-stage assessment, in particular with regard to

assessing the renal dysfunction. This patient is unstable and careful monitoring
is required. She may be developing AKI.

• Oxygenate the tubules by sitting the patient up, administering high-flow oxygen
and instituting continuous O2 monitoring.

• To restore renal perfusion, you should prescribe fluid challenges. You do not
want the patient to develop pulmonary oedema, so use smaller volumes over
short time periods, eg 500 ml of normal saline over 15 minutes, then reassess.

• Review drugs for nephrotoxins. Stop any ACE inhibitors or NSAIDs.

• You need to know the preoperative blood pressure and serum creatinine,
weight of the patient, plus fluid balance since surgery on chart review.

• Your plan should include regular observations (every 30 minutes), aiming for a
systolic BP of 130–140 mmHg, BP < 100 bpm, SaO2 > 94%, RR 12–15/min, and
urine output of 30 ml/h. Set a time for review in 1–2 hours.

After the fluid challenge, you find that the patient’s blood pressure has improved
and systolic pressure is now 140 mmHg, which is good for renal perfusion,
although urine output is still poor at 20 ml in 2 hours. Her SaO2 is 94% on
supplemental oxygen and, worryingly, the respiratory rate has risen to 24/min.

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How would you manage this situation now?

The findings are compatible with the development of pulmonary oedema and
you should reassess the patient. You should consider stopping further fluid
challenges, and arranging a chest X-ray and ABGs, re-checking biochemistry.

The chest X-ray shows interstitial oedema, and ABG analysis reveals an acidosis
(pH 7.25, PaO2 9 kPa, PaCO2 4.5 kPa, BE –5 mmol/L, lactate 2 mmol/L) and the
biochemistry is worse (urea 12 mmol/L, creatinine 148 μmol/L, Na+ 129 mmol/L,
K+ 5.9 mmol/L).

What is your assessment? What should you do?

It looks as though the patient is developing pulmonary oedema (interstitial

oedema, hypoxaemia) and established acute kidney injury (creatinine and K+
rising, metabolic acidosis). She needs a higher level of care than can be provided
on the ward. Discuss her organ failure and need for renal and respiratory support
with the critical care team.

Learning points 
• Predict and prevent renal dysfunction by identifying the surgical patient at
risk.
• Immediate management of AKI requires close attention to fluid balance while
recognising the risk of developing pulmonary oedema.
• Pulmonary oedema can be life-threatening and often requires a higher level of
care with respiratory and renal support.

Future developments
Creatinine and urine output are relatively insensitive markers of renal function and
hence new ‘biomarkers’ are being sought to identify and predict those at risk of
impending AKI. These include neutrophil gelatinase-associated lipocalin and kidney
injury marker-1.

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Chronic kidney disease

CKD is defined as chronic irreversible loss of nephron mass resulting in permanent
impairment of solute waste excretion. These patients do not necessarily need
permanent RRT. When using the Cockcroft–Gault formula to estimate the GFR, 5% of
the adult population will be found to have subclinical stage 3 CKD (a GFR 30–60 ml/
min). Such patients deserve special attention to detail in the perioperative period due
to:

n significant risk of developing AKI;

n multiple medications, especially cardiovascular drugs;

n concomitant silent cardiovascular disease;

n abnormal cardiovascular physiology, eg autonomic dysfunction reducing normal

response to volume changes, especially in diabetic patients;

n abnormal gastrointestinal function, delayed transit, impaired absorption;

n abnormal drug handling – impaired excretion requires dose modification; consult a

pharmacist.

Patients who have CKD have much less ability to compensate for circulatory stress
and the effects of nephrotoxins. A simple example is the patient with significant CKD
(creatinine of 300 μmol/L) who is fasted overnight prior to surgery. This will cause mild
intravascular volume depletion. As there are far fewer nephrons, each has to carry
increased solute, and this acts as an osmotic diuretic that prevents concentration of
the urine. This prevents maximum sodium and water retention until there has been
a significant fall in GFR secondary to a contracted circulating volume. The patient
becomes hypovolaemic and renal function decreases. Depriving patients with CKD of
oral fluid for lengths of time greater than 4–6 hours should be avoided unless fluid is
given intravenously.

Many patients with severe CKD will be chronically anaemic. Preoperative transfusion
will acutely impair renal function by altering the flow characteristics of the blood and
is seldom necessary.

Patients with a transplanted kidney must be managed in conjunction with their

nephrologist or transplant centre. Skilled assistance will be required to manage their
immunosuppression and reduce the likelihood of an acute rejection episode.

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Summary
Predict and prevent acute kidney injury, and remember the five points to consider in
the development of AKI:

n The kidneys cannot function without adequate perfusion.

n Renal perfusion is dependent on adequate blood pressure.

n A surgical patient with poor urine output usually requires more fluid.

n Absolute anuria is usually due to urinary tract obstruction.

n Poor urine output in a surgical patient is not treated initially with diuretics.

Further reading

Acute kidney injury

Bellomo R, Kellum JA, Ronco C. Acute kidney injury. Lancet 2012; 380: 756–766.

Mehta RL, Kellum JA, Shah SV et al. Acute Kidney Injury Network: report of an
initiative to improve outcomes in acute kidney injury. Crit Care 2007; 11(20): R31.

Chronic kidney disease

Plantinga C, Tuot DS, Powe NR. Awareness of chronic kidney disease among patients
and providers. Adv Chronic Kidney Dis 2010; 17: 223–236.

Fluid assessment/management
Powell-Tuck J, Gosling P, Lobo DN et al. British Consensus Guidelines on Intravenous
Fluid Therapy for Adult Surgical Patients (GIFTASUP). NHS National Library of
Health, London. Available at http://www.ics.ac.uk/downloads/ 2008112340_
GIFTASUP%20 FINAL_31-10-08.pdf.

Steddon S, Chesser A, Cunningham J, Ashman N, Oxford Handbook of Nephrology

and Hypertension, 2nd edn. Oxford University Press, Oxford; 2014.

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 10

Perioperative management
of the surgical site

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 Chapter 10  Perioperative management of the surgical site

Learning outcomes 
This chapter will help you to:

n utilise the CCrISP system to assess and manage patient problems associated
with the surgical site;

n discuss the presentation of common and/or serious complications in surgical

patients;

n contribute to planning the management of patients in the HDU or ICU;

n outline the management of surgical wounds, drains and stomas.

Introduction
Surgery is a significant physiological insult, especially when performed for a life-
threatening condition in a patient who is significantly unwell at first presentation.
Preoperative patient optimisation balanced against the need to correct the underlying
pathology in a timely manner is key to success. Likewise, in the period following
the procedure, it is essential to have a plan for on-going resuscitation and recovery,
which should be discussed prior to surgery with the relevant multidisciplinary team
members, including the anaesthetic consultant, critical care consultant and surgical
consultant. This discussion should include whether surgery has a realistic chance
of success, management of patient expectation and possible ceilings of care. The
patient (and his or her relatives if appropriate) should be involved in these discussions.

Even with all these factors in place there is a risk that complications may arise,
including infection, haemorrhage, ischaemia or incomplete resolution of the
original pathology. The challenge is to be able to recognise any deterioration early
and intervene before the advent of organ failure. In this way it may be possible to
avoid some critical care admissions but, if admission is unavoidable, the patients
are transferred as early as possible and in the best possible state to enhance the
chances of a successful outcome. While recognising physiological deterioration in
the immediate management phase, the history of the presentation or the operation
notes will give a better guide to a likely cause, and allow successful intervention if
events are predicted. The ability to anticipate problems is an important skill to acquire
(see Table 10.1), allowing earlier and targeted intervention and decreasing the chance

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Table 10.1  Examples of anticipated postoperative complications associated with initial presentation
Surgical presentation Potential postoperative complication
Infarcted bowel from intestinal Further ischaemia causing anastomotic breakdown, abscess/
ischaemia collection, fistula formation
Ruptured abdominal aortic aneurysm Open repair: reactive or secondary haemorrhage/abdominal
compartment syndrome/lower limb ischaemia/postoperative ileus
Endovascular repair: stent thrombosis and limb ischaemia/abdominal
compartment syndrome/renal impairment
Diverticular abscess and systemic Anastomotic leak and recurrent sepsis. Intraperitoneal abscess
sepsis Any inotropic support will increase risk of anastomotic leak or end
stoma infarction
Penetrating abdominal trauma Increased risk of sepsis/need for laparostomy if regular relook
laparotomy required
Risk of abdominal compartment syndrome
Appendicitis Wound infection and abscess formation
Intraperitoneal pelvic collection
Any presentation with comorbid risk Consider these comorbidities and the complications which might occur
factors: age, obesity, smoking and related to these factors. Then refer to Chapters 16 and 17 for further
diabetes information

of deterioration. Operative mortality can be in excess of 50% among patients who

develop organ failure.

It is often difficult, when you are time pressed on a routine ward round, to assess the
surgical site properly on a ward or critical care area. However, it is the surgical team’s
responsibility to ensure that there is appropriate monitoring and a management plan
in place for all patients. This includes all components of the surgical site, including
wound management and plans for drains, stomas or fistulae.

Practice task
Reflect on your last major operation. Consider what the potential complications
were, and how they may have presented. If the patient did experience
complications, what could have been done to prevent them?

Postoperative assessment of the surgical site

The end of an operation is equivalent to the ‘decide and plan’ component of the
CCrISP assessment system. The desired outcome would be for the patient to be
stable and progressing safely with a structured management plan in place.

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That plan begins with the operation note, which should clearly document the
indication for the procedure and the essential findings. The operative procedure and
any difficulties encountered should be described, as this may assist others when
assessing any subsequent deterioration in the patient. For example, a long dissection
for dense adhesions may have resulted in an unrecognised enterotomy, and repairs
to serosal tears may give way. An operative diagram is often helpful to describe the
internal and external anatomy, as well as representing the position of drains and
stomas. Clear postoperative instructions must be written, especially with regard to the
frequency of observations, when the next blood tests should be done, management
of drains or stomas, when or how to start feeding, plans for mobilisation and any
tasks or issues specific to the case (see case scenario 10.1).

In addition, a description of anticipated complications or the warning signs indicate

the need for prompt surgical review at an appropriate level, will prevent delay in the
identification of deterioration, especially if the patient is admitted to the ICU or HDU.

When you are asked to assess the postoperative patient outwith your usual schedule
of reviews, it is likely that they are deviating from their predicted course. From your
knowledge of the preoperative presentation, such as the examples in Table 10.1,
you should have suspicions of potential complications. However, you must use the
CCrISP system of assessment to guide your management and prevent omissions;
do not jump to conclusions and do not try to fit the findings to one of the known
complications. If you are unsure of the cause, the three-stage assessment system will
enable you to recognise if the patient is unstable or deteriorating, and help you to plan
if senior surgical or ICU review is necessary. This way you can be confident in your
findings and call for help as appropriate, and be clear about why you are asking for
help.

Anticipating a need for critical care

You should have observed that some patients are planned for critical care
preoperatively because of factors that predict a need for more intensive support, such
as:

n their age;

n critical nature of their diagnosis;

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n preoperative comorbidity;

n acute physiological stress.

Current guidance from the National Emergency Laparotomy Audit recommends the
completion of a postoperative assessment bundle to determine where the patient
should be cared for in the initial postoperative period.

Pre-emptive transfers allow for early recognition of any complication and so minimise
the delay in any additional treatment needed.

Recognising deterioration on critical care

The benefit of more intensive patient monitoring is the early recognition of systemic
changes, since these will raise a suspicion of new pathology developing, eg a rise
in serum lactate in a blood gas sample may raise suspicions of intra-abdominal
pathology and prompt intervention far earlier than waiting for the patient to develop
signs when the abdomen is examined.

While the abdomen alone may seem a likely source when deterioration occurs after
laparotomy, consider alternative causes such as sepsis from lines, urine or chest,
or limb ischaemia in a prothrombotic state. Information from critical care monitoring
can help you to work through these differentials. A missed intra- abdominal sepsis or
ischaemia is often fatal and if other causes for the deterioration are being considered
they have to be of sufficient magnitude to explain the deterioration – minimal findings
on clinical and radiological examination of the chest should not be ascribed as the
cause of major patient deterioration.

Practice task
Consider previous ICU patients you have seen with abdominal pathology. Were
there obvious abdominal signs or did you rely on the charts to identify clinical
deterioration?

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Assessing the abdomen on critical care

Often clinical abdominal signs are unreliable in the ventilated or sedated patient and
in the presence of a large laparotomy wound. It is easy to be lured into a false sense
of security because the abdomen feels soft and non-distended; conversely, in non-
ventilated patients, it is easy to overinterpret tenderness and guarding.

Careful analysis of the patient’s observation charts, taking into account the degree of
support the patient is receiving, will help you recognise whether the patient is making
progress or deteriorating. For example, the charts may show a gradual increase in
oxygen or ventilatory requirements, or an increasing dependence on inotropes to
maintain perfusion. The urine output may be gradually diminishing despite adequate
fluid filling.

Practice point 
Think of patients you have seen that have demonstrated features of deterioration.
Was there a concern about reoperating, or a delay in return to theatre?

Patients’ transport to theatre is often delayed by subtle and gradual clinical

deterioration. Close liaison and good communication with the critical care team is vital
in these circumstances if patients are to have good outcomes.

While it may be the systemic signs that show the patient’s deterioration, the
diagnostic question is whether this is due to bleeding, perforation, mesenteric
ischaemia, pancreatitis or sepsis, and where the source might be. Within the
abdomen there may be the temptation to confirm the diagnosis with imaging, but one
should carefully appraise the benefits of this as opposed to direct intervention with a
laparotomy. If a colonic anastomotic leak is suspected, abdominal and pelvic CT may
be useful. It may reveal pathology that can be treated without further surgery; for
example, it may reveal a collection that can be treated by radiological drainage. A
negative scan does not exclude a leak completely, and the delay caused by transfer
to and from the CT scanner should be weighed against the benefit of rapid drainage
from an immediate return to theatre. The possibility of false-positive findings also
need to be considered and imaging should be performed only if it will alter
management, not to justify a decision that has already been made. Ultrasound

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scanning may show free fluid but will rarely result in a change in management;
ultrasound is of little value in excluding diagnoses. Simple blood tests, particularly the
white cell count and blood gases, may guide you towards a specific cause of
deterioration, as shown in Table 10.2. Take all possible cultures (blood, pus, urine or
sputum, etc) in order to direct therapy in the longer term. If you are not sure, seek
senior help and advice, do not just organise more tests. A major focus of specialty
training is to learn when decisions need to be made and who needs to make them.

In patients with more subtle postoperative changes, contrast CT arterial imaging may
Table 10.2  Warning signs of significant pathology
exclude an ischaemic cause. Isolating a focus of infection may require a white cell labelled
Warning sign Possible underlying surgically related causes
scan. However, in the case of acute deterioration there is no time to delay and a laparotomy
Neutropenia (neutrophil count < 1 × 10 /L) Overwhelming sepsis/profoundly impaired host response
9
may be indicated.
Grossly elevated WCC (> 20–25 × 109/L)
Sign of infarction, presence of a collection
Also
Occasionally, a laparotomy performed asoccurs
part post
of a splenectomy
diagnostic process in a deteriorating
Consider Clostridium spp. infection if associated diarrhoea
surgical patient will be negative. This does not necessarily mean that laparatomy was the
Metabolic acidosis, elevated lactate Tissue hypoperfusion from ischaemia or sepsis
wrong course of action, but delaying the patient’s return to theatre for a prolonged period
will invariably lead to a worse outcome.

Specific surgical site complications

Abdominal compartment syndrome

Abdominal compartment syndrome or the presence of elevated intra-abdominal
pressure is a significant cause of morbidity and mortality among critically ill surgical
and medical patients. As shown in Table 10.3, major systemic effects occur with a rise
in abdominal pressure.

Case scenario 10.1 

You are asked to assess a 45-year-old, 120-kg man on the ICU who underwent
laparotomy for blunt abdominal trauma 10 hours previously. There is concern
that, despite fluid resuscitation, he remains tachycardic and hypotensive. He is
still ventilated. You arrive on the ICU and the nurse asks: ‘Do you think he could
be bleeding?’

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How would you manage this situation?

This is a difficult and complex assessment, especially since the patient remains
ventilated. However, if you follow the CCrISP three-stage system, this patient
can be assessed thoroughly and systematically in a similar manner to the non-
ventilated patient (Figure 10.1). Your immediate management is as follows:

A: Intubated and ventilated.

B: ICU report increasing airway pressure required to ventilate. Inspired oxygen

unchanged.

C: HR = 120 bpm, BP = 90/60 mmHg, CVP = 12 cmH2O, though cardiac output is

reducing.

No external signs of continued haemorrhage. Minimal reduction in Hb from 95

to 86 g/L in the last 5 hours though patient has had transfusion of 4 units of
blood since theatre. Urine output in the last 7 hours was 200 ml.

D: Pupils respond appropriately. Patient is heavily sedated.

E: This patient is obese but you note that the abdomen appears distended.

The CCrISP® system of assessment

Immediate management
Investigations
Airway | Breathing | Circulation | Dysfunction of CNS | Exposure
Blood | X-ray

Specialist opinion
Full patient assessment
Nutrition
Chart review | History and systematic examination | Available results
Requirement | Route

Fluid balance prescription

Decide and plan
Oral intake
Unstable/unsure Stable

Drugs and analgesia

Treat condition | Prophylaxis | Comorbid disease

Diagnosis required
Daily management plan Physiotherapy
Chest | Mobility

Drains and tubes removal

Move to a lower level of care

Medical | Surgical | Radiological

CCrISP 4th edition © Royal College of Surgeons of England 2017 All rights reserved Registered Charity No. 212808 www.rcseng.ac.uk 4th edition
Figure 10.1  The CCrISP system of assessment.

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Is this patient stable or unstable and what would you do at this stage?

The patient is clearly unstable. You need to consider whether more resuscitation
is required or whether to call the surgical consultant for an immediate return to
theatre. It is reasonable to gather more information and continue with the system
of assessment while the ICU staff continue resuscitation. Using the CCrISP
system, you would perform a full patient assessment. The available results
are (all conventional units): Hb 86 g/L, WCC 18.9 × 109/L, platelets 65 × 109/L,
amylase 240 units/L, Na+ 128 mmol/L, K+ 5.9 mmol/L, urea 12.5 mmol/L, pH 7.3,
PO2 10.5 kPa, PaCO2 6 kPa, BE –7 mmol/L (increased from –3 mmol/L in last
3 hours). Chart review: the operation note reports the need for a splenectomy
and extensive bleeding from the vena cava (Figure 10.2). An important part of
this assessment is to clearly determine with the ICU staff whether the patient is
having to have a lot of volume to maintain perfusion and what happens when
boluses are given – repeated ‘chasing’ of volume may indicate on-going bleeding.

Does this help you make a decision? Consider what your management
plan would be and whether you need any other investigations

A simple investigation is to check intra-abdominal pressure, which is now

28 mmHg (it was previously 18 mmHg). Therefore, this patient has abdominal
compartment syndrome and should be immediately returned to theatre and
his abdomen reopened. Further delay increases the risk of worsening organ
dysfunction and further resuscitation or conservative measures will not be
beneficial without immediate decompression. The decision to return the patient to
theatre needs to be made by the surgical consultant in charge of the case; your
role is to recognise that a decision needs to be made, by whom, and that this
needs to be done without delay. In this case, the patient is returned to theatre and
laparotomy reveals no on-going haemorrhage and a viable colon so the abdomen
is left open as a laparostomy.

Consider the problems that might be encountered when the patient is

transferred back to ICU

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Learning point 
• Abdominal compartment syndrome can lead rapidly to multiple organ failure
which, without immediate decompression, is usually fatal.

Figure 10.2  Operation note.

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Intra-abdominal hypertension (IAH) is a continuum of pathophysiological changes that

begins with a disturbance of regional blood flow and culminates in frank end-organ failure,
due to the development of abdominal compartment syndrome. The aetiology of IAH may be
intra-abdominal, particularly in abdominal trauma patients (see scenario above), pancreatitis
or following aortic surgery, but can also occur due to an extra-abdominal cause, such as
burns or sepsis associated with aggressive fluid resuscitation.

Intra-abdominal pressure is expressed in mmHg, with the usual level being

subatmospheric to 0 mmHg, though elevation to the range of 5–7 mmHg is common.

IAH is a sustained or repeated elevation of IAP > 12 mmHg and is graded as follows:

I, 12–15 mmHg; II, 16–20 mmHg; III, 21–25 mmHg; IV > 25 mmHg. Grade IV requires
surgical decompression.

The cardiac effect of IAH is due to elevation of the diaphragm and the subsequent rise
in intrathoracic pressure, which in turn reduces the venous return and cardiac output.
Such changes are far more likely in the hypotensive patient and so early signs of
pressure elevation should be managed by fluid resuscitation.

Abdominal compartment syndrome is the progression of pressure induced end-organ

changes and, if due to intra-abdominal causes such as trauma or acute pancreatitis,
is characterised by rapid deterioration which if not recognised and treated is often
fatal.

The treatment for ACS is to re-open or perform a laparotomy wound in order to decompress
the abdomen. As in the scenario above, a thorough washout of all fluid/blood should be

Table 10.3  Systemic Effects Of Abdominal Compartment Syndrome

Intra-abdominal pressure
System 10–15 mmHg 16–25 mmHg > 25 mmHg
Cardiovascular Reduced preload and increased Reduced contractility
afterload Gross reduction in cardiac
Reduced cardiac output output
Renal Oliguria Anuria
Gastrointestinal Slight intestinal and hepatic Marked intestinal and hepatic Bowel infarction
ischaemia ischaemia Hepatic failure
CNS Minimal effect Increased intracranial
pressure

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performed, with a detailed inspection for sites of bleeding. The bowel should be carefully
inspected for signs of ischaemia.

There are a number of options available at the end of the laparotomy though, usually,
primary closure should not be considered. A large saline infusion bag can be opened
up and sutured to the fascial edges in order to provide a temporary seal of the
abdominal cavity (Bogota bag). Specific bowel bags can also be used in a similar way.
Other temporary abdominal closure devices are available, including topical negative
pressure systems and zippers. Leaving the abdomen open increases the risk of bowel
damage and fistula formation, and care needs to be taken in this respect. Figure
10.3 shows a laparostomy in a patient who later underwent successful split skin graft
closure.

Postoperatively, laparostomy patients can be challenging to manage, particularly

from the nursing point of view. As the surgeon, you should liaise closely with the ICU
staff and predict problems with fluid and temperature losses through the laparostomy
wound and the potential for sepsis, especially with respect to any underlying vascular
grafts, and make a plan to achieve wound closure.

Lower limb compartment syndrome

Limb compartment syndrome should always be considered when there has been a period
of ischaemia and perfusion. Case scenario 10.2 highlights the need for thorough systematic
assessment and prompt therapeutic action. A delay in recognising limb compartment
syndrome can rapidly lead to irreversible muscle damage, resulting in permanent
neuromuscular defects within 12 hours. This may necessitate amputations. Also, aggressive

Figure 10.3  A laparostomy and outcome following mesh closure and skin graft.

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Case scenario 10.2 

You are asked by the ICU staff to assess a 25-year-old man who, 14 hours
following laparotomy for a penetrating abdominal stab wound, is becoming
increasingly unstable with a base excess of –8 mmol/L. You follow the CCrISP
system to assess and resuscitate the patient. Your findings from the initial
management are:

A: Intubated.

B: Ventilated, parameters and oxygen requirement stable.

C: HR = 120 bpm; BP = 95/75; CVP = 6 cmH2O, cold peripheries, pedal pulses not

palpable, increasing dose of noradrenaline required, urine output 250 ml since
return from theatre.

D: Pupils respond appropriately. Patient is paralysed.

E: Abdominal wound is laparostomy, with appearance of right-sided stoma.

Full patient assessment of available results: Hb 90, WCC 24, platelets 75, amylase
200, sodium 130, potassium 6.5, urea 16, pH 7.2, PO2 12.5 kPa, PaCO2 5 kPa,
BE –8, lactate 5, creatine kinase 4000 u/L. Chart review showed the patient was
stabbed in the abdomen and suffered significant blood loss at the scene. He had
a systolic pressure of only 70 mmHg on arrival in the emergency department.
He was immediately taken to theatre, where laparotomy findings were a distal
aortic laceration and a small sigmoid laceration with minimal contamination. The
sigmoid laceration was closed primarily but defunctioning ileostomy performed.
Significant blood loss occurred before and during the aortic repair with repeated
episodes of clamping. It was a long procedure; therefore, abdominal packing was
inserted with a relook planned at 24 hours.

What do you think might account for the deterioration and how would
you manage the situation?

It is unlikely to be abdominal compartment syndrome because of the

laparostomy. You need to perform a thorough systematic examination, in
particular looking at the patient’s lower limb vasculature because of the history

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of aortic injury. Only femoral pulses are palpable; both feet are cold and poorly
perfused. From toes to knees, the calves are very swollen and tense. The patient
is clearly unstable and no further investigations are required to confirm the
diagnosis of bilateral lower limb compartment syndrome. Arrangements are made
for urgent fasciotomies to be performed. Upon performing the fasciotomies, all
muscle groups are very oedematous and immediately bulge from the wounds.
Some areas of muscle do not contract to electrical (diathermy) or physical stimuli,
though other areas contract normally.

fluid resuscitation is required to minimise the effects of myoglobin from muscle breakdown
that can cause acute kidney injury.

Lower limb trauma and associated hypotension may lead to reperfusion with a
significant rise in interstitial pressure and subsequent compartment syndrome.
Prolonged operation in the lithotomy position can also produce compartment
syndrome and any delay in treatment minimises the chances of limb salvage. If there
is any doubt in the diagnosis, compartment pressures can be performed with a needle
inserted into each compartment, with the knowledge that tissue necrosis can occur
with an interstitial pressure as low as 30 mmHg.

Practice point 
An old surgical adage is that if you are thinking of the need for fasciotomies, then
you should perform them without further discussion. If you think about it, you
should discuss it with an appropriate senior.

Compartments to decompress

The lateral compartment/superficial posterior/deep posterior and anterior

compartments of the leg all require decompression and this should be performed in a
sterile environment in theatre.

After the procedure, as a result of the muscle oedema, there will be a lot of fluid
discharge from the wounds. It is important that instructions for dressing are clear and

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that no compression should be applied to reduce blood or fluid loss from the wounds.
Occasionally, brisk venous bleeding can occur from the wounds that may require
further surgical exploration to control the source. Compartment syndrome can also
occur in the thigh and upper limb and the management principles are identical.

Burst abdomen
This complication is at the other end of the spectrum from compartment syndrome
though the immediate management is similar to a laparostomy, with the aim being
to keep the exposed viscera warm and moist and to minimise the loss of fluid and
temperature. When it occurs, it is usually heralded by the so-called ‘pink fluid sign’,
serosanguinous discharge, some 8–10 days after the initial surgery. If there were little
systemic upset, and the wound can be brought together without undue tension, the
abdomen may be resutured within 3–4 hours; however, if there is systemic instability,
it would be better to manage the wound temporarily as a laparostomy.

Postoperative bleeding
Despite anticipating bleeding problems, postoperative haemorrhage can be covert,
with the only sign being progressive haemodynamic deterioration. An example would
be after angiography with a high puncture of the common femoral artery, when a
retroperitoneal bleed is common. Consider this as a potential complication, so it can
be addressed with surgical correction if necessary.

Primary haemorrhage occurs at the time of surgery. If difficult to control – particularly

if from the liver, pelvis or other inaccessible sites – consideration should be given to
packing the affected area with a view to returning the patient to theatre at 48 hours for
removal of packs and reinspection of the operative site.

Reactive haemorrhage occurs in the immediate postoperative phase and may present
while the patient is in recovery or following return to the ward from theatre. Again,
this requires a thorough systematic assessment of the patient to ensure prompt
detection and return to theatre. As stated above, determining whether or not there is
on-going bleeding can be difficult. The way to do this is to give the patient serial fluid
challenges and make decisions based on the response. For example, if the patient
responds, give them maintenance fluids and observe closely. Further deterioration
may indicate on-going bleeding. This is a situation when more senior help should
be sought early. Examples include a short gastric ligature coming loose after

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splenectomy. Even though the vessels are small, this bleed can still cause a rapid
deterioration and cardiovascular compromise. Reactive haemorrhage may also occur
after fluid resuscitation in trauma patients as the increased perfusion pressure may
initiate bleeding.

Secondary haemorrhage occurs much later, often 7–8 days following a procedure. It is
often related to infective complications but still may be unexpected and unheralded;
control may be difficult to achieve. More proximal vascular control is often required
and should be considered at the time of reoperation.

Practice point 
Reversing a coagulopathy will not stop surgical bleeding. Correct the
coagulopathy while addressing the source of the bleeding.
Case scenario 10.2 continued 
You are asked to reassess the patient from case scenario 10.2, 4 hours after
he was returned to the ICU because of blood-stained fluid appearing in the
laparostomy bag and a 25 g/L fall in Hb (now 65 g/L compared with 90 g/L at the
time of leaving theatre).

How would you manage this situation?

This decision is often a difficult balance between returning the patient to theatre
and controlling coagulopathy. This decision should be made in collaboration with
the ICU staff. There are a number of factors that will predispose to coagulopathy,
including the massive blood transfusion, hypothermia and reperfusion injury.

Learning point 
A coagulopathy is common in critically ill patients and should be considered as
a cause of any overt or concealed haemorrhage. Any clotting problem should
ideally be corrected prior to reoperation, and this may require close collaboration
between surgeon, anaesthetist and haematology staff. Be careful not to ascribe
surgical bleeding to a general bleed associated with a minor coagulopathy, as
trying to correct the clotting will not improve the situation. Further delay may

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worsen the coagulopathy and cause a cycle of deterioration. It is better to control

the source and correct the coagulopathy in theatre.

Other factors to consider with generalised bleeding problems are:

• effect of anticoagulant therapy;

• a recent large transfusion;
• the presence of sepsis or disseminated intravascular coagulation;
• previously unrecognised concomitant bleeding disorders, either congenital
(eg Waldenström’s macroglobulinaemia) or acquired (eg drugs).

Necrotising fasciitis
Necrotising infection can be difficult to diagnose; early diagnosis and targeted
treatment is essential. Any diagnostic delay increases the mortality, which has a
range of 25–73%. Immunocompromised patients on chemotherapy or steroids are
vulnerable, but diabetes is the leading predisposing factor. The causative bacteria are
synergistic and cause an infection involving the subcutaneous fascial layer, inducing
extensive undermining of surrounding tissues. Presentation may be primary, in which
no portal of entry or causative factor is found, or secondary, due to a precipitating
event such as a perianal abscess.

The initial features may be subtle, including influenza-like symptoms and localised
discomfort or pain. Subsequently, the limb or painful area begins to swell and may
show a purplish rash. The skin marking will then blister with blackish fluid, and
patients undergo severe systemic collapse due to sepsis. The surgical treatment
required is prompt, aggressive debridement, with wide excision of all involved tissue
back to bleeding edges. This may be quite extensive, and can take more than one
operation. Patients usually require systemic support on critical care along with broad-
spectrum antibiotics and consideration of immunoglobulin therapy.

Anastomotic leakage
The signs of anastomotic leakage are of systemic instability with abdominal pain
and/or rigid abdomen, tachycardia and fever. However, there may be a far more

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insidious presentation with low-grade fever, a prolonged ileus or failure to thrive.

Therefore, anastomotic leakage should be considered as a cause for any unexplained
postoperative deterioration following bowel surgery in which an anastomosis has
been performed. It should be recognised that a defunctioning stoma does not exclude
the possibility of an anastomotic leak; the presence of the stoma does not change the
leak rate and the intention is to minimise the consequences of a leak.

In trying to anticipate anastomotic leakage, it is important to review the notes and the
charts. For example, does the anaesthetic chart indicate preoperative dehydration
or any episodes of perioperative hypotension? Does the operation note comment on
the quality of perfusion in the mesenteric vessels? In an emergency case, does the
chart show that inotropes/pressors were required, that may have caused mesenteric
vasoconstriction? Factors that predispose to leak are shown in Box 10.1.

In trying to make the diagnosis of a leak, CT and contrast enema may have a
complementary role, though CT with intravenous contrast is the radiological
procedure of choice. If a collection is shown indicating a localised leak, CT- or
ultrasound-guided drainage may be a therapeutic option. Major leakage has
a significant mortality (10–15%) and so prompt reoperation is indicated with
exteriorisation of suitable ends of small and large bowel. At this time, the need for
nutritional support and the potential routes of access should be considered.

It is important to anticipate the difficulty of reoperative surgery on critically unwell

patients and follow the principles shown in Box 10.2. A senior surgeon should be
involved early in the decision-making, and in the surgery, together with a consultant
anaesthetist.

The management of intestinal fistulae

The development of an intestinal fistula poses significant management challenges,
which are likely to require high-dependency care even if there is no complicating
infection or sepsis. The management involves the monitoring of significant fluid and
electrolyte losses and their subsequent replacement along with nutritional therapy.
Also involved is the physical management of the fistula; the surrounding skin requires
protection by dressings or bags, and this will require the input of the stoma therapist.

When a fistula occurs postoperatively, assess by the CCrISP protocol and then utilise
the ‘SNAPS’ (sepsis, nutrition, anatomy, procedure, skin care) protocol.

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Box 10.1  Risk factors for intestinal anastomotic leakage

Anastomotic technique

• Tension, poor anatomical blood supply (particularly after anterior resection),

unrecognised mesenteric vessel damage, poor suture technique (eversion or
mismatch)

Local factors

• Obstruction, ischaemia or peritonitis

Systemic factors

• Shock (excessive bowel preparation or excessive blood loss), age, malnutrition,

immunosuppression

Box 10.2  Principles of reoperative surgery for abdominal sepsis

• Prepare the patient as well as possible
• Involve a senior surgeon as early as possible in the patient’s management
• Aim to deal with the source of the primary problem definitively
• Exteriorise leaking bowel
• Remove dead tissue
• Culture pus and drain sepsis
• Consider gastrostomy or jejunostomy for ease of future management

S Sepsis Obtain adequate drainage

May involve CT-guided or surgical drainage
May involve defunctioning of the bowel

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N Nutrition Provide nutritional support

Often this will be parenteral
A Anatomy Delineate by imaging the site of leak
CT with contrast is preferred choice
P Procedure Ultimately aim for reparative procedure
Delay until patient is well enough that success is likely (this may
be months)
S Skin care Determine what is coming out of the fistula and protect the skin
accordingly
Involve the stoma care and tissue viability teams

Management of stomas and drains

There are various stomas that may form a part of the postoperative management of
patients. Both on the ward and in critical care areas, this should be directed by the
surgical team with the support of the stoma care nurse, or nutritional support team in
the case of feeding stomas.

Case scenario 10.3 

Consider the surgical patient in case scenario 10.1, who developed a
compartment syndrome and required urgent laparotomy. The abdomen was
washed out and closed primarily at 48 hours with a large-bore drain inserted
via the left iliac fossa along the paracolic gutter into the splenic bed. The drain
produces 50 ml of haemoserous fluid for 48 hours; however, before it can be
removed it suddenly drains 300 ml of similar fluid.

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How would you manage the patient? Could this be a fistula and if so
what is the potential source?

Use the CCrISP system with simultaneous assessment and resuscitation.

Following immediate management, you decide that the patient is stable and
proceed to the full patient assessment. On review of the operation note, you
should note the gastric repair and the splenectomy, and consider a missed injury
to the pancreas or small bowel, or a leak from the gastric repair.

A pancreatic fistula (remember to send the draining fluid for an amylase level)
may cause further problems due to the digestive actions of the pancreatic fluid,
with concern for the various sites of surgical repair. A high small bowel fistula
can cause high volume losses of fluids and electrolytes and rapid changes to
acid–base balance. The initial fluid from a fistula can often be serosanginous
and change to obvious faecal or small bowel content in the next 24 hours. These
are complex problems and it is important to recognise them early. A diagnosis
is essential and, while testing the fluid for amylase may suggest a pancreatic
fistula, further radiological investigation is likely to be required, including contrast-
enhanced CT. Having made a diagnosis, the SNAPS protocol should be used to
manage the patient. Specialist senior help should be enlisted for the management
of intestinal fistulae.

Feeding gastrostomy or jejunostomy

The timing, content and volume of nutritional support should be planned depending
on bowel function with the surgical team liaising with the dietitian or nutritional
support team (see Chapter 13).

There must be clear advice given on timing of removal and obvious marking of the
feeding stoma to prevent accidental removal if mistaken for a drain. Ten days is
usually the minimum time required for an adequate seal to form.

Faecal stomas
These may be temporary, loop or end type, as shown in Figure 10.4; their
appearances are different, as are the difficulties in their management. Small bowel
effluent from an ileostomy will irritate the skin and so the stoma is formed as a spout,

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whereas a colostomy will be flush to the skin since the effluent is more solid and less
irritant. If a bridge is used for a loop stoma, the operation note should clearly state
how long it should remain.

Irrespective of type, if there is concern with respect to the stoma’s condition or

function it should be inspected, which will require:

n removal of the stoma bag;

n assessment of the colour/perfusion of the stoma and the contents of the bag (Is
the stoma functioning? is there any blood to indicate more proximal bleeding?);

n assessment of the skin around the stoma (Is there cellulitis or separation of the
stoma from the skin? is the stoma in close proximity to the wound giving risk of
contamination?);

n digital examination of the stoma (and the requirement for direct observation with a
proctoscope to determine the extent of any discoloration).

A complication of the stoma may lead to systemic deterioration; conversely, systemic

deterioration can lead to stoma deterioration.

The small bowel effluent from an ileostomy is usually 500–700 ml/day but, initially, on
starting to function, these volumes may be much higher, requiring careful electrolyte
monitoring and replacement.

It is important to involve a stoma therapist as early as possible, especially for skin

protection. The therapist also provides vital psychological support to the patients with
a stoma and, if possible, this meeting should occur preoperatively with marking of
potential stoma sites.

(a) (b)

Figure 10.4  (a) End colostomy. (b) Loop ileostomy.

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Management of surgical drains

There is a continued debate as to the value and usage of drains; nevertheless,
their presence in the critically ill surgical patient requires them to be assessed and
managed effectively and appropriately.

In the assessment of the surgical patient, the amount and type of drainage, and
whether that is expected, should be determined and documented. The drain site
should be inspected and notes reviewed to determine the nature and positioning of
drains, and the rationale for placement. Drains should be clearly marked if there is
more than one, and it is the surgeon’s responsibility to state when they should be
removed.

Post-surgical wound management

Surgical wound infections are a common hospital-acquired infection (~12%)
and are subsequently an important cause of morbidity and mortality. Therefore,
their prevention should be a primary management objective. The risk of infection
should relate to whether the surgery was clean, clean with risk of contamination or
contaminated. Prophylactic antibiotics should be used accordingly, guided by local
policy. Ensure good hand-washing before and after the assessment of wounds to
diminish the risk of direct contamination. The importance of environmental and hand
hygiene is often underestimated and you can provide clinical leadership and set a
good example.

A wound can be colonised by bacteria; there are bacteria present but there is no
host response. This situation does not necessarily need any intervention other than
considering the use of specific dressings, but be aware that the situation can progress
to frank infection with or without surrounding cellulitis. In accordance with the CCrISP
method of assessment, there should be a postoperative plan for all wounds, involving
observation for the early signs of infection of redness, swelling, heat and pain.
Depending on perioperative risk and/or the potential consequences of infection, the
patient may have had prophylactic antibiotics. This and any postoperative regimen
should be clear from a review of the charts. The majority of wounds are closed
primarily; however, it may be prudent to leave a wound open if postoperative infection
is likely. Collections of pus in the wound require adequate drainage rather than
antibiotics and this may be achieved by suture removal alone or may require a return
to theatre depending on the exact circumstances. Antibiotic usage should be reserved

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for the treatment of systemic disturbance or for the control of cellulitis. Empirical
treatment while awaiting culture results should be based on the underlying procedure,
not the site of the infection.

The timings of routine suture removal are a surgical decision and should be clearly
documented within any surgical management plan.

Summary
n It is sometimes difficult to assess the post-surgical patient, particularly on the ICU.

n The CCrISP process allows a structured assessment that will highlight the likely
cause of any deterioration.

n By assessing the risk factors, many surgical site complications can be anticipated
and prevented, or recognised early.

n Postoperative management plans should highlight which signs require early

surgical review, such as the increasing abdominal pressure that would trigger the
conversion to a laparostomy.

n There will always be surgical complications but the risk should be minimised and
problems should be recognised and managed promptly and effectively.

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Fluid and electrolyte

management

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Learning outcomes 
This chapter will help you:

n describe the principles of management of complex fluid balance in surgical

patients;

n avoid common pitfalls in fluid management in surgical patients;

n review water and electrolyte balance in the critically ill;

n manage common electrolyte abnormalities;

n list the properties of common intravenous fluids.

Assessing fluid balance and prescribing appropriate fluid is an important daily task for
surgeons. As the registrar, it will be often be your responsibility to ensure that this is
carried out safely and accurately. Do not delegate this task to junior members of the
team without providing adequate oversight and ensure that the prescription of fluids
in stable patients is performed by the owning team during the day and is not left to
the out-of-hours teams – this often leads to inaccurate prescribing and complications.
Conversely, do not attempt to write 24 hours’ worth of fluid in unstable patients as
predicting the circulatory status in such patients is not possible. In many surgical
patients, the process becomes potentially complex because of multiple sources of
fluid loss and several types of fluid input. However, with a logical approach and a clear
understanding of a few basics, even complex cases can be dealt with. Conversely,
poor prescribing remains a common cause of avoidable morbidity and mortality, from
either inadequate resuscitation of the critically ill or excessive provision of fluids to
elective patients.

Patient groups
All patients are a different. Fluid needs are determined by baseline needs (dependent,
in turn, on body weight), pre-existing fluid deficits and on-going abnormal losses.
However, in the majority of surgical practice, there are two differing groups of patients
who handle fluids differently. Patients may move between groups if complications
develop.

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Critical illness and emergency surgery

In critical illness, and after complicated major surgery, the obligatory extracellular
volume required to maintain adequate venous return to the heart rises as a result
of the loss of salt, water and protein into sites of tissue damage, obstructed bowel,
serous body cavities and the relaxation of the peripheral vascular bed. In some
situations, such as sepsis, the amount of sequestered fluid may be large, owing to
an enormous capillary leak, and sufficient to cause circulatory failure. This situation is
often seen in critically ill surgical patients. Consequently, it is reasonable to suspect
hypovolaemia in most patients and act accordingly.

Epidural anaesthesia causes vasodilatation, and this increased vascular space needs
filling either by means of fluid boluses as the epidural is established or, once the
patient is adequately filled, by controlling the degree of vasodilation by use of pressor
agents. This is particularly the case if the patient has also been cold after surgery and
experiences further vasodilation on warming up. In these patients, the commonest
error is fluid resuscitation that is inadequate in terms of volume, fluid type or rate of
delivery.

Uncomplicated elective surgery

Major but uncomplicated surgery produces a different situation. Surgery causes
activation of the antidiuretic hormone (ADH) and angiotensin–aldosterone, thereby
retaining fluids and causing reduced urine output for 24–48 hours. In a well patient
with otherwise normal parameters, isolated, modest oliguria can be acceptable. With
fast-track recovery programmes advocating early and liberal oral intake and less in
the way of bowel preparation (which dehydrates the patient significantly and causes
electrolyte disturbances), the elective patient is less likely to be volume depleted.
These patients often need less postoperative fluids. In these ‘well’ patients, excessive
fluids cause more harm than good. Excessive provision of sodium and water is now
recognised as the principal cause of avoidable problems, eg hyperchloraemic acidosis
from excessive saline administration. This is a very different set of circumstances to
the critically ill patient who frequently needs intravenous fluids rapidly for life-saving
resuscitation. Fluid resuscitation from shock using an appropriate crystalloid was
dealt with in the chapters on assessment and shock (Chapters 2 and 8).

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Clinical assessment
The patient should be fully assessed using the CCrISP system. Take particular
note of indices of volume status and perfusion, including vital signs, skin perfusion
as measured by capillary refill time and oedema (which appears on the sacrum if
bed-bound). Note the patient’s underlying age, BMI and lean body mass, general
condition, operative treatment and timing, comorbid diseases and drugs.

Along with clinical examination, the fluid balance chart is the principal mechanism
of assessment; however, their reliability is variable depending on the underlying
pathology and should be used only as a general guide. Analysis of the fluid balance
chart should be used in conjunction with the patient’s response to fluid challenges
to determine intravascular volume and cardiac filling. Insensible losses increase
markedly with fever, respiratory rate and the breathing of dry O2 – all of which can
apply in the day or two after major surgery. As much as 500–1000 ml can be lost daily.

No single formula can be applied to all situations; regular frequent clinical assessment
of the patient will be required to adjust the content and volumes of fluid replacement.
This should be done at least daily, more often in the unstable. Occasionally with
chronic overload, daily patient weighing, when feasible, can be of assistance and
complements the fluid balance chart.

Fluid compartments and control of volume

The total body water volume (~45 L) is distributed through the intracellular and
extravascular compartments in a ratio of 2:1 (Figure 11.1).

The total volume of water is controlled by both central osmoreceptors and volume
receptors that affect thirst and the release of ADH. Volume receptors will release
ADH even in the face of hyponatraemia and a low plasma osmolality. Extracellular
fluid (ECF) volume (of which blood volume is a special part) is maintained by the
presence of sodium and its accompanying anions which are largely excluded from
the intracellular compartment by the action of the Na/K pump. The body responds
rapidly to a fall in central volume or renal perfusion by reducing renal sodium excretion
to extremely low levels. There are two mechanisms for retaining water or sodium
rapidly. Excretion is more passive and often slower, so the response to surgical stress
favours fluid retention and overload. In critical illness this has some advantages, as

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Body weight
70kg

Total body water Fat, protein and mineral

60% = 42l 40% | 28kg

Intracellular Extracellular
66% = 28l 33% = 14l

Interstitial fluid Plasma

11l 3l

Figure 11.1 Fluid distribution in the body.

many of the effects of surgery cause fluid loss. When assessing patients, consider the
following:

n Assessment of fluid and electrolyte status requires both clinical and biochemical
examination.

n Intracellular volume is extremely difficult to assess clinically.

n The extracellular compartment is easier to assess clinically as increased salt and

water manifests itself as oedema and salt and water depletion by effects on the
circulation.

n The balance between blood volume and ECF is maintained by the oncotic
pressure and the relative leakiness of the capillaries.

n In haemorrhage, the plasma volume is partly replenished from the ECF.

n In sepsis, gross capillary leak and a low oncotic pressure contribute to oedema
and hypovolaemia.

Biochemical assessment
Clinical assessment is assisted by biochemical measurement, primarily of blood, but
also, on occasion, of urine and other fluid being lost from the body (eg fistula fluid).

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Water
Patients usually need 1500–2000 ml of water daily, depending on weight and fluid
status. The basal water requirement is 30–40 ml/kg/day.

Sodium
Normal basal requirements for sodium are 50–100 mmol/day but this can vary
considerably with surgical illness. Drug solutions, eg intravenous antibiotics, can
contain significant amounts of sodium. Care must also be taken to ensure that a false
value for sodium is not obtained by venepuncture from a limb with a running fluid
infusion or if there is frank lipaemia.

Hyponatraemia

Often, the serum sodium gives a clearer idea of the relative water state of the body
than of sodium status; hence clinical assessment is essential.

A patient with hyponatraemia, for example a serum level of 125 mmol/L, may

be sodium depleted, sodium replete or sodium overloaded (oedematous due to
cardiac, renal or hepatic disease) depending on the relative quantity of water in the
extracellular space (Table 11.1). Dilutional hyponatraemia from excessive infusion of
water (as 5% dextrose) is still seen on surgical wards.

The management of hyponatraemia may be sodium chloride infusion, water restriction

or diuretic plus water restriction depending upon clinical assessment of volume
status. Water cannot be excreted by the kidney in the presence of extracellular

Table 11.1  Hyponatraemia – types and causes

ECF volume low (NaCl – – –, ECF volume normal/slightly ECF volume high
H2O –) raised (NaCl normal, H2O +) (NaCl +, H2O +++)
Urine Na high Diuretics (excessive) Glucocorticoid deficiency Renal dysfunction
(> 20mmol/L) Salt-losing renal disease Hypothyroidism
Mineralocorticoid deficiency SIADH
Urine Na low Extrarenal loss: Dilutional (IV 5%
(< 20 mmol/L) Outwith body dextrose, water
Sequestration ingestion)
Cirrhosis
Cardiac failure
Nephrotic syndrome

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fluid depletion and the syndrome of ‘inappropriate ADH secretion’ (SIADH) can be
diagnosed only once the patient has been shown to be in sodium balance.

Correction of hyponatraemia should be achieved at a similar rate to that at which it

developed to avoid cerebral fluid shifts. Given normal renal function, water overload
can be cleared by the administration of diuretic and 0.9% sodium chloride to replace
the fluid excreted by the kidney. Hypertonic saline is seldom necessary unless the
patient is fitting.

Hypernatraemia

This can be caused by abnormal intake or administration of hypertonic fluid (eg

8.4% sodium bicarbonate), but is more commonly due to abnormal water loss (fever,
diabetes insipidus or diabetes mellitus, osmotic diuretics) in a situation in which
intake of water is impaired. Correction is with water (via the gut) or by intravenous 5%
dextrose.

Potassium
The usual requirement for potassium is 40–80 mmol/day.

Hypokalaemia

Common causes of hypokalaemia in surgical practice include (i) renal losses; (ii)
intestinal losses; and (iii) medical losses (eg high nasogastric outputs).

Plasma potassium is a poor reflection of the total body potassium content as plasma
contains only 1% of the body total. The rate of change of the extracellular potassium
concentration is more important than the absolute value. Hypokalaemia is usually
the result of loss of potassium from the body via the kidney or bowel (diuretics,
tubular disease, diarrhoea or laxatives). Acute changes in plasma potassium may
occur as potassium moves into cells during the correction of an acidosis, secondary
to the acute release of catecholamines (cerebral bleed or trauma), administration of
salbutamol or upon refeeding with the start of anabolic activity. The level should be
kept above 3.5 mmol/L by stopping any avoidable losses and the administration of
potassium.

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Hyperkalaemia

A rapidly rising plasma potassium level is a medical emergency and will result in
respiratory muscle weakness and cardiac arrest, resuscitation from which is extremely
difficult.

The primary route of potassium excretion is via the kidney, in the distal nephron, under
the influence of aldosterone. Renal failure, hypoadrenalism, distal nephron disease
(eg chronic obstructive nephropathy) or drugs that affect the renin–aldosterone
system (eg ACE inhibitors) will all impair the excretion of potassium. Where there is a
sudden movement of potassium out of cells due to trauma, drugs (suxamethonium),
ischaemic/hypoxic damage or a sudden rise in hydrogen ion concentration, patients
with impaired renal excretion will be particularly vulnerable.

An example is the hypovolaemic patient with a metabolic acidosis plus respiratory

compensation in whom anaesthesia is induced with suxamethonium and who is
then underventilated, with consequent sudden fall in pH, and then suffers a cardiac
arrest shortly after induction. There is no absolute level above which the signs and
symptoms appear, and effects are related to the rate of rise as much as the plasma
concentration. A chronic potassium level of 6.0 mmol/L will be well tolerated but may
be fatal if the result of a rapid change from 4 mmol/L. Levels of this magnitude require
rapid, specific treatment plus reversal of the primary condition and, if possible, the
removal of any precipitant drugs.

Calcium
The calcium level in the plasma is normally kept within a narrow range under the
influence of parathyroid hormone, 1,25-dihyroxyvitamin D3 and renal function. The
active component is the ionised fraction, which is unbound to albumin. Total levels
have to be interpreted in relation to the albumin level or the ionised fraction has to be
measured directly.

Hypocalcaemia

Apparent severe hypocalcaemia may be found in the critically ill if total plasma level
is measured without reference to the albumin level. An absolute hypocalcaemia
level is seen in acute pancreatitis, acute rhabdomyolysis and following thyroid or

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parathyroid surgery. Treatment is by the administration of calcium, treatment of the

primary condition and, in post-parathyroidectomy syndrome or vitamin D deficiency,
administration of activated vitamin D analogues. In situations of critical illness with
intact parathyroid function, administration of calcium should be limited to where there
is clinical evidence of hypocalcaemia or where the ionised calcium level is very low
(usually < 1 mmol/L). Symptoms include tetany, numbness and paraesthesia. Signs
include Chvostek’s sign, Trousseau’s sign and seizures. Arrhythmias may also occur.

Hypercalcaemia

Severe hypercalcaemia will affect neural tissue and damage renal tubular function. In
the critically ill, this is most often due to paraneoplastic hypercalcaemia, but it can be
caused by primary or secondary hyperparathyroidism. Hypercalcaemia diminishes the
kidney’s ability to retain salt, and the resultant hypovolaemia reduces the ability of the
kidney to excrete calcium. Symptoms include malaise, abdominal pain and possible
ureteric colic. Dysrhythmias may occur. Establishing a saline diuresis will normally
help reduce the level. If this fails, the administration of a bisphosphonate intravenously
will reduce the level of calcium. Effective treatment of the primary cause will also bring
the level back to normal. The development of hypercalcaemia in association with
recurrence of a solid tumour is usually an indication of a poor prognosis.

Magnesium
Magnesium is the second most important intracellular cation after potassium.
Magnesium is essential for the normal functioning of nerve and muscle. Depletion
causes confusion and seizures and is associated with a range of dysrhythmias, while
excess causes muscle paralysis and central nervous depression. In the critically ill,
hypomagnesaemia is common in the early recovery period following severe insults
such as peritonitis. Chronic losses from the bowel (diarrhoea) or kidney (loop diuretics)
and alcohol abuse contribute. As with potassium, plasma levels reflect total body
magnesium poorly, but a plasma level below 0.6 mmol/L associated with a condition
likely to cause magnesium deficiency or the presence of symptoms should precipitate
supplementation. This is best done intravenously in the acute stage to avoid the
purgative effects of magnesium salts. The plasma level should not exceed 1.5 mmol/L.
Critically ill patients with dysrhythmias should have magnesium levels checked as
treatment with magnesium contributes to the control of several dysrhythmic states.

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Significant hypermagnesaemia is almost always secondary to iatrogenic

administration in the presence of impaired renal function.

Phosphate
Phosphate is present in any protein-containing food and is absorbed from the gut.
The kidney excretes phosphate under the influence of parathyroid hormone. High
levels are seen in renal impairment or following massive muscle or bowel necrosis. In
the short term, this is usually not a major problem unless large quantities of calcium
are administered.

Hypophosphataemia is commonly seen during recovery from critical illness. As

cell function is restored, phosphate is taken back into cells with potassium and
magnesium. When the phosphate level falls below 0.6 mmol/L, there are measurable
effects on skeletal muscle function and on the immune system. Replacement will
come with feeding but, with levels below 0.6 mmol/L, intravenous supplementation
will need to be given slowly over 24 hours.

Trace metals
There are many trace metals that are essential to normal cellular function and the
healing process (zinc, copper and selenium). In situations where there is prolonged
dependence upon parenteral feeding or prolonged gut dysfunction, consideration
must be given to their measurement and supplementation.

Approach to the prescription of fluid and electrolytes

This should be read in conjunction with the section in Chapter 13 on nutrition. In
the critically ill, fluid replacement will be guided by the clinical situation, which is
constantly changing. Requirements will be dependent upon many factors, but with
three main headings: (i) basal requirements; (ii) existing fluid and electrolyte excess or
deficit; and (iii) continuing abnormal losses.

Basal requirements (1500–2500 ml of water, 100 mmol Na and 80 mmol K) are

influenced by a number of factors, including body weight (Box 11.1). Age and cardiac
or renal disease can jeopardise the patient’s ability to correct imbalances so greater
care is then needed. Intravenous fluids should be used for as short a period as
possible, eg after uncomplicated elective surgery.

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Pre-existing fluid and electrolyte excess or deficit needs to be taken into account
in fluid calculations, eg potassium deficit takes some time to correct. Oedema also
takes days to resolve, as a patient recovers from major surgery. The patient’s recovery
is often accompanied by a diuresis, which can be one of the clues that the patient is
getting better.

Abnormal losses usually cause change gradually. These might include insensible
loss of water dependent upon fever, continuing loss from the gastrointestinal or renal
tract, or other effects of recent surgery, with fluid redistribution or loss from open
wounds. As well as noting yesterday’s outputs, your clinical assessment should help
you predict, to some degree, how these losses might change today. For example,
a patient recovering from laparotomy with a soft abdomen and passing flatus may
be expected to successfully tolerate more oral intake. Previous nasogastric losses
will probably resolve and the need for intravenous fluid will decrease as oral intake
increases.

You should be realistic about tolerance of oral intake in unwell patients. Just because
it is prescribed or permitted, does not mean it will be taken or tolerated by the patient.
If, at this point, the fluid balance is no longer charted, then problems may develop.

Box 11.1  Some considerations for fluid therapy

• Fluid isotonic for sodium will be required to maintain adequate extracellular
volume
• Water (oral or 5% dextrose) is needed to maintain intracellular volume and
provide sufficient volume to excrete the renal load of solute waste
• The volume of clear intravenous fluids will need to be reduced depending on
the volume being given by other routes or forms (drugs, oral intake, nutrition,
blood, etc)
• Electrolyte deficiencies will need to be corrected as well as basal needs being
met

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Replacing abnormal losses

As a general rule, abnormal losses should be replaced with a fluid with the same
composition as that which is being lost, and in a similar volume. However, matching
the fluid exactly is not always necessary as the kidneys compensate efficiently under
many circumstances.

Losses can be divided into those that consist more or less of ECF, or its equivalent,
and those that are mainly or purely water (Box 11.2). Some conditions have elements
of both.

When there is loss of an ECF-equivalent fluid, there is a decrease in the total ECF
volume, and this includes the plasma volume.

Box 11.2  Fluid losses

Losses that approximate extracellular fluid

• Blood loss
• Vomiting
• Diarrhoea
• Gut fistulae
• Unwell patients (eg sepsis, burns, pancreatitis)
• Diabetes mellitus (hyperglycaemia)

Losses that are principally water

• Fever
• Increased respiratory rate
• Prolonged water deprivation
• Diabetes insipidus

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This deficit should be replaced promptly to restore perfusion to cells and vital organs.
Abnormal losses of water with or without electrolytes (particularly sodium and
potassium) will result in not only a reduction in plasma volume but also a marked
change in intracellular fluid volume and the concentrations of important ions across
cell membranes. Restoration of the plasma volume always takes precedence, and
should be accomplished with a ‘balanced salt solution’ (see below).

Restoration of the water deficit and other electrolyte deficits can then be addressed.
This should be accomplished gradually so that rapid shifts of water across
membranes, especially the blood–brain barrier, are avoided. It takes much longer for
electrolytes to equilibrate between some compartments, and the resulting osmotic
gradient can lead to fatal cerebral oedema or other complications if therapy is too
hasty. Aim to correct these over 48–72 hours.

Replacing extracellular fluid loss

Central to the replacement of ECF deficits (blood volume, interstitial volume) is the
use of a ‘balanced salt solution’. This term refers to a crystalloid solution that is
isotonic (and remains so) and has constituents that are similar to the ECF (normal
saline or 0.9% sodium chloride, lactated Ringer’s buffer – also known as Hartmann’s
solution). When a balanced salt solution is given, it will distribute itself throughout the
extracellular compartment (~14 L) over several minutes.

Only about a third of the volume given will remain in the vascular space.
Understanding this phenomenon will prevent undertreatment of blood volume deficits
when using balanced salt solutions. As reduced intravascular volume is usually
accompanied by an ECF deficit, redistribution of balanced salt solution into the
interstitial space is usually desirable. Normal saline contains too much chloride for
physiological needs and, with overprescription, hyperchloraemia and acidosis occur.
Hartmann’s solution does not cause this.

If the volumes required are large, maintenance water and electrolytes are often
forgotten. This seldom matters in the first 24 hours or so because the volume shifts
are so large and the kidney can usually sort out what it wants to keep or excrete.
However, as time goes on, maintenance water needs to be thought about or the
patient will become hypernatraemic and hyperosmolar.

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Vomiting, diarrhoea and intestinal fistula losses

These gastrointestinal conditions cause losses of fluid that resembles ECF but is
typically of a lower osmolality (ie more water is lost relative to sodium). The result is
blood volume depletion, dehydration and large electrolyte losses. If water only has
been taken orally to try to compensate, hyponatraemia may be present. If serum
sodium is normal or even high, the possibility of a significant sodium deficit must not
be overlooked.

In some conditions (eg vomiting from complete upper small bowel obstruction,
diarrhoea due to cholera) the volumes lost can be huge and rapidly life-threatening.
Potassium depletion is universal, and may be severe with marked diarrhoea.
Metabolic acidosis may mask the extent of total body potassium deficit by causing
potassium to move from within cells to the extracellular compartment in exchange for
extracellular hydrogen ions.

Additionally, vomiting or nasogastric drainage leads to loss of hydrogen (H+) and

chloride (Cl–) ions from the stomach. This can produce a marked metabolic alkalosis
but, despite this, it is rare that H+ needs to be given intravenously. Adequate
chloride replacement, in the form of normal saline, will usually correct the deficit, as
endogenously produced acid (H+) will be retained by the kidney.

By using fluid balance charts and clinical assessment logically to keep total volume
and key ions, particularly sodium and potassium, in balance, you can achieve success
in the great majority of cases. However, there is no single formula for success and
patients change continually – so reassess.

Case scenario 11.1 

A 58-year-old, 70-kg man, otherwise fit except for long-standing AF controlled
with digoxin, underwent a cystectomy for bladder cancer 3 days ago. An ileal
urostomy was constructed, necessitating a small bowel anastomosis. Presently,
he is on the HDU, is apyrexial and his chest is clear (respiratory rate 16/min), but
his abdomen is rather distended. Although his urine output is rather low, he has
a normal capillary refill time, pulse and blood pressure. The monitor shows AF at
a rate of 118 bpm. It is Saturday and you are on call – the HDU nurse has asked
you to sort out his fluid balance for the weekend. Review the fluid balance chart

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below and prescribe his intravenous fluid. His consultant wished him to stop
antibiotics after 72 hours.

• What further information do you require?

• What would you prescribe and how?

• Are blood tests necessary today?

• When should you review further?

Data

Intake
summary CVP line Peripheral line (R) Peripheral line (L) Oral
(last 24 h) Normal saline Dextrose 5% Antibiotics (600 ml), PCA Sips
(975 ml) (1800 ml) (125 ml) (120 ml)

Losses summary Nasogastric tube Pelvic drain Urostomy Bowels

(last 24 h) 1450 ml 720 ml 640 ml Nil, no
flatus

Case scenario 11.1: answers 

This is a complex patient who is not clinically stable. In addition to making your
own clinical assessment, you should review the fluid charts from the previous
day or two to look for patterns and for accumulating losses or excesses. Look at
the operation note for any specific postoperative orders. Urinary anastomoses
may leak for a few days so urine appears through the drain as well as the
catheter and/or urostomy. Ileus can be prolonged and nutritional support may
be needed but, again, this is not pressing at 72 hours postoperatively. You need
to review yesterday’s biochemistry results (Na+ 138 mmol/L, K+ 3.1 mmol/L,
urea 5.2 mmol/L) and repeat these today. Summate the data above and include
insensible losses – about 750 ml is probably reasonable here, but revise the
factors which influence this.

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His needs are probably about 3500 ml – the water requirement (5% dextrose
2000 ml) will be unchanged – the excess volume should be normal saline (1500 ml)
to replace the nasogastric losses. His antibiotics will be stopped, but his PCA will
continue. He is hypokalaemic and you should aim to give 80 mmol K+ over the
next 24 hours – you may modify this when you review with the blood results later.
This need is more pressing because of his AF and digoxin therapy. Remember
that hypokalemia potentiates digoxin toxicity. The magnesium level should also
be measured and corrected as necessary. If potassium replacement and digoxin
fail to control the rate and any hypoxia or hypovolaemia has been corrected then
alternative pharmacological interventions (eg a beta blocker and amiodarone)
should be considered.

It is inappropriate to prescribe for the whole weekend just now. Some losses –
the nasogastric loss for example – may increase or decrease and clinical and
biochemical reassessment is needed. Plan to review with your team at the end of
today and again at 8am tomorrow.

Summary
n Fluid and electrolyte imbalance is common and detrimental to surgical patients if
not addressed.

n Accurate fluid balance is achievable with a logical approach.

n Consider basal requirements based on patient size and age.

n Consider abnormal on-going losses, pre-existing deficits or excesses, fluid shifts.

n Normal renal and cardiovascular function protect against fluid intolerance.

n Look at the fluid balance chart for last 24 hours.

n Are all fluids given or lost included? Do the volumes seem right from other
available information? Check previous charts for insidious changes.

n Aim to correct abnormal electrolyte values.

n Consider measuring urine electrolytes and plasma osmolality if blood results and
patient clinical examination do not add up.

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Further reading
National Institute for Health and Care Excellence (NICE). Intravenous Fluid Therapy in
Adults in Hospital. NCE Guideline 174. NICE, London; 2013.

Powell-Tuck J, Gosling P, Lobo DN et al. British Consensus Guidelines on Intravenous

Fluid Therapy for Adult Surgical Patients (GIFTASUP). NHS National Library of
Health, London. Available at http://www.ics.ac.uk/downloads/ 2008112340_
GIFTASUP%20 FINAL_31-10-08.pdf.

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Sepsis and multiple

organ failure

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Learning outcomes 
This chapter will help you to:

n describe the clinical pathophysiology of the septic process;

n recognise that prevention, early diagnosis and prompt treatment of sepsis

is more beneficial for patient survival than treatment of established septic
shock;

n outline the essential features of the Surviving Sepsis Campaign;

n describe the linkage between organ dysfunction, sepsis and patient

outcomes;

n describe a system for managing the septic patient.

Sepsis and hospital-acquired infections remain major healthcare issues in the

developed world. Patients with indwelling devices, those in ICU or HDU, and those
being treated with chemotherapy or steroids, are at particular risk. In addition, an
ageing population and the ability to treat patients with major chronic illness increases
the complexity of management of patients with sepsis. In the US in 2011, 5.2% of
total hospital costs were attributable to sepsis, and it remains a leading cause of
mortality of surgical patients worldwide.

The signs and symptoms associated with sepsis are caused by the release of
endogenous mediators. This mediator release may be caused by a variety of
insults, including infection and trauma. The mediators involved include nitric oxide,
bradykinin, histamine, prostaglandins and cytokines, all of which have vasoactive
properties. They produce a state of vasodilatation, enhanced capillary leak and,
eventually, myocardial depression.

Cytokines involved include interleukin 1 (IL-1, an endogenous pyrogen), tumour

necrosis factor and IL-6. These are released from the patient’s own white blood
cells, and contribute to the pyrexia and hypermetabolic state found in sepsis. While
production of mediators is needed to combat infection, an excessive, prolonged and
unregulated activation of such cellular and humoral mediator pathways is thought to
contribute to the development of multiple organ dysfunction (MODs) sometimes seen
in patients with sepsis.

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A balance exists between inadequate and excessive responses to infection.

Inter-individual variation in the pattern of mediator release and of end-organ
responsiveness (probably related to genotype) plays a significant role in determining
the initial physiological response to sepsis and this may be a determinant of outcome.
Other important prognostic features include the severity of the initial ‘trigger event’,
the timeliness and adequacy of treatment of the underlying condition and the patient’s
general state of health.

Definitions
Understanding of sepsis is constantly developing. In February 2016, the European
Society of Intensive Care Medicine and the Society of Critical Care Medicine’s
Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)
were published (see Further reading). This work has attempted to simplify the
understanding of sepsis and to focus attention on the groups most at risk of death
from sepsis. The prognostic value of these definitions has been retrospectively tested
in large cohorts of patients in whom outcomes were known and, in this way, the
definitions have a greater evidence base than the earlier approach. As part of this
approach, the previous focus on the recognition of systemic inflammatory response
syndrome (SIRS) is no longer useful as it does not identify those at high risk of
mortality. SIRS is now recognised as an appropriate, regulated non-specific response
to infection and, along with the term ‘severe sepsis’, is no longer recommended
for use. Sepsis is defined as a ‘life-threatening organ dysfunction caused by a
dysregulated host response to infection’. Septic shock is a condition characterised
by profound circulatory, cellular and metabolic abnormalities and is associated with a
greater risk of mortality than is sepsis alone.

Clinically, sepsis is recognised by looking for signs of organ dysfunction in patients

who are suspected of having an infection. Signs of organ dysfunction can be
determined using the Sequential Organ Failure Assessment (SOFA) methodology
but, as this is really only suited to patients already in a critical care environment, a
modification of this for use early in a patient’s illness has been developed. The quick
SOFA (qSOFA) assesses respiratory rate, blood pressure and mentation. A respiratory
rate over 22, a systolic BP of less than 100 mmHg and altered mentation all score 1
point each; organ dysfunction is defined as a score of 2 or more and puts the patient
into a group with a predicted 10% risk of death.

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Recognising septic shock clinically is more difficult, as it can be assessed only by

response to treatment. Patients who have infection and persistent hypotension after
fluid resuscitation, or a persistent lactate of more than 2 mmol/L after resuscitation, or
a vasopressor requirement to maintain a mean arterial pressure (MAP) of ≥ 65 mmHg
in the absence of hypovolaemia are all considered to have septic shock. Septic shock
is associated with a 40% mortality rate. In a ward setting, a definitive diagnosis of
septic shock is difficult as it not possible to be sure that someone is not hypovolaemic
without invasive monitoring, but the message is to understand these definitions and
treat the patient appropriately.

Implications for screening and management of infection

(adapted from SSC)
The Surviving Sepsis Campaign (SSC) has offered the following clarification on the
implications of current definitions.

Step 1: screening and management of infection

The appropriate first step in screening should be identification of infection. In those
patients identified as having infection, management should begin by obtaining blood
and other cultures as indicated, administering tailored antibiotics as appropriate, and
simultaneously obtaining laboratory results to evaluate the patient for infection-related
organ dysfunction.

Step 2: screening for organ dysfunction and management of sepsis

Patients with sepsis should be identified by the organ dysfunction criteria (including
lactate level greater than 2 mmol/L). Organ dysfunction may be identified using the
sepsis-related qSOFA, as outlined above.

Importantly, evidence of two out of three qSOFA elements in patients who have
screened positive for infection may be used as a secondary screen to identify patients
at risk for clinical deterioration. Consider closer monitoring of these at-risk patients.

If organ dysfunction is identified, ensuring that the step 1 elements have been initiated
continues to be a priority. For instance, patients with organ dysfunction require blood
cultures if only non-blood cultures had previously been obtained and administration

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of broad-spectrum antibiotics if only narrow-spectrum antibiotics had previously been

administered in step 1.

Step 3: identification and management of initial hypotension

In those patients who have infection and hypotension or a lactate level greater than
or equal to 4 mmol/L providing 30 ml/kg crystalloid with reassessment of volume
responsiveness or tissue perfusion should be implemented.

Quick SOFA clarification for the practitioner

Sepsis-3 introduces qSOFA as a tool for identifying patients at risk of sepsis with a
higher risk of hospital death or prolonged intensive care unit (ICU) stay both inside
and outside critical care units.

Note that qSOFA does not define sepsis (but the presence of two qSOFA criteria is a
predictor of both increased mortality and ICU stays of more than 3 days in non-ICU
patients). NICE guidance has also been released, which stratifies the risk criteria when
assessing sepsis (Table 12.1).

How to proceed once sepsis is suspected

The keys to sepsis management are early recognition and prompt and accurate
treatment. To aid management of what can be a complex situation the Surviving
Sepsis Campaign has recommended the concept of care bundles.

The SSC includes two recommended management packages or ‘care bundles’ – the
3-hour care bundle and the 6-hour care bundle.

The SSC care bundles

The 3-hour care bundle

The 3-hour care bundle aims to optimise the care of patients with sepsis during
the first 3 hours after presentation. It starts with the ‘Sepsis Six’ – six tasks easily
performed by non-specialist staff that form the crucial first steps in delivering the care
bundle. These should be completed within 1 hour of presentation/suspicion of sepsis

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Table 12.1 Risk stratification tool for adults, children and young people aged 12 years and over with
suspected sepsis

Category High risk criteria Moderate to high risk criteria Low risk criteria
History Objective evidence of new altered History from patient, friend or relative Normal behaviour
mental state of new onset of altered behaviour or
mental state
History of acute deterioration of
functional ability
Impaired immune system (illness or
drugs including oral steroids)
Trauma, surgery or invasive
procedures in the last 6 weeks
Respiratory Raises respiratory rate: 25 breaths Raised respiratory rate: 21–24 No high risk or
per minute or more breaths per minute moderate to high
New need for oxygen (more than risk criteria met
40% FiO2) to maintain saturation
of more than 92% (or more than
88% in known chronic obstructive
pulmonary disease)
Blood Systolic blood pressure 90 mmHg or Systolic blood pressure 91– No high risk or
pressure less or systolic blood pressure more 100 mmHg moderate to high
than 40 mmHg below normal risk criteria met
Circulation Raised heart rate: more than 130 Raised heart rate: 91–130 beats per No high risk or
and beats per minute minute (for pregnant women 100– moderate to high
hydration 130 beats per minute) or new-onset risk criteria met
arrhythmia
Not passed urine in the previous 18 Not passed urine in the previous
hours 12–18 hours
For catheterised patients, passed For catheterised patients, passed
less than 0.5 ml/kg of urine per hour 0.5 ml/kg of urine per hour
Temperature Tympanic temperature less than
36°C
Skin Mottled or ashen appearance Signs of potential infection, including No non-
Cyanosis of skin, lips or tongue redness, swelling or discharge at blanching rash
surgical site or breakdown of wound
Non-blanching rash

and contribute to the 3-hour bundle. Note also that the Sepsis Six and associated
care bundles fit well into the CCrISP three-stage assessment process, and that
completing a CCrISP assessment will ensure that you do not miss elements of the
care bundles.

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The Sepsis Six

• Give high-flow oxygen
• Take blood cultures
• Give intravenous antibiotics
• Start intravenous fluid resuscitation
• Check haemoglobin and lactate levels
• Measure accurate hourly urine output

Additional elements of the 3-hour care bundle include:

n Ensure broad-spectrum antibiotics have been given.

n Administer 30 ml/kg crystalloid for hypotension or lactate ≥ 4 mmol/L.

Following the ‘Sepsis Six’, the SSC recommends that patients with persistent
hypotension or increased lactate should be managed with early goal-directed therapy
(EGDT). EGDT will require input from your critical care colleagues or other senior
doctors, but the principles used are important to recognise and are outlined below.

These recommendations are encompassed in the 6-hour care bundle.

The 6-hour care bundle

n Apply vasopressors (for hypotension that does not respond to initial fluid
resuscitation) to maintain a MAP ≥ 65 mmHg.

n In the event of persistent hypotension after initial fluid administration (MAP

< 65 mmHg) or if initial lactate was ≥4 mmol/L, reassess volume status and tissue
perfusion and document findings.

n Remeasure lactate if initial lactate is elevated.

Further management of patients with sepsis

The above measures are all supportive and, although important, are only part of the
management of sepsis. Source identification and control are vital if patients are to

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have good outcomes. These two things need to be achieved as quickly as possible,
and this is the remit of the surgical team. The CCrISP three-stage assessment
process will help to achieve this, as will be illustrated in the cases described below.

Management of multiple organ dysfunction

Owing to the severity of the initial insult or when there is a persistence of an activated
systemic inflammatory response, a patient may develop dysfunction or failure of one
or more organ systems (cardiovascular, pulmonary, renal, gut, liver, haematological,
CNS). If three or more systems have failed, the ensuing mortality risk approaches
80–100%. Once one organ system has failed, others typically follow (see case
scenarios). It is important to appreciate the phenomenon of multiorgan dysfunction
and to support each organ system to avoid further adverse events (eg ventilation,
haemofiltration/haemodialysis, inotropic support, nutritional support, use of blood
products).

Respiratory failure may be the result of infection (often added to pre-existing chronic
airway disease) or adult respiratory distress syndrome (ARDS). ARDS is a diffuse,
inflammatory process, usually involving both lungs, and is often seen associated with
sepsis. The lungs become ‘waterlogged’ as a result of extravasation of inflammatory
fluid and cells. Patients may develop ARDS quickly, deteriorating rapidly over a few
hours. Pulmonary signs are often minimal or non-specific: patients are breathless,
becoming progressively tachypnoeic and hypoxic. A chest X-ray will show bilateral
infiltrates but this may lag behind the clinical picture. Respiratory support is almost
always needed (usually mechanical ventilation) and expert critical care help should be
obtained at an early stage. Suspicion is the key to diagnosing ARDS.

Cardiovascular failure in sepsis results from three main factors: (i) loss of peripheral
vascular tone (vasodilatation); (ii) loss of circulating volume due to leaky capillaries
(hypovolaemia); and (iii) myocardial depression (pump failure from circulating
cytokines). Arrhythmias can exert a further effect. Close monitoring of cardiovascular
status is essential to guide treatment adequately. Fluid resuscitation may prove
successful, although inotropic and vasopressor support is often required. Many
intensivists use noradrenaline to increase peripheral vascular tone, often in
conjunction with other agents to increase cardiac contractility. Renal dysfunction in
the form of acute kidney injury is common in sepsis and is often established during
the early stages of the condition before hypovolaemia is corrected. Circulating

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nephrotoxins may compound this. Although renal function usually improves when
the patient recovers, renal replacement therapy may be required during the period
of septic shock and for some time afterwards. Failure of other systems (gut, brain,
clotting system) may be due to direct effects of the pathology or to systemic
inflammation and hypoxia. For there to be any prospect of recovery, the underlying
cause or source of sepsis must be treated.

Other causes of patients being unwell

Many patients showing signs of tachycardia, tachypnoea, raised WBC and hyper- or
hypothermia will recover uneventfully with good surgical care. However, the presence
of such signs, particularly when persistent, serves as a warning of the potential for
deterioration in the absence of prompt treatment, and if you see a patient with these
signs you should actively exclude sepsis as a cause. These signs may result from an
infective process and, with organ dysfunction, may represent sepsis although other
conditions can also cause this inflammatory response. These include pancreatitis,
ischaemia, multiple trauma and haemorrhagic shock.

You should also be actively looking for clinical evidence of organ derangement
to prevent potential future problems (eg dyspnoea, hypoxia, oliguria, jaundice,
thromobocytopenia) in all susceptible patients.

The essential points of management of these patients also include:

n early recognition;

n immediate resuscitation;

n localisation of pathology;

n appropriate management of the primary problem including the use of surgical or

radiological drainage;

n on-going reassessment to ensure that the patient continues to improve.

Failure to accomplish any of these promptly will markedly worsen the prognosis.

Table 12.2 shows some causes that you will encounter. The classification might help
you remember them but a number of the causes could appear in different boxes
depending on the stage (eg ischaemic gut). Surgical causes often require a surgical
solution but all causes occur in surgical patients.

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Table 12.2  Potential causes of abnormal patient physiology

Infective (actively exclude sepsis) Non-infective
Non-surgical Pulmonary Acute pancreatitis
Urinary and catheter-related Reperfusion injury
Intravenous lines, especially CVP
Soft tissue infection
Surgical Anastomotic leak Ischaemic gut
Biliary, especially if obstructed Ruptured aorta
Urinary with obstruction Major haemorrhage
Collection/abscess Trauma
Infected prosthesis (hip, aortic graft,
heart valve, neurosurgical shunt)
Necrotic tissue

Patient assessment and management

Immediate care
The CCrISP immediate assessment may reveal that the patient has tachypnoea and
cardiovascular changes consistent with the presence of two organ dysfunctions.
Treatment with high-flow oxygen via a facemask and establishment of IV access with
volume expansion is appropriate. Rapid volume expansion with crystalloid (30 ml/
kg lean body mass) is appropriate. An arterial blood sample to assess lactate level
should be taken at this point.

Full patient assessment

Chart review

Vital signs should be reviewed carefully: tachypnoea, tachycardia, altered mentation

and hypo- or hyperthermia are all consistent with sepsis. A normal capillary refill
time and a urine output greater than 30 ml/h are reasonable guides to the adequacy
of initial fluid resuscitation, but changes in urine output are slower to occur than
changes in capillary refill time. If hypotension or inadequate perfusion persists despite
adequate fluid replacement in the presence of a lactate concentration > 4 mmol/L,
then escalation of organ support should be considered, which will require input from
colleagues experienced in critical care and involve additional monitoring. Your role is
to recognise these patients, to try to identify the source of sepsis and to escalate their
care.

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History and systematic examination

An assessment of the patient’s presenting complaint may help to establish the likely
source of sepsis:

n Breathlessness and a productive cough may indicate a pulmonary source.

n Abdominal pain or bowel symptoms may point to an abdominal source. An

abdominal or pelvic abscess may cause diarrhoea or an ileus: anastomotic leaks
after bowel surgery can be subtle.

n Frequency, dysuria or haematuria are common in urinary sepsis. Beware the

combination of obstruction with infection (usually due to a stone), as sepsis may
be severe and permanent renal damage can occur rapidly.

n Headache and neck stiffness may point to a source in the central nervous system.

Altered mentation is common in the unwell septic patient and does not necessarily
indicate a source in the CNS.

The systemic review should also evaluate chronic health problems and current
medication that may suggest a susceptibility to sepsis (eg use of steroids) or may
indicate the need for more intensive monitoring (eg recent myocardial infarction).

The history and examination may be very useful in helping to indicate the source of
the problem. Common things occur frequently: chest infection, anastomotic leak
and central venous line infection are often implicated in the recovering surgical
patient. The timing of events can also help: the chest is a common early cause
of postoperative fever or sepsis from day 1 onwards while anastomotic leak, as
mentioned previously, usually occurs from day 4 and central line infection becomes
more frequent in lines more than 48 hours old or those that are being used for TPN.

Case scenario 12.1 

As the surgical trainee on the HDU 8am ward round, you review a 73-year-old
woman with mild COPD who had a left hemicolectomy with primary anastomosis
for colonic carcinoma 5 days ago. You are told that her WCC yesterday was
16.3 × 109/L, increased from 8.5 × 109/L the day before.

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What would you do?

Systematic assessment shows that her immediate observations are stable and
she is alert. Her systolic BP is over 100 mmHg and her respiratory rate is 18/
min. The charts show an increased heart rate (was 70 bpm, now 95 bpm), a
temporary pyrexia of 38°C overnight and decreased urine output (only 25 ml/h for
the last 3 hours). The patient has no specific complaints but has been generally
slow to recover, which is why she is still on the HDU. The CVP line from theatre
is still in situ, as is the urinary catheter. Examination of her chest reveals that it is
unchanged from previously; a few basal crackles are present, but gas exchange
is stable, lactate is not elevated and she is able to expectorate adequately
without pain. Her abdomen is slightly distended, and she has been passing flatus
but no faeces. There is no evidence of a DVT. Macroscopically and on ‘dipstick’,
her urine is clear.

What would you do now?

Now is the time to decide and plan. The patient is not quite right but has no
definite signs of pathology and you suspect sepsis.

There are a number of potential sources of infection (chest, CVP line, urine,
urinary catheter, abdomen, anastomosis). Peripheral blood cultures and cultures
through the central venous line should be sent, as should urine and sputum
cultures. A chest X-ray should be ordered if there is not a recent one, a fluid
challenge started and the physiotherapist called.

When reviewing such a case, the operation performed (which includes a primary
colonic anastomosis), the stage of recovery and the fact that her gut has still
not started working again should make you consider an anastomotic leak. You
discuss the case with your consultant and arrange contrast- enhanced CT after
adequate fluid resuscitation. A small, localised leak is suspected. Your consultant
thinks that the patient may settle and takes a conservative approach to further
management. Antibiotics are prescribed to cover a possible leak and the patient
is fasted.

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On review

Overall, the patient’s condition appears to be unchanged throughout the next

24 hours. There is one further flicker of pyrexia (37.8°C). The heart rate remains
at 95–100 bpm. The next morning, her abdomen is still distended and her ileus
persists. The urea has climbed to 10.4 mmol/L from normal and the patient had a
run of fast AF at 5am despite a CVP of +9 mmHg and normal oxygen saturations
and lactate of 2.3 mmo/L. Twelve-lead ECG and cardiac enzymes were normal
but the Mg level was low. This has been corrected.

Your consultant joins you and together you decide that the failure to respond
(abdomen, heart rate) and the recent cardiac and renal effects warrant further
surgery to deal with the leak. After appropriate resuscitation, she is taken to
theatre, where the anastomosis is taken down and the ends exteriorised. The
patient returns to HDU and makes an uncomplicated recovery.

Learning points 
• Where sepsis is suspected, management along Surviving Sepsis principles
using the CCrISP three-stage assessment helps to prevent further
deterioration and to plan care.
• Decisions to return a patient to theatre after surgery are complex and the
presence of overt sepsis is not a prerequisite.

Available results

Review available results and arrange new investigations.

Do not forget that the white blood cell count may be abnormally high (> 10 × 109/L) or
low (< 2 × 109/L) in sepsis and a coagulation screen should be checked, particularly
if surgery is contemplated. Thrombocytopenia and coagulopathies are common in
sepsis and should be corrected before surgery.

The urea and electrolytes should be reviewed with particular attention to evidence
of acute kidney injury. Liver enzymes may be abnormal, particularly when the biliary
tree is the primary source of sepsis or as part of the multiorgan dysfunction of sepsis.
An ECG should be checked for evidence of ischaemia or arrhythmia. ABG analysis

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should be taken if not already done so and may show hypoxaemia, with or without a
metabolic acidosis, and evidence of raised lactate levels.

Aerobic and anaerobic blood cultures are obligatory but will be positive in only
about 20% of cases. A higher positive culture rate can be achieved if the primary
source of sepsis can be cultured (eg pus from an abscess, urine from an infected
system). Sputum, urine, drain fluid and pus from wounds should be sent for culture
and sensitivity to antibiotics. Cultures should also be taken through indwelling
central venous catheters. Fungal infection should be considered, particularly when
the diagnosis is proving elusive, there is an upper GI source of pathology, eg
pancreatic necrosis, or there have been multiple previous courses of antibiotics.
Empirical treatment with antibiotics can be started on an ‘educated guess’ basis (with
advice from the microbiologists locally, remembering that broad-spectrum cover is
recommended if organ dysfunction has been identified). These can be changed (de-
escalated) when results of culture and antibiotic sensitivity become available.

Further evaluation of possible sites of sepsis include the use of ultrasound (remember
that this investigation does not exclude collections), CT and laparotomy. Remember
the adage, ‘pus somewhere, pus nowhere, pus under the diaphragm’. Patients
who are immunocompromised (eg transplant patients) may develop opportunistic
infections which may require very specific investigation, eg bronchoalveolar lavage,
or induced sputum sampling for those with unusual pneumonias such Pneumocystis
jirovecii (formerly called Pneumocystis carinii (PCP)).

Daily management plan: the stable patient

A daily management plan is needed for all patients and this is particularly important
in patients who have or have had sepsis, no matter how stable they appear. This
ensures that the patient and all members of the multidisciplinary team know what
is going to happen. A list of clear, positive decisions in the patient record provides
a plan for genuine progress as well as advice in the event of deterioration, eg latest
microbiology results and recommendations for antimicrobials if required. The aim is to
ensure progress through attention to detail and gives the patient the best chance of
avoiding further deterioration. Features to consider include the following.

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Fluids

Consider the need for IV fluids on a daily basis. It is important to facilitate good tissue
perfusion, and this needs to be balanced against the principles of enhanced recovery
after elective surgery. Patients who were on an enhanced recovery programme may
have been encouraged to regulate fluid balance themselves, relying on oral intake,
but, when sepsis develops or is suspected, IV fluids will be required. Crystalloids are
usually appropriate fluid replacement in cases of sepsis as there is concern that use
of artificial colloids may worsen the outcome.

Large volume fluid resuscitation is likely to require guidance by using additional

monitoring (CVP or cardiac output monitoring) and the patient is likely to need a
higher level of care.

Case scenario 12.2 

A 61-year-old, previously fit, woman was admitted to the ward 4 days ago with
acute sigmoid diverticulitis. Initial signs included minimal tenderness in the left
iliac fossa. Treatment was started with co-amoxiclav and metronidazole and
her fever and leucocytosis settled within 48 hours. She has suddenly become
acutely unwell, with recurrent tenderness in the left iliac fossa, pyrexia of 39.2°C,
tachypnoea, tachycardia and hypotension.

What would you do at this stage? What is your differential diagnosis?

It is clear that the patient has deteriorated markedly despite initial treatment for
her presumed diagnosis: a change of treatment is needed, including review of
the diagnosis. Following resuscitation (including performing the Sepsis Six, blood
cultures and biochemical tests) and after discussion with her consultant, the
patient is taken to theatre for an emergency sigmoid colectomy. There is a 7-cm
pelvic abscess beside the inflamed sigmoid colon, which is drained and a sample
of pus sent for urgent microbiological examination and culture. A Hartmann’s
procedure (sigmoid colectomy with colostomy and closure of the rectal stump) is
carried out and the patient returned to HDU in a stable condition. Perioperative
antibiotics were given and continued for a further 5 days.

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Learning points 
Recognise the patient who deviates from their anticipated recovery plan, use care
bundles appropriately and involve your seniors when making decisions about
source control.

Oxygen

It is essential that the patient does not become hypoxaemic: oxygen should be
administered as required to correct hypoxaemia. If facemask oxygen is inadequate,
consideration should be given to additional respiratory support, which will usually
require help from critical care colleagues.

Nutrition

It is essential to ensure adequate metabolic and nutritional support of the patient

in order to optimise the patient’s endogenous immune function. This can be by the
enteral or parenteral route.

Antibiotics

Antibiotics must be given as early as possible when sepsis is suspected. Empirical

treatment on a ‘best-guess’ basis should be started with microbiological advice. It is
important to review the microbiology after 48 hours when cultures are available and
sensitivities obtained: discussing cases with the microbiologist can be very helpful
and is to be recommended.

Prolonged ‘prophylaxis’ is not recommended, as ‘superinfection’ by fungi and

antibiotic-resistant organisms is encouraged. Finally, remember that enteric
streptococci account for 10–20% of severe infections related to the abdomen and
that they are not sensitive to all common prophylactic antibiotics.

Additional considerations

Instructions for physiotherapy, DVT prophylaxis and, in a patient with ongoing

abdominal sepsis, drain management should also be included in the daily
management plan.

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Diagnosing the cause of deterioration: the unstable surgical patient

In a patient with new or on-going sepsis, deterioration may be elicited by an
increase in the patient’s NEWS supplemented by other information such as clotting
disturbances, a metabolic acidosis, a raised lactate and/or organ dysfunction.
Alternatively, the patient may simply fail to progress (see case scenario 12.1). The
presence of such a pattern demands careful clinical review of symptoms and signs,
repeat microbiology and review of antibiotic sensitivities and may require further
radiological evaluation with either percutaneous or operative drainage of localised
sepsis. Failure to diagnose significant sepsis will prove fatal.

Definitive treatment
Definitive treatment is the single most important factor in securing survival. Localised
collections of pus generally need either operative or percutaneous drainage and dead
tissue should be excised. Specific soft tissue conditions such as necrotising fasciitis
need to be borne in mind. Sometimes the diagnosis is obvious, but the presentation
can be more subtle: suspect the diagnosis in a patient with sepsis, pain out of
proportion to the physical signs and skin blistering.

In spreading soft tissue infection, it is important to establish adequate drainage and

vital to excise necrotic or devitalised tissue as well as giving antibiotics. Repeated
examination under anaesthesia with further debridement is usually needed.

Abdominal sepsis, if localised, may be treated initially with antibiotics or percutaneous

drainage, but generally the primary source of sepsis must be removed. You should be
alert to the development of recurrent sepsis during subsequent assessments of the
patient.

The use of a laparostomy and/or a planned, second-look laparotomy may be useful,

particularly in patients with equivocal bowel perfusion during previous procedures or if
there is a significant risk of intra-abdominal hypertension.

Obstruction of the biliary or urinary system must be relieved. An infected prosthesis

will usually need to be removed (eg peripheral or central venous cannulae, urinary
catheters, prosthetic metalwork).

Sometimes, such decisions are difficult and will require discussion between different
medical teams. Vigilance around the possibility of catheter-associated sepsis,

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particularly in patients in the HDU or ICU, is essential and can be avoided by

adherence to vascular device care bundles.

MRSA infection is becoming more common in all patients. It is important to

distinguish between patients who are colonised carriers and those with MRSA sepsis.
Whereas MRSA colonisation does not present major problems in most patients, it may
do so in those patients with prostheses (aortic valves, aortic grafts, hip replacements),
among whom it is associated with a very high mortality. Often, the only treatment is
removal of the prosthesis and long-term antibiotics. Microbiological help is essential.

Case scenario 12.3 

You are asked to review the patient discussed above (case scenario 12.2) 72
hours following surgery. She had improved for 48 hours and was returned to
the ward, but is now breathless and pyrexial again (38.3°C). Her blood pressure
is normal but she is tachycardic (115 bpm), tachypnoeic (28/min) and poorly
perfused. Urine output has fallen off over the last 4 hours to 12 ml in the last hour.
Her chest seems clear but her abdomen is distended and quiet. The stoma has
not worked properly yet. The pelvic drain has produced 40 ml serous fluid today
only. You suspect sepsis and give high-flow oxygen (15 L/min) and start a fluid
challenge of 500 ml of Hartmann’s stat and recognise the need to complete the
full CCrISP three-stage assessment.

The foundation year doctor had checked bloods and a chest X-ray. Apart from
a leucocytosis (17 × 109/L), the blood results are unremarkable. There are no
diagnostic features on the chest X-ray. There are no signs of DVT and prescribed
DVT prophylaxis (SC heparin and anti-thrombosis stockings) are in place. You
perform a cautious rectal examination but find no obvious abnormality. Blood
gases are now reviewed and show PaO2 (on FiO2 of 0.6) 11.4 kPa, pH 7.29,
BE –7.2 mmol/L and lactate 4.5 mmol/L. After 1000 ml of saline, there is a little
improvement in perfusion, but no change in heart rate and urine output is only
15 ml in the hour since you were called.

What would you do now?

The patient remains breathless and you have neither a diagnosis nor any further
intervention of obvious help at your disposal. You request an urgent review by

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the critical care team and, as the patient still seems underperfused, give a further
fluid challenge, while the foundation year doctor checks an ECG (normal).

The critical care team arrive and assess the patient. They share your concern and
think ventilation will be needed – transfer is arranged. You inform your consultant,
who asks to be kept informed. During transfer, the patient becomes more
breathless and is intubated shortly after arriving in ICU. The positive-pressure
ventilation reduces cardiac filling and, despite further fluid loading, inotropes are
required to support the cardiovascular system. Urine output tails off. A chest
X-ray shows some diffuse bilateral shadowing suggestive of ARDS. You update
your consultant, who comes to examine the patient. No cause for deterioration
has yet been found.

Given the previous operation and the leucocytosis, recurrent abdominal sepsis is
suspected. The patient is too unstable for CT, so repeat laparotomy is arranged
and carried out by the consultant. The bowel is intact but two abscesses
are found between loops of small intestine and a left subphrenic abscess is
identified: these are drained and lavaged. More pus is sent for culture.

The patient returns to ICU for full cardiac, respiratory and renal support. The
culture result from the pus taken at the first operation has grown a coliform
resistant to prescribed antibiotics but sensitive to netilmicin. Treatment is
changed accordingly and the patient slowly begins to improve over the
succeeding 72 hours.

Learning points 
• Patients can deteriorate despite receiving appropriate initial adequate
treatment.
• A diagnosis that accounts adequately for any septic deterioration is essential
– this allows definitive treatment (‘source control’).
• Early cultures can help target later treatment – the right antibiotic is important.

Nosocomial (hospital-acquired) infection is common in patients treated in ICU and

may compound multiorgan failure. The decision to give antibiotics for a positive
culture (eg of Pseudomonas spp.) should be carefully balanced by the presence of

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a host response to such bacteria, the site of the potential infection and the need to
avoid superinfection or antibiotic resistance. Such issues should be discussed with
the microbiologist.

The recognition of the role of endogenous mediators in sepsis syndrome and the
advent of biotechnology resulted in several, large, multicentre, randomised trials using
monoclonal antibodies or antagonists to various sepsis mediators including activated
protein C, endotoxin, tumour necrosis factor and IL-1. However, it remains clear
that these treatments are unlikely ever to replace the established basic principles
of management, although time will tell whether a substantial adjuvant role can be
identified.

Case scenario 12.4 (continuation of case 12.3) 

Four days after her admission to ICU, the patient again deteriorates overnight,
needing increased vasopressors, inotropic support and oxygen, and the critical
care team suspect sepsis. A full infection screen has been taken by the time you
arrive and the central lines have been changed by your ICU colleagues. There
are no clinical features to suggest recurrent intra-abdominal sepsis: abdominal
CT confirms that there is no new intra-abdominal collection. The patient has had
several recent courses of antibiotics and there is no clear ‘best-guess’ antibiotic
to use.

Six hours later, the patient is no better and a joint discussion is held between
surgeons, ICU staff and the microbiologist. No cultures are available but Candida
was seen on samples from the urinary catheter and one of the removed central
lines. It is decided to start treatment for presumed candidaemia.

After a 4-week course of antifungal therapy and several other complications, the
patient is discharged to the ward.

Learning points 
• Surgical patients on ICU with sepsis and organ dysfunction run a roller-
coaster course, often with a range of complications – some surgical and
some medical.
• Active surgical input to care helps manage these effectively.

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• Multiple courses of antibiotics, gastrointestinal perforation, critical illness and

multiple monitoring lines are all risk factors for fungal sepsis – many of these
factors exist in surgical patients.
• Fungal sepsis may present with non-specific signs such as a failure to
progress. Identification of fungi within the blood, abdomen or urine (or at any
two other sites) would prompt many intensivists to discuss antifungal therapy
with their microbiologist and surgeon.

Established septic shock or multiorgan dysfunction is thus really treatable only by

prevention through attention to detail.

Preoperatively, the general health of the patient should be optimised (coexisting

diseases, nutrition) and any focus of sepsis should be treated.

Perioperatively, prophylactic antibiotics should be given and surgery executed in a

rapid, clean and haemostatic manner in order to prevent complications. Operations
should be performed electively whenever possible.

Postoperatively, assess clinically and monitor closely to detect problems at an early

stage, and deal with any problems found quickly and comprehensively. Be alert
to ‘occult’ hypoxia and hypovolaemia. Use prophylactic measures such as chest
physiotherapy and reinstate oral intake/enteral feeding at the earliest opportunity.
Remove lines and tubes as soon as possible, and employ short courses of targeted
antibiotics. In the event of a septic complication, adequate resuscitation and early
definitive treatment should reduce the chance of full-blown sepsis developing.

Summary
n Sepsis is a mediator disease.

n Prevention is better than cure.

n Clinical signs may be obvious but are often covert.

n Survival is improved by suspecting the diagnosis and treating the patient at an

early stage.

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n The principles of management are:

• rapid resuscitation to restore oxygenation and perfusion;

• continued optimal organ support;
• diagnosis and eradication of the source of sepsis;
• judicious and appropriate antibiotic treatment after cultures;
• reassessment to ensure continued progress.

n The SSC guidelines, particularly the ‘Sepsis Six’, are a useful starting point in the
management of the patient with severe sepsis.

Further reading
National Institute for Health and Care Excellence (NICE). Sepsis: Recognition,
Diagnosis and Early Management. NICE Guideline 51. NICE, London; 2016.

Seymour CW, Liu VX, Iwashyna TJ et al. Assessment of clinical criteria for sepsis:
for the Third International Consensus Definitions for Sepsis and Septic Shock
(Sepsis-3). JAMA 2016; 315: 762–774.

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Nutrition and the

surgical patient

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Learning outcomes 
This chapter will help you to:

n identify the underlying mechanisms and consequences of malnutrition in

critically ill surgical patients;

n use screening and assessment procedures to identify both patients with

established malnutrition and those who are at risk;

n describe basic nutritional requirements and how critical illness affects these
needs;

n understand the various methods of delivering nutritional support and

choosing the most appropriate option;

n recognise the potential complications of the different methods of nutritional

support, and how these can be minimised.

Malnutrition
Malnutrition represents a deficiency, excess or imbalance in nutrient supplies to the
body, typically of multiple components such as energy, protein, vitamins and minerals.
This results in adverse effects on body composition and function. Most surgical
patients will have a nutrient deficiency.

The National Institute for Health and Care Excellence (NICE) defines malnutrition using
the following criteria:

n body mass index (BMI) < 18. kg/m2;

n unintentional weight loss > 10% within the last 3–6 months;

n BMI < 20 kg/m2 and unintentional weight loss > 5% within last 3–6 months.

Malnutrition is present in up to 60% of surgical patients upon admission to hospital,

and may either contribute to, or be a result of, the underlying disease process.
Furthermore, people who are admitted in a good nutritional state may go on to
develop malnutrition as an inpatient. This may be directly related to their surgical
pathology, the metabolic response to illness, or simply inadequate oral intake whilst in
hospital. Patients should be considered ‘at risk’ of this if they have:

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n poor oral intake for more than 5 days and/or likely to have on-going poor intake for
5 days or longer;

n poor absorptive capacity and/or high nutrient losses and/or increased nutritional
needs from causes such as catabolism.

It is crucial to consider nutritional support for those with established malnourishment

and to identify and treat those at risk. If left untreated, malnutrition is associated with
increased postoperative complications, infection, increased length of hospital stay
and greater mortality.

Pathophysiology
In order to address the problems of malnutrition in the acutely unwell surgical patient,
you should have a knowledge of the metabolic changes that occur with starvation
(see Box 13.1), as well as the effect of the stress response to surgery.

Starvation and malnutrition

Under normal circumstances, the body utilises carbohydrate as its primary energy
substrate, creating adenosine triphosphate (ATP) via the citric acid cycle and oxidative
phosphorylation. Insulin is the major anabolic hormone, whose key roles include
stimulating glycogenesis, promotion of intracellular glucose uptake/storage, protein
synthesis and lipid synthesis.

Box 13.1  Overview of the main metabolic responses to

starvation
• Insulin È
• Glucagon Ç
• Hepatic glycogenolysis Ç
• Protein catabolism Ç
• Lipolysis and ketogenesis Ç
• Basal metabolic rate È

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During fasting, insulin levels fall and glucagon levels rise; subsequently, hepatic
glycogen stores (approximately 200 g) deplete rapidly over 24–48 hours. Muscle
contains an additional 500 g of stored glycogen, but this cannot be directly utilised
by other tissues. Instead, it is converted in the muscle to lactate, which is then
transported to the liver and converted to glucose via the Cori cycle.

As carbohydrate supply diminishes, the body adapts to use fatty acids as its main
fuel source. Protein is preserved where possible; however, some breakdown remains
necessary to supply amino acids for gluconeogenesis, as fatty acids cannot be used
for this purpose. Certain cells, including erythrocytes and renal medullary cells, can
only use glucose as an energy substrate. The brain is also largely reliant on glucose
metabolism, but can adapt over time to use ketone bodies for approximately 30% of
its energy requirements.

Fatty acids undergo a process called beta-oxidation to form acetyl-coA. In normal

health, acetyl-coA can enter the citric acid cycle, by combining with oxaloacetate.
However, in starvation, oxaloacetate stores become depleted, as it is also required for
essential gluconeogenesis. As a result, the acetyl-coA formed from beta-oxidation is
converted to ketone bodies. With continued starvation, the liver increases its capacity
for ketone body production, and the brain adapts, partly using ketone bodies for
energy. This allows some protein sparing, with the result that losses eventually fall to
around 20 g/day.

Metabolic rate also falls over time, with reduced conversion of thyroxine to its active
compound, triiodothyronine. This reduces resting energy requirements from around
1800 to 1500 calories per day (in an average 70-kg man).

Stress response to surgery/trauma

The ‘stress response’ describes a myriad of metabolic and hormonal changes that
occur in response to trauma, the magnitude of which reflect the extent of the injury.
These adjustments create a ‘catabolic state’, designed to increase the availability of
energy substrates and preserve body fluids during the period of increased metabolic
demand.

Sympathetic nervous system stimulation causes adrenal catecholamine release,

resulting in tachycardia and vasoconstriction. The renin–angiotensin–aldosterone
system is activated, promoting sodium and water retention.

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Levels of adrenocorticotrophic hormone (ACTH) rise, resulting in glucocorticoid

release. Cortisol promotes breakdown of fat and protein, and increases
gluconeogenesis. Growth hormone (GH) secretion is stimulated, promoting protein
synthesis, increasing lipolysis and antagonising the effects of insulin. Cortisol and GH
both impair peripheral glucose uptake, whilst catecholamines inhibit insulin release,
limiting the usefulness of glucose as an energy source by creating a state of ‘insulin
resistance’. These changes mean that hyperglycaemia is common. Many critically ill
patients require a variable-rate insulin infusion to maintain normoglycaemia, typically
8–10 mmol/L, as this has been shown to improve outcome after major surgery,
particularly cardiac surgery. Hypo- and hyperglycaemia have been associated with
increased morbidity and mortality, so titrating insulin to very restrictive blood glucose
limits is more likely to result in significant swings in plasma levels and you should aim
to ensure that the patient has a moderate target for blood glucose.

Whilst the body cannot use glucose effectively, fatty acids released via lipolysis once
again act as the primary energy substrate.

As the stress response subsides and insulin resistance falls, there is a move towards
net anabolism, making up the lost reserves of protein and energy. This usually
coincides with the resumption of eating/adequate nutritional intake and increased
mobility, both of which are required to restore muscle mass. Although some forms
of anaesthetic technique, eg epidural anaesthesia, have been shown to moderate
the stress response to surgery for a short time, there is little else that can be done to
reduce this response.

Metabolic changes in sepsis

The metabolic changes that develop with the onset of sepsis are complex and
are an exaggeration of the stress response. The key changes are development of
a hypermetabolic state and increased protein breakdown. There may be marked
glucose intolerance with the development of a diabetes-like state. As with the stress
response, insulin resistance develops, and the septic patient has a greater reliance on
fat as fuel.

The rate of protein breakdown may reach a substantial 250 g/day. Muscle and visceral
protein is consumed for gluconeogenesis, despite the frequently elevated plasma

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glucose concentration. Although some of this exaggerated muscle protein breakdown

might be due to the hormonal environment, the release of cytokines such as IL-1, IL-6
and tumour necrosis factor (TNF) may also be implicated.

Screening and assessment

Screening tools
Potential or established malnutrition can easily be missed, particularly among critically
ill patients. As a result, numerous screening tools have been developed to help with
early identification of ‘at-risk’ individuals. All hospitalised patients should undergo
nutritional screening by an appropriately trained professional on admission, and at
least weekly thereafter during their inpatient stay.

The most commonly used, and validated, nutritional screening tool in the UK is
MUST (Malnutrition Universal Screening Tool), which uses similar indicators to those
described by NICE in its criteria (Figure 13.1).

As with many screening tools, the outcome is operator dependent and subject to
variability. BMI measurements alone will not be able to identify all malnourished
patients. Excessive oedema or ascites can influence results, as a ‘dry weight’ is
needed for accurate calculation (see Table 13.1), and the practicalities of obtaining
measurements can be an issue with obtunded or immobile patients. It is also
important to remember that a high BMI does not exclude nutrient deficiency, as the
effects of acute illness and poor diet may still result in significant depletion of various
nutritional components.

Therefore, it is helpful to use additional methods of assessment in conjunction with

screening.

Table 13.1  Estimated contributions to body weight from ascites or oedema, based on severity of clinical
findings
Ascites (kg) Oedema (kg)
Mild 2.2 1.0
Moderate 6.0 5.0
Severe 14.0 10.4

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Step 1 + Step 2 + Step 3

BMI score Weight loss score Acute disease effect score

Unplanned If patient is acutely ill and

BMI kg/m2 Score weight loss in
there has been or is likely
>20 (>30 Obese) =0 past 3–6 months
to be no nutritional intake
18.5–20 =1 % Score for > 5 days
<5 =0
<18.5 =2 5–10 =1 Score 2
>10 =2

If unable to obtain height and weight, see

reverse for alternative measurements and
use of subjective criteria Step 4
Overall risk of malnutrition
Add Scores together to calculate overall risk of malnutrition
Score 0 Low Risk Score 1 Medium Risk Score 2 or more High Risk

Step 5
Management guidelines

0 1 2 or more
Low Risk Medium Risk High Risk
Routine clinical care Observe Treat*
• Document dietary intake • Refer to dietitian or Nutritional
• Repeat screening
for 3 days if subject in Support Team, or implement
Hospital – weekly hospital or care home
Care Homes – monthly local policy
Community – annually • If improved or adequate • Improve and increase
for special groups intake – little clinical overa II nutritional intake
e.g. those > 75 yrs concern; if no improvement • Monitor and review care plan
– clinical concern – follow Hospital – weekly
local policy Care Home – monthly
• Repeat screening Community – monthly
Hospital – weekly * Unless detrimental or no benefit
Care Home – at least monthly is expected from nutritional
Community – at least every support, eg imminent death
2–3 months

Figure 13.1  Malnutrition Universal Screening Tool (from www.bapen.org.uk).

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History and examination

A detailed history may be difficult to get from a critically unwell patient, but
information regarding weight loss, altered/poor nutritional intake or increased
gastrointestinal losses may be found from the patient’s relatives or medical records.

Non-specific examination findings such as cachexia, oedema, skin changes and

muscle wasting may be seen in extreme malnutrition, but there may be little to find in
milder cases.

Anthropometric and functional measures

Anthropometry studies the quantitative measurement of the human body, and
numerous measurement techniques to assess nutritional status have been developed.
The procedures are inexpensive and non-invasive, but must be performed by a
trained practitioner in order to achieve consistent results.

BMI is an example of an anthropometric measure, but, as discussed, it has

limitations and does not provide a comprehensive picture of body composition.
Calliper measurements of skinfold thickness (eg triceps, subscapular, biceps) give
an indication of subcutaneous fat stores that correlates closely with overall body
fat percentage. Mid-arm circumference (MAC) and mid-arm muscle circumference
(MAMC) can be useful adjuncts to estimate fat/muscle ratios. Typical values are
shown in Table 13.2. Again, changes seen in fluid distribution in critical illness can
render these measures inaccurate and must be taken into consideration. MAC
can also be used to estimate BMI in patients in whom height or weight cannot be
measured – if less than 23.5 cm, the BMI is likely to be less than 20 mg/m2.

Functional measures of nutritional status include hand grip and respiratory muscle
strength. These provide an indication of lean muscle mass and may be useful in

Table 13.2  Typical adult values for commonly used anthropometric measures in nutritional assessment
Anthropometric measures Typical adult values
Triceps skinfold thickness (TSF) (mm) Male: 12.5
Female: 16.5
Mid-arm circumference (MAC) (cm) Male: 29.3
Female: 28.5
Mid-arm muscle circumference (MAMC) (cm) Male 25.3
MAC – 3.14 × (TSF/10)] Female: 23.2

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monitoring of clinically stable patients. However, in critical illness, a number of factors,

such as impaired consciousness, critical illness polyneuropathy/myopathy and
oedema, will contribute significantly to reduced muscle strength.

Investigations
Laboratory investigations are rarely helpful during initial assessment. Albumin is used
in the wider population as a marker of protein deficiency in chronic malnutrition.
However, hypoalbuminaemia is commonly seen as a consequence of the stress
response, making it unhelpful for assessing nutritional status in the critically ill, in
whom it is more of a reflection of illness severity.

Identification of any major blood glucose or electrolyte abnormalities is important,

and a renal profile will help in assessment of hydration status, which is often also
compromised in the acutely unwell patient. More detailed studies of other vitamins/
minerals and trace elements may be recommended following dietetic involvement.

Basic nutritional requirements

The typical daily nutritional requirements of an average, healthy adult are shown in
Table 13.3.

These requirements are markedly altered in critical illness, where the response to
stress and injury results in a significant rise in basal metabolic rate (BMR), and hence

Table 13.3  Typical daily nutritional requirements in a healthy adult

Component Typical daily requirement in a healthy adult
Energy 30–40 kcal/kg
 Carbohydrate 10 g/kg
 Protein 0.5–1 g/kg
 Fat 1 g/kg
Water 30–40 ml/kg
Nitrogen 0.2 g/kg
Sodium 1 mmol/kg
Potassium 1 mmol/kg
Calcium 0.1–0.2 mmol/kg
Magnesium 0.1–0.2 mmol/kg

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Table 13.4  Increases in BMR observed in various clinical conditions

Condition Stress factor (% increase in BMR)
Infection 25–45
ICU admission
 Ventilated 0–10
 Sepsis 20–60
Surgery
 Uncomplicated 5–20
 Complicated 25–40

nutrient demand. Table 13.4 provides estimates of increases in BMR associated

with various conditions: even in uncomplicated surgical procedures, the metabolic
rate may rise by an additional 20%. Stress hyperglycaemia, loss of muscle mass,
concurrent infections and organ failure can also have a significant effect on energy
expenditure (EE), and the body’s ability to use different substrates. Various equations
have been formulated to calculate EE and guide replacement, but these are often
inaccurate, resulting in under- or over-feeding when used in the critically ill population.

Management of nutrition in surgical and critically ill patients must be tailored to the
individual, and involve early specialist dietetic input. Other vitamins, minerals and
trace elements in addition to those listed above are also required for maintenance of
health, and should be accounted for when devising a plan of nutritional support.

Treatment

Methods of nutritional support

The options available for providing nutritional support in patients with malnutrition, or
at risk of malnutrition, are:

n enteral nutrition:

• supplementation of oral intake

• nasogastric feeding
• nasojejunal or nasoduodenal feeding
• tube enterostomy

n parenteral nutrition.

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Enteral nutrition

Supplementation of oral intake

Where possible, feeding by the enteral route should be maintained. In compliant

patients who have no swallowing problems and are still maintaining some oral intake,
a dietetic review and adjustment of the meal plan to accommodate the patient’s
clinical condition may be sufficient.

The use of oral nutritional supplements may also be of benefit. These are available
in a variety of forms, such as juices, soups and mousses, providing from around
1 to 2.4 kcal/ml depending upon the preparation (typically with carbohydrate as
the predominant energy source). They also contain vitamins, minerals and trace
elements. These supplements should be used in conjunction with an oral diet, not as
a meal replacement therapy, in order to maximise their benefit. Despite the variety
of preparations available, some patients do not find these palatable, and, in the
critically ill, regular adequate oral intake is often not possible or is insufficient to meet
increased requirements.

Nasogastric feeding

Nasogastric feeding is commonly used when oral intake is deemed insufficient or

unsafe, such as in patients with swallowing difficulties or impaired consciousness.
Successful feeding by this route requires access to a functioning gastrointestinal tract.

Absolute contraindications to nasogastric feeding are mechanical bowel obstruction,

suspicion of ischaemic bowel, massive gastrointestinal haemorrhage or patient refusal
(if the patient has capacity). Relative contraindications include severe diarrhoea/
vomiting, circulatory shock states (where there may be a risk of intestinal ischaemia),
proximal small bowel fistula and conditions in which nasogastric tube placement may
be unsafe (eg following major maxillofacial surgery, skull base fracture or oesophageal
varices). Paralytic ileus is a common relative contraindication that is often identified
following failure to absorb nasogastric feed, and may be managed without
discontinuing feed altogether (see below).

Nasogastric feed can be delivered as a bolus over mealtimes, or continuously

over 16–24 hours. The latter is used in critically ill patients, as they will often be
sedated and receiving intravenous insulin infusions, with the result that continuous

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Table 13.5  Advantages and disadvantages of nasogastric feeding

Advantages Disadvantages
Physiological May be difficulty with placement
Effective, cheap and safe Misplacement may occur
Reduced incidence of hyperglycaemia, cholestasis and Potential complications
hypertriglyceridaemia compared with the parenteral route Pulmonary aspiration
Discomfort
Pressure necrosis
Diarrhoea

administration is safer and more practical. Maintenance of 30–45° head-up

positioning during feeding is important in these patients. Even ventilated patients with
cuffed endotracheal tubes are susceptible to aspiration. Tracheal intubation prevents
aspiration of most oropharyngeal secretions, but small creases in the cuff/balloon will
permit some leakage, which can result in the development of ventilator-associated
pneumonia. Head-up positioning and above-cuff suctioning can help to reduce this
risk.

Each hospital will each have its own feeding protocols, with different feed rates
and definitions of ‘high’ aspirates. An example of a typical regime involves
commencement of a ‘standard’ feed at 30 ml/h. The nasogastric tube is aspirated
after 4 hours, and if less than 250 ml gastric fluid is aspirated, the feed rate can be
increased to 65 ml/h and 4-hourly aspirates continued. If repeatedly high aspirates (eg
> 250 ml) are obtained, management options include reducing the feed rate and, if this
fails, introducing prokinetic medications.

Gastroparesis is common in critically ill surgical patients and is caused by a multitude

of factors such as the underlying illness, altered gut perfusion and the use of
medications that delay gastric emptying (eg opioids, sedatives).

The use of prokinetics is common, to increase luminal transport and strengthen

smooth muscle contraction in the gut. Treatment regimens may use of one or more of
the following drugs:

n metoclopramide 10 mg IV tds

n erythromycin 250 mg IV bd

n domperidone 10 mg IV tds.

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Typically, a response to treatment will be seen within 24 hours. Ongoing high aspirates
warrants consideration of alternative feeding methods, such as post-pyloric or
parenteral nutrition.

Nasogastric tube insertion

Patients may struggle to comply with the discomfort of feeding tube insertion,
particularly if they are confused or agitated. If a surgical patient is likely to need
postoperative nutritional support, consideration should be given to intraoperative
insertion of a nasogastric tube (NGT), whilst the patient still has the benefit of general
anaesthesia. Preoperative feeding may also be indicated in patients undergoing major
elective procedures who have established malnutrition.

In 2005, the National Patient Safety Agency (NPSA) issued an alert regarding injury/
death occurring in patients who were fed via misplaced NGTs. Despite this, between
2005 and 2010, a further 21 deaths and 79 cases of harm occurred (see Table 13.6).
As a consequence, since 2009, feeding via a misplaced NGT is a Never Event.

Any NGT used for feeding should be radio-opaque along its entire length, and have
clear markings for measurement of external length. Measurement of nose to ear
to xiphisternum distance should be performed prior to insertion, to estimate the
appropriate tube length.

Table 13.6  Incidents related to misplaced NGTs reported to NPSA September 2005 to March 2010
Total number of Number of
Checking method where error occurred incidents reported deaths
X-ray misinterpretation 45 12
Fed despite pH aspirate 6–8 7 2
Fed after obtaining pH 1–5.5 (Note – almost none of these pH levels 9 1
were contemporaneously recorded)
Water instilled down NGT before pH testing 2 0
Not checked at all 9 1
Apparent migration after initially correct placement 8 1
No information obtained re. checking method 17 4
Other
  Placed under endoscopic guidance 1 0
  Visual appearance of aspirate 1 -
Bubble test 1 0
Total 100 21

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Once in place, correct positioning must be confirmed and clearly documented prior to
use, with one of the following methods:

n pH testing (first line): pH should be between 1 and 5.5, as determined using pH

paper manufactured to test human gastric aspirate;

n X-ray (second line): must be adequate to confirm the tube position, and this
confirmation should be made only by someone assessed as competent to do so.

Figures 13.2 to 13.4 show X-rays of correctly placed (Figure 13.2) and incorrectly
placed (Figures 13.3 and 13.4) NGTs.

Feeding should be discontinued and repeated testing performed following any

episodes of vomiting and retching, if there is suspicion of tube displacement, or
the patient develops unexplained respiratory symptoms. Regular pH testing is also
recommended: at least once daily and prior to feeding or administering medication.
The latter may not be practicable in critically ill patients receiving continuous
nasogastric feed (which will raise the pH of any aspirate) and being treated with anti-
reflux medications. Most units will have protocols based around external inspection
and regular documentation of external tube length and condition of the fixation tapes.

Figure 13.2  Correctly placed NGT.

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Figure 13.3  Right main bronchus placement.

Figure 13.4  Oesophageal placement.

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A large proportion of critically ill patients develop delirium and agitation, pulling out
their NGTs, resulting in the need for repeated tube reinsertions and X-rays, which is
neither pleasant nor optimal for their care. In such patients, a bridle device may be of
use. These devices use catheter-mounted magnets to allow passage of a length of
tape behind the patient’s vomer nasal bone, which can then be secured to the tube
where it exits each nostril, making the NGT more difficult to remove.

Nasojejunal and nasoduodenal feeding

Post-pyloric feeding may be appropriate in some patients in whom the nasogastric

route is relatively contraindicated, such as those with gastroparesis that fails to
respond to prokinetics or postoperative patients with upper gastrointestinal tract
anastomoses. Otherwise, the contraindications for nasojejenual/nasoduodenal
nutrition are the same as for nasogastric feeding.

Post-pyloric feeding tubes are largely similar to nasogastric tubes, although may have
adaptations such as weighted tips and artificial ‘cilia’ to promote transit into the small
bowel. Double-lumen varieties are available, with an additional gastric opening for
decompression and/or aspiration if indicated.

They can be inserted at the bedside, but will always require radiological confirmation
of placement. More common methods of tube insertion involve siting under direct
vision during surgery, endoscopic placement and fluoroscopically guided insertion.
Correct positioning can be tricky, and requires the input of an experienced clinician.
Therefore, although there is some evidence that feeding critically ill patients via this
route may result in lower pneumonia rates than with nasogastric feeding, it is not
practicable to use this as a first-line method for enteral nutrition.

Feed regimens are similar to that used for the nasogastric route. Regular aspiration
is not routinely performed with post-pyloric tubes, so patients must be observed
carefully for signs of abdominal distension or vomiting, which may suggest outward
tube migration. In patients with a multi-lumen tube, the presence of feed in the gastric
aspirate may also suggest misplacement. If concerned, feed should be discontinued
pending radiological confirmation of tube position.

Tube enterostomy

Tube enterostomy (gastrostomy, jejunostomy or duodenostomy) should be

considered in patients expected to require prolonged nutritional support (> 4 weeks),

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or if access via the oral/nasal route is not feasible in the short term. This may be
following complex elective abdominal surgery (eg oesophagectomy, gastrectomy
or pancreatoduodenectomy), major intra-abdominal trauma, following resection of
oropharyngeal tumours, or in those at chronic risk of aspiration (eg neuromuscular
disorders).

There are a few absolute contraindications to tube enterostomy, which include

uncorrected coagulopathy, distal mechanical bowel obstruction, and peritonitis/
infection over the insertion site. Relative contraindications include the presence
of intra-abdominal malignancy (due to the potential for seeding), massive ascites,
hepatosplenomegaly, gastric varices, and peritoneal dialysis – many of these prohibit
percutaneous tube placement, but the associated risk can be attenuated by choosing
different insertion methods.

Enterostomy tubes can be placed using surgical (open or laparoscopic), endoscopic

or radiological techniques; numerous varieties are available, as demonstrated
in Figure 13.5. Surgical placement can be performed, where appropriate, as an
adjunctive procedure in patients undergoing major elective surgery. Fluoroscopically-
guided insertion may be indicated in cases where oral access is not possible.

(A) (B)

(C) (D)

Figure 13.5  Examples of enterostomy tubes. (A) Standard percutaneous endoscopic gastrostomy
(PEG) tube. (B) Radiologically inserted gastrostomy (RIG). (C) Button PEG – low profile, held in
position by water-filled balloon. More convenient for longer term use than a standard tube. (D)
Alternative low profile PEG, held in position with a distal flange.

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In postoperative/non-surgical patients, percutaneous endoscopic gastrostomy (PEG)

using local anaesthetic infiltration and endoscopic guidance is the most commonly
used method, as it has a lower complication and mortality rate (2%) compared to
surgical insertion. PEG tubes which have been inserted without complication can be
used for feeding 4 h after insertion. Feeding regimens are similar to those used for
other enteral routes, with bolus or continuous feeds being possible.

Parenteral feeding
Parenteral nutrition should be considered in patients with, or at risk of, malnutrition
and in whom:

n oral and/or enteral intake is unsafe or inadequate to meet nutritional requirements;

n there is a non-functional, inaccessible or perforated gastrointestinal tract.

Common surgical indications include: proximal small bowel obstruction or intestinal

fistulae, short bowel syndrome (< 300 cm functional small bowel), or refractory
inflammatory bowel disease.

Feed is usually supplied as total parenteral nutrition (TPN), an all-in-one preparation

that can be administered via continuous infusion, and its components adjusted to
meet a patient’s specific and complete nutritional requirements.

TPN must be administered into a central vein because of to its high osmolality, which
can otherwise precipitate thrombophlebitis. ‘Peripheral’ parenteral nutrition (PPN)
is available as a temporary alternative until central access is obtained; PPN has a
lower osmolality than TPN, but remains hyperosmolar to plasma, so can still cause
vascular injury in a similar way. Furthermore, PPN does not provide equivalent nutrient
replacement to TPN.

Many critically ill patients will have central venous catheters (CVCs) in jugular or
subclavian veins which can be used to commence parenteral feeding (femoral CVCs
should be avoided as there is greater risk of introducing bacteraemia). These lines are
routinely changed every 7 days to minimise the risk of catheter-related bloodstream
infection (CRBSI); in cases where prolonged TPN may be required, insertion of a PICC
(peripherally inserted central catheter) or tunnelled central line should be considered.

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Regardless of catheter type, TPN should be administered via a dedicated lumen

to reduce contamination risk. Feed should be introduced gradually, under dietetic
guidance, with the rate of infusion increased over a 24- to 72-hour period.

Careful monitoring of metabolic status and specialist dietetic input is crucial and
regular blood glucose measurement is required; the carbohydrate component of
TPN is supplied as glucose, and hyperglycaemia is common. Daily urea, creatinine
and electrolyte measurements (ie sodium, potassium, chloride, magnesium,
phosphate and bicarbonate) are also required, particularly when there is a risk of
refeeding syndrome (see later). TPN is presented as a lipid emulsion; therefore,
regular monitoring of triglyceride levels is also needed. Abnormal liver function tests
(LFTs) are also common. In the short term, these do not reflect permanent damage,
although this may occur in patients receiving long-term treatment (ie > 4 weeks).
A 2010 National Confidential Enquiry into Patient Outcome and Death (NCEPOD)
investigating inpatients receiving parenteral nutrition found that 43% of all patients
studied were not adequately monitored clinically and biochemically. As a result, 39%
experienced some form of electrolyte disturbance, in half of whom it was deemed to
have been avoidable.

Complications of different nutritional support methods

Complications of enteral feeding

Related to intubation of the gastrointestinal tract

Tube displacement

This is a common complication that can have serious consequences. Hospital

protocols for enteral feeding should incorporate regular checks for correct tube
positioning, and instructions as to how to manage suspected displacement.

In patients with a displaced tube enterostomy, continuing feeding may result in

peritonitis. If suspected, feeding should be stopped and appropriate contrast imaging
arranged to confirm tube position. In the event that an enterostomy tube is completely
removed, a Foley catheter can be temporarily inserted via the stoma site to prevent
tract closure whilst specialist input is sought for definitive management.

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Pressure necrosis/fistulation

Pressure necrosis of the nasal mucosa is common when nasoenteric tubes remain
in place for long periods, hence the importance of considering whether tube
enterostomy is appropriate.

In extreme circumstances, more distal necrosis can lead to fistula formation. In

patients with both endotracheal and nasoenteric tubes, tracheo-oeseophageal fistula
can develop, which may become apparent by the presence of feed on tracheal
suctioning. Gastrocolocutaneous fistulae can also occur in patients with tube
enterostomies, usually following injury to the large bowel at the time of insertion.

Wound infection/dehiscence/bleeding

This occurs more commonly in patients with tube enterostomy, and can usually be
managed conservatively with appropriate antimicrobial treatment of correction of any
underlying coagulopathies.

Related to nutrient delivery

Tube blockage

Tubes can easily become blocked, particularly after the delivery of crushed
medications. Post-pyloric feeding tubes are typically of a finer bore than NGTs and are
more susceptible to blockage. Most blockages can be resolved by flushing with sterile
water, or specific commercial solutions are available if this fails.

Pulmonary aspiration

This may be a result of tube misplacement, but can also occur with correctly
positioned tubes. Nasoenteric tubes may impede gastro-oesophageal sphincter
function; delayed gastric emptying also increases patient vulnerability. Maintaining a
head-up positioning during feeding can reduce the risk of aspiration, and the use of
proton pump inhibitors or H2-receptor antagonists increases the pH of any aspirated
gastric contents, which may reduce the resulting harm. Prokinetics may be indicated if
delayed emptying is suspected; and more distally positioned tubes can be considered
if there is likely to be long-term aspiration risk.

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Diarrhoea

This has been reported in up to 68% of critically ill patients receiving enteral feed,
and is usually multifactorial in aetiology. Concomitant antibiotic administration is
the commonest identifiable cause. Villous atrophy occurs when there are prolonged
periods without enteral nutrition and may also contribute; this can sometimes be
attenuated by the early introduction of even small volumes of enteral nutrition (‘trophic
feeding’, eg 10 ml/h nasogastric feed), if full feeding is not possible.

Infections of the gastrointestinal tract (eg Clostridium difficile) should be considered,

and appropriate samples for culture obtained. Where no infective source is found,
reducing feed rates or using pharmacological agents to slow gut transit (eg
loperamide, codeine) may help.

Complications of parenteral nutrition

Catheter related

Infection

Catheter-related bloodstream infection. is a major source of hospital-acquired

bacteraemia and mortality, with many cases (approximately 42%) arising from
central venous catheters. TPN further increases the risk of CRBSI, so a high index of
suspicion should be maintained.

The risk can be reduced by adopting strict aseptic techniques during the insertion
and handling of central lines, the use of antimicrobial-impregnated catheters, and by
allocating a dedicated lumen for the administration of TPN.

In cases of suspected CRBSI, ideally the catheter should be removed and the line
tip sent for culture and sensitivities. However, if the risk of line removal outweighs
the benefits (ie if there are difficulties in obtaining alternative venous access), then
paired blood cultures should be taken, from the central line and a peripheral site.
Microbiology input should be sought early, particularly in the latter scenario, to ensure
early and appropriate antimicrobial management.

Line blockage

Line occlusion may be due to a blockage within the lumen of the catheter (eg clotted
blood, precipitate from drugs or TPN), external venous thrombus, or secondary to line

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positioning (eg the exit port pressing against the vein wall, external kinking of the line).
Intraluminal occlusion can often be remedied by flushing with sterile 0.9% sodium
chloride; occasionally thrombolytic agents (such as urokinase and alteplase) are used,
under specialist guidance.

Central venous thrombosis

This is a particular risk in patients with long-term CVCs, those with recurrent CRBSIs
and those in whom multiple line changes are required. Many thrombi only cause
partial vessel occlusion and are asymptomatic. Occlusive thrombi may cause facial
or ipsilateral limb swelling, localised tenderness and pain. The diagnosis can be
confirmed with Doppler ultrasonography, and managed with anticoagulation under
haematology advice. The duration of treatment will depend upon the extent of the
thrombus and whether or not the central catheter is still required.

Metabolic

Fluid overload

Critically ill patients are particularly vulnerable to fluid overload. Careful monitoring
of fluid input and output is crucial to their care, as is ensuring that intravenous fluids
are discontinued when appropriate (maintenance fluids are not usually required once
a patient is fully established on TPN). The consequences of fluid overload (such as
pulmonary oedema, hyponatraemia) can significantly delay patients’ recovery and
increase their morbidity.

Hyperglycaemia

This is secondary to the high glucose load. In most critically ill patients,
hyperglycaemia is controlled with a variable rate intravenous insulin infusion
although dextrose intake can also be adjusted. Conversely, when discontinuing TPN,
hypoglycaemia is a potential complication.

Hypertriglyceridaemia

Critically ill patients often have reduced lipid clearance, and may be receiving
medications other than TPN with a high lipid content (eg the sedative agent propofol,
which is used on the ICU). In sedated patients, using alternative sedative agents
to reduce the propofol infusion rate may be sufficient to restore triglyceride levels

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to within normal limits. Alternatively, fat content can be adjusted in TPN, and some
lipid-free emulsions are available. Note that pancreatitis, although associated with
hypertriglyceridaemia, is not a contraindication to TPN.

Refeeding syndrome
Refeeding syndrome occurs following the rapid reintroduction of carbohydrates (either
enterally or parenterally) in malnourished patients. It is characterised by marked
hypophosphataemia, and may be fatal if unrecognised.

As previously discussed, during starvation/malnutrition, fat and protein metabolism

provides the predominant energy supply. Intracellular mineral stores become severely
depleted over time, although serum levels are relatively well preserved.

Resumption of carbohydrate intake prompts insulin release, resulting in stimulation

of glycogen, fat and protein synthesis. These processes require a supply of minerals
(including phosphate, magnesium, calcium and potassium) and vitamins such as
thiamine (an essential cofactor in carbohydrate metabolism). As they are taken up by
cells, the serum levels of these minerals/vitamins fall significantly, and marked fluid
shifts can occur as a result of changing osmolalities. Serum phosphate is transported
to the intracellular space to utilise in carbohydrate phosphorylation, resulting in
profound hypophosphataemia. This leads to depletion of ATP and 2,3-DPG levels in
red blood cells, inhibiting cellular oxygen utilisation.

The clinical effects of refeeding syndrome are broad in type and severity (see Table
13.7), and can easily be misdiagnosed unless a high index of suspicion is maintained.
There is no diagnostic test for refeeding syndrome; treatment should be started based
upon a suggestive history or clinical picture.

The key treatment goals are:

n Correction of mineral and vitamin deficits: central venous electrolyte replacement

may be required in cases of severe depletion or in those with worrying clinical signs.

n Safe initiation of feeding under dietetic guidance: this involves a slower

reintroduction of feed, to reduce the magnitude of the carbohydrate load, and
possibly vitamin supplementation.

n Close observation for the development of clinical features, and appropriate

management of these.

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Table 13.7  Clinical manifestations of refeeding syndrome

Organ System Clinical features
Cardiovascular Arrhythmias
Cardiac failure
Sudden death
Respiratory Dyspnoea
Respiratory muscle weakness
Ventilator dependency
Neurological Weakness
Paraesthesia
Altered conscious level
Seizures
Tetany
Wernicke’s encephalopathy
Gastrointestinal Abdominal pain
Nausea and vomiting
Ileus
Renal Acute tubular necrosis
Musculoskeletal Myalgia
Osteomalacia
Rhabdomyolysis
Haematological Leucocyte and platelet dysfunction
2,3-DPG depletion
Haemolysis

Nutrition as a component of enhanced recovery after

surgery programmes
Enhanced recovery after surgery describes a package of care for patients undergoing
major elective surgery that aims to obtund the normal stress response to surgery,
which in turn reduces complications and speeds recovery. The approach was initially
applied in colorectal surgery by Henrik Kehlet, a Danish intestinal surgeon, and the
basic principles have now been extended to several other specialties with specific
modifications. Evidence gathered to support this practice comes from the multimodal
approach, and individual elements of the pathway have not been shown to be
effective in isolation.

This section considers the basic principles of enhanced recovery rather than
procedure specific regimens, which differ between hospitals.

The aim of an enhanced recovery programme is to reduce complication rates,

improve patient experience and, as a result, reduce hospital length of stay. Patients

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undergoing major surgery experience a major stress response resulting in salt and
water retention, stress hormone release, catabolism and insulin resistance, which lead
to a loss of function in the short and medium term. Details of the metabolic response
have been described above. Traditional approaches to surgery with prolonged periods
of preoperative fasting, fluid restriction and bowel preparation followed by a further
period of nil intake by mouth, restricted mobility and the excessive use of opiate
analgesia do not address these issues. The basic principles of enhanced recovery
programmes aim to maximise the patient’s physiological status preoperatively, to
interfere with normal physiology as little as possible intra- and postoperatively, and to
restore normal function as quickly as possible.

Nutritional elements of enhanced recovery

Preoperative phase

Bowel preparation

Purgation with powerful laxatives leads to dehydration, electrolyte imbalance and

prolongation of the period of preoperative starvation and is now considered to be
unnecessary. A single enema given on the day of surgery for left-sided colonic and
rectal resections can still be used.

Preoperative fasting

Traditional wisdom was that patients needed to be nil by mouth for a considerable
time prior to surgery. It is now accepted that the last intake of food can be 6 hours
before surgery and that clear fluids can be taken up to 2 hours prior to surgery.
Preoperative oral carbohydrate loading with a glucose solution means that patients
go into surgery in the ‘fed state’, which reduces the stress response to surgery by
decreasing insulin resistance and catabolism.

Postoperative care

Recovery is promoted by attention to the following in the postoperative period:

n avoidance of opiates and using paracetamol and non-steroidal anti-inflammatory

drugs (NSAIDs) aimed at restoration of gut function;

n early commencement of postoperative diet;

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n early and structured postoperative mobilisation;

n early catheter removal;

n administration of restricted amounts of intravenous fluid.

The success of enhanced recovery programmes depends on a coordinated

multidisciplinary approach, and best outcomes are observed if the programme
is led by a designated individual who ensures compliance with all aspects of the
programme with regular audit of outcomes.

Summary
n The importance of nutritional support in critically ill patients is often
underrecognised, and this can have a significant impact on their morbidity and
mortality.

n Elective surgical and critically unwell surgical patients are undergoing major
metabolic changes, which means that maintaining an adequate nutrient supply is
vital.

n It is essential that nutritional assessment and screening forms a routine part of

patient care. Many patients will have a degree of malnutrition upon admission, and
many more are at risk of developing nutrient deficiencies as an inpatient, whilst
they spend several days ‘nil by mouth’ or managing only a minimal oral intake.

n Assessment must not be a ‘one-off’ process. The nutritional status of these

patients is dynamic and must be reviewed daily.

n Numerous methods of support are available and, whilst these may be associated
with complications, many can be avoided with careful assessment and monitoring.

n Remember there is a wealth of support available to you to help guide management

(including dietitians, pharmacists and specialist surgical nurses).

n Calculating nutritional requirements and assessing nutritional status is a complex

process, so expert input should be sought early to optimise patient care.

n Enhanced recovery programmes can improve patient outcomes and patient

experience and reduce length of stay, and managing nutrition is an important part
of this.

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 14

Pain management

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 Chapter 14  Pain management

Learning outcomes 
This chapter will help you to:

n understand the pathophysiology of pain and the need for effective treatment;

n appreciate the risks of inadequate pain treatment and its effects on the
recovery of surgical patients;

n understand your role as a part of a multidisciplinary team to relieve pain in the

surgical patient;

n evaluate the benefits and limitations of commonly used analgesics and

techniques;

n recognise that poorly treated acute pain can result in long-term persistent
pain.

Introduction
Pain is defined as ‘an unpleasant sensory and emotional experience associated with
actual or potential tissue damage, or described in terms of such damage’. Acute
pain is of recent onset and could be due to illness, injury or surgical procedures. If it
persists beyond the time of healing, then it is described as chronic pain.

Physiological pain includes nociceptive or inflammatory pain (eg musculoskeletal,

visceral pain) whereas pathological or maladaptive pain includes neuropathic pain
(eg entrapment neuropathy, neuroma pain): both pains usually exist together in some
patients. Nociception is the perception of the stimuli by the somatosensory system,
whereas pain is the experience of the patient. Pain is a product of the interaction
between biological, psychological, social and environmental factors.

In critically ill surgical patients, pain can be complex and patients may need an
integrated multidisciplinary approach to help with management. As a member of
the surgical team, you will be managing patients with significant painful conditions
caused either by illness or by interventions carried out in hospital. Safe and effective
management of acute pain is an integral part of a good surgical practice.

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Physiology of pain
Peripheral nociceptors (sensory nerve endings) detect noxious stimuli and turn
them into electrical activity. These signals are conducted by C and A-delta nerve
fibres of the peripheral nerves to the dorsal root ganglion in the spinal cord. Various
neuropeptides modulate the transmission of these signals in the spinal cord.
Ascending spinal tracts project to the thalamus and then to the sensory cortex. Some
of these pathways also track to the medulla and midbrain linked with homeostatic and
autonomic responses as well as the emotional component of the pain. Descending
tracts from the brain to the spinal cord inhibit the noxious stimulus and modulate the
pain pathway (Figure 14.1).

Pain pathway and treatment

Brain options:
Analgesics

Regional blocks

Spinal
cord

Peripheral
tissues

Figure 14.1  Pain pathway and treatment options.

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Why should acute pain be treated?

Control of pain is important not only for humanitarian reasons but because
uncontrolled pain has poor effects on body physiology, which in turn will affect the
outcome of surgery.

Pain causes sympathetic stimulation resulting in increased heart rate, peripheral

vascular resistance and visceral vasoconstriction. These changes increase the cardiac
workload and oxygen demand with consequences such as myocardial ischaemia
and reduced blood flow to other vital organs. Pain restricts mobility and increases
the chances of developing DVT. Conversely, some forms of analgesia can reduce
hypercoagulability.

Major surgery such as laparotomies and thoracic procedures already carry a risk
of adversely affecting pulmonary function. Anaesthesia and surgery can reduce the
functional residual capacity of the lung and predispose to atelectasis. Poorly managed
pain can further compound the effects by restricting respiratory excursion, impairing
the ability to cough and clear secretions, and predisposing to chest infections.

Poorly managed pain also negatively affects hormonal, metabolic and immune
systems, which can be attenuated by some combinations of systemic analgesics and
regional analgesic techniques. Intense pain can modify the nervous system, described
as ‘neuroplastic changes’, and this phenomenon can lead inadequately treated
acute pain to become chronic persistent pain. Persistent post-surgical chronic pain
is relatively more common following certain procedures including thoracic, breast,
inguinal hernia, knee and amputation surgery.

Acute pain can affect the patient psychologically causing anxiety, helplessness, sleep
problems, mood problems and loss of autonomy. Elderly critically ill patients can also
develop postoperative cognitive dysfunction due to various causes, pain being one of
the most important among these.

Principles of acute pain management

An element of pain is inevitable following trauma or surgery. Complete elimination of
pain in the immediate postoperative period is unrealistic, but the aim should be to
reduce symptoms to an acceptable level such that the patient can function, eg move
in bed, cough and comply with physiotherapy to enable recovery and rehabilitation.

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Preoperative education
It is important to inform and involve the patient regarding pain relief before an
operation to get optimal results. Higher levels of preoperative anxiety regarding
the extent of pain can lead to higher postoperative pain levels. Setting realistic
expectations and engaging a patient in the pain management plan can give the
patient the confidence needed to mobilise early and participate in rehabilitation.

Prevention
The most important principle in surgical pain control is prevention. The magnitude
of noxious stimuli is proportional to the severity of the tissue disruption, so avoiding
tension in the surgical wound and preventing drains or other tubes causing drag on
tissues or sutures is important. The choice of site of the surgical incision and the type
of incision is important in the critically unwell surgical patient with limited respiratory
reserve not just in terms of surgical access, but in relation to the degree of analgesia
and also the risk of postoperative morbidity.

‘Pre-emptive’ analgesia is a method by which analgesic medications are administered

and/or local anaesthetic procedures are performed prior to the surgical trauma.
Although there is little evidence for how successful the pre-emptive measures are,
the consensus is that proactive management of pain before it gets too severe has
potential advantages in both the short and long term.

Use multimodal analgesia wherever possible

Systemic analgesic medications in isolation are unlikely to achieve satisfactory pain
relief. A combination of medication and regional analgesic techniques is desirable for
many patients in the immediate postoperative period. Studies have shown significant
improvement in pain control with local anaesthetic infiltrations along the wound,
use of devices to infuse local anaesthetic along the wound edges (local anaesthetic
‘bombs’) as well as by using specific regional anaesthetic block techniques.

The pain management team

Whenever you are called to the ward for postoperative analgesia problems,
the three-stage assessment process is helpful: you need to know the patient’s
physiological status and further details, including the surgery and interventions they

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have undergone. Usually the anaesthetic chart and the drug prescription chart give
adequate detail in addition to the clinical notes. Discussion with the ward nursing staff
will help in understanding the present problem. It is essential to examine the patient,
record the vital signs and discuss with the patient before a proper plan is made. It
might be necessary to give some immediate pain relief before the patient can settle to
give further details.

Multidisciplinary pain teams include surgeons, anaesthetists, nursing staff and

pharmacists. The use of more sophisticated methods of analgesia require you to
discuss with the pain team to make a proper plan. Acute pain team nurses have huge
experience in dealing with postoperative patients and are available for advice in most
hospitals. Out-of-hours, this role might be done by the on-call anaesthetist, who can
provide some immediate advice and assistance. Most hospitals have local protocols
and guidelines for pain management and you need to be aware of these. It is better to
adhere to local protocols given that the nursing staff and other ward staff will be more
familiar with these.

Assessment of a patient with acute pain

Is this pain due to a new problem?

Whenever you are called to assess a patient with a recent change in the type and
intensity of pain, it is vital to rule out new surgical problems. Using the CCrISP three-
stage assessment system can help you to do that quickly and reliably. Surgical
conditions that can lead to new or increased levels of pain include ischaemia,
bleeding, anastomotic leak or compartment syndromes. ‘Breakthrough pain’ in
a patient whose pain was stable before should always be treated as a surgical
complication unless proven otherwise at the end of your three-stage assessment.

Airway
Sedative drugs such as opioids can cause sedation and airway obstruction, especially
in the older person, the obese and patients with obstructive sleep apnoea. The
risk is higher when sedative drugs are coadministered. It is important to check that
unintubated patients are able to maintain a patent airway and have intact protective
reflexes.

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Breathing
Check the respiratory rate, pattern, depth of breathing, and the ability to cough
effectively. Remember that oxygen saturation may not fall until the patient develops
profound respiratory depression.

Circulation
Tachycardia in a patient with pain could have many causes including sepsis,
myocardial ischaemia, hypoxaemia, hypovolaemia, cardiac arrhythmias or anxiety.
Hypotension in a patient receiving continuous epidural analgesia could be attributed
to sympathetic blockade causing vasodilation but there may also be other causes. For
example, low blood pressure due to hypovolaemia can be exacerbated by epidural
block. Meticulous attention to fluid balance charts, measurement of surgical and other
drain losses and a high index of suspicion for concealed bleeding or fluid losses helps
in this situation.

Disability
Analgesic medications and techniques can also contribute to clinical deterioration.
Level of consciousness and sedation scores are useful guides in patients who have
had intrathecal opioids or are presently receiving epidural or intravenous infusions of
analgesic medications. In less communicative patients, behavioural observation such
as facial expressions, verbal expressions, and restriction of mobility is invaluable.

After ensuring that the general status of the patient is stable in the ABCDE
assessment, focused assessment of pain can be made when you do the full clinical
examination. A popular acronym to use is SOCRATES:

S: Site of pain. Is this pain described in the surgical site or in a remote location (eg
calf pain due to deep venous thrombosis or chest pain due to PE)?

O: Onset. Was the onset acute or gradual (chest pain following central line insertion
may be due to pneumothorax)?

C: Character. Is the pain aching, burning or shooting (chest wall pain following rib
fractures can be musculoskeletal or neuropathic; the choice of drugs is different
for these two presentations)?

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R: Radiation. Sound anatomical knowledge and pattern of spread of symptoms can

help to identify the source of pain (for example, shooting pain to the legs can
be due to nerve root irritation at the level of spinal cord). Pain is described as
'referred' if discomfort is perceived in a location remote from the source of pain
(for example, shoulder pain following diaphragmatic irritation).

A: Associations. These include nausea, vomiting and fever (abdominal pain with
distension and vomiting may be due to obstruction).

T: Time course. Duration of pain – intermittent or continuous.

E: Exacerbating/relieving factors. This includes association with any movement,
bowel or bladder functions

S: Severity. Documenting the pain score is crucial to describe the severity, assess the
response to the interventions and monitor any progress.

Patient-reported pain assessment is also completed in the chart review.

Measuring pain-scoring systems

Pain is the ‘fifth’ vital sign; local protocols will guide the surgical trainee in the
appropriate use of the pain and sedation scoring systems used. Most of these
systems measure pain at rest and during movement to predict effectiveness of pain
relief to facilitate functional restoration. Functional assessment such as the ability
to walk, move, breath deeply and cough is an important integral component of
measuring pain.

Numerical rating scale (NRS)

The NRS is a commonly used 11-point scale for self-reporting of pain with reference
to the patient’s individual experience; zero represents no pain, 1–3 mild pain, 4–6
moderate pain and 7–10 disabling severe pain.

Verbal rating scale (VRS)

Patients verbally rate the pain with descriptions such as no pain, mild, moderate
or severe pain. This is an easy method to assess the efficacy of an intervention
compared with previous scores in the same patient.

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Visual analogue score (VAS)

The VAS is a measurement instrument on a 100-mm horizontal line, often used by
researchers. Patients indicate a position in the scale to describe the intensity of their
pain; zero represents ‘no pain’ and the maximum 100 represents ‘the worst pain
imaginable’.

Communication and documentation

Effective communication and good record-keeping are important in the provision of
a high-quality pain service. If, having properly assessed the patient, you feel that the
issue is solely attributable to pain then consider why the method of analgesia failed:

n Is it due to inadequate medication or dosage?

n Is it due to the technique used or its incorrect implementation?

n Is it because there is a surgical complication you have not yet recognised?

n Is it because other supplemental analgesic techniques are not used appropriately?

It is essential you confirm any plan for changes in analgesia to the patient and the
ward staff. Once satisfactory analgesia is achieved, methods should be put in place to
continue this and review it in a timely manner.

Management of acute pain – the clinical aspects

The choice of pain management strategy depends on different factors including the
site and nature of the surgery, type and intensity of pain, comorbidities and the on-
going clinical condition of the patient.

Whilst satisfactory pain relief is essential for patient recovery, care should be
exercised to ensure that the analgesic techniques do not make the patient worse (eg
hypotension with an epidural, respiratory depression with opioids, renal impairment
with NSAIDs).

The management options (Figure 14.2) can be categorised into:

n analgesic medications (eg paracetamol, NSAIDs, opioids);

n regional analgesic techniques (local anaesthetics with or without opioids).

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Analgesia options

Systemic Regional
analgesics blocks

Peripheral
Central
Oral Parenteral (nerve blocks,
(spinal, epidural)
wound infiltration)

Intravenous
intramuscular
(infusion, PCA)

Figure 14.2  Analgesia options.

Often, a combination of medications/local anaesthetic techniques is employed for

safe and effect pain relief. The World Health Organization analgesic ladder was
introduced to improve cancer pain control. The concept has been extrapolated to
other pain conditions as well – as the intensity of the pain increases, the complexity of
the interventions also increases. As described below, this may not be applicable in the
acute setting as rapid and effective pain relief is the goal of treatment.

n step 1: simple analgesics (paracetamol with or without NSAIDs);

n step 2: weak opioids (such as codeine) with or without simple analgesics;

n step 3: stronger opioids (such as morphine) with or without simple analgesics.

One of the fundamental principles of the pain ladder is to deliver the analgesic
medications on a regular basis – ‘by the clock’ rather than as required: PRN for pain
relief as required may also mean ‘pain relief nil’.

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If the initial presentation of acute pain is severe and difficult to control, an

alternative analgesia ladder recommended by the World Federation of Societies of
Anaesthesiologists (www.wfsahq.org) is useful. In this approach, initially effective pain
control is facilitated with stronger opioids and local anaesthetic techniques. Once
controlled, the simpler options such as regular oral opioid analgesics and then simple
analgesics are introduced.

Analgesic medications and techniques

Medications used for pain management can be grouped as:

n paracetamol;

n NSAIDs, eg ibuprofen, diclofenac, naproxen, ketorolac;

n opioids, eg codeine, morphine, fentanyl, alfentanil, oxycodone and miscellaneous

opioids such as tramadol;

n co-analgesics such as gabapentin, ketamine.

Paracetamol
Paracetamol is an analgesic and antipyretic, but its exact mechanism of action is
not fully understood. The drug is well absorbed orally and is metabolised by the
liver. When limited to the recommended dosage, paracetamol has few side-effects.
Regular administration, as a part of multimodal analgesic technique, can contribute to
effective pain management. The dose needs to be adjusted in patients with hepatic
dysfunction and in malnourished/underweight people. Paracetamol is available
in oral, suppository and intravenous infusion (over 15 minutes) formulations and
is administered at the dose of 1 g, 4- to 6-hourly up to a maximum dose of 4 g in
24 hours. In patients weighing less than 50 kg, intravenous paracetamol is limited to
15 mg/kg per dose and a maximum of 60 mg/kg in 24 hours. There is no significant
benefit to intravenous paracetamol over the oral form, which is considerably cheaper
and should be used in preference to the intravenous form whenever possible.

NSAIDs
This group of medications have analgesic and anti-inflammatory properties. Examples
include ibuprofen, diclofenac, ketorolac and naproxen. Extreme care should be taken

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when considering these drugs in critically ill patients and the elderly because of
unfavourable side-effects, particularly in the presence of other comorbidities. Their
mechanism of action is mainly inhibition of prostaglandin synthesis by inhibiting the
enzyme cyclooxygenase. Prostaglandins are the chief mediators of inflammation.
Prostaglandins also have a crucial role in physiology including renal regulation,
gastric protection and platelet function. A subgroup of NSAIDs, COX-2 inhibitors,
was developed to selectively block the cyclooxygenase 2 enzyme to enable pain
relief with minimal systemic side-effects. However, in critically ill patients, they still
have significant adverse effects (see below), thereby limiting their routine use in
pain management. Examples of COX-2 inhibitors include celecoxib, etoricoxib and
parecoxib.

NSAIDs are available in different formulations, such as oral tablets, suppositories

and injections for intramuscular and intravenous use. Whilst they may have a useful
role in stable patients, their therapeutic index is narrow in patients who are volume
depleted or dehydrated, have pre-existing renal dysfunction or are prone to bleeding.
The incidence of adverse effects can be similar regardless of the route of delivery.
In patients with deranged physiological parameters, NSAIDs can also predispose
to acute kidney injury and bleeding. It would be prudent to seek senior advice and
thoroughly assess the risks and benefits if contemplating use of NSAIDs for managing
pain in critically unwell patients.

Opioids
Opioids are derived from opium alkaloids and exert their analgesic effects by acting
on mu-opioid receptors. Despite their long list of side-effects including nausea
and vomiting, constipation, itching, bladder retention, drowsiness and respiratory
depression, opioids are still the mainstay approach for treating moderate to severe
pain. Based on their potency, opioids are arbitrarily classified as weak (eg codeine)
or strong (eg morphine). Tramadol has some mu-receptor actions along with other
mechanisms of action including serotonin and noradrenaline reuptake inhibition.

Opioids are available in different formulations including oral preparations, injections

for intramuscular and intravenous administration, lozenges and buccal preparations.
In monitored care areas, infusions (eg morphine, fentanyl, alfentanil) are also used and
doses can be titrated depending on the severity of the patient’ s pain, respiratory and
hepatorenal parameters.

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Patient-controlled analgesia

Patient-controlled analgesia (PCA) is a well-established method that enables

patients to control their pain and is likely to be the most common way to administer
intravenous opioids you will encounter on the ward. If the patient is capable of using
a simple hand-held device, opioid medication can be self-administered through
an intravenous cannula in small boluses. This concept is appealing as individual
requirements of opioids vary considerably, and with a PCA technique patients
can titrate the dose to their own end-point of pain relief. In theory, unlike clinician-
administered intramuscular or intravenous boluses, which lead to fluctuations in
plasma opioid levels, in PCA, the plasma level of analgesic will be fairly constant
within a therapeutic range providing the patient continues to make requests through
the hand-held device. A typical PCA regimen consists of 1- to 2-mg boluses of
morphine with a lockout interval of 5 minutes. The purpose of the lockout interval
is to ensure that unintentional overdose is avoided. The potency of all other opioid
medications is compared with that of morphine. Oxycodone, a synthetic opioid,
is twice as potent as morphine and may sometimes be used in a PCA device if
morphine is not working well.

Codeine is commonly given for mild to moderate pain when a patient can tolerate oral
medications. It is prescribed at a dose of 30–60 mg by mouth 4- to 6-hourly, often
as a co-drug with paracetamol. Constipation is an important side-effect and may be
undesirable, particularly if the patient is recovering from abdominal surgery. In older
patients, eg elderly patients with a fractured neck of femur, it may be sensible to
prescribe regular laxatives along with the codeine prescription.

Monitoring of patients on opioids for pain relief

Opioids have many side-effects and vigilance is essential for timely recognition of
these potentially deleterious effects. In the case of continuous infusions and PCA,
initial monitoring includes hourly recording of pain score, infusion pump checks,
assessing sedation score, respiratory rate and vital parameters (heart rate, oxygen
saturation, blood pressure) (Table 14.1). The frequency of monitoring can eventually
be reduced (to 2- to 4-hourly or so) once the general condition of the patient improves
and stabilises. In patients with PCA devices or who are receiving other opioid
intravenous infusions, additional oxygen should always be administered as a safety in
case the patient develops respiratory depression from the opioids.

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Table 14.1  Tool for monitoring pain and side effects

Pain score Sedation score Nausea score
0 = None 0 = Awake 0 = None
1 = Mild 1 = Drowsy 1 = Mild
2 = Moderate 2 = Asleep but rousable 2 = Moderate
3 = Severe 3 = Unrousable 3 = Severe

If the patient is nauseated or vomits, after ruling out causes such as hypovolaemia,
hypoxia or surgical reasons (intestinal obstruction etc), antiemetics such as
ondansetron 4 mg or cyclizine 50 mg can be administered intravenously to manage
opioid-induced nausea and vomiting.

Co-analgesics
When patients have uncontrollable nociceptive (musculoskeletal or visceral pain)
or neuropathic pain (post-thoracotomy, post-amputation, etc, where nerves are
injured), conventional analgesics may not provide satisfactory relief. The issue
is further compounded if the patient has a past history of chronic pain. Regional
analgesic techniques (discussed below) can help. When traditional interventions
fail, co-analgesics such as anticonvulsants (eg gabapentin), antidepressants (eg
amitriptyline) or ketamine (5–10 mg per hour as an intravenous infusion) may be used.
It is prudent to seek help from the hospital acute pain team prior to embarking on less
conventional approaches to manage pain.

Regional analgesic techniques

Local anaesthetics (eg bupivacaine, laevo-bupivacaine, ropivacaine) can be deposited
along the pain pathway to provide effective analgesia by selectively blocking the
neural structures and interrupting the pain impulses generated. Depending on the
level of neural blockade, the techniques can be categorised as:

n neuraxial (intrathecal, epidural);

n paraxial (eg thoracic paravertebral block);

n peripheral (eg brachial plexus nerve block, transversus abdominis plane block);

n local (eg wound infiltration, periarticular infiltration after joint surgeries).

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Regional analgesic techniques have the benefit of providing pain relief without the
side-effects of systemic pain medications. Opioid receptors are located in the spinal
cord and hence neuraxial blocks commonly involve administration of a combination
of local anaesthetic and opioids. Other peripheral blocks are performed with either a
one-off injection or continuous infusion of local anaesthetics. Local anaesthetics block
the nerves by inhibiting the sodium channels in the neuron, preventing transmission
along it. Epidural analgesia, apart from blocking sensory nerve fibres, also blocks
sympathetic nerve fibres, resulting in hypotension (which can be undesirable in
critically ill patients). With careful calculation of local anaesthetic doses, peripheral
techniques have a favourable safety profile. When used judiciously, techniques such
as thoracic paravertebral block for rib fractures and transversus abdominis plane
block for abdomino-pelvic surgeries have an important role in managing pain in
unstable surgical patients and can provide analgesia that is as effective as an epidural
in some cases. Continuous catheter techniques are mostly initiated by anaesthetists
in the operating room and the infusions are continued in the postoperative period.

Care of patients receiving epidural infusions

Patients undergoing major thoracic procedures or upper abdominal surgery and

those with bilateral multiple rib fractures can benefit from epidural analgesia. Effective
epidural analgesia helps minimise postoperative respiratory complications. A
combination of local anaesthetic and opioids (eg bupivacaine 0.1% + fentanyl 2 µg/ml)
is infused through a catheter placed in the epidural space. Although this method gives
better analgesia, complications can arise from either the technique itself or the effect
of the medications.

Complications associated with the technique include damage to the nerve roots or
spinal cord, accidental dural puncture (resulting in headache), haematoma formation
and infection risks. Local anaesthetics can cause sensory/motor blockade and
hypotension. Epidurally administered opioids can cause nausea, vomiting, pruritus,
bladder retention and respiratory depression. Some epidurals fail because of technical
issues, and insertion can be difficult in patients with degenerative spinal conditions.
Epidural insertion and removal need to be coordinated with the administration of
prophylactic anticoagulants; insertion should not be performed within 12 hours of
administration and removal within 4 hours. Epidural anaesthesia is contraindicated in
patients who are fully anticoagulated.

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When caring for patients with an epidural infusion running, observe for any above-
mentioned complications secondary to the neuraxial block and inspect the catheter
insertion site for redness, tenderness or leakage. Check for the sensory block height
to ensure that it is a functioning epidural infusion and the appropriate dermatomal
levels are covered. Suitable evidence that the epidural is working properly include the
patient being able to cough and clear their respiratory secretions and engage with
physiotherapy.

The Bromage score is used to evaluate motor weakness.

0 = full flexion of knees and feet;

1 = just able to move knees;

2 = able to move feet only;

3 = unable to move feet or knees.

Contact the acute pain team/anaesthetist if there are any major changes in motor
function or if the Bromage score is 2 or 3.

A ‘functioning epidural’ can produce an element of hypotension (as sympathetic nerve

fibres are blocked before sensory nerve fibres). This hypotension is managed with a
combination of intravenous fluids and vasopressors such as metaraminol infusions,
which might require the patient to be cared for on an HDU-type environment. In
some patients, extreme care should be taken, as both fluid overload and too much
vasoconstriction can be deleterious, and other causes of hypotension (such as
bleeding, sepsis) can be masked. Meticulous examination and comprehensive
evaluation of the clinical situation is a matter of paramount importance. Chasing the
numbers (such as blood pressure, central venous pressure, respiratory rate, urine
output) without consideration to the clinical context can be misleading. When in
doubt, complete the CCrISP three-stage assessment and, if still unsure, call for help.

Care of patients receiving local anaesthetic infusions

Ultrasound guidance is frequently used to place catheters close to peripheral nerves

and in fascial planes to provide safe and effective analgesia. For example, high-risk
patients with a fractured neck of femur may receive a fascia iliaca block as part of
their anaesthetic management. Peripheral regional blocks have the dual benefit of
avoiding the systemic side-effects of opioids as well as the adverse effects of central

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neuraxial blocks such as respiratory depression and sympathetic block-related

hypotension.

These patients may be at risk of local anaesthetic toxicity. Manifestations of toxicity

include metallic taste, tingling fingers and tongue, agitation, decreased conscious
level, hypotension, convulsions, apnoea, cardiac arrhythmias or cardiac arrest.
If toxicity is suspected, stop the local anaesthetic infusion immediately and use
the ‘ABCDE’ approach to assessment. Call for assistance, including the on-call
anaesthetist who will help with haemodynamic support and may give intravenous lipid
emulsions to combat the toxicity.

Conclusion
n Pain assessment is considered to be the fifth vital sign in the management of
surgical patients.

n Effective pain management is essential to facilitate recovery from critical illness.

n Pain may be a symptom of other more significant problems in unwell surgical

patients, and you should aim to use the CCrISP three-stage assessment to ensure
you have identified all the relevant issues.

n Documentation is important for supporting this evaluation and planning should

encompass the overall pain management plan, any consultations from the pain
team received, and periodic review of the pain score of the patient.

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Communication,
organisation and leadership
in surgical care

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Learning outcomes 
This chapter should enable you to:

n describe the facets of professional behaviour which are important in good

surgical practice, including NOTSS (non-technical skills for surgeons) and the
role of medical ethics in decision making;

n recognise the importance of clear and effective communication in surgical

critical care;

n identify the key components you may wish to develop in your transition to
specialty training.

Introduction
Medicine evolves as a result of the development of effective treatments for new
diseases. Against this backdrop of change there is one constant: the need for you to
act professionally at all times.

Professionalism, in any setting, encompasses integrity, expertise and an excellent

standard of work, but when applied to medicine it also embodies a raft of other
qualities including compassion, confidentiality, teamworking and continuous
professional development. The Royal College of Physicians defines medical
professionalism as, ‘a set of values, behaviours, and relationships that underpins the
trust the public has in doctors’.

Twenty-first century medicine is practised with a patient-centred approach, in contrast

to previous ideas of medical paternalism, a move that has seen the erosion of the
idea that doctors are infallible. Professionalism is not inherited with a medical degree;
it needs to be developed as your career progresses. The apprenticeship system that
has dominated surgical education for so long is still important in helping trainees
to develop professional behaviours but it is naive and outdated to think that role
modelling alone is sufficient. Passive learning through observation of your seniors
occurs less frequently with reduced working hours, and so training opportunities
must be maximised. There is a growing emphasis on teaching non-operative skills
through simulated scenarios and subsequent debriefing. This method is integral to the

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CCrISP course and throughout the face-to-face sessions participants will have the
opportunity to discuss and practise a variety of non-technical skills.

NOTSS (non-technical skills for surgeons)

Non-technical skills describe the interpersonal and cognitive domains that
complement technical ability in allowing safe and efficient task performance.

Medicine owes a debt of gratitude to the aviation industry, which first introduced
training in non-technical skills for pilots on the back of research suggesting that
most accidents were a result of human factors rather than equipment failure. These
‘Crew Resource Management’ programmes led to improved performance and fewer
adverse events. Extrapolating from this, human factors training was embraced by
anaesthetists as part of ‘Anaesthesia Crisis Resource Management’ courses, and
there is an increasing body of evidence showing the link between improved non-
technical skills and better clinical outcomes.

Non-technical skills can be broadly divided into the following four domains.

Situational awareness
This describes the ability to perceive and respond to changes in one’s environment
and can be summarised as detection, diagnosis, prediction. It is a dynamic
process that relies upon concentration and a good working memory. Situational
awareness can occur at an individual and a team level, with both relying upon
excellent communication. Consider the example of a patient undergoing a carotid
endarterectomy with awake testing who shows signs of neurological deterioration
upon clamping. This change in the patient’s neurological state must be recognised
by the team and communicated to the surgeon, who may then decide that a shunt
is required. This relies upon a coordinated effort from all members of the team
resulting from a shared appreciation of the problem. From an individual perspective
the surgeon will be aware that the use of a shunt makes the procedure more difficult.
They must ensure that the scrub nurse and assistant understand the sequence of
events involved in inserting a shunt, and the need to perform this part of the operation
as quickly as possible to minimise any period of cerebral hypoperfusion. This
highlights how good situational awareness allows the prediction of future difficulties.

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Decision-making
This refers to the process by which an individual chooses a course of action from
the options available using a combination of new information and past experiences
to balance risks. It is dynamic because continual re-evaluation is necessary to
assess the outcomes of previous decisions. Good decision-making is linked to good
situational awareness but the latter does not guarantee the former. Returning to the
example above, imagine if the surgeon, having correctly identified the need for a
shunt, allowed a junior trainee with minimal experience of carotid surgery to perform
the procedure.

Decision-making in medicine frequently involves consideration of an ethical dimension

to a decision. The ‘four principles’ approach of Beauchamp and Childress can be
useful in identifying and considering the issues around the decision.

n Autonomy. Individuals have the right to self-determination. Doctors must respect

this by explaining all available treatment options so that patients can make
informed decisions about their care. In situations where patients lack capacity, and
there are no advance directives to suggest which treatment they would want, then
they should be treated in accordance with their best interests.

n Beneficence. This describes actions carried out for the benefit of others. In the
context of medical ethics it means serving the best interests of patients at all
times.

n Non-maleficence. This is encapsulated in the Latin phrase primum non nocere,

which translates as ‘first do no harm’. Patients should not be exposed to risks of
harm where there is no clear benefit to them.

n Justice. This refers to fairness and equality of treatment and access. This simple
definition belies its complexity, particularly when one considers the concept of
‘distributive justice’, which is concerned with the allocation of scarce resources
and who gets what treatment.

Treating patients who are nearing the end of their lives can be incredibly challenging;
clinical decisions are often emotionally distressing and far from straightforward, and
may have moral uncertainties. The law surrounding end of life care varies from country
to country, and it is not the aim of the CCrISP course to discuss legal frameworks;
however, the ethical considerations do warrant some discussion. Doctors have an
obligation to administer effective palliative care to patients who are terminally ill.

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The provision of adequate opioid analgesia to dying patients is a clear example of

beneficence but the respiratory depression associated with these medications may
shorten the life of the patient and could be viewed as contravening the principle of
non-maleficence. This introduces the notion of ‘double effect’, which describes how
an intervention can have both intended and unintended consequences. It can be
argued that an action with two opposite outcomes is morally justifiable if the intention
is to achieve the good effect, even if the possible negative effect is foreseen.

Another example of a clash of ethical principles concerns the patient who is bleeding
but does not want a blood transfusion owing to religious beliefs. In this case there
is a conflict between autonomy and beneficence. However, if the patient is mentally
competent, then his or her wishes should be respected, particularly since a breach
of autonomy may deter similar patients from seeking medical attention in the future,
reducing the ability to carry out beneficent acts.

Task management
This describes the combination of planning and prioritisation which allows work to be
carried out to the highest standards using the resources at one’s disposal.

Teamworking
Unlike the other cognitive skills, teamworking is rooted in the interpersonal domain.
It refers to the way in which an individual can function as part of a group to achieve a
goal, and requires the reciprocal qualities of followership and leadership depending
upon one’s role within the team. Effective teamwork relies upon accurate exchange
of information and supporting others, with excellent communication skills. The
importance of the multi-disciplinary team in patient management is not in question
but a team of experts does not automatically translate into an expert team. This
realisation has led to a greater emphasis on interprofessional team training using
simulated patients, wards and operating theatres to improve communication skills and
enhance patient safety.

Within this classification the ability to deal with stress and fatigue is not included as a
discrete non-technical skill but its influence in each of the four domains should not be
underestimated.

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Being an effective communicator is a vital skill for surgeons. Large numbers of people,
coming from different branches of the healthcare professions, are now involved in
the care of a single patient and this process needs to be actively managed by the
surgical consultant and his/her team, who have ultimate and continuing responsibility
for each individual patient. Patients and relatives expect good outcomes from surgical
interventions and expect to be kept informed about details of their care at each stage.
It is vitally important to understand patients’ expectations from the outset so that all
concerned can understand what a realistic outcome for that patient may be. It is easy
to make assumptions of what other people think and believe, which may reflect the
surgeon’s own beliefs rather than the reality for that individual. Many problems arising
in surgical care are the result of poor communication, and often serial episodes, rather
than a lack of knowledge or an incorrect decision.

Evidence suggests that adverse outcomes, iatrogenic injuries, failure to provide

adequate care, mistakes or system errors are more likely to lead to litigation or
complaints if there have been preceding communication problems. Other international
data on litigation have shown adverse outcomes occurring in 3.7% of admissions,
with one in four (1% of the total admissions) due to negligence. However, two out of
three claims come from patients with no adverse outcome or an adverse outcome
not due to negligence. Another study found that only 3% of patients who suffered
negligence filed a lawsuit. Reasons given for instigating litigation include a desire
to correct apparently deficient standards of care, to find out what happened and
why, to enforce accountability and to gain compensation for accrued and future
costs of care. A further study has shown that 70% of medical litigation is related
to poor communication, citing patient feelings such as desertion, devaluation, lack
of information and lack of understanding. In one study, over half of patients who
commenced litigation claimed that they were so unimpressed by the doctor that they
wanted to sue him or her before the alleged event occurred.

Communication matters, therefore, not just with the patient and relatives, but also
with colleagues, so that clinical information can be provided quickly and accurately.
Furthermore, good communication skills allow you to be able to respond to
psychological and emotional issues in colleagues and detect the possibility of tension
or distress building up within the team as well as how to respond to this.

A comprehensive account of basic communication skills is outside the remit of

this chapter, although certain relevant communication skills are discussed and
practised on the CCrISP course. You should develop an awareness of basic

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communication skills including the appropriate use of open, focused and closed
questions, knowledge and avoidance of leading and multiple questions, knowledge
of and methods to overcome responses such as denial and blocking, and the use of
empathic statements (see Glossary).

What are the specific communication problems in critically ill

surgical patients?
Often, surgical critical care takes place in an environment where background
obstacles to communication are more likely. The patients are ill and frightened,
and the staff are often incredibly busy. The patient may be unable to concentrate,
especially if there is pain, severe illness or complications of medication. Equally,
operational fatigue on the part of staff is also important. It is often easier for others to
recognise the signs than for individuals to identify themselves. Signs of operational
fatigue include loss of clinical sharpness and reduction in the quality of decision-
making. Other obstacles to communication may include irritability and anger, high
tension, confusion (most obvious in organic brain syndromes but may also occur in
functional disorders), distress and tearfulness, and high expectations from patients,
relatives, colleagues and oneself.

Specific communications strategies

The critical care setting

Critical care settings can be bewildering for patients and their relatives, with a lot
of unfamiliar equipment, background noise and sometimes with limited access to
natural light. It is easy to assume that patients, relatives and doctors have a greater
knowledge and experience of these environments than they actually have. It is
especially important that, at each stage of care, explanations are provided. These can
be very simple tasks, such as explaining the role of a particular piece of equipment,
an account of the next intervention or an explanation of where a specific issue fits
into the overall management plan. It can be helpful to try to predict what may happen
and have a plan for the different possibilities. An environment with limited natural light
may increase disorientation, especially in elderly patients. Readable clocks or other
ways of helping to overcome this are important. Where there is a degree of organic
confusion, aids to orientation can be important, such as photographs of loved ones

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and easy-to-read name badges. Acute confusional states (delirium) are common, and
the three-stage assessment process can be used to address the causes rather than
immediately resorting to sedative-type medications.

It may be necessary to repeat both questions and explanations at different times.

Being prepared to go back over the history after the immediate crisis is good
clinical practice and may reveal issues that were previously unconsidered. You have
probably realised that many communication situations are not single episodes of
communication but rather a continuous process involving multiple episodes over
time. Similarly, it is helpful to reduce fear by offering repeated explanations and
using check-backs to assess that a patient and relatives have understood. Patients
can often recall only small amounts of the information provided from a single
communication episode.

Breaking bad news

There is no perfect way to communicate – what works well in some situations can
fail in others. However, some general principles are helpful. It can be useful to think
about this in terms of what educators call the ‘set’. This includes the environment
in which the communication episode will take place and who will be present. It also
includes an introduction as to the purpose of the episode, the details of the episode
itself and then a summary of the salient points of the discussion. When speaking to
relatives, it is important to confirm that the patient has given permission for relatives
to be informed of their condition. Understanding intra-family dynamics can also help
manage communications with relatives. For example, in some circumstances it may
be necessary for the medical staff to talk to several family members together, while in
others a family ‘spokesperson’ may be the best person to talk to.

When breaking bad news, it is important to talk, and to listen. The barriers to doing
this may come from patients (or relatives if they are receiving the communication) or
from us. Some things are hard for us to talk about but, in this setting, it is important
to be able to tackle these. One way of starting such a conversation is to ask an open
question such as ‘what is your understanding of the present situation?’ or ‘what
have you been told so far?’. In this way, you are giving the patient or relative the first
opportunity to have a say and it may help you understand their expectations and how
much they wish to be told. Some patients want a lot of detail, others only a broad
outline. If you are unaware of the patient’s expectations at the outset, you will not

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be able to meet them and you should not make assumptions. Starting in this way
also gives you the opportunity to show that you are listening and to pick up on any
verbal or physical clues as to the patient’s or relative’s underlying emotions. These
can be subtle and you need to consciously look for them. You need to be prepared
to use direct and understandable language. It is a great temptation to ‘beat around
the bush’ in an attempt to soften the blow, but it is important to say difficult, emotive
words such as ‘cancer’ or ‘death’, should they be appropriate. People find uncertainty
difficult to handle; once they know what they are facing, they can start to deal with
it and patients will often thank you for being frank and honest. Clearly, however, this
can still be a delicate situation. A good tip is to avoid the urge to fill silences with
your words and to avoid pushing your own agenda. It is often a good idea to say the
minimum, allow silences for information to be absorbed and then for more information
to be exchanged in a question and answer manner, with the patient and/or relatives
asking the questions.

Attitudes have changed substantially in the last two decades, but the work of John
Hinton in the 1970s with people who had terminal illnesses is useful. He found that, in
an inpatient unit, although staff believed that only a small minority of patients knew of
their diagnosis and prognosis, a substantial majority had a very good understanding.
This knowledge was acquired in various ways, including overhearing bedside
conversations or reading case files. Patients were able and willing to share this with
Hinton in a way that they had not done with the other staff. When asked why they did
not discuss their knowledge with staff, patients often indicated that they did not want
to cause the staff distress. In other words, patients chose silence partly to protect
the staff working with them. From this, the concept arose of being prepared and able
to give the patient permission to talk about bad news. To be able to give permission
effectively requires good listening skills. Listening is an active process, interspersed
with signs of encouragement. We all do this differently but should use attitude,
facial expression, body language or verbal acknowledgements to show interest and
encourage further disclosure.

The use of empathic statements can be a straightforward way of identifying feelings

and showing support. These are statements in which the interviewer tries to identify
a current feeling such as sadness, anger or fear and then ties it to what has been
happening, such as ‘It sounds as if this news has made you feel more fearful than
anything else’. This can allow the person to talk about feelings and it also gives the
interviewer a chance to check if what he or she perceives is correct. In contrast,

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sympathetic statements, such as ‘I know just how you feel’, should be avoided. It
is very unlikely that you could really feel the same and such statements can lead to
aggressive reactions from patients or relatives.

The most important aspects of helping people talk about feelings is to allow time
and space. The setting should be quiet and private. The interviewer should give
a sense of having time to talk. Often it will not take much time (in general, more
skilled communicators take less time than less skilled communicators) but it does
require planning to ensure, for example, that discussions like this are not started a
few seconds before a ward round or some other fixed event. There is evidence to
show that if a person is left to talk freely that they will speak for between 40 and 80
seconds. Allowing them to do so will start things off on the right footing and help the
patient appreciate that you are focused on their problem. Sitting down to talk to the
patient is good body language and gives the impression of more time being available.
In a study where a doctor, who was either sitting or standing, spoke to patients for
a set length of time, the patients’ estimation of how long the doctor had spent with
them was doubled if the doctor was sitting down.

An important part of communication is the use of ‘mirroring’. The doctor mirrors what
the patient is doing in terms of tone and speed of speech, and body language. For
example, if a patient sounds timid and scared, using a similar tone may reassure the
patient that he or she is being listened to and dealt with appropriately. If the patient
leans forward, you should lean forward. It is not suggested that everything a patient
does should be mirrored but doing the opposite to what the patient is doing can send
a message that you are not listening or concerned about them.

A further issue, for more junior doctors in particular, is the way they handle their
own uncertainties. In general, patients want definite statements and guarantees of
outcomes. Clearly, there is much uncertainty surrounding surgical outcomes and you
need to be able to appear confident in your knowledge, yet not lead patients to have
unrealistic expectations.

At the end of the discussion, make it clear that further meetings can be arranged
and give details of how this can be done. Giving the family a ‘liaison’ person can
often provide reassurance that it should be easy to talk again. It is also important to
document in the patient’s notes that a discussion has taken place, to provide a brief
outline of what was said and to record any issues that may be relevant in the future.

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Medical mistakes
Occasionally, people come to harm following a medical complication or a medical
error. This raises quite different communication issues. In addition to breaking bad
news, there is the additional matter of handling guilt and fear of litigation. It is not
possible to make absolute statements but, in general, you should provide a frank and
full explanation and, if an error has been made, offer an apology. Not only is this in
keeping with current thinking in the NHS but, since a sense of injustice often drives
litigation, it is probably also a part of good risk management. It is important to be
clear that one cannot apologise for the actions of others; you can state that you are
sorry to hear of any concerns/worries and that a full reply to questions/complaints will
be provided in time. Recent developments in the UK have led to the introduction of
the concept of the Duty of Candour, which places a duty on a hospital to ensure that
patients are informed if mistakes in their care have led to significant harm. Your role
as the trainee may be to recognise where a patient has suffered a harm that would
require a disclosure under the rules of Duty of Candour.

It is also important to realise that you should not criticise the actions of others without
very careful consideration. General Medical Council guidance stresses the importance
of collegiality, and it is very easy to comment on something without knowing the full
details. Criticism of others is easy to imply by the most innocent off-hand remarks or
ill-guarded body language. In certain cases, such actions can lead the patient to feel
justified in making a complaint or seeking legal advice.

Working with colleagues

Staff relationships are of particular importance in critical care settings. Not only
does the work involve vulnerable and dependent patients, it also carries with it a
lot of work-related emotional issues. It is easy for these pressures to translate into
aggression and lack of respect. They may be made worse when interprofessional
rivalries intervene or when people normally outside the unit are involved with particular
patients.

Ideally, there needs to be some way for these issues to be dealt with on a team
basis – identifying problem areas and finding supportive and effective ways of
achieving change. Methods of achieving this cannot be prescribed but must vary
with the situation. Deficient communication must be addressed, whether within or
between professional groups, either by individual or group meetings, and formally

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or informally. These techniques often remain alien to the medical profession but can
help greatly in the development of efficient and good-humoured units. Individuals
should also show respect in their own behaviour and learn how to use assertive rather
than aggressive or passive interaction (see Glossary). It is important to remember
that the communication issues when talking to patients outlined above also apply to
communication with colleagues. It is easy to make assumptions about colleagues’
knowledge of a situation or their attitudes and motivations towards work. Try not to
make assumptions but approach situations with the view of exploring and confirming
facts and be clear about what has been agreed and who will action any agreements
by confirming actions at the end of conversations.

Coping with adverse events

Emotionally charged events are common in everyday life, and particularly so in the
critical care setting. This holds true for relatives and staff as well as for patients.
Coming to terms with these everyday events is a largely automatic process. In
simple terms, it seems to include having an awareness of the emotional reaction and
somehow returning towards a normal balance. Traumatic stressors are events that
produce intense pressure or tension and are associated with the negative emotions
of fear and sadness. In normal circumstances, these emotional reactions gradually
decline and each subsequent recall of these feelings is rather less intense until
eventually, as a new equilibrium is reached, the emotional reaction fades completely
and the individual adapts.

Faced with events that are perceived to be especially traumatic, this adaptive
mechanism may be overwhelmed. The initial emotional reaction may be so intense
that the only viable reaction is to attempt to prevent or avoid (blot out) these painful
feelings. This may be achieved by avoiding places or objects that remind the person
about the trauma, or through suppression of emotions in general – ‘emotional
numbing’.

These defensive reactions will rarely be completely successful and the individual is
left with painful intrusive recollections, which alternate with defensive avoidance.
This cyclical reaction of intrusion and avoidance is the central element of post-
traumatic stress disorder (PTSD). It is possible that, as the emotions are suppressed
because they are too extreme, they are not held in awareness and do not decline.
The condition becomes chronic and may be disabling. Stress disorders are not rare:

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some symptoms of PTSD are seen in the majority of patients who are involved in
significant accidents and features occur in relatives of the victims and staff. Patients
may report recurrent and intrusive distressing recollections of the event including
flashback episodes. These can be precipitated by cues, which symbolise or resemble
an aspect of the traumatic event (eg hearing a car’s brakes on TV or even driving past
the hospital). The victim is likely to avoid thoughts or cues that activate memories of
the event and may become withdrawn, detached or appear depressed.

Critical events are a significant cause of occupational stress for staff groups (including
doctors) in this environment and this is important to recognise not only for personal
and team well-being but also because operational fatigue and impaired performance
may result. Awareness of stress reactions is the first step and the provision of
appropriate support of colleagues and patients, largely through opportunities for
discussion, will represent a significant advance in many settings. The initial aim is
to provide a means for people to talk about a critical event, learning about some of
the ways that people may respond and (usually) achieving an understanding that
their own behaviour is within a normal range. Your hospital should be able to provide
support for you should you feel particularly affected by adverse events.

Common psychological disorders in surgical critical care

So far, the emphasis has been on specific reactions to adversity, but of course a wide
range of problems may occur. Traumatic life events may trigger feelings of depression,
anxiety or even relapse of certain psychoses. The assessment needs to cover the full
range of psychological difficulties. In this section, brief reference will be made to four
of these.

Anxiety
Mild feelings of fear, apprehension, sadness and emotional turmoil are very common
in anyone admitted to hospital with a serious condition. In general, the approach
taken by the clinical team can often determine the amount of distress experienced. A
team that works well together, communicates well with patients and offers appropriate
emotional support will reduce these difficulties, while dysfunctional teams will
exacerbate the problem.

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Assessment is likely to centre on asking appropriate questions about current feelings

and enquiring into any associated autonomic symptoms of anxiety (eg tachycardia,
raised blood pressure) which may mislead in the assessment of physical health.
Sometimes, visible overbreathing (excessive, often irregular breathing) may be a clue
to the presence of the chronic hyperventilation syndrome. This can present with a
multitude of physical symptoms and is often associated with anxiety or depression.

Major depression
Depression is a common condition and is often unrecognised. It spans a wide range
of severities and patterns of reaction. The core feature is a low mood, in which there
is loss of pleasure and enjoyment, reduced interest, hopelessness and helplessness,
and pessimism for the future. In addition, there are often biological features, such as
loss of weight, impaired sleep with early-morning wakening and a diurnal variation of
mood which is worse in the early morning. Finally, there may be evidence of a frank
psychosis with mood-congruent delusions and hallucinations. These may include
delusions of worthlessness or guilt, delusions of cancer, delusions of persecution
(felt to be deserved) or accusatory auditory hallucination. All these are in keeping
with the primary disturbance of mood. As a routine in the assessment of psychiatric
disturbance, there should be an investigation of suicidal ideation. One way of asking
about this is to combine a permissions statement with a question. For example, if
someone has talked about feeling very unhappy, they may be unable to see much
point in life. Then continue with something like ‘I wonder if you have ever felt it
would be better just to go to sleep and never wake up?’ This can be followed by
further questions about any suicidal thoughts, any suicidal plans (going into detail if
needed) and any suicidal behaviour. In this way, the whole subject can be covered
easily without causing excessive concern. There is no excuse for failing to ask about
suicidal thinking in the presence of significant psychiatric disturbance.

Alcohol dependence
This is included as a reminder that alcohol problems are common (in general, about
one in five people in hospital have significant alcohol-related problems) and can cause
complications for the critically ill surgical patient. The characteristic problem arises
from withdrawal symptoms, which follow hospitalisation and enforced abstinence.
These can include typical tremor, nausea, mood disturbances and confusion but may
extend to delirium tremens and even convulsions.

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Acute organic reactions

Variously styled as confusional states, toxic confusional states, delirium, etc,
these are short-lived organic disturbances characterised by confusion, clouding of
consciousness (sometimes quite subtle), disorientation and often marked fearfulness.
There may be delusions which are often persecutory. Common causes include alcohol
withdrawal and prescribed medication (eg analgesia) but they may also occur in
the context of a wide range of medical conditions. Following assessment using an
ABCDE approach, further evaluation is centred on the cognitive state (ability to attend
and retrieve information, awareness of environment, etc), and on the possible organic
causes, and requires completion of a full assessment and review. This is an organic
disorder in the psychiatric classification because it is always secondary to some
physical dysfunction. It is likely to be made worse in elderly patients or those with
impaired hearing and/or sight by a disorientating environment and by a failure to offer
frequent and repeated explanations.

When to refer to a psychiatrist?

This may depend on the capacity and engagement of the local psychiatric liaison
service. However, there are clear indicators for referral, which are important to outline.
First, there is the situation in which the diagnosis is uncertain and especially where
there may be a psychiatric component. Somatisation disorder and Munchausen’s
syndrome are extreme examples occasionally seen in the surgical population, but
there are often complex interactions between physical and psychological processes
which may require assessment. It is important in these situations to make positive
psychiatric assessments rather than assumptions based on the absence of signs of
physical disorder.

There are situations where either the severity of the psychiatric condition or level of
danger associated with the condition make referral both appropriate and often urgent.
This might be following, for example, deliberate self-harm or the development of
persecutory beliefs in an acute organic reaction leading to thoughts of murder.

One situation in which referral is often considered is in relation to consent for

surgery. Psychiatrists have special knowledge of the legislation to do with consent to
treatment for psychiatric illness. The relevant legislation has much less to say about
consent to treatment for physical illness and common law principles usually apply.
Nonetheless, as long as a referral is not made with overoptimistic expectations, it may

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still be useful to discuss difficult cases where patient consent is withheld as this is an
issue which is more common in psychiatric practice.

Transition to specialty training

Change is unsettling and it is natural for promotion within surgical training to provoke
feelings of apprehension and anxiety. In 2012, Critchley introduced the concept
of ‘zones of change’ and described how, when faced with change, people station
themselves in one of three zones depending upon how confident they feel with the
situation. At one extreme is the comfort zone, in which individuals are secure and
competent, whilst at the other is the high-risk zone, in which huge challenges exist.
Bridging the gap between these is a zone in which learning can occur. By attending
the CCrISP course you have positioned yourself in this zone of development. The
fundamental aim of the course is to provide you with the confidence to safely and
effectively care for critically ill surgical patients, but it is also an opportunity to learn to
take more responsibility for patient care, a hallmark of the step up to specialty training.

Social psychology distinguishes between a ‘change’, which is rapid and happens to

people irrespective of their level of readiness, and a ‘transition’, which is a slower,
developmental process occurring in people’s minds when experiencing change. It is
preferable to view the move to specialty training as a transition because this allows
you to prepare as fully as possible by building on skills which you have already
acquired during core training.

A specialist registrar will often be responsible for the daily business ward rounds,
reporting as necessary to the consultant. It is unlikely that the consultant will conduct
a formal ward round every day, so it is essential that the trainee actively manages the
patients, looks for and identifies problems, makes decisions about management and
contacts the consultant when appropriate. Initially, as a new specialty trainee you
will be communicating very frequently with the consultant but, with experience, your
scope for safe practice can and should expand. It is important to understand when
decisions need to be made and who needs to make them at all times in your training.

Decision-making is impossible without clinical information and business ward rounds

should be timetabled so that key information is most likely to be readily available
from nurses and junior colleagues. As the senior trainee you need to become aware
of what information you need and what is largely superfluous to any critical decision.
There is a balance to be struck between hasty and unfounded decision-making and

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unnecessary delay waiting for tests that will add little or nothing. Getting information
takes you or others time and you need to delegate and organise appropriately. The
CCrISP three-stage assessment process and adherence to ward round standards will
help this process.

To get the best out of a team, leadership is essential. This encompasses a range of
skills including knowledge, affability, decision-making, appropriate humour, humility,
acceptance of other views and firmness. All must be deployed at the right time and
few, if any of us, possess all or even a majority of these attributes. You will need to
work hard, praise and support your colleagues, admit when you are wrong or do not
know and get timely help. Consultants will wish to be informed promptly about unwell
patients (even in the middle of the night) and will expect you to have carried out an
assessment, instituted immediate treatment and devised a provisional plan of action.
The exception to this is the patient who clearly needs an immediate operation beyond
your ability such as a collapsed patient with penetrating trauma. In this situation the
consultant will want a brief, clear message and probably give you a brief and clear
reply.

Role-modelling is very important and clinically you must lead by example: if you
are not thorough, why will anyone else be? Reassessing patients after making
decisions or instigating interventions is vitally important but is perhaps the single most
neglected skill in medicine. With current working practices this is becoming more
difficult, and greater organisation is required for achievement. At the end of your shift
you must hand over to the duty team. A surgical handover can be a challenging task,
particularly when a large number of patients need to be passed on to the duty team.
A written handover list with a concise summary of each patient can be invaluable
in this situation. Some hospitals may have electronic systems to support handover,
and these can facilitate communication between different professional groups and
enhance sharing of knowledge about patients as well as providing a permanent
record of the process. This should be supplemented by a verbal reinforcement of
which patients are giving cause for concern and some acknowledgement from
the doctor receiving the handover that these patients have been identified and the
responsibility accepted.

As the senior trainee you must be prepared to circumvent blocks to your patients’
progress. At times this may require a degree of assertiveness, but caution must
be exercised so that you do not appear aggressive as this may lead to alienation.
Building up good working relationships between other key members of the

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multidisciplinary team will often help in ensuring your patients receive the treatment
they need. Senior nurses, advanced nurse practitioners, outreach nurses, emergency
theatre nurses and radiologists are some examples of people who can make things
happen for your patient and for you.

The promotion to specialty training is associated with an increased responsibility for

patient care on the wards and in the operating theatre. However, in the current climate
of surgical training it is recognised that operative exposure during core training is
significantly less than it has been previously. Working within your limitations is one of
the key skills of being a doctor at any level of training and any feelings of dismay at
perceived surgical inadequacy must be banished. You will very quickly develop new
operative skills and begin to feel that you really are a surgeon.

Summary
This chapter does not provide a comprehensive account of the field of professional
behaviour but highlights those areas where further learning may be required. This
learning is not readily available in text books but can be gained with experience. It
does require insight and reflection on the part of the individual, the latter skill being
easily neglected in a busy surgical environment. Communication skills are especially
important as they help to make practice more effective and efficient. More can be
achieved in less time. It is important to look at patients, relatives and staff groups and
understand the ways in which we cope with the everyday workload, with adversity
and how these mechanisms can be overwhelmed at times of crisis.

Glossary
Most clinicians could improve their communication skills and surgeons are certainly
no exception. The glossary outlines some principles about which you may wish to
read further. The specific skills cannot be summarised in a short glossary but are
included in most books on communication.

Basic communication skills

In this section, some of the terminology will be explained. It is useful in data gathering
to use an appropriate range of open, focused and closed questions. In taking a
history, the open question ‘Is there anything else?’ is useful as a final question.

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Open questions can take a wide range of responses, eg ‘What is the main
problem?’. Focused questions can take a limited range of responses, eg ‘Which
is the worst pain today?’. Closed questions must be answered ‘yes’ or ‘no’, eg ‘Is
the pain in the knee the worst pain that you have?’.

Some questions are likely to produce misleading answers. A leading question expects
a particular response, and this may be given even if it is wrong. Multiple questions are
common in checklist approaches to the history but the answer given may only relate
to the final item in the list – again misleading.

A leading question expects a particular answer, eg ’The pain is worst at night, is it

not?’. Multiple questions include a list, eg ‘Do you have problems with chest pain,
shortness of breath or ankle swelling?’. This might attract the answer ‘no’, which
to the patient might be ‘no’ to ankle swelling and to the doctor might be ‘no’ to
the three items together.

There is a skill to checking back – being prepared to check that you have the right
understanding – or using a summary of the main features as a way of confirming the
history with your patient.

There is also a skill to sharing a problem. If you do not know how to handle something
in an interview, sometimes the best thing is to own up. For example:

‘I have a feeling that you are upset but I am not sure what has caused it. Is it OK
to ask you about it?’

‘My problem is that I only have 5 minutes before I have to go to theatre. I really
need to ask you about something. Is that alright?’

Finally, perhaps the most useful of the active steps in understanding emotional
reactions is the empathic comment. This is a statement identifying an emotional

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reaction, eg ‘That must have made you feel very frightened’. In making this statement,
a great deal of care must be exercised to listen to what is being said and not
simply to assume that everyone will experience fear, anger, sadness, etc, in specific
situations. It is useful as a way of checking back on emotions but, more importantly,
it communicates that you can appreciate at least some of what your patient is feeling.
This can be a very powerful intervention and should be a skill available to all doctors.

Blocking

This means not facing up to an issue. This occurs, or example, when a patient asks
‘Are there any complications with this operation?’ and the surgeon replies, ‘Don’t you
worry, it’ll all be fine’. Another example is a doctor telling a patient they have cancer
and the patient says ‘It can’t be cancer, I feel too well’.

Mirroring

This is reflecting what the patient is saying in terms of tone of voice and body
language. For example, if a patient is talking softly and timidly, reply in similar tones.
If a patient is sitting leaning forward, do the same. Doing the opposite (anti-mirroring)
can adversely affect interactions.

Assertiveness, passivity and aggression

In being assertive, communication allows each person to express their honest
opinions without needlessly hurting the other person. In being passive, honest
opinions are suppressed.

Aggression involves the use of excessive force or power, causing needless suffering.
This can be active aggression (eg violent, insulting speech) or passive aggression (eg
emotional manipulation).

Assertiveness is, therefore, usually the preferred option. In general, assertive

statements contain the pronoun ‘I’ whereas aggressive statements more often include
the pronoun ‘you’, for example, ‘I feel that the patient would be better helped by this
approach’ versus ‘You are incompetent and have got this all wrong’.

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Further reading
Beauchamp TL and Childress JF. Principles of Biomedical Ethics. 7th edn. Oxford
University Press, Oxford; 2017. ISBN: 9780199924585.

Critchley K. Managing change. BJMP 2012: 5 (3): a531. Available at http://www.bjmp.

org/files/2012-5-3/bjmp-2012-5-3-a531.pdf.

Royal College of Surgeons of England. 'Consent: Supported Decision-

Making – a good practice guide'. Available at: https://www.rcseng.ac.uk/
library-and-publications/college-publications/docs/consent-good-practice-guide/

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 16

Assessment of surgical risk

and perioperative care

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 Chapter 16  Assessment of surgical risk and perioperative care

Learning outcomes 
This chapter should enable you to:

n appreciate the importance of assessing perioperative risk;

n recognise the factors that contribute to increased surgical risk;

n identify patients at increased risk of a perioperative cardiac event.

Introduction
Approximately 250,000 patients (15% of total hospital inpatients having surgery) can
be considered to be at high risk of adverse outcomes during their procedure.

The presence of any comorbidity increases the risk associated with surgical
procedures, and minimising that risk is vitally important to improve outcomes, as
high-risk patients account for 80% of deaths after surgery. Risk assessment is also
important in terms of outcome measures for comparative audit, eg the National
Emergency Laparotomy Audit (NELA) and NCEPOD (National Confidential Enquiry
into Patient Outcome and Death) studies. Simple scales, such as the American
Society of Anaestheologists (ASA) grading system, are open to varied interpretation
among experienced medical assessors, while more complex systems, such as
the physiological and operative severity score for enumeration of mortality and
morbidity, or POSSUM, are too complex for most daily clinical applications or have
a retrospective element that makes their reliability in preoperative risk assessment
limited.

Coexisting diseases can complicate even a simple operation and increase morbidity
and mortality, as in the case of a patient with a heart transplant who needs to undergo
surgery for a cholecystectomy. The level of care required for a particular patient
needs to be anticipated and consideration given to transfer to units with appropriate
facilities, and to gaining the expertise needed to advise on preoperative optimisation
and perioperative management of individual comorbidities.

The concept of a ‘high-risk’ patient is generally understood, but the key is to

recognise the factors contributing to that perceived risk and repeatedly (re)assess
these patients throughout their stay in hospital to minimise the risk of developing
complications.

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Many of the factors that increase surgical risk are covered elsewhere in this book. This
chapter will discuss risk assessment in more detail and outline the specific effects of
older age and obesity. There is also a specific chapter on diabetes (Chapter 17).

The metabolic response to injury

An understanding of the metabolic response to injury is helpful in understanding how
comorbidity affects perioperative management and risk (see also Chapter 13).

Metabolic responses to major injury, surgery and severe infection have similar
mechanisms. The response occurs in two phases, referred to as ‘ebb and flow’.
The mediators and their effects for these responses are outlined in Box 16.1. The
‘ebb phase’ lasts 24–48 hours and is a neuroendocrine response to tissue injury and
hypovolaemia. Cardiovascular reflex activity and inhibition of central thermoregulation
are reminders of the ‘fight or flight’ response. Energy stores are mobilised to fuel the
increased metabolic demand: plasma glucose concentration increases in proportion
to the severity of the injury as a result of mobilisation of liver and skeletal muscle
glycogen stores and the suppression of insulin release that inhibits the uptake of
glucose into cells. Lipolysis is increased but fatty acid re-esterification within adipose
tissue may be stimulated by the raised plasma lactate of severe injury or impaired
perfusion of fat deposits. An early rise in hepatic protein synthesis and an increase in
microvascular permeability are responsible for the characteristic changes in plasma
protein concentrations observed within 6 hours.

Survival beyond the first 1- to 2-day initial phase gives rise to the ‘flow phase’ of
increased metabolic rate, principally due to muscle catabolism and resistance to the
anabolic effects of insulin.

The triggers for this are similar to the first phase but with increased energy
consumption. The high-energy source ATP is produced principally by glycolysis
(an inefficient mechanism) and the lactate produced is reconverted into glucose
in the liver in an energy-consuming process, thereby increasing hepatic oxygen
consumption and blood flow. Protein catabolism predominates, principally affecting
skeletal muscle, but respiratory, gut and (possibly) cardiac muscle are also affected,
giving rise to problems with mobility, ventilation and enteral nutrition. There are
concomitant increases in urinary excretion of nitrogen and creatinine. The increase
in proteolysis provides amino acids as precursors for hepatic gluconeogenesis.

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Intramuscular glutamine concentration is decreased because of increased efflux and

possibly decreased de novo synthesis.

Glutamine is an important fuel for cells of the immune system and it is a precursor for
glutathione (a free radical scavenger); it has a role in nitric oxide metabolism and has
also been implicated in the maintenance of the gut mucosal barrier, which may be
compromised after injury.

Insulin resistance after injury refers to its anabolic effects; for example, hepatic
glucose production, lipolysis and the net efflux of amino acids from skeletal muscle.
These effects persist as plasma glucose and insulin concentrations that are inhibitory
in uninjured subjects. Uptake of glucose into skeletal muscle is also reduced, an
impairment that involves glucose storage rather than oxidation. The cause may
result partly from the counter-regulatory hormones cortisol, adrenaline and glucagon,
although infusion in healthy individuals requires much higher plasma concentrations
to cause insulin resistance than those found in injured or septic patient. The effect
of these hormones can be augmented by modulation of insulin sensitivity by pro-
inflammatory cytokines: IL-6 in cancer patients, IL-1 in endotoxaemia and TNF in
diabetes and obesity are all correlated with the degree of insulin resistance.

Box 16.1  Mediators of injury response and their effects

Counter-regulatory hormones

(eg catecholamines [adrenaline], cortisol, glucagon, antidiuretic hormone)

• Breakdown of glycogen stores in liver and skeletal muscle

• Suppression of insulin release resulting in reduced uptake and oxidation of
glucose

Increased sympathetic nervous system activity

• Lipolysis

Protein metabolism

• Increased hepatic synthesis (IL-6 induced)

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• Increased microvascular permeability

• Raised plasma concentration of fibrinogen and C-reactive protein
• Fall in plasma albumin concentration

Proinflammatory cytokines (eg TNF-α, IL-1β, -2, -6 and -8)

• Mimic some responses, but plasma levels not universally linked to injury
indicating autocrine/paracrine (cf endocrine) function

IL-6 induction of prostanoids at the blood–brain barrier

• Activation of the hypothalamus–pituitary–adrenal axis

Perioperative medicine
There is considerable interest in the development of multidisciplinary care pathways
that manage patients before, during and after their operation. Specialties such as
cardiac surgery have shown that by adopting such an approach, the overall mortality
of surgery can be reduced.

Comorbidities and perioperative care

Good surgical results reflect patient selection and the quality of perioperative care.
This depends on:

n surgical factors, relating to pre-, intra- and postoperative care;

n patient factors, regarding disease presentation and pre-existing comorbidities,

age, gender, biomarkers and socioeconomic factors;

n systemic factors that relate to the resources available for the treatment of surgical
patients and treatment of complications.

Pre-existing comorbidity increases the risk of surgery. Anticipation of risk and risk-
factor modification are vital in attempting to reduce surgical morbidity and mortality.
Comorbidities most commonly associated with increased surgical morbidity and
mortality are:

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n cardiovascular (hypertension, myocardial ischaemia, cardiac failure and cardiac

arrhythmias;)

n chronic respiratory disorders;

n anaemia;

n diabetes mellitus;

n chronic renal impairment;

n obesity;

n immunocompromised states such as poor nutrition, infectious diseases,

connective tissue disorders, etc;

n chronic liver disease.

Elderly patients are more likely to have coexisting medical illness and a reduced
physiological reserve and much of the focus of assessment in the elderly patient
should be directed towards assessing their degree of physiological reserve and any
frailty. Many hospitals now have specialist geriatricians who plan the care of very
elderly patients undergoing both elective and emergency orthopaedic surgery. As
surgeons you will not be expected to have detailed knowledge of the long-term care
of patients with chronic diseases but you are expected to understand your role within
the team and act accordingly.

Obesity
Excessive body weight is a growing epidemic among people of all ages in the UK.
The reference scale for obesity is the BMI, which is given by weight (in kg) divided
by height (in m2). The normal range for BMI is 20–25 kg/m2. Obesity is defined as a
greater than 20% increase over the ideal body weight, which equates to a BMI over
30 kg/m2. A patient with a BMI over 35 kg/m2 can be considered morbidly obese.

Obesity increases the likelihood of associated medical disorders including ischaemic

heart disease (especially central obesity), hypertension, oesophageal reflux, diabetes,
obstructive sleep apnoea (OSA), osteoarthrosis, gallstones, varicose veins and
haemorrhoids. It can also result in a chronic inflammatory response driven by the
excess adipose tissue.

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Increased insulin resistance is strongly associated with increasing BMI. Some

obese patients will develop a metabolic syndrome, which significantly increases
perioperative cardiac risk: this is defined by a collection of symptoms of central
obesity, insulin resistance, dyslipidaemia and hypertension. The presence of a
metabolic syndrome and obesity increases complications and mortality in those with
a BMI > 50 kg/m2.

OSA is frequently undiagnosed but present in 10–20% of morbidly obese patients. If

untreated, heart failure and pulmonary hypertension can occur. Strong predictors of
OSA include male gender, older age, diabetes, hypertension, snoring (usually reported
by the partner) and large collar size.

The STOP-BANG questionnaire is a screening tool designed to pick up these

predictive factors (Figure 16.1). A STOP-BANG value of 5 or more indicates the likely
presence of OSA and, if OSA is identified, perioperative patient management may
include admission to critical care postoperatively if general anaesthesia is required.

Do you snore loudly? Yes/No

Do you often feel tired, fatigued, or sleepy during the

Yes/No
daytime?

Has anyone observed you stop breathing during

Yes/No
your sleep?

Do you have or are you being treated for high blood

Yes/No
pressure?

Are you obese/very overweight – BMI more than 35

Yes/No
kg/m2?

Age over 50 years old? Yes/No

Neck Circumference >16 inches? Yes/No

Are you male? Yes/No

Figure 16.1  STOP-BANG questionnaire.

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Reaching a diagnosis of an acute problem can often be rendered more difficult in

obese patients. General anaesthesia and surgical procedures are more hazardous
and postoperative complications, especially those relating to cardiopulmonary events,
venous thromboembolism and the wound, are more frequent.

In patients with non-life threatening conditions requiring elective surgery, preoperative

weight loss should be recommended. Before all operations, at least blood glucose
and ECG should be checked preoperatively, even in younger patients. Further
investigations and preoperative optimisation will depend on other patient and surgical
factors. The risk of an adverse perioperative cardiac event is related to the nature and
severity of the underlying heart disease, associated comorbidities and the type of
surgery undertaken. The need for additional cardiac-based investigations should be
made on the basis of patient comorbidities, function and the planned surgery. In the
immobile, morbidly obese population, many of the functional assessments, eg shuttle
walk test, are not always possible. Proceeding to elective surgery requires a balance
of risk versus benefit and may warrant careful discussion with the patient.

The elderly
A social definition of elderly is all those over 65 years of age, and this group accounts
about one in four patients admitted to surgical wards. Increasingly, patients over 80
years of age are being considered for major surgery, and these patients provide a
special challenge.

Two main reasons for increased risk with ageing are the frequent association of age
and concurrent medical problems and decreasing functional reserve in many organ
systems, making the elderly less able to respond to the physiological consequences
of an operation. This is especially true for the respiratory system, cardiovascular
system, kidneys, nervous system and drug handling. Again, careful patient
assessment, optimisation and perioperative care should reduce the surgical risk.
Polypharmacy (defined as use of five of more medications regularly) is common in this
patient population.

Calculated risk for elderly patients after surgery is not clearly defined. The US National
Surgical Quality Improvement Programme identified events in the postoperative
period as more important than preoperative patient risk factors in determining
survival, but very little research has examined functional and social outcomes after
major surgery. The American College of Surgeons and the American Geriatric Society

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have produced an evidence-based best practice guideline which provides useful

guidance (see Further reading).

Risk assessment
Defining levels of risk to patients is important, both for enhancing the outcome of
surgical intervention and for managing the expectations of patients, their relatives and
our colleagues. Assessment of risk is also part of the process in achieving informed
consent from patients for surgery.

Assessment of clinical risk is a complex higher function that forms an integral part
of training. Apart from direct clinical experience, how can we improve our risk
assessment?

Evidence-based medicine provides different levels of confidence about the outcome

of an intervention when examining published results. The most robust evidence
comes from randomised controlled trials (RCTs) and meta-analyses of several RCTs
on the same topic, while case–control series provide lower levels of evidence and
case reports provide the lowest (but not always insignificant) form of evidence. These
data often suffer from the constraints of carefully conducted trials but can be used in
your own practice to establish criteria for audit and quality improvement. Audit aims
to improve the care of patients by establishing a standard, identification of areas
for improvement and implementing that improvement, then evaluating the effects
of implementation. Audit can also be national with contribution of data to national
databases that are being established by the surgical specialty associations, eg the
National Emergency Laparotomy Audit.

In the workplace, mortality and morbidity conferences provide a forum in which

factors that have contributed to adverse outcomes can be debated and strategies
may be developed to improve unit outcomes. National surveys such as NCEPOD
(National Confidential Enquiry into Patient Outcome and Death) allow panels of
experts to analyse surgical deaths and make conclusions about their causes and
recommendations for prevention. This can be around preoperative preparation, the
grade and seniority of staff involved and the resources available for treatment (eg
provision of emergency theatres, ICU and HDU care). NCEPOD reviewers are selected
by open application and you may wish to become involved as a reviewer in an
NCEPOD audit when you progress to higher training.

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Measurement of risk aims to provide some objective evaluation of individual patient

risk and can allow comparison of individual clinicians or units. This is a growth area
for research. Scoring systems have been developed in most subspecialties and for
many individual conditions or procedures to try and produce a scale that will allow an
accurate prediction of outcomes for each patient. Highly complex scoring systems
may be unwieldy in the clinical situation and, when found to be valid in one unit or
specialty, may require modification for successful adaptation to other specialties
eg POSSUM. Simple and more widely applicable scoring systems such as the ASA
grading system are in wide clinical use and ASA data are frequently a feature of
anaesthetic and surgical outcomes databases (Table 16.1).

Most patients will be assigned an ASA grade (I–V) by the anaesthetist assessing
the patient preoperatively. Although the scale is widely used, it is recognised to be
open to individual variation, and even experienced anaesthetists may vary in their
assessment of the same patient. This blunts its sensitivity and ability to discern actual
risk for an individual patient.

Risk management is developing in healthcare and is borrowing ideas and techniques

from the aviation industry, which has practised risk avoidance with great success
over many years. In addition to anticipating risk and the management of appropriate
preventative strategies, a cultural change around the use of the information is
developing. Using adverse incident monitoring as an education tool, rather than as
a tool for apportioning blame, allows for learning appropriate lessons and putting
strategies in place that minimise the likelihood of repeated failure. In addition, aviation
simulators that reproduce critical incidents allow important skills to be developed
that can then be put into practice at appropriate moments when real lives are at
stake. In surgery, this translates to the use of courses like CCrISP, skills laboratories
and simulation centres in which clinical skills and techniques can be practised in

Table 16.1  The ASA system for grading surgical risk

Grade Definition Mortality (%)
I Normal healthy individual 0.05
II Mild systemic disease, does not limit activity 0.4
III Severe systemic disease, limits activity but is not incapacitating 4.5
IV Incapacitating systemic disease, constantly life-threatening 25
V Moribund, not expected to survive 24 h with or without surgery 50

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the context of simulated patients and procedures in order that best practice can be
learned and honed, for use in the clinical arena.

An international campaign to reduce harm in perioperative care has led to initiatives

such as ‘Patient Safety First’ within the NHS. This is based on an acknowledgement
by healthcare workers that events that produce harm in patients are potentially
avoidable. An example of one such initiative is that of reducing surgical site infections
by establishing a target reduction and examining compliance with appropriate
interventions to achieve it, including appropriate use of prophylactic antibiotics,
maintaining normothermia, maintaining glycaemic control in diabetic patients and
using recommended hair removal methods. In addition, to increase safety in the
operating theatre, the use of the World Health Organization Surgical Safety Checklist
is being implemented in hospitals. This contains the team brief, sign-in, a time-out
before surgery (degree of urgency permitting), sign-out at the end of the procedure
prior to transfer to the recovery area and debrief after patient has gone to the
recovery. The anaesthetist, surgeon, scrub nurse and other theatre staff discuss the
patient preparation, any anticipated critical moments, potential complications and
how these will be managed during the checklist. As champions for risk management,
surgeons can demonstrate leadership in the care of patients that will improve the
outcome of our treatment and operations.

Preoperative assessment clinics

In many hospitals there are now dedicated clinics where the focus is on assessing
and preparing patients for surgery, particularly assessing the cardiorespiratory
system. Tests can be divided into those which are relatively static, such as resting
ECG or resting echocardiography, and dynamic (stressed) tests such as exercise ECG
or stress echocardiography.

Cardiopulmonary exercise testing (CPET) looks at the cardiorespiratory system in

its entirety, and is dynamic, robust and replicable by progressively stressing the
patient using a standardised test. CPET quantifies a patient’s ability to respond to
the metabolic demands of major surgery. There are considerable data to suggest
that cardiorespiratory reserve absolutely correlates with probability of death and
complications perioperatively. An anaerobic threshold is measured for each patient,
and this is then used to triage patients into a perioperative care package that
is appropriate for their degree of risk. Anaerobic threshold is the point at which

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inadequate oxygen delivery results in a shift to anaerobic metabolism and is not

altered by patient effort. An anaerobic threshold of at least 11 ml/kg/min is considered
necessary for major elective surgery, and values less than this almost certainly mark
the patient out as requiring postoperative care on an ICU or HDU.

However, aside from cardiorespiratory reserve, age, nature of surgery and other
physiological systems and coexisting disease are also important in terms of
perioperative risk. So, for instance, concomitant renal disease or neurological
disease may also impact upon perioperative risk, and there may be immunological,
haematological, endocrinological, hepatic function or malnutritional considerations.

The important issue with preassessment clinics is to assess physiological reserve and
consider whether any of the systems can be improved prior to surgery. There is also
now growing interest in preconditioning, whereby patients are given a graded exercise
programme prior to planned surgery, as this is also thought to improve outcomes.

The role of enhanced recovery

Enhanced recovery after surgery (ERAS) programmes, initially developed in colorectal
patients by Henrik Kehlet, are being increasingly used across the surgical spectrum.
Evidence shows that patient outcomes, length of stay and patient satisfaction are
improved by these programmes.

ERAS programmes are essentially packages of care that describe the patient journey
from time of decision to operate to discharge from hospital after surgery. The basic
principles are described below and all aspects of the package need to be adhered
to for success. The relative effectiveness of each individual component is difficult to
demonstrate but there is evidence that the catabolic phase of the surgical response
earlier in this chapter can be reversed by the use of oral preoperative carbohydrate
loading.

Outline of enhanced recovery programmes

Preoperative phase
The goal in the preoperative phase is to ensure that patients are as fit as possible
so that they have the best chance of making an uncomplicated and quick recovery
from their forthcoming surgery. This involves an accurate and detailed preassessment

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process which identifies and modifies, where possible, the patient’s comorbidities.
Good control over comorbidities such as diabetes, cardiovascular and pulmonary
disease, as well as treating anaemia and encouraging patients to stop smoking
(stopping smoking for 1 month prior to surgery can reduce the incidence of wound
infection and respiratory complications) are all important considerations. Ideally, this
process should start in general practice once the patient is referred. CPET is used to
quantify the risk around the surgery, and may be useful in informing the discussion
with the patient, and in planning postoperative requirements.

The patient needs to be actively engaged in discussing what happens around the time
of surgery and goals set for them to achieve in terms of mobility and estimated length
of hospital stay. Daily targets are also identified, supported by a written pathway that
is actively monitored by the ward nursing staff, who, together with the physiotherapy
team and any specialist nurses, play a vital role in supporting and encouraging the
patient postoperatively. These expectations need to be actively reinforced by the
whole of the team during the patient’s journey. Having named individuals to lead and
champion ERAS programmes can lead to greater compliance with the pathway.

A risk assessment for venous thromboembolic disease should be carried out

and thromboembolic deterrent stockings used when not contraindicated and the
appropriate dose of prophylactic subcutaneous fractioned heparin prescribed. Single-
dose antibiotics are given as prophylaxis against wound or prosthesis infection in
accordance with local hospital policy. The aim is to continue cardiac, pulmonary and
antacid medications on the day of surgery, but a decision regarding the risks and
benefits of stopping anticoagulant medication such as warfarin or dabigatran and
antiplatelet medication such as clopdiogrel and dipyridamole needs to be made and
may require discussion with other specialties.

Operative phase
Medication to control postoperative nausea and vomiting is given at the time of
induction. Intraoperative care includes prevention of hypothermia, goal-directed
intraoperative fluid therapy using fluid boluses and stroke volume optimisation
supplemented by judicious use of vasopressors. Minimally invasive techniques are
preferred such as short and transverse incisions for open surgery, avoidance of
postoperative drains and naso-gastric tubes, and avoidance of or short-duration use
of epidural analgesia, with local blocks being preferred as appropriate.

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Postoperative phase
The postoperative phase aims to restore the patient’s normal function as soon as
possible. Daily goals for mobilisation and tube removal should be set and met.
Good pain relief aimed at restoration of function such as deep breathing, coughing
and moving rather than the elimination of all pain is important. The use of opiate
medication should be minimised and other analgesics and/or local anaesthetic
techniques should be used. Allowing oral intake of fluids and diet immediately after
surgery, combined with the measures described above to prevent postoperative
nausea and vomiting, leads to early return of gut function, another important goal in
the postoperative phase. Early cessation of IV fluids contributes to this. Early removal
of other tubes reduces pain and aids mobilisation. Giving patients a sense of having
control over their own recovery facilitates the process.

When managing patients on ERAS programmes it is important to realise when

complications may be developing. The use of a track and trigger system and the
CCrISP three-stage assessment process should facilitate this. Once it is recognised
that a patient has ‘fallen off’ the enhanced recovery pathway they need to be
managed differently, especially with regard to fluid therapy which should be used in a
resuscitative manner rather than in a restrictive manner.

Summary
n It is essential to recognise the factors that contribute to surgical risk.

n All members of the surgical team have a responsibility to ensure that patients are
as fit as possible prior to surgery.

n Be aware of comorbidities to predict and prevent perioperative problems and

manage any that do occur in the perioperative period in a timely manner.

Further reading
Agnew N. Preoperative cardiopulmonary exercise testing. Contin Educ Anaesth Crit
Care Pain 2010; 10 (2): 33–37.

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Khuri SF Henderson WG, DePalma RG et al. Determinants of long-term survival after

major surgery and the adverse effect of postoperative complications. Ann Surg
2005; 242: 326–343.

Mohanty S, Rosenthal RA, Russell MM et al. Optimal perioperative management

of the geriatric patient: A best practices guideline from ACS NSQIP®/American
Geriatrics Society. Available at https://www.facs.org/quality-programs/acs-nsqip

Royal College of Anaesthetists. Perioperative Medicine: the pathway to better surgical

care. Available at https://www.rcoa.ac.uk/periopmed/vision-document

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Perioperative management
of diabetes

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 Chapter 17  Perioperative management of diabetes

Learning outcomes 
This chapter should enable you to:

n appreciate the importance of recognising and treating diabetes in the surgical

patient;

n work through examples of management plans for surgical patients with

diabetes;

n identify other clinical and metabolic states associated with poor glucose
control.

Introduction
The prevalence of diabetes mellitus is rapidly increasing and diabetes now affects
4–5% of the UK population. Diabetes is a state of impaired glucose tolerance
caused by either absolute lack of insulin (type 1) or relative lack of insulin (type 2). In
addition to the metabolic disturbance, micro- and macrovascular abnormalities cause
retinopathy, nephropathy, neuropathy, coronary heart disease, stroke and peripheral
vascular disease. Diabetic patients also develop cataracts and specific soft tissue
disorders such as diabetic cheiroarthropathy as a result of exposure of the tissues to
hyperglycaemia, causing accelerated irreversible biochemical and structural changes
normally found in ageing. Improved glycaemic control in diabetes protects against
these secondary effects.

Even the simplest surgery can be hazardous to diabetic patients. The metabolic
response to surgical trauma can rapidly lead to hyperglycaemia and ketoacidosis,
especially in insulin-deficient patients. Poorly controlled diabetes accelerates
catabolism and delays healing. Insulin and the sulphonylureas can cause severe
hypoglycaemia in fasted and anorexic patients, which can be particularly dangerous
during general anaesthesia. Assessment of fitness for surgery, preoperative
optimisation, an agreed management policy between specialists and ward staff and
meticulous glycaemic control will greatly reduce the risks of operating on diabetic
patients.

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Utility of preoperative glycated haemoglobin values

Good preoperative glycaemic control as directed by the HbA1c concentrations is
associated with decreased morbidity and mortality and also shorter hospital stay (Box
17.1).

Box 17.1  HbA1c values

Non-diabetic reference range: 4.0–6.0% or 20–42 mmol/mol

Diagnostic of diabetes mellitus: > 6.5% or 48 mmol/mol on repeated testing

High risk of diabetes: 6.0–6.4% or 42–47 mmol/mol

Target HbA1c concentration for diabetic patients: 6.5–7.5% or 48–58 mmol/mol

HbA1c values of > 8.6% or 70 mmol/mol are associated with four-fold mortality in

cardiac surgery

Some case examples will serve to illustrate the key management issues in patients
with diabetes undergoing surgical treatment. You are advised to read and review the
Joint British Diabetes Societies inpatient guidelines at this point (see Further reading).

Case scenario 17.1 

A 33-year-old civil servant, admitted to the surgical unit for an open elective
inguinal herniorrhaphy, is stabilised on three times daily subcutaneous soluble
insulin injection and is otherwise fit and well.

How would his diabetes be managed perioperatively?

Such patients have absolute deficiency of insulin and require variable-rate

intravenous insulin (VRIII) infusions to be instituted on the morning of surgery
after an overnight fast and omission of the morning insulin dose. A protocol for
infusion is given in Box 17.2, but note that most hospitals will have their own local

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protocols and you should make sure you are familiar with the one where you
work.

The patient had an uneventful procedure under general anaesthesia on the

morning list with hourly blood glucose recordings showing good control with
plasma levels of glucose between 5 and 10 mmol/L. Owing to postoperative
nausea and vomiting, the VRIII regimen was continued overnight. By the
next morning, he was able to eat and drink normally; the VRIII infusion was
discontinued and he had his normal morning insulin dose with his breakfast and
was discharged home later that morning.

Case scenario 17.2 

A 67-year-old retired coach driver was seen in the preadmission clinic for
workup for an elective transurethral prostatectomy for symptomatic benign
prostatomegaly. He has been diabetic for 5 years and his disease is currently
controlled with diet and oral glibenclamide.

How would you manage his diabetes?

Generally, patients with type 2 diabetes that is well controlled by diet or oral
agents may simply omit their oral agents and breakfast on the morning of
surgery. However, long-acting sulphonylurea drugs (eg glibenclamide) should
be replaced by short-acting ones (eg glicazide) some days before surgery to
reduce the risk of hypoglycaemia. Blood glucose should be monitored closely in
the perioperative period and persistent hyperglycaemia should be treated with
a VRIII infusion. If the patient is in a steady state, the VRIII infusion will maintain
satisfactory glycaemic control and prevent hypokalaemia. If glucose levels are not
within the range then, as an alternative, insulin may be given as a variable-rate
intravenous infusion (Box 17.2), which provides greater flexibility.

Always consider the clinical haemodynamic state and review U&Es before deciding on
the type and rate at which IV fluids are prescribed and administered (Table 17.1).

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Table  17.1  Fluid regime whilst on VRIII

Blood glucose and serum
Patient group K+ level Fluid recommendation
No concern of fluid overload Blood glucose > 14 mmol/L 0.9% NaCl with 20 or 40 mmol/L KCl at
Serum K+ 3.5–5.5 mmol/L 125 ml/h
Blood glucose < 14 mmol/L 5% dextrose with 40 mmol KCl at 125 ml/h
Serum K+ 3.5–5.5 mmol/L
Serum K+ > 5.5 mmol/L No additional KCl, reassess serum K+ and aim
to keep serum K+ between 3.5 and 5.5 mmol/L
Risk of fluid overload Consider whether VRIII is needed or use
subcutaneous insulin regimen; consider 10%
dextrose rather than 5% dextrose
Hyopnatraemia or serum Na+ Consider whether VRIII is needed or
falls greater than 3 mmol/L in use subcutaneous insulin regimen; high
24 hours concentration NaCl can be used after
discussion

Diabetic ketoacidosis (DKA) is uncontrolled hyperglycaemia with hyperketonaemia

severe enough to cause metabolic acidosis. It is caused by severe insulin deficiency
that stimulates lipolysis and a massive increase in ketogenesis. It is the hallmark
of poorly treated type 1 diabetes but can occur in type 2 diabetes when patients
are relatively insulin deficient and there is intercurrent illness, stimulating counter-
regulatory hormone secretion (especially glucagon). It carries a mortality of 5–10%
(50% in elderly patients with DKA precipitated by MI or infection). Prompt diagnosis
and management is essential to prevent death.

As well as hyperglycaemia, hyperketonaemia occurs due to oxidation of free fatty

acids in hepatocyte mitochondria (a process stimulated by glucagon and inhibited
powerfully by insulin), yielding ATP and acetyl-CoA. The latter is converted to
acetoacetate, which may be oxidised to 3-hydroxybutyrate or undergo condensation
to produce acetone. Ketones are transported out of the liver and used as metabolic
fuels by various tissues including the brain; they provide a few per cent of the total
energy needs after an overnight fast, but this rises to one-third in prolonged fasting.
When produced in excess, they accumulate rapidly as uptake mechanisms become
saturated. The main consequences of raised circulating ketones are:

n acidosis, both extracellular and intracellular;

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n diuresis, as osmotically active ketones are filtered in the urine, exacerbating the
osmotic diuresis caused by glycosuria, and resulting in polyuria, electrolyte losses,
dehydration and hypovolaemia;

n nausea – by direct stimulation of the chemoreceptor trigger zone in the medulla.

Simultaneous resuscitation and investigation includes a 12-lead ECG, bacteriological

cultures of all appropriate fluids including blood and urine, cardiac enzyme
determination and ABG analysis. Intravenous saline and insulin should begin
immediately (Box 17.2). Urgent treatment with scrupulous clinical and biochemical
monitoring is essential. Correction of hypovolaemia will often improve acidosis and
hyperglycaemia. However, overenergetic fluid and insulin replacement can predispose
to cerebral oedema and increase mortality. CVP monitoring for the elderly and those
at risk of heart failure may be required. Monitoring for response is essential and 0.9%
saline (containing potassium when appropriate; see Box 17.3) is the fluid of choice.
Dextrose 5% is substituted when plasma glucose has fallen to 10–14 mmol/L to
prevent hypoglycaemia (insulin is still required to prevent ketogenesis and promote
glucose utilisation in the tissues).

Box 17.2  Variable-rate intravenous insulin infusion: guidance

• Start VRIII at the standard rate
• Measure blood glucose every hour and adjust VRIII to keep the glucose level
between 6 and 10 mmol/L
• If blood glucose is > 14 mmol/L and not under control move to increased insulin
rate scale
• If blood glucose is < 4.0 mmol/L, stop VRIII and treat hypoglycaemia
• If blood glucose control is too tight, ie blood glucose persistently 4 mmol/L,
consider using reduced insulin infusion rate
• Monitor urea and electrolytes (U&Es) daily and adjust potassium chloride dose
accordingly
• Usual diabetic medications should be omitted during VRIII

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Case scenario 17.3 

A 66-year-old woman was admitted from A&E with a 6-day history of feeling
unwell, with immobility and discharge from the right foot. She has had diabetes
for 7 years treated with diet, glicazide and metformin. Examination revealed
discharge from the instep, a necrotic heel and cellulitis extending across the
ankle into the lower leg. Her pulses were all palpable, but there was diminished
pedal sensation. Her Hb was 111 g/L, WCC 18.6 × 109/L, blood glucose
24 mmol/L, potassium 5.8 mmol/L, urea 9.0 mmol/L and creatinine normal.

How would you manage this patient?

She should be managed as per the CCrISP protocol, with immediate attention to
ABCDE assessment and resuscitation. Her diabetes is out of control. A variable-
rate intravenous insulin infusion (Table 17.2), with hourly monitoring of the blood
glucose and 3- to 4-hourly potassium estimation (Box 17.3) is appropriate. She
requires resuscitation with IV 0.9% saline until she has been stabilised, and her
glycaemic and potassium control optimised. Administration of broad-spectrum or
‘best-guess’ intravenous antibiotics aids stabilisation of sepsis and the metabolic
state prior to definitive treatment of foot sepsis: debridement or amputation
will give the best result. Rarely, gas-forming organisms may be present; if gas
gangrene is suspected, urgent surgery will be required after initial resuscitation,
so urgent senior surgical review is needed.

Box 17.3  A potassium replacement regimen

In an unstable patient with varying insulin requirements, serum potassium levels
should be monitored every 3–4 hours.

Replacement should be guided by the latest serum K+ concentration

• if K+ > 5.0 mmol/L, omit KCl due to the risk of cardiac arrhythmias

• if K+ 3.5–5.0 mmol/L, add 20 mmol KCl to each litre of IV fluid
• if K+ < 3.5 mmol/L, add 40 mmol KCl to each litre of IV fluid.

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Table 17.2  Variable rate intravenous insulin infusion

Insulin rate (ml/h)
Glucose (mmol/L) Reduced rate Standard rate (first choice) Increased rate
< 4 0 0 0
4.1–8.0 0.5 1 2
8.1–12.0 1 2 4
12.1–16 2 4 6
16.1–20.0 3 5 7
20.1–24.0 4 6 8
> 24.1 6 8 10

Case scenario 17.4 

A 68-year-old, overweight woman was admitted in a coma. Her family provided
a history of abdominal pain, anorexia and vomiting for 1 week against a
background of 15 years of diabetes mellitus. In the early years, her diabetes
was controlled by diet and oral hypoglycaemic agents; however, for the past 8
years, she has required subcutaneous insulin supplementation. On admission,
she appeared to be dehydrated and had a temperature of 38.3°C, a pulse of 130/
min and systolic blood pressure of 80 mmHg. There was epigastric fullness and
guarding and she had sighing respiration with a smell of acetone on her breath.
A chest X-ray showed basal atalectasis. Blood results showed Hb 101 g/L, WCC
19.5 × 109/L, Na+ 152 mmol/L, K+ 6.7 mmol/L, HCO3– 15 mmol/L, Cl– 100 mmol/L,
urea 22.5 mmol/L, creatinine 85 μmol/L, glucose 36 mmol/L. Her urine was
strongly positive for ketones.

What is the management of this patient?

This is a complex clinical problem that cannot be managed in a general surgical

ward. The patient should be managed according to the CCrISP protocol with
simultaneous immediate assessment and resuscitation. Although she probably
has a surgical problem, she also has DKA and this needs to be managed jointly
with critical care and endocrinology input in an HDU facility with continuous ECG
monitoring and close biochemical monitoring of glucose (hourly) and potassium
(3- to 4-hourly) levels (Boxes 17.2 and 17.3).

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Use of bicarbonate and hypotonic solutions is contentious. Hypotonic solutions may

exacerbate intracellular movement of water and could lead to cerebral oedema, while
bicarbonate may improve extracellular acidosis. However, as membranes are not
permeable to bicarbonate ions, intracellular acidosis may not be improved. Carbon
dioxide can enter the cells to combine with water to produce H2CO3, which can
worsen intracellular acidosis with an adverse impact on outcome.

A hyperosmolar hyperglycaemic state is distinguished from DKA by the absence of

high ketones levels and metabolic acidosis. Hyperglycaemia may rise to higher levels
but insulin levels are high enough to suppress ketogenesis. It is found in previously
undiagnosed type 2 diabetes and may be precipitated by intercurrent illness,
diabetogenic drugs (corticosteroids and thiazide diuretics) or fizzy glucose-containing
drinks. Complications include thrombotic events such as CVA, peripheral arterial
occlusion, DVT and PE, due to increased blood viscosity. Mortality exceeds 30%
because these patients are often older and often have a serious precipitating illness.

Lactic acidosis is generated rapidly during tissue anoxia (eg shock, cardiac failure
or pneumonia) or when liver gluconeogenesis is impaired. In diabetes mellitus, it
is a rare, but fatal, complication of biguanides (phenformin, metformin), which act
by inhibiting gluconeogenesis. It presents as coma with metabolic acidosis and a
wide amino gap due to hyperlactataemia. Blood glucose levels are usually raised.
Treatment is difficult: intravenous bicarbonate may aggravate intracellular acidosis;
forced ventilation to reduce carbon dioxide levels may help; dialysis clears lactate and
H+ and will correct any sodium overload from bicarbonate infusion. Mortality is high
(> 30%) because of coexisting organ failures.

Hypoglycaemia
This is infrequently seen as a presenting condition but still occurs as a form of
iatrogenic injury on surgical wards.

Common factors that predispose to hypoglycaemia are outlined in Box 17.4.

The events as blood glucose falls are listed in Box 17.5 but without early recognition
can precipitate a coma. Hypoglycaemia should be recognised and treated
immediately.

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Box 17.4  Common factors contributing to hypoglycaemia

Accelerated insulin absorption

• Exercise
• Hot environmental conditions

Unfavourable factors relating to insulin administration

• Too early
• Too much
• Inadequate food intake

Alcohol consumption

• Inhibits hepatic gluconeogenesis

Weight loss

Loss of counter-regulatory hormones

• Addison’s disease
• Hypothyroidism
• Hypopituitarism
• Blunted glucagon secretion (as in long-standing type 1 diabetes)
• Intestinal malabsorption
• Renal failure (impaired insulin clearance)

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Box 17.5  Clinical events as blood glucose falls

~3.8 mmol/L: adrenaline and glucagon secretion increases

~3.0 mmol/L: onset of hypoglycaemic symptoms (note, hypoglycaemic

unawareness in some patients)

~2.8 mmol/L: neuroglycopenia and cognitive impairment

< 1.0 mmol/L: coma

Practice point 
Check the blood glucose with a capillary blood glucose (CBG) stick in any patient
with a reduced level of consciousness as part of the initial ABCDE assessment.

Summary
Diabetes is common, and poor management has a significant impact on outcome
from surgery as well as patient quality of life and mortality. As a surgeon you should
be able to identify diabetes as well as other clinical and metabolic states associated
with poor glucose control.

Further reading
Joint British Diabetes Societies for Inpatient Care. Management of Adults with
Diabetes Undergoing Surgery and Elective Procedures: Improving Standards.
Revised September 2015. Available at http://www.diabetologists-abcd.org.uk/JBDS/
JBDS_IP_Surgical_Guideline_2015_Full.pdf

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