Manual Icu
Manual Icu
or equivalent)
ii) If sedation is required, midazolam can be administered via subcutaneous
route as a continuous infusion, with an opioid if already in use.
c) If the patient has not required regular opioid or sedation in ICU, the following
PRN orders should be in place prior to discharge:
i) For pain:
+ Opioid nave patient - e.g. morphine 2.5-5mg s.c. 2 hrly prn
+ Opioid tolerant - dose guided by background usage
ii) For agitation, restlessness:
+ Midazolam 2.5mg - 5mg s.c. 1 hrly prn
iii) For management of secretions:
+ Hyoscine hydrobromide 400 g s.c. 3-4 hourly prn
+ Atropine 600 g s.c. 3-4 hourly prn
3. Where appropriate, formal consult and involvement of the Palliative Care Service is
encouraged.
16
G. Clinical Duties in the ICU
1. Infection Control in ICU
a) Prevention and containment of nosocomial infection is a fundamental principle of
effective medical practice.
b) The critically ill patient is highly vulnerable to nosocomial infection, which results
in significant morbidity, prolonged length of hospital stay, increased cost and
attributable mortality.
c) It is the responsibility of every member of the health care team to ensure
compliance with Hospital and Unit infection control policies. This may include
reminding senior colleagues or visiting teams to conform to basic issues such as
hand-washing or additional precautions.
d) Hand-hygiene remains an established method of effective infection control and
must be strictly performed by all members of the health care team:
i) Aqium hand gel must be used by all staff:
+ Every time they enter or exit a patients cubicle
(defined as the line of the door or curtain of bed space.)
+ Before wearing gloves
+ Before and after patient contact
+ Before and after contact with a patients environment
ii) Hand wash with soap where:
+ Contact with blood or body fluids
+ Hands are visibly soiled
+ After removing gloves
iii) Hand wash with chlorhexidine:
+ Prior to clinical procedures
+ After contact with patients with multi-resistant organisms
e) Gloves
i) Disposable gloves must be worn for all contact with patients bodily fluids,
dressings and wounds.
ii) Gloves must be disposed of within the patient cubicle on leaving
f) Plastic aprons are to be worn:
i) With gross physical contact with the patient (e.g. patient turns)
ii) For additional precautions (see below)
g) Additional precautions:
i) The following patients require additional precautions:
+ Infection or colonisation with:
a. Methicillin Resistant Staph. Aureus
b. Vancomycin Resistant Enterococcus
c. Multiresistant gram negatives
d. Clostridium difficile
+ Burns
+ Febrile neutropenia
+ Immunosuppressed patients as directed by Infection Control
17
ii) These patients will normally be managed in either Units A or B.
iii) An Additional Precautions sign is placed outside cubicles of patients
identified as infective risks:
+ Red sign = patient has multi-resistant organism
+ Blue sign = patient is immunocompromised
iv) New disposable gowns and gloves must be used for each person entering
the cubicle and disposed of within the cubicle upon leaving.
v) Consumable stock within the cubicle should be kept to a minimum.
vi) Notify appropriate staff if patients are transported to theatre, for diagnostic
procedures, or for ambulance transport.
vii) Once the patient has been transferred or discharged, the area should remain
vacant until terminally cleaned in accordance with RAH policy.
viii) Environmental swabbing in Intensive Care is conducted as required by
Infection Control staff.
h) Aseptic technique
i) Aseptic technique is to be used for all patients undergoing major invasive
procedures (refer to procedures section).
ii) This includes:
+ Hand disinfection: surgical scrub with chlorhexidine for >1 minute
+ Sterile barrier: full gown, mask, hat, gloves and sterile drapes.
+ Skin preparation with chlorhexidine 2% in 70% alcohol.
i) Sharps disposal
i) The person performing the procedure is responsible for disposal of all
sharps (needles, blades) using the sharp disposal containers.
ii) The nursing staff are not responsible for sharps disposal.
j) Traffic control
i) Movement of people through the unit should be kept to a minimum.
ii) This applies equally to visiting clinics and large numbers of relatives.
iii) All visitors are expected to conform to the above infection control
measures and should be tactfully reminded or instructed when necessary.
k) Nominated isolation/quarantine rooms for highly contagious patients:
i) Rooms 3, 4, 5 & 6 - shared air-conditioning
ii) Rooms 21 & 22 - sealed, independent, negative pressure A/C units.
2. Guidelines for admission of a new patient to ICU
a) Handover from the referring doctor. Obtain as much information as possible.
b) Primary survey:
i) Ensure adequate airway, breathing and place the patient on a FiO
2
= 1.0 until
a blood gas is done.
ii) Check circulation and venous access.
c) Notify the duty consultant.
d) Secondary survey: fully examine the patient.
18
e) Document essential orders:
i) Ventilation
ii) Sedation / analgesia
iii) Drugs, infusions
iv) Fluids
f) Outline the management plan to the nursing staff.
g) Secure appropriate basic monitoring/procedures:
i) SpO
2
ii) ECG
iii) Arterial line
iv) IDC, nasogastric tube
v) CVC for the majority
h) Basic investigations as indicated:
i) Routine biochemistry, blood picture and coagulation studies
ii) Group and screen.
iii) Septic screen / microbiology.
iv) Arterial blood gas
v) ECG
vi) CXR (after placement of appropriate lines)
i) Advanced investigations: CT, angiography, MRI, etc
j) Advanced monitoring where indicated: e.g. PA catheter, ICP, PiCCO.
k) Document in case notes. (See below)
l) Notify the parent clinics of patients admitted directly to ICU
NB: this applies particularly to patients who have been retrieved.
m) Clinic Interns and RMOs should clerk hospital admissions direct to ICU.
n) Inform and counsel relatives.
3. Daily management in ICU.
a) Daily investigations:
i) Routine blood tests (U&E, LFT, Mg, Hb, WCC, Plts, ABG) are ordered on
the daily flow chart and signed for on the 11:00 am fluid round.
ii) Coagulation studies, drug levels or other tests are requested as required and
may also be requested on the daily flow chart.
iii) The night duty nurses take the bloods at 06:00 and complete the request form,
which must be signed by the night registrar.
iv) Registrars are responsible for taking blood specimens:
+ When nursing staff request assistance.
+ For blood transfusion - the requesting MO must ensure that the labelling
of the request form and specimen matches the patients wristband.
19
v) Chest x-rays are ordered after the morning handover round via OACIS.
+ Routine daily chest x-rays are not performed in ICU
+ Chest x-rays are performed
a. On admission to ICU (beds 1-24)
b. Following invasive procedures:
i. Endotracheal intubation
ii. Complicated percutaneous tracheostomy
iii. CVC placement (subclavian or jugular)
iv. Nasogastric or IABP placement
c. Suspected pneumothorax
d. At the discretion of the attending doctor
b) Handover ward rounds are at 08:00 and 18:30. These are brief business rounds to
handover essential information to the next team (either day or night) and are
attended by the duty consultant, team registrars and senior nursing staff.
c) Liaison with parent clinics is essential to ensure continuity of management.
Clinics must be informed of significant changes in a patients condition or the
requirement for specialist investigations or interventions.
d) Complex investigations (e.g. CT, MRI scans) and procedures should be authorised
by the duty consultant and discussed with the parent clinic where appropriate.
H. Documentation
The following guidelines are designed to facilitate the recording of clear, relevant
information that is essential for continuity of care, audit and medico-legal review.
Entries should establish a balance, being concise but still accurately recording all
relevant information and events.
Specific documentation expected from ICU registrars includes:
1. Admission note for all patients admitted to ICU (Units A, B & C)
2. Daily entry in case notes during admission.
3. Handover summary
4. Discharge summary
5. Death certificates.
1. Admission Notes
a) All patients admitted to Units A & B must have a detailed admission summary.
i) The admitting clinic must be notified by the admitting registrar and invited
to record an admission summary for patients admitted directly to ICU.
This is to ensure that clinics are aware when a patient has been admitted
under their bedcard.
ii) The admission note should incorporate all relevant aspects of the patients
medical history, clinical examination and investigation results.
20
b) Complicated Unit C patients require the same detail as Unit A & B patients.
c) Routine postoperative, short stay patients in Unit C do not need detailed
admission notes. In these patients record:
i) Relevant operative & anaesthetic details
ii) Significant comorbidities and history
iii) Anticipated problems
iv) Procedures e.g. epidural, invasive monitoring, TPN
2. Daily case-note entries
a) A daily entry must be made in the case notes.
i) Notes are most efficiently recorded after the 11:00 ward round so that
current results and management plans are recorded
b) Additional notes must be made for the following:
i) Significant changes in physical condition necessitating changes in
management, e.g. renal failure requiring dialysis.
ii) Invasive procedures, e.g. laparotomy, tracheostomy, PAC/CVC insertion
iii) Results of specific investigations or tests, e.g. CT scans, endocrine tests
iv) Changes in policy, e.g. non-escalation of treatment, advance directives.
3. Handover summary
a) Due to the large number of complex patients, an ongoing handover summary
should be established for each patient
b) This facilitates ease of handover between day and night resident staff and for the
duty consultant staff.
c) This is not a formal casenote, nor does it take the place of a thorough review of
each patient and their casenotes. This is meant to be an aide-mmoire to be
updated each shift.
d) This is stored in a specific ICU database available on the PCs in the ICU.
4. Discharge summary
a) All patients transferred from ICU (Units A/B/C) require a Medical Transfer
Summary (MR 42) form completed.
b) This is a single page document outlining all relevant transfer information.
c) The original should be filed in the case notes and a photocopy placed in the
marked box in the Unit B station for filing by the secretary.
d) The duty registrar on the day of transfer is responsible for completing the form.
e) Incomplete or missing summaries will be forwarded to the responsible registrar
for completion.
f) Short term Unit C patients do not require detailed discharge summaries, only
pertinent information relating to their stay.
21
5. Death certificates
a) The following forms need to be completed:
i) RAH Notification and Certification of Death (MR 150.2)
+ all patients including those reported to the Coroner
ii) Death Certificate ("the yellow form")
+ do not complete this for deaths reported to the Coroner
iii) First Medical Certificate
+ do not complete this for deaths reported to the Coroner
b) Deaths notifiable to the Coroner:
i) Contact the Coroners office and provide preliminary demographic details
of the deceased.
ii) The Coroners office will then fax the Medical Practitioners Deposition
form for you to complete and return by fax.
iii) File the original deposition in the patients case-notes.
I. Consent in ICU
1. Competent patients:
a) All competent patients undergoing invasive procedures should have a standard
RAH consent form (MR: 60.16) completed and signed by the patient.
2. Incompetent patients (sedation, coma or encephalopathy):
a) Third party consent is not necessary for routine ICU procedures:
i) endotracheal intubation
ii) arterial lines
iii) central venous lines
iv) pulmonary artery catheters
v) transvenous pacing wires
vi) underwater seal drains
vii) jugular bulb catheters
viii) intra-aortic balloon counterpulsation
ix) oesophageal tamponade tubes
x) bronchoscopy
b) However, relatives should be informed prior to the procedure if present.
c) The indications, conduct and complications of the procedure should be
documented in the casenotes.
d) Major invasive procedures such as percutaneous tracheostomy, coronary
angiography, permanent pacemaker insertion or major surgical procedures
require completion of a consent form:
i) Emergency procedures signed by two doctors
ii) Non-urgent procedures by third party consent (next-of-kin).
e) Responsibility for consent lies with the operator performing the procedure.
22
f) ICU staff are not responsible for consent for procedures performed outside of
ICU, e.g. surgical tracheostomy, or PICC lines placed in radiology
g) A person, not necessarily next-of-kin, who has been nominated by the patient as
a medical power of attorney may sign or refuse consent on behalf of the patient.
h) Relatives should always be informed of any non-routine procedures and the
consent issue explained, irrespective of the presence or absence of a medical or
legal power of attorney.
i) If relatives cannot be contacted, emergency life saving treatment should
proceed immediately, with discussion with the Duty Consultant.
J. ICU Ward Rounds
1. Grand rounds
a) Held on Mondays and Fridays are an integral feature of the running of the unit.
b) These are open, multi-disciplinary meetings to discuss management issues and are
a valuable teaching forum.
c) Current x-rays and investigation results are displayed via computer projection.
d) The ward round is attended by:
i) Team A, B, C and Duty ICU consultants and all floor registrars
ii) An infectious diseases consultant
iii) Senior nursing staff
iv) Physiotherapists
v) A pharmacist
vi) A dietician
vii) Invited clinics when appropriate
viii) Medical students
e) Registrars are expected to present their allocated patients and to actively participate
in management discussion.
f) Presentations should be of a standard suitable for a fellowship examination:
i) Should take no more than 5-8 minutes.
ii) Emphasise the relevant and pertinent issues only:
+ Patient details and demographics.
+ State day of ICU admission (e.g. Day 6 ICU).
+ Diagnosis or major problems.
+ Relevant pre-morbid history pertinent to this admission.
+ Relevant progress and events in ICU
(deterioration/improvement, procedures, investigations).
+ Current clinical status (system by system).
+ Outline features on daily pathology and radiology.
+ Current plan of management:
a. Medications
b. Further investigations / procedures
c. Discharge planning & prognosis
23
2. Bedside patient rounds
a) Are held daily, including grand-round days.
b) Team consultants and registrars review each patients condition.
c) Unit A&B flowcharts are re-written daily and include orders for ventilation,
procedures, medications, infusions and fluid therapy.
i) To ensure all aspects of patient care have been considered, the
FATDOGS algorithm should be considered in all patients:
- F - Feeding & fluids
- A - Analgesia & sedation
- T - Thromboprophylaxis
- D - Drugs therapeutic & usual
- O - Oxygen & ventilation
- G - Glucose control
- S - Sit out of bed
ii) You need to either write up each one of these each day or have a reason
why you have not.
d) Printed stickers should be used for routine medications and infusions.
e) All orders must be signed by a doctor.
f) Requests for routine blood tests are made on the chart.
g) Patients transferred to the general ward or Unit C
i) Should have the hospital blue folder completed.
ii) All medication orders should be re-written
iii) Fluid or nutrition orders for the next 24 hours are prescribed.
iv) Patients started on TPN should have their details entered in the TPN
folder kept in Unit A.
h) Similarly, Unit C patients have their charts reviewed, however all medications
and fluids are recorded on the hospital blue treatment folders.
K. Clinical Duties Outside of the Intensive Care Unit
1. Policy regarding outside consults:
a) NB: The Unit must not be left unattended at any time to attend outside calls.
(i.e. at least one registrar must remain on the floor)
b) The consults and code-blue/trauma pagers are carried by the Consults Registrar
(D7) during the day and Night Senior overnight (this may be modified at the
discretion of the 1
st
on-call consultant / senior registrar).
c) All consults should be addressed as soon as possible.
d) If the ICU workload is heavy, refer ward consults to the DI, who will delegate
appropriately.
e) Notify the senior nurse and fellow registrar(s) when leaving the floor.
f) The following duties accompany the Consults pager (pager no #89 22888*):
i) Ward consults
ii) Requests for Total Parenteral Nutrition (refer to Team A SR)
iii) Requests for retrieval (refer to MedStar)
24
g) The following duties accompany the Emergency pager (#33)
i) Code blue calls |
ii) Escalated MET calls | *see (4) below.
iii) Trauma (P1) resuscitation
+ Trauma pages are subdivided into levels
+ Attendance by the ICU registrar is only required for Level 1 calls.
h) All consults/MET calls potentially requiring admission to ICU must be
discussed with the Duty Intensivist (DI).
2. Ward Calls
a) Consults regarding potential admissions from the general wards, theatre or ED.
b) Pre-operative consults for potential or booked surgical patients.
c) Advice regarding fluid and electrolyte management, oxygen therapy, sedation and
analgesia (usually referred to APS).
d) Review as requested patients in the:
i) Spinal Injuries Unit with potential respiratory failure.
ii) Burns Unit for airway / breathing assessment, IV access or resuscitation.
e) Requests for venous access:
i) Requests must come from registrar level or above and after reasonable
attempts have been made to obtain IV access.
ii) Radiology provide a PICC line service in working hours.
iii) CVCs are not to be inserted on ward patients.
iv) Should be attended to in a timeframe appropriate to the patients condition.
f) Requests for TPN.
3. Total Parenteral Nutrition (TPN)
a) ICU provides a TPN service for the hospital.
b) Requests for TPN are elective(i.e. Mon to Fri: 0800-1800) and should be made
according to recommended indications.
c) Requests are made via the DI or consults registrar.
d) The TPN Folder is kept in the Unit A ward station.
e) The Team A Senior Registrar and Consultant will manage:
i) Initial consultation with the requesting clinic.
ii) Recording TPN patients in the TPN Folder.
iii) Insertion of a PICC catheter.
iv) Daily:
+ Review of electrolytes and fluid balance,
+ Review of the central venous catheter/PICC,
+ Prescription of TPN orders vitamins / trace elements,
+ Issue a request form for serum electrolytes.
+ Use pink labels from ICU & leave a spare for labelling of specimen tubes
- this ensures priority in the lab
f) Refer to the section on nutrition in the clinical protocols for indications &
complications.
25
4. Code Blue & MET Calls
a) The RAH medical emergency codeis 33#.
i) Upon dialling 33#, switchboard automatically page the following people:
+ ICU registrar
+ ICU equipment nurse
+ Medical registrar
b) These calls are divided into:
i) Code Blue *all calls must be attended immediately
+ Cardiac &/or respiratory arrest (actual or impending)
+ Threatened airway
+ Major haemorrhage
ii) MET calls
+ Significant clinical deterioration (see MET criteria)
+ MET calls are not routinely attended by ICU Registrars.
+ The ICU Registrar should remain immediately available if a MET call
has been activated, so that assistance can be provided to the MET team if
required (e.g. avoid starting procedures such as CVC insertions if the
MET pager has activated).
c) When 33 is displayed on the pager:
i) Dial 33# on an internal phone.
ii) Switchboard will then state the location of the arrest.
iii) Clearly state who you are (i.e. ICU registrar) and go to the location.
d) Ensure that the ICU staff know where you are going and that the Unit is not left
unattended.
e) At the emergency:
i) This hospital follows the Australian Resuscitation Council guidelines for
cardiopulmonary resuscitation.
ii) The ICU/resuscitation registrar is responsible for initial assessment, securing
the airway and establishing effective ventilation.
iii) Basic life support is done by attending nursing and medical staff and may be
directed by either ICU or medical registrar.
iv) Advanced life support is directed by the more senior registrar present. This is
usually the ICU registrar.
v) Depending on the outcome of the Code Blue, the patient may be admitted to
ICU, CCU or remain on the ward according to standard admission policies.
vi) As a general rule, it is better to admit a patient if previous details are not
immediately available than to prematurely abandon resuscitation.
vii) Document your involvement with the resuscitation in the casenotes.
viii) The home team should be involved or at least informed of their patients
condition, including when resuscitation is unsuccessful.
26
5. Trauma Calls
a) As in cardiac arrest, a 33# call is activated for trauma patients who meet
specified trauma criteria. (Refer to trauma directives.)
b) Trauma pages will appear as 2 Levels:
i) Level 1: major trauma requiring immediate attendance / airway support
ii) Level 2: trauma requiring full assessment in ED/Resus.
c) The following people are paged and the level response detailed on the pager:
i) ICU/resuscitation registrar
ii) Trauma Service registrar
iii) Accident and emergency registrar
d) On receiving a Level 1 call the ICU registrar should proceed directly to Resus in
the Emergency Department (ED)
e) Ensure that ICU staff know where you are going and that the Unit is not left
unattended.
f) At the trauma resuscitation:
i) This hospital follows the Early Management of Severe Trauma (RACS)
guidelines.
ii) The team leader is designated by the current Trauma Service Directive (found
on the wall in Resus).
iii) Role of the ICU registrar:
+ Primarily as a backup for acute life threatening situations in the event that
sufficiently experienced personnel are not available in Resus.
+ If anaesthetic staff are present in Resus, there is no requirement for ICU
registrars to attend the resuscitation unless specifically requested by these
personnel or the Trauma Director.
+ If anaesthetic staff are not immediately available, the following role is
indicated until appropriate personnel arrive:
a. Initial airway assessment and management.
b. Establishing effective ventilation
c. Assistance with vascular access and restoration of circulation.
d. Other acute interventions (e.g. UWSD) as required
+ Once anaesthetic & trauma team members are present and the situation is
under control, return to ICU - do not leave ICU unattended for lengthy
periods of time.
+ If prolonged resuscitation is anticipated, call in the ICU or Trauma
Consultant and/or delegate to the anaesthetic/resuscitation registrars.
+ Transportation of trauma patients to CT scan, angiography etc. is the
responsibility of the emergency anaesthetic staff.
+ ICU registrars must not do prolonged intra-hospital transports for trauma
patients without approval by the duty ICU consultant.
27
iv) General principles:
+ Document your involvement with the resuscitation in the casenotes
+ Once the primary survey is completed, proceed to the secondary survey
and order appropriate investigations as per the Trauma team leader.
+ In critically ill patients, ensure that a suitably qualified person (in terms of
resuscitative skills) remains with the patient at all times. This is
mandatory if the patient is transported from Resus (e.g. to radiology,
ICU, theatre).
+ Notify ICU staff of pending admissions.
+ Demarcation disputes are referred to the duty Trauma Consultant.
6. Retrieval Requests
a) Requests for consultation may originate from a number of sources. Namely,
i) The DI phone (SD: 1650)
ii) Other ICU telephones
iii) ICU registrar pager
iv) Other clinics who have been consulted by outside medical officers.
b) All retrieval requests should be referred immediately to the state retrieval
service, MedStar on 82224222.
c) All requests from MedStar for the transfer of patients to the RAH must be
referred to the on-call ICU consultant.
7. Intrahospital transportation of Intensive Care patients
a) All transports must be authorised by the duty ICU consultant.
b) The transport/investigation must be considered in the best interests of the patient.
c) All ventilated and potentially unstable transports need a medical escort.
d) Stable, self-ventilating patients may be transported by an ICU RN
e) If ICU nursing staff are concerned, then a medical escort is required.
f) At no stage must the unit be left uncovered.
g) If the Unit is busy, or transports clash with ward rounds, other personnel may be
deployed to do the transport. This is coordinated by the duty ICU consultant.
h) As a general rule, ICU staff are responsible for transportation of ICU patients.
i) Anaesthesia is responsible for transport of the following ICU patients:
i) Trauma resuscitation patients
ii) Patients to and from theatre
iii) Patients to and from hyperbaric medicine.
j) The transport of patients undergoing prolonged investigations or treatments, (e.g.
MRI, angiographic embolisation, invasive radiological procedures, TIPS) should
be discussed with the Duty ICU consultant and Duty Anaesthetist (SD 1175)
28
k) Guidelines
i) Registrars must familiarise themselves with transport monitors, portable
ventilators and infusion pumps.
ii) Inform and discuss the transport with the nursing staff as soon as possible.
iii) Patients must be appropriately monitored during the transport and
observations recorded on the flow chart.
iv) Document any problems which may occur during transport.
v) Ensure that the results of investigations performed (e.g. CT scans etc) are
recorded in the case notes by the appropriate person.
L. Hospital Emergencies
1. The emergency number is 33# : state the nature and location of emergency
2. Fire
a) A copy of the hospital emergency procedures (fire, smoke, bomb-threat) is kept in
the P4A and P4C nursing stations.
b) The chief fire and emergency officer is the overall controller during a fire or smoke
emergency (Code Red).
c) Become familiar with the location of fire exits, extinguishers and blankets in ICU
i) Unless small and easily contained do not attempt to fight a fire yourself.
ii) Remove yourself from the immediate vicinity of the fire, alerting other staff
members as indicated, and position yourself behind the automatic fire doors.
iii) The MFS has a 3 minute response time to the RAH.
iv) Wait for the arrival of the Fire Chief and assist in any patient
movement/evacuation only as indicated by the Fire Chief.
d) Role of medical staff:
i) There is no place for heroic action - ensure your own safety first!
ii) Wait for the arrival of the MFS.
iii) Assist in patient assessment/management under the coordination of the Fire
Chief.
iv) In the event of a significant fire / smoke hazard, staff will only re-enter the
danger zone in the immediate company of a MFS fire-fighter, with
appropriate breathing apparatus.
29
M. Research in ICU
1. Background:
There is a prolific research programme at the RAH ICU. This research is world
leading in the areas of gastrointestinal motility, nutrient absorption and incretin
hormones in the critically ill.
2. Personnel:
a) Director of Research - A/Prof. Marianne Chapman
b) Research Fellow - Dr Adam Deane
c) Research Manager - Ms Stephanie OConnor
d) Research Nurses - Ms Justine Rivett
- Mr Luke Chester
- Ms. Alison Ankor
e) Research Scientists - Mr Matthew Summers
- Mr Antony Zaknic
3. There are students studying toward their higher degrees frequently working in the
ICU. These students are strongly supported by the ICU Research Unit. Trainees
interested in undertaking a higher degree are always well received.
4. There are broadly 3 types of research studies occurring in the unit:
a) Locally initiated studies
b) Drug company sponsored studies
c) Studies performed with the ANZICS Clinical Trials Group (see below).
5. Medical and nursing staff are encouraged to become involved in research:
a) Registrars are expected to assist in obtaining consent for ongoing studies.
b) Knowledge of these studies can be obtained from any of the research staff.
c) Further involvement is encouraged and there are supports within the unit to
facilitate research to occur.
d) Because the ICU is a world-leader in several areas, it is advised to leverage on
the expertise and availability of sophisticated methodologies within the group.
However, independent projects, driven by highly committed individuals, will
always be supported.
6. The CICM formal project takes, at a minimum, 12 months to complete.
a) Trainees interested in undertaking a study for their formal project are advised to
approach potential supervisors with sufficient time to complete their project.
b) Potential projects (and initial contact persons) are:
i) Retrospective observational studies (A/Prof Flabouris and Dr Finnis)
ii) Prospective observational studies (Dr Sundarajarajan)
iii) Experimental work using a sheep model (Dr Maiden)
iv) Laboratory based work (Dr Reddi) and
v) Prospective clinical research (A/Prof Chapman and Dr Deane).
30
7. Most projects require prior RAH Research Ethics Committee approval. Your
supervisor will be able to provide details.
8. Completed research projects should be presented at either a local or interstate
scientific meeting.
a) Partial funding is available for staff who present work at approved meetings.
b) Applications should be made to the Coordinator of Research.
c) Eligible meetings include, but are not limited to:
i) ANZICS / ACCCN Annual Scientific Meeting - October.
ii) CICM Annual Scientific Meeting May/June.
iii) ACCCN (Institute of Continuing Education), Conference. Annual May.
9. ANZICS Clinical Trials Group (CTG).
a) A national clinical trials group to facilitate multicentre trials in Australia & NZ.
b) World-leading in critical care research and is open to all interested parties.
c) CTG meetings are held once per season, with the main meeting in March.
d) Resource person: A/Prof. Marianne Chapman.
10. If you are unsure of what to do about a patient enrolled in a study, please contact the
relevant staff member regardless of the time of day.
a) Queries about drug company sponsored studies should be directed to the ICU
Research Nurse on-call (SD 1520)
b) Queries relating to a local investigator studies should be directed to the primary
investigator.
N. Information Technology in ICU
a) All consultant and registrar offices and the Registrar Teaching Room are
equipped with PCs, connected to the RAH local area network (LAN).
b) Facilities available through the LAN include:
i) Intranet e-mail accounts
ii) WWW browsing facilities (available on application).
iii) Intranet resources, which are being continuously expanded:
+ UpToDate
(chlorhexidine 2%) or
MEDISPONGE
(chlorhexidine 2%) or
MEDISPONGE
.
iii) Single lumen 20G CVC (paediatric) for femoral arterial lines.
f) Insertion sites in order of preference:
radial > dorsalis pedis > femoral > brachial
g) The femoral artery may be the sole option in the acutely shocked patient.
h) Secure with a StatLock
device.
i) There is no optimal time for an arterial line to be removed or changed.
j) IA cannulae are changed/removed in the following settings:
i) Invasive IA line is no longer necessary.
ii) Distal ischaemia
iii) Mechanical failure (overdamped waveform, inability to aspirate blood)
iv) Evidence of local or unexplained systemic infection
k) Measurement of pressure:
i) Transducers should be zeroed each nursing shift
ii) Zero reference = the mid-axillary line, 5
th
intercostal space
l) Maintenance of lumen patency
i) Continuous pressurised (Intraflo
antimicrobial
impregnated (rifampicin/minocycline) 7F 15 or 20cm 3-lumen catheter.
ii) Non-impregnated catheters inserted outside the ICU should be changed to
an impregnated catheter according to clinical indication.
iii) Dolphin Protect
b) Sites:
i) Preferred site for routine stable patients SCV > IJV.
ii) Femoral v. access is preferable where:
+ Dolphin Protect
/ CVVHDF
+ Limited IV access (burns, multiple previous CVCs),
+ A thoracic approach is considered hazardous with:
a. Severe respiratory failure from any cause (PaO
2
/FiO
2
< 150)
b. Hyper-expanded lung fields (severe asthma, bullous disease)
c. Coagulopathy (see below)
+ Inexperienced staff requiring urgent access, where supervision is not
immediately available.
35
c) Coagulopathic patients:
i) INR > 2.0 or APTT > 50s correct with FFP and/or
prothrombinex
ii) INR 1.5-2.0 or APTT 40-50s correct with FFP, or
use IJ or femoral approach
iii) Platelets < 50,000 transfuse 1 pack (5
U
) platelets
+ Failure to increment femoral approach or PICC
iv) Uncontrolled coagulopathy femoral approach or PICC
+ Including recent therapy with Dabigatran
v) Insertion under ultrasound guidance may be preferred.
d) Technique policy
i) Use local anaesthesia in awake patients.
ii) Strict aseptic technique at insertion:
+ Handwash with AVAGARD
(chlorhexidine 2%) or
MEDISPONGE
(chlorhexidine 4%)
+ Sterile barrier: gown, sterile gloves, mask, hat
sterile drapes (CVC - Patient Cover)
+ Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol)
iii) Seldinger technique or ultrasound guided insertion Sonosite
iv) U/sound guided insertion may be preferred where:
+ There is an increased complication risk (e.g. bleeding, pneumothorax)
+ Large bore catheter insertion.
+ Distorted patient anatomy.
v) CVC Catheter lengths:
+ 15cm - right subclavian or internal jugular
+ 20cm - left subclavian or internal jugular, either side femoral
vi) Secure all lines with a StatLock
=
1400-2400
dyn.sec/cm
5
/m
2
Pulmonary vascular
resistance index
9 . 79
CI
PAOP PAP m
PVRI
=
150-250
dyn.sec/cm
5
/m
2
Stroke volume index
HR
CI
SVI =
33- 47 ml/beat/m
2
LV stroke work index ( ) 0.0136 SVI PAOP MAP LVSWI =
50-120 g/m
2
/ beat
RV stroke work index ( ) 0.0136 SVI PAOP mPAP RVSWI =
25-55 g/m
2
/ beat
Arterial oxygen content ( ) ( ) CaO Hb SaO PaO
2 2 2
134 0003 = + . .
17-20 ml/100ml
Venous oxygen content
( ) ( )
CvO Hb SvO PvO
2 2 2
134 0003 = + . .
12-15 ml/100ml
Oxygen delivery index DO I CI CaO
2 2
10 = 550-750 ml/min/m
2
Oxygen consumption
index
( )
VO I CI CaO CvO
2 2 2
10 = 115-160 ml/min/m
2
Oxygen extraction ratio
O ER
VO I
DO I
2
2
2
=
0.24-0.4
Shunt equation
0 10
O v C O c C
CaO O c C
Qt
Qs
2 2
2 2
'
'
=
5-15%
End capillary oxygen
content
( ) ( ) 0.003 PAO 1.0 1.34 Hb O c C
2 2
+ = '
80-100 ml/100ml
Alveolar gas equation ( ) ( ) PAO FiO PaCO
2 2 2
760 47 125 = .
100-650 mmHg
42
J. Pleural Drainage
1. Indications:
a) Pneumothorax
b) Tension pneumothorax may require urgent needle thoracostomy
c) Haemothorax
d) Large symptomatic pleural effusion
2. Management protocol:
a) Needle thoracostomy (tension pneumothorax):
i) 14 or 16G cannula placed in mid-clavicular line, 2
nd
intercostal space
ii) Always place an UWSD following this procedure
b) Pleurocentesis: (pleural effusion)
i) Prior to commencement, ultrasound the chest to confirm the presence of
fluid and indentify/mark an appropriate insertion site.
ii) Strict aseptic technique at insertion:
+ Handwash with AVAGARD
(chlorhexidine 2%) or
MEDISPONGE
(chlorhexidine 4%)
+ Sterile barrier: gown, sterile gloves, mask, hat & drape(s)
+ Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol)
iii) Local anaesthesia in conscious patients.
iv) Seldinger technique:
+ Pigtail catheter or ThalQuick
12F kit.
+ Insert guidewire through needle into pleural space
+ Insert catheter into pleural space over the wire
+ Aspirate intermittently with closed system or attach to an UWSD.
v) Record volume removed and send for MC&S, cytology & biochemistry.
vi) Check CXR post-procedure.
c) Underwater seal drainage:
i) Local anaesthesia in awake patients.
ii) Aseptic insertion technique - as above.
iii) Site:
+ Mid-axillary line, 3-5
th
intercostal space
+ Mid-clavicular line, 2
nd
intercostal space ( air only)
+ Do not insert drains through old wounds
iv) ICU patients need large drains: 28F catheter or larger
v) Use soft Mallinkrodt tubes in preference to the stiffer Argyle tubes
vi) Remove the trochar from catheter: do not use the trochar for insertion
vii) For the usual lateral ICD, go for the anterior or mid-axillary lines, avoid
the posterior sites as the chest wall is too thick, and there is a danger to
neurovascular structures
viii) Make a 2-3cm skin incision parallel to the ribs (#10 or #15 scalpel)
43
ix) Instruments & technique:
+ Blunt dissect using short artery forceps, avoid long forceps.
+ Do not plunge into the chest with either instrument.
+ Access to the intercostal space is by careful blunt dissection of the
intercostal muscles above the rib below.
+ The chest wall hole must be 2-3 cm wide in order that a finger can be
inserted into the pleural space to identify possible adhesions.
+ The soft tube should be guided by the intrapleural finger so that the
tube goes in between the finger and chest wall
x) Connect to an underwater seal drain apparatus
xi) Insert 2 purse string sutures:
+ 1 to fasten the tube
+ 1 (Z or purse-string) to close the skin incision on drain removal.
xii) Insert additional sutures as required to close the external wound.
xiii) Dressing: occlusive dressing (Hypafix)
xiv) Check CXR.
xv) Maintenance
+ Remove or replace drains inserted in unsterile conditions ASAP.
+ Leave the drain in situ until:
a. Radiological resolution of pleural collection (air/fluid)
b. No ongoing air-leak (no drain bubbling)
c. Minimal drainage (< 150 ml/24 hrs).
+ In ventilated patients, consider clamping the drain for >4 hours prior to
removal, providing the patient remains stable and/or post CXR.
+ Surgically placed drains are the responsibility of the surgeon and
should only be removed in consultation.
3. Complications
a) NB: minimised using the blunt technique
b) Incorrect placement - extrapleural, intrapulmonary, subdiaphragmatic
c) Pulmonary laceration - haemorrhage, fistula
d) Pneumothorax
e) Bleeding
i) local incision, intercostal vessels
ii) lung
iii) IMA (with anterior placement)
iv) Great vessels (rare)
f) Infection
i) Soft tissue
ii) Empyema
g) Mechanical (kinking, luminal obstruction)
44
K. Endotracheal Intubation
1. Policy:
a) Endotracheal intubation in ICU patients is a high risk but vital procedure:
i) Usually an emergency procedure, with limited time.
ii) Usually indicated for acute respiratory failure, or associated with limited
respiratory reserve
iii) Patients may have cardiovascular instability and significant co-morbidities
iv) Patients may have cervical spine or oropharyngeal trauma / surgery
v) Patients are at risk of vomiting and aspirating
vi) Positioning is difficult.
b) Familiarisation with the intubation trolleys, equipment and drugs is essential.
c) Intubation should ideally not be done as a sole operator procedure.
Skilled assistance should always be sought.
d) If you are alone (i.e. after hours): call for help!
i) Expertise in intubation is always available.
ii) Remember emergency anaesthesia staff.
e) The majority of ICU patients mandate rapid sequence induction.
2. Indications
a) Institution of mechanical ventilation
b) To maintain an airway
i) Upper airway obstruction
+ Potential e.g. early burns
+ Real e.g. epiglottitis, trauma
ii) Patient transportation
c) To protect an airway
i) Patients at risk of aspiration
ii) Altered conscious state
iii) Loss of glottic reflexes
d) Tracheal toilet
3. Techniques
a) Orotracheal intubation is the standard method of intubation in this unit.
b) Nasotracheal intubation may be indicated where:
i) Patients require short-term ventilation and are intolerant of oral ET tubes.
ii) Nasal Fibreoptic intubation may be indicated for:
+ Oro-maxillary surgery and pathology
+ Inability to open the mouth:
e.g. intermaxillary fixation, TMJ trauma, rheumatoid arthritis.
+ Upper airway obstruction and nasal route preferred
iii) Contraindicated in base of skull & LeForte facial fractures
c) Methods:
i) Direct laryngoscopy, C-MAC after rapid sequence induction
ii) Fibreoptic bronchoscopic awake intubation (oral or nasal)
iii) Intubating laryngeal mask LMA Fastrac
45
4. Endotracheal Tubes
a) Standard tube:
i) Low pressure, high volume cuff.
ii) Males: 8-9 mm secure at 21-23cm to incisors
iii) Females: 7-8 mm secure at 19-21cm to incisors
iv) Do not cut tubes to less than 26 cm length
b) Double lumen tubes: *rarely indicated in ICU:
i) Lung isolation for broncho-pulmonary fistula, abscess or haemorrhage
ii) Inserted as a temporary manoeuvre prior to definitive therapy
iii) Allow differential lung ventilation
iv) Males: Left 41F
v) Females: Left 39F
vi) NB: right bronchial tubes are harder to correctly site.
vii) Position should be checked with bronchoscope.
c) Intubated patients from theatre may have the following tubes that are not
recommended for prolonged intubation. These tubes must be changed if intubation
is anticipated > 48 hrs and exchange is safe and feasible.
i) Plain PVC tubes - no above cuff suction port
ii) Armoured tubes - risk kinking & obstruction
iii) RAE tubes - difficulty with suction & malposition
5. Protocol for endotracheal intubation in ICU
a) Personnel:
i) Intubation is a 3-4 person procedure - skilled assistance is mandatory
ii) The top end intubator coordinates the procedure
iii) One person to administer drugs
iv) One person to apply cricoid pressure(CP) post-induction:
+ This is routine for all emergency intubations
+ CP is considered safe in the presence of suspected spinal injury.
+ CP must be correctly applied - distortion of the larynx and difficulty in
intubation may occur if poorly applied.
v) One person to provide in-line cervical spine immobilisation (trauma and
spinal patients only).
b) Secure adequate IV access
c) Equipment (kept in difficult airway & intubation trolleys in P4-A,B&C).
Ensure the following equipment is available and functional:
i) Adequate light
ii) Oropharyngeal airways
iii) Working suction with a rigid (Yankauer) sucker
iv) Self-inflating hand ventilating assembly and mask
v) 100% oxygen, i.e. working flowmeter at 15 l/min
vi) 2 working laryngoscopes (standard & long blades)
vii) Magill forceps
viii) Malleable introducer and gum-elastic bougie
46
ix) 2 Endotracheal tubes
+ Normal size + 1 size smaller
+ Check cuff competence
x) Access to difficult intubation equipment and be aware of the difficult
airway trolley location and its contents.
+ Be aware of the Failed Intubation Drill.
+ Airtrach, C-MAC, Heine Flex tip
+ Intubating Fastrach LMA
+ Cricothyroidotomy equipment
a. Percutaneous kit or
b. #15 scalpel & #6.0 cuffed ETT
d) Monitoring (on all patients) :
i) SpO
2
, ETCO
2
, ECG
ii) Invasive BP *desirable but not essential and must not delay intubation
if urgent
e) Drugs
i) Induction agent - propofol, fentanyl, ketamine, midazolam
ii) Suxamethonium - 1-2mg/kg is the muscle relaxant of choice.
+ Contraindicated in:
a. Burns > 3 days
b. Chronic spinal injuries (i.e. spastic plegia)
c. Chronic neuromuscular disease (e.g. GBS, motor neurone disease)
d. Hyperkalaemic states. (K
+
> 5.5)
+ Consider Rocuronium (1-2 mg/kg) if Sux. contraindicated
iii) Atropine - 0.6-1.2mg available
iv) Adrenaline - 10ml 1:10000 solution available
f) Procedure: Rapid sequence induction and orotracheal intubation
i) Pre-oxygenate with 100% oxygen for 3-4 minutes.
ii) For patients on mask CPAP/NIV, pre-O
2
with the NIV mask
iii) Preload with 250-500ml IV crystalloid
iv) Inotropes may be necessary after induction/intubation
v) Induction agent + suxamethonium
+ Induction doses in the critically ill must be modified from routine
doses used in general anaesthesia
vi) Cricoid pressure applied (ensure correct positioning)
vii) Direct visualisation of vocal cords and tracheal intubation
viii) Inflation of cuff until airway sealed
ix) Confirmation of ETCO
2
x) Chest and gastric auscultation with manual ventilation
xi) Cricoid pressure released
xii) Secure tube at correct length
xiii) Connect patient to ventilator (see default ventilator parameters)
xiv) Ensure adequate sedation muscle relaxant
47
xv) Consider insertion of a naso/oro-gastric tube.
+ Required by the majority of ICU patients.
+ Insertion will avoid repeating the CXR.
xvi) Chest X-ray
xvii) Confirm blood gas analysis and adjust F
I
O
2
accordingly.
g) Sedation post-intubation:
i) None if comatose or haemodynamically unstable
ii) Propofol fentanyl infusions as clinically indicated.
6. Maintenance of endotracheal tubes
a) Securing to face
i) Secure ETT with white tape after insertion.
ii) Ensure that the loop of tape is snug around back of neck but not too tight to
occlude venous drainage should allow 2 fingers under tape.
iii) Re-secure with adhesive tape once CXR check done.
b) Cuff checks
i) Volumetric tests are done following insertion and whenever a leak is
detected: sufficient air to obtain a seal + 1ml
ii) Seal is assessed by auscultation over trachea during normal ventilation.
iii) Manometric tests are inaccurate and do not correlate with mucosal
pressure. These are an adjunct only if cuff malfunction is suspected.
c) Persistent cuff leaks
i) Tubes requiring more than 8ml of air to obtain a seal or if there is a
persistent cuff leak must be examined by direct laryngoscopy as soon as
possible:
+ Even if taped at the correct distance at the teeth.
+ Ensure that the cuff has not herniated above the cords
+ Tube has not ballooned inside the oral cavity and pulled the cuff
above the cords.
ii) Patients at high risk for cuff leaks:
+ Nasal RAEs - prone to outward migration
+ Cut tubes - do not cut tubes < 26 cm
+ Facial swelling - burns, facial trauma
+ Patients requiring high airway pressures during ventilation
48
7. Endotracheal tube change protocol
a) Ensure adequate skilled assistance, equipment, drugs and monitoring as for de
novo intubation.
b) Procedure
i) Set the F
I
O
2
= 1.0 and change SV modes to SIMV.
ii) Ensure sufficient anaesthesia and muscle relaxation (fentanyl / propofol +
neuromuscular blockade)
iii) Perform laryngoscopy and carefully identify:
+ Patency of upper airway after suction
+ Anatomy of larynx
+ Degree of laryngeal exposure and swelling.
iv) I F clear view of larynx and no or minimal laryngeal swelling:
+ Application of cricoid pressure by assistant and careful, graded
extubation under direct laryngoscopic vision.
+ Maintain laryngoscopy and replace tube under direct vision.
v) I F impaired visualisation of larynx:
+ Re-evaluate the need to change ETT
+ Use gum elastic or ventilating bougie
+ Place bougie through tube under direct vision and insert to a length
that would be just distal to the end of the ETT (approximately 30cm
from end of tube)
+ Have an assistant control the bougie so that it does not move during
movement of the endotracheal tube
+ Application of cricoid pressure by assistant and careful, graded
extubation
+ Maintain laryngoscopy and ensure bougie is through the cords on
extubation
+ Replace tube over bougie and guide through larynx under available
vision.
+ Inflate cuff, check ETCO
2
, auscultation and expired tidal volume
+ Release cricoid pressure.
+ Secure tube with tape.
49
L. Weaning Guidelines
1. Commencement of weaning is a medical decision.
2. Weaning is contraindicated with any of the following:
a) Unstable ICP (abort weaning if ICP increases)
b) Need for heavy sedation (e.g. upper airway obstruction)
c) Haemodynamic instability
d) Significant bronchospasm
e) High work of breathing.
3. Trial pressure support daily if the patient meets both the following criteria:
a) PaO
2
/FiO
2
ratio > 150
b) Patient can take spontaneous breaths if SIMV resp-rate reduced.
4. Weaning protocol:
a) See the flow diagram following page.
b) Set initial pressure support to maintain adequate V
T
i) Start at 10 cmH
2
O and adjust to:
+ V
T
6 ml/kg IBW for patients recovering from ARDS.
+ V
T
8 ml/kg IBW for all others.
+ IBW Males = 0.91 (height [cm] 152.4) + 50
+ IBW Females = 0.91 (height [cm] 152.4) + 45.5
ii) Alternatively, use target V
T
= 80-100% of set SIMV V
T
iii) Allowable PS range = 5-25 cmH
2
O
+ If V
T
cannot be achieved with 25cmH
2
O, cease trial
c) Assess at 15 and 30 minutes for weaning success criteria
d) Assess each hour for suitability to wean PS
e) Once PS has reached minimum (5cmH
2
O) then wean PEEP to 5cmH
2
O
f) If PS & PEEP = 5cmH
2
O then assess for extubation.
5. Weaning Success Criteria:
i) RR < 30/min
ii) SpO
2
> 90%
+ May be set lower with COPD, e.g. >86-88%
iii) F
I
O
2
0.5
iv) No respiratory distress as shown by 2 or more of the following:
+ HR > 120% baseline
+ Accessory muscle use
+ Diaphoresis
+ Paradoxical abdominal movements
+ Marked dyspnoea
50
Flowchart: Ventilation Weaning Protocol
PaO
2
/FiO
2
> 150
&
PEEP < 10 cmH
2
O
Pass
Fail
NO Weaning Contraindication:
- Unstable ICP
- Need for heavy sedation
- Haemodynamic instability
- Significant bronchospasm.
AND
Start Weaning Settings:
- Reduce patient sedation
- Reduce SIMV-Rate to 8bpm
- Adjust initial PS to target V
T
8ml/kg IBW, or
6ml/kg IBW if ARDS
- Allowed PS range (5-25 cmH
2
O)
- PEEP remains on previous setting.
Check each 15 minutes -
Weaning Success Criteria:
- RR < 30/min
- SpO
2
> 90% (*lower in COPD)
- FIO
2
0.5
- No respiratory distress as shown
by 2 or more of the following:
HR > 120% baseline
Accessory muscle use
Diaphoresis
Paradoxical muscle movements
Marked dyspnoea
Assess After Each Hour -
Set Pressure Support Level:
- If weaning successful after 1
st
Hour
cease SIMV
- If successful on subsequent hours
decrease PS, as per
- If no previous weaning failure
decrease PS by 4 cmH
2
O
- If previous episode of failure
decrease PS 1-2 cmH
2
O
- If at minimum PS = 5 cmH
2
O
decrease PEEP by 1-2 cmH
2
O
Weaning Failure:
- IF post PS decrease
return to previous settings
*note change to PS decrease rate
- IF post return to settings
set PS to max = 25 cmH
2
O
- IF on maximum PS
return to SIMV settings
- IF PS
Max
or SIMV, patient should
be reviewed by SR or Consultant
Weaning Complete:
- If PS = 5 & PEEP = 5 cmH
2
O
- Check ABG
- Assess for Extubation see over.
51
M. Extubation
1. The decision to extubate is made by medical staff, in consultation with either the
senior registrar, fellow or duty consultant.
2. Extubation is to be performed by medical or senior nursing staff, with airway
competent medical staff immediately available.
3. Criteria to predict successful extubation are helpful, however, ongoing success
should never be assumed:
a) FiO
2
< 0.5 with PEEP 5 cmH
2
O
b) PaO
2
> 70 mmHg ** lower values may be appropriate in
SpO
2
> 90% chronically hypoxaemic patients
c) RR < 30 with PS 5cmH
2
O (Drger)
d) pH > 7.2
e) No respiratory distress (see over)
f) Patient able to obey commands
g) Patient able to protect airway and cough
h) Patient able to cope with amount of secretions
i) Reason for intubation resolved.
*this may include checking for an air leak with the cuff deflated
4. Early extubation to NI V may be considered for some patients who present with
hypercapnic exacerbation of COPD or pulmonary oedema:
a) Performed with close supervision by senior medical staff.
b) If no improvement after 1-2 hrs, the patient should be considered for
reintubation.
5. Extubation protocol:
a) Ensure equipment, monitoring and adequate assistance is available, as for
intubation
b) Plastic surgical and ENT patients with intermaxillary fixation/wiring require
consultation with the Parent Clinic.
i) A wire cutter must be present in the room at all times.
ii) The parent clinic should be given opportunity to be present during extubation
if the jaws are wired.
c) All patients should receive supplemental oxygen pre/post-extubation.
52
N. Emergency Surgical Airway Access
1. Policy
a) Call for skilled assistance then proceed without delay.
b) Difficult airway & failed intubation trolleys are in areas A, B & C
c) Cricothyroidotomy, percutaneous or surgical, is the recommended procedure for
urgent surgical airway access and emergency oxygenation.
d) Standard percutaneous tracheostomy is not an emergency procedure.
e) Cricothyroidotomy is a temporary airway - arrange a definitive surgical airway
(ENT surgeons) as soon as possible.
2. Indications:
a) Refer to the failed intubation drill in the clinical protocols section.
b) Inability to establish an effective airway following failed laryngoscopy despite:
i) Basic manoeuvres - jaw thrust / chin lift / oral-nasal airways
ii) Attempted LMA insertion
c) Inability to ventilate.
3. Cricothyroidotomy
a) Percutaneous technique
i) Equipment
+ Cook Melker
)
Prophylaxis:
40mg subcut daily
20mg subcut daily if Creat clearance < 30ml/min
High risk 20mg mane 40mg nocte
Treatment:
1mg/kg subcut bd - lean body mass
1mg/kg subcut once daily if CrCl < 30ml/min
Prostacyclin (infusion)
Dose: 0.2-0.6 g/kg/hr
500g (+10ml diluent): add to 40ml NSal = 10g/ml solution
Start at 2ml/hr and monitor platelet count
May cause hypotension
Danaparoid sodium
(Orgaran
)
Infusion
IV loading dose: < 60kg 1500 U
60-75 kg 2250 U
75-90 kg 3000 U
> 90 kg 3750 U
Infusion: 2250
U
of danaparoid in 250ml 5% dextrose:
44 ml/hr (400 U/hr) x 4 hours
33 ml/hr (300 U/hr) x 4 hours
22 ml/hr (200 U/hr)
Adjust dose to anti-Xa levels (target 0.5-0.8 anti-Xa U/ml)
Long half life (25 hrs): cease early if changing to oral anticoagulants
Danaparoid (subcut) 750 U 8-12 hourly
Lepirudin Complex see below
Dabigatran See below
94
Table: Heparin Infusion Protocol
Weight (kg) 45-55 56-65 66-75 76-85 86-95 >95
Bolus (U) 3,500 4,200 4,900 5,600 6,300 7,000
Infusion (U/hr) 900 1,100 1,250 1,400 1,600 1,800
Infusion adjustment
APTT IV bolus Stop Infusion Rate Change Repeat APTT
< 37 5,000 units | 400u/hr 6 hrs
38-64 | 200u/hr 6 hrs
65-110 No change Daily
111-130 + 50u/hr 6 hrs
131-140 30 min + 100u/hr 6 hrs
141-150 60 min + 150u/hr 6 hrs
> 150
120 min or
APTT <150
+ 200u/hr 2 hrs
Note: Infusion: 25,000 units in 50ml syringe = 500U/ml
Check first APTT 6 hrs after bolus dose
Table: Lepirudin Infusion Protocol
CrCl (ml/min) Bolus Dose
Maintenance Infusion
mg/kg/hr % original dose
> 60
0.4 mg/kg
(max 44mg)
0.1 (max 11mg/hr) 100%
45-60 0.2 mg/kg 0.05 50%
30-44
None
0.025 25%
15-29 0.01 10%
< 15 0.005 5%
CVVHDF 0.01 10%
95
7. Lepirudin
a) Recombinant direct thrombin inhibitor
b) Dose range varies by a factor of 20x
i) Care must be used in determining the precise dose
ii) Renally excreted and must be carefully monitored in the critically ill
c) NB: a bolus dose is only used if patient has life threatening thrombus
8. Dabigatran
a) Competitive direct thrombin inhibitor.
b) Used as an oral alternative to warfarin.
c) Current indications include:
i) Atrial fibrillation
ii) VTE prophylaxis following major orthopaedic surgery.
d) Renally cleared with a half-life ~ 12-14 hrs.
e) Monitoring
i) INR cannot be used to monitor efficacy or toxicity.
ii) APTT provides an approximate indication of the level of anticoagulation
iii) A normal APTT suggests that drug is unlikely to be present in significant
concentration.
iv) APTT of > 80 seconds suggests that drug is present in excess.
f) No specific antidote is available to reverse effect.
i) For severe bleeding, supportive strategies are recommended, including
transfusion of fresh whole blood, or fresh frozen plasma.
ii) Dialysis may be indicated in patients with prolonged APTT particularly if
renal function is impaired.
iii) The role of prothrombinex and rFVIIa is unclear.
iv) For advice under these circumstances contact the on-call Haemostasis
Service through Transfusion on 8222 5430 or 8222 5431.
96
H. Endocrine Drugs
1. Insulin
a) Indications:
i) Diabetic emergencies DKA and hyperosmolar coma
ii) Treatment of hyperkalaemia
+ 50% dextrose 50ml, plus Actrapid 10
U
iii) Perioperative diabetic patients (both insulin and non-insulin dependent)
iv) General ICU patients
+ Hyperglycaemia > 10 mmol/l or glycosuria in acute illness:
a. Maintaining BGL 6-10mmol/l is recommended for all critically ill
patients
b. Majority of ICU patients will require insulin using this protocol.
c. NB: This protocol is not designed for patients with diabetic
ketoacidosis and is a guideline only.
d. Some patients will require individual manipulation of dose.
+ Subcutaneous sliding scale insulin:
a. Is inadequate for most critically ill patients and should be avoided.
b. May be used in a small number of less critically ill patients, who
have a limited requirement for exogenous insulin.
c. A regular dose of subcutaneous intermediate/long-acting insulin,
adjusted according to BGL may be suitable in some ICU patients.
b) ICU Insulin Protocol see following page.
i) Target BGL = 6-10mmol/l.
ii) Blood for testing should ideally be:
+ Sampled from the arterial line rather than capillary (finger prick), as the
former is more accurate in the critically ill.
+ Measured via the blood gas analyser, c.f. bedside glucometer.
iii) Protocol Precautions:
+ If insulin rate 8 U/hr and the BGL remains high, measurement may
be erroneous take a sample from another site and measure in the
blood gas analyser.
+ Consider holding the infusion if feed or glucose infusions are stopped.
+ Potassium level
a. Administration of insulin reduces K
+
levels.
b. Check K
+
on ABG specimen at least twice daily and more often if
the insulin infusion rate is high or changing acutely.
c. If [K
+
] < 3.5 mmol/l
KCl ~ 30 mmol over 1h via a pump.
97
Flowchart: Blood Glucose Management in ICU
Table: Insulin Infusion Protocol
BGL Bolus
Starting
infusion
Subsequent infusion Repeat BGL
mmol/l Units IV Units/hr Units/hour Hours
>15 2 2 Increase by 1 1
10.1-14.9 1 1 Increase by 1 1
8-10 0 0
If BGL dropping continue current rate.
If static or rising increase by 0.5
1
5-7.9 0 0
Continue current rate
If BGL dropping for 2 consecutive hrs
decrease rate by 0.5.
1 (2hrly if
BGL stable
for 6 hrs)
3.5-4.9 0 0 Cease
1 (4hrly if off
insulin>6hrs)
<3.5 Call MO 0 Cease 1
c) Discharge Management:
i) Pre-discharge, cease insulin infusion for at least 4 hours and check BGL
ii) Order BGL to be checked 8 hourly on the ward
iii) Refer to the RAH intranet documents:
+ Insulin Protocol for Patients Discharged from ICU.
+ Diabetes Management Guidelines.
iv) Liaise with Endocrinology as indicated.
Target BGL = 6-10mmol/l
Perform BGL on Admission
BGL = 6-10mmol/l
BGL > 10 mmol/l
Commence Protocol
Perform BGL 4hrly
98
2. Diabetes insipidus: protocol for DDAVP
a) Diabetes insipidus may occur in the following situations:
i) Post ablative pituitary surgery
ii) Severe head injury, esp. anterior cranial fossa #, trauma
iii) Evolving brain death
iv) Lithium administration
b) Indications for DDAVP
i) Acute perioperative management (24-48hrs) of DI following pituitary
surgery is usually fluid based the use of DDAVP is rarely indicated.
ii) Persistent polyuria in the absence of diuretics > 300ml/hr for > 3hrs
iii) Altered conscious state, inability to detect thirst or take oral fluids
iv) Low urine osmolality in the presence of high plasma osmolality
v) Pre-existing hyperosmolar state or predisposition to pre-renal failure where
persistent polyuria may exacerbate this.
c) DDAVP Prescription
i) Dose 1-2g s.c. bd as required. (4g is excessive)
ii) Adjust maintenance fluids according to the response
d) Maintenance fluids should be prescribed in the usual manner, according to
volume status, renal function and osmolality.
e) Presumptive or proven brain death:
i) DI should be treated early (i.e. as soon as polyuria occurs)
ii) Delayed administration of DDAVP can result in significant electrolyte
abnormalities, which may influence the organ donation process.
3. Steroids
a) Indications
i) Pre-existing steroid therapy:
+ Wide variety of indications, doses and durations of therapy.
+ The need to continue steroids, with or without dose adjustment, should
be assessed.
ii) ICU conditions where steroid therapy may be beneficial. :
+ Addisonian crisis
+ Anaphylaxis
+ Asthma, Chronic obstructive pulmonary disease
+ Bacterial meningitis - esp. pneumococcal prior to antibiotics
+ Croup, post-extubation laryngeal oedema
+ Fulminant vasculitis
+ Hypercalcaemia
+ Idiopathic thrombocytopenic purpura
+ Myasthenic crisis
+ Myxoedema coma / Thyroid storm.
+ Organ transplantation
+ Pneumocystis jurovecii pneumonia
99
iii) Conditions where supporting data are variable and the decision to administer
steroids should be made on a case-by-case basis
+ Sepsis
+ ARDS
b) Contra-indications / non-indications
+ Active infection
+ Acute head injury
+ Guillain-Barr syndrome
+ Fat embolism syndrome
c) Relative drug potencies
Table: Steroid Doses / Relative Potencies
Drug
Equivalent
dose (mg)
Glucocorticoid
activity
Mineralocorticoid
activity
Hydrocortisone 100 1 1
Prednisone 25 4 0.3
Methylprednisolone 20 4 0
Dexamethasone 4 30 0
Cortisone acetate 125 0.8 0.8
Fludrocortisone 1 10 250
d) Limitations of a random cortisol
i) Marked fluctuation in plasma cortisol in the critically ill.
ii) The normal range in critical illness is not defined.
iii) There is no consensus cut-off value below which insufficiency is present.
e) Limitations of total cortisol
i) Free cortisol is the bioactive fraction of cortisol
ii) Large variation in total cortisol assay results when the same specimen is
tested in different laboratories and using different assays
iii) Peripheral tissue-specific glucocorticoid resistance is not tested
f) Conventional (high-dose) short synacthen test (HDSST)
i) Synacthen concentrations are supraphysiological
ii) Published data likely overestimate the incidence of adrenal insufficiency,
as most studies did not excluded patients on etomidate.
iii) The low-dose SST may be more a better predictor of outcome.
iv) Insufficient data to support the routine use in patients with septic shock.
v) Should only be performed if there is suspicion of hypoadrenalism
+ Hyperkalaemia/hyponatraemia
+ Hypoglycaemia
+ Refractory acidosis
+ Catecholamine resistance
100
I. Renal Drugs - Diuretics
1. General principles
a) Oliguria in acutely ill patients is frequently a manifestation of:
i) Hypovolaemia relative or absolute
ii) Decreased cardiac output
iii) Direct renal toxicity, or
iv) A combination of these factors.
b) Therapy should be directed toward causative factors and not maintenance of urine
output by the administration of a diuretic agent.
c) Urine output, in the absence of diuretic use, represents one of the best markers of
end-organ perfusion and is a useful guide to clinical management.
d) Diuretics should never be used to treat oligo/anuria, they are only a treatment for
fluid overload
2. Indications
a) Symptomatic fluid overload
i) Pulmonary oedema / CCF
ii) Cor pulmonale
b) Hyperaldosterone states: ascites
c) Chronic renal failure
3. Contraindications
a) Hypovolaemic and/or Na
+
-depleted states
b) Known drug hypersensitivity (esp. sulphonamide group)
4. Complications
a) Hypovolaemia
b) Hyperosmolar states
c) Potentiation of renal failure - 2 to hypovolaemia
d) Electrolyte disturbance especially + K
+
, Mg, PO
4
, metabolic alkalosis
e) Natriuresis and kaliuresis will alter urine electrolytes and osmolality for 24-48
hrs post dose.
101
Table: Diuretics
Drug Infusion/dose Clinical uses
Frusemide 40-250 mg/day
IV / oral
First line, potent loop diuretic
Doses may be increased in diuretic dependence
+ K
+
, Mg, PO4, metabolic alkalosis common
Acetazolamide 250-500 mg IV tds Carbonic anhydrase inhibitor
Alkaline diuresis with HCO3
-
excretion
Used for severe metabolic alkalosis after
correction of hypovolaemia: + K
+
, Mg
++
, PO4
=
Post-hypercapnic alkalosis
Spironolactone 25-100 mg oral bd Potassium sparring diuretic
Often given with loop and thiazide diuretics
Indicated as part of a chronic treatment regimen
for left ventricular failure
Use in acute LVF is less certain
May be of use in patients with ascites, particularly
if secondary hyperaldosteronism is a feature.
Careful administration is required in patients with
impaired renal function.
Mannitol 20% solution /
200 mg/ml
Dose 100 ml prn
(20g)
(0.5g/kg is
too much!!)
Potent osmotic diuretic
May cause - initial hypervolaemia
- late hypovolaemia
- hyperosmolal state
- osmolal gap.
Maintain measured osmolality < 300 mosmol/l
Limited role in suspected acute life-threatening
intracranial hypertension as a bridge to definitive
surgical therapy.
Limited (unproven) roles in rhabdomyolysis,
transfusion reactions, myoglobinuria for renal
protection
102
J. Gastrointestinal Drugs
1. Stress ulcer prophylaxis
a) Routine stress ulcer prophylaxis is not indicated:
i) Low prevalence of clinically significant bleeding due to stress ulceration
ii) No evidence of survival benefit with use of stress ulcer prophylaxis
iii) Possible increased incidence of VAP and/or clostridium difficile infection
b) Pantoprazole may be considered in patients at high risk.
c) Patients on pre-existing therapy (with PPIs or H
2
-blockers) should be continued
d) Patients with clinically suspected GI bleeding should commence on a PPI
e) Enteral feeding should be commenced as soon as possible.
2. Acute GI bleeding
a) Definition
i) Overt bleeding
+ Blood in the NGT
+ Haematemesis or malaena
ii) Plus either:
+ + MAP > 20 mmHg
+ + Hb > 20 g/L in 24 hours
+ Required > 2 units blood transfusion in 24 hrs
iii) Blood in the NG tube is frequently due to local erosion and by itself does not
constitute clinically significant GI bleeding.
b) Management
i) Resuscitation - ABC
ii) Correct coagulopathy
iii) Cease heparin / anticoagulants
iv) Commence PPI - pantoprazole 40 mg bd/tds.
v) Endoscopy sclerotherapy
vi) If the source is not identified and with ongoing bleeding, consider:
+ Labelled red cell scan
+ Angiography (+/-embolisation), or
+ Colonoscopy.
103
3. GI drugs
Table: GI Drugs
Drug Dose Clinical uses
Metoclopromide 10 mg IV 6 hrly, prn Persistent vomiting, nausea
Large gastric aspirates
(in combination with erythromycin)
Erythromycin 100-200 mg IV bd Large gastric aspirates
(in combination with metoclopramide)
Droperidol 0.625 mg IV prn Potent, effective antiemetic
Minimal side effects
Tropisetron 2 mg IV / oral daily Use if anticholinergic side effects are to be
avoided.
Ondansetron 4 mg IV prn / 12 hrly Second line, antiemetic
(not available at RAH)
Ranitidine 50 mg 8hrly IV
150-300 mg daily po
Stress ulcer prophylaxis
Peptic ulcer disease
Does not prevent acute rebleeding
Reduce dose in renal failure.
Pantoprazole Acute RX:
40 mg IV bd/tds
Maint. RX:
40 mg daily
First line RX for peptic ulceration
Refractory peptic ulcer, ulcerative oesophagitis
Z-E syndrome
Upper GI bleeding
Octreotide Bolus: 50 g IV
Varices: 50 g / hr
Fistulae: 100-200 g
sc 8-hrly
Variceal bleeding
(as effective as sclerotherapy)
Enteric, pancreatic fistulae
Sulphonylurea overdose
Severe secretory diarrhoea, e.g. post-chemo
104
K. Antibiotics
1. Policy
a) Prescription of antibiotics must conform to RAH guidelines.
b) The over-prescription and irrational use of antibiotics is associated with the
development of bacterial resistance, nosocomial infection and drug related
morbidity
c) All antibiotics must be reviewed daily and where appropriate, discussed with
Infectious Diseases or Clinical Microbiology.
d) Record the day and expected course of antibiotics in the left-hand margin of the
drug chart, e.g. D4/7 = day 4 of a 7 day course.
e) Record date, test and results (including sensitivities) in the results folder.
2. Principles of antibiotic prescription
a) The treatment of infection consists of (in order of priority)
i) Adequate resuscitation
ii) Source control drainage of infected collections, etc.
iii) Relevant samples for microbiological and/or histological analysis
iv) Routine cultures:
+ Blood - 2 sets at different times from venous stabs
+ Urine
+ Sputum
+ Any other suspicious site
v) Prompt administration of
+ Rational empiric antibiotics
+ Culture-directed antibiotics
+ NB: time to effective ABx treatment affects outcome.
b) General indications for antibiotics:
i) Prophylaxis for invasive procedures and operations
+ Proven indications
a. Abdominal surgery which involves a breach of the colonic mucosa
(traumatic or elective), or draining an infected cavity
b. Selected obstetrical and gynaecological procedures:
i. Caesarean section with ruptured foetal membranes
ii. Vaginal hysterectomy
c. Insertion of a prosthetic device
d. Compound fractures
e. Amputation of gangrenous limb
+ Unproven but recommended
a. Lacerations penetrating into periosteum or into joint cavities
b. Crush injuries
c. Insertion of a neurosurgical shunt
d. Cardiac valve replacement
e. Arterial prosthesis
105
ii) Empirical antibiotics
+ Obtain as many cultures as possible before antibiotics commenced.
+ Should be commenced early in critically ill patients
+ Should be rationalised according to gram stain & culture results.
iii) Specific infections where the organisms is known
c) Complications of antibiotics
i) Antibiotic effect related
+ Bacterial resistance
+ Nosocomial infection
+ Pseudomembranous colitis
ii) Systemic reactions
+ Skin rashes
+ Anaphylactoid / anaphylactic reactions
iii) Specific organ toxicities, e.g.
+ Interstitial nephritis, ATN
+ Seizures
+ Marrow suppression, thrombocytopaenia
+ QT prolongation
iv) Cost
d) Gentamicin / Tobramycin
i) Where possible, the aminoglycosides should be used for a limited duration
and therapy changed to a suitable alternative when possible.
ii) Pharmacodynamic properties
+ Concentration-dependent killing peak:MIC ~ 10:1
+ Significant post-antibiotic effect
iii) Toxicity
+ Nephrotoxicity - non-oliguric renal failure
+ Ototoxicity - permanent, vestibular or auditory
iv) Dosing
+ All dosing is by estimated Lean Body Weight (LBW):
a. Male: kg ~ 50 + 0.9(height - 150cm)
b. Female: kg ~ 45 + 0.9(height - 150cm)
+ Initial Dose: 5-7 mg/kg *irrespective of renal function
a. Measure level 6-10 hrs post-dose
b. Liaise with ICU Pharmacist (Pg: 22916), or
Drug Information (Ext: 25546) re further dose requirements.
c. Do not use the standard dosing normogram in ICU patients.
+ Synergistic gentamicin, e.g. tds dosing in endocarditis
a. Measure pre-dose trough levels
b. Aim for < 1.0 mg/L to avoid toxicity.
106
e) Vancomycin
i) Pharmacology
+ Time-dependent killing max 24h-AUC:MIC ratio
+ Moderate post-antibiotic effect
+ Renally cleared Plasma t
|
~ 4-6 hrs
ii) Toxicity
+ Ototoxicity < 2%
+ Nephrotoxicity - very rare (20 case reports 1956-84)
*probably non-existent with current preparations
+ Red-man synd. rate of IV administration.
iii) Preference in ICU is for continuous infusion, c.f. interval dosing.
+ More constant plasma levels & efficacy
+ Reduced red-man syndrome
+ Irritant to veins, dilute to 250ml
+ Daily drug levels until stable
*assessment of CrCl in critical illness is sub-optimal.
iv) For patients on CRRT or CrCl < 20ml/min
+ Intermittent Dose = 1.0g slow IV when levels < 15mg/l
v) For patients transferring to the ward, see RAH intranet guidelines.
Table: Vancomycin Dosing Schedule
Renal Function
CrCl
> 60 ml/min
CrCl
20-60ml/min
CrCl < 20 ml/min
CRRT
I
n
i
t
i
a
l
D
o
s
i
n
g
Loading dose IV
25 mg/kg (max 2.0g) | Slow infusion (1/24)
in All Patients
Infusion Rate 2.0-4.0g / 24 hrs 1.0g / 24 hrs Not indicated
I
n
f
u
s
i
o
n
D
o
s
e
A
d
j
u
s
t
m
e
n
t
Vanc Level *Daily levels until stable
< 15mg/L
| Dose 1.0g/day
| Dose 0.5g/day
Not indicated
15-20mg/L | Dose 500mg/day | Dose 250mg/day
Target Level = 20-25mg/L Cont Current Infusion Rate
> 30mg/L
Hold 12 hrs
Recheck Level
Hold 12 hrs
Recheck Level
device, or
ii. Endoscopically placed by the GI Unit
b. Feeding jejunostomy
c. Nasogastric naloxone 4-8mg tds
d. TPN.
xi) Consider a PEG, PEJ or feeding jejunostomy in long term patients
e.g. Guillain Barr or severe head injury
xii) Cease feeds 4 hrs prior to extubation, tracheostomy, ET tube change.
xiii) There is no requirement to cease feeds until immediately prior to going to
theatre, unless:
+ Surgical procedure on the GIT
+ Planned for tracheostomy or ETT change.
xiv) Remember to modify insulin dose when feeds are reduced or ceased.
2. Enteral Protocol - See over page.
Flowchart: Nutritional Therapy Protocol
118
Patients expected to be mechanically ventilated for > 48h should have
enteral nutrition (EN) commenced within 24 h of admission to ICU
Insert NET, confirm position by XR and confirm
suitability for commencement of feeds
Commence feeds Osmolite 1 ml/kg/h
(1 kcal/ml @ max 80 ml/h)
(unless pt fluid restricted)
Pts unsuitable
for EN should
be considered
for TPN if EN
unlikely for > 5
days. Include;
short gut, GI
fistulae,
contraindication
to placing NET,
GIT perforation.
Referral to Dietitian for Nutritional Ax
Weekdays - ICU Dietitian will review ICU / SDU pts daily and chart max recommended feeding rate on daily obs chart.
Contact ICU Dietitian on Pg 1342 if any concerns / queries.
Weekends - Nursing T/L should be advised of new NET / changes to existing regimens. On call Dietitian should be
contacted (SD 1156 / 0401711460) and advised of - new ICU / SDU NET feeds; changes to existing regimens; pt
transfers.
Cover (when ICU Dietitian on leave) - Clinical Dietetics should be contacted (Pg 1342) and advised of all NEW ICU /
SDU NET feeds and changes to existing regimens.
If GRV remains high (i.e. 2
aspirates 250 ml within
12 h) consider post-pyloric
feeding
Do NOT aspirate post pyloric feeding tubes.
Monitor pt for signs of intolerance including abdominal distension, constipation,
diarrhoea or vomiting. Notify physician of concerns.
Feeding interruptions
Do not hold feeds for
routine nursing care,
bedside procedures
or diagnostic tests
unless specified.
No need to fast prior
to surgery unless
ETT to be removed,
i/o tracheostomy,
tracheostomy change
or GIT surgery.
If fasting for theatre,
commence fast when
pt called to theatre.
Or fast for 4 hr prior
to r/o ETT, i/o
tracheostomy,
tracheostomy change
or surgery on gut
lumen.
EN and insulin to
cease during time in
OT and restart at
same rate as when
discontinued.
Cease feeds 4hr prior
to planned
extubation.
Check Gastric residual volume (GRV) every 6 h
for ALL gastric tubes, document on chart.
Do NOT aspirate post pyloric tubes.
GRV < 250 ml
return aspirate,
continue feed
regimen (if not at
goal increase rate
by 20 ml/h)
GRV 250 ml
return 250 ml,
halve feed rate,
commence
prokinetics
Prokinetics
Both Metoclopramide 10mg QID IV and Erythromycin 100 - 200mg BD IV
Metoclopramide not recommended for use in head injury pts.
Refer Pt to Dietitian for Nutritional Ax
Consider TPN if unable to
place post pyloric tube
Jejunostomy
feeds should
commence at
rate of 1 ml/kg/h
or as
recommended
by Dietitian and
flushed 20 ml N
saline QID.
119
3. Post-pyloric feeding protocol:
a) Commence feed at 1ml/kg/hr, up to a maximum 80 ml/h.
b) No need to cease feed for any procedures, other than GI surgery.
c) Consider placement of a NG tube to aspirate and ensure an empty stomach.
4. Parenteral Nutrition
a) General principles
i) TPN may be harmful in critically ill patients.
ii) Enteral nutrition is preferred and TPN should only be considered for patients
in whom this is not possible.
iii) Supplementing EN with TPN is not beneficial and should be avoided.
iv) Refer to Clinical Duties Outside ICU, regarding the responsibilities and
management of ward patients receiving TPN.
v) TPN is usually ordered by the Unit A Senior Registrar, under the supervision
of Dr Adam Deane.
vi) IV access may be via a CVC or PICC line, with the latter being preferred.
vii) TPN for ICU patients is prescribed during the midday fluid round.
viii) Patient being discharged from ICU on TPN must be entered into the TPN
folder in Unit A.
b) Indications for TPN in the patient who cannot be fed enterally are:
i) GIT Failure > 7-10 days and expected duration of support > 5-7 days.
+ Prolonged post-operative ileus
+ Enteric fistulae
ii) Short GIT syndrome following major intestinal resection.
c) Complications of TPN:
i) Depression of immune function, esp. in cancer patients
ii) Intestinal villous atrophy
iii) Metabolic imbalance
+ Electrolyte disturbances (+ K
+
, HPO
4
=
, Mg
++
)
+ Glucose intolerance: hyperglycaemia and glycosuria
+ Hyperosmolar dehydration syndrome
+ Rebound hypoglycaemia on cessation of TPN
+ Hyperbilirubinaemia
+ CO
2
production, esp. in COPD patients
iv) Central venous access complications
120
d) Protocol
i) On commencement:
+ Add the following orders to the patient's drug folder:
a. Cernevit MV 1 ampoule IV daily.
b. Trace elements 1 ampoule daily
c. Vitamin K 10 mg IV weekly
d. Commence insulin:
i. Initial dose = 5
U
s.c. qid *hold if BGL < 10
ii. Check BGL qid
iii. Adjust the dose on subsequent days guided by BGLs
iv. Sliding Scale regimens are no longer used.
+ Commence TPN solution at a lower rate (40ml/hr) in starved patients
a. Potential movement of K
+
/ HPO
4
=
into cells with re-feeding
b. May cause acute severe hypokalemia and hypophosphataemia.
+ Slowly increase to desired rate, usually 60-80 ml/hr.
+ Dietician will provide a calculated energy requirement as a guide
ii) Daily:
+ Review the patient, CVC site, biochem, BGL chart and fluid balance.
+ Prescribe TPN selecting the most appropriate option from the table
below.
+ These bags are pre-prepared and must not be altered, i.e. no further
additives. Patients requiring K
+
, PO
4
and fluids etc. abovethe quantities
provided must receive these in a separate line/infusion.
iii) Intralipid
+ Commence TPN with lipid-free solutions (#3, #4)
+ Lipid is indicated if the period of malnutrition > 4 weeks or if the patient
is hyperglycaemic.
Table: Average Daily Requirements
Water 30-40 ml/kg/day
Calories 25-30 kcal/kg/day
1. Glucose: 2g/kg/day @ 4.1 kcal/g
2. Fat: 2g/kg/day @ 9 kcal/g
Protein 0.5-2.0 g/kg/day
1. 2:5 essential:total amino acids
2. 150:1 kcal:g N2 (non-nitrogen kcal)
Sodium 1.0 mmol/kg/day
Potassium 1.0 mmol/kg/day Dependent on renal function
Phosphate 0.2 mmol/kg/day Dependent on renal function
Vitamins
B groups daily
B12, Folate, A, D, E, K weekly
Trace elements as required.
Replacement
solutions
1. Urine
2. Nasogastric/ileostomy
3. Pancreatic/biliary fistulae
1. Normal saline KCl 10 ml/L
2. Normal saline KCl 10 ml/L
3. Hartmanns solution
121
Table: Baxter TPN Solution Options
Composition
Baxter Option 1
With Lipid
With Potassium
Baxter Option 2
With Lipid
No Potassium
Baxter Option 3
No lipid
With Potassium
Baxter Option 4
No Lipid
No Potassium
Total Volume (ml) 2000 2100 2000 2100
Glucose (gm) 250 250 500 500
Lipids (gm) 100 100 0 0
Energy (kcal) 2270 2270 2300 2300
Protein (gm) 100 100 100 100
Nitrogen (gm) 16.5 16.5 16.5 16.5
Na
+
(mmol) 73 73 73 73
K
+
(mmol) 60 0 60 0
Mg
++
(mmol) 5 5 5 5
HPO4
=
(mmol) 37.5 7.5 30 0
Cl
-
(mmol) 70 110 70 110
Acetate (mmol) 150 82 150 82
Solution shelf life 12 mths room T 6 mths room T 12 mths room T 6 mths room T
1. Lipid source is Clinoleic 20% which comprises olive oil 80% and soya oil 20%.
2. Multivitamin and trace elements to be given separately from TPN.
3. Nothing may be added to TPN bags.
4. All solutions come in triple phase bag and have light protection cover.
NB: Specialised prescription TPN can be ordered via pharmacy, e.g. when large daily potassium requirements are not feasibly
administered by 10mmol/100ml bags and the standard 60mmol/2L TPN.
122
C. Blood Component Therapy
1. Indications
a) Blood component therapy should only be given if benefit outweighs the risk
b) The decision to transfuse should be based on clinical assessment, disease course
and response to previous transfusion as well as [Hb] levels.
c) Potential risks including
i) Mis-identification / acute transfusion reaction
ii) Bacterial / viral infection
iii) Transfusion associated acute lung injury (TRALI)
iv) Transfusion associated circulatory overload (TACO)
v) Immune modulation (this and TRALI are probably the most significant)
d) The best way to reduce the risk of blood component therapy is to reduce
requirements
i) Minimise unnecessary blood sampling
ii) Minimise blood loss during procedures
iii) Consider nutritional and iron stores state
2. Red Blood Cells
a) Elective *as per NHMRC / ASBT guidelines.
i) Use of RBCs at Hb > 100g/L is likely to be inappropriate
ii) Use of RBCs at Hb < 70g/L is likely to be appropriate but in some
asymptomatic patients a lower threshold may be acceptable
iii) At Hb 70-100g/L clinical assessment of risk versus benefit is required.
iv) The following criteria may indicate RBC transfusion is indicated
+ Significant ongoing bleeding present or anticipated.
+ Clinical signs of impaired oxygen transport such as dyspnoea,
tiredness/weakness, angina, syncope.
+ Cardiac ischaemia or cardiac failure due to anaemia.
v) Order as Red cells or RBCs on the ICU or ward fluid chart
vi) Type & Screen specimens are held for 10 days for compatibility testing.
vii) For transfusion, a new specimen is needed for cross-match every 72 hours.
b) Resuscitation
i) Abnormal bleeding is usually surgical and requires urgent surgical and/or
radiological intervention.
ii) A full cross-match takes 30 minutes if marked urgent (not including the
time for transfer of blood); this should be performed if possible while
volume is replaced with crystalloid or colloid.
123
iii) If blood is required faster than this, the request Time Required box
should be marked:
+ Desperate *group O Rh(D)-ve blood is issued immediately
(see massive transfusion protocol)
+ 10 minutes *group-specific (ABO/Rh-D) but without full
compatibility testing
+ 30 minutes urgently processed, fully crossmatched blood
NB: The requesting MO accepts full responsibility for these (*)
iv) Blood replacement should start immediately in the setting of:
+ Rapid blood loss leading to hypovolaemia and shock.
+ Blood loss estimated or anticipated to exceed 20-25% of blood
volume, i.e. 1000-1500 ml in a normal adult.
3. Massive Transfusion Protocol
a) Definition:
i) Loss of one blood volume within a 24 hr period.
ii) Alternative, more practical definitions:
+ 50% blood volume loss within 3 hr, or
+ 150 ml/min rate of loss.
b) The RAH massive transfusion protocol should be activated as soon as the need
is identified
c) Correction of critical bleeding requires simultaneous approach to:
i) Control the source of bleeding
ii) Contact key personnel required for haemorrhage control
iii) Maintain blood volume
iv) Prevent hypothermia and acidosis
d) Principles
i) Trauma patients with critical bleeding are coagulopathic on presentation
ii) Prevention of further coagulopathy with aggressive management is much
more effective than delayed treatment
iii) Acidosis and hypothermia worsen coagulopathy
e) On identification:
i) Take blood and place in red bags for:
+ CBE, Group and match
+ Extended Coags
ii) Notify transfusion medicine on 47*
iii) Dispatch blood samples ASAP
iv) Transfusion will provide products in Massive Transfusion Packs
v) Notify transfusion when bleeding controlled
f) Tranexamic acid
i) Routinely used in trauma only as per CRASH2
ii) Triggers modified for local use (see Chart)
iii) Dose 1g over 10 minutes then 1g over 8 hours
iv) Delivered with first MTP pack
124
Table: Critical Bleeding (Massive Transfusion)
Procedure Comments
Laboratory
investigations
Samples to Blood Bank for T&S
CBE, INR, APTT, fibrinogen
Biochemical profile, blood gases etc.
Repeat CBE, INR, APTT, Fib
after blood component infusion, or
every 4 hrs until stable.
Take samples at earliest opportunity as
results may be affected by colloid
infusion.
Mis-identification is commonest
transfusion risk.
May need to give components before
results available.
Use Massive TransfusionPriority
Processing labels with Red bag to alert
lab for speedy processing.
Suitable RBC Un-crossmatched group O Rh(D)
negative in extreme emergency until
blood group known, then group-specific.
Then fully crossmatched blood when
time permits.
To prevent hypothermia by the use of
blood warmer and/or rapid infusion
device.
Employ intra-op blood salvage if
available and appropriate.
Rh(D) positive is acceptable if patient is
male or post-menopausal female.
Laboratory will complete compatibility
testing after issue.
Further compatibility test not required
after replacement of 1 blood volume (8
10 units).
Blood-warmer indicated if flow rate >50
ml/kg/hr in adult.
Salvage contraindicated if wound heavily
contaminated.
Platelets Anticipate platelet count <50x10
9
/L after
2 x blood volume replacement.
Target platelet count: >100x10
9
/L for
multiple/CNS trauma or if platelet
function abnormal.
Target >50x10
9
/L for other situations.
FFP
(10-15 ml/kg 1 litre
or 4 units for an adult)
Aim for INR <1.5 and APTT <40 secs.
Allow for 30 min thawing time.
Consider extended life plasma
INR >1.5 and APTT >40 secs correlates
with increased surgical bleeding.
Keep Ca
++
>1.13mmol/L
Cryoprecipitate
(2-4 units)
Replace fibrinogen.
Aim for fibrinogen >1.0 g/L.
Allow for 30 min thawing time.
Fibrinogen <0.5 strongly associated with
microvascular bleeding.
Fresh whole blood Request hospital Blood Bank to contact
ARCBS on-call MO.
Anticipated major blood loss in elective
patients with platelet or coagulation
abnormalities. Continued significant
bleeding even after use of conventional
component therapy. Role in haemostasis
controversial.
Recombinant FVIIa
(Novoseven)
Dose ~ 90 g/Kg
Obtain approval from consultation with
senior Surgeons / Anaesthetists /
Intensivists and Haematologists /
ARCBS on-call MO.
May be considered when the patients
condition continues to deteriorate to
likely haemorrhagic death
Usually as a desperate effort after other
measures fail.
See Massive Transfusion Protocol
125
126
127
4. Platelets
a) Standard dose is Platelets - 1 Adult Pack
b) Prophylactic transfusion before surgery or other at risk procedures:
i) Platelet count < 50 10
9
/L or
ii) Platelet count > 50 10
9
/L
with evidence of inherited or acquired (drug-induced) platelet dysfunction
c) Prophylactic transfusion in marrow failure:
i) Platelet count < 10 10
9
/L, or
ii) Higher levels with clinical evidence of bleeding or other risk factor
d) Therapeutic transfusion for uncontrolled haemorrhage:
i) As per the massive transfusion protocol
ii) Platelet count < 50 10
9
/L
iii) Platelet count < 100 10
9
/L with microvascular bleeding
iv) Irrespective of platelet count with evidence of platelet dysfunction.
e) Platelet dysfunction can contribute to bleeding with a normal platelet count
f) ITP: Only if life-threatening bleeding is present.
5. Fresh Frozen Plasma (FFP)
a) Prophylactic transfusion before surgery or other invasive procedure that could
result in significant bleeding:
i) Urgent correction of prolonged INR or APTT in warfarin overdose or
vitamin K deficiency (see below)
ii) Correction of prolonged INR or APTT in liver disease
iii) Correction of inherited coagulation factor deficiencies where specific
coagulation factor concentrates are not available
b) Therapeutic transfusion for uncontrolled haemorrhage in:
i) Warfarin overdose
ii) Liver disease
iii) Vitamin K deficiency
iv) Inherited coagulation factor deficiencies where specific coagulation factor
concentrates are not available
v) DIC
c) Plasma exchange in TTP & related syndromes
d) As per the massive transfusion protocol
e) Post massive transfusion with coagulopathy:
i) INR > 1.5, or
ii) APTT > 40 seconds
6. Extended Life Plasma
a) Recent regulatory changes allow transfusion laboratories to used thawed FFP
for up to 5 days.
b) By using thawed FFP the product can now be provided immediately, c.f. the
standard 20-30 minute delay normally involved in thawing.
c) Five day thawed FFP will be labelled Extended Life Plasma
128
Table: Guidelines for the Management of an Elevated INR
Clinical Setting Action
INR < 5.0
Bleeding absent
Lower the dose or omit the next dose of warfarin.
Resume therapy at a lower dose when the INR approaches therapeutic range.
If the INR is only minimally above therapeutic range (up to 10%), dose reduction
may not be necessary.
INR ~ 5.09.0*
Bleeding absent
Cease warfarin; consider reasons for | INR and patient-specific factors.
If bleeding risk is high, give vitamin K1 (1.02.0mg orally or 0.51.0mg IV) .
Measure INR within 24 hrs, resume warfarin at a reduced dose once INR is in
therapeutic range.
INR > 9.0
Bleeding absent
Where there is a low risk of bleeding
Cease warfarin, give 2.55.0mg vitamin K1 orally or 1.0mg IV
Measure INR in 6-12 hrs & resume warfarin at a reduced dose once INR < 5.0.
Where there is high risk of bleeding
Cease warfarin, give 1.0mg vitamin K1 IV.
Consider Prothrombinex-HT (2550 IU/kg) and FFP (150300mL)
Measure INR in 6-12 hrs, resume warfarin at a reduced dose once INR < 5.0.
Any clinically
significant
bleeding where
warfarin induced
coagulopathy is
considered a
contributing factor
Cease warfarin therapy, give 5.010.0mg vitamin K1 intravenously, as well as
Prothrombinex-HT (2550 IU/kg) and fresh frozen plasma (150300mL), assess
patient continuously until INR < 5.0, and bleeding stops.
or
If fresh frozen plasma is unavailable, cease warfarin therapy, give 5.010.0mg
vitamin K1 intravenously, and Prothrombinex-HT (2550 IU/kg), assess patient
continuously until INR < 5.0, and bleeding stops.
or
If Prothrombinex-HT is unavailable, cease warfarin therapy, give 5.010.0mg
vitamin K1 intravenously, and 1015mL/kg of fresh frozen plasma, assess
patient continuously until INR < 5.0, and bleeding stops.
* Bleeding risk increases exponentially from INR 5 to 9, INR 6 should be monitored closely.
Vitamin K effect on INR can be expected within 6-12 hours.
Examples of patients with a high bleeding risk:
active gastrointestinal disorders (such as peptic ulcer or inflammatory bowel disease)
those receiving concomitant antiplatelet therapy
those who underwent a major surgical procedure within the preceding two weeks, and
those with a low platelet count.
In all situations carefully reassess the need for ongoing warfarin therapy.
From consensus guidelines Australian Society of Thrombosis and Haemostasis 2004
129
7. Cryoprecipitate
a) Bleeding and fibrinogen < 1.0 g/L in:
i) DIC.
ii) Massive transfusion.
iii) Hereditary hypofibrinogenaemia.
b) 10
U
of cryoprecipitate will | plasma fibrinogen by ~ 1.0g/l
c) Standard dose = 8
U
for hypofibrinogenaemia.
8. DDAVP
a) Standard dose = 0.3-0.4g/kg intravenously over 30 mins
b) Increases factors VIII:C, VIII:vWF and platelet adhesion.
c) Indications: actual, or significant risk of bleeding with,
i) Haemophilia A
ii) type I von Willebrand's disease
iii) Post cardio-pulmonary bypass (check with surgeon)
iv) Clinical scenarios where platelet dysfunction is likely
+ Uraemia
+ Drugs - aspirin, clopidogrel
9. Recombinant activated factor VII (rFVIIa, NovoSeven)
a) TGA approved indications
i) Haemophilia patients with antibodies to factor VIII
ii) Glanzmann's thrombasthenia with antibodies to GPIIb-IIIa and/or HLA,
and who have past or present refractoriness to platelet transfusions
iii) Patients with congenital factor VII deficiency
b) Effective in improving coagulopathies associated with trauma, major surgery,
and organ transplantation = off-label indications.
c) No risk of virus transmission and contains no human protein
d) Binds to tissue factor (TF) activating both factors IX and X.
i) High doses activate factor X on the surface of activated platelets
ii) Has both TF-dependent and TF-independent effects
e) Recommended dose for the treatment of a severe coagulopathy ~ 90g/kg
f) Acts within a few minutes and has a half-life of about 2.5 hours.
g) Requires consultant/haematology approval because of high cost and absence of
current TGA approval for these indications.
130
10. Dabigatran Clinical Guidelines
a) General Information
i) Dabigatran etexilate (Pradaxa) is a pro-drug of dabigatran
ii) Reversible direct thrombin inhibitor
iii) Onset of anticoagulant effect within 30 minutes after oral administration
iv) Peak plasma concentration and effect within 2-3hrs.
v) Usual half-life: 12-14 hrs
vi) Renally cleared, ClCr < 30 ml/min t
> 24 hrs.
b) Effect on Laboratory Coagulation Parameters
i) Monitoring is not routinely required
ii) No direct relationship between coagulation tests and therapeutic effect.
iii) Thrombin time (TT)
+ Particularly sensitive to dabigatran
+ A normal TT excludes clinically significant dabigatran levels.
iv) Activated partial thromboplastin time (APTT)
+ Shows best correlation with plasma levels
+ Increasing APTT occurs with dabigatran concentration.
a. Usual peak concentration APTT ~ 2x control
b. Trough levels (12 hrs post dose) ~ 1.5x
+ A normal APTT suggests that minimal drug is present
+ A significantly prolonged APTT suggests drug excess:
a. APTT > 65s at trough (12 hrs post-dose) or
b. APTT > 80s at any time.
v) Prothrombin time (PT)
+ At therapeutic concentrations (50-200 ug/L) dabigatran has little effect
on PT and therefore INR.
+ INR results therefore do not reflect anticoagulant activity.
+ At supra-therapeutic concentrations the INR may be s 2.0.
c) Dabigatran Assay
i) Haemoclot dabigatran assay has been established by SA Pathology
ii) A dabigatran level should be requested on the pathology form and the
timing of the last dabigatran dose given.
iii) A single citrate tube is required. For further information ring 8222 3918.
d) Dabigatran and other anticoagulants
i) When converting patients from warfarin do not commence dabigatran
until the INR is < 2.0.
ii) For patients on dabigatran commencing parenteral anticoagulation, wait
+ 12 hours (CrCl 30 mL/min) or
+ 24 hours (CrCl < 30 mL/min) after the last dose.
iii) For patients receiving a parenteral anticoagulant commencing dabigatran
+ LMWH (b.d.) commence dabigatran 0-2 hours before the next dose of
LMWH was to have been administered
+ Heparin infusion - commence dabigatran on cessation of infusion.
131
e) Peri-operative dabigatran management
i) The requirement to cease anticoagulation should be assessed
ii) If cessation is required, the timing will be dependent upon renal function
and the bleeding risk associated with the procedure.
Table: Pre-operative Dabigatran Management
Renal Function
(CrCl ml/min)
Half-life
dabigatran (hrs)
Timing of discontinuation prior to surgery
Standard bleeding risk High bleeding risk
> 80 13.4 24 hrs 2-4 days
> 50 to s 80 15.3 24 hrs 2-4 days
> 30 to s 50 18.4 At least 2 days 4 days
s 30* 27.2 2-5 days > 5 days
NB: *Ongoing treatment with dabigatran should be reviewed as use in patients with a CrCl <
30ml/min is contra-indicated.
f) Bridging therapy with parenteral anticoagulation
i) Pre-operative bridging is not required in the majority of patients.
ii) Post-operative bridging
+ The onset of therapeutic anticoagulation after administration of
dabigatran is rapid (within 1-2 hrs)
+ Caution should be exercised in restarting within 48-72 hrs following
high bleeding risk procedures
+ Alternative parenteral prophylactic anticoagulation may be warranted
(eg subcutaneous enoxaparin) in the time period prior to resuming
dabigatran, depending on the procedure performed.
g) Epidural and other regional anaesthesia/analgesia and dabigatran
i) LP, spinal, epidural and some forms of major regional block should not be
performed within 24 hrs post-dabigatran, longer with renal dysfunction.
ii) Dabigatran should not be administered to patients with an epidural catheter
in-situ (and some regional analgesia catheters discuss with anaesthetist).
iii) Dabigatran should be delayed > 4 hrs following performance of an
epidural, spinal, LP, regional block or after catheter removal.
h) Emergency procedures
i) Surgery or invasive procedures should be delayed at least 12 hrs post-dose
ii) An urgent APTT +/- dabigatran level can be requested and bleeding risks
are small providing:
+ normal APTT or
+ dabigatran level < 50 ug/L.
iii) See guideline for management of bleeding in patients receiving dabigatran
for details regarding the treatment of surgical bleeding.
132
Flowchart: Management of Bleeding Patient on Dabigatran
Moderate bleeding reduction in Hb 20g/L, transfusion of 2 units of red cells
Severe bleeding bleeding in critical area or organ (intraocular, intracranial, intraspinal, compartment
syndrome, retroperitoneal or pericardial), hypotension not responding to resuscitation.
* This is an off license use of rVIIa (NovoSeven) and the risk of thrombotic complications when rVIIa is
used for this indication is unclear. The use of rVIIa is supported by laboratory data however clinical
evidence supporting an improvement in clinical outcomes is still lacking.
Bleeding Patient on Dabigatran
- Initiate Standard Resuscitation Procedures as Required
- Urgent bloods:
FBC, APTT, PT, TT and dabigatran level*
E, C&U, Creatinine
*2 x citrate tubes + time of last dose of dabigatran.
STOP DABIGATRAN THERAPY
Mild Bleeding
- Local haemostatic measures.
- Delay next dose of dabigatran
or discontinue if felt
appropriate by prescribing
physician.
Moderate Bleeding
- Consult critical bleeding on-call
haematologist via transfusion. (25430/25431)
- Consider oral charcoal administration if
dabigatran ingestion < 2 hrs prior.
- Local haemostatic measures
o Mechanical compression
o Consider seeking an opinion regarding
surgical intervention
- Maintain adequate hydration to aid drug
clearance.
- Transfusion support
o Packed cell transfusion as indicated by Hb
and ongoing bleeding
o Consider platelet transfusion if platelets <
70 x 109/L or if taking antiplatelet therapy.
o Consider 25U/kg prothrombinex if INR >
1.5.
o If ongoing bleeding resulting in clinical
instability despite above measures consider
rVIIa* +/- dialysis as described as for severe
bleeding.
Severe Bleeding
- Consult critical bleeding on-call
haematologist via transfusion.
(25430/25431)
- Consult ICU or if necessary other
appropriate facility.
- Institute measures as for moderate to
severe bleeding.
- Administer rVIIa 90 ug /kg
(rounded up to nearest mg), and
consider repeat dose at 30
minutes, if no response.*
- Consider dialysis particularly indicated if
high drug level as indicated by excessively
prolonged aPTT > 80 secs or
dabigatran level > 200 ug/L and/or impaired
renal function.
Consider dose of rVIIa immediately prior to
vascular access if significantly prolonged aPTT.
4 hrs of haemodialysis will reduce
drug level by approx. 60%.
- Neither rVIIa nor dialysis is likely to improve
outcome in patients with a normal aPTT or a
dabigatran level of < 50 ug/L
133
11. Disseminated intravascular coagulation (DIC)
a) Definition
i) DIC occurs when the balance of the haemostatic and fibrinolytic systems
becomes disordered. It occurs in response to severe pathophysiological
stimuli and is a part of multisystem organ dysfunction (often associated
with ARDS and acute renal failure). It is characterised by:
+ Microthrombi formation causing microvascular obstruction
+ Consumption of platelets and clotting factors
+ Abnormal fibrinolysis
b) DIC screen:
i) Complete blood picture
+ microangiopathic haemolytic anaemia with red cell fragmentation
+ haemolysis
+ thrombocytopenia
ii) Extended coagulation screen:
+ prolongation of TCT, APTT, PT
+ hypofibrinogenaemia
+ low factor VIII
+ excess fibrinolysis with elevated FDPs
iii) Liver and renal function tests
c) Treatment
i) Treatment of the underlying cause
ii) Replacement of blood components in the bleeding patient
+ FFP - based on INR/APTT
+ cryoprecipitate - for marked fibrinogen deficiency
iii) Controversial therapies (following consultant approval only)
+ heparin, fibrinolytics (tPA)
+ anti-fibrinolytics (EACA)
11. Blood transfusion reaction protocol
a) Plasma can cause reactions ranging from mild pruritus, erythema and urticaria
through to severe flushing, hypotension, fever, angioedema, bronchospasm and
fulminant anaphylaxis.
b) Suspected Reaction Protocol
i) Stop the transfusion immediately do not disconnect the IV line.
ii) Recheck the patient identification on the blood product pack label against
the patients wristband and verbally with the patient if possible.
iii) I f there is an unexplained discrepancy, discontinue the transfusion and
treat as per (iv, v below)
iv) Mild Reactions
+ | Temp. < 1.5 C
+ Mild or no hives or rash.
+ Action - slow the rate and continue transfusing the same unit of blood.
134
v) Severe Reactions
+ Severe hives and/or a rash.
+ | Temp. > 1.5C and is the only clinical sign or symptom
+ Action
a. Consider an antihistamine and antipyretic
b. Cease and then restart transfusing the same unit of blood after
approximately 20 minutes.
+ If there are further signs & symptoms of a reaction
discontinue & order a transfusion reaction investigation
+ If there is a sudden and acute change in the patients condition, e.g.
cyanosis, bad headache, backache, or significant change in pulse or
blood pressure for no apparent clinical reason
discontinue & order a transfusion reaction investigation
vi) Investigation of a transfusion reaction:
+ A transfusion reaction investigation form (IMVS 224) should be
completed and sent to Transfusion Medical Unit (TMU) with:
a. A description of the relevant clinical findings and vital signs
b. A post-reaction 10ml EDTA blood specimen, preferably from a
vein other than that used for transfusion
c. Any used or unused blood packs and the attached IV set(s).
+ If there is a major reaction, it is also recommended that the first urine
specimen voided after reaction is saved, and patients urine output
over the next few hours is recorded.
+ Further blood samples for biochemical assays, coagulation tests, and
cultures will be needed.
+ Administration of incompatible blood constitutes a Sentinel Event.
vii) Haemovigilance
+ The IMVS and RAH are participating in the Blood Safe
haemovigilance scheme, an adverse incident reporting system aimed at
the quality and safety improvement of transfusion practices.
+ Contact the Transfusion Safety RN (Pager: 1575, Tel: 22975)
135
Table: Blood Transfusion Reactions
Type Signs & Symptoms Treatment Prevention
Febrile non-haemolytic
transfusion reaction
(FNHTR)
Pyrexia (> 1C rise)
Rigors/chills
Anxiety
Withhold transfusion.
Mild fever without other
symptoms may be treated
by slowing infusion.
An antipyretic may be
helpful.
Investigate as for
suspected HTR if the
reaction is significant.
Consider use of
leucodepleted red cells or
platelets if a recurrent
problem.
Circulatory Overload Distended cervical veins.
Pulmonary oedema
Dyspnoea. Headache.
Heaviness in limbs.
Discontinue.
Institute treatment for fluid
overload,
e.g. diuretic
Give all fluids slowly to
patients with compromised
cardiac or renal status.
Use red cell concentrates.
If anticipated, give diuretic.
Allergic Flushing
Urticaria, itchy hives
Facial oedema
Slow rate of flow.
Consider anti-histamine.
Watch for laryngeal
oedema and development
of anaphylaxis.
When anticipated,
use prophylactic
antihistamines.
Anaphylaxis Dyspnoea from laryngeal
oedema or bronchospasm,
sometimes cyanosis and
collapse
Discontinue transfusion
immediately.
Institute treatment for
anaphylaxis,
e.g. Adrenalin, steroids
Use of Medi-Alert
wristband in proven
IgA deficient patients.
Acute Haemolytic
Transfusion Reaction
(HTR)
Pyrexia
Rigors/chills
Lumbar pain
Pain along vein
Jaundice
Haemoglobinuria
Oliguria later uraemia
Discontinue transfusion
immediately.
Get expert advice
immediately.
Save all used packs, blood
samples.
Save all urine.
Collect fresh blood
samples.
Extreme care in
collecting the correct
blood sample for T&S.
Careful compatibility
testing by laboratory.
Careful method for storing
& labelling blood.
Careful identification
of the correct recipient.
Infected blood Bacterial sepsis with
hyperpyrexia
Pain in limb & chest
Headache
Pallor
Burning pain along vein
Low blood pressure
Rapid pulse
Profound collapse & shock
Discontinue transfusion
immediately.
Acute medical emergency
get advice immediately.
Save used packs, all blood
samples, with labels.
Save all urine.
Anti-shock treatment and
antibiotics.
Storage at correct temp.
Do not remove from
refrigerator until
immediately before
transfusion
Non-cardiogenic
pulmonary oedema.
Transfusion related acute
lung injury (TRALI): rare
Dyspnoea
ARDS picture within 6
hours after transfusion.
Maintain blood pressure &
cardiac output with fluid
support. May require
ventilatory support.
Difficult, usually in the
setting of multiparous blood
donor with anti-recipient-
WBC antibodies.
NB: See RAH Intranet, Transfusion Medicine (http://rahadm05v.had.sa.gov.au/)
136
D. Guidelines for the Management of Electrolytes
1. General principles
a) Total body water (60% total body weight):
i) intracellular fluid : predominant ions : K
+
, PO
4
2-
ii) extracellular fluid:
+ 75% interstitial fluid: predominant ions : Na
+
, Cl
-
+ 25% plasma volume (PV)
b) Osmotic equilibrium is maintained by Na
+
/K
+
pump
i) ECF ions therefore reflect total osmolality:
Calculated osmolality ~ 2Na
+
+ urea + glucose
ii) Magnesium is a cofactor for this pump
c) Most electrolyte disturbances in critically ill patients relate to changes in the
distribution and concentrations of the predominant ECF and ICF ions.
d) As a general rule, changes in one ion will be reflected in the associated cation or
anion.
e) Electrolyte disturbances should be considered in terms of the following groups:
i) Erroneous results
+ Lab error
+ Bloods taken from a drip arm
+ Haemolysed specimen - traumatic (old IA lines), delayed samples
+ Osmolar agents
ii) Decreased or increased losses: usually
+ Renal
+ Extra renal: GIT, skin losses
iii) Transcellular shifts.
iv) Decreased or increased intake
f) Treatment should be directed at the underlying cause.
g) Rapid correction of electrolyte disturbances may be deleterious.
h) One electrolyte disturbance may be predictive of another electrolyte disturbance
e.g. +K
+
often associated with +Mg
+
i) The following paragraphs outline the common electrolyte disturbances.
137
2. Hyponatraemia: Na
+
< 130 mmol/l
a) Aetiology / classification
i) Misleading result
+ Isotonic - Hyperlipidaemia
- Hyperproteinaemia
+ Hypertonic - Hyperglcaemia
- Mannitol, glycerol, glycine or sorbitol excess
ii) Water Retention
+ Renal Failure
+ Hepatic Failure
+ Cardiac Failure
+ SIADH
+ Drugs
+ Psychogenic polydipsia
iii) Water retention / Salt depletion
+ Post-operative, post-trauma
+ Patients with excess fluid losses given inappropriate replacement
+ Cerebral salt-wasting syndrome
+ Adrenocortical failure
+ Diuretic excess
b) Diagnosis & Management:
i) Factitious: ignore and manage underlying condition then recheck Na
+
ii) Misleading:
+ Hyperglycaemia: | BGL ~ 10 mmol/l + [Na
+
] ~ 3 mmol/l
a. Hyponatraemia per se is real, but treatment is directed at the
underlying cause, where correction of the hyperglycaemia will
correct the plasma [Na
+
]
b. NB: Total body Na
+
deficit may co-exist with diuresis in DKA
+ Mannitol:
a. +[Na
+
] early, then diuresis & late |[Na
+
] are more problematic
b. Maintain adequate plasma volume with N.saline initially
+ Alcohols: permeate solutes, o[Na
+
] less problematic
iii) Hypovolaemic states:
+ Restore volume with colloid or normal saline according to clinical
markers: urine output, plasma [Na
+
], RAP
+ Aim for slow Na
+
correction: s 2 mmol/l/hr, unless seizures.
+ Urine Na
+
is uninterpretable after diuretics or catecholamines for 24hrs
138
iv) Hypervolaemic states: *most common clinically
+ Fluid restriction < 15 ml/kg/day
a. Water Excess ~ (140 - Na
+
)/140 (Wt 0.6)
e.g., 70kg patient with plasma [Na
+
] = 120 mmol/l:
= (140 - 120)/140 (70kg 0.6)
= 6 litres
b. Will slowly correct excess - ADH group & reset osmostat
c. Treat the underlying cause - CCF, nephrotic synd., ascites
v) SIADH
+ Causes
a. Ectopic ADH production by tumours
e.g. small cell bronchogenic tumour
b. CNS disorders
e.g. tumour, abscess, trauma, SAH etc
c. Pulmonary diseases
e.g. TB, pneumonia, abscess etc
+ Diagnosis
a. Hypo-osmolar hyponatraemia
b. Urine osmo > plasma osmo
c. Urine Na
+
> 40 mosm/l
d. Normal endocrine, renal, hepatic, cardiac function
e. No diuretics or drugs affecting ADH secretion
f. Corrected by water restriction alone
+ Management: fluid restriction
vi) Severe Symptomatic Hyponatraemia : fitting, or decreased consciousness
+ Resuscitation / ABC
+ Consider anticonvulsants - phenytoin, benzodiazepines
+ Hypertonic saline (3%) may be indicated
a. Always discuss use with the Duty Consultant
b. Correct [Na
+
] rapidly only to ~ 120mmol/l
+ Thereafter, slow correction with N.saline over 24-36hrs (s 2 mmol/l/hr)
+ Treat the underlying cause.
3. Hypernatraemia: Na
+
> 145 mmol/l
a) Hypernatraemia is always a hyperosmolar state
b) Most body fluids have a [Na
+
] < plasma net water loss
c) Aetiology / classification:
i) Water depletion / inadequate replacement
+ Renal
a. Diuretics, glycosuria
b. ARF/CRF, partial obstruction
c. Central diabetes insipidus
i. Post traumatic head injury or surgery
ii. CNS infection, tumour, granulomatous disease, GBS
139
d. Nephrogenic diabetes insipidus:
i. 1 : congenital renal resistance to ADH
ii. 2 : hypokalaemia, hypercalcaemia, lithium, multiple
myeloma, sickle cell anaemia, nephrocalcinosis, amyloid
+ GIT losses - diarrhoea, vomiting, fistulae, SBO
+ Respiratory - IPPV with dry gases
+ Skin losses
a. Fever, high ambient temperature
b. Vasodilatory states
c. Exfoliative skin disorders, burns
d. Thyrotoxicosis
+ Unconsciousness
+ Reset osmostat
ii) Salt gain - Na
+
gain > H
2
O gain
+ Iatrogenic
a. Most common cause
b. Excess normal saline ~ 150 mmol/l [Na
+
]
c. NaHCO
3
, feeding formulae, TPN
+ Mineralocorticoid excess:
a. Conn's, Cushing's syndromes
b. Steroid excess
d) Management
i) Hypovolaemic states
+ Restore volume according to clinical markers:
BP, HR, urine output, RAP
a. Hartmanns solution - slightly hypo-osmolar
b. Colloid: initial resuscitation, severe hypovolaemic states
ii) Slow Na
+
correction: s 2 mmol/l/hr
+ Water deficit: ~ (Na
+
- 140)/140 (B.Wt 0.6)
e.g. 70 kg patient, with plasma [Na
+
] = 160 mmol/l
~ (160-140)/140 (70 0.6)
~ 6.0 litres
1 litre water replacement will reduce [Na
+
] ~ 3-4 mmol/l
+ In addition to basal fluid requirements & ongoing losses
+ Replace over a 24-48 hr period with 5% dextrose
+ Monitor [Na
+
] regularly
+ Manage aetiological causes
+ Cease causal drugs and inappropriate IVT
+ DDAVP for central DI only ~ 1-2 g s.c.
140
4. Hypokalaemia: K
+
< 3.0 mmol/l plasma
K
+
< 3.5 mmol/l serum
a) Aetiology / classification:
i) Compartmental / transcellular shift
+ Alkalaemia | pH ~ 0.1 + [K
+
]
pl
~ 0.5 mmol/l
+ Catecholamines / salbutamol
+ Insulin / anabolism - refeeding effect
+ Hypomagnesaemia - ICF K
+
depletion
+ Toxic / poisoning - barium, toluene
+ Familial periodic paralysis
+ Hypothermia
ii) Reduced intake - urine [K
+
] < 20 mmol/L
+ Starvation
+ TPN
iii) Increased clearance/losses
+ Renal - urine [K
+
] > 20 mmol/L
a. Diuretics | distal tubular flow
i. Loop agents - frusemide, bumetanide
ii. PT agents - acetazolamide, mannitol
iii. Early DT - thiazides
b. Steroids / Mineralocorticoid excess
i. Conns, Cushings, Bartters syndrome
ii. Ectopic ACTH - Small cell Ca lung
- Pancreatic, thymus carcinoma
iii. Exogenous steroids
c. Drugs
i. Anionic drugs - antibiotics (penicillins, amphotericin)
ii. High dose gentamicin
iii. Lithium
d. Hypomagnesaemia, Hypocalcaemia
e. RTA I, II
+ GIT losses
a. Villous adenoma
b. Ureterosigmoidostomy
c. Fistulae, malabsorption syndromes
d. Diarrhoea, Laxatives
+ Skin losses
b) Management:
i) Treat underlying cause
ii) Correct hypovolaemia: volume contraction will potentiate both alkalosis
and hypokalaemia
iii) Always add Mg
++
+ normomagnesaemia is essential for correction of hypokalaemia
iv) Look for and treat concurrent hypophosphataemia
141
v) Potassium preparations
+ KCl: 10 ml = 10 mmol/l
+ KH
2
PO
4
: 10 ml = 10 mmol/l
+ K-acetate: 5 ml at 5 mmol/ml
25 mmol K
+
+ 25 mmol acetate (bicarbonate)
5. Hyperkalaemia: K
+
> 5.0 mmol/l serum
K
+
> 4.5 mmol/l plasma
a) Aetiology / classification:
i) Artefactual
+ Drip arm specimen
+ Tourniquet / Haemolysed specimen (extravascular)
+ Thrombocytosis > 750,000
Leukocytosis > 50,000
ii) Compartmental / transcellular shift
+ Acidosis + pH ~ 0.1 |[K
+
] ~ 0.5 mmol/l
+ Insulin deficiency: DKA
NB: normo- or hypo-kalaemia in the presence of severe DKA is
associated with a marked total body K
+
deficit, which must be
addressed prior to correction of the acidaemia.
+ Familial periodic paralysis
+ Suxamethonium
+ Digoxin, |-blocker overdose
+ Fluoride poisoning
+ | ECF tonicity
a. Water moves from cells |[K
+
]
ICF
and passive diffusion
b. Seen with large doses of mannitol given rapidly (1.5-2.0 g/kg)
c. Hyperkalaemia of DKA is due to this in addition to the acidaemia
& insulin deficiency
iii) Cellular disruption / death
+ Tissue breakdown
+ Rhabdomyolysis, haemolysis (intravascular), ischaemia / reperfusion
+ Severe burns
+ Tumour lysis syndrome, leukaemia
iv) Increased intake - rarely a problem unless impaired renal function
+ Massive transfusion
+ Direct IV/oral
+ Drugs (penicillins)
142
v) Reduced clearance
+ Acute renal failure
a. Any cause for + distal tubular flow, or + distal NaCl delivery
b. Hypoaldosteronism
i. Mineralocorticoid deficiency, Addisons
ii. |K
+
is multifactorial - K
+
ICF
K
+
ECF
- +distal tubular flow
- +DT aldosterone effect
+ Type IV RTA
+ ACE Inhibitors
+ Potassium sparing diuretics
a. aldosterone antagonists - spironolactone
b. distal Na
+
channel inhibitors - amiloride, triamterene
b) Management:
i) The clinical scenario will dictate treatment
ii) Acute K
+
> 6.0 mmol/l is a medical emergency
iii) Associated with acute ECG changes, or haemodynamic compromise:
In following order (not mixed together),
+ CaCl
2
10 ml IV stat
+ NaHCO
3
50-100 ml IV stat
+ Glucose 50% 50g + Insulin 20 units
+ Salbutamol nebs continuously
iv) Refractory or persistent:
+ CVVHDF
+ intermittent dialysis
v) Chronic | K
+
or slow rate of rise or no ECG changes:
Resonium 30g oral / PR 8 hourly
vi) Address aetiological factors
vii) Normalise renal function / volume status
6. Acid base disturbances
a) Acid base disturbances in ICU are frequently mixed disorders
b) Correction of these should be directed at the underlying cause and maintenance
of cardiopulmonary homeostasis.
c) Primary correction of an acid base disturbance with acid or alkali is seldom
required.
143
7. Rules of thumb *these are approximations only
a) Primary metabolic disturbances: last 2 digits of pH will reflect PaCO
2
i) Met Acid to min 7.10 e.g. pH 7.25 PaCO
2
25 mmHg
ii) Met alkalosis to max 7.60 e.g. pH 7.57 PaCO
2
57 mmHg
b) Primary respiratory acidosis:
i) |HCO
3
~ 1mmol/l per 10mmHg |PaCO
2
above 40 to max 30
c) Primary respiratory alkalosis
i) +HCO
3
~ 2.5mmol/l per 10mmHg +PaCO
2
below 40 to min 18
d) Chronic respiratory acidosis
i) |HCO
3
~ 4mmol/l per 10mmHg |PaCO
2
above 40 to max 36
8. Metabolic acidosis
a) Assessment of metabolic acidosis must include the anion gap:
Anion Gap = [Na
+
+ K
+
] - [Cl
-
+ HCO
3
-
] ~ 12-17 mmol/l
Unmeasured cations Unmeasured anions
Mg
++
~ 1.2 mmol/l Albumin ~ 15 mEq/l
Ca
++
~ 2.2 mmol/l H2PO4
-
~ 2 mmol/l
IgG Small HSO4
-
~ 1 mmol/l
Organic ~ 5 mEq/l
~ 7.0 mEq/l ~ 23 mEq/l
b) This allows sub-classification of metabolic acidosis into raised or normal anion
gap acidoses.
i) Beware a low [Alb] in critically ill lowering the measured AG
ii) Measurement of chloride in the lab is highly variable
iii) Assessment of the AG must be viewed within the clinical context.
c) Aetiology of raised anion gap:
i) Renal failure - H
2
PO
4
-
, HSO
4
-
(rarely AG > 23)
ii) Lactic acidosis - types A&B
* normal AG does not exclude a lactic acidosis
iii) Ketoacids - |-OH-butyrate, acetoacetate
- diabetes mellitus, starvation, alcohol
iv) Rhabdomyolysis - organic acids
v) Drugs / poisons:
+ Aspirin - salicylate, lactate, ketones
+ Paracetamol - lactate, pyroglutamate
+ Ethanol - acetoacetate, lactate
+ Methanol - formate (formaldehyde), lactate
+ Paraldehyde - formate, acetate, lactate, pyruvate
+ Ethylene glycol - oxalate
+ Xylitol, Sorbitol - lactate
+ Fructose - lactate
144
Table: Classification of Lactic Acidosis
Type A Type B Drug induced Hereditary
Severe exercise
Seizures
Cardiac arrest
Shock
Hypoxia
Anaemia
Thiamine deficiency
Diabetes
Hepatic failure
Renal failure
Infection
Leukaemia, lymphoma
Pancreatitis
Short bowel syndrome
Phenformin
Metformin
Ethanol
Methanol
Salicylates
IV fructose
Xylitol
Sorbitol
G6PD deficiency
Fructose-1,6-DP-
deficiency
d) Aetiology of low or normal anion gap:
i) Hyperchloraemic metabolic acidosis
+ Resolving renal failure
+ Resolving DKA
+ Renal tubular acidosis / carbonic anhydrase inhibitors
+ Mineralocorticoid deficiency
+ Pancreatic, enteric fistulae
+ Ureterosigmoidostomy
+ IV HCl, NH
4
Cl, Arginine
ii) Metabolic alkalosis due to HCO
3
-
gain
iii) Hypoalbuminaemia
iv) Myeloma - IgG has positive charge, +'s AG
v) Increased Mg
++
or Ca
++
(rarely)
vi) Artefactually elevated Cl
-
vii) ? Hyperlipidaemia
e) Management
i) High anion gap
+ Treat the underlying cause
+ No indication for NaHCO
3
ii) Normal anion gap
+ Treat the underlying cause.
+ Replace HCO
3
serum level and losses
a. Approx. deficit = (24 - [HCO
3
]) (Wt. 0.6) mmol/l
e.g. for a 70kg patient with a [HCO
3
] = 4 mmol/l
deficit = (24 - 4) (70 0.6)
= 840 mmol (= ml of standard bicarb solution)
b. Replace 1/3-1/2 of this amount then remeasure blood gases.
145
9. Metabolic alkalosis
a) Aetiology / classification
i) Common causes:
+ Diuretics
+ Vomiting
+ Post-hypercapnia > 48 hours
+ Commonly associated with hypovolaemia and/or hypokalaemia
however, actual causation by these is debated
ii) Increased proton losses: acid loss is either renal or GIT
+ Renal
a. | Na
+
reabsorption (hypovolaemia, dehydration, etc.)
b. Cushing's syndrome, exogenous steroids
c. Hyperaldosteronism 1 / 2
d. Bartter's syndrome (JGA hyperplasia)
e. Liddle's syndrome
f. Hypercalcaemia / hypomagnesaemia nephrogenic DI
g. Drugs: steroids, diuretics, carbenoxolone
+ GIT
a. N/G suctioning, protracted vomiting
b. Diarrhoea
iii) Increased bases
+ Administration of NaHCO
3
+ Metabolism of exogenous acid anions - citrate, lactate, acetate
+ Milk/alkali syndrome
+ Renal conservation of HCO
3
-
- acidosis, hypercarbia
iv) Factors tending to maintain an alkalosis
+ Any fluid loss replaced with insufficient Na
+
H
+
excretion
(contraction alkalosis)
+ Hypovolaemia
+ Hypokalaemia, hypochloraemia, hypomagnesaemia
+ Chronic hypercapnia
+ Mild chronic renal failure
b) Management
i) Correct hypovolaemia
*normal ECF volume is essential for the correction of alkalosis
ii) Inotropic support of cardiac output and GFR
iii) Correct + K
+
, Mg
++
, HPO
4
=
iv) Consider acetazolamide if the alkalosis is persistent - provided the above
are corrected.
146
10. Respiratory acidosis
a) Aetiology
i) Any cause of hypoventilation respiratory failure (see diag.)
+ A. Respiratory centre / CNS
+ B. Upper motor neuron / spinal cord
+ C. Anterior horn cell
+ D. Lower motor neuron
+ E. Neuro-muscular junction
+ F. Respiratory muscles
+ G. Elasticity/compliance of lungs/chest wall
+ H. Structural integrity of chest wall & pleural cavity
+ I. Increased airways resistance intra/extrathoracic
ii) May be acute or chronic
b) Management
i) Restore ventilation / manage underlying cause(s)
ii) No indication for HCO
3
2. Respiratory alkalosis
b) Aetiology
i) Early hypoxia, shock or hypotension
ii) Anxiety, hysteria, neurogenic hyperventilation
iii) PTE
iv) Hepatic failure
v) Prescribed hyperventilation (rarely indicated)
c) Management
i) Treat underlying cause
ii) Neurogenic hyperventilation is a marker of severity of head injury
147
PART 5 - CLINICAL MANAGEMENT
The following protocols are designed to facilitate clinical management of patients in the
Intensive Care.
These protocols may vary from other ICUs and do not represent the sole approach to
patient management. However, they do represent a standardised approach which has
evolved in this ICU over the years.
Each clinical scenario is managed according to the particular situation and individual
patient - it is neither practical nor appropriate to apply rigid policies to clinical
situations. However, as clinical medicine is at times more art than a science, these
protocols are designed to assist in areas that are unfamiliar and to standardise
approaches by all staff members of the Unit.
The following protocols are outlined.
A. Cardiopulmonary resuscitation
B. Failed intubation drill
C. Respiratory therapy
D. Management of cardiothoracic patients
E. Renal failure
F. Neurosurgical protocols
G. Microbiology protocols
H. Drug overdose
I. Bites and Envenomation
J. Withdrawal of therapy
K. Organ donation and brain death
148
A. Cardiopulmonary Resuscitation
Flowchart: Basic Life Support
149
Flowchart: Advanced Life Support
150
Flowchart: Paediatric Cardiorespiratory Arrest
151
Induced Hypothermia Post Cardiac Arrest
1. Aim: To improve CNS outcome by actively cooling to a T
Core
~ 32-34C
2. Inclusion Criteria
a) Non-traumatic cardiac arrest with return of spontaneous circulation
a) Unconscious, intubated and ventilated
b) Absence of an immediately correctable cause for coma
c) T
C
> 34.5C
4. Exclusion Criteria
a) Cardiac arrest related to trauma or intracranial injury
b) Ongoing CPR and/or persistent cardiovascular instability
c) Cardiology consultation need for acute intervention
d) Criteria that preclude 40mls/kg of cold Hartmanns solution,
e.g. acute pulmonary oedema, T
C
< 34.5C
e) Time from cardiac arrest to ED > 12 hrs
f) Pregnancy relative C/I
5. Procedure - Initial Treatment Protocol
a) ECG and routine blood tests as indicated
b) Record core temperature (T
C
): rectal, oesophageal or bladder catheter
c) Ensure adequate IV access (1x 16G)
d) Document neurological function, specifically:
i) Pupillary responses to light
ii) Response to painful stimuli (all limbs), vocalization
iii) Reflexes gag, conjunctival, lash, tendon & plantar
e) Hartmanns (Temp. ~ 4C) / Bolus ~ 40mls/kg. / Infuse @ 100ml/min.
f) Maintain MAP ~ 80-100mmHg (relative to premorbid BP)
g) Maintain K
+
~ 4-5mmol/L and Mg
++
~ 0.8-1.2mmol/L
h) If T
C
> 35C after 1 hour, add surface cooling (cooling blanket / packs)
i) If patient is shivering and/or goal T
C
not achieved:
i) Midazolam (0.05mg/kg bolus, repeat every 5 min as required)
ii) Midazolam (1-5mg/hr) or Propofol infusion as clinically indicated.
iii) If sedation ineffective, consider a non-depolarizing muscle relaxant
6. Observations
a) Maintain T
C
~ 32-34C for 12-24 hrs from the time of achieving goal temp.
b) To increase temp. (T < 31.5C), use heated air blanket until 33C
c) To decrease temp. (T > 34.5C), use cold packs, cooling blanket, sedation and
then consider using non-depolarizing muscle relaxants
7. Complications
a) Arrythmia
b) Reduced cardiac index / increased peripheral resistance.
c) Ongoing cardiac instability may necessitate stopping the hypothermia protocol.
d) Hyperglycaemia
8. Aftercare
a) At 24 hrs cease all active cooling and allow passive rewarming.
b) If temp increases < 1C per 4 hours then rewarm actively to temp > 36C
c) Once T
C
> 35C, cease sedation and muscle relaxants
152
B. Failed Intubation Drill
1. Following rapid sequence induction in ICU we are generally committed to securing
the airway by some means. Allowing the patient to wake-up in the event of a failed
intubation is rarely practical.
2. Risk of failed intubation in ICU is higher than in the operating theatre.
3. Before intubating, you MUST have a contingency plan for a difficult airway/failed
intubation.
4. After hours, remember the anaesthesic staff may be available to assist.
5. Ensure all equipment is working and that the ETCO
2
monitor provides a reliable
waveform.
6. Ensure adequate IV access with running intravenous fluids.
7. Ensure ready access to vasopressors and resuscitation drugs.
8. Always have the difficult intubation trolley at hand.
9. Visually confirm that each individual piece of airway equipment is immediately
available and operational.
10. ICU patients have limited O
2
reserves and desaturate quickly.
a) If initial intubation attempts fail, or the patient desaturates significantly, ensure
you can manually ventilate the patient.
b) Failure to achieve manual ventilation is an absolute emergency
cant intubate + cant ventilate
11. If an intubation technique fails, move on quickly to an alternative.
12. There are a range of airway devices available to help secure the airway.
a) Guedel airway / Nasopharyngeal airway
b) Bougie
c) C-Mac
d) Laryngeal Mask / Intubating Laryngeal Mask
e) Cricothyroidotomy
f) Jet insufflation
g) Bronchoscopy (for anticipated difficult intubations)
13. You must be familiar with the devices you plan to use in the case of a failed
intubation.
14. Airway equipment and intubating manikins are available for practice in the
registrars room.
153
Flowchart: Failed Intubation Drill
Oxygenate/ventilate
Committed to
Intubation
Best Attempt
Laryngoscopy
ILMA +/-
Bronchoscope
Failure to
Ventilate
Crico-
Thyroidotomy
FURTHER
ATTEMPTS USING
ADVANCED DEVICE
- McCoy / Flextip
- C-MAC
- Airtraq
Intubate
Intubate
Call for help
No
CALL
EMERGENCY
Failure or
SpO
2
< 88%
Yes
154
C. Respiratory Therapy
1. Respiratory Failure
a) Definition = failure of efficient gaseous exchange and/or effective ventilation.
i) Type 1 Respiratory Failure
+ Hypoxaemia, PaO
2
:FiO
2
< 300 mmHg
+ i.e. failure to oxygenate
ii) Type 2 Respiratory Failure
+ Hypercapnoea, PaCO
2
> 50 mmHg, with a pH < 7.35
+ i.e. failure to ventilate
2. Oxygen Delivery Capacity
Table: Oxygen Delivery Devices
Apparatus/Device Oxygen Flow (l/min) Approx. FIO2 (%)
Nasal catheters 2 - 6 25-40%
Semi - rigid masks
(e.g. Hudson, CIG)
5
6
8
10
12
35
50
55
60
65
Venturi type mask
(e.g. Ventimask, Accurox)
2 - 8 24 - 50
Nasal High Flow
(humidified circuit)
30-50 l/min 21 - 95
Reservoir plastic masks
(Non-rebreathing mask)
6 - 15 FiO2 = 21% + 4% per l/min
Closed Circuits
e.g. IPPV, NIV
Variable 21 - 100
Oxylog 1000 and 2000
Oxylog 3000
Variable
Variable
Airmix : 60
No airmix : 100
40 - 100
a) The FiO
2
delivered to the patient by an open circuit will depend on the
patients peak inspiratory flow rate (PIFR).
b) The higher the PIFR, the higher the O
2
flow required to provide a given FiO
2
.
155
3. Humidification
a) All ventilated patients must have adequate humidification of inspired gases for
optimal mucociliary function and conservation of temperature.
b) Optimal humidification requires:
i) Delivery of gas to the trachea at a constant temperature (32-36C).
ii) Relative humidity 75-100%.
iii) No increase in circuit resistance.
iv) No increase in circuit dead space.
v) Applicable to spontaneous and controlled ventilation.
vi) Sterile inspired gas
c) Types of humidifiers available
i) Heat/moisture exchangers (HME)
+ First line humidification.
+ Effective for most patients.
+ Incorporates a bacterial and viral filter.
+ Cannot be used with nebulised drugs.
+ Secretions increase resistance and reduce HME efficacy. Change to
wet circuit (FP) in patients with bronchorrhoea or mucous inspissation.
+ Single use & change every 48 hrs, or as required.
ii) Fisher Paykel (FP) evaporative humidifier (wet circuit)
+ Bronchorrhoea or mucous inspissation.
+ Hypothermic or heat-loss susceptible patients (e.g. burns).
+ Ventilation anticipated for more than 48 hrs.
+ Set chamber to 40C.
iii) Inspiron (aerosolised T-piece).
+ Relatively inefficient humidification.
+ Allows variable FiO
2
: 0.21-0.7
4. Nasal High-Flow Oxygen
a) NHF delivers high gas flows through a unique Optiflow nasal cannula.
b) Critical to NHF is the delivery of optimal humidity to allow delivery of high
flows directly into the nares.
c) This provides greater patient comfort while optimising mucociliary clearance.
d) Main benefits of NHF:
i) Delivery of up to 100% oxygen.
+ Actual FiO
2
will depend upon the patients breathing pattern
ii) Anatomical dead space flushed.
iii) Positive airway pressure (2-5cmH
2
O) throughout the respiratory cycle.
iv) Improved mucociliary clearance.
156
Table: Oxygen Delivery Percentage - Nasal High Flow
O2% 30 LPM 40 LPM 50 LPM
O2 Air O2 Air O2 Air
30 4 26 5 35 6 44
40 7 23 10 30 12 38
50 11 19 15 25 18 32
60 15 15 20 20 25 25
70 19 11 25 15 32 18
80 22 8 30 10 38 12
90 26 4 35 5 44 6
100 30 0 40 0 50 0
5. Mechanical Ventilation
a) Mechanical ventilation is one of the mainstays of intensive care medicine.
b) There are 2 main types of mechanical ventilation:
i) Non-invasive ventilation.
ii) Invasive ventilation.
c) An understanding of the types of mechanical ventilation, indications,
complications, practical aspects of mechanical ventilators and their use in
respiratory failure is essential.
d) Registrars should familiarise themselves with the ventilators, understand the
default settings and common modes of ventilation.
e) All changes to ventilation orders must be recorded on the flowchart and
conveyed to the bedside nurse.
f) All ventilator alarms must be addressed immediately.
g) Any changes to alarm settings must be relayed to the bed-side nurse.
6. Non-Invasive Ventilation
a) Definition: Mechanical positive pressure respiratory support in the absence of
tracheal intubation (e.g. via a face mask, nasal mask, head piece/box)
b) Modes
i) Continuous positive airway pressure (CPAP)
ii) Bi-level positive airway pressure (BiPAP).
c) Indications
i) As an adjunct to weaning from ventilation (e.g. extubation to NIV).
ii) Acute exacerbation of COAD.
iii) Cardiogenic pulmonary oedema.
iv) Obstructive sleep apnoea / obesity hypoventilation syndrome.
v) Post-extubation hypoxia due to pulmonary oedema or atelectasis.
vi) Febrile neutropaenia with pulmonary infiltrates.
157
d) Prerequisites
i) Adequate glottic reflexes should be present to protect from aspiration -
moribund patients require intubation where appropriate.
ii) Patients receiving CPAP or BiPAP are generally managed in Units A&B.
iii) Selected patients may be managed in Unit C.
e) Complications
i) Inadequate ventilation.
ii) Mask leaks.
iii) Aerophagia, gastric distension, vomiting, aspiration.
iv) Claustrophobia and mask intolerance.
v) Pressure necrosis of nasal bridge.
vi) Dry secretions.
vii) Barotrauma.
viii) Reduced preload and hypotension.
ix) Raised intracranial and intraocular pressure.
7. Non-Invasive Ventilators
a) BiPAP
Vision
i) Microprocessor controlled.
ii) Nasal, face & full head masks can be used.
iii) IPAP = Inspiratory positive airway pressure.
iv) EPAP = Expiratory positive airway pressure (PEEP).
v) Pressure support = IPAP - EPA
vi) Monitors machine pressure against proximal airway (mask pressure) to
ensure effective delivery of pressure despite circuit leaks.
vii) Need to calibrate for tubing and mask.
viii) Uses internal algorithm for respiratory cycling and leak adjustment.
ix) Liquid crystal displays:
+ IPAP, EPAP, Rate, FiO
2
.
+ V
T
, Vmin, PIP, Insp. time/total cycle time.
+ Leak (patient & total), % patient triggered breaths.
+ Graphical display of pressure, volume & flow.
x) Operation:
+ Machine starts up in mode previously used.
+ Press [Mode] hard key to display CPAP or S/T mode
+ Press [Activate New Mode] soft key to select the new mode.
+ Select soft key parameters displayed & turn adjustment knob
accordingly.
+ CPAP Mode - Default settings
a. CPAP 5cmH
2
O, FiO
2
1.0
+ S/T Mode - Default settings
a. IPAP 15cmH
2
O, EPAP 5cmH
2
O
b. FiO
2
1.0, Rate 12, T
Insp
1 sec, IPAP rise time 0.1 sec
158
b) CPAP via Drger EVITA
i) Operation:
+ Select Non-Invasive Mode
+ Default settings:
a. Pressure support 10 cmH
2
O (above PEEP)
b. PEEP 5 cmH
2
O
c. Inspiratory time 4 sec
d. Trigger 5 L/min
+ Adjust Press Support and Rise Time to provide the assisted breaths.
8. Indications for Invasive Ventilation
a) Respiratory Failure.
b) Intubated for airway protection.
c) Severe metabolic disturbance with altered conscious state.
9. When to institute invasive ventilation
a) Clinical assessment is the most sensitive assessment of respiratory failure.
b) Do not delay the initiation of ventilatory support pending results, blood gases or
mechanical measurements in the following settings:
i) Threatened airway.
ii) Fatigue / exhaustion.
iii) Failure of secretion clearance.
iv) Overt respiratory failure.
v) Speech impairment due to dyspnoea.
vi) Reduced GCS in the absence of other causes.
c) Objective measurements are adjuncts to clinical assessment:
i) RR > 35 bpm
ii) VC < 15 ml/kg
iii) SpO
2
< 90% on 15L O
2
iv) PaCO
2
> 60 mmHg (with pH < 7.2)
10. Modes of Ventilation in ICU
a) Synchronised intermittent mandatory ventilation (SIMV).
i) Default ventilation setting at RAH.
ii) Prescribed tidal volume.
iii) Airway pressure is variable.
b) Pressure control ventilation (PCV).
i) Prescribed peak pressure.
ii) Tidal volume is variable.
iii) High sedation requirements, occasional use of muscle relaxants.
c) Pressure Support Ventilation (PSV) + PEEP
i) Spontaneous ventilation mode for patients with adequate respiratory drive,
respiratory mechanics and strength.
ii) Commonly used when weaning from ventilation.
iii) Requires patient effort to initiate ventilatory assistance.
159
11. Optimising Ventilation
a) Optimise oxygenation:
i) Use the lowest FiO
2
to achieve an adequate SpO
2
or PaO
2
.
e.g. SpO
2
> 95% and/or PaO
2
> 80 mmHg.
ii) Lower values may be appropriate with chronic lung disease.
b) Optimise PaCO
2
:
i) Adjust relative to pre-morbid PaCO
2
.
ii) Consider permissive hypercapnia in patients with poor lung compliance.
c) Optimise patient-ventilator interface:
i) Reduce work of breathing through the ETT and ventilator circuit.
ii) Pressure support.
iii) Automatic Tube Compensation (ATC).
iv) Appropriate trigger threshold.
v) Adequate expiratory time.
vi) Prevent gas trapping: measurement and manipulation of auto-PEEP
vii) Patient positioning.
d) Optimise sedation and analgesia.
i) Review the need for sedation daily.
ii) Calculate the RASS score for each patient daily.
iii) Order depth of sedation on the ICU obs chart.
iv) Always assess suitability for ceasing sedation.
e) Minimise volutrauma (barotrauma)
12. Complications of Mechanical Ventilation
a) Haemodynamic.
i) Reduced preload.
ii) Increased RV afterload unmasked hypovolaemia.
b) Respiratory.
i) Ventilator Associated Pneumonia (VAP).
ii) Volutrauma / Barotrauma Ventilator associated lung injury.
iii) Patient ventilator dys-synchrony.
c) Metabolic.
i) Post-hypercapnoeic metabolic alkalosis.
ii) SIADH.
d) Raised intracranial and intraocular pressure.
e) Need for sedation
i) Reduced patient mobility DVT, pressure sores, weakness
ii) Reduced joint movement.
f) Local pressure effects from intubation, tracheostomy or face masks.
160
13. Drager EVITA 2 Ventilator
a) The Evita 2 are the default ventilator at the RAH.
b) Modes: SIMV, PCV, Pressure Support, CPAP, APRV.
c) Non-invasive ventilation modes are also available.
d) Specific features:
i) Auto flow: automated adjusted inspiratory flow according to lung
mechanics during controlled ventilation.
ii) Rise time: manual adjustment in all modes.
iii) 100% O
2
suction button: delivers 100% oxygen for 3 minutes.
iv) Programmable default parameters.
v) Flow and Pressure-Volume loops.
vi) Preset emergency and apnoea ventilation parameters.
vii) Automatic tube compensation to assist weaning.
viii) Automated respiratory mechanics:
+ Static and dynamic compliance.
+ Automated estimation of auto-PEEP and occlusion pressure (P
0.1
).
+ Inspiratory airway resistance.
+ Negative inspiratory pressure.
+ Vital capacity.
e) SIMV
i) Default settings: SIMV: 60012, PS = 5 / PEEP = 5, FiO
2
= 1.0
ii) Select mode: SIMV.
iii) FiO
2
= 1.0
iv) V
T
= 0.6 L
v) Rate = 12 bpm
vi) PS = 5 cmH
2
O
vii) PEEP = 5 cmH
2
O
viii) Rise time = 0.2 secs
ix) Adjust T
Insp
I:E ratio ~ 1:2 (default 1.7 secs)
x) Extra settings mode
+ Flow trigger = 5 l/min
+ Backup ventilation (CMV) : Off
f) PC (Pressure control)
i) Default settings P
Insp
= 3012, PEEP = 5, FiO
2
= 1.0, I:E=1:2
ii) Select mode: PCV+
iii) Select total inspired level of pressure (P
Insp
) = 30 cmH
2
O
iv) Rate = 12
v) Rise time = 0.2 secs
vi) PS = 5 cmH
2
O
vii) PEEP = 5 cmH
2
O
viii) FiO
2
= 1.0
ix) Adjust T
Insp
I:E ratio ~ 1:2 (default 1.7 secs)
x) Do not exceed total inspired pressure > 40 cmH
2
O
xi) Tidal volume is determined by respiratory compliance.
161
g) Pressure Support (PS) + PEEP
i) Total inspiratory pressure, when using PS on the Evita, is the dialed value
plus dialled PEEP value
ii) Mode = CPAP
iii) Rise time = 0.2 secs
iv) PS = 10 cmH
2
O
v) PEEP = 5 cmH
2
O
vi) FiO
2
= 1.0
h) I:E Ratio
i) Alteration of the I:E ratio is potentially hazardous and should only be done
following discussion with the duty consultant.
i) Measurement of auto-PEEP
i) Not accurate if patient effort, patients should be well sedated / paralysed.
ii) Measurement of intrinsic PEEP at end expiration + closed airway.
iii) Press the [Special Procedure] button & select [PEEPi].
iv) Press [Start] to begin the automatic 7sec manoeuvre.
v) Read off the PEEPi and trapped gas volume (V
Trap
)
vi) The value displayed includes applied PEEP, so:
vii) auto-PEEP = PEEPi - applied PEEP
j) Measurement of occlusion pressure (P
0.1
)
i) Measurement of the negative airway pressure generated in the first
100msec of inspiration against an occluded airway.
ii) Reflects diaphragmatic effort and neuromuscular drive.
iii) Normal value ~ 3-4 mbar.
iv) Press [Special Procedure] button.
v) Select P
0.1
and press [Start] to measure value.
k) Always examine the flow, pressure and volume vs time loops
i) Upper/lower airway obstruction.
ii) Recruitable lung.
iii) Increased airway resistance.
iv) Dynamic hyperinflation
e.g. flow does not return to baseline before the next breath
v) Sudden reversal of flow / pressure which does not trigger a breath may
indicate wasted patient effort.
162
14. RAH ARDS Ventilation
a) Initial Ventilator Set-up and Adjustments (Drger)
i) Mode: SIMV + PS
ii) Resp. Rate: 18 bpm
iii) Insp. Flow Rate: Autoflow
iv) Tidal Volume: 6 ml/kg IBW
b) Tidal Volume Settings are determined by calculated Ideal Body Weight
i) Males = 0.91 (height [cm] 152.4) + 50
ii) Females = 0.91 (height [cm] 152.4) + 45.5
iii) Calculate IBW and V
T
= 6 x IBW
c) Adjust RR to achieve the pH goals according to ABGs.
i) After any RR change, check the I:E ratio and T
Insp
.
ii) Target I:E Ratio ~ 1:1 1:3
iii) Maintain T
Insp
> 0.8 sec.
d) Adjust V
T
according to inspiratory plateau pressure (P
Plat
) goals.
i) Target P
Plat
< 30cmH
2
O
ii) Check P
Plat
with a 2 sec inspiratory pause every 4 hrs and after each change
in PEEP or V
T
.
iii) Method (Drger): [Measurements] + press [Insp Hold] for 0.5sec
P
Plat
will appear on the screen for 1 sec.
iv) P
Plat
> 30cmH
2
O
+ V
T
by 1 ml/kg IBW steps (min V
T
= 4ml/kg IBW).
v) P
Plat
< 25cmH
2
O and V
T
< 6ml/kg IBW
| V
T
by 1ml/kg IBW.
vi) NB: Observe spontaneous tidal volumes and adjust PS downwards if
volumes generated are higher than the calculated goal V
T
.
e) Adjust FiO
2
& PEEP according to SpO
2
and PaO
2
.
i) Goal PaO
2
= 55-80mmHg
or SpO
2
= 88-95%.
ii) Use the table (right) to adjust FiO
2
/ PEEP combinations
for the target PaO
2
range required, e.g.
+ If FiO
2
= 0.4 / PEEP = 5 and the PaO
2
= 54,
| PEEP to 8 cmH
2
O
+ If FiO
2
= 0.9 / PEEP = 14 and the SpO
2
= 99%
+ FiO
2
to 0.8
f) Other therapies that may improve oxygenation.
i) Recruitment Manoeuvres
ii) Prone Ventilation
iii) Nitric Oxide / Nebulised prostacylcin.
iv) ECMO
None proven see over.
FiO
2
PEEP
0.3 5
0.4 5
0.4 8
0.5 8
0.5 10
0.6 10
0.7 10
0.7 12
0.7 14
0.8 14
0.9 14
0.9 16
1.0 16
163
15. Recruitment Manoeuvres
a) Recruitment of under-ventilated alveoli may be achieved by prolonged
inspiration with higher inspiratory pressures and higher PEEP.
b) There are a variety of strategies employed.
c) These should only be performed following discussion with the consultant.
d) Contraindications to a LRM include the following:
i) Mean BP < 60mmHg despite fluids/vasopressors
ii) Active air leak through thoracostomy tube, i.e. broncho-pleural fistula
iii) Pneumatoceles, subpleural cysts, or pericardial or mediastinal emphysema
iv) Subcutaneous emphysema not related to trauma, surgical or ICU
procedures
e) Early termination of a LRM is mandatory if any of the following develop:
i) SpO
2
< 85%
ii) HR < 60 or > 140
iii) New arrhythmia - except isolated supraventricular extrasystoles
iv) New air leak through thoracostomy tube
v) Fall in mean BP < 60 mmHg
16. Prone Ventilation.
a) May improve oxygenation
b) Has never been shown to improve ICU survival from ARDS
c) Risky and labour intensive intervention.
d) Should only be considered and undertaken under direct consultant supervision.
17. Nitric Oxide / Nebulised Prostacylcin.
a) Both can improve oxygenation but do not improve survival from ARDS
b) Nitric Oxide is not currently provided in ICU at RAH
c) Nebulized prostacylcin should only be commenced per the duty consultant.
18. Extra-Corporeal Membrane Oxygenation (ECMO)
a) ECMO can be used to provide either:
i) Oxygenation in cases of overwhelming respiratory failure (veno-venous
ECMO)
ii) Circulatory support in reversible cases of refractory overwhelming cardio-
respiratory failure (veno-arterial ECMO).
b) ECMO services commenced at the RAH in 2009, and continue to evolve.
c) Any cases for potential ECMO support will be discussed in detail prior to
initiation, and will be supervised closely by duty ICU consultant.
d) The ECMO circuit and equipment must not be altered without ICU consultant
and/or perfusionist supervision.
e) The policies, protocols and procedures for ECMO are contained in a manual
that is attached to the ECMO machine and available online.
164
19. Weaning From Ventilation
a) General principles
i) No mode of weaning has been demonstrated to be superior to another.
ii) Short-term patients with acute resolution of respiratory failure (e.g. post-
operative, drug overdose, trauma) may be rapidly weaned and extubated.
iii) Long-term patients with multiple intercurrent problems take longer and
effectively go at their own pace.
iv) See Flowchart: Ventilation Weaning Protocol (p50)
b) Clinically important determinants for weaning from ventilation
i) Resolution of the process requiring ventilation.
ii) No new CXR abnormality.
iii) Completion of therapeutic options that require ventilation
e.g. debridements, operations.
iv) Appropriate conscious state - cooperative patient.
v) Appropriate peripheral motor function.
vi) Adequate analgesia.
vii) Haemodynamic stability.
viii) Metabolic, acid-base stability.
c) Methods
i) Spontaneous effort is required for the patient to be weaned.
ii) SIMV with reducing RR and V
T
in conjunction with PSV and PEEP.
iii) Use PSV + PEEP alone once the patients spontaneous rate is sufficient to
prevent a respiratory acidosis.
iv) T-piece weaning: intermittent T-piece and positive pressure support.
v) Non-invasive bi-level ventilation.
d) Objective measurements
i) Adjuncts to the assessment of weaning success.
ii) Respiratory rate and tidal volume are the most sensitive:
+ Rate ( f ) < 30/min
+ V
T
> 5 ml/kg
+ f /V
T
< 100 (rapid shallow breathing index)
+ PaO
2
/FiO
2
> 200 and PEEP < 10 cmH
2
O
+ PaCO
2
< 60 mmHg
+ pH > 7.3
165
20. Extubation Protocol
a) The duty consultant or SR must be involved in all decisions to extubate.
b) In case of urgent re-intubation, ensure equipment, monitoring and adequate
assistance is immediately available.
c) Extubation is preferentially done during daytime working hours and is a
medical responsibility.
d) Extubation criteria:
i) Return of adequate conscious state to maintain adequate protective
laryngeal reflexes and secretion clearance.
ii) Adequate pulmonary reserve.
iii) Adequate cuff leak if upper airway surgery or airway swelling.
iv) Ability to be re-intubated.
v) Resolution of reason why patient was intubated.
e) Beware of patients with inter-maxillary fixation and wiring.
i) Home team must be aware of planned extubation.
ii) Wire cutters must be present during extubation.
f) All patients must receive supplemental oxygen post extubation.
166
D. Management of Cardiothoracic Patients
1. General Principles
a) The following guidelines apply to elective post-cardiac surgical patients.
b) These are only guidelines and each individual consultant will manage the
patients as is clinically indicated.
2. Respiratory:
a) Following surgery use the following default ventilator settings:
i) FIO
2
=1.0
ii) SIMV 12 600, PS 10cmH
2
O, PEEP 5cmH
2
O.
b) After the first ABG, adjust the FIO
2
to maintain a PaO
2
> 80mmHg
c) Wean from ventilation according to past history, surgery performed and current
clinical status
d) Suggested extubation criteria:
i) Temperature > 36C
ii) Awake, able to obey commands
iii) Adequate analgesia
iv) Cardiovascular stability on minimal inotropes
(< 10g/min noradrenaline or adrenaline)
v) Adequate gaseous exchange:
+ PaO
2
> 80 mmHg on FIO
2
s 0.5, PEEP 5cm
vi) Bleeding: drain losses < 100 ml/hr
e) Respiratory failure post-extubation secondary to collapse / consolidation is
common.
i) Ensure good analgesia and frequent, effective physiotherapy
ii) CPAP may be required in the first 48 hours.
f) Patients with poor LV function / recurrent acute pulmonary oedema are prone to
extubation failure and may benefit from the use of ACE inhibitors or inodilators
prior to extubation.
3. Post-operative bloods:
a) Check CBE, U&E, Mg, ACT, APPT, INR and ABGs on all patients.
b) Maintain [K
+
] > 4.0 mmol/l
4. Hypotension
increasing inotrope requirements may occur for a variety of reasons:
a) Hypovolaemia
i) Return any remaining pump blood as soon as possible.
ii) Correct fluid/blood losses as appropriate
iii) Check ECG
b) Low cardiac output states
i) Noradrenaline is the first choice vasopressor.
ii) Low dose dobutamine (to improve regional blood flow to splanchnic/renal
vascular beds), may also be considered.
iii) Adrenaline can be used for severely impaired ventricles.
167
iv) If required vasoactive agent > 20g/min and increasing, and the patient is
euvolaemic, consider:
+ Echo to exclude tamponade, AMI, papillary muscle rupture, or VSD.
+ PA catheter insertion or pulse contour CO measurement, e.g. Vigileo.
v) Consider pacing (either epicardial or transvenous) if hypotension is rate
related (HR < 60). A-V sequential pacing is the ideal mode (DDD)
vi) Consider IABP if hypotension persists despite inotropes.
vii) Consider milrinone or dobutamine for patients with predominantly
diastolic cardiac failure or pulmonary hypertension.
c) Tamponade
i) This is a medical emergency.
ii) If suspected, the cardiothoracic surgeon must be notified immediately.
iii) Diagnosis:
+ Refractory hypotension despite adequate volume replacement and
inotropic support
+ Cessation / reduction of blood coming from drains
+ Perform urgent CXR if time available. Globular heart shadow on CXR
and muffled heart sounds may be present but are unreliable signs
+ Diastolic equalisation of right-sided pressures on PA catheter insertion
+ Echocardiographic evidence of tamponade.
iv) Treatment
+ Support MAP with aggressive volume and inotropic support.
+ Ensure sufficient blood is cross-matched (> 6 units)
+ If stable, reopening in theatre is the preferred treatment
+ In emergency situations the chest may need to be opened in ICU.
d) Tension pneumothorax
i) This is a medical emergency.
ii) If a pleural drain is already present, quickly exclude obstruction/kinking.
iii) Otherwise, needle decompression followed by insertion of an underwater
seal drain.
e) Cardiac arrest
i) This is a medical emergency.
ii) The resuscitation guidelines are different from standard BLS/ALS.
iii) A major and important difference is that in patients who arrest following
cardiac surgery, chest compressions should only be commenced if the
sternotomy cannot be performed within 3 minutes.
iv) See guidelines below.
168
Flowchart: Arrest Post Cardiac Surgery
5. Hypertension
a) MAP should be kept at approximately 70 mmHg for the first 24-36 hrs.
b) This may vary according to the patients pre-morbid BP.
c) Management:
i) Ensure adequate analgesia
ii) Nitroprusside or GTN: titrate to maintain MAP ~ 70 mmHg.
iii) If nitroprusside infusion > 40-50 ml/hr (2 g/kg/min), consider:
+ Metoprolol: 1-2 mg IV, (if no contraindication)
+ Clonidine: 25-50 g IV (up to 300g/24 hrs)
+ Hydralazine: 10-20 mg IV
+ Captopril: 6.25-12.5mg 2 hourly PRN (up to 150mg/24 hrs)
Ventricular Fibrillation
Ventricular Tachycardia
Asystole
Profound Bradycardia
HR < 30
Pulsless Electrical
Activity
DC shock
(3 attempts)
+/- Amiodarone
Atropine 3 mg IV
Pace : Invasively (If Wires Present)
Noninvasively
If paced turn OFF to exclude
Ventricular Fibrillation
- Internal Defibrillation
- Internal Cardiac Massage
- Relieve Tamponade (If Present)
- Internal Cardiac Massage
- Relieve Tamponade (If present)
- Internal Cardiac Massage
- Relieve Tamponade (If present)
Resuscitation of a Patient Who Arrests Post Cardiac Surgery
Assess rhythm Hand ventilate
(Administer FiO2 100% with Bag mask/ETT turn OFF PEEP. Auscultate chest to exclude tension pneumothorax)
Commence Advanced Life Support
If an IABP in situ change to pressure trigger
No CPR or Precordial thump
Activate 4 Key Roles in Emergency Resternotomy
CPR if Resternotomy expected to take longer than 3 minutes
Perform Resternotomy
Adapted From: Dunning J, et al. Guideline for resuscitation in cardiac arrest after cardiac surgery. European Journal of Cardiothoracic Surgery, 2009
169
6. Management of Bleeding
Flowchart: Bleeding Post Cardiac Surgery
7. Sedation/Analgesia:
a) Propofol if required
b) Fentanyl IV boluses PRN while on ventilator
c) Morphine or fentanyl subcutaneously post-extubation
d) Paracetamol IV or po 4/24 PRN for first day then 6/24 if no contraindication
e) Oxycodone po 4/24 PRN in appropriate dose from second post-op day
- Transfuse RC to maintain Hb > 80g/L
- INR > 1.5 or APTT > 45 sec
give 3-4 units FFP
- Fib < 1.0g/L
give 5 bags (apheresed) of cryoprecipitate
- Platelet <100 x 10
9
/L or prolonged by pass time
or pre-op clopidogrel
give 1 bag of platelet (pooled/apheresed)
- Treat acidosis, hypocalcaemia, hypothermia
- Resend CBP/coag screen
- Discuss with haematologist or activate MTP
- Consider DDAVP (0.3 mcg/kg) but must discuss with surgeon
Excessive bleeding post-op: > 200 mL/hr for 3-4 hrs, or
> 1500 mL total loss
Or, as per Surgeons advice
If ACT = 145-159s 25mg protamine once only
ACT > 160s 50mg protamine once only
IF Bleeding Continues +
170
8. Anticoagulation / DVT prophylaxis:
a) Heparin 5000
U
s/c 8 hrly - all patients.
i) Start 6-12 hours post-op in the absence of excessive bleeding.
b) Aspirin 300mg daily - following coronary artery grafts.
i) Start at the same time as the heparin.
ii) Give via NG/OGT or S/L if the patient remains intubated.
c) Commence patients with mechanical valve replacements on warfarin (5mg
nocte) from the second post-operative day if extubated.
d) Discuss anticoagulation requirements for tissue valves with the surgeon.
e) Patients with a mitral valve replacement ventilated > 48hrs may require
heparinisation as will patients in AF for > 48hrs.
9. Antibiotic prophylaxis:
10. Other Drugs
a) Calcium Channel Blockers. Following radial artery grafts, diltiazem (30mg po
tds) may be required from first postoperative day. Discuss with surgeon.
b) Stress ulcer prophylaxis not routinely indicated unless the patient has pre-
existing peptic ulcer disease.
c) Insulin is managed as per the general ICU protocol.
11. Minimally Invasive Mitral Valve Repairs
a) These are performed through a right sided mini-thoracotomy with the patient
on femoro-femoral bypass
b) Patients may have a pain buster placed perioperatively for analgesia
c) Management is as for other cardiothoracic patients.
d) Clarify with surgeon if warfarin is to be given postop. This may vary with
exact type of repair, use of annuloplasty ring, heart rhythm etc.
Table: Antibiotic Prophylaxis for Cardiac Surgery
Cardiac
Surgery
- CABG
Non-allergic, or
Type 3 Penicllin allergy
delayed rash only
Cefazolin 2g IV
+ Gentamicin 240mg 30min pre-incision, then
Cefazolin 1g IV post-onset-bypass, then
Cefazolin 1g IV 8 hourly for 24 hours
Gentamicin 240mg day 1 post-op
(omit if CrCl < 60 ml/min)
Penicillin allergy Type 1
Vancomycin 1g (1.5g > 80kg)
+ Gentamicin 240mg 30min pre-incision, then
Vancomycin 500mg, 6hrs post bypass
Gentamicin 240mg day 1 post-op
(omit if CrCl < 60 ml/min)
Cardiac valve surgery
Vancomycin 1g (1.5g > 80kg)
+ Gentamicin 240mg 30min pre-incision, then
Vancomycin 500mg, 6hrs post bypass
Gentamicin 240mg day 1 post-op
(omit if CrCl < 60 ml/min)
171
E. Renal Failure
1. Background
a) The mortality from acute renal failure remains high:
i) ~ 8% in isolation
ii) 70% when associated with other organ or system failures.
b) Patients who die with acute renal failure, usually die from the underlying cause
rather than ARF itself.
c) There is a spectrum of renal dysfunction with variable definitions of what
constitutes Renal Failure.
d) Bellomo has proposed the following definitions:
Creat ACreat Urea AUrea UO / d
Normal 15-70 2-6 >800
Acute Renal Impairment > 120 > +60 > 8 > +4 <800
Acute Renal Failure > 240 > +120 > 12 > +8 <400
e) Approx. 30% of ICU patients have pre-existing renal impairment.
f) Patients at high risk of developing ARF are those with:
i) Pre-existing renal impairment (creatinine > 120).
ii) Severe sepsis
iii) Hypertension
iv) Diabetes
v) Arteriovascular disease
vi) Heart failure
vii) Large contrast media loads
g) The minimum urine output required to excrete the
obligatory solute load ~ 0.5 ml/kg/hr.
h) ARF can be oliguric or non-oliguric.
i) Non-oliguric renal failure has a better prognosis.
j) Duration of ARF is variable and depends upon resolution of the underlying
injury, severity of the injury and pre-morbid renal function.
k) Consequences of ARF:
i) Fluid overload.
ii) Uraemia encephalopathy, platelet dysfunction, pericardial effusions.
iii) Acidaemia.
iv) Electrolyte derangements K
+
, PO
4
=
, HCO
3
-
v) Accumulation of pro-inflammatory cytokines (theoretical)
172
2. Pathogenesis ARF in critically ill patients is usually multifactorial.
a) Pre-Renal
i) The most common cause of renal failure in ICU.
ii) Aetiologies:
+ Low cardiac output states
+ Hypovolaemia.
+ Vasodilation - sepsis, vasodilators
+ Renal vasoconstriction - NSAIDs
+ Renal artery obstruction - stenosis, embolus, post-surgical
iii) Reduced renal blood flow
+ + GFR and renal function
+ | angiotensin-II and glomerular efferent arteriolar constriction
+ ++ blood flow to the renal medulla
+ If maintained, then ischaemic renal injury occurs (e.g. ATN).
b) Renal
i) Acute Tubular Necrosis.
+ Ischaemic - see above
+ Nephrotoxic - drugs, contrast, myoglobin, sepsis
ii) Interstitial Nephritis - infections, drugs
iii) Vascular disease - renal vein occlusion, HUS, vasculitis
iv) Glomerulonephritis
c) Post-Renal
i) Obstruction of the renal collecting system leads to +GFR.
ii) Must be considered in unexplained renal failure.
iii) Cannot be reliably ruled out clinically and hence requires imaging.
iv) Ensure a bladder catheter is inserted and draining freely.
v) Aetiologies:
+ Drugs - opiates, anticholinergics
+ Pelvic neoplasms.
+ Retroperitoneal collections (e.g. blood, pus, fibrosis).
+ Pregnancy.
+ Prostatic Obstruction
+ Renal calculi
d) Specific Renal Failure Syndromes
i) Increased intra-abdominal pressure (IAP)
+ Effects at all levels - pre-renal, renal and post-renal
+ May consider decompression when IAP > 20 mmHg with ARF.
ii) Hepato-Renal Syndrome - predominantly pre-renal
+ + albumin, vasodilatation, splanchnic shunting
+ diuretics for oedema, lactulose, diarrhoea, |intra-abdo pressure
iii) Rhabdomyolysis - pre-renal, renal and post-renal
iv) Ineffective plasma volume
+ e.g. nephrotic syndrome, liver failure, cardiac failure.
173
3. Renal Investigations
a) Blood tests
i) Creatinine
+ Logarithmic (inverse) relationship with GFR.
+ Can lose up to 60% renal function and maintain a normal creatinine.
+ Conversely in severe renal failure, a small decrease in renal function
can cause large rises in serum creatinine.
+ Lags behind the evolution of renal injury.
+ Insensitive where muscle mass is low elderly, wasting diseases
ii) Creatinine clearance (Cl
Cr
)
+ Cl
Cr
slightly overestimates GFR due to tubular secretion
+ Estimated on IMVS biochemistry (eGFR) from single specimen
creatinine, thus has same inaccuracies as creatinine
+ Measured Cl
Cr
requires min 8 hour urine collection
iii) Urea
+ Less accurate indicator of GFR than creatinine
+ Modified by diet, catabolic state, GIT blood, liver disease
iv) Electrolytes - Na
+
, K
+
, HPO
4
=
, ABGs.
v) GN screen - ESR, C
3
, C
4
, ANA, RhF, ANCA, anti-GBM.
vi) Haemolysis screen - RBC frags, |LDH, +haptoglobins, bilirubinaemia.
b) Urine
i) M, C&S - infection must always be excluded
ii) Myoglobin
iii) Urinary electrolytes
+ impossible to interpret with diuretic or natriuretic agents (CAs).
iv) Urinary sediment
+ Epithelial cell casts - ATN
+ RBC / WBC casts - GN
+ Eosinophils - interstitial nephritis
+ Crystals - oxalate (e.g. ethylene glycol)
- urate (e.g. tumour lysis)
c) Imaging
i) Ultrasound
+ Exclude urinary tract obstruction.
+ Doppler studies can assess renal artery and venous flows
ii) CT Renal Tract (non-contrast) highlights renal stones and masses.
iii) IVP - rarely required given availability of U/S and CT.
iv) DMSA scan - a static radionuclide scan to reveal kidney structure.
v) MAG
3
scan - a dynamic radionuclide scan
- renal function, collecting system obstruction, ATN.
d) Biopsy
i) Glomerulonephritis
ii) Interstitial nephritis
iii) Infiltration
174
4. Renal protection
a) Established renal protection strategies
i) Fluid resuscitation to maintain circulating blood volume.
ii) Haemodynamic support of MAP and CO using inotropes
+ adrenaline, noradrenaline, dobutamine
iii) Exclusion of post-renal obstruction
+ check IDUC, renal tract U/S, nephrostomy
iv) Avoidance / close monitoring of nephrotoxic drugs
+ aminoglycosides, amphotericin
+ contrast agents
+ ACE inhibitors
+ NSAIDs
v) Prompt detection & treatment of urinary infection.
b) Unproven strategies for renal protection
i) N-acetyl cysteine
ii) Frusemide infusion / high dose
iii) Mannitol infusion / intermittent
iv) HCO
3
-
for rhabdomyolysis.
v) Aminophylline infusion
vi) Calcium channel blockers
vii) Clonidine
c) Contrast Prophylaxis
i) Best evidence is to use HCO
3
-
ii) Add 150ml 8.4% NaHCO
3
to 850ml 5% Dextrose.
iii) Run at 3ml/kg the hour prior to contrast administration,
then continue at 1ml/kg/hr for 6 hours
d) Low Dose Dopamine
i) May temporarily increase urine output
ii) Does not reduce the incidence of dialysis dependent renal failure or
mortality. (ANZICS CTG).
175
5. Indications for renal replacement therapy
a) Symptomatic or refractory:
i) Acidosis
ii) Hyperkalaemia
iii) Fluid overload - e.g. pulmonary oedema
iv) Uraemia - urea > 35 mmol/l or symptomatic
b) Severe sepsis / developing oliguric renal failure
c) Diuretic resistant pulmonary oedema.
d) Drug removal (see Dialysis in Overdose)
e) The decision to commence RRT should be discussed with the duty consultant.
f) RRT is generally initiated early before serious complications develop.
g) The choice of RRT modality depends on patients type and severity of illness,
equipment availability and local expertise.
h) The renal unit should be notified early of patients who are potential long-term
dialysis candidates.
6. Renal Replacement Therapy Principles
a) Haemofiltration.
i) Convective solute and fluid removal down a hydrostatic pressure gradient
to form an ultrafiltrate (UF).
ii) Clears middle molecules (> 500D) and fluid.
iii) UF formation is dependent on the pressure gradient and membrane
characteristics (effective pore size & surface area).
iv) Predilution replacement of ultrafiltrate with balanced salt solution
increases the availability of urea for convective transfer by favouring its
movement from red cells.
b) Haemodialysis.
i) Diffusion of solute down a concentration gradient across a semi-permeable
membrane, running dialysate fluid counter-current to blood flow
ii) Clears urea, creatinine, electrolytes (i.e. small molecules).
iii) Solute clearance is adjusted by changing the dialysate fluid solute
concentration, blood and dialysate flow rates.
iv) Intermittent HD (IHD)
+ Utilised if the patient is stable and requires longer-term dialysis.
+ Takes 3-5 hours using higher blood flows of 300 ml/min
+ Fluid removal occurs quickly, not tolerated in unstable patients.
+ Performed by the Renal Unit.
v) Sustained Low Efficiency Dialysis (SLED)
+ Similar to standard IHD but occurs over 8-12 hours
+ Lower blood and dialysate flow rates.
+ Well tolerated by the critically ill.
+ Used in some ICUs (not the RAH) for nursing and cost reasons.
+ Although better tolerated than IHD in the critically ill, there is little
evidence to confirm equipoise with CVVHD/F in terms of outcomes.
176
c) Continuous veno-venous haemodiafiltration (CVVHDF).
i) Standard form of continuous renal replacement therapy in this Unit.
ii) The combination of ultrafiltration and dialysis improves solute clearance.
iii) Advantages of CVVHDF over conventional intermittent haemodialysis:
+ Effective and more flexible control over fluid balance.
+ Greater cardiovascular stability.
+ Does not require attendance of Renal Unit staff.
+ May have a role in modification of the septic response.
+ Some trials suggest improved patient mortality (not proven).
+ Allows patients to receive continuous protein rich diet.
7. Complications of CVVHDF
a) Hypothermia.
b) Prolonged exposure to heparin: | incidence of HITS, bleeding
c) Prolonged venous access: infection, thrombosis, vascular injury
d) Prolonged exposure to extracorporeal membrane: thrombocytopenia
e) Air embolism.
f) Increased nursing workload.
g) Electrolyte imbalance: hypomagnasemia, hypophosphataemia
177
Diagram: CVVHDF Circuit
Heparin
Ultrafiltrate
Replacement
To Patient
Dialysate
Solution
Effluent
Deaeration
Chamber
178
8. CVVHDF Equipment
a) Dialysis catheters
i) Priority of site placement and optimal catheter length:
R.IJ R.SC L.IJ L.SC Femoral
15cm 15cm 20cm 20cm 25cm
ii) Use Dolphin Protect
AN69:
+ Membrane = acrylonitrile
+ Membrane thickness = 50m.
+ Surface area = 1m
2
/1.5m
2
(RT-150)
(larger filters 1.22m
2
allow |blood flow and clearance)
+ Blood volume in set = 150ml
c) Dialysis machine settings
i) The PrismaFlex
OG < 10
Salicylates
Cyanide
Carbon monoxide
Lactic acidosis
Iron
Isoniazid
Metformin
OG > 10
Methanol
Other alcohols
208
4. Specific therapies / protocols
a) Paracetamol: Acute overdose
i) Defined as a single ingestion, or staggered ingestion occurring over 8
hours or less.
ii) If the time of ingestion can be defined risk assessment and the decision to
treat may be based upon the modified Rumack-Matthew nomogram (use
the initial ingestion time as the assumed total ingestion time when plotting
staggered ingestions occurring over < 8hrs).
iii) Potentially hepatotoxic dose in a fit adult is > 200 mg/kg (or > 10g)
iv) Markedly less in high risk individuals:
+ Chronic alcoholics and the malnourished
+ Pre-existing liver disease
+ Those taking cytochrome P450 inducing medications
v) The risk of hepatic injury without NAC (N-acetylcysteine) is predicted by
plotting a level taken 4-15 post ingestion on the Rumack-Matthew
nomogram.
vi) The probability, with a 4hr drug level, is:
+ 1-2% < 1320 mol/L (200mg/L)
+ 30% ~ 1320-1980 mol/L (200-300mg/L)
+ 90% > 1980 mol/L (> 300mg/L)
vii) The risk of hepatic impairment with NAC is determined primarily by the
time from overdose to commencement of NAC:
+ Survival is 100% where NAC is commenced within 8 hours
+ Benefit is reduced if NAC commenced at 8-24 hours
+ Benefit is not confirmed if commenced beyond 24 hours, except in the
setting of hepatic failure.
viii) The administration of NAC is indicated in the following settings (refer to
flowcharts on following pages):
+ Patients who present within 8 hours of ingestion and have a 4-8 hour
level falling above the treatment line
+ All patients presenting 8-24 hours post-ingestion
*may be ceased if the subsequent level is non-toxic and transaminases
are normal
+ Patients presenting beyond 24 hours post-ingestion with detectable
paracetamol and elevated transaminases
+ Unknown time of ingestion (follow the >8 hour scenario in Box 3)
+ Late presenters with clinical or biochemical evidence of hepatic injury
ix) For repeated supra-therapeutic ingestions see Flowchart: Repeated
Supratherapeutic Paracetamol Ingestion for management guidelines.
209
x) For sustained released paracetamol preparations:
+ Start NAC if > 200mg/kg or 10gm (whichever is less) ingested.
+ Use paracetamol levels to determine the need for NAC.
a. Check serum levels at 4 hours and repeated 4 hours later.
b. If either level > nomogram line, continue or commence NAC.
c. NAC may be discontinued if both levels < nomogram line
xi) NAC may be ceased in the following settings:
+ Patients in whom NAC was commenced < 8 hrs post-ingestion who
are clinically well and without hepatic tenderness at the completion of
the 20 hour infusion (no further investigation required)
+ Patients in whom NAC was commenced > 8 hrs post-ingestion who
are clinically well and have normal transaminases at the completion of
the 20 hour infusion. Those whose transaminases are abnormal at this
time should continue an infusion at 100mg/kg/16 hrs until
transaminases and INR (tested 12-24 hourly) are falling.
xii) Consultation with liver transplant services (FMC) for consideration of
transplant should commence with any of the following high risk criteria:
+ INR > 3.0 at 48 hours or > 4.5 at any time
+ Oliguria or creatinine > 200 mol/L
+ Acidosis with pH < 7.3 after resuscitation
+ Ongoing hypotension with systolic BP < 80mmHg
+ Hypoglycaemia
+ Severe thrombocytopenia
+ Encephalopathy (any degree)
xiii) The default position, if in doubt, should be to treat with NAC.
xiv) Toxicological advice should be sought if there are any uncertainties.
Graph: Modified Rumack-Matthew Nomogram
210
Flowchart: Acute Paracetamol OD - Known Time of Ingestion
*from Daly FFS, Fountain JS, Murray L, Graudins A, Buckley NA. Guidelines for the management of
paracetamol poisoning in Australia and New Zealand explanation and elaboration (Consensus Statement).
MJA 2008; 188: 296-301.
211
Flowchart: Repeated Supratherapeutic Paracetamol Ingestion
Table: N-Acetylcysteine Administration
NAC 150mg/kg in 200mls of 5% dextrose over 30 minutes
NAC 50 mg/kg in 500mls of 5% dextrose over 4 hours
NAC 100mg/kg in 1000mls of 5% dextrose over 16 hours
212
b) Lithium - Acute overdose
i) Generally produces significant GIT symptoms with nausea, vomiting,
abdominal pain and diarrhoea.
ii) Ingestion < 25g in the setting of normal renal function is benign
iii) Ingestion > 25g may cause more significant GIT toxicity
iv) Neurotoxicity is rare with good supportive care and hydration
v) Renal impairment, dehydration and sodium depletion cause a reduction in
renal lithium excretion and increase the risk of delayed neurotoxicity
vi) Patients presenting late with established neurotoxicity should be managed
as for chronic toxicity, and have similar long term morbidity
vii) Lithium levels > 5mmol/L 4-8 hrs post ingestion are not uncommon
viii) Treatment
+ Normal saline rehydration
+ Maintenance of urine output > 1ml/kg/hr
ix) Haemodialysis is reserved for:
+ Those with established or worsening renal failure, and
+ Those presenting late with established neurotoxicity
c) Lithium - Chronic poisoning:
i) The clinical features of chronic toxicity are primarily neurological
ii) Develops when renal lithium excretion is impaired for any reason
iii) Serum lithium levels correlate poorly with clinical toxicity
iv) Neurotoxicity may persist well after lithium levels return to normal.
v) The Hansen-Amdisen classification may be used to grade severity:
+ Grade 1 (mild): tremor, weakness, ataxia, hyperreflexia
+ Grade 2 (moderate): stupor, rigidity, hypertonia, hypotension
+ Grade 3 (severe): myoclonus, convulsions, coma
vi) Cardiac effects can occur in late toxicity following the establishment of
neurological features, which includes rhythm disturbances, A-V delay,
heart block and non-specific ST segment and T wave abnormalities
vii) Lithium levels
+ Confirm a diagnosis but should not be used to grade severity
+ Are useful serially to monitor response to therapy
viii) Principles of therapy
+ Careful correction of fluid and sodium balance
+ Cease lithium and any medications that may impair excretion
+ Monitor urine output, renal function, electrolytes and lithium levels
ix) Indications for haemodialysis
+ Neurotoxicity and a serum level > 2.5 mmol/L
+ Grade 3 neurotoxicity regardless of level
+ Pre-existing renal or cardiac disease preventing the achievement of an
adequate urine output with hydration alone
+ Repeated haemodialysis treatments may be required
213
d) Opioids
i) Produce CNS and respiratory depression, often just above analgesic doses
ii) Death is usually due to respiratory failure, either primary effect or
compounded by aspiration, and good supportive care ensures survival
iii) Some opioids may possess additional cardiac and neurologic toxicity
- e.g. dextropropoxyphene, tramadol, pethidine
iv) Controlled release preparations may cause delayed and prolonged toxicity
v) Treatment is generally supportive
vi) Naloxone (50 to 100g IV repeated as needed)
+ Useful for diagnostic purposes
+ Can assist in the management of airway and breathing
+ May result in a withdrawal syndrome
vii) If repeated naloxone boluses are required to ensure a protected airway,
intubation is the preferred method of ongoing management
viii) If a naloxone infusion is established:
+ Initial hourly requirement is generally half the effective dose used over
the preceding hour, i.e. that required to achieve airway protection and
adequate tidal volumes
+ Infusions require constant observation/assessment
+ Hospital deaths have occurred due to inadequate observation
e) Carbon monoxide
i) CO is a common cause of poisoning death
ii) Most deaths occur pre-hospital.
iii) Acute effects are due to tissue hypoxia
iv) Those that arrive at hospital alive should survive.
v) In-hospital management involves supportive care and identification of
those at risk of long term neuropsychiatric sequelae
vi) Delayed neurological effects are secondary to unrelated and incompletely
understood mechanisms
vii) HbF binds CO more avidly than HbA, and the foetus is at particular risk
viii) Self poisonings involve high concentration, short term exposures, and are
associated with fewer long-term sequelae than industrial and domestic
exposures (low concentration, prolonged exposures)
ix) High risk features for delayed neurological sequelae:
+ Loss of consciousness or coma
+ Persisting neurological deficit (e.g. confusion)
+ Cerebellar signs
+ Metabolic acidosis
+ Myocardial ischaemia
+ Age > 55yrs
214
x) Treatment options
+ Normobaric oxygen at high flow via non rebreather mask
a. Continue until all symptoms resolve
b. Pregnant women to continue for 24 hours with concomitant foetal
assessment
+ Hyperbaric oxygen
a. May be indicated in patients with 1 or more high risk factors
b. Indications and effectiveness are controversial
f) Cyanide
i) Acute cyanide poisoning is rare, dramatic and lethal
ii) Removal from the source of exposure, good resuscitative care and selective
antidote use provide the best chances of survival
iii) Most deaths will occur pre-hospital, and those who arrive alive in hospital
post-inhalational exposure are likely to survive with supportive care.
iv) Risks to those involved in care delivery are negligible.
v) Decontamination should involve removal of clothes and washing of skin
with soap and water.
vi) Cyanide levels are not available in a timely manner and do not aid
management
vii) Serum lactate levels parallel cyanide levels and may be used as a proxy
marker of exposure
viii) A lactate level > 10 mmol/L correlates with a toxic cyanide level
(in the absence of an alternative cause for elevation)
ix) Management should proceed along normal resuscitative lines with the
delivery of 100% oxygen
x) Consider using an antidote in the following settings:
+ Altered mental state
+ Seizures
+ Hypotension
+ Significant and persisting metabolic acidosis (lactic)
xi) Antidote choice and administration
+ 100% oxygen in all cases
+ Hydroxocobalamin (1
st
line)
a. 5g in 200mls of 5% dextrose over 30 minutes
b. Repeat in 15 minutes if no improvement
+ Sodium thiosulphate (adjunct to Hydroxocobalamin, or 2
nd
line)
a. 12.5g IV
b. Repeat dose at 30 minutes if acidosis persists
+ Sodium nitrite
a. 300mg IV over 3 minutes
b. Follow immediately with sodium thiosulphate
c. Half dose may be repeated in 30 minutes if required
d. Monitor methaemoglobin (must not exceed 40%)
215
g) Toxic alcohols
i) A variety of alcohols (methanol, ethylene and diethylene glycol etc) are
used as industrial solvents, cleaning agents and reactants.
ii) Accidental ingestions are rarely of sufficient volume to cause toxicity
iii) Deliberate ingestion is associated with severe metabolic acidosis,
multiorgan dysfunction and potentially death.
iv) Cause an initial ethanol like intoxication followed by a progressive
metabolic acidosis and compound specific end-organ toxicities, e.g.
+ Retinal toxicity/blindness (methanol)
+ Acute renal failure (multiple agents)
+ Seizures (multiple agents)
+ Refractory hypotension (multiple agents)
+ Delayed neurological sequelae (diethylene glycol)
v) Diagnosis is based upon a history suggestive of ingestion and a
characteristic evolution of metabolic acidosis
+ Initially: | osmolar gap (OG) + normal pH and anion gap (AG)
+ Evolution of acidosis with +pH, +OG and |AG
+ Variability in osmolar gap amongst the normal population is such that
a single assessment of acid-base, AG and OG is insufficient to
exclude significant exposure (although it may confirm it)
vi) Specific treatment
+ Ethanol
a. Commence ASAP, regardless of symptomatology, in all with:
i. Acidosis, or
ii. An elevated OG (with or without acidosis),
b. Check baseline BAL, if > 0.1g/dl a loading dose is not required
c. Titrate to BAL ~ 0.1-0.2g/dL while on dialysis
d. May be given orally (via NGT) or by IV infusion
e. Oral protocol *avoid in ICU if possible
i. Loading dose of 1.8ml/kg of 43% ethanol
(4 x 30ml vodka shots for a 70 kg adult)
ii. Maintenance infusion of 0.2-0.4 ml/kg/hr
(1 x 40ml vodka shot per hour)
f. Intravenous protocol
i. Loading dose: 8ml/kg of 10% ethanol
ii. Maintenance: 1-2ml/kg/hr of 10% ethanol
g. Actual requirements vary widely between individuals, and serial
blood alcohol assessments are required to ensure a level within the
target range
h. I f on CVVHDF, then safer to dialyse against desired [ETOH]
i. 0.1g/dl = 5ml ETOH / 5l Bag (inc. replacement)
ii. first bag may be run at 0.2g/dl = 10ml ETOH / 5l bag
216
+ Haemodialysis (HD)
a. Significantly more efficient at clearing alcohols than CVVHD
b. Indications
i. Serum pH < 7.3
ii. Serum bicarb < 20 mEq/L
iii. Worsening acidosis or vital signs despite supportive care and
ethanol infusion
+ Folate 50mg IV QID or folinic acid
+ Thiamine 300mg IV daily
& pyridoxine 50mg QID for ethylene glycol poisoning
+ Correct hypocalcaemia (if symptomatic) & hypomagnesaemia
h) Organophosphorous agents
i) Includes the organophosphates (OP) and carbamates (CM)
ii) Similar initial presentation
iii) Most deaths occur as a consequence of respiratory failure
iv) OPs as a group have greater lethality
+ Form a covalent bond with serine esterase enzymes
+ In contrast to the competitive bond formed by CM.
v) There is great variability amongst the OPs in terms of enzyme aging,
toxicity profiles, and pralidoxime responsiveness
vi) High quality supportive care and aggressive use of antidotes is necessary to
ensure survival.
vii) The diagnosis is essentially clinical:
+ Muscarinic features - diarrhoea, emesis, urination
- miosis, lacrimation, salivation
- bronchorrhoea, bronchospasm
- bradycardia, hypotension
+ Nicotinic features - fasciculation, tremor, weakness
- respiratory muscle paralysis
- tachycardia, hypertension
+ CNS features - agitation, seizures, coma
- delayed neuropsychiatric effects
viii) Cholinesterase levels:
+ Plasma cholinesterase levels fall more rapidly and recover more
quickly than RBC cholinesterase levels, they are useful in confirming
exposure but do not correlate with toxicity.
+ RBC cholinesterase levels correlate better with toxicity and response
to therapy, but take longer to perform (limiting their clinical utility)
ix) Decontamination
+ Resuscitation must not be delayed by external decontamination
procedures
+ These agents do not vapourise at atmospheric pressure
+ There is no risk to care providers from inhalational exposure
+ The characteristic odour is due to a hydrocarbon solvent, which may
cause headaches & eye irritation, but is otherwise harmless
217
+ Staff should wear impermeable gowns, gloves, glasses and facemasks
+ Care should be delivered in a well ventilated setting
+ The patients clothing should be removed and the skin washed with
soap and water
x) Treatment
+ Ventilatory and CVS support as indicated
+ Atropine
a. Reverses muscarinic effects only it will not reverse paralysis!
b. Titrate 1.2 mg at 5 min intervals (doubling the dose every 5 min)
until signs of successful atropinisation are noted
i. Drying of secretions
ii. Resolution of bradycardia
iii. Clear chest
c. Over 10-20mg, or infusions of up to 5 mg/hr may be required in
severe poisoning.
d. Typically commenced at 10-20% of loading dose per hour.
e. NB: HR and pupil size are not useful for clinical monitoring after
nerve agent exposure
+ Diazepam IV
a. Treatment of seizures
b. Reduces the incidence of neuropsychiatric sequelae
c. Regular dosing is recommended.
+ Pralidoxime Iodide
a. Efficacy is unclear and is likely to be compound specific
b. Default is to give ASAP
c. Not required for documented carbamate ingestion (although not
contraindicated)
i. 1g IV over 30 minutes
ii. 500 mg/hr for 24 hours
iii. May be ceased at 24 hours in the absence of nicotinic or
muscarinic features. The benefit of continuing beyond 24
hours is unclear and warrants specialist consultation.
i) Calcium Channel Blockers
i) Of the common slow release formulations, verapamil and diltiazem
frequently cause profound CVS collapse 4-16 hrs post-ingestion.
ii) Other agents within the class rarely cause major toxicity
iii) Onset of toxicity may be delayed:
+ Up to 2 hours post-ingestion of the standard preparation, and
+ Up to 16 hours after ingestion of the SR formulation
iv) Ingestion of >10 tablets of verapamil SR or diltiazem SR may cause
serious toxicity
218
v) The key issues in management are:
+ Identification of patients at risk
+ Judicious use of the pre-toxicity window of stability
+ Consideration of GIT decontamination options
(including whole bowel irrigation), and
+ A graduated approach to developing or established toxicity
vi) Risk of serious toxicity is significantly increased by:
+ Co-ingestion of other cardiac medications, and
+ Underlying cardiac disease or advancing age
vii) Graduated response to hypotension: failure to achieve stability at each step
should prompt immediate initiation of the next
+ Fluid load with 10-20 ml/kg isotonic crystalloid (avoid overload)
+ Calcium load
a. Calcium gluconate - 60ml of 10% solution, or
b. Calcium chloride - 20ml of 10% solution
c. Commence an infusion to keep calcium levels > 2.0mEq/L
+ Atropine to a total of 1.8mg
+ Catecholamine infusion effects are variable in terms of:
a. Central - negative inotropic & chrontropic effects
- Adrenaline is an appropriate 1
st
line agent
b. Peripheral - reduced vascular tone
-Noradrenaline 1
st
line agent
c. Do not persist with escalating inotrope doses in the setting of
continued instability
+ High dose insulin & dextrose / euglycaemia
a. Most effective when used early.
b. Glucose
i. Bolus ~ 25g (50 mL of 50% solution)
- unless hyperglycaemia (BGL > 22 mmol/L) present
ii. Infusion ~ 25 g/h IV titrated to maintain euglycaemia
c. Actrapid insulin
i. 1 IU/kg bolus
ii. Infusion ~ 0.5 IU/kg/h
- titrated every 30 min to a maximum of 5-10 IU/kg/h
d. Monitor:
i. Glucose - every 20 min for first hour, then every 1 h
ii. Potassium - replace only if < 2.5 mmol/L and there is a
source of potassium loss
e. Therapeutic end points:
i. BP > 90mmHg, HR > 60, resolution of acidaemia
ii. Adequate urine output (1-2 mL/kg/h)
iii. QRS interval < 120 ms
iv. Improved mentation
219
viii) Seek guidance from Clinical Toxicologist (via switchboard or Poisons
Information Centre) or ICU consultant staff regarding protocol
ix) Cardiopulmonary bypass, ECMO, cardiac pacing and intra-aortic balloon
pumps have been used successfully as extraordinary manoeuvres
j) Beta Blockers
i) Usually minimal toxicity and require only simple supportive care.
ii) By contrast overdoses of sotalol or propranolol may be life threatening
iii) In addition to class |
1
and |
2
effects (bradycardia, conduction blocks and
hypotension)
+ Propranolol
a. Na
+
channel blocking effects wide complex arrhythmias
b. Highly lipid soluble enters the CNS (coma and seizures)
+ Sotalol
a. Blocks cardiac K
+
-channels
b. Causing QT prolongation and torsades de pointes
iv) The clinical response to overdose is highly variable, but the threshold for
severe toxicity from propranolol may be as low as 1g
v) With the exception of sotalol and slow release preparations, toxicity is
usually apparent within a few hours post-ingestion
vi) PR prolongation in the absence of bradycardia is an early marker of
toxicity
vii) Approach to immediate life threatening symptoms:
+ Bradycardia and hypotension
a. Atropine
b. Adrenaline
c. Noradrenaline
d. Glucagon 5-10mg bolus & 1-5mg/hr infusion (cumbersome), or
e. High dose insulin dextrose euglycaemia
(targeting impaired contractility)
+ Wide QRS
a. Sodium bicarbonate bolus 1-2 mEq/kg
b. Repeat as required
c. Intubate and hyperventilate targeting serum pH ~ 7.5 to 7.55
+ Torsades de pointes
a. Isoprenaline
b. Magnesium
c. Overdrive pacing
220
k) Tricyclic Antidepressants (TCAs)
i) Tricyclic antidepressant use has escalated after an initial reduction
secondary to SSRI introduction
ii) TCAs remain a significant cause of toxicological morbidity and mortality
iii) Poisoning rapid onset CNS and CVS toxicity
peak between 4-6 hrs post ingestion
+ Dose > 10mg/kg is potentially life threatening
+ Dose > 30mg/kg is expected to cause severe cardiotoxicity and coma.
+ Prompt intubation, hyperventilation and sodium bicarb administration
at the onset of major toxicity is life saving.
iv) The investigation of choice is the 12 lead ECG, with diagnostic and
prognostic features including:
+ Prolongation of the PR and QRS intervals
+ Terminal R wave in aVR
+ Increased R/S ratio (>0.7) in aVR
+ QRS > 100 ms is predictive of seizures
+ QRS > 160 ms is predictive of ventricular tachycardia
v) The approach to resuscitative management includes the following:
+ Prompt intubation and hyperventilation (to serum pH 7.5-7.55) at the
onset of CNS depression
+ Ventricular arrhythmias are unlikely to respond to defibrillation:
a. NaHCO
3
~ 2 mmol/kg IV every 2 minutes until perfusing rhythm
restored. (Most effective when used in combination with
hyperventilation)
b. Lignocaine is a 2
nd
line agent if arrhythmias persist despite |pH.
+ Hypotension is managed with crystalloid and alkalinisation followed
by noradrenaline
+ Seizures are managed with benzodiazepines (*avoid phenytoin)
I. Bites and Envenomation
1. Up to date and detailed information on envenomation may be found at the
toxinology website http://www.toxinology.com/ managed by the Womens &
Childrens Hospital
2. Medical advice for doctors can be sought by contacting the clinical toxinologist,
A/Prof Julian White via the WCH switchboard (Ph: 81617000)
3. Emergency cases are seen through the Emergency Departments of major hospitals,
while less urgent cases are seen after discussion with the treating doctor.
221
J. Limitation of Therapy
a) Limitation may involve either withholding and/or withdrawal of life supporting
therapies.
b) There is no ethical or legal distinction between these processes.
c) Limitation may involve challenging ethical and legal issues; however, in patients
with no realistic chance of meaningful recovery, decisions to limit life-sustaining
therapies are both clinically and ethically indicated.
d) Assisted suicide and euthanasia are medically and ethically distinct from limitation
of therapy, are illegal in SA and should never occur.
e) The administration of medication to relieve the suffering of a dying patient is
imperative, even though a side-effect may be to hasten the onset of the patients
death. Such therapy is legally distinct from euthanasia.
f) Approximately 70% of all RAH-ICU deaths involve some limitation of therapy.
g) Absolute requirements for limitation of therapy are:
i) Medical consensus, including the treating ICU and admitting clinical teams
ii) Clear and open discussion with the patient, family or next of kin regarding
this consensus medical opinion; and, an absence of objection to this
proposed management direction.
iii) Clear documentation in the patients medical record, along with a description
of the process by which the decision was made.
h) Counselling patients and families in limitation of therapy requires clarity and
sensitivity to ensure that all parties understand and accept the plan of management.
i) The concerns and wishes of the patient and family are important considerations.
j) The overriding goal is to provide the best care possible for the patient. This may be
to concentrate on palliation, rather than life sustaining therapies.
k) The decision to limit treatment is a consultant responsibility.
l) Refer to the CICM Policy Document IC-14
http://www.cicm.org.au/policydocs.php
K. Brain Death and Organ Donation
1. Reference: ANZICS Statement on Death and Organ Donation
http://www.anzics.com.au/death-and-organ-donation
2. For further information, trainees should liaise with the Organ Donation Hospital
Medical Directors:
a) Dr David Evans
b) Dr Stewart Moodie
c) Dr Peter Sharley
d) Dr Alex Wurm
222
3. Declaration of brain death
a) This is an absolute requirement prior to beating-heart organ donation
b) Declaration must be made by two members of the ICU staff:
i) The Duty ICU consultant, and
ii) Another ICU doctor (more than 5yrs qualified with appropriate experience).
c) The declaration of brain death may be by either clinical or imaging certification.
4. Clinical certification of brain death
a) The procedure is completed on a Certification of Brain Death form (MR150.0) and
documented in the case notes.
b) Record the time of onset of coma
i) Last time the patient showed response such as breathing, pupil reaction or
coughed on suction.
ii) This can be determined from the nursing observations
c) Pre-conditions:
i) A recognised irreversible cause of coma must be identified.
ii) Potentially reversible causes of coma have been excluded:
+ Hypotension
+ Hypothermia *core temp must be > 35C
+ Drugs or poisons.
+ Neuromuscular blocking drugs
+ Metabolic or endocrine disturbance including:
a. Deranged renal or hepatic function
b. Hyperglycaemia, hypoglycaemia, thyroid function
c. Electrolyte disturbances
iii) Ability to perform examination of:
+ Cranial nerves
+ Apnoea testing (e.g. not severely hypoxaemia or high cervical injury)
d) Clinical confirmation of absent brain stem function
i) Performed separately by 2 doctors, with the first test at least 4 hours after the
onset of coma (longer in the case of hypoxaemic/ischaemic injuries).
ii) Absent pupillary responses to light, both direct and consensual
iii) Absent corneal reflexes
iv) Absent vestibulo-ocular reflex
+ No nystagmus on injection of 20ml iced water into the ear
+ Check tympanic membranes prior to this procedure
+ Occulo-cephalic reflexes are often tested, but are not formally required
v) Absent gag / cough reflex.
vi) Absent response to pain in the cranial nerve distribution.
vii) Apnoea following disconnection from the ventilator:
+ Pre-oxygenate patient with 100% oxygen
+ Disconnect ventilator and connect to bag with 100% O
2
at 1-2 l/min
+ Confirm PaCO
2
> 60mmHg and pH < 7.30 (with PaO
2
> 60mmHg)
+ Continuously look for apnoea clinically
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e) The following are compatible with Brain Death
i) Spinal reflexes
ii) Sweating, blushing and tachycardia
iii) Normal BP without pharmacological support
iv) Absence of Diabetes Insipidus
f) The 2 practitioners may choose to be present at each examination, however,
each must perform and be responsible for one of the 2 examinations
g) From the onset of coma until the second set of testing, there should be a
continuous period of observation by nursing staff
h) Families may benefit from witnessing the clinical testing for brain death
i) The time of death is the time when certification of brain death is completed i.e.
on completion of the second examination and documentation in the case notes.
j) There is no legal requirement for certification of persons not considered for
organ donation, however this is encouraged as it can assist in counselling
relatives and the subsequent cessation of inappropriate medical intervention.
5. Imaging (Non-clinical) certification of brain death
a) Consider when clinical examination is consistent with brain death, however, the
preconditions (2c) for clinical certification cannot be met.
b) Demonstrated absence of cerebral blood flow is therefore required.
c) Ideally there should be a period of observation of 4 hours to increase the likelihood
that no flow will be demonstrated.
d) Absence of cerebral blood flow may be established by either:
i) Radionuclide cerebral perfusion scan (Tc99 HMPAO).
ii) 4 vessel cerebral angiography (rarely performed at the RAH)
e) Certification of brain death is by 2 clinicians, (not including the doctor who
performed the imaging investigation) who have considered the onset and cause of
coma, the clinical examination and the results of the investigation performed.
6. Organ donation
a) General principles
i) Any patient who is, or may become brain dead is a potential donor. There are
no automatic exclusion criteria.
ii) All potential donors should be offered the opportunity to donate
iii) Notify the Donor Coordinator from Donate Life, SA (Ph: 82077117) when a
potential donor is identified.
b) Criteria for brain dead organ donation
i) The patient has been declared brain dead
*for donation after cardiac death see below.
ii) Usually, no patient history of:
+ HIV, untreated bacterial, fungal or viral infection.
+ IV drug abuse
+ Malignancies other than primary brain tumours and minor skin lesions.
+ Treatment with hormones of human pituitary origin.
+ Dementia (or family history of dementia).
+ Disease of the donor organ
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iii) All brain dead patients should be discussed with the Donor Coordinator,
regardless of relative contraindications.
c) Procedure:
i) Organ donation should not be discussed with the family until brain death has
been certified and the family informed.
ii) Family approaches regarding donation prior to the patients death should be
referred to the consultant
iii) Counselling families with regard to brain death and organ donation requires
considerable compassion, knowledge, skill and time. While this is primarily a
consultant responsibility, advanced trainees are encouraged to participate in
the process under supervision.
iv) The wishes of the patient and family are paramount.
v) A donor kit is kept in the cupboard in P4A which contains a check-list, plus
all the forms and specimen bottles required.
vi) Following consent for organ donation, blood should be sent for:
+ HTLV-1, HIV 1 + 2
+ HBsAg, HBsAb, HBcAb, HCV
+ CMV-IgG, EBV, RPR
+ Group and X-match
+ Tissue typing volume of blood varies according to blood group
+ Mark the request forms: Urgent Organ Donor, cc: Donate Life
vii) Coronial approval will be sought by the Donor Coordinator where required.
viii) The RAH Designated Officer may give permission for donation if all efforts
to find relatives have failed.
ix) It is the responsibility of ICU medical staff to provide either a death certificate
or report to the coroner. Time of death is the time of second certification.
x) Notification of the recipient and procuring teams (which may come from
interstate) and coordination of operating theatre time, collation of results and
investigations are dealt with by the Donor Coordinator(s)
xi) Donor coordinators may seek assistance from ICU staff with ordering
investigations.
xii) The following investigations are normally required:
+ Recent ECG
+ Recent CXR
+ Echocardiography
+ ABG
d) Management of the organ donor:
i) The situation is time critical as it is not possible to stabilise a brain dead
patient indefinitely.
ii) Aim to ensure perfusion and protection of all organs for donation to achieve
the optimal outcome for all recipients
iii) Avoid focused management strategies aimed at single organ systems
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iv) Ventilation:
+ Adequate oxygenation: PaO
2
> 60 mmHg | F
I
O
2
< 0.5
+ Adequate ventilation: PaCO
2
~ 35-45 mmHg
+ Prevention of atelectasis and lung recruitment is important.
v) Cardiovascular instability:
+ Common around the time of cerebral herniation (coning).
+ Hypertensive episodes should be treated with short acting agents.
+ Maintain MAP > 70 mmHg:
a. Adequate volume loading prior to using inotropes.
b. If CVC present: CVP ~ 8-14mmHg
c. High dose inotropic support may reduce organ viability.
vi) Aim for a urine output > 0.5ml/kg/hr
vii) Maintain normothermia:
+ Established hypothermia can be difficult to manage.
+ Prevention is preferred, using active warming devices if necessary.
viii) Check biochemistry and maintain normal electrolytes.
ix) Diabetes insipidus
+ Common but not universal in the setting of brain death
+ Treatment should commence on clinical suspicion and not be delayed for
confirmatory results.
+ Hypernatraemia adversely affects liver transplant outcomes.
+ DDAVP ~ 1-2 g IV bd
x) Evidence for hormonal resuscitation is conflicting. Steroids and vasopressin
should be considered if hypotension is refractory.
xi) Consider non-depolarising muscle relaxants if spinal reflexes persist, as these
may be disconcerting for relatives and attending carers.
7. Tissue Donation
a) All patients who die in the ICU may become tissue donors.
b) Tissues donated include:
i) Corneas
ii) Heart valves
iii) Bones
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L. Donation After Cardiac Death (DCD)
1. Introduction
a) DCD provides an option where there is a strong desire for organ/tissue donation;
however, the patient is unlikely to progress to brain death.
b) In all circumstances, the decision to withdraw life sustaining therapy is made
independent & prior to any consideration of organ donation.
c) DCD may be considered when:
i) A patient is planned for withdrawal of active therapy.
ii) The patient and/or their representative(s) support organ/tissue donation.
iii) Preferably age 65 (c.f. donation after brain death)
iv) Cardiac standstill is probable within 90 minutes of withdrawal:
+ Liver and Pancreas 30 minutes
+ Kidneys 60 minutes
+ Lungs 90 minutes.
v) There is good underlying organ function
vi) Normal contraindications to donation are absent
e.g. malignancy, active infection etc. (consult donor coordinator)
d) If a patient is likely to progress to brain death - this is preferred to DCD.
2. Determining the patients wishes
a) As for all organ donations, the pre-morbid wishes of the patient are paramount.
b) The Australian Organ Donor Register may assist with decision making.
c) DCD can be difficult for families, relevant issues include but are not limited to:
i) The discussion of donation prior to patient death
ii) Families may change their mind at any time without reason or question.
iii) Logistic requirements which inevitably delay the withdrawal process.
iv) Reasonable escalation of supports may occur, however if the patient becomes
too unstable donation may not occur.
v) The requirement for ante-mortem testing and interventions.
vi) Consent should be sought and rationale provided for ante mortem therapies
intended solely to aid donation.
vii) The immediate transfer of the deceased following death for organ
procurement and effective removal from the family.
viii) Difficulty in predicting the time of death.
ix) A significant risk of donation not proceeding, depending upon timing.
x) If the patient does not die within the organ suitability times, then palliative
care will continue in ICU and possibly the ward.
xi) There may be unknown medical reasons why donation cannot occur.
d) Under some circumstances (such as complex difficult decisions to withdraw
therapy) it may not be appropriate to include discussion about DCD.
e) A plain language statement on DCD is available from the Donate Life website.
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3. Process of DCD
a) The process will be governed by the duty ICU consultant, in conjunction with the
Organ and Tissue Donor Coordinator (OTDC - pager 83781671) and Organ
Donation Hospital Medical Director as required.
b) If reportable under the Coroners Act:
i) The treating ICU team should complete the required documentation.
ii) The OTDC will seek in principle approval for donation and notify the
Coroners representative between death and donation.
c) Withdrawal is best done as planned event in working hours.
d) The organ retrieval teams must not be involved in direct patient care before death.
4. Ante-Mortem Interventions
a) Ongoing supportive care prior to donation is rational and accepted.
b) Escalation of care, for the sole purpose of facilitating donation, is less clear.
c) The following may be considered excessive in most circumstances:
i) CPR
ii) Massive use of blood products
iii) Escalating organ support in the setting of deteriorating physiology
d) For invasive interventions, such as bronchoscopy or biopsy, discussion/consensus
with the next of kin is recommended .
e) Interventions directly aimed at the organ donation process i.e. of benefit to the
recipient but not the patient, may be considered when unlikely to cause harm
e.g. antibiotics or steroids.
f) High dose heparin with intra-cerebral pathology or ante-mortem cannulation for
organ perfusion are not considered acceptable.
g) Advice can be sought from the Organ Donation Hospital Medical Director
5. Care of the dying patient
a) Use of sedative and analgesic drugs should be in accordance with the standard
practice of good palliative care.
b) Locality
i) There is no suitable location in the current theatre suite so withdrawal should
occur in ICU with transport to theatre after death.
ii) An appropriate route should be pre-identified and kept clear.
iii) Normally there will be an OTDC with both the theatre and ICU teams.
iv) Withdrawal should not occur until there is direct communication from the
ODTC that theatre is ready.
c) Monitoring
i) HR, BP (IA), SpO
2
and respiratory rate
ii) Alarms should be disabled.
iii) Remote monitoring may be preferable.
iv) Warm ischaemic time is considered to be from when SBP 50 mmHg.
v) All timing is recorded by the OTDC in the ICU.
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d) Determination of Death
i) Death is considered irreversible in the context of DCD when 5 minutes
have passed since circulation ceased.
+ Best determined by loss of a pulsatile waveform on IABP.
+ ECG monitoring may be used along with clinical signs.
ii) A note including the time of death should be documented in the patients case
notes declaring death prior to organ procurement surgery.
iii) Should death not occur in the required time the family and organ retrieval
teams should be informed and standard comfort care continued.
iv) The family may wish to view their relative following organ procurement; this
can be facilitated by the OTDC.
See the 2010 Organ and Tissue Donation and Transplant Authority (AOTDTA)
http://www.donatelife.gov.au/the-authority/national-protocol-for-donation-after-cardiac-death
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Table: Contact Phone Numbers
ICU Secretary Ph: 8222 5325
MedStar Ph: 8222 4222
F: 8222 2826
Organ Donor Coord T: 8207 7117
Duty Intensivist
SD: 1650 Pg: 8378 1671
M: 0434 605 903
Transfusion IMVS Ext: 25430 / 25431
Consults Pager Pg: #89 22888
Transfusion RN
Pg: #89 1575
Emergency Pg: #33 Ext: 22975
Massive Transfusion 47*
Duty Anaesthetist SD: 1175
APS Pg: #89 22556 WCH Toxicology T: 8161 7000
ICU Research RN SD: 1520
ICU Dietician
SD: 1156
M: 0401 711 460
Pg: 1342