Internal Medicine Notes does not cause fatigue, dyspnoea, palpitation

2 Slight limitation of physical activity. Ordinary

Chronic Heart Failure physical activity results in fatigue,
palpitation, dyspnoea, angina
Aetiology 3 Marked limitation of physical activity. Less
than ordinary physical activity leads to
Common Causes
symptoms of CHF
4 Symptoms of CHF present at rest. Unable to
 Chronic heart disease or prior myocardial
carry out any physical activity
infarction
 Essential hypertension via increased afterload Signs of CHF
and acceleration of CHD
 Signs of underlying cardiac disease, including
Less Common Causes a displaced apex beat, or a murmur which
 Non-ischaemic idiopathic dilated may indicate underlying valve disease
cardiomyopathy- patients tend to be younger,  Signs of fluid retention, including soft basal
and at least 30% are familial inspiratory crackles which do not clear with
coughing, resting tachypnoea, raised JVP,
Uncommon Causes ankle and sacral oedema, ascites or tender/
pulsatile hepatomegaly
 Valvular heart disease, especially mitral and
 Signs of cardiac strain, including tachycardia,
aortic incompetence
or a third heart sound
 Non-ischaemic dilated cardiomyopathy
 Other abnormal vital signs
secondary to chronic alcohol misuse
 Inflammatory cardiomyopathy, myocarditis Initial Investigations
(viral- enteroviruses, coxsackie B)
 Chronic arrhythmia  ECG for conduction blocks, previous MI, LVH,
AF, sinus tachycardia
 Thyroid dysfunction
 Chest X-ray for cardiomegaly and pulmonary
 HIV-related cardiomyopathy
venous redistribution with upper lobe blood
 Drug-induced
diversion. Batwing appearance. Does not
 Peripartum cardiomyopathy – rare
exclude diagnosis. Worsening CHF can show
Symptoms of CHF interstitial oedema seen in the perihilar
region, with prominent vascular markings and
 Exertional dyspnoea present in most, initially small basal pleural effusions obscuring the
with more strenuous exertion, but later costophrenic angle. Kerley B lines, indicative
progresses to occur on level walking and of lymphatic oedema due to raised left atrial
eventually at rest pressure may be present
 Orthopnoea- more likely to be due to CHF but  Trans-thoracic Echocardipgrahy for distinction
occur at a later stage between systolic and diastolic dysfunction (LV
 Paroxysmal nocturnal dyspnoea (PND)- more ejection fraction <40%) while excluding
likely due to CHF but rare sign correctable causes of CHF such as valvular
 Dry irritating cough may occur, particularly at disease. Single most important investigation
night in CHF. Can also gain information regarding LV
 Fatigue and weakness may be prominent thrombus, atrial size, pulmonary systolic
 Dizzy spells or palpitations which may indicate pressure, pericardial disease, ventricular size
arrhythmia  Full blood count for mild anaemia associated
with adverse prognosis or rare cause
Symptom Grading
 Urea, creatinine and electrolytes for initial
Class Description workup and monitored regularly (6 months).
1 No limitations. Ordinary physical activity Advance CHF can lead to dilutional
 hyponatreamia, hyperkalaemia, hypokalaemia o Excessive caffeine intake may
(diuretics), hypomagnesia, ↓ GFR and renal exacerbate arrhythmia, increase heart
blood flow rate and increase blood pressure
 Liver function tests for abnormal liver function  Smoking cessation
due to congestive hepatomegaly. There may  Self-management and education
be a rise in serum bilirubin, particularly in o Possible side effects of therapy
severe CHF o Signs of deterioration
 Thyroid function test for uncommon causes of o Importance of adherence to therapy
CHF.  Psychosocial support
 Natriuretic peptides (ANP and NBP) reflect
severity of CHF. Measurement of BNP or N- Other Important Issues
teminal proBNP is not recommended as  Sleep apnoea occur commonly in patients
routine in the diagnosis of CHF. There is no o Obstructive sleep apnoea
evidence that BNP offers additional diagnostic o Central sleep apnoea
information that is beyond information
 Vaccination as they are at increased risk of
provided by a comprehensive echo.
respiratory infection
 Stress ECG, stress echocardiography or stress o Influenza
nuclear study for dyspnoea on exertion o Pneumococcal disease
 Spirometry and respiratory function testing to  Pregnancy and contraception
exclude concomitant smoking related or other o CHF increases risk of maternal and
causes of airway limitation. The FEV1 may be neonatal morbidity and mortality
reduced and reversibility demonstrated in o Pregnancy and delivery may cause
reaction to an elevated pulmonary capillary deterioration in women with
wedge pressure moderate to severe CHF
 Travel
o May be at increased risk of deep vein
thrombosis
o High-altitude destination should be
avoided because of relative hypoxia
o Travellers to very humid or hot
climates should be counselled on
dehydration and modification of
diuretic doses

Management Pharmacotherapy Management

Non Pharmacological Management Prevention of CHF and treatment asymptomatic LV

systolic Dysfunction
 Physical activity and rehabilitation
 ACE inhibitor to delay development of
 Nutrition: lose weight, limit saturated fat, high
symptomatic CHF
fibre diet, maintain nutrition, limit sodium
 Beta-blockers- when given in the early post-
 Fluid management
MI period, beta-blockers reduce the
o Weight themselves every morning
subsequent develop of CHF in patients with
after going to the toilet
persevered ventricular function
o Limit fluid intake to 1.5L/ day
o Those who suffer from alcohol-related  Management and control blood pressure
cardiomyopathy should abstain from Treatment of Symptomatic Systolic CHF
alcohol. Should not exceed the
recommended daily intake First Line
  ACE Inhibitors  Corticosteroids
o Prolong survival in patients with NYHA
Class 2, 3, 4
o Improve symptom status, physical
activity tolerance and need for
hospitalisation
o Increased ejection fraction
 Beta-blockers
o Inhibit the adverse effects of chronic
activation of key neurohormonal
system (sympathetic system) action
on the myocardium
 Diuretics
o Has not been shown to improve
survival and should be reserved for
symptom control only
o Shown to increase urine sodium
excretion and decrease the physical
signs of fluid retention
o In fluid overload patients, the aim is
to achieve an increase in urine output
and weight reduction of 0.5-1kg daily
For Severe (class 4) CHF, add spironolactone ± digoxin
 Aldosterone antagonist- aldosterone
± angiotensin 2 receptor blocker if there is no
receptions within the heart can mediate
improvement after ACE inhibitor and diuretics. If no
fibrosis, hypertrophy and arrhythmogenesis.
improvement after, add hydralazine/ nitrate and
Therefore blockade with spironolactone is
consider heart transplant. Add beta-blocker if showing
useful
signs of improvement
 Angiotensin 2 receptor antagonist
 Direct sinus node inhibitors Causes of Exacerbations of CHF

Second Line

 Digoxin has been shown to improve inotropic

responsiveness in patients with ventricular
dysfunction
 Non-compliance with drugs, diet, fluid
 Iron deficiency is common in CHF and
treatment with iron is useful  Hazardous drugs (NSAIDs)
 Other drugs  Acute infection
o Hydralazine/ isosorbide dinitrate  New arrhythmia (AF)
o Calcium-channel blockers  Acute ischaemia/ infarction
 Other: anaemia, PE
Drugs to avoid in CHF
Acute Liver Disease
 Anti-arrhythmic agents
 Non-dihydropyridine calcium-channel Causes of Acute Liver Disease
blockers
 Viral: ABCDE, EBV, CMV
 Tricyclic antidepressants
 Bacterial: Q fever, leptospirosis, melioidosis
 NSAIDs
 Drugs: paracetamol, antiobitics (Augmentin,
 Clozapine flucloxallin), berbal
 Thiazolidinediones (glitazones)  Alcohol
  Ischaemia/ hypoxia (approx. twice the upper limit of normal); with
 Acute fatty liver (pregnancy)/ Non-alcohol exacerbations, levels are >10 upper limit
fatty liver disease  Chronic hepatitis C infection: wide variability,
 Autoimmune: primary biliary cirrhosis typically normal to less than twice the upper
 Wilson disease limit, rarely more than 10 times the upper
 Budd-chiari syndrome limit
 HELLP (haemolysis, elevated liver enzymes,  AST and ALT are raised in malignant
low platelets) syndrome and occasionally infiltration as well
acute fatty liver of pregnancy
Acute Liver Failure
 sepsis
 Acute hepatocellular injury with LFT’s typically
Extrahepatic Cholestasis
more than 10 times the upper limit
 Choledocholithiasis (most common cause)  Hepatic encephalopathy
 Malignant obstruction (pancreas, gallbladder,  Prolonged prothrombin time
ampulla or bile duct cancer)
Chronic Liver Disease
 Primary sclerosing cholangitis with an
extraheptic bile duct stricture Causes of Chronic Liver Disease
 Chronic pancreatitis with structuring of the
distal bile duct (uncommon)AIDS A specific Aetiology can be determined in 80 to 90
cholangiopathy percent of patients with cirrhosis. Most causes are
 If ultrasound suggests obstruction due to a due to chronic liver injury or imflammation
stone or malignancy, or if the onset of the Common Causes in Developed Countries
cholestasis was acute, and ERCP should be
carried out to confirm diagnosis and facilitate  Viral hepatitis: B and C
biliary drainage  Alcoholic liver disease
 If the cholestasis is chronic or ultrasound  Haemachromatosis
show shows biliary dilation with an apparent  Non-alcoholic fatty liver disease
cause or in patients who are at high risk for
ERCP, MRCP or CT should be obtained Less Common Causes
 ERCP can then be performed if there is
 Autoimmune Hepatitis
evidence of an obstructing stone, stricture or
 Drugs: methotrexate, amiodarone, herbal,
malignancy.
isoniazid
 If both are negative, AMA should be tested for
 Alpha-1 antitrypsin deficiency
primary biliary cirrhosis and a biopsy should
 Wilson’s Disease
be taken if positive to confirm diagnosis
 Right sided heart failure
Magnitude of AST and ALT elevations  Infection (brucellosis, syphilis, schistosomiasis,
echinococcosis)
 Non-alcoholic fatty liver disease: AST and ALT  Hereditary haemorrhagic telangiectasia
<4 times upper limit  NASH cirrhosis
 Alcoholic Fatty liver disease: AST < 8 times  Coeliac disease
upper limit, ALT <5 times upper limit  Granulomatous liver disease
 Acute viral or toxin-related hepatitis with  Polycystic liver disease
jaundice: AST and ALT >25 upper limit
 Ischaemic hepatopathy: AST and ALT >50 Other Causes of Jaundice: Biliary Obstruction
upper limit of normal
 Bile duct stones
 Chronic hepatitis B infection: levels vary; the
 Bile duct stricture
AST and ALT may be normal, although most
o Pancreatic cancer
patients have mild to moderate elevations
o Primary sclerosing cholangitis
 o Acute/ chronic pancreatitis  ALP is usually elevated in cirrhosis but is less
o Cholangiocarcinoma than two to three times the upper normal
o Ampullary lesion limit
 Primary and secondary biliary cirrhosis  GGT levels correlate reasonably well with ALP
but are nonspecific. Levels of GGT are much
Presentation of Patients with Liver Disease
higher in chronic liver disease from alcohol
 May have no symptoms and be well- than other causes
incidental/ compensated liver  Bilirubin levels may be normal in well-
 Abnormal liver enzymes compensated, however, they rise as the
 Non-specific: anorexia, weight loss, weakness, cirrhosis progresses
fatigue)  Albumin levels fall as the synthetic function of
 Hepatic decompensation: jaundice, pruritus, the liver declines with worsening cirrhosis.
signs of upper gastrointestinal bleeding, Hypoalbuminaemia is not specific for liver and
ascites, confusion due to hepatic can be seen in heart failure, nephrotic
encephalopathy syndrome, protein losing enteropathy,
malnutrition
 Upper gastrointestinal bleeding:
haematemesis, melena, haematochezia)  Prothrombin time reflects the degree of
hepatic synthetic dysfunction
Stigmata of Liver Disease
Other Important Tests
 Leukonychia, clubbing
 FBC: anaemia (macrocytic) and
 Duypetron’s Contracture
thrombocytopenia (splenomegaly) can occur
 Palmar erythema
 U/E: hyponatraemia due to an inability to
 Asterixis/ hepatic encephalopathy
excrete free water resulting primarily from
(decompensated liver)
high levels of anti-diuretic hormone secretion
 Spider naevi
 Coagulation profile: INR and prothrombin
 Bruising
time
 Cachexia, muscle wasting
 Globulins tend to be increased in patients
 Hepatic fetor
with cirrhosis and may be secondary to
 Gynaecomastia
shunting of bacterial antigens in portal venous
 Ascites (decompensated liver)
blood away from the liver to lymphoid tissue.
 Splenomegaly
 Caput medusa Radiology
 Testicular atrophy and loss of libido-
predominant in alcohol cirrhosis and  Ultrasound liver is routinely used. In advanced
haemachromatosis cirrhosis, liver may appear small and nodular
with increased echogenicity. May be used in
 Cruveilhier-Baumgarten murmur is a venous
screening for hepatocellular carcinoma and
hum that may be auscultated in patients with
portal hypertension and useful for detecting
portal hypertension. It results from collateral
splenomegaly, ascites and portal vein
connections between the portal system and
thrombosis
the remnant of the umbilical vein. It is best
appreciated when stethoscope is placed over  CT not routinely used for cirrhosis as it
the epigastrium provides similar information to ultrasound.

Investigations Ultrasound- 6 things to look for

Liver Function Tests  Bile duct dilatation

 Gall bladder/ bile duct stones
 AST and ALT are usually moderately elevated  Echogenicity/ texture of liver
in patients with cirrhosis. (AST > ALT)  Splenomegaly
  Focal liver lesion Points Class 1 Year 2 year
 Metastasis Survival Survival
 *presence of biliary dilation on USS suggests 5-6 A 100% 85%
7-9 B 81% 57%
extrahepatic cholestasis, whereas the absence
10-15 C 45% 35%
of biliary dilation suggests intrahepatic
cholestasis.
Complications of Liver Disease
Liver Screen if Ultrasound shows normal ducts
Cirrhosis represents a late stage of progressive
 Hepatitis serology hepatic fibrosis characterised by distortion of the
 Viral serology- CMV, EBV, Hep A, Hep D hepatic architecture and the formation of
regenerative nodules and considered irreversible in its
 Paracetamol levels
advanced stages. Once these complications develop,
 Alpha 1 anti-trypsin levels
patients are considered to have decompensated
 Iron studies
cirrhosis and should be considered for liver
 Globulins
transplantation. Complications of portal vein
 Autoantibodies- SmAb, AMA, LKM Ab
thrombosis and cardiomyopathy are factors which
 ↓Caeruloplasmin for Wilson’s Disease
give the term decompensation
Liver Biopsy
Portal Hypertension
 If above testing is negative despite raised AST/
 Ascites
ALT which fails to resolve or decline, we
 Hepatic encephalopathy due to ammonium
proceed to liver biopsy
 Variceal haemorrhage
 In clinical practice, cirrhosis is diagnosed with
 Spontaneous bacterial peritonitis
a liver biopsy, during which a sample of the
 Hepatorenal syndrome: development of renal
liver is obtained either by a percutaneous,
failure due to reductions in renal perfusion
transjugular, laparoscopic or radiographically
induced by increasingly severe hepatic injury.
guided fine needle.
Arterial vasodilatation in the splanchnic
 Biopsy is not necessary if the clinical,
circulation, triggered by portal hypertension
laboratory and radiologic data strongly
appears to play a central role in the decline
suggest the presence of cirrhosis.
 Portal hypertensive gastropathy
When to Suspect Cirrhosis  Hepatic hydrothorax: pleural effusions due to
peritoneal fluid moving in to the pleural space
 Stigmata of chronic liver disease on physical through defects in the diaphragm (usually
examination right sided)
 Evidence of cirrhosis on laboratory or  Hepatopulmonary syndrome: triad of liver
radiologic testing or by direct visualisation disease, increased alveolar-arterial gradient in
while undergoing surgical procedure room air and evidence of intrapulmonary
 Evidence of decompensated cirrhosis vascular abnormalities. Mild hypoxaemia and
diaphragm elevation with VQ mismatch due
Assessment of Severity of Liver Disease
to ascities
Child Pugh Classification  Portopulmonary hypertension
 Cirrhotic cardiomyopathy
Points 1 2 3
Encephalopathy None Minimal Advance  Splenomegaly and anaemia and
(coma) thrombocytopenia due to hypersplenism
Ascites Absent Controlled Refractory
Bilirubin <34 34-51 >51 Other Complications
Albumin >35 28-35 <28
Prothrombin <4 sec 4-6 sec >6 sec

Scoring
  Hepatic encephalopathy: disturbance in a result of severe/ prolonged shock, bilateral
diurnal sleep pattern, asterixis, hyperactive urinary tract obstruction, pregnancy-related
deep tendon reflexes cortical necrosis, or bilateral renal arterial
 Hepatocellular carcinoma obstruction (dissecting aortic aneurysm)
 Portal vein thrombosis: can contribute to  Haematuria
cirrhosis and related to unbalanced  Dyspnoea
haemostasis and slowing of portal flow  Lethargy
 Nausea/ vomiting due to uraemia
Chronic Kidney Disease
 Malaise, fatigue
Defined as an estimated or measured glomerular  Anorexia
filtration rate <60mL/min/1.73m2 that is present for ≥  Oedema due to fluid overload
3 months with or without evidence of kidney damage.  Joint point, bone pain due to osteodystrophy
 Restless legs
OR  Sallow skin
Evidence of kidney damage with or without decreased  Uraemic frost or fetor
GFR that is present for ≥ 3 months as evidenced by  Half and half nails
the following, irrespective of the underlying cause:
Early Detection of CKD
 Albuminuria
 Increased amounts of albumin in the urine
 Haematuria after exclusion of urological
correlate directly with an increased rate of
causes progression to ESKD, and increased
 Structural abnormalities (on kidney imaging) cardiovascular risk
 Pathological abnormalities (renal biopsy)  eGFR correlates well with complications of
Causes CKD and increased risk of adverse outcomes
 Early intervention with blood pressure
 Diabetic kidney disease reduction and use of ACE inhibitors or ARBs
 Glomerulonephritis can reduce progression and cardiovascular
 Hypertensive vascular disease risk by up to 50% and may also improve
 Polycystic kidney disease quality of life
 50% or more of kidney function can be lost
before the serum creatinine rises above upper
limit of normal

Diagnostic Evaluation Tests for CKD

 Renal ultrasound: small shrunken kidney

<10cm in length
 Repeat (within 1 week) serum urea/
electrolytes/ creatinine/ eGFR/ albumin
 Full blood count, CRP, ESR
 Urine ACR (preferably on a first morning void
to minimise postural effect on albumin
Clinical Presentation
excretion)
 Hypertension  Urinalysis shows SG 1.010 (isothenuria) due to
 Pruritus due to phosphate and urea inability to concentrate urine. Broad waxy
 Nocturia due to the kidney’s inability to casts and proteinuria on PCR
concentrate urine. Followed by oligouria.  Fasting lipids and glucose
Anuria is never observed with CKD and always  Urine microscopy for dysmorphic red cells,
indicates acute kidney injury. Anuria occurs as red cell casts or crystals (urinalysis)
  Doppler: renal artery stenosis  Can affect 1 in 5 people with CKD and 1 in 3
individuals with depression
 Screen recurrently and maintain an high level
of clinical awareness for depression

Fluid Overload

 Sodium and intravascular volume balance are

usually maintained via homeostatic
mechanisms until the eGFr falls below 10-
15mL. However, the patient with mild to
Electrolyte Imbalances
moderate CKD, despite being in relative
Hyper Hypo volume balance, is less able to respond to
Potassium Sodium rapid intake of sodium and is therefore prone
Phosphate Calcium to fluid overload
Urea Bicarbonate  Management: dietary sodium restriction and
Creatinine diuretic therapy (loop diuretic)

Complications Haematuria

Metabolic Acidosis  Most common causes are non-glomerular

such as UTI, renal calculi, prostatic disease or
 People with eGFR <30 are at increased risk
urinary tumours
 Main factor is decreased renal acid excretion
 Haematuria due to kidney disease is called
compounded by a reduction in bicarbonate
glomerular haematuria
production
 Acidosis contributes to demineralisation of Hyperkalaemia
bone and increased protein degradation
 Management: supplementation with sodium  Excretion of potassium in urine is impaired
bicarbonate and levels may also rise with ACE inhibitors
and ARBS used to treat hypertension
Albuminuria  Levels consistently above 6.0mmol/L are of
concern and should be managed
 Important prognostic feature in CKD and
 Levels >6.5mmol/L, predisposes to
relates to the severity of kidney disease and
arrhythmias
with a greater likelihood of progression to end
 Management: low potassium diet, potassium
stages of CKD
wasting diuretics (thiazides), resonium, cease
 Target 50% reduction in urine ACR
ACE inhibitor
 Management: ACE inhibitor or ARB as first line
therapy. Reduction in salt output through oral Lipids
salt intake. Spironolactone
 Associated with increased LDL’s, triglycerides,
Anaemia VLDL’s and lipoprotein(a) and reduced HDL’s
 Raised homocysteine levels
 Related to reduced EPO production,
 Dyslipidaemia is more severe in individuals
resistance to the action of ESA, reduced
with albuminuria, particularly those with
absorption of iron
nephrotic syndrome
 Anaemia of chronic disease
 Management: lipid profile and statin
 Starts to develop when GRF is <60
commencement
 Management: ESA therapy (erythropoiesis
stimulating agent) Hypertension

Depression
  Target: ≤140/90mmHg or ≤130/80mmHg in  Benzodiazepines
people with albuminuria  Colchicine
 Mainly caused by fluid overload  Digoxin
 Glicazide
Mineral and Bone Disorder (osteodystrophy)
 Insulin
 Changes in metabolism of calcium, phosphate,  Lithium
parathyroid hormone and vitamin D typically  Metformin
start once GFR <60  Gliptins
 This leads to ↑ phosphate + parathyroid  Spironolactone
hormone and ↓ calcium + vitamin D levels
Drugs that can adversely affect kidney function in CKD
(secondary hyperparathyroidism)
 These changes are associated with an  Aminoglycosides
increased risk of fracture and also increased  Calcineurin inhibitors
cardiovascular mortality, perhaps mediated  Lithium
by accelerated vascular calcification  NSAIDs and COX-2 inhibitors (beware the
 Management triple whammy)
o Use phosphate binders, which bind to  Radiographic contrast agents
dietary phosphate.
o If phosphate is controlled, calcium will Other Practice Tips
typically remain in normal range.
 ACE inhibitors and ARBS can safely be
o Cholecalciferol that comes from sun
prescribed at all stages of CKD and should not
exposure can be given as dietary
be deliberately avoided just because GFR is
supplement. Calcitriol can also be
reduced
given in CKD
o Cinacalcet, is a calcimimetic agent  Combination of ACE inhibitor (or ARB),
that can be used to treat diuretic and NSAID or COX-2 inhibitor (except
hyperparathyroidism for individuals low dose aspirin) can result in acute kidney
on dialysis injury, especially if volume-depleted or CKD
present
Uraemia  Frusemide can be used safely for
management of fluid overload in all stages of
 Syndrome seen in stage 4 or 5 CKD, and is
CKD
caused by the accumulation of the breakdown
 Both non-loop diuretics (thiazides) are
products of protein metabolism
effective in all stages of CKD as adjunct
 Uraemia-related signs may develop when the
antihypertensive therapy
eGFR is between 10-15mL but usually are not
disabling until the eGFR is <10mL Indications for Dialysis
 Symptoms include: anorexia, nausea,
Acute Kidney Injury (AEIOU)
vomiting, lethargy, confusion, muscle
twitiching, convulsions and coma  Acidosis (metabolic) with pH <7.1
 Urea accumulation can lead to pericarditis,  Electrolyte imbalance (hyperkalaemia) >6.5 or
pleuritis and encephalopathy rapidly rising potassium levels
 Management: dialysis should be commenced  Intoxication/ ingestion of certain alcohol and
as soon as uraemic symptoms develop drugs
Medications usage in CKD  Overload (refractory fluid)
 Uraemia signs such as pericarditis,
Medications which may need to be reduced or ceased neuropathy, encephalopathy, serositis,
pleuritis
 Antivirals
Renal replacement therapy is usually continued until
the patient manifests evidence of recovery of kidney
function either by increased urine output or
progressive decline in serum creatinine concentration
after intial attainment of stable values

Chronic Kidney Disease

 Patients with eGFR >15mL or asymptomatic

patients with eGFR 5-15mL are not indicated
for dialysis
 Patients with eGFR 5-15mL with symptoms or
signs and patients with eGFR ≤5mL should
receive dialysis
 Absolute indications: uraemic pericarditis or
pleuritis or uraemic encephalopathy Acute Kidney Injury
 Common indications
Pre-Renal 80% of causes
o Declining nutritional status- eGFR
<15mL who have anorexia, weight History and Presentation
loss or poor caloric intake
o Persistent or difficult to treat volume  Variable, depending on cause, may be
overload preceded by a catastrophic event: sepsis, DIC
o Fatigue and malaise trauma, shock, ↓ BP
o Mild cognitive impairment  Urine output ↓ acutely, with a concomitant
o Refractory acidosis, hyperkalaemia, ↑ in plasma urea and creatinine levels
and hyperphosphataemia  If the ↓ renal perfusion can be rectified
timeously, the renal failure may be rapidly
Treatment Options for Stage 5 CKD reversed

Causes: any cause of ineffective circulation

→ Poor renal perfusion and ↓ GFR

 LV failure → ↓ cardiac output

 ↓ Circulating blood volume
o Haemorrhage
o Dehydration
o Sespsis/ DIC
 ↓ Systemic vascular resistance
o Liver failure
o Hepatorenal syndrome
 ↑ Renal vascular resistance
o Renal artery obstruction
o Renal vein thrombosis due to trauma,
extrinsic compression, dehydration,
nephrotic syndrome, invasion by renal
cell carcinoma, pro-thrombotic state
o Renal artery stenosis (atherosclerosis)

Investigations

 ↑ Urea/ creatinine ratio >100

  ↓ Urine volume due to hypoperfusion of  ↓ Urea/creatinine ration <40
glomeruli. May be anuric if patient is shocked  May be oliguria (50-400ml/day) or urine
or bilateral vascular occlusion as in dissecting volume may be normal (<2.4L/day); the
aortic aneurysm oliguric phase lasts on average 10-14 days and
 Urinalysis unremarkable- urine normal or near may be followed by a short diuretic phase,
normal (no casts/ ↑ cells) and then gradual return to normal urine
 ↓ urinary sodium due to renin-aldosterone output
system activation therefore ↓ FeNa  Haematuria and red cell casts in
 ↑ Urine osmolality >500mOsm glomerulonephritis/ vasculitis
 Epithelial casts (muddy brown casts) and
Intrinsic Renal 10-15% of causes granular casts in ATN
History and Presentation  Eosinophiluria in acute interstitial nephritis
 Pyuria and white cell casts in infection
 Presentation depends on cause (pyelonephritis)
 Commonest cause is acute tubular necrosis  ↑ Urinary sodium and ↑ FeNa
following a pre-renal situation, in which blood  ↓ Urinary osmolality < 350mOsm
supply to tubules is inadequate→ tubular
death Post Renal 5-10% of Causes
 Tubular blood supply is via efferent arteriole
History and Presentation
Causes: GITV
 May be a history of difficulty in passing urine:
 Glomerular Lesions: glomerulonephritis hesitancy, double voiding, dribbling, nocturia,
o IgA nephropathy weak stream
o SLE  Obstruction may lead to anuria
o Post infectious: URTI, GIT infection  May be enlarged kidneys on ultrasound if
o Bacterial endocarditis bilateral ureteral obstruction
 Tubular Lesions: Toxins  An enlarged bladder may be palpable if a
o Ischaemia (any untreated pre-renal) urethral obstruction is present
o Nephrotoxins
Causes
 Myoglobin/ haemoglobin
 Calcium  Urinary calculi
 Uric acid  Benign prostatic hyperplasia
 Bence Jones proteins  Prostate cancer
(immuno light chains)  Bladder cancer
 Aminoglycoside  Tumour compression (lymphoma)
 Contrast material  Urethral stricture
 Interstitial Lesions: Infections  Retroperitoneal fibrosis
o Drugs: NSAIDs/ antibiotics
o Pyelonephritis Investigations
o Autoimmune
o Infiltrations: lymphoma/ leukaemia  ↑ Urea/ creatinine ratio >100
 Microvascular Lesions: vasculitis  Anuria (<50ml/day) occurs most commonly
o Vasculitis  Urine normal or near normal. Possibly ↑
o Malignant hypertension white cells (infection) or red cells (trauma
o Thrombotic microangiopathies (TTP/ from calculi)
HUS)  USS may show hydronephrosis due to
o Thrombo/ atheroembolism obstruction in the urinary tract
 90% of renal calculi are visible on abdominal
Investigations X-ray due to calcium contents
Blood Tests (common to all types of AKI)  Damage glomerular basement membrane
results initially in leakage of albumin into
 ↑ Urea: daily of 3.5-5.0mmol/L/day tubules
 ↑ Creatinine: daily of 90-180μmol/L/day  As condition progresses, higher molecular
 Sodium: normal/ ↓ if fluid overload present weight proteins are lost and losses can be
 ↑ Potassium: ↓ filtration and urinary massive
excretion
 ↑ Phosphate: ↓ filtration and urinary Hypercoagulable State: ↑ risk of thromboembolism
excretion and 2° hyperparathyroidism
 Loss of urokinase and anti-thrombin 3 (ATT) in
 ↓ Calcium or normal: ↓ active vitamin d,
urine and ↑ levels of factor 8, fibrinogen and
secondary hyperparathyroidism may
platelets in the blood
compensate calcium levels to normal
 Predisposed to DVT, PE, and renal vein
 ↓ Bicarbonate: metabolic acidosis (kidney
thrombosis
unable to excrete H+ ions)
 FBC: normocytic anaemia (↓ EPO, uraemic Hypogammaglobulinaemia
toxins)
 These patients are prone to infection, as they
Nephrotic Syndrome lose immunoglobulins in the urine

 Proteinuria of ≥ 3g/day or PCR >300 Oedema

 Hypoalbuminaemia
 Oedema  Often the presenting feature and is due to
 Hyperlipidaemia (↑ cholesterol and part of ↓ oncotic pressure due to
triglycerides) hypoproteinaemia
 Some patients are resistant to the effects of
Causes: damage to glomerulus or foot process atrial natriuretic peptide and reabsorb
inappropriate amounts of sodium and water
 *Glomerulonephritis: minimal change disease,
and may become oedematous even when
focal segmental glomerulosclerosis,
albumin is not very low→ pericardial effusion,
membranous glomerulonephritis
ascites, pleural effusion
 Systemic diseases: *diabetes, *amyloidosis,
SLE, sarcoidosis, vasculitis immunologica Hyperlipidaemia
disease (polyarteritis nodosa)
 Infections:  ↑ both triglycercides and cholesterol, mainly
o Bacterial: streptococcal, syphilis, SBE) due to ↑ LDL from linked synthesis of
o Viral: hepatitis, HIV, infectious albumin in the liver
mononucleosis, CMV)  ↓ LCAT in liver
o Parasitic: malaria, toxoplasmosis,  ↑ Lp(a) contributes to hyperlipidaemia
schistosomiasis, filariasis)
Electrolytes
 Drugs: gold, mercury, NSAIDs, lithium, heroin
 Neoplasm: Hodgkin’s disease, solid tumours Sodium
 Hereditary: Alport’s syndrome, Sickle cell
Hypernatraemia
anaemia, familial nephrotic syndrome
 Other: *pregnancy (pre-eclamptic toxaemia), → Normal plasma osmolality = 275 – 295 mmol/L
massive obesity, renal artery stenosis,
transplant rejection  ↑ Na: Conn’s Syndrome
 ↓ H20: Diabetes Inspidus, dehydration
Consequences
Hyponatraemia
Proteinuria: frothy urine
→ commonest electrolyte abnormality in the elderly Symptoms and Signs
and is associated with a high mortality because of the
diseases associated with it  Muscle weakness, cramps, fasciculations
 Paralytic ileus
↓ Na (Di’s) Normal Na ↑ Na with ↑H20  ↓ ventilation and BP
Diarrhoea SIADH Cardiac failure
 Rhabdomyolysis
Diurectics Psychogenic Nephrotic
polydipsia syndrome  Nephrogenic diabetes insipidus
Diabetes (schizophrenia) Liver failure
Addison’s Disease Renal Failure Calcium
Will get Over hydration
dehydration Hypercalcaemia

 Common: hyperparathyroidism (adenoma),

Potassium
malignancy (caused by PTH-related peptide)
Hyperkalaemia  Rare: sarcoidosis (↑ Vit D and ACE activity),
Paget’s disease
 Metabolic acidosis
 Renal failure Symptoms and Signs
 Addison’s Disease
 Bones: bone pain, fractures
 Diuretics (K+ sparring)
 Stone: polyuria, polydipsia, nocturia, calculi,
 Rhabdomyolysis (K+ released by lysed cells)
nephrocalcinosis
 Burns
 Groans: constipation, anorexia, nausea,
 Massive transfusion
vomiting, abdominal pain, ileus, peptic ulcer
ECG Changes (K+ >5.5 mmol/L) disease, pancreatitis
 Moans: emotional lability, confusion,
 ST elevation and tall T waves delirium, psychosis, stupor, coma
 Widened QRS  Muscle weakness
 P wave disappears  ECG: short QT interval
 Short QT interval
 Finally, QRS becomes wide sine wave→ Hypocalcaemia
asystole/ ventricular fibrillation
 Parathyroidectomy
 Arrhythmias- sinus bradycardia, nodal/
 Primary hypoparathyroidism
ventricular arrhythmias
 Vitamin D deficiency
Hypokalaemia  Acute pancreatitis
 Renal failure
 Metabolic alkalosis  Pseudohypoparathyroidism
 Diarrhoea or vomiting/ laxative abuse  Severe alkalosis
 Steroid use/ Conn’s syndrome
 Diuretics (frusemide) Symptoms and Signs
 Villous adenoma
 Neuromuscular irritability: muscle cramps,
 Liquorice (aldosterone-like effect)
tetany, laryngospasm, convulsions
ECG changes of hypokalaemia (K+ < 3.5mmol/L  CNS symptoms: depression, dementia,
psychosis, papilloedema
 ST depression and T wave flattening  Cataracts
 Prominent U waves  Chvostek’s sign: masseter fasciculations
 APBs/ VPBs  Trousseau’s Signs: BP cuff
 1st/2nd/3rd degree heart block  ECG: prolonged QT interval
 Atrial/ ventricular tachyarrhythmias
 Potentiation of adverse effects of digoxin Phosphate
Hyperphosphataemia  Hypocalcaemia in setting of
hypoparathyroidism
 Renal failure
 Hyponatraemia and hypernatraemia
 Massive cell necrosis (lysis and release
intracellular phosphate) Syndrome of Inappropriate ADH (SIADH)
 Metabolic acidosis
 Important cause of hyponatraemia
Hypophosphataemia  Produced in posterior pituitary gland or by
ectopic production of ADH by a tumour
 Critical illness
 The excessive reabsorption of water in the
 Alcoholism
distal nephron continues in the face of a
 Diuretics dilute ECF and will cause plasma osmolality to
 Respiratory alkalosis fall below 275 mmol/L
 Primary hyperparathyroidism  Concentration of other electrolytes in the
 Post DKA (lost in urine) plasma is usually unaffected
 Severe burns (catacholamines stimulate
intracellular shift) Diagnosis and Criteria

Magnesium  When urine osmolality > plasma osmolality

 Urine osmolality > 100mmol/L
Hypermagnesiumaemia  Urine sodium > 30mmol/L (due to renin
inhibition)
 Renal failure especially those who ingest Mg
containing drugs (antacids)  Correction of hyponatraemia with H2O
restriction
Hypomagnesmiumaemia  Normal cardiac, hepatic and thyroid function
and no sign of dehydration or oedema
 Alcoholism due to poor intake and ↑ renal
excretion Common Causes
 Primary hyperparathyroidism
 Drugs: TCA antidepressants, SSRI’s, nicotine,
 Diuretics
ACE inhibitors, haloperidol, omeprazole
 Diarrhoea
(PPI’s), carbamazepine
Chloride  Post-operative stress caused by surgery, use
of mechanical ventilator, anaesthetic agents
Hyperchloridaemia
 CNS disturbances: infections, stroke, trauma,
 Normal anion gap acidosis (↓ bicarbonate = neurosurgery
↑ chloride)- to maintain electrical neutrality  Pulmonary Disorders: pneumonia, TB,
 Iatrogenic ↑ volumes NaCl administered IV emphysema, status asthmaticus
 ↑ H+ ↑ K+ ↑ Cl- ↑ PO4 ↓ HCO3- Rare Causes
Hypochlorideamia  Malignant disease
 Metabolic alkalosis o Neoplasm in the lung (small cell
carcinoma), duodenum, pancreas,
 Vomiting
olfactory neuroblastoma, bladder,
 Diarrhoea
prostate, thymus or brain
 ↓ H+ ↓ K+ ↓ Cl- ↓ PO4 ↑ HCO3-
o Lymphoma
Rhabdomyolysis Induced by Electrolyte Imbalances o Leukaemia
o Mesothelioma
 Hypophosphataemia: membrane injury o Ewing’s sarcoma
 Hypokalaemia: prevent local vasodilation in  Psychosis
muscle
  Hormone administration: vasopressin or those with TIA and a positive MRI has
oxytocin increased risk of subsequent stroke.
 Measurement of D-dimer or CRP does not
Transient Ischaemic Attack improve accuracy of clinical or imaging
The aim of assessment of a patient with suspected assessment but lipoprotein-associated
stroke or TIA is to confirm diagnosis, identify and treat phospholipase A2 levels may provide useful
the cause, and guide early rehabilitation and relevant information
early secondary prevention to prevent complications Prognosis
or stroke reoccurrence. Appropriate diagnosis and
immediate referral to a stroke team is vital given  ABCDD score used to determine risk of
advances in hyper-acute treatments developing a subsequent stroke post TIA
 Maximum score of 7, where there is an 8%
Definition
chance of developing a stroke in the next 2
 Rapidly developed clinical signs of focal or days
global disturbance of cerebral function lasting  A cut-off score of 4 has been suggested to
less than 24 hours, with no apparent non- differentiate between high and low risk. Score
vascular cause of 4-5 is 4% risk and 0-3 is 1% risk
 Revised definition: brief episode of  Does not consider AF as a risk factor
neurological dysfunction caused by a focal  ECG should be conducted routinely to screen
disturbance of brain or retinal ischemia, with for AF. A new diagnosis of AF or non-
clinical symptoms lasting less than1 hour, and therapeutic INR levels would indicate a
without evidence of infarction patient is at high risk and further rapid
investigations and management is required
Assessment
Features
 As with stroke, diagnosis is based on careful A Age ≥ 60 years (1)
B BP ≥ 140mmHg and/ or 90mmHg Diastolic (1)
clinical history and examination and it is vital C Clinical Features: unilateral weakness (2), speech
to elicit the onset and nature of symptoms, impairment without weakness (1)
and to identify treatable causes that can D Duration: >60 mins (2), 10-59 mins (1)
D Diabetes (1)
reduce the risk of future events.
 Assessment Tools such as ROSIER or National Stroke
Institutes Health Stroke Scale (NIHSS)
 Early (within 24 hours) carotid investigations Aetiology
should be routine for patients with suspected
Intracerebral Haemorrhage: usually derived from
anterior circulation TIA’s. Where symptomatic
arterioles/ smaller arteries
carotid stenosis is found, early (within 2
weeks) carotid endarterectomy significantly  Hypertension (number 1)
reduces risk of subsequent stroke  Trauma
 Brain imaging should be conducted. The  Bleeding tendency
presence of new brain CT changes within 48  Amyloid
hours after TIA was found to predict stroke
 Illicit drugs (cocaine)
risk. As with ischemic stroke, CT is useful to
 Tumours
exclude conditions that could mimic TIA such
 Aneurysm
as subdural haematoma or brain tumour. CT
 Vasculitis
has a high specificity but low sensitivity.
 MRI with diffusion-weighted imaging is Ischaemia
imaging strategy of choice for patients with
suspected TIA with studies detecting ischemic Thrombotic: large vessel disease
changes signifying infarction in 16-67% of
 Atherosclerosis (number 1)
  Takayasu arteritis/ Giant cell arteritis  Complete or partial hemianopia, monocular/
 Fibromuscular dysplasia binocular vision loss or diplopia
 Vasculitis  Dysarthria, aphasia
 Moya-moya  Ataxia, vertigo, nystagmus
 Sudden decrease in consciousness
Embolic: cardiac source vs other
 Palpate pulses for signs of AF
 Cardiac  Auscultation of heart and carotids for bruits
o Atrial fibrillation or murmurs
o Valve lesion  Skin- look for signs of endocarditis- septic
o Cardiomyopathy emboli
o Myocardial infarction (ventricular  Head- look for signs of trauma, tongue
aneurysm) lacerations (seizures)
o Infective endocarditis  Perform fundoscopy
o Atrial myxoma
Acute Medical and Surgical Management
o Patent fossa ovale
 Other  Supplemental O2 when indicated (Sp02 <95%)
o Systemic hypoperfusion  Establish intravenous lines
o Cardiac arrest  Rapid assessment (NIHSS) and arranging of CT
o arrhythmias is essential for these patients
 Contact stroke unit/ team
Clinical Features
 Treat early hypoglycaemia
In younger patients, it is important to get a history of  Look for other neurological infections like
recent trauma, migraines, use of OCP, recent meningitis, subdural brain abscess, infective
infections or seizures and use of illicit drugs. endocarditis
 Treat hypertension if
Any focal neurological deficit can present but more
o Ischaemic: >220/120
commonly:
o Haemorrhagic: >170 systolic
 Sudden numbness or weakness of face, arm, o Pre-existing anti-hypertensives can be
leg, especially unilaterally continued if no hypotension
 Sudden confusion, difficulty speaking or
Assess Physiological Status
understanding (Aphasia)
 Sudden deterioration in vision of one or both  Glasgow Coma Scale
eyes  Vital signs (glucose and O2 sats)
 Sudden difficulty walking, dizziness, loss of  Respiratoy pattern monitored
balance and coordination
 Sudden severe headache without any known Thrombolysis
cause  Tissue plasminogen activators such as rt-PA,
History and clinical examination must be used for streptokinase, recombinant pro-urokinase and
differential diagnosis urokinase given in a maximum time window
of 4.5 hours
 Seizures  Inclusion criteria: age over 18 years, clinical
 Syncope diagnosis of ischaemic stroke with measurable
 Migraine with auras neurological deficit, symptoms within 4.5
 Hypoglycaemia hours, CT scan does not show haemorrhage or
non-vascular cause of stroke
Examination  Absolute contraindications:
 Acute hemiparesis, hemiplegia o Uncertainty about time of onset
 o Coma or severe obtunded with fixed  Patients who are receiving anticoagulation
eye deviation and complete therapy prior to the haemorrhagic stroke and
hemiplegia who have elevated INR, therapy to reverse
o Only minor stroke deficit which is anticoagulation should be initiated rapidly
rapidly improving (vitamin K or prothrombin complex
o Seizure observed or known to have concentrate)
occurred at onset of stroke  Surgery for supratentorial haemorrhage can
o Hypertension ≥185/110 be considered in carefully selected patients
o Presentation suggestive of SAH within 72 hours.
o INR > 1.5  Surgical evacuation may be undertaken for
o Thrombocytopenia cerebellar hemisphere haematomas >3cm
o Hypo < 2.8 or hyper >22.0 glycaemia diameter in selected patients
o Presumed septic emboli  Contact neurosurgeon
 Commencement of aspirin for patients who
have received thrombolysis should be delayed Pyrexia Management
for 24 hours
 Associated with poorer outcomes after stroke
Neurointervention and mostly due to chest or urinary infections
 Paracetamol and physical cooling have been
 Intra-arterial thrombolysis within six hours found to be effective
can be used in carefully selected patients  Antibiotics for pneumonia and UTI
 Insufficient evidence to recommend the use
of mechanical clot removal in routine practice VTE Management

Antithrombotic Therapy  Subcutaneous LMW heparin for prevention of

DVT
 Aspirin orally or via a nasogastric tube or  Graded compression stockings for DVT
suppository should be given as soon as  Early mobilisation with (multidisciplinary team
possible after the onset of stroke symptoms within 48 hours)
(within 48 hours) if CT/ MRI exclude o Physiotherapist
haemorrhage o Occupational therapist
 Must be given after 24 hours if had o Speech pathologist
thrombolysis o Rehabilitation services
 The first dose should be at least 150-300mg
and dosage can be reduced to 100mg daily Seizure Management

Surgery for Ischaemic Stroke and management of  Reported incidence of post-stroke seizures
cerebral oedema varies ranging from 2-33% for early seizures
(<7 days) and 3-67% for late seizures (>7 days)
 Selected patients (18-60 years, where surgery  People with severe stroke, haemorrhagic
can occur within 48 hours of symptom onset) stroke and/ or a stroke involving the cerebral
and with large middle cerebral artery cortex are at increased risk
infarction should be urgently referred to a  Anti-convulsant medication should be used
neurosurgeon for consideration of for people with recurrent seizures after stroke
decompressive hemicraniectomy
 Corticosteroids are NOT recommended for Secondary Prevention Post Stroke
management of patients with brain oeema
Lifestyle Modification
and raised intra-cranial pressure
 Stopping smoking: nicotine replacement
Intracerebral Haemorrhage Management
therapy, buproprion or nortriptyline therapy,
varenicline, behavioural therapyimproving
 diet: a diet low in fat and sodium but high in intracranial haemorrhage as the cause of the
fruit and vegetables current event
 Increasing regular exercise
Cholesterol lowering Therapy
 Avoiding excessive alcohol (≤2 SD/ day)
 Higher cholesterol levels are associated with
Adherence to Pharmacotherapy
higher risk of ischaemic stroke but a lower risk
 Reminders to promote adherence to anti- of haemorrhagic stroke
hypertensives, statins, antiplatelet drugs or  Therapy with a statin should be used for all
warfarin patients with ischaemic stroke or TIA
 Reminders, self-monitoring, reinforcement,  Should not be used routinely for
counselling, family therapy, telephone follow haemorrhagic stroke
up, supportive care and dose administration
Carotid Surgery
aids
 Performed by carotid doppler ultrasound and
Blood Pressure Lowering
using NASCET criteria
 All stroke and TIA patients, whether  Carotid endarterectomy should be
normotensive or hypertensive should receive undertaken in patients with non-disabling
blood pressure lowering therapy, unless carotid artery territory ischaemic stroke or TIA
contraindicated by symptomatic hypotension with ipsilateral carotid stenosis measured at
 New BP lowering therapy, should be 70-99% or those with 50-69% with symptoms
commenced before discharge for those with  Carotid endarterectomy is NOT recommended
stroke or TIA for those with symptomatic stenosis < 50% or
asymptomatic stenosis <60%
Anti-platelet Therapy
 Carotid stenting should not routinely be
 Long-term antiplatelet therapy should be undertaken with carotid stenosis
prescribed to all people with ischaemic stroke
Diabetes Management
or TIA who are not prescribed anticoagulant
therapy  Diabetes and glucose intolerance post stroke
 Low-dose aspirin and modified release have been found to be independent risk
dipyridamole or clopidogrel alone should be factors for subsequent strokes
prescribed to all people with ischaemic stroke  Patients with glucose intolerance or diabetes
or TIA should be managed in line with national
 Combination of aspirin plus clopidogrel is NOT diabetes guidelines
recommended for secondary prevention in
people who do not have acute coronary Oral Contraceptive or Hormone Replacement Therapy
disease or recent coronary stent  The decision whether to start or continue oral
Anticoagulation Therapy contraception in women of child-bearing age
with a history of stroke should be discussed
 Anticoagulation therapy for secondary with the individual patient based on overall
prevention for people with ischaemic stroke assessment of risk and benefit. Non-hormonal
or TIA from presumed arterial origin should methods of contraception should be
not be routinely used considered
 Anticoagulation therapy should be used long-  Following a stroke event, HRT should be
term for those with AF or cardio-embolic stopped. The decision whether to start or
stroke continue in patients should be discussed with
 In patients with TIA, anticoagulation therapy the individual and based on an overall
should begin once CT or MRI has excluded assessment of risk and benefit
Complications  Patients with TIA should not drive for 2 weeks
 If person is deemed medically fit but is
 Dehydration and malnutrition, common after
required to undertake further testing, they
stroke due to swallowing impairment,
should be referred for an OT driving
immobility and communication difficulties
assessment
 Poor oral hygiene due to physical weakness,
dysphagia, lack of coordination and cognitive Acute Coronary Syndrome
problems
Includes: unstable angina, NSTEMI (subendocardial)
 Spasticity characterised by velocity dependent
and STEMI (transmural) myocardial infarctions
increased in tonic stretch reflexes (muscle
tone) with exaggerated tendon jerks resulting Causes: atherosclerotic plaque rupture, thrombosis,
from upper motor neurone syndrome inflammation and rarely due to emboli or coronary
 Contracture due to muscle weakness and artery spasm (prinzmetal angina)
immobility or poor stretching
 Central post stroke pain which is a superficial Risk Factors
and unpleasant burning, lancinating or
Non-Modifiable Modifiable Controversial
pricking sensation, often made worse by ↑ Age Smoking Stress
touch, water or movement Male Gender Hypertension Type A Personality
Family Hx of IHD Diabetes LVH
 Swelling of extremities Familial lipidaemia Hyperlipidaemia ↑ fibrinogen
 Fatigue: incidence from 16070% Obesity Hyperinsulinaemia
 Incontinence from bladder or bowel Sedentary lifestyle ↑ homocysteine
Cocaine use
dysfunction
 Mood disturbance, mainly depression, anxiety Diagnosis
and emotional lability
 Behaviour changes such as irritability, Raised cardiac serum markers and either
aggression, preservation, adynamia, apathy,
1. Symptoms of ischaemia
emotional lability, perseverative behaviours,
2. ECG changes of new ischemia, development
disinhibition, impulsivity and lack of insight
of pathological Q waves, or loss of
 Deep vein thrombosis or pulmonary embolism
myocardium on imaging
 Pressure sores or injuries
 Hospital acquired infection: pneumonia or UTI Clinical Features
 Falls
 Sleep apnoea (obstructive) Symptoms

Driving and Stroke  Acute central chest pain, often described as

heavy or crushing, lasting >20 mins,
 All patients admitted to hospital should be unrelieved by GTN or rest
asked if they intend to drive again  Associated with nausea, sweatiness,
 Any patient who does wish to drive should be dyspnoea, palpitations
given information about driving and be  Can radiate to left arm, neck or jaw
assessed for fitness to return to driving using  May present without chest pain (silent infarct)
national guidelines (assessing fitness to drive) in elderly patients or diabetics. In such
 Patients should be informed that they are patients, presentation may include: syncope,
required to report their condition to driver pulmonary oedema, epigastric pain and
license authority and their car insurance vomiting, post-operative hypotension or
company oliguria, acute confusional state, stroke and
 Stroke survivors should not return to driving diabetic hyperglycaemic states
for at least one month post event. A follow-up
assessment should be conducted prior to Signs
driving.
  Distress, anxiety, pallor, sweatiness infarction whilst troponin levels remain
 Pulse ↑ or ↓ elevated from first event
 BP ↑ or ↓ o ↑ 3-12 hours of onset
 May have 4th heart sound o Peak at 24 hours
 May have signs of heart failure (↑JVP, 3rd o ↓ to baseline over 48-72 hours
heart sound, basal crackles)  Myoglobin levels rise within 1-4 hours from
 Pansystolic murmur from mitral regurgitation the onset of pain. They are sensitive but not
due to papillary muscle dysfunction rupture, specific
VSD
Others
 Low-grade fever may be present
 Later, a pericardial friction rub or peripheral  Full blood count
oedema may develop  U and E’s
 Glucose
ECG Changes
 Lipid profile
STEMI
Management of STEMI
 Classically, hyperacute (tall) T waves, ST
Initial Management
elevation or new LBBB occur within hours of
transmural infarction (acute injury)  Aspirin 300mg PO (if not already given) PLUS
o ST elevation >2mm either clopidogrel, pasugrel, ticagrelor
o If LBBB present, ST elevation >5mm  Morphine 5-10mg IV state (repeat after 5
 T wave inversion develop over hours to days mins if necessary)
(ischaemia)  Anti-emetic (metoclopramide) 10mg IV with
 Pathological Q waves occur after several days first dose of morphine
and remain permanent (necrosis)  Oxygen therapy is recommended if patients
have SpO2 <95%, are breathless or in acute
LVF
 GTN routine use not recommended in the
acute setting unless patient is hypertensive or
in acute LVF. Useful as anti-anginal in chronic/
stable patients
NSTEMI
Reperfusion Therapy
 ST depression
 T wave inversion Indications

Blood Tests  Persistent ST elevation ≥ 1mm in 2 contiguous

limb leads OR
Cardiac Enzymes
 ST elevation ≥ 2mm in 2 contiguous chest
 Cardiac troponin levels (T and I) are the most leads OR
sensitive and specific markers of myocardial  New left bundle branch block pattern
stress and necrosis.
o ↑ within 3-12 hours
o Peak at 24-48 hours
o ↓ to baseline over 5-14 days
o If normal after 6 hours onset of pain,
and ECG normal, risk of missing MI is
0.3%
 Creatine Kinase: MB isotype mainly found in
the heart. Good for monitoring second
 o Replace fibrinogen using
cryoprecipitate or fresh frozen plasma
o Give blood as necessary

Subsequent Management

 Bed rest for 48 hours, continuous ECG

monitoring on Holter monitor
 Daily examination: heart, lungs, legs for
complciations; U&E
 Continue antiplatelet therapy if no
 If these targets cannot be reached, fibrinolysis contraindications with aspirin daily PLUS
should be given within 30 mins of arrival in clopidogrel daily (unless CABG likely)
hospital  Beta-blockers as they offer prognostic benefit
 In patients presenting longer than 12 hours following myocardial infarction and should be
after onset of symptoms, myocardial started during hospital admission. Should not
infarction may already be complete, but be started in those with decompensated heart
reperfusion should be considered if there are failure, heart block or significant bradycardia.
signs of continuing ischaemia Use atenolol daily or metoprolol twice daily
 All patients with acute MI should be  ACE inhibitors improve outcome after
considered for admission to a coronary care myocardial infarction. Start ACEI therapy
unit for monitoring and expert care within 24-48 hours of MI
Fibrinolytic Therapy  Statin therapy has been shown to reduce
premature death, myocardial infarction and
 Indicated if there is prolonged ischaemic chest other cardiovascular events
paint that has begun within the previous 12  Prophylaxis against thromboembolism until
hours, in the presence of significant ST fully mobile and should be continued if
segment elevation or left bundle branch block patient suffered a large myocardial infarction
that is presumed new to prevent emboli from left ventricular mural
 The following drugs are used thrombus in ventricular aneurysms
o Alteplasase  Calcium channel blockers should be reserved
o Reteplase for those who have contraindications to beta
o Tenecteplase blockers
 Adjuvant anticoagulation therapy for  Address modifiable risk factors
fibrinolysis  Assess LV function in all patients post MI
o Enoxaparin or unfractionated heparin  Refer for structured cardiac rehabilitation
 Contraindications programme
o Active bleeding or bleeding diathesis  Review at 5 weeks post MI to review
o Significant closed head or facial symptoms and consider coronary angiography
trauma within 3 months  Review at 3 months: check fasting lipids
o Suspected aortic dissection
o Any prior intracranial haemorrhage Management of NSTEMI
o Ischaemic stroke within 3 months
High Risk
o Known structural cerebral vascular
lesion Those who present with symptoms consistent with
o Known malignant intracranial ACS and any of the following:
neoplasm
 Occasionally bleeding may occur following  Repetitive or prolonged (>10 mins) ongoing
treatment and can be reversed: chest pain or discomfort
o Heparin: protamine  Elevated level of at least one cardiac marker
  New T-wave inversion >2mm or changes of ST
segment depression
 Haemodynamic compromise: systolic BP
<90mmHg, cool peripheries, diaphoresis,
heart failure, Mitral regurgitation
 Sustained VT
 Left ventricular systolic dysfunction EF <40%
 Known diabetes
 Chronic kidney disease eGFR <60

Management

 Antiplatelet therapy: aspirin + clopidogrel

 Beta blocker: atenolol or metoprolol
 Anti-coagulant therapy: dalteparin,
enoxaparin, unfractionated heparin
 Platelet glycoprotein 2b/3a inhibitor (if
abnormal ECG or +ve troponin): tirofiban
 Refer to angiography
Low Risk
 Revascularisation (stenting or bypass surgery)
should be considered in all patients who are Those who present with clinical features with ACS
at high risk without intermediate or high risk features. This
includes onset of angina symptoms within the last
Intermediate Risk
month, or worsening in severity or frequency of
Those who present with clinical features consistent angina, or lowering of angina threshold
with ACS and any of the following and who do not
Management
meet criteria for high risk
 Need cardiac assessment to rule out coronary
 Age more than 65
disease
 Known coronary heart disease
 Involves stress testing: exercise ECG, stress
 No high risk changes on ECG
cardiography or nuclear stress study
 Two or more modifiable risk factors
 Patients proven to have coronary disease
 Prior aspirin use should proceed to further investigation and
 Known diabetes or CKD with eGFR <60 (with management
atypical symptoms of ACS)  Patients should be treated with antiplatelet
Management therapy while being assessed

 Monitored and have reassessment of clinical Complications of MI and Management

status, ECG and biochemical markers Cardiac Arrest or Cardiogenic Shock
 They can be reclassified depending on results
into high or low risk  Caused by significant reduction in cardiac
output resulting in hypotension with signs of
impaired perfusion, including oliguria
 Management of hypotension: inotropic
support using adrenaline IV through central
venous catheter or large antecubital vein

Unstable Angina

 Manage using initial management of ACS

  Refer to a cardiologist Systemic embolism

Bradycardias or Heart Block  May arise from LV mural thrombosis due to

ventricular aneurysm
 Sinus bradycardia: treat with atropine  After larger anterior MI, consider
 1st degree AV block common in inferior MI, anticoagulation with warfarin for 3 months
observe closely as they can develop higher
degrees of heart block Cardiac Tamponade
 Mobitz Type 1: does not require pacing
 Beck triad: (muffled heart sounds,
 Mobitz Type 2: high risk of sudden complete
hypotension, distended neck veins), ↑ JVP,
AV block and should be paced
pulsus paradoxus
 3rd degree AV block: insert pacemarker
 Diagnosis made via echo. ECG should
Tachyarrhythmias electrical alternas
 Treatment: pericardial aspiration, surgery
 Hypokalaemia, hypoxia and acidosis all
predispose to arrhythmias and should be Mitral Regurgitation
corrected
 Due to papillary muscle dysfunction (mild) or
 AF or flutter, if compromised: DC
muscle rupture (severe)
cardioversion or control rate with digoxin ±
 Presents with pulmonary oedema, pansystolic
Beta blocker
murmur
 Atrial flutter or intermittent AF, try
 Treat LVF (frusemide, O2 and nitrates) and
amiodarone or sotalol
consider valve replacement
 Frequent PVC’s common after acute MI and
do not usually result in VF Ventricular Septal Defect
 Sustained VT if compromised give DC shock, if
stable treat with amiodarone  Presents with pansystolic murmur, ↑ JVP,
 Ventricular fibrillation: 80% occurs within 12 cardiac failure
hours. If occurs >48 hours, usually indicates  Diagnosis with Echo
pump failure or cardiogenic shock. DC shock  Treatment: surgery. 50% mortality in first
 Consider implantable cardiac defibrillator if week
ejection fraction <35% and VT
Dressler’s Syndrome
Right Ventricular Failure
 Recurrent pericarditis, pleural effusions, fever,
 Life-threatening and may accompany inferior anaemia and raised ESR 1-3 weeks post MI
MI  Treatment: NSAID’s, steroids if severe
 Clinical signs: right heart failure with signs of
Left Ventricular Aneurysm
low cardiac output without pulmonary
congestion  This occurs late (4-6 weeks post MI) and
 Gentle IV fluid challenge: sodium chloride presents with LVF, angina, recurrent VT or
200mL systemic embolism
 If BP remains low, give inotropes  ECG: persistent ST segment elevation
 Treatment: anticoagulation, consider excision
Pericarditis
DVT and PE
 Central chest pain, relived by sitting forwards
 ECG: PR interval depression, saddle shapped  Prophylactically heparinised (enoxaparin) until
ST elevation fully mobile
 Treatment: NSAIDs and echo to check for
effusion Acute Cardiogenic Pulmonary Oedema
  Medical emergency that requires urgent (corticosteroids, NSAIDs, COX-2 inhibitors),
treatment in hospital thiazolidinediones (glitazones)
 Patients which chronic heart failure should be
Management
counselled about the earliest manifestations
of pulmonary oedema:  Reassured that their condition can be treated
o Increasing breathlessness quickly and should be managed sitting upright
o PND and orthopnoea as possible
o Cough  Oxygen 15L/ minute via mask fitted with
 Differentials for acute breathlessness reservoir bag to maximise inspired oxygen
o Acute or chronic COPD delivery
o Asthma  Frusemide 20-80 mg IV or IM, reapeated 20
o Pneumonia (can precipitate minutes later if necessary, followed by regular
pulmonary oedema) (mane) PO frusemide
 Prevention of an acute attack usually requires
adjustment to fluid intake, increased PLUS if systolic pressure above 100mmHg
frusemide and modification of other
 Glyceryl trinitate (GTN) spray 400 micrograms
medication
sub-lingually, repeated dose every 5 minutes
 High risk groups include older patients with
OR GTN tablet sublingually
elevated blood pressure
 Symptoms: rapid onset of severe In Emergency Department
dyspnoea,often first occuring at night.
 Signs: tachypnoea, tachycardia and poor  Continuous positive airway pressure
peripheral perfusion (ashen colour, sweaty, ventilation (CPAP), commencing with 10cm of
cool peripheral and decreased capillary refill water pressure PLUS
time), agitation and restlessness and  GTN IV infusion
widespread lung crackles  Insert an indwelling catheter to monitor urine
 clinical features stem from two major output
pathophysiological processes, intra-alveolar  Morphine IV which can be used if patient has
fluid accumulation and extreme sympathetic acute anxiety or distress
nervous systemic activation  If pulmonary oedema is not responding to the
above measures, consider adding dubutamine
Precipitating or Exacerbating Factors or milrinone
 Lack of adherence to treatment, particularly Atrial Fibrillation
diuretics
 Dietary lapse (excessive fluid or salt or alcohol  Atrial fibrillation usually presents with an
intake) irregularly irregular ventricular rate of around
 Fluid overload 160 to 180 beats per minute
 Tachyarrhtyhimas: AF, atrial flutter or atrial  Most common arrhythmia
tachycardia
Aetiology : PIRATE SHIV
 Bradyarrhythmias: sinus bradycardia, heart
block  Pulmonary Embolism
 Myocardial ischaemia or infarction  Ischaemic Heart Disease
 Infection: bronchopneumonia, urinary tract  Rheumatic Heart Disease
infection, endocarditis  Alcohol Intoxication
 Pulmonary embolism or thrombosis  Thyrotoxicosis
 Anaemia  Endocarditis
 drug therapy: negatively inotropic drugs  Sleep Apnoea, surgery
(verapamil, diltiazem), salt-retaining drugs  Hypertension
  Infection Management
 Valvular Diseases (MR and MS and TS most
Rate control vs Rhythm control
common)
 Myocarditis, pericarditis  Once ventricular rate control is achieved, a
 Recent myocardial infarction decision regarding the long term management
(rate vs rhythm) should be made
History an Examination
 A rhythm control strategy uses antiarrhythmic
 A description of symptoms: onset or date of drugs (class 1 and 3), percutaneous catheter
discovery, the frequency and duration, ablation and/ or a surgical procedure
severity and qualitative characteristics  Antiarrhythmic medications are generally
 Typical symptoms: palpitations, tachycardia, started before cardioversion and continued to
fatigue, weakness, dizziness, light maintain sinus rhythm
headedness, reduced exercise capacity,  The reasons to pursue a rhythm-control
increased urination, mild dyspnoea strategy would be preferred when there are
 More severe symptoms: dyspnoea at rest, symptoms, younger patient age, and
angina, presyncope, or infrequently syncope irreversible structural and electrical
remodelling that occurs with longstanding
ECG Changes persistent AF
 A rate control strategy uses drugs that slow
 Lack of discrete P waves
conduction across the AV node, such as beta
 Fibrillatory waves are present at a rate that is
blockers and non-dihydropyridine calcium
between 350 and 600 beats/ min. The f waves
channel blockers or digoxin
vary continuously in amplitude, morphology
 The decision to adopt a rhythm or rate control
and intervals
strategy is often dictated by
 Ventricular response follows no repetitive
o the presence of symptoms associated
pattern; the variability in the intevals between
with AF
QRS complexes is often termed irregularly
o presence of diminutions in left
irregular
ventricular systolic function thought
 QRS complexes are narrow unless AV
secondary to the arrhythmia
conduction through the His Purkinje system is
 rate control is strongly preferred as the initial
abnormal due to functional aberration, pre-
approach in elderly patients with minor
existing bundle branch block or ventricular
symptoms
pre-excitation with conduction down the
accessory pathway Rate Control

Classification  β-blockers: atenolol or metoprolol

 Non-dihydropyridine calcium channel
 Paroxysmal (self-terminating or intermittent):
blockers: diltiazem or verapamil
terminates spontaneously or with
 Where there are contraindications to the
intervention within seven days of onset
above such as in decompensated heart
 Persistent: fails to self-terminate within seven
failure, heart block or low heart rate,
days. Episodes often require pharmacologic or
asthmatics, digoxin can be used
electrical cardioversion to restore sinus
o Digoxin 62.5 to 250 micrograms
rhythm
orally, daily according to age, eGFR
 Long-standing persistent AF: last more than
and plasma digoxin concentration
12 onths
 Digoxin alone usually fails to control exercise-
 Permanent AF: identify individuals with
induced tachycardia in younger patients and
persistent AF where a joint decision by the
more active patients
patient and clinician has been made to no
longer pursue a rhythm control strategy Rhythm Control and Cardioversion
  If the patient has severe symptoms or a an embolic risk even if a transoesophageal
compromised haemodynamic state, echo an hour or two earlier was clear
cardioversion should always be considered  If a TOE is performed and shows no evidence
immediately, but unless this is the case, of thrombus in the atria, it is safe to proceed
careful consideration of the risk of at once to attempted cardioversion.
thromboembolism is important before  If this is successful, the patient should be
treating with either a drug or DC shock. anticoagulated (usually subcutaneous
 It is generally safe to cardiovert (electrically or enoxaparin) for at least a few days to reduce
pharmacologically) if it is certain that the the risk of thromboembolism from stunning
episode has lasted less than 48 hours  If TOE is not performed, or is done and shows
 Two acceptable ways to cardiovert a patient thrombus, cardioversion should not be
will vary with patient preference and the attempted until patient has been fully
availability of transoesophageal echo. anticoagulated, preferably 3 weeks

Pharmacological Cardioversion Anticoagulation

 Amiodarone (class 3 potassium channel  Dalteparin subcut, BD

blocker) IV or PO  Enoxaparin subcut, BD
 Flecainide (class 1c sodium channel blocker)  Unfractionated heparin IV infusion, adjusted
IV or PO according to APTT
 If using flecainide, there is a possibility of  If required, oral may be started as follows
accelerating the ventricular rate, particularly o Warfarin PO, target INR 2 – 3
in flutter. Consider pre-treatment with an AV o Dabigatran 150mg PO, BD
nodal blocking drug
Long Term Maintenance Therapy after Cardioversion
Electrical Cardioversion
 Long term not required if AF or atrial flutter is
 Requires a DC shock, starting with 100 joules associated with transient condition (MI,
in an average adult but consider starting at surgery, excessive alcohol)
200 or even 300 joules in a large patient, or  Consider whether risk associated with
where there is a history of requiring a large recurrence outweigh those of long-term
shock antiarrhythmic treatment
 Atrial flutter generally requires much less  More invasive procedures such as
current, start with 50 joules radiofrequency ablation, His-bundle ablation
with pacemaker implantation, ore event
Thromboembolic Risk Post Cardioversion
surgical approaches, should be considered in
 If there is doubt as to duration of AF or if it is patients whose ventricular rate and rhythm
clear the attack has lasted more than 48 are poorly controlled by drugs
hours, do not attempt to cardiovert until
Complications and Long Term Anticoagulation
steps are taken to minimise thromboembolic
risk, except for haemodynamically unstable  Atrial fibrillation rare causes death except
patients through thromboembolic complications
 Even in very recent onset AF, there is a risk of o Stroke
atrial stunning following cardioversion to o Ischaemic bowel
sinus rhythm  All patients in whom AF is discovered should
 Stunning is an unpredictable failure of the be considered for long-term anticoagulation
atria to contract and may persist for hours to with warfarin or dabigatran (novel
days. anticoagulant), whether discovery is because
 During this time, fresh thrombus can form in of symptoms or as chance finding
the hypocontractile atria, and this constitutes
  All patients with AF should have a CHADS 2 – consumption, CKD, chronic lung disease and
Vasc score to evaluate need for immunosuppressive therapy
anticoagulation
Clinical Features
CHA2DS2-Vasc Score
 Acute respiratory symptoms: cough,
 Congestive heart failure dyspnoea, sputum production, pleuritic chest
 Hypertension pain
 Age ≥ 75  Fever, rigors, night sweats
 Diabetes  Reduced chest wall expansion on affected
 Stroke or TIA history side. decreased air entry on affected side,
 Vascular disease (peripheral artery disease, coarse crackles, dull percussion, bronchial
complex aortic plaque, myocardial infarction) breathing
 Age 65-74  Localised lobar consolidation on Chest X-ray
 Sex: female
Investigations
Score Risk Treatment Recommendations
 Chest X-ray
0 Low No therapy or aspirin
1 Moderate Oral anticoagulation or aspirin  Oxygen saturation, arterial blood gases are
≥2 high Oral anticoagulation appropriate in severely ill patients
 Sputum MCS
 Blood cultures if signs of sepsis
 If aspirin is indicated use: 100-300mg PO, daily  Consider pneumococcal urinary antigen assay,
 If oral anticoagulation is indicated use: which can be easily performed on routine
o Warfarin PO, daily, target INR 2-3 urine specimens for early identification of S.
o Dabigatran 150mg PO, BD pneumonia. Test all adults with severe disease
Community Acquired Pneumonia  Consider nose and throat swabs for NAAT PCR
for respiratory viruses
Pneumonia in individuals who are not hospitalised, or  Consider IgM serology for M. pnuemoniae
who have been hospitalised for less than 48 hours. and acute and convalescent serology for M.
pneumonia, Legionella, C. pnuemoniae and
Pathogens
influenza
 Streptococcus pneumonia (most common and  Bronchoalveolar lavage can be considered
causes most cases of severe disease and when other tests have not identified a
death, particularly in elderly) pathogen in a severely ill patient who has not
 Haemophilus influenza (COPD) responding to empirical antibiotic therapy
 Mycoplasma pneumonia (common in young Pneumonia Severity and Red Flags
adults)
 Chlamydophilia pnuemoniae CURB-65
 Legionella species (acquired from
 Confusion (abbreviated mental test ≤8)
environmental sources and can occur in
outbreaks)  Urea > 7mmol/L
 Respiratory rate ≥ 30 breaths/min
 Gram negative bacilli, including Klebsiella and
pseudomonas are uncommon causes of CAP  BP < 90 systolic and/ or 60 diastolic
 Staphyloccous aureus is uncommon cause of  Age ≥ 65
CAP but can be associated with MRSA and can A score of:
occur secondary to influenza
 In tropical regions, Bukrholderia pseudomallei  0-1: home treatment possible
and Acinetobacter baumannii can cause CAP.  2+: hospital therapy
Risk factors include diabetes, alcohol
  ≥3 severe pneumonia indicates mortality 15-  If atypical pathogens ( mycoplasma,
40%, consider ICU chlamydia, legionella) are suspected or
patients hypersensitive to penicillins, use
SMART COP doxycycline

Moderate Disease

 Treat as inpatient and use SMARTCOP to

assess for moderate severity (score 3-4)
 Investigations for causative organism are
important; collect blood and sputum samples
for cultures, ideally before starting antibiotics
 Always consider influenza as a potential
diagnosis, based on season and local
epidemiology
 Review the need for isolation and empirical
antiviral therapy while waiting for PCR results
 Non-tropical regions: benzylpenicillin IV until
significant improvement, then amoxicillin. +
Scoring doxycycline
 0-2: low risk of needing intense respiratory  Tropical regions: treat as above unless has risk
and or/ vasopressor support (IRVS) factors for B. pseudomallei and Acinetobacter
 3-4: moderate risk (1 in 8) of needing IRVS baumannii or if gram-negative bacilli are
identified on cultures, use:
 5-6: high risk (1 in 3) of needing IRVS
o Ceftriaxone 2g IV daily + gentamicin IV
 7 or more: very high risk (2 in 3) of needing
o Atypical pathogens: add doxycycline
IRVS
 SEVERE CAP = score of ≥ 5 Severe Disease

Red Flags  Inpatient assessed as severe pneumonia

based on SMARTCOP (5) or CURB65 (3)
 Respiratory Rate >30 breaths/ min
 More likely to require intensive respiratory or
 Systolic BP <90mmHg
vasopressor support, usually in ICU
 Oxygen saturation <92%
 Empirical therapy should treat: S. pneumonia,
 Tachycardia >100bpm
legionella and enteric gram –ve bacilli
 Acute onset confusion
 Also consider whether influenza or S. Aureus
 Multilobar involvement on CXR
are important causes and treat accordingly
Management  Investigation to identify pathogen is
important, collect blood cultures and sputum
Mild Disease samples
 Nontropical regions: (ceftriaxone IV or
 Does not require hospital admission and does
cefotaxime) PLUS (azithromycin IV)
not have any of the red flags
 Tropical regions: (meropenem IV (wet season)
 Monotherapy of amoxicillin or doxycycline is
or piperacillin + tazobactam) PLUS
recommended to minimise adverse effects
azithromycin IV
and optimise adherence to therapy
 If patient is not improving after 48 hours of Complications
monotherapy, consider escalating to
combination of amoxicillin + doxycycline, and Respiratory Failure
reassess the patient’s need for hospital
admission
  Type 1 relatively common. Treat with high-  Clinical features: swinging fever, cough,
flow (60%) oxygen and transfer to ICU if purulent, foul smelling sputum, pleuritic chest
hypoxia does not improve or PCO2 rises >6kPa pain, haemoptysis, malaise, weight loss. Look
 Aim to keep SpO2 at 94-98% for finger clubbing, anaemia, crepitations.
Empyema develops in 20-30%
Hypotension  Tests: FBC, Sputum MCS and cytology, CXR
 May be due to combination of dehydration shows walled cavity, often with a fluid level.
and vasodilation due to sepsis Bronchoscopy to obtain diagnostic specimens
 If systolic BP is <90mmHg, give IV fluids  Treatment: antibiotics as indicated by MCS,
continue until healed (4-6 weeks). Postural
Atrial Fibrillation draining, repeated aspiration, antibiotic
instillation or surgical excision may be
 Quite common, particularly in elderly and required
usually resolves with treatment of the
pneumonia Others
 Beta-blocker or digoxin may be required to
 Septicaemia: bacterial spread from lung
slow the ventricular response rate in the short
parenchyma into bloodstream and may cause
term
infective endocarditis, meningitis
Pleural Effusion  Pericarditis and myocarditis
 Jaundice: usually cholestatic and may be due
 Inflammation of pleura by adjacent
to sepsis or secondary to antiobiotic therapy
pneumonia may cause fluid exudation into the
(particularly flucloxacillin and co-amoxiclav)
pleural space
 If this accumulates faster than it is Hospital Acquired (Nosocomial) Pneumonia
reabsorbed, a pleural effusion develops.
Pneumonia that develops in a patient who has been
 If it becomes large and symptomatic, or
hospitalised for longer than 48 hours. Most bacterial
infected (empyema), drainage is required
HAP occurs by micro-aspiration of bacteria that
Empyema colonise the oropharynx or upper gastrointestinal
tract.
 Pus in the pleural space. Should be suspected
if patient with resolving pneumonia develops  Atypical pathogens are much less common in
a recurrent fever HAP than in community acquired
 CXR indicates a pleural effusion  Intubation greatly increases the risk of HAP
 Aspirated pleural fluid is typically yellow and because it interferes with normal
turbid with a pH <7.2, ↓ glucose and ↑LDH physiological mechanisms that limit bacterial
 Empyema should be drained using a chest contamination of the airways; intubated
drain, inserted under radiological guidance patients can develop ventilator-associated
 Adhesions and loculation can make this pneumonia (VAP)
difficult  Pneumonia caused by macroaspiration of
bacteria may occur in hospitalised patients,
Lung Abscess particularly in patients with risk factors such
as stroke, neuromuscular disorders or
 Cavitating area of localised, suppuratives
impaired consciousness
infection within the lung
 Causes: inadequately treated pneumonia, Diagnosis and Pathogens in HAP
aspiration, bronchial obstruction (tumour,
foreign body), pulmonary infarction, septic  Respiratory symptoms may be mild, and other
embolic, subphrenic or hepatic abscess symptoms, including confusion and
gastrointestinal symptoms, can be prominent
  Isolation of bacteria from expectorated
sputum or lower respiratory tract secretion
cultures often represents colonisation and is
not sufficient to diagnosis HAP or VAP
 HAP and VAP, is more likely in patients who
have a new, progressive, or persistent
infiltrate on chest x-ray, plus two or more of
the following features:
o Fever above 38c Severe Disease
o Total white cell count above or below
 Perform chest x-ray
normal range
 Collect blood, and if possible, expectorated
o Presence, or increased amount of
sputum for cultures before starting therapy
purulent sputum or lower respiratory
 Antibiotic therapy should not be delayed if
tract secretions
specimens are unobtainable
o Worsening gas exchange
 For patients without any additional risk
(desaturation, increased oxygen
factors for MDR organisms use: (same as
requirement or increased ventilator
moderate)
demand)
o Ceftriaxone IV OR
 Hospitalised patients may develop
o Cefotamine IV
colonisation of the oropharynx with aerobic
 Those with severe disease with additional risk
gram –ve bacilli, and may also be exposed to
factors for MDR or severe sepsis or septic
MRSA, multi-drug resistant
shock, use the management as per high risk of
enterobacteriaceae, pseudomonas aeruginosa
multidrug-resistant organisms
and Acinetobacter species
o Recent treatment with antibiotics
 Although HAP can be caused by Legionella,
o Recurrent or prolonged
particularly fungi or respiratory viruses
hospitalisation
(influenza, parainfluenza, RSV and
o Requirement for high-level nursing
adenovirus), these pathogens are relatively
care
uncommon
o Immunosuppuression
 It is essential to collect blood and cultures,
expectorated sputum before antibiotics are Higher Risk of Multi-drug Resistant Organisms
given, because the results of cultures
frequently enable directed therapy or de-  Patients with HAP who are in a high-risk ward
escalation of treatment within 48 to 72 hours (ICU, high-dependency unit, area with a high
rate of MDR organisms) for 5 days or longer
Management have increased risk of having an infection
caused by MDR organisms
Low Risk of Multidrug-resistant organism
 Should be treated initially with a broader-
Defined as spectrum empirical regimen regardless of
disease severity
 Low-risk ward (any duration)
 High-risk ward (ICU, high dependency unit,
areas with high rates of MDR organism) for
fewer than 5 days

Mild or Moderate Severity

 Perform chest x-ray

 Collect blood, and if possible, expectorated
sputum for cultures before starting therapy
 Aspiration Pneumonitis is characterised by acute lung
inflammation within several hours of aspiration of
acidic gastric contents, and is an important differential
diagnosis for aspiration pneumonia. Antibacterial
therapy is not required for the classical aspiration
pneumonitis syndrome (Mendelson syndrome)
because acidic gastric contents are normally sterile.
However, aspiration pneumonia can develop
following aspiration pneumonitis; risk factors include
gastric acid suppression therapy and bowel
obstruction

Causes of Aspiration

 Stroke
 Decreased level of consciousness, ↓ GCS
Review Treatment at 48 to 72 hours.  Bulbar palsy or other neuromuscular disorders
 Swallowing dysufnction
 Alcohol intoxication
 Seizures
 Anaesthesia
 Intubation
 Poor dentition or oral hygiene
 Hiatus hernia or GORD
 Bowel obstruction

Investigation

 Chest x-ray to determine if pneumonia is

present
 Collect blood and if possible expectorated
sputum (or, for intubated patients, lower
respiratory tract secretions) for cultures
before antbiotics are given
 In those who are severely unwell or not
improving, may use more invasive methods
such as bronchoalverolar lavage

Management

 While awaiting culture results, treat

Aspiration Pneumonia established community or nursing home
acquired aspiration pneumonia according to
Aspiration pneumonia is a bacterial infection that disease severity. As per CAP guidelines
occurs in the days following macroaspiration of  The role of anaerobic organisms in aspiration
organisms from the oropharynx. It is frequently pneumonia is frequently over-estimated
associated with risk factors such as bulbar dysfunction  In mild disease, penicillin effectively treats
and impaired consciousness. A chest X-ray is required anaerobic organisms aspirated from the
to confirm the diagnosis of pneumonia oropharynx, and the addition of
metronidazole is not required
  The addition of metronidazole is indicated in o Capable of substantial morbidity,
moderate disease who: mortality
o Have putrid sputum, severe o Occurs within days-weeks with
periodontal disease or a history of sudden onset of fever, fatigue and
chronic hazardous alcohol weakness
consumption o Prognosis is poor and high mortality
o Develop lung abscess, empyema or o Necrotising, destructive lesions
necrotising pneumonia  Subacute endocarditis- more common
o Do not respond to initial empirical o Infections by organism of low
therapy virulence involving a previously
 Severe disease: ceftriaxone IV + abnormal heart, especially scarred or
metronidazole IV deformed valves (strep mutans-
 For uncomplicated aspiration pneumonia, a viridans group) or strep bovis.
total treatment duration of 7 days (IV + oral) is o Common in post-dental work
usually adequate o Occurs within weeks-months
 Extensive or complicated disease involving the o Prognosis is good- antibiotics- low
development of lung abscess, empyema or mortality
necrotising pneumonia often requires o Less destructive lesions
prolonged therapy and/ or surgery
Clinical Features
Directed Therapy for Pneumonia
 Fever most consistent sign but can be absent
Bacterial Therapy in subacute or elderly
Pneumococcal Benzylpenicillin, then amoxycillin
 Nonspecific fatigue, weight loss and flulike
Staph Infection Flucloxacillin
MRSA Vacomycin syndrome
Legionella Azithromycin or doxycycline  Splenomegaly in subacute cases
H. Influenzae Amoxicillin or benzylpenicillin
Mycoplasma P Doxycycline or azithromycin or
 Acute- stormy onset of rapidly developing
clarithromycin fever, chills, night sweats, weakness, lassitude
Chlamydophilia P Doxycycline or azithromycin or  Murmurs are present in 90% of patients with
clarithromycin
Aerobic Gram –ve Ceftriaxone or cefotaxime or piperacillin + left-sided lesions
bacilli including tazobactam or meropenem  Microemboli give rise to petechial, splinter
Klebsiella P
Pseudomonas A Ceftazidime or piperacillin + tazobactam or
haemorrhages, retinal haemorrhages (Roth
meropenem spots), painless pal erythematous lesions
Acinetobacter Meropenem (Janeway lesions), or painful fingertip nodules
Baumanni
(Osler nodes)
Infective Endocarditis Diagnosis: Dukes Criteria
Aetiology  2 major and 0 minor
 Microbial invasion of heart valves or mural  1 major and 3 minor
endocardium- often with destruction of  0 major and 5 minor
underlying cardiac tissues
Major Criteria
 Acute endocarditis- rare
o Tumultuous, destructive infections,  Positive blood culture for typical infective
frequently involving highly virulent endocarditis organisms (strep viridans or
organism attacking a previously bovis, HACEK organism, Staph aureus without
normal valve (staph aureus) primary site, enterococcus) from 2 separate
o Common in IVDU in right heart, blood cultures or 2 positive cultures from
elderly samples drawn > 12 horus apart, or 3 or a
 majority of 4 separate cultures of blood(first because antibiotic resistance is increasingly a
and last sample drawn 1 hour apart) problem
 Echocardiogram with oscillating initracardiac  Gentamicin for 4-6 weeks + EITHER
mass on valve or supporting structures o Benzylpenicillin IV for 4-6 weeks
o Ideally TOE- more sensitive than TTE, o Amoxy/amplicillin 2g IV for 4-6 weeks
particularly for prosthetic valve and
pacemaker lead endocarditis Staphylococcal Endocarditis

Minor Criteria  Flucloxacillin 2g IV, 4 hourly for 4-6 weeks

 Four weeks may be adequate in
 Predisposing heart condition or intravenous uncomplicated cases but 6 weeks should be
drug use given if there are complications (perivalvular
 Temperature >38.0 abscess, septic metastatic complications
 Vascular phenomena: arterial emboli,  Patients with right-sided (tricuspid valve)
pulmonary infarcts, mycotic aneurysms, methicillin-susceptible staphylococcal
intracranial bleed, conjunctival haemorrhages, endocarditis (usually people who inject drugs)
Janeway lesions can be treated with a short course (2 weeks)
 Microbiological evidence: positive blood  For MRSA: vancomycin IV
culture but does not meet a major criterion
Endocarditis caused by the HACEK group
 Echocardiographic findings: consistent with
endocarditis but does not meet major  Oral gram –ve bacilli
criterion o Haemophilus parainfluenzae
Treatment o Haemophilus aphrophilus
o Aggregatibacter species
 Treatment involves several weeks of IV o Cardiobacterium species
antibiotics (PICC line) o Eikenella corrodens
o Kingella species
Empirical Therapy  Causes fewer than 5% of cases of endocarditis
 Once-daily dosing of gentamicin IV to cover and approximately 1/3 of these have
possibility of Gram –ve sepsis PLUS prosthetic valves
o Only interim regimen pending blood  If susceptible to penicillin and are beta-
culture results lactamase negative
o In confirmed streptococcal or o Amoxy/ampicillin or benzylpenicillin
enterococcal infection, 8 hourly  Beta-lactamase positive: broad-spectrum
gentamicin I recommended for cephalosporins
synergistic therapy of penicillin o Ceftriaxone 2g IV daily for 4-6 weeks
 Benzylpenicillin 1.8g IV 4-hourly (vacomycin IV o Cefotaxime 2g iv 8-hourly for 4-6
if prosthetic value or pacemaker lead weeks
endocarditis)
Complications
 Flucloxacillin 2g IV 4-hourly
 Generally begin within first weeks after onset
Viridans Streptococci Endocarditis of infectious process
 Benzylpenicillin 1.8 IV 4-hourly for 2 weeks +  Glomerulonephritis due to glomerular
 Gentamicin 1mg/kg IV, 8-hourly for 2 weeks trapping of antigen-antibody complexes with
haematuria, albuminuria, or renal failure
Enterococcal Endocarditis  Arrhythmias
 Systemic embolization bode particularly ill for
 Test all enterococcal isolates for minimum
patient
inhibitory concentration (MIC) of penicllin and
for high-level aminoglycoside resistance,
  Septic embolism, septicaemia, renal/ spleen  Younger patients develop severe and
infarcts persistent tachycardia before becoming
 Left untreated, it is generally fatal hypotensive late in the course

Abnormal Mental Status

Shock in Hospital  Altered sensorium in shock is usually due to

poor perfusion or metabolic encephalopathy
Shock is a life-threatening condition of circulatory
 Begins with agitation, progresses to confusion
failure that most commonly presents with
or delirium and ends in obtundation or coma
hypotension. Effects of shock are initially reversible
but can rapidly become irreversible, resulting in multi- Oliguria
organ failure and death.
 Shock can be due to shunting of renal blood
Definition and Classification flow to other vital orangs, direct kidney injury
or due to intravascular volume depletion
Shock is defined as a state of cellular and tissue
(vomiting, diarrhoea, or haemorrhage)
hypoxia due to reduced oxygen delivery and/ or
increased oxygen consumption or inadequate oxygen Cool, clammy, cyanotic skin
utilisation.
 Due to compensatory peripheral
 Distributive: septic shock, toxic shock, vasoconstriction that redirects blood
neurogenic shock, anaphylactic shock, centrally, to maintain vital organ perfusion
endocrine shock, systemic inflammatory (coronary, cerebral, and splanchnic flow)
response syndrome  A cyanotic, mottled appearance is a late and
 Cardiogenic: myocardial infarction, atrial and worrisome feature of shock
ventricular arrhythmias, valve or ventricle  Warm, hyperemic skin does not ensure the
septal rupture absence of shock because such an appearance
 Hypovolemic: haemorrhagic and non- may be present in patients with early
haemorrhagic fluid losses distributive shock (prior to onset of
 Obstructive: pulmonary embolism, pulmonary compensatory vasoconstriction) or terminal
hypertension, tension pneumothrorax, shock (due to failure of compensatory
constrictive pericarditis, restrictive vasoconstriction)
cardiomyopathy
Metabolic acidosis
Clinical Manifestations – undifferentiated shock
 High anion gap metabolic acidosis, specifically
Hypotension elevated lactate, should raise clinical suspicion
for the presence of shock
 Occurs in majority of patients with shock
 Absolute: systolic BP <90mmHg; mean arterial Initial Approach
pressure <65mmHg
 Relative: a drop in systolic blood pressure >40  Assess airway, breathing, circulation
mmHg  Obtain IV access with two large bore cannulas
 Orthostatic: >20mmHg fall in systolic pressure and initial fluid delivery
or > 10mmHg fall in diastolic pressure with  Oxygen to be given when SpO2 <95%
standing General Assessment
 Profound: vasopressor-dependent
History and Examination
Tachycardia
 Sensorium (orientation)
 Early compensatory mechanism in patients  Mucous membranes, lips, tongue, CRT
with shock
 Neck veins
  Lungs, heart and abdomen  Treatment: tube thoracostomy (5th intercostal
space, mid-axillary line) or needle
Laboratory Evaluation compression (2nd or 3rd intercostal space, mid-
 Serum lactate: reflection of poor tissue clavicular line
perfusion (lactic acidosis) and produced by Pericardial Tamponade
anaerobic metabolism
 Renal and liver function tests: ↑ BUN,  Features: dysnpoea, tachycardia,
creatinine and transaminases are usually due hypotension, elevated JVP, distant heart
to shock-induced end-organ damage sounds, pulsus paradoxus
 Cardiac enzymes and natriuretic peptides: ↑  Treatment: bedside echocardiography and
troponin, creatine phosphokinase, BNP may pericardiocentesis
indicate cardiogenic shock from ischaemia or
Haemodynamically significant Haemorrhage
massive PE
 Full blood count and differential: high  Traumatic: blunt or penetrating trauma
haematocrit may suggest hypovolaemia and leading to haemothorax, peritoneal lavage,
anaemia suggest haemorrhagic shock. ruptured spleen
Leukocytosis may indicate septick shock.  Nontraumatic: ruptured AAA, upper and
Neutrophilic lefft shift with toxic granules on lower GI bleeds (haematemesis,
blood smear is more indicative haematochezia, anaemia, bleeding diathesis)
 Coagulation and D-dimer: may indicate  Treatment: requires large volumes of blood
haemorrhagic shock or sepsis which has products and vasopressors are avoided. A
caused DIC type and crossmatch, a complete blood count
 Venous or arterial blood gas: hypoxaemia and and coagulation studies should be obtained in
acidosis all patients with suspected haemorrhage
Chest X-ray Life-threatening Arrhythmias
 Performed in most patients with suspected  Can be cardioverted (tachyarrhythmias),
hosck to detect common causes: pneumonia, receive atropine or infusions of dopamine, or
pneumothorax, pulmonary oedema, widened undergo temporary or permanent pacemaker
mediastinum to support aetiology for septic, placement (bradyarrhythmias)
obstructive, cardiogenic or aortic dissection
 May show complications of shock such as Severe Septic Shock
acute respiratory distress syndrome
 Features: fever, severe hypotension and an
Common Conditions with Lifesaving Interventions obvious septic source
 Septic screen: Blood cultures, FBC, CXR, Urine
Anaphylactic Shock MCS
 Features: hypotension, inspiratory stridor,  Treatment: oxygen and fluids if required.
oral and facial oedema, hives and history of Immediate broad spectrum antibiotics:
recent exposure vacomycin with ceftriaxone/ cefotaxime or
beta-lactam/ beta-lactamase inhibitor
 Treatment: Adrenaline IM 0.3mg of 1:1000
 Other agents: antihistamines, nebulised Cardiogenic Shock from MI
albuterol, methylprednisolone
 Features: hypotension associated with
Tension Pneumothorax anterior crushing chest pain, respiratory
distress and STEMI and/ or elevated troponin
 Features: tachypnoea, unilateral pleuritic
 Antiplatelets, PCI/ stent
chest pain and diminished breath sounds,
distended neck veins, tracheal deviation Dissection of the ascending aorta
  Features: hypertension, tearing chest or back 3. If ketones ≥0.6 (risk of DKA), check VBG for
pain. However, hypotension and shock occur pH, HCO3 and anion gap
with retrograde dissection that results in 4. If absence of acidosis, do not use protocol and
acute aortic insufficiency, pericardial recheck BGL and ketones in 2 hours. Treat
tamponade or myocardial infarction patient as clinically indicated
 Treatment: CT contrast, transoesophageal 5. Acidosis and ketosis present, DKA= ph <7.35
echo or MRI to demonstrate aortic root and HCO3 <15 and raised anion gap and
dilatation. Surgical Referral ketones >1. BGL may be nomal or elevated

Haemodynamically Significant PE Clinical Signs and Symptoms

 Features: hypotension, acute dyspnoea,  Hyperventilation or Kaussmaul’s breathing

hypoxemia  Vomiting and abdominal pain
 Treatment: systemic thrombolytic therapy  Dehydration
 Impair consciousness
Adrenal Crisis
Consider Precipitating Factors
 Features: hypotension, volume depletion,
history of glucocorticoid deficiency or  Omission of insulin
withdrawal should receive dexamethasone  Infection
4mg IV  Newly diagnosed diabetes ellitus
 Blood for serum cortisol, ACTH, aldosterone,  Myocardial infarction
renin and serum chemistries should be drawn  Recent surgery/ trauma
prior to therapy
Key Issues
Undifferentiated Management of Shock
 Initial fluid management
 Haemodynamic support with IV fluids (usually  Early potassium replacement
crystalloids in well-defined boluses of 500 to  Early IV insulin initiation (titrated to blood
1000mL. those who have distributive shock or glucose level)
hypovolaemic shock need 2-5L of fluid  Frequent monitoring
replacement
 Vasopressors are second line agents in the Management
treatment with suspected/ undifferentiated
Immediate management (1 hour)
shock. The use of vasopressors in patients
with haemorrhagic or hypovolaemic shock 1. Initial investigation
may be harmful a. Two IV cannulae
 Vasopressors should only be used as an b. FBC, U&E, LFT, BGL, VBG
additional form of haemodynamic support c. Finger prick ketones
when aggressive resuscitation has failed to d. Blood cultures
restore adequate tissue perfusion 2. Fluid replacement (cannula 1)
o Adrenergic agonists: noradrenaline IV a. 0.9% sodium chloride 1000ml/hr.
o Inotropic agents: dobutamine Repeat if hypotensive
(commoner in cardiogenic shock 3. Start IV insulin (cannula 2)
a. If K >3mmol/L commence soluble
Diabetic Ketoacidosis
insulin (maximum starting dose 10
Protocol units /hr)
b. If K <3mmol/L, replace K (cannula 1),
1. Patient unwell with T1DM recheck levels and commence insulin
2. Test BGL and finger prick ketones infusion once K >3mmol/L
4. Other actions
 a. Manage airway- consider NGT if  Continue insulin at variable rate to maintain
protracted vomiting/ risk of aspiration BGL 9-14mmol/L
b. Check bHCG and cardiac enzymes and  Patient is ready to transition to regular insulin
if indicated (triggers) regimen when the following criteria are met
c. Undertake septic screen and treat o Patient well and eating/drinking
infection if present (triggers) o Anion gap is normal
d. Fluid balance chart and neurological o Ketones <0.6mmol/L
observations o Long acting insulin has been given at
e. If patient on insulin pump- remove it least 2 hours ago (pump
f. DVT prophylaxis recommenced)
g. Prescribe/ administer patient’s usual  Ignore mild persistent acidosis if above
long acting insulin criteria are met and there is hyperchloraemia
5. Contact accepting consultant (saline induced metabolic acidosis)

Ongoing management (hour 2-4) Discharge Planning

1. Further investigations Refer for specialist review before discharge

a. Hourly BGL
b. 4 hourly ketones  Endocrinologist
c. U&E’s and VBG at end of hour 2 and  Diabetes educator
hour 4  Dietician
2. Continuation of fluid replacement 0.9%  Psychologist
sodium chloride
Discharge Preparation
3. Potassium replacement (cannula 1)
a. If serum K >5mmol/L or patient  Ketones <0.6mmol/L and anion gap normal
anuric- withhold  Eating normally and established on routine
b. If serum K 3.5-5.0mmol/L give insulin regimen
10mmol/100mL  Given written advice about sick day
c. If serum K <3.5mmol/L give 2 x management
10mmol/100mL
 Ensure that a copy of patient discharge letter
4. IV insulin and glucose (cannula 2)
is sent patient’s GP and diabetes care team
a. Continue initial rate of insulin if BGL’s
are decreasing and venous pH at hour Refer to ICU for consultation if any of the following
2 and 4 is consistently increasing
(finger prick ketones at hour 4 should  pH <7.1
be decreasing)  Altered level of consciousness
b. Increase rate of insulin if pH is not  Severe hypokalaemia (<3mmol/L)
increasing or if BGL’s rise or do not  Severe hyponatraemia (<125mmol/L)
decrease  Altered blood pressure or severe dehydration
c. When BGL <14mmol/L give 10%  Pregnancy
glucose 100mL/hr via cannula 2
Delirium
Subsequent Management
Confusion Assessment Method
 Finger prick ketones until ketones <0.6mmol/L
1. Acute onset and fluctuating course: usually
 Continue 0.9% sodium chloride infusion at
obtained from a family member of nurse and
125mL/hr until patient is fluid replete or
shown by positive responses to follow
eating/ drinking
questions
 Continue K replacement to maintain within
reference range and continue to monitor K as
above with U&E’s and VBG
 a. Is there evidence of an acute change  Others: changes in environment, dehydration,
in mental status from the patient’s not eating or drinking, restrained patients,
baseline constipation, chronic pain
b. Did the abnormal behaviour fluctuate
during the day Features of Delirium- DELIRIUM
2. Inattention: shown by a positive response to
 Disordered thinking: slow, incoherent,
the following:
confused ideas
a. Did the patient have difficulty
 Euphoric, fearful, angry, depression (labile
focusing attention, for example, being
mood)
easily distractible or having difficulty
 Language impaired: reduced speech,
keeping track of what was being said
repetitive
3. Disorganised thinking: shown by a positive
 Illusions/ hallucinations/ delusions
response to the following:
 Reversal of sleep-awake cycle: tired during
a. Was the patient’s thinking
day, awake hypervigilant at night
disorganised or incoherent, such as
 Inattention: focusing attention is poor- test
rambling or irrelevant conversation,
with serial 7’s or spelling world backwards
unclear or illogical flow of ideas, or
 Unaware/ disorientated: doesn’t know name,
unpredictable switching from subject
time, location
to subject
 Memory deficit: may be amnesic during
4. Altered level of consciousness: shown by an
answer other than alert to the following: episode
a. Normal= alert Delirium Work up
b. Hyperalert= vigilant
c. Drowsy, easily aroused= lethargic Laboratory Studies
d. Difficult to arouse= stupor
 FBC with differential: helpful to diagnose
e. Unarousable= coma
infection and anaemia
The diagnosis of delirium requires the presence of  Electrolytes: to diagnose low or high levels
features 1 AND 2 plus either 3 or 4  Glucose: to diagnosis hypoglycaemia, DKA and
HONK states
Causes of Delirium- I WATCH DEATH
 Renal and liver function tests to diagnose liver
 Infection: pneumonia, UTI, skin, CNS and renal failure
 Withdrawal: often unintentional from alcohol,  Thyroid function tests: to diagnosis
sedative, barbiturates hypothyroidism
 Acute metabolic changes: altered pH, hypo/  Urine analysis for UTI
hyper sodium or calcium, acute liver or renal  Urine and blood drug screen: used to
failure diagnosis toxicological causes
 Trauma: brain injury, subdural haematoma  Thiamine and vitamin B12 levels used to
 CNS pathology: post-ictal, stroke, tumour, detect deficiency states of these vitamins
brain metastasis  Tests for bacteriological and viral aetiologies
 Hypoxia- CHF, anaemia (blood cultures and viral serology): to
 Deficiencies: thiamine, niacin, B12, folate diagnosis infection
 Endocrinopathies: hypo/ hyper cortisol,  ESR/ CRP
hypoglycaemia, hypothyroidism  Drug screen including alcohol level
 Acute vascular: hypertensive emergencies,  HIV and syphilis serology
septic hypotension
Imaging Studies
 Toxins and drugs: especially anticholinergics,
opioids, benzodiazepines, SSRI’s  Chest X-ray for pneumonia and congestive
 Heavy metals: lead, arsenic heart failure
  CT head scan  The increase in sympathetic outflow raises
 MRI may be useful in diagnosing stroke, peripheral vascular resistance, venous return
haemorrhage and structural lesions and cardiac output, thereby limiting the fall in
 EEG to exclude seizures, confirm the diagnosis blood pressure
of certain metabolic encephalopathies or  Because of these compensatory mechanisms,
infectious encephalitides that have normally, assumption of erect posture leads
characteristic EEG patterns to a small fall in systolic blood pressure (5-
10mmHg), an increased in diastolic blood
Other Tests pressure (5-10mmHg) and an increase in pulse
rate (10-25bpm) (sinus arrhythmia)
 Lumber puncture is indicated when CNS
infection is suspected as a cause of delirium or Aetiology
when source for the systemic infection cannot
be determined  Autonomic failure: disorder of nonadrenergic
 Pulse oximetry is used to diagnose hypoxia as neurotransmission in which postganglionic
a cause of delirium sympathetic neurons do not release
 ECG for ischaemic and arrhythmic causes norepinephrine appropriately
 Check their medication list- polypharmacy  Neurodegenerative disease
o Parkinson’s disease
Postural Hypotension o Lewy body dementia
o Multiple system atrophy
When autonomic reflexes are impaired or
 Neuropathies: leads to autonomic failure
intravascular volume is markedly depleted, a
o Diabetes mellitus
significant reduction in blood pressure occurs upon
o Amyloidosis
standing. Orthostatic hypotension can cause dizziness,
o Sjogren syndrome
syncope and even angina or stroke.
o Renal failure
Chronic orthostatic intolerance describes the o B12 deficiency
association of lightheadedness, dizziness, faintness or o Syphilis, Lyme, HIV
syncope that occurs with prolonged standing or o Sarcoidosis
upright posture. These symptoms may be sometimes o Alcohol
associated with an exaggerated tachycardia but little o Guillain Barre Syndrome
or no fall in blood puressure- postural tachycardia  Volume depletion: acute or subacute volume
syndrome depletion due to diuretics, hyperglycaemia,
haemorrhage or vomiting
Normal BP Response to Standing
 Medication
 Upright posture results in pooling of 500- o Alcohol
1000mL of blood in the lower extremities and o Alpha blockers: Terazosin
splanchnic circulation which initiates to o Antidepressant drugs: SSRI, MOA
following sequence: inhibitors, TCA
 Rapid decrease in venous return to the heart o Antihypertensives
 Ensuing reduction in ventricular filling results o Antiparkisonism drugs: levodopa
o Antipsychotic drugs
in diminished cardiac output and blood
pressure o Beta-blockers
o Diuretic drugs: hydrochlorothiazide,
 The fall in blood pressure and thoracic volume
furosemide
provokes a compensatory reflex involving the
o Muscle relaxant drugs
central and peripheral nervous systems that
o Narcotic analgesic drugs: morphine
increases sympathetic and reduces
o Phosphdiesterase inhibitors: sildenafil
parasympathetic outflow (baroreceptor
o Sedatives/ hypnotic drugs:
reflex)
temazepam
 o Vasodilator drugs: hydralazine, Categories of Seizures
nitroglycerin, calcium channel
blockers Epileptic Seizures
 Ageing: decrease in baroreceptor sensitivity  At least two unprovoked (or reflex) seizures
 Others: cardiac pump failure (aortic stenosis, occurring more than 24 hours apart
pericarditis/ myocarditis, arrhythmias) and  One unprovoked seizures and a probability of
adrenal insufficiency and less commonly further seizures similar to general recurrence
pheochromocytoma risk after two unprovoked seizures, occurring
over the next 10 years
Symptoms
 Diagnosis of epilepsy syndrome
 Symptoms typically occur in response to
sudden postural change, but also in Aetiology
association with meals, exertion and  Less than one-half of epilepsy cases have an
prolonged standing identifiable cause. It is presumed that most of
 Symptoms result from cerebral hypoperfusion these are genetically determined. In the
and include generalised weakness, dizziness remainder of patients in whom an aetiology
or lightheadedness, visual blurring or can be determined, the causes include
darkening of the visual fields and in severe o Head trauma
cases, syncope o Stroke
 Elderly patients are at increased risk of falls o Brain tumour
o Intracranial infection
Diagnosis
o Cerebral degeneration
 When, within two to five minutes of quiet o Congenital brain malformations
standing (after a five minute period of supine o Inborn errors of metabolism
rest), one or both of the following is present  In the elderly, vascular degeneration and
o At least a 20mmHg drop in systolic neoplastic causes are more common than in
o At least a 10mmHg drop in diastolic younger adults and children
 The heart rate normally rises immediately on  A higher proportion in children is due to
standing congenital brain malformations than in other
age groups
Evaluation  Onset of seizures in late life may be a risk
 Detailed medication list, prescription and non- factor for stroke
prescription  Anti-seizure drugs prevent seizures in the first
 Recent medical history of potential volume week after head injury but do not prevent the
loss (vomiting, diarrhoea, fluid restriction, development of epilepsy
fever) Provoked or Secondary Seizures
 Medical history of congestive heart failure,
malignancy, diabetes, alcoholism Acute Symptomatic Seizures
 Evidence on neurological history and
 Patients without a history of epilepsy often
examination of parkinsonism, ataxia,
experience seizures in the setting of acute
peripheral neuropathy or dysautonomia
medical or neurological illness or injury
(abnormal pupillary response, history of
 While this occurrence places them at risk for
constipation or erectile dysfunction
future epilepsy, a seizure in the acute setting
 Laboratory testing (haematocrit, electrolytes,
carries a lower risk
blood urea nitrogen, creatinine, glucose) and
 Patients with seizures provoked by metabolic
an electrocardiogram
derangements are generally not felt to be at
Seizures risk for future epilepsy compared to those
post traumatic injury
  Another features is the risk of seizures is felt  Miscellaneous neurological events
to occur in proportion to the rapidity of the  Elderly causes
onset, rather than to the severity of the o TIA
underlying metabolic disturbance o Transient global ischaemia
o Drop attacks
Aetiology
o Cardiogenic syncope
 Hypoglycaemic seizures: diaphoresis, o Delirium
tachycardia, anxiety and confusion Seizure History
 Nonketotic hyperglycaemia: elderly diabetes
and can cause focal motor seizures  What happened just before seizure? (aura)
 Precipitous falls in serum sodium  What was happening during? (witness)
concentrations can trigger generalised tonic-  What happened after recovery? (drowsy/
clonic seizures, usually with prodrome of confused)
confusion and depressed level of  Could you remember what happened or
consciousness events leading up to
 Hypocalcaemia: rare- often in neonates.  Did you bite your tongue or was there any
Prodrome: mental status changes and tetany blood in your mouth, did you vomit, were you
 Hypomagnesium <0.8: irritability, agitation, incontinent. Do your muscles feel sore or
confusion, myoclonus, tetany, and were you unable to move them? (Todd’s
convulsions Palsy)
 Renal failure and uraemia- particularly  Have you had seizures before? Child hood
myoclonic seizures seizures.
 Hyperthyroidism can cause seizures and can  Ask about risk factors: head injury, Alzheimer
exacerbate seizures in patients with epilepsy disease, stroke, drug or alcohol abuse
 Acute intermittent porphyria  Medication history
 Cerebral anoxia as a complication of cardiac  What triggers do you have?: loud music,
or respiratory arrest, carbon monoxide intense exercise, strong emotions, flashing
poisoning, drowning or anaesthetic lights, lack of sleep
complication. Cerebral anoxia dye to syncope  Family history of seizures, in particularly
can result in very brief tonic and/ or clonic absence seizures and myoclonic seizures may
movements without a prolonged postictal be inheritied
state
 Withdrawal states- particularly alcohol and Seizure Symptoms and Signs
benzodiazepine withdrawal typically in 7-48 Partial (Focal) Seizures without impairment of
hours of last drink consciousness (simple)
 Drug toxicity/ intoxication
 Involves warning or aura, which are seizures
Nonepileptic Seizures that affect enough of the brain to cause
 Sudden changes in behaviour that resemble symptoms, but not enough to interfere with
epileptic seizures but are not associated with consciousness
the typical neurophysiological changes that  Auras are called focal seizures without
characterise epileptic seizures impairment of consciousness
 Seizure that begins in occipital cortex may
Imitators of Epilepsy result in flashing lights, while a seizure that
affects the motor cortex will result in rhythmic
 Syncope
jerking movements of face, arm, or leg on side
 Psychological disorders of the body opposite to the involved cortex
 Sleep disorders (Jacksonian seizure)
 Migraine
  Presence of aura supports diagnosis of Generalised Seizures
epileptic seizure and do not typically precede
provoked seizures  Originate in all regions of the cortex
simultaneously.
 Symptoms of simple partial seizures or auras
o Black out Generalised Tonic Clonic Seizure
o Confusion
o Deja-vu  Begins with abrupt loss of consciousness,
o Dizziness often in association with a scream or shriek.
o Drooling  All of the muscles of the arms and legs as well
o Electric shock feeling as chest and back then become stiff
o Eyelid flutter  The patient may begin to appear cyanotic
o Lightheadness or LOC during this tonic phase
o Memory loss  After approximately one minute, the muscles
o One side of body different than over begin to jerk and twitch for additional one to
o Racing thoughts two minutes. During this clonic phase, the
o Sound or spatial perception distortion tongue can be bitten and frothy and bloody
o Spinning feeling sputum may be seen coming out of the
o Sweating mouth. Possible loss of bowel or bladder
o Tremors control.
o Visual distortion, visual loss or  The postictal phase begins once the twitching
blurring movements end. The patient is initially in a
deep sleep, breathing deeply, and then
Focal (Partial) Seizures with Impairment of
gradually wakes up, often complaining of a
Consciousness (complex)
headache, mild confusion, muscles sore,
 Most common type of seizure in epileptic fatigue
adults  Other features: fast heart rate, elevated blood
 During the seizure, the patients appear to be pressure, respiratory and metabolic acidosis,
awake but are not in contact with others in dilated pupils, risk of vertebral fracture
their environment and do not respond pneumonia
normally to instructions or questions.  Certain physical signs, such as lateral tongue
 They often seem to stare into space and bite and urinary incontinence, are more
either remain motionless or engage in specific for an epileptic generalised tonic-
repetitive behaviours, called automatisms, clonic seizure
such as facial grimacing, gesturing, chewing,
Absence Seizure
kip smacking, snapping fingers, repeating
words or phrases, walking, running or  Usually occur during childhood and typically
undressing last between 5 to 10 seconds
 Patients may become hostile or aggressive if  They frequently occur in clusters and may
physically restrained during these seizures take place dozens or even hundreds of times a
 Typically last less than three minutes and may day
be immediately preceded by a focal seizure  Cause sudden staring with impaired
with preserved awareness (aura) consciousness
 Afterward, the patient enters the postictal  If it lasts more than 10 seconds, there may
phase, characterised by somnolence, also be eye blinking and lip smacking
confusion, and headache for up to several
hours Other Seizures
 Patient has no memory of what took place
 Clonic seizures: rhythmical jerking muscle
during the seizure other than, perhaps, the
contractions that may occur singly or in
aura
 clusters and that can affect any muscle group,  Other seizure biomarkers: cretine
although typically the arms are, neck, face phosphokinase (CPK), cortisol, white blood
affected. cell count, lactate dehydrogenase, pCO2,
 Myoclonic seizures consist of sudden, brief ammonia, neuron specific enolase (to
muscle contractions that may occur singly or differentiate between syncope, psychogenic
in clusters and that can affect any group of nonepileptic seizures)
muscles, although typically the arms.  VBG: can have respiratory and metabolic
Consciousness is usually not impaired acidosis
 Tonic seizures cause sudden muscle stiffening,  ECG: cardiogenic syncope can manifest as a
often associated with impaired consciousness secondary hypoxic seizure
and falling to the group  Lumbar puncture: if clinical presentation
 Atonic seizures (drop seizures): a sudden loss suggests an acute infectious process or history
of control of the muscles, particularly of the of cancer-type known to metastasize to
legs, that results in collapsing to the ground meninges
and possible injuries  EEG: essential study in diagnostic evaluation
of epileptic seizures, a normal EEG does not
Postictal State
rule out epilepsy
 Following seizure, there is a period of  MRI brain preferred over CT to identify a
transition back to individual’s normal level of specific lesion such as cortical dysplasia,
awareness and function infarcts or tumours. CT brain sufficient if
 Manifestations include: confusion, suppressed suspecting a cerebral haemorrhage, mass or
alertness, focal neurological deficits may also large stroke
be present.
Acute Management of Inpatient Seizure
 May last from seconds to minutes to hours
depending on where the brain was affected,  Most seizures remit spontaneously within two
length of seizure, whether they were on anti- minutes and rapid administration of
epileptics, age benzodiazepine or antiseizure drug is not
 Postictal paresis (Todd’s palsy) is a transient required
neurological deficit that lasts for hours after  Intravenous access should be secured so that
an epileptic seizure. The classic deficit is medications can be administered if the
weakness of a hand, arm or leg that appears seizure is more prolonged
following focal motor seizure activity involving  Maintain airway and suction out vomitus or
one limb or side of the body. blood. Give oxygen via non-rebreather
 Other postictal symptoms: transient aphasia,  Monitor vital signs: pulse and oxygen
amaurosis, hemianopsia and sensory loss. saturations
Some patients manifest psychosis and  Seizure that last longer than 5 to 10 minutes
aggression or frequent clinical seizures without an
interictal return to baseline meet the
Diagnostic Studies
definition of status epilepticus
 Causative metabolic abnormalities:
Prescribing Intravenous Fluids and Electrolytes
electrolytes, calcium, magnesium, glucose,
renal function tests, liver function tests, 1. Assess current fluid status
toxicology screen
 Full blood county  Is the patient dry, wet or just right?
 Prolactin: serum prolactin levels may rise  Review fluid balance charts, urine output and
shortly after generalised tonic-clonic seizures daily weight
and some focal seizures  Review clinical symptoms and signs of fluid
deficit or overload
Fluid Deficit 3.3% glucose containing 40mmol/L of
potassium at 80mL/ hr (1L, 12 hourly)
 Features: thirst, dry mucous membranes,  Remember to consider all sources of fluid
tachycardia and low urine output administration: TPN, NG feeds and drug
 Postural hypotension plus flat neck veins with infusions
or without other evidence of shock indicate
intravascular hypovolaemia Typical daily needs Weight based (lean) Average Adult
Sodium 2mmol/kg 140mmol
 First correct intravascular hypovolaemia: Potassium 1mmol/kg 70mmol
o Rapid replacement with fluids such as Fluid 30-35ml/kg 2L
0.9% sodium chloride or compound 4. Modify in the following situations
sodium lactate or colloids
 Conditions where ADH levels are elevated
o Blood and blood products may be
o Patients with nausea, emesis, pain
indicated
and stress tend to retain water and
o May be necessary to contact ICU
develop hypotonicity. The post-
 Replace estimated extracellular deficit:
operative period is high risk
o Correct with appropriate fluid based
o Fluids with higher sodium
on type of fluid lost and current
concentration administered in
tonicity (serum sodium)
reduced volumes are indicated
o Compound sodium lactate may be
 Smaller patients (weight <50kg)
appropriate
o Proportional reductions are indicated
o If serum sodium is low, avoid glucose
solutions  Reduced left ventricular function
o Administer half required volume over o Increased risk of fluid overload
8 hours and second half over 16 hours o Reduce volume given and monitor
o Frequently reassess during this fluid status more frequently
process  Reduced renal function
o Increased risk of fluid overload and
Fluid Overload hyperkalaemia
o If oliguric, do not use maintenance
 Signs: increased daily weight, raised JVP, potassium
peripheral oedema, pulmonary oedema
o If hypovolaemic, correct any fluid
 Management: minimise sodium and fluid deficit as above
given. Consider diuretic o If euvolaemic, limit the volume given
2. Assess ongoing fluid losses to approximately: urine volume +
other losses + 500mL per day
 Estimate ongoing volume losses including:  Medications that increase potassium
vomiting, diarrhoea, nasogastric draining and o Increased risk of hyperkalaemia.
other losses (ileus) Monitor potassium levels frequently
 These should be added to the volume given o ACE inhibitors and ARBs,
daily spironolactone, eplerenone
 Septic patients
3. Assess maintenance requirements
o Have variably increased fluid
 Requires in unstressed, well individuals differ requirements
from sick hospital patients o Vasopressor support in ICU may be
 A well, unstressed 70kg adult, who is nil by required
mouth, euvolaemic, not septic or post-  Obese
surgical, with normal cardiac and renal  Malnourished patients and extended duration
function and no additional fluid losses who of therapy
have needs met by 0.3% sodium chloride and o Often experience complex and
resistant electrolyte disturbances
  Specific fluid requirements  Maximum concentration = 40mmol/L in
o Patients on dialysis, with burns, sodium chloride 0.9%, peripherally to prevent
transplants, acute neurological phlebitis. If maximum concentrations are
conditions (meningitis, encephalitis, exceeded, must administer through a large
stroke), DKA, HONK, have very specific vein with high blood flow
fluid requirements  Premixed minibags can be given peripherally
o Seek advice but via infusion pump
 Mild hypokalaemia may be treated with oral
Properties of Common Fluids
Type of Fluid Na+ K+ Cl- Glucose supplementation alone
Sodium Chloride 0.9% 154 0 154 0 o Potassium chloride effervescent 1-2
Compound Sodium 129 5 109 0 tabs BD
Lactate
0.3% NaCl + 3.3% glucose 51 0 51 33 o Potassium chloride slow release
5% glucose 0 0 0 50 tablets (span K or slow K) 2 tabs BD
o Potassium chloride 10% oral solution
5. When to Review  If resistant to treatment, check magnesium
and replace if necessary
 Unstable patients need to be reviewed at
 Check for medications which may decrease
least every 2-4 hours. All patients should be
plasma potassium: salbutamol, insulin
reassessed at least daily
 Consider slowing the rate of fluid infusion Hypomagnesaemia
overnight in patients at risk of overload
 Switch to an enteral route (oral, NG) as soon Mild: <0.7 mmol/L
as possible to minimise iatrogenic Severe: < 0.4 mmol/L
complications
 Severe of symptomatic (tremors, weakness,
Electrolyte Disturbances and Replacement cardiac arrhythmias, convulsions) should be
corrected with IV magnesium sulphate
Hypokalaemia  Mild or asymptomatic can be treated with
oral magnesium supplements (magmin) 1-2
Mild: 3.1-3.5 mmol/L
tablets BD. Diarrhoes is a comment side
Moderate: 2.5-3.0 mmol/L
effects
Severe: <2.5mmol/L
Hyponatraemi
 Total body deficit of potassium correlates
poorly with plasma potassium because most is Mild: <135 mmol/L
intracellular Severe: <120 mmol/L
 Plasma levels <3.5mmolL may result in
dysrhythmias  Management requires careful assessment of
 Moderate and severe should be treated with fluid status and biochemical indices including
IV and oral supplementation. These patients plasma glucose and osmolality, and urinary
usually require at least an extra 60-80mmol sodium and osmolality
potassium above maintenance over the next  If hypovolaemic: correction of intravascular
24 hours (100-140mmol in total). Repeat deficit with 0.9% sodium chloride
plasma levels 4-6 hours after commencing  If euvolaemic or hypervolaemic: consider
treatment drugs (SSRI’s, diuretics, anti-epileptics, PPI’s)
 All potassium containing infusions must be or conditions associated with SIADH, or
given via an infusion pump or burette and conditions with reduced effective circulating
maximum rate is 20mmol/hr with pump. If volume (cirrhosis and CCF). Manage with fluid
maximum rate exceeded, cardiac monitoring restriction
and administration through a large vein is  Symptomatic hyponatraemia (drowsiness,
recommended headache, fitting) is an emergency and should
 be managed in intensive care. Hypoertonic  If resistant to treatment, exclude
saline and airway access may be indicated hypomagnesaemia
 In general, increase plasma sodium by no
more than 10mmol/L/day, to prevent Electrolyte solutions are incompatible with blood
permanent neurological injury (central products, other medications and often each other.
pontine myelinosis) from osmotic Seek advice before mixing together in an infusion or
demyelination. 0.9% sodium chloride (not giving simultaneously via the same IV line.
hypertonic saline) is the normal mainstay of IV Hospital Insulin Management
therapy
Insulin Types
Hypophosphataemia
Rapid Novorapid (aspart), Lispro, insulin glulisine
Mild: <0.7 mmol/L Short Actrarpid, Humulin R
Severe: <0.4 mmol/L Intermediate Protaphane (isophane), Humulin NPH
Long/Basal Lantus (insulin glargine), Levemir (insulin
 Phosphate does not normally need detemir)
replacement until less than 0.6mmol/L except
if: alcoholism, alcohol withdrawal, Patients NOT PREVIOUSLY on Routine Insulin
malnutrition, re-feeding syndrome, receiving
1. If not starting an insulin infusion give a stat
TPN, renal hosphate wasting, recovery from
dose of subcutaneous rapid/ short acting
DKA or respiratory failure
insulin shown in table 1
 Consider IV replacement if plasma phosphate
2. Discontinue all oral hypoglycaemia agents,
< 0.4mmol/L
except metformin unless contraindicated
 Oral effervescent phosphate is available.
a. Metformin 2g dose if eGFR >60
Diarrhoea is a common side effect
b. Metformin 1g ½ dose if eGFR 30-60
Hypocalcaemia c. Metformin contraindicated if eGFR
<30
Mild: <2.15mmol/L 3. Order continuing in-hospital intensive insulin
Severe: <2mmol/L or <0.9 mmol/L ionised treatment to prevent recurrent
hyperglycaemia according to dietary intake
 Remember: plasma calcium (even corrected
a. Eating: order basal, mealtime and
for albumin) is an unreliable measure of
supplemental doses (given as a
functional (ionised) calcium
supplement to mealtime insulin only,
 Hypocalaemia often reflects severe body fluid not 6 hourly)
and electrolyte disturbances b. Not- eating: and insulin infusion not
 If patient is symptomatic (seizures, tetany, appropriate, order basal and 6 hourly
positive Chvostek’s or Trousseau’s) or at high supplemental doses. Ensure constant
risk of developing symptomatic rate of glucose provided by either as
hypocalcaemia (post-parathyroidectomy), use IV fluids or enteral feeds
IV replacement
o Calcium gluconate is preferred Initiating Intensive Insulin Treatment in Hospital (>2
o Calcium chloride is very irritating and injects per day. Does not include stand-alone short
should be given via a central line acting insulin sliding scales)
o Do not co-infuse or mix calcium with
phosphate containing preparation  Calculate total daily insulin unit intake. (0.3-
0.4 or 0.5 x weight (kg))
 For oral replacement use
o Effervescent calcium tablets  Separate into bolus (long acting) dose and
o Calcium carbonate tablets total rapid acting doses by dividing by two (or
o Give away from food divide weight by 4)
 Rapid acting doses given at each meal time is
divided by remain total units/ day by the
 number of meals (breakfast, lunch, dinner) (or 8.1-12 1 2 3 4
divide weight by 12) 12.1-16 2 4 6 8
 Lantus (long acting) dose usually given at 16.1-20 3 6 9 12
night just before bed or early morning. >20 4 8 12 16

Table 1 Patients previously on intensive insulin treatment

BGL <50kg 50.1-100 100.1-150 >150kg
8.1-12 1 2 3 4  If hyperglycaemia has occurred within 4 hours
12.1-16 2 4 6 8 after mealtime insulin, increase that mealtime
16.1-20 3 6 9 12 dose the following day by 10%
>20 4 8 12 16  If hyperglycaemia has occurred more than 4
hours after mealtime insulin, increase basal
Patients Previously on Routine Insulin dose by 20%
1. Check: type, time and dose of previously When to use an Insulin Infusion
administered insulin, for missed doses and
BGL record and pattern  Recommended for managing unpredictable
2. Do not give stat dose if hypoglycaemia treated glycaemia if adequate monitoring available
within previous 4 hours. Recheck BGL in  Used correctly, an insulin infusion is safe and
another 4 hours and respond accordingly effective but should be discontinued as soon
3. If not starting an insulin infusion give a stat as medical condition and dietary intake allow
dose of subcut rapid/ short acting insulin as  Generally, patients who are eating normally
calculated from table 2 will not require an insulin infusion
4. Premixed insulin and non-intensive insulin
treatment are generally not optimal for in- Nasogastric Tube
hospital use especially if eating pattern is  Flexible tubes with double or single lumen
variable. Substitute with in-hospital intensive that are passed proximally from the nose
insulin treatment to prevent recurrent distally into the stomach or small bowel
hyperglycaemia
 Dual lumen sump tubes are most commonly
5. Discontinue all oral hypoglycaemic agents
used for gastrointestinal decompression
except metformin unless contraindicated
 Specifically designed, flexible, small diameter
6. For patients previously on intensive insulin
enteral tubes are preferred for feeding
treatment, do not alter insulin types,
unnecessarily- dosage adjustment is usually all Indications
that is required
 Treatment of ileus or bowel obstruction-
Managing patients previously on non-intensive insulin gastrointestinal decompression. It improves
treatment patient comfort, minimizes or prevents
recurrent vomiting, and serves as a means to
 Divide current total daily dose by 2 to
monitor the progress or resolution of these
calculate initial basal dose of long acting
conditions
insulin
 Administration of medications or oral contrast
 If eating, divide current total daily dose by 6
for CT in patients who cannot swallow or who
(half of daily dose, separated into each meal)
are neurologically impaired
to calculate initate mealtime doses of rapid/
 Enteral nutrition- NG and nasoenteric tubes
short acting insulin.
are used to deliver enteral nutrition into the
 Use table 2 to determine initial supplemental
stomach or into the small intestine
doses of rapid acting insulin
(postpyloric)
 Ensure previous insulin orders are ceased
 Stomach lavage- lavage may be needed to
Table 2 remove blood clots to facilitate endoscopy
BGL <26 U 26-50 U 51-100 U >100 U  Risk of aspiration
Contraindications against the nares because pressure ulceration
or necrosis can occur
 Oesophageal stricture due to risk of  The tube can then be secured to the patient’s
perforation gown with a safety pin
 Basilar skull fracture or facial fracture due to
potential for intracranial misplacement Management
 NG tubes should also be avoided in patients
 The proper functioning of the NG tubes
with oesophageal varices because tube
should be routinely checked every four to
placement may trigger variceal bleeding
eight hours by irrigating the tube
 In patients with bleeding diathesis, minimal
 Many patients experience oropharyngeal
trauma to the pharynx, oesophagus or
discomfort, which usually resolves in 24 to 48
stomach from NG tubes can also lead to
hours. Local anaesthetic spray applied to the
severe bleeding
oropharynx may alleviate some of the gag
Confirmation of Placement reflex
 New onset of gagging or respiratory
Radiographic difficulties should raise the concern of
 Always confirm the position of enteral feeding migration into the oropharynx and indicates
tubes, radiographically before formula or the need to re-evaluate the position of the
medications are given tube
 Patients who cannot express their problems  They should be removed when the indication
(children, infants, intubated patients) should for placement no longer exists
always have radiographic confirmation of Complications
tube placement prior to any use of the tube
 The tip of a decompressive NG tube should be  Malposition, coiling or knotting of tubes
positioned into the most dependent portion  More susceptible to reflux of gastric contents
of the stomach which may lead to oesophagitis, oesophageal
stricture, gastrointestinal bleeding or
Clinical Confirmation pulmonary aspiration
 The main lumen is aspirated. If gastric  Tubes can cause gastritis or gastric bleeding
contents are returned, the tube can be tested due to chronic irritation or pressure necrosis
by flushing with 20 to 30 ml of warm water due to suctioning of the gastric mucosa
with a large syringe, and the water  Increased risk of pulmonary complications
immediately suctioned back into the syringe. such as pneumonia and pulmonary abscess,
 If most (~70%) of water can be retried, the tracheal perforation and pneumothorax
tube is likely in the proper position. If an  Nasal alar ulceration or necrosis
insufficient amount of fluid returns, the tube  Perforation
should be readjusted and the test repeated
Guidelines for Anticoagulation using Warfarin
 Auscultating over the epigastrium during air
injection into any tube is not an accurate way 1. Prescribing Principles
to evaluate tube position
 For gastrointestinal decompression,  Consider if the benefits of anticoagulation
confirmation of the tube’s position by clinical outweigh the risks (bleeding) for each patient
means is usually adequate  Ensure pre-treatment INR, platelets and liver
function tests are normal
Tube Fixation  The imitating team must complete target INR,
indication, initial dose and consider duration
 It should be taped securely to the nose, but
of therapy
care should be taken not to push the tube up
  If admitted on warfarin, an INR must be  If risk factors, consider a smaller loading dose
performed within 24 hours of admission, then (2-4mg) and seek senior/ specialist advice
every 2 to 3 days and documented in warfarin  If no risk factors, follow the recommended
section of medication chart. If an INR has not nomogram and monitor INR daily
been performed within 24 hours, warfarin is
no to be administered until and INR is 5. Recommended target INR ranges and minimum
available to guide dosing decisions duration
 Check patient has received education and Indication INR Target Min
warfarin leaflets before discharge. Ask Duration
Valve repairs, bioprosthetic valve 2-3 6 weeks
pharmacist for assistant
post op
DVT/ PE 2-3 3 months
2. Starting Warfarin Therapy AF; Irreversible, clinical hyper- 2-3 Life-long,
coagulable states, mechanical AVR balanced
 Acute DVT or PE: start warfarin on same days with no risk factors against risk
High risk mechanical heart valves; 2.5-3.5 Life-long,
as therapeutic unfractionised or LMW heparin
mechanical MVR; mechanical AVR balanced
and overlap for a minimum of 5 days, until with risk factors against risk
target INR reached for at least 2 consecutive
days *Risk factors: AF, previous VTE, hypercoagulable
 Chronic AF and valve replacements: start states, left ventricular dysfunction or older generation
warfarin alone (may overlap with prophylactic AVR
heraprin)
6. Perioperative Thromboembolism Risk Stratification
 Post-operative patients: restart with their
normal pre-operative maintenance dose- do Low Risk: bridging unlikely required
not re-load
 High loading doses, such as 10mg, should not  Mechanic valve present- discuss with
be used due to an increased in the risk of cardiologist
bleeding  AF and no history of cardiac embolism or
CHADSVASC score 0-4
3 Recommended starting nonogram for patients with  One DVT or PE more than three months ago
no risk factors or increased sensitivity to warfarin  Prior VTE and low risk thrombophilia
 Begin with 5mg if INR <1.4 Moderate to High Risk: consider bridging
 If INR remains < 1.4 at day 4, use 10mg
 Taper dose down if INR within target range  Mechanic valve present- discuss with
 Warfarin takes around 3 days to work cardiologist
 After day 4, dose is based on clinical  Rheumatic AF (mitral valve disease stenosis/
judgement regurgitation)
 AF with history of cardiac embolism or
4. Risk Factors for Increased Sensitivity to Warfarin mechanical heart valve in any position or
CHADSVASC score 5-9
 Age greater than 75 years
 VTE within the past three months or very
 History of bleeding or falls
strong family history
 Baseline INR > 1.4
 High risk thrombophilia: deficiency of protein
 Concomitant drugs affecting warfarin
c, protein S or antithrombin 3; homozygous
metabolism
factor 5leiden mutation, antiphospholipid
 Co-morbidities: hypertension, cerebrovascular
antibody syndrome; more than one laboratory
disease, ischaemic stroke, heart disease, renal
thrombophilic defect (compound
insufficiency, hepatic impairment or low
heterozygotes)
platelets, malignancy
 Two or more arterial or iodipathic venous
 Major surgery within the preceding 10-14
thromboembolic events
days
7. Managing Warfarin therapy during Invasive >1.5, defer surgery or give
Procedures prothrombinex or FFP
o Option 3: urgent surgery
Low Risk  For urgent surgery, check INR
 Before surgery before surgery and give
o Withhold 4 daily doses of warfarin prothrombinex depending on
before surgery initial and target INR
o Night before surgery: if INR greater  For procedures with low risk
than 2, give 3mg vitamin K IV or oral of bleeding, warfarin may not
o Day of surgery need to be ceased
 If INR ≤1.5, surgery can  After surgery
proceed o Recommence warfarin as soon as
 If INR > 1.5, defer surgery or if possible at the previous normal
urgent, give Promthrombinex maintenance dose as long as there is
or fresh frozen lasma no evidence of bleeding- do not
 Employ pre-operative reload
thromboprophylaxis as per o Consider bleeding risk against
hospital policy thrombosis
 After surgery o Start LMWH or UFH 12 to 24 hours
o Start warfarin on the day of surgery at post operatively
the previous normal maintenance o Consider delaying resumption of
dose as long as there is no evidence of therapeutic LMWH for 48 to 72 hours
bleeding after major surgery
o Employ thromboprophyalxis as per o Continue LMWH or UFH for minimum
hospital policy of 5 days and cease 48 hours after
target INR is reached
Moderate to High Risk o In surgery with high risk of bleeding,
consider using prophylactic dose
 Before surgery LMWH or UFH IV only and cease 48
o Option 1: planned surgery hours after target INR is reached
 Without 4 daily doses of
warfarin before surgery 8. Recommendations for reversal of warfarin
 2 to 3 days before surgery:
Clinical Setting Recommedation
when INR is less than 2 INR 3.0 – 4.5 and Reduce or withhold next dose of warfarin
commence treatment dose of NO BLEEDING Resume lower dose of warfarin one INR
LMWH subcut or UFH IV approaches therapeutic range
INR 4.5 – 10 and Cease warfarin.
 If using LMWH, last dose NO BLEEDING Consider reasons for elevated INR and patient
should be given at least 24 factors.
Vitamin K usually not required unless bleeding
hours before surgery risk is high- give vitamin K
 If using URF IV, cease infusion Check INR within 24 hours. Resume lower dose
4 to 6 hours before surgery once INR reaches therapeutic range
INR > 10 and Cease warfarin.
o Option 2: planned surgery with stable NO BLEEDING Given vitamin K PO or IV. If bleeding risk high,
INR in preceding weeks give prothrombinex
Check INR in 12 to 24 hours and continue to
 Night before surgery: if INR is monitor every 1 to 2 days over the following
stable at 2-3 in the 2 to 4 week
weeks preceding surgery, give Resume lower dose of warfarin once INR
approaches therapeutic range
3 mg vitamin K IV or oral INR ≥1.5 with life- Cease warfarin. Give vitamin K IV,
 Day of surgery: if INR ≤1.5, threatening prothrombinex and fresh frozen plasma
bleeding Assess INR frequently until clinically stable
surgery can proceed, if INR INR ≥ 2 with Cease warfarin. Give vitamin K IV and
clinically prothrombinex. If prothrombinext not
significant available, give FFP Main Symptoms in Palliative Care
bleeding (not LT) Assess INR frequently until clinically stable
Any INR with Omit warfarin. Repeat INR the following day Pain
minor bleeding and adjust warfarin dose to maintain INR in
target therapeutic range.
If bleeding risk is high or INR >4.5, consider  Don’t assume a cause-take a detailed history
vitamin K PO or IV and examine to understand the aetiology
 Evaluate severity, nature, functional deficit
9. Potential Drug Interactions and psychological state- depression occurs in
up to 25% of cancer patients
 Whenever starting or stopping a drug,
particularly antibiotics, the INR must be re-  Pain from nerve infiltration or local pressure
checked 48-72 hours after change in therapy may respond better to anitryiptyline or
gabapentin than opioids
 Do no pre-empt a change. Make dose
adjustments only after checking INR at 48-72  Management: explain and plan rehabilitation
hours goals. Aim to modify the pathological process
when possible (radiotherapy, hormones,
 Medications which can increase risk of
chemotherapy, surgery)
bleeding
o Anticoagulants: apixaban, dabigatran,  Effective analgesia is possible in 70-90% of
rivaroxaban, heparin, LMWH patients by adhering to 5 simple guidelines
o Antiplatelet: aspiring, clopidogrel, o By the mouth- give orally wherever
dipyridamole, ticagrelor possible
o Antithrombotic agents: alteplase, o By the clock- give at the fixed intervals
tenecteplase to give continuous relief
o NSAIDs: ibuprofen, ketoprofen, o By the ladder- follow WHO Ladder
naproxen o For the individual- there are no
o Complementary meds: cranberry, fish standard doses for opiates, needs
oil, garlic, ginger, ginkgo, papaya vary
o With attention to detail- inform, set
extract
times carefully, warn of side-effects
Increased Bleeding Decreased Bleeding  Start regular laxatives and anti-emetics with
Amiodarone Dicloxacillin strong opiates
Penicillins (except Infliximab
dicloxacillin) The WHO analgesic Ladder
Doxycycline Phenytoin (long term) Rung 1 Non-opioid Paracetemol, NSAIDs
Most other antibiotics Rifampicin Rung 2 Weak opioid Codeine, Dihydrocodeine,
Tramadol
Antifungals carbemezapine Rung 3 Strong opioid Morphine, Diamorphine,
COX-2 inhibitors Hydromorphone, oxycodone,
Methotrexate fentanyl, pubrenorphine
SSRI and SNRI If one drug fails to relieve pain, move up- do not try
Satins other drugs at the same level. In new severe pain,
Sodium valproate rung 2 may be omitted.
Testosterone/ tamoxifen
Nausea and Vomiting
Palliative Care
 Causes include: chemotherapy constipation,
 Palliative care is the medicine of relieving GI obstruction, drugs, severe pain, cough, oral
symptoms thrush, infection and uraemia
 Though this most often applies in the later  Aim to treat reversible causes e.g. with
stages of malignancy, it does not necessarily laxatives, fluconazole, analgesia or antibiotics
have to  Consider the likely cause and base anti-emetic
 Take time to find out what is troubling a choice on mechanism of nausea and site of
patient and approach problems holistically drug action
  Patients starting strong opioids should be Local Systemic
prescribed a regular antiemetic for the frist Eczema, atophy, urticarial Liver disease
week, then PRN Scabies Uraemia
 Oral agents: cyclizine (antihistamine, Lichen Planus Malignancy (lymphoma)
Dermatitis Herpetiformis Diabetes Mellitus
anticholinergic), domperidone
Spinal cord tumours (rare Drugs (morphine)
(antidopaminergic), metoclopramide (good in
Thyroid disease
gastric stasis), haloperidol (effective in drug or HIV
metabolic induced nausea), ondansetron Iron deficiency Anaemia
(good for chemo/radiotherapy related Polycythemia Rubra Vera
nausea), levomepromazine (broad spectrum, Venepuncture Problem
but can sedate)
 Repeated venepuncture with the attendant
Constipation risk of painful extravasation and pheblitis may
be avoided by insertion of a single or
 Very common side effect with opiates, and multilumen skin-tunnelled catheter (Hickman
better prevented than treated line) into a major central vein
 May be due to ↑ Ca2+ or dehydration  Patients can look after their own lines at
 Use disacodyl at night or combine with a home, and give their own drugs.
stimulant with a softener.  Problems: infection, blockage (flush with
 Macrogols are useful in resistance saline or dilute herapin), axillary, subclavian or
 Try glycerol suppositories or an enema if oral superior vena cava thrombosis/ obstruction
therapy fails and line slippage

Breathlessness The Last Days and Weeks of Life

 Consider fans, air supply and supplementary  Once a decision has been made that patient is
oxygen entering the very final days of their illness,
 Morphine reduces respiratory drive and thus comfort should be the main concern
relieves the sensation of breathlessness.  Thinking about stopping observations,
 Use of relaxation techniques and unnecessary blood tests and medications
benzodiazepines can be useful (such as for long-term prophylaxis)
 Look for pleural or pericardial effusion.  Prescribed PRN subcutaneous end of life
Consider thoracocentesis ± pleurodesis for a drugs before they are needed
significant pleural effusion  Start a syringe driver if any of these are being
given regularly
Mouthcare
 Ensure that a do not attempt resuscitation
 Treat any candida infection or other order has been made and clearly documented
underlying cause (usually by a senior doctor)
 Simple measures such as chewing ice chips,  Personalised end-of-life care plans should be
pineapple chunks (release proteolytic made, which focus on control of symptoms,
enzymes) or gum should be tried comfort and cessation of unnecessary
 Good oral hygiene with mouth washes, interventions
chorhexidine and saliva substitutes such as  Consider whether transfer to a hospice may
biotene oral balance can help be appropriate. If home is a priority, it can be
arranged at very short notice
Pruritus
Syringe Drivers
 Treat causes: try soothing bland emollients,
emollient bath oils, sedative antihistamines at  Allow continuous subcutaneous infusion of
night (chlorphenamine) drugs when the oral route is no longer
 feasible and avoids repeated cannulation  Management of open wounds located in the
attempts. sacral or perineal regions in patients who are
incontinent
Indication Drug
Pain Diamorphine General Medicine Ward Round Checklist
Agitation Midazolam
Nausea and Vomiting Cyclizine/ Haloperidol Strategic Issues
Respiratory Secretions Hyoscine/ Hydrobromide
Bowel Colic Hyoscine/ butylbromide For admission and post take, but may need ongoing
review
As Required End of Life Medications
 Document (in ieMR) goals for care to meet
 Prescribe the following PRN subcutaneous before discharge
medications for all dying patients before they o Medical
are needed, in anticipation of any symptoms o Social
 Also write them up for any patients on syringe o Allied health
drivers who may require breakthrough doses  Infection control, AWS, Right ward?
 Anticipate barriers to discharge and act early
Indication Drug o Home modifications, transport, family
Pain Diamorphine meeting, guardianship, placement
Agitation Midazolam
 Acute resuscitation plan (ARP)
Nausea and Vomiting Haloperidol
Respiratory Secretions Hyoscine/ Hydrobromide  Estimated discharge date
 If subspecialty consult requested
Indwelling Urinary Catheter  Radiology, pathology and allied health
requests appropriately ordered and registered
Indications  Initiate discharge summary early in order to
complete by discharge
 Management of urinary retention with or
 Post discharge follow up plan. Referrals?
without blood outlet obstruction
 Public health interventions- smoking, alcohol,
 Hourly urine output measurement in critically
ill patients (AKI) other drugs, obesity, diet, exercise
 Daily urine output measurement for fluid Practical Issues to Review (each day)
management or diagnostic test
 During surgery to assess fluid status  Observations
(prolonged procedures, large volume fluid  Pathology results
infusion)  Radiology results and ECG
 During and following specific surgeries of the  Medication chart
genitourinary tract or adjacent structures o Necessity of each medication
(urologic, gynaecologic, colorectal) o Dose and frequency review
 Management of haematuria associated with o Antibiotics- appropriate for purpose,
clots route of administration, length of
 Management of immobilised patients course
 Management of patients with neurogenic o Check specialised medications:
bladder insulin, warfarin, prednisolone
 Management of patients with urinary o Analgesia: adequate, appropriate
incontinence following failure of conservative, o Has the medication been given?
behavioural, pharmacologic and surgical  Patient’s cognitive state/ mood and sigh/
therapy hearing function
 Improved patient comfort for end of life care  Patient’s understanding (and priorities) of
their health issues
 Family, careers, guardian informed
 Lines (IVC, IDC): necessity? Site infection?
Duration
 DVT prophylaxis
 IV fluids and electrolytes
 Bowel and bladder function
 Pressure sores