Internal Medicine Notes
2 Slight limitation of physical activity. Ordinary
Chronic Heart Failure
Aetiology
Common Causes
 Chronic heart disease or prior myocardial
infarction
 Essential hypertension via increased afterload
and acceleration of CHD
Less Common Causes
 Non-ischaemic idiopathic dilated
cardiomyopathy- patients tend to be younger,
and at least 30% are familial
Uncommon Causes
 Valvular heart disease, especially mitral and
aortic incompetence
 Non-ischaemic dilated cardiomyopathy
secondary to chronic alcohol misuse
 Inflammatory cardiomyopathy, myocarditis
(viral- enteroviruses, coxsackie B)
 Chronic arrhythmia
 Thyroid dysfunction
 HIV-related cardiomyopathy
 Drug-induced
 Peripartum cardiomyopathy – rare
Symptoms of CHF
 Exertional dyspnoea present in most, initially
with more strenuous exertion, but later
progresses to occur on level walking and
eventually at rest
 Orthopnoea- more likely to be due to CHF but
occur at a later stage
 Paroxysmal nocturnal dyspnoea (PND)- more
likely due to CHF but rare sign
 Dry irritating cough may occur, particularly at
night
 Fatigue and weakness may be prominent
 Dizzy spells or palpitations which may indicate
arrhythmia
Symptom Grading
Class Description
1 No limitations. Ordinary physical activity
does not cause fatigue, dyspnoea, palpitation
physical activity results in fatigue,
palpitation, dyspnoea, angina
3 Marked limitation of physical activity. Less
than ordinary physical activity leads to
symptoms of CHF
4 Symptoms of CHF present at rest. Unable to
carry out any physical activity
Signs of CHF
 Signs of underlying cardiac disease, including
a displaced apex beat, or a murmur which
may indicate underlying valve disease
 Signs of fluid retention, including soft basal
inspiratory crackles which do not clear with
coughing, resting tachypnoea, raised JVP,
ankle and sacral oedema, ascites or tender/
pulsatile hepatomegaly
 Signs of cardiac strain, including tachycardia,
or a third heart sound
 Other abnormal vital signs
Initial Investigations
 ECG for conduction blocks, previous MI, LVH,
AF, sinus tachycardia
 Chest X-ray for cardiomegaly and pulmonary
venous redistribution with upper lobe blood
diversion. Batwing appearance. Does not
exclude diagnosis. Worsening CHF can show
interstitial oedema seen in the perihilar
region, with prominent vascular markings and
small basal pleural effusions obscuring the
costophrenic angle. Kerley B lines, indicative
of lymphatic oedema due to raised left atrial
pressure may be present
 Trans-thoracic Echocardipgrahy for distinction
between systolic and diastolic dysfunction (LV
ejection fraction <40%) while excluding
correctable causes of CHF such as valvular
disease. Single most important investigation
in CHF. Can also gain information regarding LV
thrombus, atrial size, pulmonary systolic
pressure, pericardial disease, ventricular size
 Full blood count for mild anaemia associated
with adverse prognosis or rare cause
 Urea, creatinine and electrolytes for initial
workup and monitored regularly (6 months).
Advance CHF can lead to dilutional
 hyponatreamia, hyperkalaemia, hypokalaemia
(diuretics), hypomagnesia, ↓ GFR and renal
blood flow
 Liver function tests for abnormal liver function
due to congestive hepatomegaly. There may
be a rise in serum bilirubin, particularly in
severe CHF
 Thyroid function test for uncommon causes of
CHF.
 Natriuretic peptides (ANP and NBP) reflect
severity of CHF. Measurement of BNP or N-
teminal proBNP is not recommended as
routine in the diagnosis of CHF. There is no
evidence that BNP offers additional diagnostic
information that is beyond information
provided by a comprehensive echo.
 Stress ECG, stress echocardiography or stress
nuclear study for dyspnoea on exertion
 Spirometry and respiratory function testing to
exclude concomitant smoking related or other
causes of airway limitation. The FEV1 may be
reduced and reversibility demonstrated in
reaction to an elevated pulmonary capillary
wedge pressure
Management
Non Pharmacological Management
 Physical activity and rehabilitation
 Nutrition: lose weight, limit saturated fat, high
fibre diet, maintain nutrition, limit sodium
 Fluid management
o Weight themselves every morning
after going to the toilet
o Limit fluid intake to 1.5L/ day
o Those who suffer from alcohol-related
cardiomyopathy should abstain from
alcohol. Should not exceed the
recommended daily intake
o Excessive caffeine intake may
exacerbate arrhythmia, increase heart
rate and increase blood pressure
 Smoking cessation
 Self-management and education
o Possible side effects of therapy
o Signs of deterioration
o Importance of adherence to therapy
 Psychosocial support
Other Important Issues
 Sleep apnoea occur commonly in patients
o Obstructive sleep apnoea
o Central sleep apnoea
 Vaccination as they are at increased risk of
respiratory infection
o Influenza
o Pneumococcal disease
 Pregnancy and contraception
o CHF increases risk of maternal and
neonatal morbidity and mortality
o Pregnancy and delivery may cause
deterioration in women with
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
Pharmacotherapy Management
Prevention of CHF and treatment asymptomatic LV
systolic Dysfunction
 ACE inhibitor to delay development of
symptomatic CHF
 Beta-blockers- when given in the early post-
MI period, beta-blockers reduce the
subsequent develop of CHF in patients with
persevered ventricular function
 Management and control blood pressure
Treatment of Symptomatic Systolic CHF
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
 Acute fatty liver (pregnancy)/ Non-alcohol
fatty liver disease
 Autoimmune: primary biliary cirrhosis
 Wilson disease
 Budd-chiari syndrome
 HELLP (haemolysis, elevated liver enzymes,
low platelets) syndrome and occasionally
acute fatty liver of pregnancy
 sepsis
Extrahepatic Cholestasis
 Choledocholithiasis (most common cause)
 Malignant obstruction (pancreas, gallbladder,
ampulla or bile duct cancer)
 Primary sclerosing cholangitis with an
extraheptic bile duct stricture
 Chronic pancreatitis with structuring of the
distal bile duct (uncommon)AIDS
cholangiopathy
 If ultrasound suggests obstruction due to a
stone or malignancy, or if the onset of the
cholestasis was acute, and ERCP should be
carried out to confirm diagnosis and facilitate
biliary drainage
 If the cholestasis is chronic or ultrasound
show shows biliary dilation with an apparent
cause or in patients who are at high risk for
ERCP, MRCP or CT should be obtained
 ERCP can then be performed if there is
evidence of an obstructing stone, stricture or
malignancy.
 If both are negative, AMA should be tested for
primary biliary cirrhosis and a biopsy should
be taken if positive to confirm diagnosis
Magnitude of AST and ALT elevations
 Non-alcoholic fatty liver disease: AST and ALT
<4 times upper limit
 Alcoholic Fatty liver disease: AST < 8 times
upper limit, ALT <5 times upper limit
 Acute viral or toxin-related hepatitis with
jaundice: AST and ALT >25 upper limit
 Ischaemic hepatopathy: AST and ALT >50
upper limit of normal
 Chronic hepatitis B infection: levels vary; the
AST and ALT may be normal, although most
patients have mild to moderate elevations
(approx. twice the upper limit of normal); with
exacerbations, levels are >10 upper limit
 Chronic hepatitis C infection: wide variability,
typically normal to less than twice the upper
limit, rarely more than 10 times the upper
limit
 AST and ALT are raised in malignant
infiltration as well
Acute Liver Failure
 Acute hepatocellular injury with LFT’s typically
more than 10 times the upper limit
 Hepatic encephalopathy
 Prolonged prothrombin time
Chronic Liver Disease
Causes of Chronic Liver Disease
A specific Aetiology can be determined in 80 to 90
percent of patients with cirrhosis. Most causes are
due to chronic liver injury or imflammation
Common Causes in Developed Countries
 Viral hepatitis: B and C
 Alcoholic liver disease
 Haemachromatosis
 Non-alcoholic fatty liver disease
Less Common Causes
 Autoimmune Hepatitis
 Drugs: methotrexate, amiodarone, herbal,
isoniazid
 Alpha-1 antitrypsin deficiency
 Wilson’s Disease
 Right sided heart failure
 Infection (brucellosis, syphilis, schistosomiasis,
echinococcosis)
 Hereditary haemorrhagic telangiectasia
 NASH cirrhosis
 Coeliac disease
 Granulomatous liver disease
 Polycystic liver disease
Other Causes of Jaundice: Biliary Obstruction
 Bile duct stones
 Bile duct stricture
o Pancreatic cancer
o Primary sclerosing cholangitis
 o Acute/ chronic pancreatitis
o Cholangiocarcinoma
o Ampullary lesion
 Primary and secondary biliary cirrhosis
Presentation of Patients with Liver Disease
 May have no symptoms and be well-
incidental/ compensated liver
 Abnormal liver enzymes
 Non-specific: anorexia, weight loss, weakness,
fatigue)
 Hepatic decompensation: jaundice, pruritus,
signs of upper gastrointestinal bleeding,
ascites, confusion due to hepatic
encephalopathy
 Upper gastrointestinal bleeding:
haematemesis, melena, haematochezia)
Stigmata of Liver Disease
 Leukonychia, clubbing
 Duypetron’s Contracture
 Palmar erythema
 Asterixis/ hepatic encephalopathy
(decompensated liver)
 Spider naevi
 Bruising
 Cachexia, muscle wasting
 Hepatic fetor
 Gynaecomastia
 Ascites (decompensated liver)
 Splenomegaly
 Caput medusa
 Testicular atrophy and loss of libido-
predominant in alcohol cirrhosis and
haemachromatosis
 Cruveilhier-Baumgarten murmur is a venous
hum that may be auscultated in patients with
portal hypertension. It results from collateral
connections between the portal system and
the remnant of the umbilical vein. It is best
appreciated when stethoscope is placed over
the epigastrium
Investigations
Liver Function Tests
 AST and ALT are usually moderately elevated
in patients with cirrhosis. (AST > ALT)
 ALP is usually elevated in cirrhosis but is less
than two to three times the upper normal
limit
 GGT levels correlate reasonably well with ALP
but are nonspecific. Levels of GGT are much
higher in chronic liver disease from alcohol
than other causes
 Bilirubin levels may be normal in well-
compensated, however, they rise as the
cirrhosis progresses
 Albumin levels fall as the synthetic function of
the liver declines with worsening cirrhosis.
Hypoalbuminaemia is not specific for liver and
can be seen in heart failure, nephrotic
syndrome, protein losing enteropathy,
malnutrition
 Prothrombin time reflects the degree of
hepatic synthetic dysfunction
Other Important Tests
 FBC: anaemia (macrocytic) and
thrombocytopenia (splenomegaly) can occur
 U/E: hyponatraemia due to an inability to
excrete free water resulting primarily from
high levels of anti-diuretic hormone secretion
 Coagulation profile: INR and prothrombin
time
 Globulins tend to be increased in patients
with cirrhosis and may be secondary to
shunting of bacterial antigens in portal venous
blood away from the liver to lymphoid tissue.
Radiology
 Ultrasound liver is routinely used. In advanced
cirrhosis, liver may appear small and nodular
with increased echogenicity. May be used in
screening for hepatocellular carcinoma and
portal hypertension and useful for detecting
splenomegaly, ascites and portal vein
thrombosis
 CT not routinely used for cirrhosis as it
provides similar information to ultrasound.
Ultrasound- 6 things to look for
 Bile duct dilatation
 Gall bladder/ bile duct stones
 Echogenicity/ texture of liver
 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
diurnal sleep pattern, asterixis, hyperactive
deep tendon reflexes
 Hepatocellular carcinoma
 Portal vein thrombosis: can contribute to
cirrhosis and related to unbalanced
haemostasis and slowing of portal flow
Chronic Kidney Disease
Defined as an estimated or measured glomerular
filtration rate <60mL/min/1.73m2 that is present for ≥
3 months with or without evidence of kidney damage.
OR
Evidence of kidney damage with or without decreased
GFR that is present for ≥ 3 months as evidenced by
the following, irrespective of the underlying cause:
Early Detection of CKD
 Albuminuria
 Haematuria after exclusion of urological
causes
 Structural abnormalities (on kidney imaging)
 Pathological abnormalities (renal biopsy)
Causes
 Diabetic kidney disease
 Glomerulonephritis
 Hypertensive vascular disease
 Polycystic kidney disease
Diagnostic Evaluation Tests for CKD
Clinical Presentation
 Hypertension
 Pruritus due to phosphate and urea
 Nocturia due to the kidney’s inability to
concentrate urine. Followed by oligouria.
Anuria is never observed with CKD and always
indicates acute kidney injury. Anuria occurs as
a result of severe/ prolonged shock, bilateral
urinary tract obstruction, pregnancy-related
cortical necrosis, or bilateral renal arterial
obstruction (dissecting aortic aneurysm)
 Haematuria
 Dyspnoea
 Lethargy
 Nausea/ vomiting due to uraemia
 Malaise, fatigue
 Anorexia
 Oedema due to fluid overload
 Joint point, bone pain due to osteodystrophy
 Restless legs
 Sallow skin
 Uraemic frost or fetor
 Half and half nails
 Increased amounts of albumin in the urine
correlate directly with an increased rate of
progression to ESKD, and increased
cardiovascular risk
 eGFR correlates well with complications of
CKD and increased risk of adverse outcomes
 Early intervention with blood pressure
reduction and use of ACE inhibitors or ARBs
can reduce progression and cardiovascular
risk by up to 50% and may also improve
quality of life
 50% or more of kidney function can be lost
before the serum creatinine rises above upper
limit of normal
 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
excretion)
 Urinalysis shows SG 1.010 (isothenuria) due to
inability to concentrate urine. Broad waxy
casts and proteinuria on PCR
 Fasting lipids and glucose
 Urine microscopy for dysmorphic red cells,
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
people with albuminuria
 Mainly caused by fluid overload
Mineral and Bone Disorder (osteodystrophy)
 Changes in metabolism of calcium, phosphate,
parathyroid hormone and vitamin D typically
start once GFR <60
 This leads to ↑ phosphate + parathyroid
hormone and ↓ calcium + vitamin D levels
(secondary hyperparathyroidism)
 These changes are associated with an
increased risk of fracture and also increased
cardiovascular mortality, perhaps mediated
by accelerated vascular calcification
 Management
o Use phosphate binders, which bind to
dietary phosphate.
o If phosphate is controlled, calcium will
typically remain in normal range.
o Cholecalciferol that comes from sun
exposure can be given as dietary
supplement. Calcitriol can also be
given in CKD
o Cinacalcet, is a calcimimetic agent
that can be used to treat
hyperparathyroidism for individuals
on dialysis
Uraemia
 Syndrome seen in stage 4 or 5 CKD, and is
caused by the accumulation of the breakdown
products of protein metabolism
 Uraemia-related signs may develop when the
eGFR is between 10-15mL but usually are not
disabling until the eGFR is <10mL
 Symptoms include: anorexia, nausea,
vomiting, lethargy, confusion, muscle
twitiching, convulsions and coma
 Urea accumulation can lead to pericarditis,
pleuritis and encephalopathy
 Management: dialysis should be commenced
as soon as uraemic symptoms develop
Medications usage in CKD
Medications which may need to be reduced or ceased
 Antivirals
 Benzodiazepines
 Colchicine
 Digoxin
 Glicazide
 Insulin
 Lithium
 Metformin
 Gliptins
 Spironolactone
Drugs that can adversely affect kidney function in CKD
 Aminoglycosides
 Calcineurin inhibitors
 Lithium
 NSAIDs and COX-2 inhibitors (beware the
triple whammy)
 Radiographic contrast agents
Other Practice Tips
 ACE inhibitors and ARBS can safely be
prescribed at all stages of CKD and should not
be deliberately avoided just because GFR is
reduced
 Combination of ACE inhibitor (or ARB),
diuretic and NSAID or COX-2 inhibitor (except
low dose aspirin) can result in acute kidney
injury, especially if volume-depleted or CKD
present
 Frusemide can be used safely for
management of fluid overload in all stages of
CKD
 Both non-loop diuretics (thiazides) are
effective in all stages of CKD as adjunct
antihypertensive therapy
Indications for Dialysis
Acute Kidney Injury (AEIOU)
 Acidosis (metabolic) with pH <7.1
 Electrolyte imbalance (hyperkalaemia) >6.5 or
rapidly rising potassium levels
 Intoxication/ ingestion of certain alcohol and
drugs
 Overload (refractory fluid)
 Uraemia signs such as pericarditis,
neuropathy, encephalopathy, serositis,
pleuritis
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
glomeruli. May be anuric if patient is shocked
or bilateral vascular occlusion as in dissecting
aortic aneurysm
 Urinalysis unremarkable- urine normal or near
normal (no casts/ ↑ cells)
 ↓ urinary sodium due to renin-aldosterone
system activation therefore ↓ FeNa
 ↑ Urine osmolality >500mOsm
Intrinsic Renal 10-15% of causes
History and Presentation
 Presentation depends on cause
 Commonest cause is acute tubular necrosis
following a pre-renal situation, in which blood
supply to tubules is inadequate→ tubular
death
 Tubular blood supply is via efferent arteriole
Causes: GITV
 Glomerular Lesions: glomerulonephritis
o IgA nephropathy
o SLE
o Post infectious: URTI, GIT infection
o Bacterial endocarditis
 Tubular Lesions: Toxins
o Ischaemia (any untreated pre-renal)
o Nephrotoxins
 Myoglobin/ haemoglobin
 Calcium
 Uric acid
 Bence Jones proteins
(immuno light chains)
 Aminoglycoside
 Contrast material
 Interstitial Lesions: Infections
o Drugs: NSAIDs/ antibiotics
o Pyelonephritis
o Autoimmune
o Infiltrations: lymphoma/ leukaemia
 Microvascular Lesions: vasculitis
o Vasculitis
o Malignant hypertension
o Thrombotic microangiopathies (TTP/
HUS)
o Thrombo/ atheroembolism
Investigations
 ↓ Urea/creatinine ration <40
 May be oliguria (50-400ml/day) or urine
volume may be normal (<2.4L/day); the
oliguric phase lasts on average 10-14 days and
may be followed by a short diuretic phase,
and then gradual return to normal urine
output
 Haematuria and red cell casts in
glomerulonephritis/ vasculitis
 Epithelial casts (muddy brown casts) and
granular casts in ATN
 Eosinophiluria in acute interstitial nephritis
 Pyuria and white cell casts in infection
(pyelonephritis)
 ↑ Urinary sodium and ↑ FeNa
 ↓ Urinary osmolality < 350mOsm
Post Renal 5-10% of Causes
History and Presentation
 May be a history of difficulty in passing urine:
hesitancy, double voiding, dribbling, nocturia,
weak stream
 Obstruction may lead to anuria
 May be enlarged kidneys on ultrasound if
bilateral ureteral obstruction
 An enlarged bladder may be palpable if a
urethral obstruction is present
Causes
 Urinary calculi
 Benign prostatic hyperplasia
 Prostate cancer
 Bladder cancer
 Tumour compression (lymphoma)
 Urethral stricture
 Retroperitoneal fibrosis
Investigations
 ↑ Urea/ creatinine ratio >100
 Anuria (<50ml/day) occurs most commonly
 Urine normal or near normal. Possibly ↑
white cells (infection) or red cells (trauma
from calculi)
 USS may show hydronephrosis due to
obstruction in the urinary tract
 90% of renal calculi are visible on abdominal
X-ray due to calcium contents
Blood Tests (common to all types of AKI)
 ↑ Urea: daily of 3.5-5.0mmol/L/day
 ↑ Creatinine: daily of 90-180μmol/L/day
 Sodium: normal/ ↓ if fluid overload present
 ↑ Potassium: ↓ filtration and urinary
excretion
 ↑ Phosphate: ↓ filtration and urinary
excretion and 2° hyperparathyroidism
 ↓ Calcium or normal: ↓ active vitamin d,
secondary hyperparathyroidism may
compensate calcium levels to normal
 ↓ Bicarbonate: metabolic acidosis (kidney
unable to excrete H+ ions)
 FBC: normocytic anaemia (↓ EPO, uraemic
toxins)
Nephrotic Syndrome
 Proteinuria of ≥ 3g/day or PCR >300
 Hypoalbuminaemia
 Oedema
 Hyperlipidaemia (↑ cholesterol and
triglycerides)
Causes: damage to glomerulus or foot process
 *Glomerulonephritis: minimal change disease,
focal segmental glomerulosclerosis,
membranous glomerulonephritis
 Systemic diseases: *diabetes, *amyloidosis,
SLE, sarcoidosis, vasculitis immunologica
disease (polyarteritis nodosa)
 Infections:
o Bacterial: streptococcal, syphilis, SBE)
o Viral: hepatitis, HIV, infectious
mononucleosis, CMV)
o Parasitic: malaria, toxoplasmosis,
schistosomiasis, filariasis)
 Drugs: gold, mercury, NSAIDs, lithium, heroin
 Neoplasm: Hodgkin’s disease, solid tumours
 Hereditary: Alport’s syndrome, Sickle cell
anaemia, familial nephrotic syndrome
 Other: *pregnancy (pre-eclamptic toxaemia),
massive obesity, renal artery stenosis,
transplant rejection
Consequences
Proteinuria: frothy urine
 Damage glomerular basement membrane
results initially in leakage of albumin into
tubules
 As condition progresses, higher molecular
weight proteins are lost and losses can be
massive
Hypercoagulable State: ↑ risk of thromboembolism
 Loss of urokinase and anti-thrombin 3 (ATT) in
urine and ↑ levels of factor 8, fibrinogen and
platelets in the blood
 Predisposed to DVT, PE, and renal vein
thrombosis
Hypogammaglobulinaemia
 These patients are prone to infection, as they
lose immunoglobulins in the urine
Oedema
 Often the presenting feature and is due to
part of ↓ oncotic pressure due to
hypoproteinaemia
 Some patients are resistant to the effects of
atrial natriuretic peptide and reabsorb
inappropriate amounts of sodium and water
and may become oedematous even when
albumin is not very low→ pericardial effusion,
ascites, pleural effusion
Hyperlipidaemia
 ↑ both triglycercides and cholesterol, mainly
due to ↑ LDL from linked synthesis of
albumin in the liver
 ↓ LCAT in liver
 ↑ Lp(a) contributes to hyperlipidaemia
Electrolytes
Sodium
Hypernatraemia
→ Normal plasma osmolality = 275 – 295 mmol/L
 ↑ Na: Conn’s Syndrome
 ↓ H20: Diabetes Inspidus, dehydration
Hyponatraemia
→ 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
oxytocin
Transient Ischaemic Attack
The aim of assessment of a patient with suspected
stroke or TIA is to confirm diagnosis, identify and treat
the cause, and guide early rehabilitation and relevant
early secondary prevention to prevent complications
or stroke reoccurrence. Appropriate diagnosis and
immediate referral to a stroke team is vital given
advances in hyper-acute treatments
Definition
 Rapidly developed clinical signs of focal or
global disturbance of cerebral function lasting
less than 24 hours, with no apparent non-
vascular cause
 Revised definition: brief episode of
neurological dysfunction caused by a focal
disturbance of brain or retinal ischemia, with
clinical symptoms lasting less than1 hour, and
without evidence of infarction
Assessment
 As with stroke, diagnosis is based on careful
clinical history and examination and it is vital
to elicit the onset and nature of symptoms,
and to identify treatable causes that can
reduce the risk of future events.
 Assessment Tools such as ROSIER or National
Institutes Health Stroke Scale (NIHSS)
 Early (within 24 hours) carotid investigations
should be routine for patients with suspected
anterior circulation TIA’s. Where symptomatic
carotid stenosis is found, early (within 2
weeks) carotid endarterectomy significantly
reduces risk of subsequent stroke
 Brain imaging should be conducted. The
presence of new brain CT changes within 48
hours after TIA was found to predict stroke
risk. As with ischemic stroke, CT is useful to
exclude conditions that could mimic TIA such
as subdural haematoma or brain tumour. CT
has a high specificity but low sensitivity.
 MRI with diffusion-weighted imaging is
imaging strategy of choice for patients with
suspected TIA with studies detecting ischemic
changes signifying infarction in 16-67% of
those with TIA and a positive MRI has
increased risk of subsequent stroke.
 Measurement of D-dimer or CRP does not
improve accuracy of clinical or imaging
assessment but lipoprotein-associated
phospholipase A2 levels may provide useful
information
Prognosis
 ABCDD score used to determine risk of
developing a subsequent stroke post TIA
 Maximum score of 7, where there is an 8%
chance of developing a stroke in the next 2
days
 A cut-off score of 4 has been suggested to
differentiate between high and low risk. Score
of 4-5 is 4% risk and 0-3 is 1% risk
 Does not consider AF as a risk factor
 ECG should be conducted routinely to screen
for AF. A new diagnosis of AF or non-
therapeutic INR levels would indicate a
patient is at high risk and further rapid
investigations and management is required
Features
A Age ≥ 60 years (1)
B BP ≥ 140mmHg and/ or 90mmHg Diastolic (1)
C Clinical Features: unilateral weakness (2), speech
impairment without weakness (1)
D Duration: >60 mins (2), 10-59 mins (1)
D Diabetes (1)
Stroke
Aetiology
Intracerebral Haemorrhage: usually derived from
arterioles/ smaller arteries
 Hypertension (number 1)
 Trauma
 Bleeding tendency
 Amyloid
 Illicit drugs (cocaine)
 Tumours
 Aneurysm
 Vasculitis
Ischaemia
Thrombotic: large vessel disease
 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
eye deviation and complete
hemiplegia
o Only minor stroke deficit which is
rapidly improving
o Seizure observed or known to have
occurred at onset of stroke
o Hypertension ≥185/110
o Presentation suggestive of SAH
o INR > 1.5
o Thrombocytopenia
o Hypo < 2.8 or hyper >22.0 glycaemia
o Presumed septic emboli
 Commencement of aspirin for patients who
have received thrombolysis should be delayed
for 24 hours
Neurointervention
 Intra-arterial thrombolysis within six hours
can be used in carefully selected patients
 Insufficient evidence to recommend the use
of mechanical clot removal in routine practice
Antithrombotic Therapy
 Aspirin orally or via a nasogastric tube or
suppository should be given as soon as
possible after the onset of stroke symptoms
(within 48 hours) if CT/ MRI exclude
haemorrhage
 Must be given after 24 hours if had
thrombolysis
 The first dose should be at least 150-300mg
and dosage can be reduced to 100mg daily
Surgery for Ischaemic Stroke and management of
cerebral oedema
 Selected patients (18-60 years, where surgery
can occur within 48 hours of symptom onset)
and with large middle cerebral artery
infarction should be urgently referred to a
neurosurgeon for consideration of
decompressive hemicraniectomy
 Corticosteroids are NOT recommended for
management of patients with brain oeema
and raised intra-cranial pressure
Intracerebral Haemorrhage Management
 Patients who are receiving anticoagulation
therapy prior to the haemorrhagic stroke and
who have elevated INR, therapy to reverse
anticoagulation should be initiated rapidly
(vitamin K or prothrombin complex
concentrate)
 Surgery for supratentorial haemorrhage can
be considered in carefully selected patients
within 72 hours.
 Surgical evacuation may be undertaken for
cerebellar hemisphere haematomas >3cm
diameter in selected patients
 Contact neurosurgeon
Pyrexia Management
 Associated with poorer outcomes after stroke
and mostly due to chest or urinary infections
 Paracetamol and physical cooling have been
found to be effective
 Antibiotics for pneumonia and UTI
VTE Management
 Subcutaneous LMW heparin for prevention of
DVT
 Graded compression stockings for DVT
 Early mobilisation with (multidisciplinary team
within 48 hours)
o Physiotherapist
o Occupational therapist
o Speech pathologist
o Rehabilitation services
Seizure Management
 Reported incidence of post-stroke seizures
varies ranging from 2-33% for early seizures
(<7 days) and 3-67% for late seizures (>7 days)
 People with severe stroke, haemorrhagic
stroke and/ or a stroke involving the cerebral
cortex are at increased risk
 Anti-convulsant medication should be used
for people with recurrent seizures after stroke
Secondary Prevention Post Stroke
Lifestyle Modification
 Stopping smoking: nicotine replacement
therapy, buproprion or nortriptyline therapy,
varenicline, behavioural therapyimproving
 diet: a diet low in fat and sodium but high in
fruit and vegetables
 Increasing regular exercise
 Avoiding excessive alcohol (≤2 SD/ day)
Adherence to Pharmacotherapy
 Reminders to promote adherence to anti-
hypertensives, statins, antiplatelet drugs or
warfarin
 Reminders, self-monitoring, reinforcement,
counselling, family therapy, telephone follow
up, supportive care and dose administration
aids
Blood Pressure Lowering
 All stroke and TIA patients, whether
normotensive or hypertensive should receive
blood pressure lowering therapy, unless
contraindicated by symptomatic hypotension
 New BP lowering therapy, should be
commenced before discharge for those with
stroke or TIA
Anti-platelet Therapy
 Long-term antiplatelet therapy should be
prescribed to all people with ischaemic stroke
or TIA who are not prescribed anticoagulant
therapy
 Low-dose aspirin and modified release
dipyridamole or clopidogrel alone should be
prescribed to all people with ischaemic stroke
or TIA
 Combination of aspirin plus clopidogrel is NOT
recommended for secondary prevention in
people who do not have acute coronary
disease or recent coronary stent
Anticoagulation Therapy
 Anticoagulation therapy for secondary
prevention for people with ischaemic stroke
or TIA from presumed arterial origin should
not be routinely used
 Anticoagulation therapy should be used long-
term for those with AF or cardio-embolic
stroke
 In patients with TIA, anticoagulation therapy
should begin once CT or MRI has excluded
intracranial haemorrhage as the cause of the
current event
Cholesterol lowering Therapy
 Higher cholesterol levels are associated with
higher risk of ischaemic stroke but a lower risk
of haemorrhagic stroke
 Therapy with a statin should be used for all
patients with ischaemic stroke or TIA
 Should not be used routinely for
haemorrhagic stroke
Carotid Surgery
 Performed by carotid doppler ultrasound and
using NASCET criteria
 Carotid endarterectomy should be
undertaken in patients with non-disabling
carotid artery territory ischaemic stroke or TIA
with ipsilateral carotid stenosis measured at
70-99% or those with 50-69% with symptoms
 Carotid endarterectomy is NOT recommended
for those with symptomatic stenosis < 50% or
asymptomatic stenosis <60%
 Carotid stenting should not routinely be
undertaken with carotid stenosis
Diabetes Management
 Diabetes and glucose intolerance post stroke
have been found to be independent risk
factors for subsequent strokes
 Patients with glucose intolerance or diabetes
should be managed in line with national
diabetes guidelines
Oral Contraceptive or Hormone Replacement Therapy
 The decision whether to start or continue oral
contraception in women of child-bearing age
with a history of stroke should be discussed
with the individual patient based on overall
assessment of risk and benefit. Non-hormonal
methods of contraception should be
considered
 Following a stroke event, HRT should be
stopped. The decision whether to start or
continue in patients should be discussed with
the individual and based on an overall
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

 All patients admitted to hospital should be
asked if they intend to drive again
 Any patient who does wish to drive should be
given information about driving and be
assessed for fitness to return to driving using
national guidelines (assessing fitness to drive)
 Patients should be informed that they are
required to report their condition to driver
license authority and their car insurance
company
 Stroke survivors should not return to driving
for at least one month post event. A follow-up
assessment should be conducted prior to
driving.
heavy or crushing, lasting >20 mins,
unrelieved by GTN or rest
 Associated with nausea, sweatiness,
dyspnoea, palpitations
 Can radiate to left arm, neck or jaw
 May present without chest pain (silent infarct)
in elderly patients or diabetics. In such
patients, presentation may include: syncope,
pulmonary oedema, epigastric pain and
vomiting, post-operative hypotension or
oliguria, acute confusional state, stroke and
diabetic hyperglycaemic states
Signs
  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

 If these targets cannot be reached, fibrinolysis
should be given within 30 mins of arrival in
hospital
 In patients presenting longer than 12 hours
after onset of symptoms, myocardial
infarction may already be complete, but
reperfusion should be considered if there are
signs of continuing ischaemia
 All patients with acute MI should be
considered for admission to a coronary care
unit for monitoring and expert care
Fibrinolytic Therapy
 Indicated if there is prolonged ischaemic chest
paint that has begun within the previous 12
hours, in the presence of significant ST
segment elevation or left bundle branch block
that is presumed new
 The following drugs are used
o Alteplasase
o Reteplase
o Tenecteplase
 Adjuvant anticoagulation therapy for
fibrinolysis
o Enoxaparin or unfractionated heparin
 Contraindications
o Active bleeding or bleeding diathesis
o Significant closed head or facial
trauma within 3 months
o Suspected aortic dissection
o Any prior intracranial haemorrhage
o Ischaemic stroke within 3 months
o Known structural cerebral vascular
lesion
o Known malignant intracranial
neoplasm
 Occasionally bleeding may occur following
treatment and can be reversed:
o Heparin: protamine
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
contraindications with aspirin daily PLUS
clopidogrel daily (unless CABG likely)
 Beta-blockers as they offer prognostic benefit
following myocardial infarction and should be
started during hospital admission. Should not
be started in those with decompensated heart
failure, heart block or significant bradycardia.
Use atenolol daily or metoprolol twice daily
 ACE inhibitors improve outcome after
myocardial infarction. Start ACEI therapy
within 24-48 hours of MI
 Statin therapy has been shown to reduce
premature death, myocardial infarction and
other cardiovascular events
 Prophylaxis against thromboembolism until
fully mobile and should be continued if
patient suffered a large myocardial infarction
to prevent emboli from left ventricular mural
thrombus in ventricular aneurysms
 Calcium channel blockers should be reserved
for those who have contraindications to beta
blockers
 Address modifiable risk factors
 Assess LV function in all patients post MI
 Refer for structured cardiac rehabilitation
programme
 Review at 5 weeks post MI to review
symptoms and consider coronary angiography
 Review at 3 months: check fasting lipids
Management of NSTEMI
High Risk
Those who present with symptoms consistent with
ACS and any of the following:
 Repetitive or prolonged (>10 mins) ongoing
chest pain or discomfort
 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
 They can be reclassified depending on results
into high or low risk
Cardiac Arrest or Cardiogenic Shock
 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
Bradycardias or Heart Block
 Sinus bradycardia: treat with atropine
 1st degree AV block common in inferior MI,
observe closely as they can develop higher
degrees of heart block
 Mobitz Type 1: does not require pacing
 Mobitz Type 2: high risk of sudden complete
AV block and should be paced
 3rd degree AV block: insert pacemarker
Tachyarrhythmias
 Hypokalaemia, hypoxia and acidosis all
predispose to arrhythmias and should be
corrected
 AF or flutter, if compromised: DC
cardioversion or control rate with digoxin ±
Beta blocker
 Atrial flutter or intermittent AF, try
amiodarone or sotalol
 Frequent PVC’s common after acute MI and
do not usually result in VF
 Sustained VT if compromised give DC shock, if
stable treat with amiodarone
 Ventricular fibrillation: 80% occurs within 12
hours. If occurs >48 hours, usually indicates
pump failure or cardiogenic shock. DC shock
 Consider implantable cardiac defibrillator if
ejection fraction <35% and VT
Right Ventricular Failure
 Life-threatening and may accompany inferior
MI
 Clinical signs: right heart failure with signs of
low cardiac output without pulmonary
congestion
 Gentle IV fluid challenge: sodium chloride
200mL
 If BP remains low, give inotropes
Pericarditis
 Central chest pain, relived by sitting forwards
 ECG: PR interval depression, saddle shapped
ST elevation
 Treatment: NSAIDs and echo to check for
effusion
Systemic embolism
 May arise from LV mural thrombosis due to
ventricular aneurysm
 After larger anterior MI, consider
anticoagulation with warfarin for 3 months
Cardiac Tamponade
 Beck triad: (muffled heart sounds,
hypotension, distended neck veins), ↑ JVP,
pulsus paradoxus
 Diagnosis made via echo. ECG should
electrical alternas
 Treatment: pericardial aspiration, surgery
Mitral Regurgitation
 Due to papillary muscle dysfunction (mild) or
muscle rupture (severe)
 Presents with pulmonary oedema, pansystolic
murmur
 Treat LVF (frusemide, O2 and nitrates) and
consider valve replacement
Ventricular Septal Defect
 Presents with pansystolic murmur, ↑ JVP,
cardiac failure
 Diagnosis with Echo
 Treatment: surgery. 50% mortality in first
week
Dressler’s Syndrome
 Recurrent pericarditis, pleural effusions, fever,
anaemia and raised ESR 1-3 weeks post MI
 Treatment: NSAID’s, steroids if severe
Left Ventricular Aneurysm
 This occurs late (4-6 weeks post MI) and
presents with LVF, angina, recurrent VT or
systemic embolism
 ECG: persistent ST segment elevation
 Treatment: anticoagulation, consider excision
DVT and PE
 Prophylactically heparinised (enoxaparin) until
fully mobile
Acute Cardiogenic Pulmonary Oedema
  Medical emergency that requires urgent
treatment in hospital
 Patients which chronic heart failure should be
counselled about the earliest manifestations
of pulmonary oedema:
o Increasing breathlessness
o PND and orthopnoea
o Cough
 Differentials for acute breathlessness
o Acute or chronic COPD
o Asthma
o Pneumonia (can precipitate
pulmonary oedema)
 Prevention of an acute attack usually requires
adjustment to fluid intake, increased
frusemide and modification of other
medication
 High risk groups include older patients with
elevated blood pressure
 Symptoms: rapid onset of severe
dyspnoea,often first occuring at night.
 Signs: tachypnoea, tachycardia and poor
peripheral perfusion (ashen colour, sweaty,
cool peripheral and decreased capillary refill
time), agitation and restlessness and
widespread lung crackles
 clinical features stem from two major
pathophysiological processes, intra-alveolar
fluid accumulation and extreme sympathetic
nervous systemic activation
Precipitating or Exacerbating Factors
 Lack of adherence to treatment, particularly
diuretics
 Dietary lapse (excessive fluid or salt or alcohol
intake)
 Fluid overload
 Tachyarrhtyhimas: AF, atrial flutter or atrial
tachycardia
 Bradyarrhythmias: sinus bradycardia, heart
block
 Myocardial ischaemia or infarction
 Infection: bronchopneumonia, urinary tract
infection, endocarditis
 Pulmonary embolism or thrombosis
 Anaemia
 drug therapy: negatively inotropic drugs
(verapamil, diltiazem), salt-retaining drugs
(corticosteroids, NSAIDs, COX-2 inhibitors),
thiazolidinediones (glitazones)
Management
 Reassured that their condition can be treated
quickly and should be managed sitting upright
as possible
 Oxygen 15L/ minute via mask fitted with
reservoir bag to maximise inspired oxygen
delivery
 Frusemide 20-80 mg IV or IM, reapeated 20
minutes later if necessary, followed by regular
(mane) PO frusemide
PLUS if systolic pressure above 100mmHg
 Glyceryl trinitate (GTN) spray 400 micrograms
sub-lingually, repeated dose every 5 minutes
OR GTN tablet sublingually
In Emergency Department
 Continuous positive airway pressure
ventilation (CPAP), commencing with 10cm of
water pressure PLUS
 GTN IV infusion
 Insert an indwelling catheter to monitor urine
output
 Morphine IV which can be used if patient has
acute anxiety or distress
 If pulmonary oedema is not responding to the
above measures, consider adding dubutamine
or milrinone
Atrial Fibrillation
 Atrial fibrillation usually presents with an
irregularly irregular ventricular rate of around
160 to 180 beats per minute
 Most common arrhythmia
Aetiology : PIRATE SHIV
 Pulmonary Embolism
 Ischaemic Heart Disease
 Rheumatic Heart Disease
 Alcohol Intoxication
 Thyrotoxicosis
 Endocarditis
 Sleep Apnoea, surgery
 Hypertension
  Infection
 Valvular Diseases (MR and MS and TS most
common)
 Myocarditis, pericarditis
 Recent myocardial infarction
History an Examination
 A description of symptoms: onset or date of
discovery, the frequency and duration,
severity and qualitative characteristics
 Typical symptoms: palpitations, tachycardia,
fatigue, weakness, dizziness, light
headedness, reduced exercise capacity,
increased urination, mild dyspnoea
 More severe symptoms: dyspnoea at rest,
angina, presyncope, or infrequently syncope
ECG Changes
 Lack of discrete P waves
 Fibrillatory waves are present at a rate that is
between 350 and 600 beats/ min. The f waves
vary continuously in amplitude, morphology
and intervals
 Ventricular response follows no repetitive
pattern; the variability in the intevals between
QRS complexes is often termed irregularly
irregular
 QRS complexes are narrow unless AV
conduction through the His Purkinje system is
abnormal due to functional aberration, pre-
existing bundle branch block or ventricular
pre-excitation with conduction down the
accessory pathway
Classification
 Paroxysmal (self-terminating or intermittent):
terminates spontaneously or with
intervention within seven days of onset
 Persistent: fails to self-terminate within seven
days. Episodes often require pharmacologic or
electrical cardioversion to restore sinus
rhythm
 Long-standing persistent AF: last more than
12 onths
 Permanent AF: identify individuals with
persistent AF where a joint decision by the
patient and clinician has been made to no
longer pursue a rhythm control strategy
Management
Rate control vs Rhythm control
 Once ventricular rate control is achieved, a
decision regarding the long term management
(rate vs rhythm) should be made
 A rhythm control strategy uses antiarrhythmic
drugs (class 1 and 3), percutaneous catheter
ablation and/ or a surgical procedure
 Antiarrhythmic medications are generally
started before cardioversion and continued to
maintain sinus rhythm
 The reasons to pursue a rhythm-control
strategy would be preferred when there are
symptoms, younger patient age, and
irreversible structural and electrical
remodelling that occurs with longstanding
persistent AF
 A rate control strategy uses drugs that slow
conduction across the AV node, such as beta
blockers and non-dihydropyridine calcium
channel blockers or digoxin
 The decision to adopt a rhythm or rate control
strategy is often dictated by
o the presence of symptoms associated
with AF
o presence of diminutions in left
ventricular systolic function thought
secondary to the arrhythmia
 rate control is strongly preferred as the initial
approach in elderly patients with minor
symptoms
Rate Control
 β-blockers: atenolol or metoprolol
 Non-dihydropyridine calcium channel
blockers: diltiazem or verapamil
 Where there are contraindications to the
above such as in decompensated heart
failure, heart block or low heart rate,
asthmatics, digoxin can be used
o Digoxin 62.5 to 250 micrograms
orally, daily according to age, eGFR
and plasma digoxin concentration
 Digoxin alone usually fails to control exercise-
induced tachycardia in younger patients and
more active patients
Rhythm Control and Cardioversion
  If the patient has severe symptoms or a
compromised haemodynamic state,
cardioversion should always be considered
immediately, but unless this is the case,
careful consideration of the risk of
thromboembolism is important before
treating with either a drug or DC shock.
 It is generally safe to cardiovert (electrically or
pharmacologically) if it is certain that the
episode has lasted less than 48 hours
 Two acceptable ways to cardiovert a patient
will vary with patient preference and the
availability of transoesophageal echo.
Pharmacological Cardioversion
 Amiodarone (class 3 potassium channel
blocker) IV or PO
 Flecainide (class 1c sodium channel blocker)
IV or PO
 If using flecainide, there is a possibility of
accelerating the ventricular rate, particularly
in flutter. Consider pre-treatment with an AV
nodal blocking drug
Electrical Cardioversion
 Requires a DC shock, starting with 100 joules
in an average adult but consider starting at
200 or even 300 joules in a large patient, or
where there is a history of requiring a large
shock
 Atrial flutter generally requires much less
current, start with 50 joules
Thromboembolic Risk Post Cardioversion
 If there is doubt as to duration of AF or if it is
clear the attack has lasted more than 48
hours, do not attempt to cardiovert until
steps are taken to minimise thromboembolic
risk, except for haemodynamically unstable
patients
 Even in very recent onset AF, there is a risk of
atrial stunning following cardioversion to
sinus rhythm
 Stunning is an unpredictable failure of the
atria to contract and may persist for hours to
days.
 During this time, fresh thrombus can form in
the hypocontractile atria, and this constitutes
an embolic risk even if a transoesophageal
echo an hour or two earlier was clear
 If a TOE is performed and shows no evidence
of thrombus in the atria, it is safe to proceed
at once to attempted cardioversion.
 If this is successful, the patient should be
anticoagulated (usually subcutaneous
enoxaparin) for at least a few days to reduce
the risk of thromboembolism from stunning
 If TOE is not performed, or is done and shows
thrombus, cardioversion should not be
attempted until patient has been fully
anticoagulated, preferably 3 weeks
Anticoagulation
 Dalteparin subcut, BD
 Enoxaparin subcut, BD
 Unfractionated heparin IV infusion, adjusted
according to APTT
 If required, oral may be started as follows
o Warfarin PO, target INR 2 – 3
o Dabigatran 150mg PO, BD
Long Term Maintenance Therapy after Cardioversion
 Long term not required if AF or atrial flutter is
associated with transient condition (MI,
surgery, excessive alcohol)
 Consider whether risk associated with
recurrence outweigh those of long-term
antiarrhythmic treatment
 More invasive procedures such as
radiofrequency ablation, His-bundle ablation
with pacemaker implantation, ore event
surgical approaches, should be considered in
patients whose ventricular rate and rhythm
are poorly controlled by drugs
Complications and Long Term Anticoagulation
 Atrial fibrillation rare causes death except
through thromboembolic complications
o Stroke
o Ischaemic bowel
 All patients in whom AF is discovered should
be considered for long-term anticoagulation
with warfarin or dabigatran (novel
anticoagulant), whether discovery is because
of symptoms or as chance finding
  All patients with AF should have a CHADS 2 –
Vasc score to evaluate need for
anticoagulation
CHA2DS2-Vasc Score
 Congestive heart failure
 Hypertension
 Age ≥ 75
 Diabetes
 Stroke or TIA history
 Vascular disease (peripheral artery disease,
complex aortic plaque, myocardial infarction)
 Age 65-74
 Sex: female
Score Risk Treatment Recommendations
0 Low No therapy or aspirin
1 Moderate Oral anticoagulation or aspirin
≥2 high Oral anticoagulation
 If aspirin is indicated use: 100-300mg PO, daily
 If oral anticoagulation is indicated use:
o Warfarin PO, daily, target INR 2-3
o Dabigatran 150mg PO, BD
Community Acquired Pneumonia
Pneumonia in individuals who are not hospitalised, or
who have been hospitalised for less than 48 hours.
Pathogens
 Streptococcus pneumonia (most common and
causes most cases of severe disease and
death, particularly in elderly)
 Haemophilus influenza (COPD)
 Mycoplasma pneumonia (common in young
adults)
 Chlamydophilia pnuemoniae
 Legionella species (acquired from
environmental sources and can occur in
outbreaks)
 Gram negative bacilli, including Klebsiella and
pseudomonas are uncommon causes of CAP
 Staphyloccous aureus is uncommon cause of
CAP but can be associated with MRSA and can
occur secondary to influenza
 In tropical regions, Bukrholderia pseudomallei
and Acinetobacter baumannii can cause CAP.
Risk factors include diabetes, alcohol
consumption, CKD, chronic lung disease and
immunosuppressive therapy
Clinical Features
 Acute respiratory symptoms: cough,
dyspnoea, sputum production, pleuritic chest
pain
 Fever, rigors, night sweats
 Reduced chest wall expansion on affected
side. decreased air entry on affected side,
coarse crackles, dull percussion, bronchial
breathing
 Localised lobar consolidation on Chest X-ray
Investigations
 Chest X-ray
 Oxygen saturation, arterial blood gases are
appropriate in severely ill patients
 Sputum MCS
 Blood cultures if signs of sepsis
 Consider pneumococcal urinary antigen assay,
which can be easily performed on routine
urine specimens for early identification of S.
pneumonia. Test all adults with severe disease
 Consider nose and throat swabs for NAAT PCR
for respiratory viruses
 Consider IgM serology for M. pnuemoniae
and acute and convalescent serology for M.
pneumonia, Legionella, C. pnuemoniae and
influenza
 Bronchoalveolar lavage can be considered
when other tests have not identified a
pathogen in a severely ill patient who has not
responding to empirical antibiotic therapy
Pneumonia Severity and Red Flags
CURB-65
 Confusion (abbreviated mental test ≤8)
 Urea > 7mmol/L
 Respiratory rate ≥ 30 breaths/min
 BP < 90 systolic and/ or 60 diastolic
 Age ≥ 65
A score of:
 0-1: home treatment possible
 2+: hospital therapy
  ≥3 severe pneumonia indicates mortality 15-
40%, consider ICU
SMART COP
Scoring
 0-2: low risk of needing intense respiratory
and or/ vasopressor support (IRVS)
 3-4: moderate risk (1 in 8) of needing IRVS
 5-6: high risk (1 in 3) of needing IRVS
 7 or more: very high risk (2 in 3) of needing
IRVS
 SEVERE CAP = score of ≥ 5
Red Flags
 Respiratory Rate >30 breaths/ min
 Systolic BP <90mmHg
 Oxygen saturation <92%
 Tachycardia >100bpm
 Acute onset confusion
 Multilobar involvement on CXR
Management
Mild Disease
 Does not require hospital admission and does
not have any of the red flags
 Monotherapy of amoxicillin or doxycycline is
recommended to minimise adverse effects
and optimise adherence to therapy
 If patient is not improving after 48 hours of
monotherapy, consider escalating to
combination of amoxicillin + doxycycline, and
reassess the patient’s need for hospital
admission
 If atypical pathogens ( mycoplasma,
chlamydia, legionella) are suspected or
patients hypersensitive to penicillins, use
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. +
doxycycline
 Tropical regions: treat as above unless has risk
factors for B. pseudomallei and Acinetobacter
baumannii or if gram-negative bacilli are
identified on cultures, use:
o Ceftriaxone 2g IV daily + gentamicin IV
o Atypical pathogens: add doxycycline
Severe Disease
 Inpatient assessed as severe pneumonia
based on SMARTCOP (5) or CURB65 (3)
 More likely to require intensive respiratory or
vasopressor support, usually in ICU
 Empirical therapy should treat: S. pneumonia,
legionella and enteric gram –ve bacilli
 Also consider whether influenza or S. Aureus
are important causes and treat accordingly
 Investigation to identify pathogen is
important, collect blood cultures and sputum
samples
 Nontropical regions: (ceftriaxone IV or
cefotaxime) PLUS (azithromycin IV)
 Tropical regions: (meropenem IV (wet season)
or piperacillin + tazobactam) PLUS
azithromycin IV
Complications
Respiratory Failure
  Type 1 relatively common. Treat with high-
flow (60%) oxygen and transfer to ICU if
hypoxia does not improve or PCO2 rises >6kPa
 Aim to keep SpO2 at 94-98%
Hypotension
 May be due to combination of dehydration
and vasodilation due to sepsis
 If systolic BP is <90mmHg, give IV fluids
Atrial Fibrillation
 Quite common, particularly in elderly and
usually resolves with treatment of the
pneumonia
 Beta-blocker or digoxin may be required to
slow the ventricular response rate in the short
term
Pleural Effusion
 Inflammation of pleura by adjacent
pneumonia may cause fluid exudation into the
pleural space
 If this accumulates faster than it is
reabsorbed, a pleural effusion develops.
 If it becomes large and symptomatic, or
infected (empyema), drainage is required
Empyema
 Pus in the pleural space. Should be suspected
if patient with resolving pneumonia develops
a recurrent fever
 CXR indicates a pleural effusion
 Aspirated pleural fluid is typically yellow and
turbid with a pH <7.2, ↓ glucose and ↑LDH
 Empyema should be drained using a chest
drain, inserted under radiological guidance
 Adhesions and loculation can make this
difficult
Lung Abscess
 Cavitating area of localised, suppuratives
infection within the lung
 Causes: inadequately treated pneumonia,
aspiration, bronchial obstruction (tumour,
foreign body), pulmonary infarction, septic
embolic, subphrenic or hepatic abscess
 Clinical features: swinging fever, cough,
purulent, foul smelling sputum, pleuritic chest
pain, haemoptysis, malaise, weight loss. Look
for finger clubbing, anaemia, crepitations.
Empyema develops in 20-30%
 Tests: FBC, Sputum MCS and cytology, CXR
shows walled cavity, often with a fluid level.
Bronchoscopy to obtain diagnostic specimens
 Treatment: antibiotics as indicated by MCS,
continue until healed (4-6 weeks). Postural
draining, repeated aspiration, antibiotic
instillation or surgical excision may be
required
Others
 Septicaemia: bacterial spread from lung
parenchyma into bloodstream and may cause
infective endocarditis, meningitis
 Pericarditis and myocarditis
 Jaundice: usually cholestatic and may be due
to sepsis or secondary to antiobiotic therapy
(particularly flucloxacillin and co-amoxiclav)
Hospital Acquired (Nosocomial) Pneumonia
Pneumonia that develops in a patient who has been
hospitalised for longer than 48 hours. Most bacterial
HAP occurs by micro-aspiration of bacteria that
colonise the oropharynx or upper gastrointestinal
tract.
 Atypical pathogens are much less common in
HAP than in community acquired
 Intubation greatly increases the risk of HAP
because it interferes with normal
physiological mechanisms that limit bacterial
contamination of the airways; intubated
patients can develop ventilator-associated
pneumonia (VAP)
 Pneumonia caused by macroaspiration of
bacteria may occur in hospitalised patients,
particularly in patients with risk factors such
as stroke, neuromuscular disorders or
impaired consciousness
Diagnosis and Pathogens in HAP
 Respiratory symptoms may be mild, and other
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
Aspiration pneumonia is a bacterial infection that
occurs in the days following macroaspiration of
organisms from the oropharynx. It is frequently
associated with risk factors such as bulbar dysfunction
and impaired consciousness. A chest X-ray is required
to confirm the diagnosis of pneumonia
established community or nursing home
acquired aspiration pneumonia according to
disease severity. As per CAP guidelines
 The role of anaerobic organisms in aspiration
pneumonia is frequently over-estimated
 In mild disease, penicillin effectively treats
anaerobic organisms aspirated from the
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
and last sample drawn 1 hour apart)
 Echocardiogram with oscillating initracardiac
mass on valve or supporting structures
o Ideally TOE- more sensitive than TTE,
particularly for prosthetic valve and
pacemaker lead endocarditis
Minor Criteria
 Predisposing heart condition or intravenous
drug use
 Temperature >38.0
 Vascular phenomena: arterial emboli,
pulmonary infarcts, mycotic aneurysms,
intracranial bleed, conjunctival haemorrhages,
Janeway lesions
 Microbiological evidence: positive blood
culture but does not meet a major criterion
 Echocardiographic findings: consistent with
endocarditis but does not meet major
criterion
Treatment
 Treatment involves several weeks of IV
antibiotics (PICC line)
Empirical Therapy
 Once-daily dosing of gentamicin IV to cover
possibility of Gram –ve sepsis PLUS
o Only interim regimen pending blood
culture results
o In confirmed streptococcal or
enterococcal infection, 8 hourly
gentamicin I recommended for
synergistic therapy of penicillin
 Benzylpenicillin 1.8g IV 4-hourly (vacomycin IV
if prosthetic value or pacemaker lead
endocarditis)
 Flucloxacillin 2g IV 4-hourly
Viridans Streptococci Endocarditis
 Benzylpenicillin 1.8 IV 4-hourly for 2 weeks +
 Gentamicin 1mg/kg IV, 8-hourly for 2 weeks
Enterococcal Endocarditis
 Test all enterococcal isolates for minimum
inhibitory concentration (MIC) of penicllin and
for high-level aminoglycoside resistance,
because antibiotic resistance is increasingly a
problem
 Gentamicin for 4-6 weeks + EITHER
o Benzylpenicillin IV for 4-6 weeks
o Amoxy/amplicillin 2g IV for 4-6 weeks
Staphylococcal Endocarditis
 Flucloxacillin 2g IV, 4 hourly for 4-6 weeks
 Four weeks may be adequate in
uncomplicated cases but 6 weeks should be
given if there are complications (perivalvular
abscess, septic metastatic complications
 Patients with right-sided (tricuspid valve)
methicillin-susceptible staphylococcal
endocarditis (usually people who inject drugs)
can be treated with a short course (2 weeks)
 For MRSA: vancomycin IV
Endocarditis caused by the HACEK group
 Oral gram –ve bacilli
o Haemophilus parainfluenzae
o Haemophilus aphrophilus
o Aggregatibacter species
o Cardiobacterium species
o Eikenella corrodens
o Kingella species
 Causes fewer than 5% of cases of endocarditis
and approximately 1/3 of these have
prosthetic valves
 If susceptible to penicillin and are beta-
lactamase negative
o Amoxy/ampicillin or benzylpenicillin
 Beta-lactamase positive: broad-spectrum
cephalosporins
o Ceftriaxone 2g IV daily for 4-6 weeks
o Cefotaxime 2g iv 8-hourly for 4-6
weeks
Complications
 Generally begin within first weeks after onset
of infectious process
 Glomerulonephritis due to glomerular
trapping of antigen-antibody complexes with
haematuria, albuminuria, or renal failure
 Arrhythmias
 Systemic embolization bode particularly ill for
patient
  Septic embolism, septicaemia, renal/ spleen
infarcts
 Left untreated, it is generally fatal
Shock in Hospital
Shock is a life-threatening condition of circulatory
failure that most commonly presents with
hypotension. Effects of shock are initially reversible
but can rapidly become irreversible, resulting in multi-
organ failure and death.
Definition and Classification
Shock is defined as a state of cellular and tissue
hypoxia due to reduced oxygen delivery and/ or
increased oxygen consumption or inadequate oxygen
utilisation.
 Distributive: septic shock, toxic shock,
neurogenic shock, anaphylactic shock,
endocrine shock, systemic inflammatory
response syndrome
 Cardiogenic: myocardial infarction, atrial and
ventricular arrhythmias, valve or ventricle
septal rupture
 Hypovolemic: haemorrhagic and non-
haemorrhagic fluid losses
 Obstructive: pulmonary embolism, pulmonary
hypertension, tension pneumothrorax,
constrictive pericarditis, restrictive
cardiomyopathy
Clinical Manifestations – undifferentiated shock
Hypotension
 Occurs in majority of patients with shock
 Absolute: systolic BP <90mmHg; mean arterial
pressure <65mmHg
 Relative: a drop in systolic blood pressure >40
mmHg
 Orthostatic: >20mmHg fall in systolic pressure
or > 10mmHg fall in diastolic pressure with
standing
 Profound: vasopressor-dependent
Tachycardia
 Early compensatory mechanism in patients
with shock
 Younger patients develop severe and
persistent tachycardia before becoming
hypotensive late in the course
Abnormal Mental Status
 Altered sensorium in shock is usually due to
poor perfusion or metabolic encephalopathy
 Begins with agitation, progresses to confusion
or delirium and ends in obtundation or coma
Oliguria
 Shock can be due to shunting of renal blood
flow to other vital orangs, direct kidney injury
or due to intravascular volume depletion
(vomiting, diarrhoea, or haemorrhage)
Cool, clammy, cyanotic skin
 Due to compensatory peripheral
vasoconstriction that redirects blood
centrally, to maintain vital organ perfusion
(coronary, cerebral, and splanchnic flow)
 A cyanotic, mottled appearance is a late and
worrisome feature of shock
 Warm, hyperemic skin does not ensure the
absence of shock because such an appearance
may be present in patients with early
distributive shock (prior to onset of
compensatory vasoconstriction) or terminal
shock (due to failure of compensatory
vasoconstriction)
Metabolic acidosis
 High anion gap metabolic acidosis, specifically
elevated lactate, should raise clinical suspicion
for the presence of shock
Initial Approach
 Assess airway, breathing, circulation
 Obtain IV access with two large bore cannulas
and initial fluid delivery
 Oxygen to be given when SpO2 <95%
General Assessment
History and Examination
 Sensorium (orientation)
 Mucous membranes, lips, tongue, CRT
 Neck veins
  Lungs, heart and abdomen
Laboratory Evaluation
 Serum lactate: reflection of poor tissue
perfusion (lactic acidosis) and produced by
anaerobic metabolism
 Renal and liver function tests: ↑ BUN,
creatinine and transaminases are usually due
to shock-induced end-organ damage
 Cardiac enzymes and natriuretic peptides: ↑
troponin, creatine phosphokinase, BNP may
indicate cardiogenic shock from ischaemia or
massive PE
 Full blood count and differential: high
haematocrit may suggest hypovolaemia and
anaemia suggest haemorrhagic shock.
Leukocytosis may indicate septick shock.
Neutrophilic lefft shift with toxic granules on
blood smear is more indicative
 Coagulation and D-dimer: may indicate
haemorrhagic shock or sepsis which has
caused DIC
 Venous or arterial blood gas: hypoxaemia and
acidosis
Chest X-ray
 Performed in most patients with suspected
hosck to detect common causes: pneumonia,
pneumothorax, pulmonary oedema, widened
mediastinum to support aetiology for septic,
obstructive, cardiogenic or aortic dissection
 May show complications of shock such as
acute respiratory distress syndrome
Common Conditions with Lifesaving Interventions
Anaphylactic Shock
 Features: hypotension, inspiratory stridor,
oral and facial oedema, hives and history of
recent exposure
 Treatment: Adrenaline IM 0.3mg of 1:1000
 Other agents: antihistamines, nebulised
albuterol, methylprednisolone
Tension Pneumothorax
 Features: tachypnoea, unilateral pleuritic
chest pain and diminished breath sounds,
distended neck veins, tracheal deviation
 Treatment: tube thoracostomy (5th intercostal
space, mid-axillary line) or needle
compression (2nd or 3rd intercostal space, mid-
clavicular line
Pericardial Tamponade
 Features: dysnpoea, tachycardia,
hypotension, elevated JVP, distant heart
sounds, pulsus paradoxus
 Treatment: bedside echocardiography and
pericardiocentesis
Haemodynamically significant Haemorrhage
 Traumatic: blunt or penetrating trauma
leading to haemothorax, peritoneal lavage,
ruptured spleen
 Nontraumatic: ruptured AAA, upper and
lower GI bleeds (haematemesis,
haematochezia, anaemia, bleeding diathesis)
 Treatment: requires large volumes of blood
products and vasopressors are avoided. A
type and crossmatch, a complete blood count
and coagulation studies should be obtained in
all patients with suspected haemorrhage
Life-threatening Arrhythmias
 Can be cardioverted (tachyarrhythmias),
receive atropine or infusions of dopamine, or
undergo temporary or permanent pacemaker
placement (bradyarrhythmias)
Severe Septic Shock
 Features: fever, severe hypotension and an
obvious septic source
 Septic screen: Blood cultures, FBC, CXR, Urine
MCS
 Treatment: oxygen and fluids if required.
Immediate broad spectrum antibiotics:
vacomycin with ceftriaxone/ cefotaxime or
beta-lactam/ beta-lactamase inhibitor
Cardiogenic Shock from MI
 Features: hypotension associated with
anterior crushing chest pain, respiratory
distress and STEMI and/ or elevated troponin
 Antiplatelets, PCI/ stent
Dissection of the ascending aorta
  Features: hypertension, tearing chest or back
pain. However, hypotension and shock occur
with retrograde dissection that results in
acute aortic insufficiency, pericardial
tamponade or myocardial infarction
 Treatment: CT contrast, transoesophageal
echo or MRI to demonstrate aortic root
dilatation. Surgical Referral
Haemodynamically Significant PE
 Features: hypotension, acute dyspnoea,
hypoxemia
 Treatment: systemic thrombolytic therapy
Adrenal Crisis
 Features: hypotension, volume depletion,
history of glucocorticoid deficiency or
withdrawal should receive dexamethasone
4mg IV
 Blood for serum cortisol, ACTH, aldosterone,
renin and serum chemistries should be drawn
prior to therapy
Undifferentiated Management of Shock
 Haemodynamic support with IV fluids (usually
crystalloids in well-defined boluses of 500 to
1000mL. those who have distributive shock or
hypovolaemic shock need 2-5L of fluid
replacement
 Vasopressors are second line agents in the
treatment with suspected/ undifferentiated
shock. The use of vasopressors in patients
with haemorrhagic or hypovolaemic shock
may be harmful
 Vasopressors should only be used as an
additional form of haemodynamic support
when aggressive resuscitation has failed to
restore adequate tissue perfusion
o Adrenergic agonists: noradrenaline IV
o Inotropic agents: dobutamine
(commoner in cardiogenic shock
Diabetic Ketoacidosis
Protocol
1. Patient unwell with T1DM
2. Test BGL and finger prick ketones
3. If ketones ≥0.6 (risk of DKA), check VBG for
pH, HCO3 and anion gap
4. If absence of acidosis, do not use protocol and
recheck BGL and ketones in 2 hours. Treat
patient as clinically indicated
5. Acidosis and ketosis present, DKA= ph <7.35
and HCO3 <15 and raised anion gap and
ketones >1. BGL may be nomal or elevated
Clinical Signs and Symptoms
 Hyperventilation or Kaussmaul’s breathing
 Vomiting and abdominal pain
 Dehydration
 Impair consciousness
Consider Precipitating Factors
 Omission of insulin
 Infection
 Newly diagnosed diabetes ellitus
 Myocardial infarction
 Recent surgery/ trauma
Key Issues
 Initial fluid management
 Early potassium replacement
 Early IV insulin initiation (titrated to blood
glucose level)
 Frequent monitoring
Management
Immediate management (1 hour)
1. Initial investigation
a. Two IV cannulae
b. FBC, U&E, LFT, BGL, VBG
c. Finger prick ketones
d. Blood cultures
2. Fluid replacement (cannula 1)
a. 0.9% sodium chloride 1000ml/hr.
Repeat if hypotensive
3. Start IV insulin (cannula 2)
a. If K >3mmol/L commence soluble
insulin (maximum starting dose 10
units /hr)
b. If K <3mmol/L, replace K (cannula 1),
recheck levels and commence insulin
infusion once K >3mmol/L
4. Other actions
 a. Manage airway- consider NGT if
protracted vomiting/ risk of aspiration
b. Check bHCG and cardiac enzymes and
if indicated (triggers)
c. Undertake septic screen and treat
infection if present (triggers)
d. Fluid balance chart and neurological
observations
e. If patient on insulin pump- remove it
f. DVT prophylaxis
g. Prescribe/ administer patient’s usual
long acting insulin
5. Contact accepting consultant
Ongoing management (hour 2-4)
1. Further investigations
a. Hourly BGL
b. 4 hourly ketones
c. U&E’s and VBG at end of hour 2 and
hour 4
2. Continuation of fluid replacement 0.9%
sodium chloride
3. Potassium replacement (cannula 1)
a. If serum K >5mmol/L or patient
anuric- withhold
b. If serum K 3.5-5.0mmol/L give
10mmol/100mL
c. If serum K <3.5mmol/L give 2 x
10mmol/100mL
4. IV insulin and glucose (cannula 2)
a. Continue initial rate of insulin if BGL’s
are decreasing and venous pH at hour
2 and 4 is consistently increasing
(finger prick ketones at hour 4 should
be decreasing)
b. Increase rate of insulin if pH is not
increasing or if BGL’s rise or do not
decrease
c. When BGL <14mmol/L give 10%
glucose 100mL/hr via cannula 2
Subsequent Management
 Finger prick ketones until ketones <0.6mmol/L
 Continue 0.9% sodium chloride infusion at
125mL/hr until patient is fluid replete or
eating/ drinking
 Continue K replacement to maintain within
reference range and continue to monitor K as
above with U&E’s and VBG
 Continue insulin at variable rate to maintain
BGL 9-14mmol/L
 Patient is ready to transition to regular insulin
regimen when the following criteria are met
o Patient well and eating/drinking
o Anion gap is normal
o Ketones <0.6mmol/L
o Long acting insulin has been given at
least 2 hours ago (pump
recommenced)
 Ignore mild persistent acidosis if above
criteria are met and there is hyperchloraemia
(saline induced metabolic acidosis)
Discharge Planning
Refer for specialist review before discharge
 Endocrinologist
 Diabetes educator
 Dietician
 Psychologist
Discharge Preparation
 Ketones <0.6mmol/L and anion gap normal
 Eating normally and established on routine
insulin regimen
 Given written advice about sick day
management
 Ensure that a copy of patient discharge letter
is sent patient’s GP and diabetes care team
Refer to ICU for consultation if any of the following
 pH <7.1
 Altered level of consciousness
 Severe hypokalaemia (<3mmol/L)
 Severe hyponatraemia (<125mmol/L)
 Altered blood pressure or severe dehydration
 Pregnancy
Delirium
Confusion Assessment Method
1. Acute onset and fluctuating course: usually
obtained from a family member of nurse and
shown by positive responses to follow
questions
 a. Is there evidence of an acute change
in mental status from the patient’s
baseline
b. Did the abnormal behaviour fluctuate
during the day
2. Inattention: shown by a positive response to
the following:
a. Did the patient have difficulty
focusing attention, for example, being
easily distractible or having difficulty
keeping track of what was being said
3. Disorganised thinking: shown by a positive
response to the following:
a. Was the patient’s thinking
disorganised or incoherent, such as
rambling or irrelevant conversation,
unclear or illogical flow of ideas, or
unpredictable switching from subject
to subject
4. Altered level of consciousness: shown by an
answer other than alert to the following:
a. Normal= alert
b. Hyperalert= vigilant
c. Drowsy, easily aroused= lethargic
d. Difficult to arouse= stupor
e. Unarousable= coma
The diagnosis of delirium requires the presence of
features 1 AND 2 plus either 3 or 4
Causes of Delirium- I WATCH DEATH
 Infection: pneumonia, UTI, skin, CNS
 Withdrawal: often unintentional from alcohol,
sedative, barbiturates
 Acute metabolic changes: altered pH, hypo/
hyper sodium or calcium, acute liver or renal
failure
 Trauma: brain injury, subdural haematoma
 CNS pathology: post-ictal, stroke, tumour,
brain metastasis
 Hypoxia- CHF, anaemia
 Deficiencies: thiamine, niacin, B12, folate
 Endocrinopathies: hypo/ hyper cortisol,
hypoglycaemia, hypothyroidism
 Acute vascular: hypertensive emergencies,
septic hypotension
 Toxins and drugs: especially anticholinergics,
opioids, benzodiazepines, SSRI’s
 Heavy metals: lead, arsenic
 Others: changes in environment, dehydration,
not eating or drinking, restrained patients,
constipation, chronic pain
Features of Delirium- DELIRIUM
 Disordered thinking: slow, incoherent,
confused ideas
 Euphoric, fearful, angry, depression (labile
mood)
 Language impaired: reduced speech,
repetitive
 Illusions/ hallucinations/ delusions
 Reversal of sleep-awake cycle: tired during
day, awake hypervigilant at night
 Inattention: focusing attention is poor- test
with serial 7’s or spelling world backwards
 Unaware/ disorientated: doesn’t know name,
time, location
 Memory deficit: may be amnesic during
episode
Delirium Work up
Laboratory Studies
 FBC with differential: helpful to diagnose
infection and anaemia
 Electrolytes: to diagnose low or high levels
 Glucose: to diagnosis hypoglycaemia, DKA and
HONK states
 Renal and liver function tests to diagnose liver
and renal failure
 Thyroid function tests: to diagnosis
hypothyroidism
 Urine analysis for UTI
 Urine and blood drug screen: used to
diagnosis toxicological causes
 Thiamine and vitamin B12 levels used to
detect deficiency states of these vitamins
 Tests for bacteriological and viral aetiologies
(blood cultures and viral serology): to
diagnosis infection
 ESR/ CRP
 Drug screen including alcohol level
 HIV and syphilis serology
Imaging Studies
 Chest X-ray for pneumonia and congestive
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,
nitroglycerin, calcium channel
blockers
 Ageing: decrease in baroreceptor sensitivity
 Others: cardiac pump failure (aortic stenosis,
pericarditis/ myocarditis, arrhythmias) and
adrenal insufficiency and less commonly
pheochromocytoma
Symptoms
 Symptoms typically occur in response to
sudden postural change, but also in
association with meals, exertion and
prolonged standing
 Symptoms result from cerebral hypoperfusion
and include generalised weakness, dizziness
or lightheadedness, visual blurring or
darkening of the visual fields and in severe
cases, syncope
 Elderly patients are at increased risk of falls
Diagnosis
 When, within two to five minutes of quiet
standing (after a five minute period of supine
rest), one or both of the following is present
o At least a 20mmHg drop in systolic
o At least a 10mmHg drop in diastolic
 The heart rate normally rises immediately on
standing
Evaluation
 Detailed medication list, prescription and non-
prescription
 Recent medical history of potential volume
loss (vomiting, diarrhoea, fluid restriction,
fever)
 Medical history of congestive heart failure,
malignancy, diabetes, alcoholism
 Evidence on neurological history and
examination of parkinsonism, ataxia,
peripheral neuropathy or dysautonomia
(abnormal pupillary response, history of
constipation or erectile dysfunction
 Laboratory testing (haematocrit, electrolytes,
blood urea nitrogen, creatinine, glucose) and
an electrocardiogram
Seizures
Categories of Seizures
Epileptic Seizures
 At least two unprovoked (or reflex) seizures
occurring more than 24 hours apart
 One unprovoked seizures and a probability of
further seizures similar to general recurrence
risk after two unprovoked seizures, occurring
over the next 10 years
 Diagnosis of epilepsy syndrome
Aetiology
 Less than one-half of epilepsy cases have an
identifiable cause. It is presumed that most of
these are genetically determined. In the
remainder of patients in whom an aetiology
can be determined, the causes include
o Head trauma
o Stroke
o Brain tumour
o Intracranial infection
o Cerebral degeneration
o Congenital brain malformations
o Inborn errors of metabolism
 In the elderly, vascular degeneration and
neoplastic causes are more common than in
younger adults and children
 A higher proportion in children is due to
congenital brain malformations than in other
age groups
 Onset of seizures in late life may be a risk
factor for stroke
 Anti-seizure drugs prevent seizures in the first
week after head injury but do not prevent the
development of epilepsy
Provoked or Secondary Seizures
Acute Symptomatic Seizures
 Patients without a history of epilepsy often
experience seizures in the setting of acute
medical or neurological illness or injury
 While this occurrence places them at risk for
future epilepsy, a seizure in the acute setting
carries a lower risk
 Patients with seizures provoked by metabolic
derangements are generally not felt to be at
risk for future epilepsy compared to those
post traumatic injury
  Another features is the risk of seizures is felt
to occur in proportion to the rapidity of the
onset, rather than to the severity of the
underlying metabolic disturbance
Aetiology
 Hypoglycaemic seizures: diaphoresis,
tachycardia, anxiety and confusion
 Nonketotic hyperglycaemia: elderly diabetes
and can cause focal motor seizures
 Precipitous falls in serum sodium
concentrations can trigger generalised tonic-
clonic seizures, usually with prodrome of
confusion and depressed level of
consciousness
 Hypocalcaemia: rare- often in neonates.
Prodrome: mental status changes and tetany
 Hypomagnesium <0.8: irritability, agitation,
confusion, myoclonus, tetany, and
convulsions
 Renal failure and uraemia- particularly
myoclonic seizures
 Hyperthyroidism can cause seizures and can
exacerbate seizures in patients with epilepsy
 Acute intermittent porphyria
 Cerebral anoxia as a complication of cardiac
or respiratory arrest, carbon monoxide
poisoning, drowning or anaesthetic
complication. Cerebral anoxia dye to syncope
can result in very brief tonic and/ or clonic
movements without a prolonged postictal
state
 Withdrawal states- particularly alcohol and
benzodiazepine withdrawal typically in 7-48
hours of last drink
 Drug toxicity/ intoxication
Nonepileptic Seizures
 Sudden changes in behaviour that resemble
epileptic seizures but are not associated with
the typical neurophysiological changes that
characterise epileptic seizures
Imitators of Epilepsy
 Syncope
 Psychological disorders
 Sleep disorders
 Migraine
 Miscellaneous neurological events
 Elderly causes
o TIA
o Transient global ischaemia
o Drop attacks
o Cardiogenic syncope
o Delirium
Seizure History
 What happened just before seizure? (aura)
 What was happening during? (witness)
 What happened after recovery? (drowsy/
confused)
 Could you remember what happened or
events leading up to
 Did you bite your tongue or was there any
blood in your mouth, did you vomit, were you
incontinent. Do your muscles feel sore or
were you unable to move them? (Todd’s
Palsy)
 Have you had seizures before? Child hood
seizures.
 Ask about risk factors: head injury, Alzheimer
disease, stroke, drug or alcohol abuse
 Medication history
 What triggers do you have?: loud music,
intense exercise, strong emotions, flashing
lights, lack of sleep
 Family history of seizures, in particularly
absence seizures and myoclonic seizures may
be inheritied
Seizure Symptoms and Signs
Partial (Focal) Seizures without impairment of
consciousness (simple)
 Involves warning or aura, which are seizures
that affect enough of the brain to cause
symptoms, but not enough to interfere with
consciousness
 Auras are called focal seizures without
impairment of consciousness
 Seizure that begins in occipital cortex may
result in flashing lights, while a seizure that
affects the motor cortex will result in rhythmic
jerking movements of face, arm, or leg on side
of the body opposite to the involved cortex
(Jacksonian seizure)
  Presence of aura supports diagnosis of
epileptic seizure and do not typically precede
provoked seizures
 Symptoms of simple partial seizures or auras
o Black out
o Confusion
o Deja-vu
o Dizziness
o Drooling
o Electric shock feeling
o Eyelid flutter
o Lightheadness or LOC
o Memory loss
o One side of body different than over
o Racing thoughts
o Sound or spatial perception distortion
o Spinning feeling
o Sweating
o Tremors
o Visual distortion, visual loss or
blurring
Focal (Partial) Seizures with Impairment of
Consciousness (complex)
 Most common type of seizure in epileptic
adults
 During the seizure, the patients appear to be
awake but are not in contact with others in
their environment and do not respond
normally to instructions or questions.
 They often seem to stare into space and
either remain motionless or engage in
repetitive behaviours, called automatisms,
such as facial grimacing, gesturing, chewing,
kip smacking, snapping fingers, repeating
words or phrases, walking, running or
undressing
 Patients may become hostile or aggressive if
physically restrained during these seizures
 Typically last less than three minutes and may
be immediately preceded by a focal seizure
with preserved awareness (aura)
 Afterward, the patient enters the postictal
phase, characterised by somnolence,
confusion, and headache for up to several
hours
 Patient has no memory of what took place
during the seizure other than, perhaps, the
aura
Generalised Seizures
 Originate in all regions of the cortex
simultaneously.
Generalised Tonic Clonic Seizure
 Begins with abrupt loss of consciousness,
often in association with a scream or shriek.
 All of the muscles of the arms and legs as well
as chest and back then become stiff
 The patient may begin to appear cyanotic
during this tonic phase
 After approximately one minute, the muscles
begin to jerk and twitch for additional one to
two minutes. During this clonic phase, the
tongue can be bitten and frothy and bloody
sputum may be seen coming out of the
mouth. Possible loss of bowel or bladder
control.
 The postictal phase begins once the twitching
movements end. The patient is initially in a
deep sleep, breathing deeply, and then
gradually wakes up, often complaining of a
headache, mild confusion, muscles sore,
fatigue
 Other features: fast heart rate, elevated blood
pressure, respiratory and metabolic acidosis,
dilated pupils, risk of vertebral fracture
pneumonia
 Certain physical signs, such as lateral tongue
bite and urinary incontinence, are more
specific for an epileptic generalised tonic-
clonic seizure
Absence Seizure
 Usually occur during childhood and typically
last between 5 to 10 seconds
 They frequently occur in clusters and may
take place dozens or even hundreds of times a
day
 Cause sudden staring with impaired
consciousness
 If it lasts more than 10 seconds, there may
also be eye blinking and lip smacking
Other Seizures
 Clonic seizures: rhythmical jerking muscle
contractions that may occur singly or in
 clusters and that can affect any muscle group,
although typically the arms are, neck, face
affected.
 Myoclonic seizures consist of sudden, brief
muscle contractions that may occur singly or
in clusters and that can affect any group of
muscles, although typically the arms.
Consciousness is usually not impaired
 Tonic seizures cause sudden muscle stiffening,
often associated with impaired consciousness
and falling to the group
 Atonic seizures (drop seizures): a sudden loss
of control of the muscles, particularly of the
legs, that results in collapsing to the ground
and possible injuries
Postictal State
 Following seizure, there is a period of
transition back to individual’s normal level of
awareness and function
 Manifestations include: confusion, suppressed
alertness, focal neurological deficits may also
be present.
 May last from seconds to minutes to hours
depending on where the brain was affected,
length of seizure, whether they were on anti-
epileptics, age
 Postictal paresis (Todd’s palsy) is a transient
neurological deficit that lasts for hours after
an epileptic seizure. The classic deficit is
weakness of a hand, arm or leg that appears
following focal motor seizure activity involving
one limb or side of the body.
 Other postictal symptoms: transient aphasia,
amaurosis, hemianopsia and sensory loss.
Some patients manifest psychosis and
aggression
Diagnostic Studies
 Causative metabolic abnormalities:
electrolytes, calcium, magnesium, glucose,
renal function tests, liver function tests,
toxicology screen
 Full blood county
 Prolactin: serum prolactin levels may rise
shortly after generalised tonic-clonic seizures
and some focal seizures
 Other seizure biomarkers: cretine
phosphokinase (CPK), cortisol, white blood
cell count, lactate dehydrogenase, pCO2,
ammonia, neuron specific enolase (to
differentiate between syncope, psychogenic
nonepileptic seizures)
 VBG: can have respiratory and metabolic
acidosis
 ECG: cardiogenic syncope can manifest as a
secondary hypoxic seizure
 Lumbar puncture: if clinical presentation
suggests an acute infectious process or history
of cancer-type known to metastasize to
meninges
 EEG: essential study in diagnostic evaluation
of epileptic seizures, a normal EEG does not
rule out epilepsy
 MRI brain preferred over CT to identify a
specific lesion such as cortical dysplasia,
infarcts or tumours. CT brain sufficient if
suspecting a cerebral haemorrhage, mass or
large stroke
Acute Management of Inpatient Seizure
 Most seizures remit spontaneously within two
minutes and rapid administration of
benzodiazepine or antiseizure drug is not
required
 Intravenous access should be secured so that
medications can be administered if the
seizure is more prolonged
 Maintain airway and suction out vomitus or
blood. Give oxygen via non-rebreather
 Monitor vital signs: pulse and oxygen
saturations
 Seizure that last longer than 5 to 10 minutes
or frequent clinical seizures without an
interictal return to baseline meet the
definition of status epilepticus
Prescribing Intravenous Fluids and Electrolytes
1. Assess current fluid status
 Is the patient dry, wet or just right?
 Review fluid balance charts, urine output and
daily weight
 Review clinical symptoms and signs of fluid
deficit or overload
Fluid Deficit
 Features: thirst, dry mucous membranes,
tachycardia and low urine output
 Postural hypotension plus flat neck veins with
or without other evidence of shock indicate
intravascular hypovolaemia
 First correct intravascular hypovolaemia:
o Rapid replacement with fluids such as
0.9% sodium chloride or compound
sodium lactate or colloids
o Blood and blood products may be
indicated
o May be necessary to contact ICU
 Replace estimated extracellular deficit:
o Correct with appropriate fluid based
on type of fluid lost and current
tonicity (serum sodium)
o Compound sodium lactate may be
appropriate
o If serum sodium is low, avoid glucose
solutions
o Administer half required volume over
8 hours and second half over 16 hours
o Frequently reassess during this
process
Fluid Overload
 Signs: increased daily weight, raised JVP,
peripheral oedema, pulmonary oedema
 Management: minimise sodium and fluid
given. Consider diuretic
2. Assess ongoing fluid losses
 Estimate ongoing volume losses including:
vomiting, diarrhoea, nasogastric draining and
other losses (ileus)
 These should be added to the volume given
daily
3. Assess maintenance requirements
 Requires in unstressed, well individuals differ
from sick hospital patients
 A well, unstressed 70kg adult, who is nil by
mouth, euvolaemic, not septic or post-
surgical, with normal cardiac and renal
function and no additional fluid losses who
have needs met by 0.3% sodium chloride and
3.3% glucose containing 40mmol/L of
potassium at 80mL/ hr (1L, 12 hourly)
 Remember to consider all sources of fluid
administration: TPN, NG feeds and drug
infusions
Typical daily needs Weight based (lean) Average Adult
Sodium 2mmol/kg 140mmol
Potassium 1mmol/kg 70mmol
Fluid 30-35ml/kg 2L
4. Modify in the following situations
 Conditions where ADH levels are elevated
o Patients with nausea, emesis, pain
and stress tend to retain water and
develop hypotonicity. The post-
operative period is high risk
o Fluids with higher sodium
concentration administered in
reduced volumes are indicated
 Smaller patients (weight <50kg)
o Proportional reductions are indicated
 Reduced left ventricular function
o Increased risk of fluid overload
o Reduce volume given and monitor
fluid status more frequently
 Reduced renal function
o Increased risk of fluid overload and
hyperkalaemia
o If oliguric, do not use maintenance
potassium
o If hypovolaemic, correct any fluid
deficit as above
o If euvolaemic, limit the volume given
to approximately: urine volume +
other losses + 500mL per day
 Medications that increase potassium
o Increased risk of hyperkalaemia.
Monitor potassium levels frequently
o ACE inhibitors and ARBs,
spironolactone, eplerenone
 Septic patients
o Have variably increased fluid
requirements
o Vasopressor support in ICU may be
required
 Obese
 Malnourished patients and extended duration
of therapy
o Often experience complex and
resistant electrolyte disturbances
  Specific fluid requirements
o Patients on dialysis, with burns,
transplants, acute neurological
conditions (meningitis, encephalitis,
stroke), DKA, HONK, have very specific
fluid requirements
o Seek advice
Properties of Common Fluids
Type of Fluid Na+ K+ Cl- Glucose
Sodium Chloride 0.9% 154 0 154
Compound Sodium 129 5 109
Lactate
0.3% NaCl + 3.3% glucose 51 0 51
5% glucose 0 0 0 50
5. When to Review
 Unstable patients need to be reviewed at
least every 2-4 hours. All patients should be
reassessed at least daily
 Consider slowing the rate of fluid infusion
overnight in patients at risk of overload
 Switch to an enteral route (oral, NG) as soon
as possible to minimise iatrogenic
complications
Electrolyte Disturbances and Replacement
Hypokalaemia
Mild: 3.1-3.5 mmol/L
Moderate: 2.5-3.0 mmol/L
Severe: <2.5mmol/L
 Total body deficit of potassium correlates
poorly with plasma potassium because most is
intracellular
 Plasma levels <3.5mmolL may result in
dysrhythmias
 Moderate and severe should be treated with
IV and oral supplementation. These patients
usually require at least an extra 60-80mmol
potassium above maintenance over the next
24 hours (100-140mmol in total). Repeat
plasma levels 4-6 hours after commencing
treatment
 All potassium containing infusions must be
given via an infusion pump or burette and
maximum rate is 20mmol/hr with pump. If
maximum rate exceeded, cardiac monitoring
and administration through a large vein is
recommended
 Maximum concentration = 40mmol/L in
sodium chloride 0.9%, peripherally to prevent
phlebitis. If maximum concentrations are
exceeded, must administer through a large
vein with high blood flow
 Premixed minibags can be given peripherally
but via infusion pump
 Mild hypokalaemia may be treated with oral
supplementation alone
0 o Potassium chloride effervescent 1-2
0 tabs BD
33 o Potassium chloride slow release
tablets (span K or slow K) 2 tabs BD
o Potassium chloride 10% oral solution
 If resistant to treatment, check magnesium
and replace if necessary
 Check for medications which may decrease
plasma potassium: salbutamol, insulin
Hypomagnesaemia
Mild: <0.7 mmol/L
Severe: < 0.4 mmol/L
 Severe of symptomatic (tremors, weakness,
cardiac arrhythmias, convulsions) should be
corrected with IV magnesium sulphate
 Mild or asymptomatic can be treated with
oral magnesium supplements (magmin) 1-2
tablets BD. Diarrhoes is a comment side
effects
Hyponatraemi
Mild: <135 mmol/L
Severe: <120 mmol/L
 Management requires careful assessment of
fluid status and biochemical indices including
plasma glucose and osmolality, and urinary
sodium and osmolality
 If hypovolaemic: correction of intravascular
deficit with 0.9% sodium chloride
 If euvolaemic or hypervolaemic: consider
drugs (SSRI’s, diuretics, anti-epileptics, PPI’s)
or conditions associated with SIADH, or
conditions with reduced effective circulating
volume (cirrhosis and CCF). Manage with fluid
restriction
 Symptomatic hyponatraemia (drowsiness,
headache, fitting) is an emergency and should
 be managed in intensive care. Hypoertonic
saline and airway access may be indicated
 In general, increase plasma sodium by no
more than 10mmol/L/day, to prevent
permanent neurological injury (central
pontine myelinosis) from osmotic
demyelination. 0.9% sodium chloride (not
hypertonic saline) is the normal mainstay of IV
therapy
Hypophosphataemia
Mild: <0.7 mmol/L
Severe: <0.4 mmol/L
 Phosphate does not normally need
replacement until less than 0.6mmol/L except
if: alcoholism, alcohol withdrawal,
malnutrition, re-feeding syndrome, receiving
TPN, renal hosphate wasting, recovery from
DKA or respiratory failure
 Consider IV replacement if plasma phosphate
< 0.4mmol/L
 Oral effervescent phosphate is available.
Diarrhoea is a common side effect
Hypocalcaemia
Mild: <2.15mmol/L
Severe: <2mmol/L or <0.9 mmol/L ionised
 Remember: plasma calcium (even corrected
for albumin) is an unreliable measure of
functional (ionised) calcium
 Hypocalaemia often reflects severe body fluid
and electrolyte disturbances
 If patient is symptomatic (seizures, tetany,
positive Chvostek’s or Trousseau’s) or at high
risk of developing symptomatic
hypocalcaemia (post-parathyroidectomy), use
IV replacement
o Calcium gluconate is preferred
o Calcium chloride is very irritating and
should be given via a central line
o Do not co-infuse or mix calcium with
phosphate containing preparation
 For oral replacement use
o Effervescent calcium tablets
o Calcium carbonate tablets
o Give away from food
 If resistant to treatment, exclude
hypomagnesaemia
Electrolyte solutions are incompatible with blood
products, other medications and often each other.
Seek advice before mixing together in an infusion or
giving simultaneously via the same IV line.
Hospital Insulin Management
Insulin Types
Rapid Novorapid (aspart), Lispro, insulin glulisine
Short Actrarpid, Humulin R
Intermediate Protaphane (isophane), Humulin NPH
Long/Basal Lantus (insulin glargine), Levemir (insulin
detemir)
Patients NOT PREVIOUSLY on Routine Insulin
1. If not starting an insulin infusion give a stat
dose of subcutaneous rapid/ short acting
insulin shown in table 1
2. Discontinue all oral hypoglycaemia agents,
except metformin unless contraindicated
a. Metformin 2g dose if eGFR >60
b. Metformin 1g ½ dose if eGFR 30-60
c. Metformin contraindicated if eGFR
<30
3. Order continuing in-hospital intensive insulin
treatment to prevent recurrent
hyperglycaemia according to dietary intake
a. Eating: order basal, mealtime and
supplemental doses (given as a
supplement to mealtime insulin only,
not 6 hourly)
b. Not- eating: and insulin infusion not
appropriate, order basal and 6 hourly
supplemental doses. Ensure constant
rate of glucose provided by either as
IV fluids or enteral feeds
Initiating Intensive Insulin Treatment in Hospital (>2
injects per day. Does not include stand-alone short
acting insulin sliding scales)
 Calculate total daily insulin unit intake. (0.3-
0.4 or 0.5 x weight (kg))
 Separate into bolus (long acting) dose and
total rapid acting doses by dividing by two (or
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
 Oesophageal stricture due to risk of
perforation
 Basilar skull fracture or facial fracture due to
potential for intracranial misplacement
 NG tubes should also be avoided in patients
with oesophageal varices because tube
placement may trigger variceal bleeding
 In patients with bleeding diathesis, minimal
trauma to the pharynx, oesophagus or
stomach from NG tubes can also lead to
severe bleeding
Confirmation of Placement
Radiographic
 Always confirm the position of enteral feeding
tubes, radiographically before formula or
medications are given
 Patients who cannot express their problems
(children, infants, intubated patients) should
always have radiographic confirmation of
tube placement prior to any use of the tube
 The tip of a decompressive NG tube should be
positioned into the most dependent portion
of the stomach
Clinical Confirmation
 The main lumen is aspirated. If gastric
contents are returned, the tube can be tested
by flushing with 20 to 30 ml of warm water
with a large syringe, and the water
immediately suctioned back into the syringe.
 If most (~70%) of water can be retried, the
tube is likely in the proper position. If an
insufficient amount of fluid returns, the tube
should be readjusted and the test repeated
 Auscultating over the epigastrium during air
injection into any tube is not an accurate way
to evaluate tube position
 For gastrointestinal decompression,
confirmation of the tube’s position by clinical
means is usually adequate
Tube Fixation
 It should be taped securely to the nose, but
care should be taken not to push the tube up
against the nares because pressure ulceration
or necrosis can occur
 The tube can then be secured to the patient’s
gown with a safety pin
Management
 The proper functioning of the NG tubes
should be routinely checked every four to
eight hours by irrigating the tube
 Many patients experience oropharyngeal
discomfort, which usually resolves in 24 to 48
hours. Local anaesthetic spray applied to the
oropharynx may alleviate some of the gag
reflex
 New onset of gagging or respiratory
difficulties should raise the concern of
migration into the oropharynx and indicates
the need to re-evaluate the position of the
tube
 They should be removed when the indication
for placement no longer exists
Complications
 Malposition, coiling or knotting of tubes
 More susceptible to reflux of gastric contents
which may lead to oesophagitis, oesophageal
stricture, gastrointestinal bleeding or
pulmonary aspiration
 Tubes can cause gastritis or gastric bleeding
due to chronic irritation or pressure necrosis
due to suctioning of the gastric mucosa
 Increased risk of pulmonary complications
such as pneumonia and pulmonary abscess,
tracheal perforation and pneumothorax
 Nasal alar ulceration or necrosis
 Perforation
Guidelines for Anticoagulation using Warfarin
1. Prescribing Principles
 Consider if the benefits of anticoagulation
outweigh the risks (bleeding) for each patient
 Ensure pre-treatment INR, platelets and liver
function tests are normal
 The imitating team must complete target INR,
indication, initial dose and consider duration
of therapy
  If admitted on warfarin, an INR must be
performed within 24 hours of admission, then
every 2 to 3 days and documented in warfarin
section of medication chart. If an INR has not
been performed within 24 hours, warfarin is
no to be administered until and INR is
available to guide dosing decisions
 Check patient has received education and
warfarin leaflets before discharge. Ask
pharmacist for assistant
2. Starting Warfarin Therapy
 Acute DVT or PE: start warfarin on same days
as therapeutic unfractionised or LMW heparin
and overlap for a minimum of 5 days, until
target INR reached for at least 2 consecutive
days
 Chronic AF and valve replacements: start
warfarin alone (may overlap with prophylactic
heraprin)
 Post-operative patients: restart with their
normal pre-operative maintenance dose- do
not re-load
 High loading doses, such as 10mg, should not
be used due to an increased in the risk of
bleeding
3 Recommended starting nonogram for patients with
no risk factors or increased sensitivity to warfarin
 Begin with 5mg if INR <1.4
 If INR remains < 1.4 at day 4, use 10mg
 Taper dose down if INR within target range
 Warfarin takes around 3 days to work
 After day 4, dose is based on clinical
judgement
4. Risk Factors for Increased Sensitivity to Warfarin
 Age greater than 75 years
 History of bleeding or falls
 Baseline INR > 1.4
 Concomitant drugs affecting warfarin
metabolism
 Co-morbidities: hypertension, cerebrovascular
disease, ischaemic stroke, heart disease, renal
insufficiency, hepatic impairment or low
platelets, malignancy
 Major surgery within the preceding 10-14
days
 If risk factors, consider a smaller loading dose
(2-4mg) and seek senior/ specialist advice
 If no risk factors, follow the recommended
nomogram and monitor INR daily
5. Recommended target INR ranges and minimum
duration
Indication INR Target Min
Duration
Valve repairs, bioprosthetic valve 2-3 6 weeks
post op
DVT/ PE 2-3 3 months
AF; Irreversible, clinical hyper- 2-3 Life-long,
coagulable states, mechanical AVR balanced
with no risk factors against risk
High risk mechanical heart valves; 2.5-3.5 Life-long,
mechanical MVR; mechanical AVR balanced
with risk factors against risk
*Risk factors: AF, previous VTE, hypercoagulable
states, left ventricular dysfunction or older generation
AVR
6. Perioperative Thromboembolism Risk Stratification
Low Risk: bridging unlikely required
 Mechanic valve present- discuss with
cardiologist
 AF and no history of cardiac embolism or
CHADSVASC score 0-4
 One DVT or PE more than three months ago
 Prior VTE and low risk thrombophilia
Moderate to High Risk: consider bridging
 Mechanic valve present- discuss with
cardiologist
 Rheumatic AF (mitral valve disease stenosis/
regurgitation)
 AF with history of cardiac embolism or
mechanical heart valve in any position or
CHADSVASC score 5-9
 VTE within the past three months or very
strong family history
 High risk thrombophilia: deficiency of protein
c, protein S or antithrombin 3; homozygous
factor 5leiden mutation, antiphospholipid
antibody syndrome; more than one laboratory
thrombophilic defect (compound
heterozygotes)
 Two or more arterial or iodipathic venous
thromboembolic events
7. Managing Warfarin therapy during Invasive
Procedures
Low Risk
 Before surgery
o Withhold 4 daily doses of warfarin
before surgery
o Night before surgery: if INR greater
than 2, give 3mg vitamin K IV or oral
o Day of surgery
 If INR ≤1.5, surgery can
proceed
 If INR > 1.5, defer surgery or if
urgent, give Promthrombinex
or fresh frozen lasma
 Employ pre-operative
thromboprophylaxis as per
hospital policy
 After surgery
o Start warfarin on the day of surgery at
the previous normal maintenance
dose as long as there is no evidence of
bleeding
o Employ thromboprophyalxis as per
hospital policy
Moderate to High Risk
 Before surgery
o Option 1: planned surgery
 Without 4 daily doses of
warfarin before surgery
 2 to 3 days before surgery:
when INR is less than 2
commence treatment dose of
LMWH subcut or UFH IV
 If using LMWH, last dose
should be given at least 24
hours before surgery
 If using URF IV, cease infusion
4 to 6 hours before surgery
o Option 2: planned surgery with stable
INR in preceding weeks
 Night before surgery: if INR is
stable at 2-3 in the 2 to 4
weeks preceding surgery, give
3 mg vitamin K IV or oral
 Day of surgery: if INR ≤1.5,
surgery can proceed, if INR
>1.5, defer surgery or give
prothrombinex or FFP
o Option 3: urgent surgery
 For urgent surgery, check INR
before surgery and give
prothrombinex depending on
initial and target INR
 For procedures with low risk
of bleeding, warfarin may not
need to be ceased
 After surgery
o Recommence warfarin as soon as
possible at the previous normal
maintenance dose as long as there is
no evidence of bleeding- do not
reload
o Consider bleeding risk against
thrombosis
o Start LMWH or UFH 12 to 24 hours
post operatively
o Consider delaying resumption of
therapeutic LMWH for 48 to 72 hours
after major surgery
o Continue LMWH or UFH for minimum
of 5 days and cease 48 hours after
target INR is reached
o In surgery with high risk of bleeding,
consider using prophylactic dose
LMWH or UFH IV only and cease 48
hours after target INR is reached
8. Recommendations for reversal of warfarin
Clinical Setting Recommedation
INR 3.0 – 4.5 and Reduce or withhold next dose of warfarin
NO BLEEDING Resume lower dose of warfarin one INR
approaches therapeutic range
INR 4.5 – 10 and Cease warfarin.
NO BLEEDING Consider reasons for elevated INR and patient
factors.
Vitamin K usually not required unless bleeding
risk is high- give vitamin K
Check INR within 24 hours. Resume lower dose
once INR reaches therapeutic range
INR > 10 and Cease warfarin.
NO BLEEDING Given vitamin K PO or IV. If bleeding risk high,
give prothrombinex
Check INR in 12 to 24 hours and continue to
monitor every 1 to 2 days over the following
week
Resume lower dose of warfarin once INR
approaches therapeutic range
INR ≥1.5 with life- Cease warfarin. Give vitamin K IV,
threatening prothrombinex and fresh frozen plasma
bleeding Assess INR frequently until clinically stable
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
prescribed a regular antiemetic for the frist
week, then PRN
 Oral agents: cyclizine (antihistamine,
anticholinergic), domperidone
(antidopaminergic), metoclopramide (good in
gastric stasis), haloperidol (effective in drug or
metabolic induced nausea), ondansetron
(good for chemo/radiotherapy related
nausea), levomepromazine (broad spectrum,
but can sedate)
Constipation
 Very common side effect with opiates, and
better prevented than treated
 May be due to ↑ Ca2+ or dehydration
 Use disacodyl at night or combine with a
stimulant with a softener.
 Macrogols are useful in resistance
 Try glycerol suppositories or an enema if oral
therapy fails
Breathlessness
 Consider fans, air supply and supplementary
oxygen
 Morphine reduces respiratory drive and thus
relieves the sensation of breathlessness.
 Use of relaxation techniques and
benzodiazepines can be useful
 Look for pleural or pericardial effusion.
Consider thoracocentesis ± pleurodesis for a
significant pleural effusion
Mouthcare
 Treat any candida infection or other
underlying cause
 Simple measures such as chewing ice chips,
pineapple chunks (release proteolytic
enzymes) or gum should be tried
 Good oral hygiene with mouth washes,
chorhexidine and saliva substitutes such as
biotene oral balance can help
Pruritus
 Treat causes: try soothing bland emollients,
emollient bath oils, sedative antihistamines at
night (chlorphenamine)
Local Systemic
Eczema, atophy, urticarial Liver disease
Scabies Uraemia
Lichen Planus Malignancy (lymphoma)
Dermatitis Herpetiformis Diabetes Mellitus
Spinal cord tumours (rare Drugs (morphine)
Thyroid disease
HIV
Iron deficiency Anaemia
Polycythemia Rubra Vera
Venepuncture Problem
 Repeated venepuncture with the attendant
risk of painful extravasation and pheblitis may
be avoided by insertion of a single or
multilumen skin-tunnelled catheter (Hickman
line) into a major central vein
 Patients can look after their own lines at
home, and give their own drugs.
 Problems: infection, blockage (flush with
saline or dilute herapin), axillary, subclavian or
superior vena cava thrombosis/ obstruction
and line slippage
The Last Days and Weeks of Life
 Once a decision has been made that patient is
entering the very final days of their illness,
comfort should be the main concern
 Thinking about stopping observations,
unnecessary blood tests and medications
(such as for long-term prophylaxis)
 Prescribed PRN subcutaneous end of life
drugs before they are needed
 Start a syringe driver if any of these are being
given regularly
 Ensure that a do not attempt resuscitation
order has been made and clearly documented
(usually by a senior doctor)
 Personalised end-of-life care plans should be
made, which focus on control of symptoms,
comfort and cessation of unnecessary
interventions
 Consider whether transfer to a hospice may
be appropriate. If home is a priority, it can be
arranged at very short notice
Syringe Drivers
 Allow continuous subcutaneous infusion of
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