Hospital Based Practice – Confusion.

Confusion.
• Can be:
o Acute or sub – acute.
 Delerium
o Chronic and progressive.
 Dementia
• Causes of delirium can also exacerbate dementia, to give a acute on chronic
picture.
• Confusion in the elderly is very common
o Can be exacerbated by admission to hospital.

Differential diagnosis of confusion.

• Dementia.
o Commonly.
 Alzheimer’s disease
 Vascular dementia
 Lewy body dementia
 Fronto – temporal dementia
o Rarer:
 Chronic alcohol abuse
 Huntington’s chorea
 CJD
 Parkinson’s disease
 Pick’s disease
 HIV
 Pellagra
 Subacute sclerosing panencephalitis
 Progressive multiple leukencephathy
 Pellagra.
• Niacin deficiency
 o Treatable causes.
 Have to be excluded in all patients.
 Deficiencies
• B12
• Hypothyroidism
• Thiamine
 Subdural haematoma
 Normal pressure hydrocephalus
 Neurosyphilis
 Resectable tumour
 Depression
• Pseudodementia.

• Delerium
o Infection.
 Any
 Most commonly
• UTI
• Pneumonia
• Cellulitis
• Meningitis
• Encephalitis
o Drug intoxication.
 Opiates
 Anxiolytics
 Steroids
 Tricyclics
 Anticonvulsants
 Drugs of abuse.
o Drug withdrawal.
 Alcohol
 Benzodiazepines.
o Metabolic.
 Failures.
• Liver
• Kidney
• Cardiorespiratory.
o Hypoxia
o Hypercapnia
 Electrolytes.
• Hypernatraemia
• Hyponatraemia
• Hypoglycaemia
• Hypercalcaemia
o Vitamin deficiencies.
 Thiamine.
• Wernicke – Korsakoff
o Cerebral pathology.
 Abscess
 Tumour
 Haemorrhage
 Infarction
 Trauma
 Epilepsy
 Post - ictal
o Pain
o New surroundings.
 Hospital ward.
• Possibly without good hearing (missing/
forgotten hearing aid)
• Possibly without good sight (missing/ forgotten
glasses)
History in the confused patients.
• Establish whether patient has delirium or dementia.
o Good collateral history from:
 Relatives
 Carers
 Close friends
o Review previous hospital notes.
o Good social history is vital.
 Allows the problems to be put in context.
• Try and identify possible causes for the confusion.

• Pattern of confusion.
o Confusion developing 2 days after hospital admission could be due
to alcohol withdrawl.
o Delerium.
 Develops over hours – day.
 Characterised by:
• Clouding of consciousness
• Fluctuating in severity.
o Worse at night.
o May have lucid periods during the day.
• Poor recent memory
• Disorientation
• Hallucinations
 Patient may appear.
• Agitated
• Uncooperative
• Paranoid
o Dementia.
 Gradual onset over months to years.
 Characterised by:
• Global deterioration in higher cerebral functions.
 • No change in levels of consciousness
• Deterioration tends to be progressive
• Often exacerbated by removal from familiar
environment.
• Multi – infarct dementia progresses in a stepwise
fashion.

o More rapid onset occurs with:

 CJD
 Hydrocephalus
 Depression
o Depression can be suggested by:
 Complaining of memory loss.
• Patients with dementia or delirium tend not to
realise that their losing their memeory.
• Poor effort at attempting tests.
• Personal or family history of depression.

Possible underlying causes.

• Age.
o Dementia becomes increasingly common after 60 years.
o In younger patients a thorough search for an underlying cause
should be made.
• Underlying infection
• Raised ICP
o Headache worse on:
 Coughing
 Sneezing
 Leaning over
o Headache worse in the morning.
o Visual disturbances.
 Due to papilloedema
o Nausea and vomiting
o Diplopia.
 False localising
 CN VI palsy
• Risk factors or known vascular disease.
o Previous CVD, Stroke, TIA
 o Age
o Sex
o Smoking
o Elevated Blood pressure
o Diabetes
o Exercise
o Cholesterol
o Genetics

• Dietary history.
o Vitamin deficiency
o Alcohol use
 Chronic alcohol abuse
 Folate and thiamine deficiency.
• Previous head injury.
o Subdural haematoma
• Drug history.
o Sedatives
o Anticonvulsants
o Steroids
• Other neurological symptoms.
o Cerebrovascular disease
o MS
o Cerebral tumour
o Cerebral abscess.
• Past medical history.
o Renal disease.
 Uraemia
o Malignancy.
 Brain metts
 Hypercalcaemia
 Paraneoplastic
o Diabetes.
 Insulin overload
• Family history.
o Wilson’s disease.
 Autosomal recessive
o Huntingdon’s chorea.
  Autosomal dominant.
o Depression

• Brief psychiatric history.

o Particularly symptoms of depression.
 Poor sleep
 Loss of interest in things
 Guilt
 Poor energy
 Poor concentration
 Anxiety
 Psychomotor retardation
 Suicidality

Examination of the confused patient.

• Since causes of confusion are so varied, a thorough clinical exam should be
conducted.
• Particular attention should be paid to.
o Glasgow Coma Scale.
Category Response Score
Best motor response Moves on command 6
Localises to pain 5
Withdraws from pain 4
Flexes to pain 3
Extends to pain 2
No movement 1
Best verbal response Coherent words 5
Confused speech 4
Inappropriate speech 3
Grunting 2
No speech 1
Best eye opening Spontaneous 4
response
On command 3
To pain 2
No opening 1

o Cyanosis.
 Hypoxia is a common cause of confusion in hospital
 Oxygen saturation should be performed.
o Blood pressure.
 Hypotension.
• Overwhelming infection
• Cardiac failure
 Hypertension.
• Risk factor for cerebrovascular disease.
• Can be caused by raised intracranial pressure.
o Blood glucose.
 Hypoglycaemia.
o Evidence of head injury.
 Subdural haematoma.
o Signs of infection.
 Temperature.
 Neck stiffness
 Consolidation on CXR
 Signs of endocarditis
 Abdominal tenderness
 Otitis media
 Pressure sores
 Cellulitis.
o Mental state.
 AMT is used for
• Confirming confusion
 • Monitoring progress.
 MMSE is used for:
• Diagnosing dementia
• Providing a baseline for monitoring of
deterioration.

 Abbreviated Mental Test.

 Address for recall. 42 West Street.
 Age
 Date of birth
 Time ( to the nearest hour)
 Year
 Name of this place
 Recognition of 2 people
 Year of WWI
 Name of current monarch
 Count backwards from 20
o Focal neurological deficit.
 Pattern of signs may provide clues to the diagnosis.
 Fundoscopy to look for
• Papilloedema.
o Raised ICP
• Optic atrophy.
o Demylination
• Subhyaloid bleeding
o Subarachnoid haemorrhage
 Parkinsonism
 CJD signs.
• Myoclonus
• Extrapyrimidal signs
 • Aphasia.
o Signs of chronic liver disease.
 Hepatic encephalopathy can cause confusion.
 Chronic liver disease may also indicate:
• Alcoholism
• Wilson’s disease.
 Malignancy.
• Breasts
• PR
• Lymph nodes
• Skin

Investigating the confused patient.

Blood
• FBC.
o Reactive picture in
 Malignancy
 Infection
 Inflammation
o Anaemia, with raised MCV in deficiency of:
 B12
 Folate
• ESR.
o Raised in
 Malignancy
 Infection
 Inflammation
o U&Es.
 Hyponatraemia

 Hypernatraemia
o LFT.
 Abnormal in liver disease.
 γ – glutamyl transferase raised in alcohol consumption.
 o Thyroid function test.
 Low T4 in hypothyroidism
o Serum calcium
 Hypocalcaemia
 Hypercalcaemia
o Serum glucose
o Serum B12 and red blood cell folate.
o Syphilis serology
o ABG
o Blood culture.
 If considering infection.

Urine
• MSU for:
o Microscopy
o Culture
o Sensitivity.

Radiology
• CXR may show:
o Pneumonia
o Cardiac failure
o Malignancy
• CT of MRI of head may show:
o Tumour
o Infarction
o Haematoma
o Hydrocephalus
o Abscess.

Other tests
• When clinically indicated, consider:
o Malaria.
  Thick & thin films.
o HIV serology
o Urine toxicology screen
o Thiamine deficiency
 Red cell transketolase.
o Wilson’s disease.
 Low serum copper
 Low caeruloplasmin
 Raised 24 – hour copper excretion.
o Electroencephalogram.
 Typical changes in herpes simplex encephalitis.
o Lumbar puncture & CSF examination.
 Protien
 Glucose
 Microscopy
 Culture
 Oligoclonal bands.

Pathway for managing confusion.

 Confusion

History &
Examination

Acute/
Longstanding
subacute

FBC
FBC
U&E
U&E
Biochemistry
Glucose
B12/ folate
LFT
TFTs
ABGs
Syphilis
Sepsis screen
serology
Drug screen
Consider CT
Consider CT

Biochemistry Temperature
CT Scan Drug history Untreatable Treatable
ABGs Cultures

B12/ folate
deficiency
Hypothyroidis
Abscess Failure of:
Alzheimers Thiamine deficiency
Tumour Cardiac
Intoxication Vascular Subdural
Haemorrhage Respiratory Sepsis
Withdrawl Lewy body haematoma
Haematoma Liver
Fronto – temporal Hydrocephalus
Infarction Renal
Syphilis
Tumour
Depression

Alcohol withdrawl.
• Acute onset of confusion in the recently hospitalised is acute alcohol
withdrawl/ delirium tremens until proven otherwise.
o Check serum phosphate.
o Can be > 0.4 mmol/L in acute withdrawl.

• If left untreated, risk of:

o Seizures.
o Permanent neurological deficits.
o Death

• Minor symptoms can be managed at home by the GP.

o Often a short admission is more effective
o Allows close observation for:
 Complications
 Psychosocial assessment
 Rehabilitation.
o Admission particularly important if:
 History of seizures
 Signs of Delerium Tremens

• Presentation.
o Initially.
 Anxiety
 Tremor
 Hyperactivity
 Sweating
 Nausea & retching
 Tachycardia
 Hypotension
 Mild pyrexia.
 Insomnia
 Sweating
o Symptoms normally peak at 12 – 30 hours, and subside by 48
hours.
 o May be complicated by generalised tonic – clonic seizures.
 “Rum Fits”
 Rarely progress to status epilepticus.
 Distinguished from epilepsy by EEG.
 May be precipitated by flickering lights.
 Particularly likely to occur in those with epilepsy

• Delerium tremens.
o Occur in < 5% of acute withdrawl p[aitents.
o Usually 3 – 4 days after abstinence.
o Untreated, is associated with mortality of 15%.
o Features include.

 Disorientation
 Labile mood
 Irritability
 Coarse tremor
 Agitation
 Confusion
 Delusion
 Hallucinations
• Visual
• Auditory
 Fever
• Occisionally severe
 Sweating
 Tachycardia
 Acidosis.
• Rare
• Ketoacidotic
• Lactic.
 Also be aware of:
• Hypoglycaemia
• Wernicke – Korsakoff psychosis
• Subdural haematoma
• Hepatic encephalopathy.
• Management.
o General management.
 Nurse in a well lit room to prevent disorientation.
 Rehydrate.
• IV fluids if needed
• Avoid saline in patients with chronic liver
disease.
 Monitor urine output.
 Vitamin supplements.
• Parbinex 2 – 3 ampulles
• Treat for 5 days
• Give as slow IV over 8 hours
• Beware of anaphylaxis.

• Oral therapy for 1 week.

o Thiamine 100 mg BD
o Vitamin B 2 tablets TDS
o Vitamin C 50 mg BD
 Monitor and treat BM for hypoglycaemia.
 Severe hypophosphataemia may complicate alcohol
withdrawl.
• Give IV polyfusor phosphate if serum phosphate
< 0.6 mM
 Exclude intercurrent infection.
• Pneumonia
• Urine
• Skin
 Beta – blockers may be useful for hypertension.
o Sedation.
 Long – acting benzodiazepines are often used.
• Commonly used.
o Chlordiazepoxide (Librium)
 30 mg QDS for 2 days.
 20 mg daily for 2 days
 10 mg daily for 2 days
 5 mg daily for 2 days
 Women should be started on 20
mg and tapered down
 Reduce dose if:
• Liver disease
• Elderly
• Thinness
o Diazepam (Valium)
• Lorazepam is metabolised by the liver
o Contraindicated in liver disease.
• Chlormethiazole is no longer used regularly.
o Highly dependency inducing
o Dangerous if combined with alcohol.
• Carbamazepine.
o Effective as benzodiazepines.
o Use limited by side effect profile.
 Drowsiness
 Headache
 Migraine
 Motor co – ordination
impairment
 Upset stomach
 Less commonly.
• Arrythmias
• Blurred vision
• Pancytopaenia
• Aplastic anaemia
 o Start with 200 mg daily as divided does
o Increase to 400 mg daily over next 2 -3
days
o Taper off by day 8.

• Haliperidol.
o For severe agitation
o 10 mg IM

• Wernicke – Korsakoff syndrome.

o Wernicke disease consists of a triad of:
 Ophthalmoplegia.
• Nystagmus
• Nerve VI palsy
 Cerebellar ataxia
 Confusion
o In Korsakoff syndrome.
 Confusion predominates
 Often presence of:
• Psychosis
• Amnesia.
o Retrograde
o Antegrade
• Confabulation.
 Causes permenant neurological damage.
o Diagnosis by reduced red – cell transketolase activity.
o Treat with IV thiamine on clinical suspicion.

• Seizures.
o Withdrawl symptoms are typically self limiting.
o If needed, give IV diazepam.
 10 mg over 5 minutes.
o Give chlordiazepoxide.
 Not chlormethiazole or carbemazipine.
o Phynetoin.
 Less effective.
 Added if history of epilepsy or recurrent seizures.
 • Follow up
o Referral to alcohol abuse team.
o Maintain vitamin supplementation
o Screen for residual cognitive impairment
o Involve Occupational therapy before discharge.

Diabetic ketoacidosis.
• Predominantly occurs in Type I diabetics.
• Increasingly being recognised in some Type II diabetics.
o Afro – Caribbean patients.

Presentation
• Polyuria & polydypsia.
o Increasing dehydration over a few days.
• Weight loss
• Weakness
• Hyperventilation or dyspnoea.
o Due to acidosis
o Kussmaul’s breathing
 Deep sighing respiration.
• Abdominal pain.
o Have to be excluded in an acute abdomen.,
• Vomiting.
o Exacerbates dehydration
• Confusion.
o 10% develop coma.
• On examination assess for:
o Hydration status.
o Ventilation rate
o Smell of ketones.

Investigations.
• Blood glucose.
o Not always high.
o Patient can be severely acidotic at values as low as 10 mM.
 Eg. if patient has recently taken insulin.
• ABGs.
 o Assess degree of acidosis.
• U&Es.
o Sodium will need to be corrected.

1.6 x [Glucose]
Corrected Sodium = [Na+] + – 1.6
5.5

o Assess Potassium
o Assess renal function.

• Urinalysis.
o Ketones strongly positive.
o Starvation can cause mild ketones in normal patients.
o Sulphydryldrugs, like captopril, can cause false positive for
ketones.
• FBC.
o WCC will be raised
 Mainly neutrophiles.
o Leukaemoid reaction can occur in absence of infection.
• Septic screen.
o Blood culture.
o Urine culture.
• Plasma ketones.
o Many labs do not regularly perform, so need to be specifically
asked for
• CXR.
o Look for signs of infection
• Amylase.
o May be high with abdominal pain ± vomiting in absence of
pancreatitis.
o Acute pancreatitis will occur in 10% of patients with DKA.

Common precipitants of DKA.

• Infection.
o 30%
• Non – compliance with treatment.
o 20%
• First presentation of diabetes.
o 25%

Poor prognostic factors in DKA.

 • pH < 7.
• Oliguria
• Serum osmolality > 320
o Serum osmolality = 2([Na] + [K]) + [urea] + [glucose]
• Newly diagnosed diabetes.

Notes.
• Diagnosis of DKA requires:
o Positive urine or plasma ketones
 Some labs don’t record plasma ketones.
 Can be estimated on the ward by diluting plasma to 1:1
with normal saline and testing with urine diptix.
• Result of +++ corresponds to plasma ketone of 5
mmol/L
o Arterial pH < 7.3 and/ or serum bicarbonate > 15 mmol/L
• Elderly patients may present as hyperglycaemic and ketotic, but with a
relatively normal acid – base balance. However, they are:
o Not in DKA
o Not necessarily insulin dependant.
• Always consider other causes of hyperglycaemia and acidosis.
o Aspirin overdose
o Lactic acidosis.
 Particularly in elderly.

Management.
• Consider arterial line to monitor:
o ABGs
o Potassium.
• Make patient Nil by mouth for at least 6 hours.
o Gastroparesis is common.
• Insert NG tube if GCS is reduced.
o Aspirate stomach contents due to risk of aspiration.
• Insert urinary catheter.
o Oliguria
o High serum creatinine
• Broad spectrum antibiotics if infection suspected.
• LMWH should be given as DVT prophylaxis.
o Good idea.
o Not yet standard clinical practice.
• Half life of insulin is short.
o Continued replacement by IV or SC is essential.

• General methods.
o Mainstays of treatment.
 Rehydration
• Site the IV cannula for rehydration well away
from any major wrist veins.
o This large vein may be needed for AV
fistula if patient develops diabetic
neuropathy.
• Insert central line in patients who have a history
of:
o Cardiac disease.
o Autonomic neuropathy
o Elderly.

• Use normal saline ± potassium until BM < 12

mmol/L.
• Average fluid loss in DKA is 3 – 6 L.
o Aim to restore this over 24 hours.
• If hypotensive and oliguric (and no history of
heart disease), give following regime:
o IV colloids ± N saline to restore BP.
o 1 L saline over 30 minutes.
o 1 L saline every 2 hours, for 8 hours.
 Add potassium based on
current serum potassium.
Plasma Potassium
potassium added to each
(mmol/L) litre (mmol)
< 3.0 40
< 4.0 30
< 5.0 20
  Potassium can be depleted by
1000 mmol.
 Plasma potassium can rapidly
fall as potassium shifts into
cells under action of insulin.
 Use less potassium in patients
with:
• Renal impairment
• Oliguria.
o 1 L saline every 4 hour, with potassium
added as above.
 Until fully rehydrated.

• Use of bicarbonate is controversial.

o If pH < 7 give isotonic (1.26%)
bicarbonate at 500 ml/h..
 Faster rates cause paradoxical
intracellular acidosis.
o Add 10 – 20 mEq Potassium per 500 ml.
o There is no evidence that use of
bicarbonate improves outcome in DKA.
• When BM < 12 mmol/L start
o 5% dextrose infusion
o Continuous insulin infusion.
 Continuous insulin is required
to inhibit ketoacid production.

 Insulin therapy.
• Dilute 50 units of actrapid insulin in 50 ml 0.9%
saline, and administer by IV infusion.
• Start off infusing at 0.1U/kg/h.
o This is 7 units/hour for a 70kg patient.
• If BM falls by 5 mmol in one hour, halve rate to
0.05 U/kg/h.
• When BM < 12 mmol/h, change the infusion for
one diluted in 5% dextrose rather than saline.
o Infuse according to the sliding scale
below.
• BM should be checked hourly, and rate altered.
 Blood glucose Insulin
(mmol/L) infusion
(units/hour)
0.0 – 2.0 Stop insulin –
call specialist
2.1 – 4.0 Call specialist
4.1 – 7.0 0.5 – 1
7.1 – 11.0 2
11.1 – 20.0 4
> 20. 7 – call
specialist

• This sliding scale is a guide, and should be

tailored to the patient and response to therapy
• Aim for fall in BM of 5 mmol/h, with correction
of acidosis and plasma bicarbonate levels.
• If glucose or acidosis not changing, increase
insulin rate accordingly.
• Keep BM = 10 – 14 mmol for the first 24 hours.
o Or until ketoacidosis resolves.
o Use 5% dextrose infusion to do this.
• Maintain IV insulin until 4 hours after regular SC
insulin is restarted.

Complications
• Assessment during treatment.
o Rapid normalisation of biochemistry can be detrimental in all
patients.
o Better to be cautious and less than perfect, than be enthusiastric and
dangerous.
o Check ward BM hourly.
 Check lab BM 4 hourly.
o Check electrolytes every 2 hours, reducing to 4 hours when patient
consistently improving.
 Main risk is hypokalaemia.
 o Do ABGs every 4 hours, until persistent improvement or
normalised.
o Check plasma osmolality every 4 hours.
o Consider need for regular/ continuous ECG monitoring for T –
wave changes
o Check phosphate daily.
 Falls due to treatment.
 Moved intracellular with potassium.
 If phosphate drops to < 0.4 mmol/L.
• Monobasic potassium phosphate IV infusion
• Don’t exceed rate of 0.75 mmol/h.
• Check preparation with pharmacist.
o Check magnesium levels daily.
 May fall during insulin therapy.
 If levels fall < 0.6 mmol/L
• 4 – 8 mmol in 50 ml 0.9% saline over 15 – 30
minutes.
• Repeat as necessary.

• Complications.
o Main complications.
 Hypokalaemia
 Hypophosphataemia
 Hypoglycaemia
• Due to over zealous insulin replacement.
 Hyperchloraemic acidosis
• A high anion gap acidosis in a well – hydrated
patient.
• May be seen in:
o Excessive administration of saline.
o Increased consumption of bicarbonate.
• No specific treatment is required, just correct
acidosis.
 Cerebral oedema.
• Mainly in children
o May be precipitated by sudden shifts in
plasma osmolality.
o Symptoms include:
 Drowsiness
  Severe headache
 Confusion
o Management.
 Open airway.
 Give oxygen
 Consider invasive ventilation.
• Enforced
hyperventilation can
blow off carbon
dioxide and reduce
ICP.
 Correct hypotension
 Treat seizures
 Give IV mannitol at 0.5 g/kg
body weight.
• Repeat as necessary.
 Transfer to ITU.
o Mortality of 70%
o Full recovery of normal function about
7 – 14 %

 Thromboembolism.
• Tissue hypoperfusion due to dehydration can
trigger coagulation cascade.
• Consider LMWH prophylaxis for those at risk.

Hyperosmolar Non – Ketotic Coma (HONC)

• Occurs in elderly patients with non – insulin dependant diabetes.
• Large risk of venous and arterial thrombi
• Much higher mortality than DKA

• Presentation.
o Elderly
o Previously unknown diabetic.
o Insideous onset of polyuria and polydypsia.
o Severe dehydration
o Reduced GCS.
 Degree correlates with increase in plasma osmolality.
 Osmolality > 440 associated with coma.
 o Respiration typically normal
o May present with:
 CVA
 Seizures
 MI
• Investigations.
o BM.
 Usually > 50 mmol/L
o U&E.
 Dehydration.

• Greater rise in urea than creatinine.

• If units are ignored (as urea is in mmol/L and
creatinine is in μmol/L), ratio of Cr:U is about
20:1.
 Significant hypernatraemia.
• Can be obscured by a high glucose.
• Corrected sodium concentration can be
calculated.

• Before relying on corrected results, check that

lab doesn’t already measure ionic sodium.
• As glucose falls, hypernatraemia may appear to
worsen.
• If glucose is high enough, patients may present
with a pseudohyponatraemia.
 Plasma osmolality
• Calculated as 2([Na+]+[K+]) + [urea]+[glucose]
• Should be > 350 mosm/kg for diagnosis.
o ABGs.
 Relatively normal.
 Compare with DKA
 Coexistant lactic acidosis significantly worsens prognosis.
o FBC.
 Polycythemia may indicate dehydration
 Leukocytosis may indicate infection.
o ECG.
 Look for signs of ischemia.
o CXR
 Look for signs of infection.
o Urine
  Dipstix
• Ketones may be due to simple starvation.
• Requires levels of > 5 mM for DKA
 Microscopy
 Culture & Sensitivity
 UTI suggested by urinalysis showing.
• Blood
• Protein.

Management.
• Rehydration and insulin are mainstay.
• Give oxygen if hypoxic on air.
• Nil by mouth for 6 hours.
o Aspirate with an NG tube if reduced GCS to prevent reflux and
aspiration.
• Insert urinary catheter if:
o Oligouria
o High creatinine.
• Anticoagulate with LMWH.
o Enoxaparin 40 mg SC OD

• Fluid replacement.
o Be cautious in the elderly.
o To avoid fluid overload monitor CVP
o Average fluid loss is 8 – 10 L.
 Replace cautiously.
o 1 L saline over first hour
o 1 L saline over 2 hours
 Add potassium as per DKA protocol.
 Continue for 4 hours.
o 1 L saline with potassium (as per DKA protocol) QDS until
rehydrated.
 Should take about 48 hours in total.
 o If corrected sodium is > 160 mmol/.L, use 0.45% saline for first 3
litres.
 Otherwise use 0.9% saline.
 Remember artificial lowering effect of hyperglycaemia.
o When BM < 12 mmol/L, commence 5% dextrose infusion.
 Consider stopping insulin therapy.
 Consider starting oral hypoglycaemics.
 Consider using diet control alone.

• Insulin regimen.
o Similar to DKA protocol.
o With HONK, stopping insulin completely is less dangerous in the
short term than in DKA.

Hypoglycaemic coma.
• All comatose patients are hypoglycaemic until proven otherwise.
o Check with a BM
o Confirm with a lab BM.
• Most common cause of coma in a diabetic is hypoglycaemia due to drugs.
o Long acting sulphonyureas (eg. Glibenclamide) are more prone to
do this than short acting ones.
• Hypoglycaemic patients who are not known to have diabetes should have a
lab BM saved for insulin and C – peptide determination.
o Differential diagnoses.
 Insulinoma
 Facticious drug administration.
o Take these blolods before glucose is given.

• Presentation.
o Sympathetic overactivity ( BM < 3.6 mM)
 Tachycardia
 Palpatations
 Sweating
 Anxiety
 Pallor
 Tremor
 Cold extremeties.
o Neuroglycopaenia ( BM < 2.6 mM)
 Confusion
  Slurred speech
 Focal neurological deficits.

• Stroke – like syndrome

 Coma

o Patients with well controlled diabetes are at increased risk of

hypoglycaemia.
 Can be desensitised to sympathetic sctivation.
 Can develop neuroglycopaenia without warning signs.
o β – blockers blunt the symptoms of sympathetic activation.
 Patients on these drugs lose early warning symptoms.
o Patients with poor diabetes control become hypersensitised to
sympathetic activation.
 Develop warning signs early.
 May present complaining of “going hypo” with a normal
blood sugar.

 Need reassurance and better diabetes control, not glucose.

o Patients with diabetes post – total pancreotomy have more frequent
and severe attacks of hypoglycaemia (“brittle diabetes”)
 Due to lack of glucagons producing α cells, as well as
insulin producing β cells.

Causes.
• Drugs.
o Insulin
o Sulphonyureas
 Particular risk in patients who have a stroke or other
pathology that decreases their food intake.
o Alcohol
 Acute injestion can suppress hepatic gluconeogenesis.
o Salicylates
o Prescription errors.
  Eg. chlopropamide instead of chlorpromazine
o Others.
 Disopyramide
 β – blockers
 Pentamidine
 Quinine
• .Organ failure.
o Hypopituitarism.
 Especially acute pituitary necrosis
o Acute liver failure
o Myxoedmea
o Rarely.
 Congestive cardiac failure
 Chronic renal failure
• Infections.
o Sepsis syndrome
o Malaria
• Tumours.
o Insulinoma
o Retroperitoneal sarcoma

Investigations.
• Blood glucose.
o Check with ward BM
o Confirm with lab BM.
• U&Es.
o Hypoglycaemia is more common in diabetic nephropathy.
• Save serum prior to giving glucose.
o Insulin
 o C – peptide.
o Send 20 ml to lab for immediate centrifuge if indicated.

• Notes.
o Lab glucose < 2.2 mmol/L is defined as a severe attack.
o Coma normally occurs if BM < 1.5 mmol/.L
o Low C – peptide and high insulin.
 Exogenous insulin
o High C – peptide and high insulin.
 Endogenous insulin.
• Sulphonyurea ingestion
• Insulinoma.

Management.
• Acute measures.
o Take blood prior to glucose administration.
o If history of alcohol abuse or malnutrition.
 Give IV thiamine 1 – 2 mg/kg prior to beginning glucose
therapy.
 Risk of precipitating Wernike’s encephalopathy.
o If patient is conscious and co – operative.
 50g oral glucose.
 Eg. lucozade
 Eg. milk and sugar
o If patient unable to take oral fluids.
 50 ml of 50% dextrose IV
o If IV access impossible.
 1 mg glucagons IM
• Less effective if hypoglycaemia due to alcohol.
 Oral glucose to prevent recurrent hypoglycaemia.

o If cause is long – acting sulphonyurea/ long – acting insulin.

 Admit patient.
 Commence continuous infusion of 10% dextrose at 125
ml/h.
 Check B< every 1 – 2 hours.
 • Further management.
o Patients should regain consciousness, or become coherent, within
10 minutes of therapy starting.
 May take 30 – 45 minutes for full cognition to return.
 Don’t give further glucose boluses without rechecking
BM.
o If patient doesn’t regain consciousness in this time.
 Recheck BM
 Consider an alternative cause.
• Eg. head injury due to fall while hypoglycaemic.
o Prolonged severe hypoglycaemia (> 4 hours at < 2.s mmol) may
bresult in permanent cerebral dysfunction.
o Recurrent hypoglycaemia may induce diabetic nephropathy.
 Adaptive process to reduce insulin demand.
 Insulin partly degraded by the kidney.
o Review patient’s medication and inspect all tablets from home for a
possible cause.
o Consider psychiatric review if self – inflicted.

• Liver dysfunction and recurrent hypoglycaemia.

o Hypoglycaemia is common in acute liver failure.
 Coma may occur due to hepatic encephalopathy rather
than hypoglycaemia.
o Hypoglycaemia is rare in chronic liver disease.

Hyponatraemia.
• Presentation.
o Mild hyponatraemia (Na = 130 – 135 mmol/L)
 Common.
• Especially in patients on thiazide diuretics.
  Usually asymptomatic
o Moderate hyponatraemia (Na = 120 – 129 mmol/L)
 Usually asymptomatic.
 Unless it has developed quickly.
o Severe hypotension (Na < 120 mmol/L)
 May be associated with:
• Disturbed mental state.
• Restlessness
• Confusion
• Irritability.
 Seizures and coma prevail as Na < 110 mmol/L

• History.
o Drugs
o Fluid losses.
 Diarrhoea
 Frequency
 Sweating
o Symptoms of Addison’s
o Cardiac disease
o Lung disease
o Liver disease
o Renal disease.

• Examination.
o Focus on careful assessment of volume status.
 Hypovolemic or Normovolemic
 • Patients who are hyponatraemic and
hypovolemic are salt depleted.
 Oedema

o Lying and standing BP

o Heart rate
o JVP ± CVP
o Skin turgor
o Oedema & Ascites
• Investigations.
o Tests should be aimed at excluding other causes of hyponatraemia.
 Assessment of fluid status.
• Capillary refill
• Engorged neck veins
• Orthostatic hypotension
• Ascites
• Skin turgor
 BM
 Serum osmolality
• Compare calculated osmolality with measured
osmolalaity
o Correct sodium if BM is high.
• Osmolar gap increased when having:
o Hyperlgycaemia
o Ethelyne glycol
o Mannitol
 Urine osmolality
 Urine sodium

Hypovolaemic Normovolaemic (normal or slightly raised ECV) Oedematous

states
SIADH: urine osm > 100, serum osm < 260, unine Na > 40 mmol/L
Renal losses Non – renal CNS disorders Malignancy Pulmonary Drugs Others
losses disease
(uNa > 20
mmol/L) (uNa < 20
mmol/L)
Diuretics Vomiting Trauma Lung (oat Pneumonia Opiates Vasculitis CCF
cell)
Adrenal Diarrhoea Stroke TB Haloperidol (eg. SLE) Cirrhosis with
insufficiency Pancreas ascites
(Addison’s Burns Sub – Lung abscess Amitriptyline Abscess
disease) arachnoid Lymphoma Severe renal
3rd space fluid bleed Cystic Cyclophoshamide Meningioencephalitis failure
Intrinsic renal losses Leukaemia fibrosis
Malignancy Vasopressin Severe myxoedema Nephrotic
disease. Prostate Lung
o o Thiodizine Psychogenic syndrome
Hypothyroidism (1 or 2 ) vasculitis
Urinary tract polydipsia
Carbamazepine
SIADH
Clofibrate
Oxytocin
Chlopropramide
Thiazides
Vincristine

• Management
o General principles.
 Mild asymptomatic hyponatraemia will normally resolve
with treatment of underlying condition.
 Correction of hyponatraemia should be gradual to avoid.
• Fluid overload
• Central pontine myelinolysis
o May be delayed 2 – 5 days.
o Often irreversible or only partially
reversible.
o Dysarthrai
o Dysphasia
o Parparesis or quadriparesis
o Lethargy
o Coma
o Seizures.
 Aim to actively get [Na] = 125 mmol/L with IV fluids,
then allow gradual rise as underlying cause is treated.
• Do not increase sodium by > 12 mmol./day.
 Seek expert help if [Na] < 120 mmol/L, or severely
symptomatic.

 Patients with cirrhosis, ascites and severe hyponatraemia.

 • Stop diuretics
• Give volume expansion.
 SIADH, and other conditions associated with plasma
volume expansion, can cuase hypouricaemia due to
increased renal clearance.

o Exclude psuedohyponatraemia.
 Lipaemic serum will be obvious.
 Calculate osmolar gap to check for hidden osmoles
 Exclude possibility of artificially lowered [Na] by not
taking blood proximal to an IV infusion.
o Symptomatic hyponatraemia.
 Ie. Seizures or Coma
 Aggressively increase [Na] by 6 mmol/L over 3 – 4 hours.
 Then increase [Na] more slowly, so total increase is by 12
mmol/L over 24 hours.
 Seek expert help.
 Start IV 0.9% saline at 250 – 500 ml/h.
• Watch out for fluid overload.
 As a rule, if 1 tire of 0.9% saline was instantly infused, it
would raise serum sodium by 4 – 5 mmol/L.
 Alternatively, infuse 5% saline at 50 – 850 ml/h until [Na]
increases significantly
o If dehydrated.
 Start infusion of 0.9% saline.
 Insert central venous line if indicated.
 Monitor fluid output.
• Catheterise bladder if renal impairment.
 Watch out for heart failure.
o If not dehydrated.
 For patients with moderate SIADH, restrict fluid intake to
500 ml/24 hours.
 Seek expert help.
Hypernatraemia.
• As with low sodium, hypernatraemia is normally associated with disorders
of water, not of salt.

• Presentation.
o Symptoms of severe volume depletion.
 Weakness
 Malaise
 Fatigue
 Altered mental state
 Confusion
 Delirium
 Coma

• Investigations
o Assess ECV.
 Neck vein engorgement
 Supine and standing BP
 Cardiac signs of fluid overload.
• Third heart sound
• Oedema
 Skin turgor.
o Assess urine and serum osmolality.
 Serum sodium > 145 mmol/L is always associated with
hyperosmolality.

• Causes.
o Normal or low ECV
 Renal water losses.
• Urine osmolality inappropriately low.
• Diabetes insipidus.
o Central
o Nephrogenic
• Osmotic diuresis with water replacement only.
o Eg, Diabetes Mellitus.
 Non – renal water losses.
• Urinary osmolality > 400 mosmo/L
• Hypotonic GI losses.
 o Eg. diarrhoea

• Cutaneous losses.
o Burns
o Heat shock
o Sweating
o High fever
• Chest infections with prolonged hyperventilation.
o Salt overload (normally iatrogenic)
 Overdose with sodium bicarbonate.
 Post – operatively if huge fluid volumes used.
 In ITU, when volume loaded with saline.
 Concentrated infant formula.
 Conn’s syndrome.
• Hypertension
• Hypokalaemia
• Alkalosis

• Management.
o Avoid rapid and extreme changes in [Na].
 Safer to cautiously change [Na]
o If there is hypovolaemia.
 Start fluid replacement.
 Use 0.9% NaCl to correct hypovolaemia.
 Use 5% dextrose to replace water and gradually reduce
[Na]
o If patient haemodynamically stable, encourage oral fluids.
o Check U&Es twice daily.

Hypocalcaemia.
• Presentation.
o Abnormal neurological sensations & neuromuscular excitability.
o Numbness around mouth
o Parasthesia of the distal limbs
o Hyperreflexia
o Carpopedal spasm
o Tetanic contractions.
 May include laryngospasm
 o Focal or generalised seizures.

o Hypotension
o Bradycardia
o Arrythmias
o CCF
o Chvostek’s sign
 Tap facial nerve anterior to the ear.
 Causes contraction of facial muscles
 Seen in 10% of normal patients.
o Trousseau’s sign.
 Inflate a BP cuff to 10 – 20 mmHg above SBP for 3 – 5
minutes.
 The mild ischaemia will unmask latent neuromuscular
hyperexcitability.
 Carpal spasm is observed.
• Dd for carpospasm is respiratory alkalosis
induced by hyperventilation.
o Rarely.
 Papilloedema
 Extra – pyramidal effects.

• Causes.
o Vitamin D deficiency.
 Asians
 Chronic renal failure
o Loss of calcium from circulation.
 Extra – vascular deposition.
• Hyperphosphataemia.
o Renal failure
o Tuumour lysis
• Acute pancreatits
• Osteoblastic metastases.
o Eg. prostate.
 Intra – vascular binding.
• Citrate
• Blood products
 • Foscarnet.
o Anti – CMV drug.
• Acute respiratory alkalosis.

o Hypoparathyroidism.
 Post – thyroid, parathyroid or other neck surgery.
 Idiopathic
 Pseudo – hypoparathyroidism
• PTH receptors stop responding.
 Infiltration
 HIV infection
o Disorders of Magnesium metabolism.
 Magnesium deficiency.
o Other
 Sepsis
 Burns
 Floride intoxication
 Chemotherapy.
• Eg. cisplatin.

• Investigations.
o Bloods.
 Calcium
 Phosphate
 Albumin
 Magnesium
 Parathyroid hormone
o ECG.
 Prolonged QT time
o Skull X – ray.
 Intercranial calcification.
 Seen especially in hypoparathyroidism.

• Management.
o If hypocalcaemia is difficult to correct, check for magnesium
deficiency.
o Aim of acute management is to reduce the effects of low calcium,
not necessarily to return calcium to normal.

o For frank tetany.

 10ml of 10% calcium gluconate (2.25 mmol) IV over 10
minutes
• NB: Calcium chloride has 4 times more calcium
than calcium gluconate.
• Don’t muddle the two drugs up.
• Generally gluconate is preferred as reduced risk
of:
o Tissue necrosis on extravasation
o Arrythmias.
• Do not give at a higher rate, as risk of arrythmias.
 Next, start calcium infusion at 0.025 – 0.05 mmol/kg/h.
• For 70 kg add 50 ml 10% calcium gluconate, or
10 ml 10% calcium carbonate to 200 ml 0.9%
saline.
• Infuse 50 – 80 ml/h.
o Post parathyroidectomy.
 Mild hypocalcaemia is normal.
 Requires simple monitoring and observation.
 For patients who have parathyroid bone disease (“hungry
bones”).
• Profound hypocalcaemia may occur when
parathyroids are removed.
• May become prolonged, and requiring treatment.
o Chronic hypocalcaemia is best managed with:
 Oral calcium
 Vitamin D.
• If cause is simply low calcium intake/ high
excretion.
 Hydroxylated Vitamin D.
• Hypoparathyroidism.
• Problem with vitamin D metabolism.
 • Eg. Alfacalcidol, Calcitriol.
o If magnesium deficient.
 Take 20 ml (40 mmol) of 50% magnesium sulphate.
 Make it up to 250 ml with 0.9% saline.
 Infuse 50 ml (8 mmol) over 10 minutes.
 Continuing infusing at 25ml/h.

Hypercalcaemia.
• .Free (ionic) calcium is dependent on arterial pH and plasma albumin.
o Increased calcium in acidosis
o Increased calcium in low albumin.
• Ionized calcium = [Ca] + 0.02(40 – [Albumin])
o Most ITU departments now measure ionized calcium.

• Presentation.
o Routine biochemical screen in asymptomatic patients.
o General.
 Depression
• 30 – 40%
 Weakness
• 30%
 Tiredness
 Malaise.
o GI.
 Constipation
 Anorexia
 Nausea & Vomiting
 Weight loss
o Renal.
 Calculi.
• If long standing
 Nephrogenic diabetes insipidus.
• 20%
 Pre – renal failure
 Chronic hypercalcaemic nephropathy
  Polyuria
 Polydipsia
 Dehydration
o Neuopsychiatric.
 Depression
 Cognitive dysfunction
 Coma
 Obtundation.
o Cardiac.
 Hypertension
 Cardiac dysrhythmias.

• Causes.
o Primary (or tertiary) hyperparathyroidism.
 85% of cases.
o Malignancy.
 Humoral hypercalcaemia.
 Local osteolytic hypercalcaemia.
• Myeloma
• Metasteses
o Hyperthyroidism.
 15 – 20% of patients.
o Granulomatous disorders.
 Sarcoidosis
o Drug related.
 Vitamin D intoxication
 Theophylline toxicity
 “Milk – alkali” syndrome
 Thiazide diuretics
 Lithium.
• Mild
• Present in 50% of patients on long – term
lithium.
o Immobilization.
 Paget’s disease
o Benign familial hypocalcuric hypercalcaemia.
 High serum calcium
 Normal 24 hour urinary calcium
  Causes mild symptoms.
• Mild fatigue
• Lethargy
 PTH may be raised.
• Patients don’t respond to parathyroidectomy.
o HTLV – 1 infection.
 May present with sever hypercalcaemia.
o Phaeochromocytoma.
 Part of MEA Type II
 Also acromegaly.
o Adrenal failure
o Rhabdomyolysis
 May cause hypo – or hypercalcaemia.
o Congential lactase deficiency.

• Investigations.
o Bloods.
 Calcium
 Phosphate
 Magnesium
 U&Es
 LFTs
 PTH levels
o CXR
o Urine.
 24 hour urinary calcium
 Urinary cAMP.

• Management.
o Urgent treatment required if.
 [Ca] < 3.5 mmol/L
 Clouding of conciousness
 Confusion
 Hypotension
 Severe dehydration, causing pre – renal failure.
o Rehydrate with 0.9% saline.
 Aim for 3 – 6L/24 hours.
 Monitor fluid status with urine output.
 • If patient doesn’t pass urine for 4 hours, monitor
fluid status with
o Central venous line
o Urinary catheter.
o Once patient is rehydrated.
 Continue saline infusion.
 Give 40 mg frusemide every 2 – 4 hours.
 Continue monitoring CVP to prevent fluid overload or
dehydration.
 Monitor U&Es, particularly potassium and magnesium
• Diuretics and rehydration can cause electrolytes
to rapidly fall.
• Replace potassium as 20 – 40 mmol in each litre
of saline.
• Replace magnesium as up to 2 mmol in each litre
of saline.
o If these measures fail to reduce calcium fully (Ca > 2.8 mM), then
consider.
 Salmon calcitoninc 400 IU TDS.
• Rapid onset of action (within hours)
• Effects will only last 2 – 3 days (tachyphylaxis)
 Bisphosphonates.
• Inhibit osteoclast activity, causing fall in plasma
Ca.
• Pamidronate at 30 – 60 mg IV over 4 – 6 hours.
o Give 30 mg over 4 hours if
 [Ca] < 3 mmol/L
 Significant renal impairment.
o Give 60 mg over 8 hours if.[Ca] = 3 – 4
mmol/L
o Calcium levels begin to fall after 48
hours.
 Remain suppressed for up to 14
days.
• Zolendronate is drug of choice.
o Can infuse over 15 minutes.
o More effective
o Longer duration of action.
 Prednisolone 30 – 60 mg PO OD.
• Most effective in hypercalcaemia due to:
o Sarcoidosis
 o Myeloma
o Vitamin D intoxication.

Hypophosphataemia.
• Plasma phosphate is normally 0.8 – 1.4 mmol/L.
• Hypophosphataemia is:
o Common
o Often unrecognised by clinicians.
• Most intracellular phosphate is present as:
o Creatine phosphates
o Adenosine phosphates
o 2.3 – diphosphoglycerate.
 In Red Blood Cells.
• Hypophosphataemia doesn’t always indicate phosphate deficiency.
o Phosphate deficiency may present with normal or high plasma
phosphate.

• Causes.
o Modest (0.4 – 0.75 mmol/L)
 Decreased dietary intake
 Vitamin D deficiency
 Chronic liver disease
 Hyperparathyroidism
 Decreased absorption.
• Vitamin D deficiency
• Steatorrhoea
• Phosphate binding antacids.
 Hungry bones syndrome.
• Post parathyroidectomy
• Acute leukaemia
 Lymphoma
 Leukamias
 Hyperaldosteronism
 Diuretics
 Fanconi syndrome
o Severe (<0.4 mmol/L)
 Respiratory alkalosis
 Treatment of DKA
  Alcohol withdrawal.
• Especially with ketoacidosis
 Acute liver failure
 Hyperalimentation.
• Eg. refeeding syndrome.
 Ventilation of chronic severe respiratory failure.
 Neuroleptic malignant effects.

• Presentation.
o Most cases of severe hypophosphataemia occur in very sick
patients.
 Often in ITU.
o Manifestation of severe hypophosphataemia.
 Myopathy.
• Skeletal muscle
• Diaphragm
 Rhabdomyolysis
 Cardiomyopathy
 Erythrocyte dysfunction
 Leukocyte dysfunction
 Metabolic acidosis
 CNS dysfunction.
• Encephalopathy
• Irritability
• Seizures
• Parasthesia
• Coma
 Respiratory failure
 Reduced platelet half – life.
 Mineral mobilization.
o Occasionally seen in asymptomatic patients.
o Modest hypophosphataemia has no effects.
 Warrants investigation

• Treatment.
o Phosphate repletion should be reserved for sustained
hypophosphataemia with either.
 Oral effervescent Phosphate Sandoz.
 • 2 tablets TDS
 IV potassium phosphate.
• 9 – 18 mmol/day.
o Excessive phosphate replacement may cause hypocalcaemia and
metastatic calcification.
 Monitor calcium, phosphate and other electrolytes.