confusion for medical finals (based on newcastle university learning outcomes)
TRANSCRIPT
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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.
Alzheimers disease
Vascular dementia
Lewy body dementia
Fronto temporal dementia
o Rarer:
Chronic alcohol abuse
Huntingtons chorea
CJD
Parkinsons disease
Picks disease
HIV
Pellagra
Subacute sclerosing panencephalitis
Progressive multiple leukencephathy
Pellagra.
Niacin deficiency
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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)
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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.
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No change in levels of consciousness
Deterioration tends to be progressive
Often exacerbated by removal from familiar
environment.
Multi infarct dementia progresses in a stepwisefashion.
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
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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 Wilsons disease.
Autosomal recessive
o Huntingdons chorea.
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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 2No speech 1
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Best eye opening
response
Spontaneous 4
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
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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
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Aphasia.
o Signs of chronic liver disease.
Hepatic encephalopathy can cause confusion.
Chronic liver disease may also indicate:
Alcoholism
Wilsons 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.
glutamyl transferase raised in alcohol consumption.
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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.
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Thick & thin films.
o HIV serology
o Urine toxicology screen
o Thiamine deficiency
Red cell transketolase.
o Wilsons 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.
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Alcohol withdrawl.
Confusion
History &Examination
Acute/
subacuteLongstanding
FBC
U&EBiochemistry
B12/ folateTFTsSyphilis
serologyConsider CT
TreatableUntreatable
Alzheimers
VascularLewy body
Fronto temporal
B12/ folate
deficiencyHypothyroidis
Thiamine deficiencySubdural
haematomaHydrocephalusSyphilis
TumourDepression
FBCU&EGlucose
LFTABGs
Sepsis screenDrug screen
Consider CT
Temperature
CulturesDrug history
Biochemistry
ABGsCT Scan
SepsisIntoxication
Withdrawl
Failure of:
CardiacRespiratory
LiverRenal
Abscess
TumourHaemorrhage
HaematomaInfarction
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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.
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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.
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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.
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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
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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.
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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 Kussmauls 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.
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o Assess degree of acidosis.
U&Es.
o Sodium will need to be corrected.
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.
1.6 x [Glucose]
5.5 1.6Corrected Sodium = [Na+] +
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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 dont 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.
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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
(mmol/L)
Potassium
added to each
litre (mmol)
< 3.0 40
< 4.0 30
< 5.0 20
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Potassium can be depleted by
1000 mmol.
Plasma potassium can rapidlyfall 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.
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Blood glucose
(mmol/L)
Insulin
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, increaseinsulin 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.
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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
Dont 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
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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/kgbody 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.
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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 mol/L), ratio of Cr:U is about20:1.
Significant hypernatraemia.
Can be obscured by a high glucose.
Corrected sodium concentration can be
calculated.
Before relying on corrected results, check that
lab doesnt 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
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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.
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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 alab 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
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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 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 cells, as well as
insulin producing 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.
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Eg. chlopropamide instead of chlorpromazine
o Others.
Disopyramide
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
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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 Wernikes 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.
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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.
Dont give further glucose boluses without recheckingBM.
o If patient doesnt 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 patients 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.
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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 Addisons
o Cardiac disease
o Lung disease
o Liver disease
o Renal disease.
Examination.
o Focus on careful assessment of volume status.
Hypovolemic or Normovolemic
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Patients who are hyponatraemic and
hypovolemic are salt depleted.
Oedema
o
Lying and standing BPo 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)
SIADH: urine osm > 100, serum osm < 260, unine Na > 40 mmol/L
Oedematousstates
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Renal losses
uNa > 20mmol/L)
Non renal
losses
(uNa < 20
mmol/L)
CNS disorders Malignancy Pulmonary
disease
Drugs Others
Diuretics
Adrenalnsufficiency
Addisonsdisease)
ntrinsic renal
disease.
Hypothyroidism
Vomiting
Diarrhoea
Burns
3rd space fluidlosses
Trauma
Stroke
Sub
arachnoidbleed
Malignancy
(1o or 2o)
Lung (oat
cell)
Pancreas
Lymphoma
Leukaemia
Prostate
Urinary tract
Pneumonia
TB
Lung abscess
Cysticfibrosis
Lung
vasculitis
Opiates
Haloperidol
Amitriptyline
Cyclophoshamide
Vasopressin
Thiodizine
Carbamazepine
Clofibrate
Oxytocin
Chlopropramide
Thiazides
Vincristine
Vasculitis
(eg. SLE)
Abscess
Meningioencephalitis
Severe myxoedema
Psychogenicpolydipsia
SIADH
CCF
Cirrhosis withascites
Severe renalfailure
Nephroticsyndrome
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.
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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 to500 ml/24 hours.
Seek expert help.
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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.
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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.
Conns 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
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o Focal or generalised seizures.
o Hypotension
o Bradycardia
o Arrythmias
o CCF
o Chvosteks sign
Tap facial nerve anterior to the ear.
Causes contraction of facial muscles
Seen in 10% of normal patients.
o Trousseaus 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
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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.
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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.
Dont 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.
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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
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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.
Pagets disease
o Benign familial hypocalcuric hypercalcaemia.
High serum calcium
Normal 24 hour urinary calcium
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Causes mild symptoms.
Mild fatigue
Lethargy
PTH may be raised.
Patients dont 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.
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If patient doesnt 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 plasmaCa.
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
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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 doesnt 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 (
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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.
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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.