Confusion for Medical Finals (based on Newcastle university learning outcomes)

8/14/2019 Confusion for Medical Finals (based on Newcastle university learning outcomes)

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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



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.

Documents

Confusion for Medical Finals (based on Newcastle university learning outcomes)