Hyperosomolar hyperglycaemic state Flashcards

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1
Q

Pathophysiology

A

Hyperglycaemia results in osmotic diuresis with associated loss of sodium and potassium

Sever volume depletion results in significant raised serum osmolality so hyperviscosity of blood

Despite severe electrolyte losses and total body depletion, typical patient with HHS may not look as dehydrated as they are because hypertonicity leads to preservation of intravascular volume

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2
Q

Clinical features

A

General: fatigue, lethargy, nausea, vomiting

Neuro: altered consciousness, headaches, papilloedema, weakness

Haematological: hyperviscosity (may result in MI, stroke, peripheral arterial thrombosis)

CVD: drhydration, hypotension, tachycardia

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3
Q

Diagnosis

A

Hypovolaemia

Marked hyperglycaemia (>30mmol/L) without significant ketonaemia or acidosis

Significantly raised serum osmolality (>320mosmol/kg)

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4
Q

Management

A

Gradually normalise osmolality (serum osmolality key parameter)

Replace fluid and electrolyte losses

Gradually normalise blood glucose

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5
Q

Fluid losses

A

Estimated to be between 100-220ml/kg

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6
Q

Fluid replacement

A

IV 0.9% NaCl first line

Already relatively hypotonic compared to serum in someone with HHS

If serum osmolality not declining switch to 0.45% NaCl (more hypotonic compared to serum osmolality)

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7
Q

Aim of treatment

A

Replace approximately 50% estimated fluid loss within first 12 hours and remaining in the following 12 hours

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8
Q

Monitoring response

A

Key parameter is serum osmolality (glucose and sodium are main contributors)

Rapid change can cause CVD collapse and central pontine myelinolysis

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9
Q

Target blood glucose

A

Between 10-15mmol/L

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10
Q

Insulin

A

Fluid replacement alone will result in gradual decline of blood glucose and osmolarity

Insulin can result in rapid decline of serum glucose and osmolarity

Prior to fluid replacement may cause CVD collapse and CPM

Only use if significant ketonaemia (fixed rate IV insulin at 0.05 units/kg/hour)

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11
Q

Potassium

A

Patients potassium deplete but less acidotic than DKA so potassium shift less pronounced

Hyperkalaemia may present with AKI

Patients on diuretics may be profoundly hypokalaemic

Potassium should be replaced or omitted as required

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