Write a short note on hyperglycaemic hyperosmolar state and the differentiation of diabetic comas.

Definition

Hyperglycaemic hyperosmolar state (HHS) — formerly hyperosmolar non-ketotic coma — is characterised by:

• Severe hyperglycaemia, typically > 600 mg/dL
• Marked serum hyperosmolality, usually > 320 mOsm/kg
• Profound dehydration
• Absence of significant ketosis and acidosis (pH > 7.3, bicarbonate > 18, mild or no ketonaemia)

It occurs typically in elderly patients with type 2 diabetes, often as the first presentation, and develops insidiously over days to weeks. Mortality is considerably higher than in DKA (10–20%), largely because of the age and comorbidity of those affected.

WHY No Ketosis?

Patients with type 2 diabetes retain sufficient residual insulin to suppress lipolysis and hepatic ketogenesis, but not enough to prevent hyperglycaemia. Lower counter-regulatory hormone levels contribute. Hence extreme hyperglycaemia without ketoacidosis.

Precipitants

Infection (pneumonia and urinary sepsis are the commonest), myocardial infarction, stroke, poor fluid intake (elderly, bedbound, dementia, no access to water), drugs — corticosteroids, thiazide and loop diuretics, beta-blockers, antipsychotics, dialysis, and undiagnosed diabetes.

Clinical Features

• Profound dehydration — dry mucosae, sunken eyes, reduced turgor, tachycardia, hypotension, oliguria. Fluid deficits are typically greater than in DKA.
• Neurological features dominate and correlate with osmolality: confusion, drowsiness, focal neurological signs and seizures mimicking stroke, progressing to coma.
• No Kussmaul breathing and no ketotic breath — the clinical contrast with DKA.
• Features of the precipitating illness.
• Complications: arterial and venous thrombosis (hyperviscosity — stroke, myocardial infarction, DVT, PE), rhabdomyolysis, acute kidney injury, and cerebral oedema with over-rapid correction.

Differentiating the Diabetic Comas

Management of HHS

The principles differ from DKA in important ways, and treating HHS "like DKA" causes harm.

1. Fluid replacement is the priority and the main treatment

• Isotonic saline to restore circulating volume; deficits are large (typically 100–220 mL/kg).
• Replace slowly — aim to correct over 24–48 hours, with a gradual fall in osmolality, because rapid correction risks cerebral oedema and osmotic demyelination.
• Monitor for fluid overload in the elderly and those with cardiac or renal disease; central monitoring is often needed.

2. Insulin — later and lower dose than in DKA

• Fluids alone lower glucose substantially; insulin is often withheld initially and started at a low fixed rate once the fall in glucose with fluids plateaus, or immediately if there is significant ketonaemia.
• Excessive early insulin causes a rapid osmotic shift into cells, precipitating cardiovascular collapse and cerebral oedema.

3. Potassium and electrolytes

Total body potassium is depleted; monitor closely and replace as in DKA once urine output is established. Monitor sodium — the corrected sodium typically rises as glucose falls, which is expected.

4. Other measures

• Prophylactic anticoagulation — thrombotic risk is high and this is a specific difference from routine DKA care.
• Treat the precipitant — a thorough septic screen and early antibiotics.
• Foot protection, pressure area care, and careful monitoring of consciousness and osmolality.
• Most patients require insulin initially, but many can later be transitioned to oral agents, unlike in DKA.