Severe hyperglycaemia without significant ketosis; the characteristic metabolic emergency of T2DM
Aetiology
- People present in middle or later life, often with previously undiagnosed diabetes
- Common precipitating factors include consumption of glucose-rich fluids, concurrent medication such as thiazide diuretics or steroids, and intercurrent illness
Pathophysiology
- Pathophysiology is similar to DKA, but HHS, there are still small amounts of insulin being secreted by the pancreas
- This is sufficient to prevent DKA by suppressing lipolysis and, in turn, ketogenesis, but level is not high enough to lower blood glucose to a safe level
- HHS is characterized by symptoms of marked dehydration (and loss of electrolytes) due to the predominating hyperglycaemia and osmotic diuresis (hyperosmolar urine)
Clinical presentation
- Dehydration due to polyuria
- Polydipsia
- Nausea and vomiting
- Stupor/coma
- Impaired consiousness is directly related to degree of osmolarity
Investigations
HHS is characterised by:
- Profound hyperglycaemia (blood glucose >600 mg/dL)
- Hyperosmolality (serum osmolarity >320mmol/kg)
- Can be measured directly or calculated as (2 x Na+) + glucose + urea
- Volume depletion in the absence of ketoacidosis (pH >7.3 and bicarbonate >18mmol/L)
Other features
- Significant renal impairment
- Sodium often high normal or raised
Management
- Assess severity of dehydration and use 0.9% saline for fluid replacement WITHOUT insulin - fluids alone will reduce osmolarity
- Be aware of increased risk of fluid overload
- Sodium - avoid rapid fluctuations, if dropping too quickly consider 0.45% saline
- Monitor and chart BG, osmolarity and sodium
- Start low dose IV insulin only if significant ketones (>1) or BG falling at a slow rate
- Comorbidities more likely
- Screen for vascular event e.g. silent MI
- LMWH for all patients (unless contraindicated)
- High risk of feet complications
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