Hyperosmolar Hyperglycaemic State (HHS)
NICE and BNF — life-threatening hyperglycaemic emergency, fluid replacement and management
Hyperosmolar Hyperglycaemic State (HHS) is a life-threatening metabolic emergency characterised by extreme hyperglycaemia, severe dehydration, and hyperosmolality without significant ketoacidosis. It occurs predominantly in people with type 2 diabetes, particularly older adults, and carries a higher mortality rate than diabetic ketoacidosis. HHS often develops insidiously over days to weeks, allowing profound dehydration and metabolic derangement to accumulate before medical attention is sought.
What is HHS?
HHS represents a state of extreme metabolic decompensation in which severe insulin deficiency leads to profound hyperglycaemia (often >50 mmol/L), osmotic diuresis causing massive fluid losses (up to 8–12 litres), and hyperosmolality (>320 mOsm/kg). Unlike DKA, there is typically enough endogenous insulin to prevent significant ketogenesis, so metabolic acidosis is absent or mild. The condition predominantly affects older people with type 2 diabetes, often those with limited access to water or impaired thirst mechanism. Precipitating factors include infection (pneumonia, urinary tract infection, sepsis), acute illness (myocardial infarction, stroke, pancreatitis), medications (glucocorticoids, thiazides, atypical antipsychotics), and poor adherence to diabetes treatment.
Recognition and Diagnosis
Clinical features reflect severe dehydration and hyperosmolality: polyuria, polydipsia (though thirst may be impaired in elderly), profound lethargy, weakness, confusion, drowsiness progressing to coma, focal neurological signs (hemiparesis, seizures, visual disturbances), and signs of severe dehydration (dry mucous membranes, reduced skin turgor, tachycardia, hypotension, reduced urine output). Biochemical criteria include: severe hyperglycaemia (blood glucose >30 mmol/L, often >50 mmol/L), hyperosmolality (>320 mOsm/kg), absence of significant ketonaemia/ketonuria (ketones <3.0 mmol/L), absence of significant metabolic acidosis (venous pH >7.3, bicarbonate >15 mmol/L), prerenal uraemia (elevated urea and creatinine), and electrolyte disturbances. NICE NG19 and Joint British Diabetes Societies (JBDS) guidelines provide the framework for diagnosis and management.
Treatment
Management requires intensive care or high-dependency unit admission with hourly monitoring. FLUID REPLACEMENT is the cornerstone — aggressive IV 0.9% sodium chloride to restore circulating volume and correct dehydration (deficit often 8–12L, replaced gradually over 24–48 hours). INSULIN THERAPY: fixed-rate IV insulin infusion (typically 0.1 units/kg/hour) is started AFTER initial fluid resuscitation to avoid rapid osmolar shifts. Goal is gradual glucose reduction (3–5 mmol/L/hour). POTASSIUM MANAGEMENT: total body potassium is depleted; monitor every 2–4 hours and replace aggressively (often 20–40 mmol/hour) to maintain 4.0–5.5 mmol/L. THROMBOPROPHYLAXIS: LMWH (e.g. enoxaparin) is essential due to extreme thrombotic risk from hyperviscosity and immobility. TREAT UNDERLYING CAUSE: identify and treat infection, MI, or other precipitants. MONITORING: hourly blood glucose, 2–4 hourly U&E, venous blood gas, osmolality. Mortality remains 5–20%, higher with older age, comorbidity, and delayed treatment. This article has been prepared following careful evaluation of NICE NG19 (Recognition and Initial Management of Diabetic Ketoacidosis and Hyperosmolar Hyperglycaemic State) and current BNF guidance.