Description
- Life-threatening hyperglycaemic emergency of type 2 diabetes (residual insulin secretion prevents significant ketogenesis, unlike DKA) - severe hyperglycaemia, marked hyperosmolality, and profound dehydration, typically without significant ketoacidosis
- Onset is more insidious than DKA (days rather than hours) - often an elderly patient with a preceding illness and reduced oral intake, presenting later and sicker
- Overlap syndromes (mixed DKA/HHS features) occur and should be managed addressing both processes
Epidemiology
- Occurs predominantly in older adults with type 2 diabetes, often with a precipitating acute illness
- Less common than DKA overall, but carries a substantially higher mortality - reflecting the older, more comorbid population and degree of dehydration/organ hypoperfusion at presentation
Aetiopathogenesis
- Relative (not absolute) insulin deficiency - enough residual insulin to suppress hepatic ketogenesis, but not enough to control hyperglycaemia
- Precipitants: infection (commonest), non-adherence, new diagnosis, MI/stroke, medications (corticosteroids, thiazides, SGLT2 inhibitors, antipsychotics), inadequate fluid intake (impaired thirst/access - common in frail elderly)
- Hyperglycaemia -> osmotic diuresis -> profound volume depletion -> rising osmolality -> further impaired renal clearance of glucose -> a self-perpetuating cycle
- Impaired consciousness itself worsens the cycle by reducing oral fluid intake
Diagnosis
Clinical
- Marked dehydration, altered mental state ranging from confusion to coma, focal neurological signs can occur (mimicking stroke) and typically resolve with correction
- Often an evolving presentation over days with reduced intake/increasing lethargy preceding admission
Diagnostic features - definitions vary slightly between major guidelines, so treat these as the general pattern rather than one fixed cutoff
- Marked hyperglycaemia (typically severe, often >30mmol/L)
- Significantly elevated serum osmolality (typically >320mOsm/kg)
- Minimal or no ketosis/acidosis (distinguishes from DKA) - mild ketonuria can occur from starvation and does not exclude HHS
- Calculate/measure serum osmolality and correct sodium for the degree of hyperglycaemia when interpreting the result
Management
A. Fluid resuscitation - the primary and most urgent therapy
- IV isotonic saline, substantial volumes over the first 24 hours, adjusted to haemodynamic status/comorbidity (cautious in heart failure/renal impairment)
- Correct fluid deficit and osmolality gradually - target a gradual fall in osmolality; correcting too fast risks cerebral oedema, correcting too slowly risks ongoing organ hypoperfusion - a balance that differs somewhat between guidelines, reinforcing the need for frequent reassessment rather than a rigid rate
B. Insulin - started cautiously, after fluid resuscitation is underway
- Lower-dose IV insulin infusion than DKA protocols, generally started once fluid resuscitation has begun and blood glucose is no longer falling adequately with fluids alone - insulin given too early/aggressively before adequate fluid replacement risks a precipitous osmotic shift
- Add dextrose-containing fluid once glucose falls to a target range to allow continued insulin infusion without hypoglycaemia
C. Electrolytes
- Potassium replacement - total body potassium is typically depleted despite a normal/high initial serum level (as in DKA); monitor closely once insulin/fluids start
D. Address the precipitant and prevent complications
- Identify and treat the underlying trigger (infection, medication, missed diagnosis)
- VTE prophylaxis - HHS carries a high thrombosis risk given profound dehydration/hyperviscosity
- Monitor closely for improvement in mental state and osmolality; involve intensive care for severe cases given the high mortality risk
Associations
- Type 2 diabetes, often previously undiagnosed or poorly controlled
- Elderly, frail, residential care patients with reduced access to fluids/impaired thirst response
- Precipitating infection, medication changes (corticosteroids, SGLT2 inhibitors, antipsychotics), non-adherence
- Concurrent acute illness (MI, stroke, sepsis) - may be both precipitant and complication
Natural history & complications
- Mortality is substantially higher than DKA, reflecting age, comorbidity, and degree of dehydration/organ hypoperfusion at presentation
- Complications: VTE/arterial thrombosis (hyperviscosity), acute kidney injury, cerebral oedema (particularly with overly rapid correction), and complications of the precipitating illness itself
- With appropriate fluid resuscitation and gradual correction, mental state typically normalises over 24-72 hours as osmolality falls
- Recurrence risk is high without addressing ongoing diabetes management and the precipitating factors - discharge planning should include diabetes education and medication review
Study aid only. These notes are written with the help of AI. Not for guiding clinical decisions.