DKA & HHS (hyperglycaemic emergencies)

The two acute hyperglycaemic emergencies of diabetes. Content extracted and expanded from Diabetes – complications; for the primary-care red flags and when to transfer, see also Type 2 Diabetes Management.

Recognising a hyperglycaemic emergency in primary care

Per the RACGP/ADS joint guidance, urgently assess (point-of-care blood ketones

• volume status) and consider hospital transfer when:

• capillary BGL >15 mmol/L for more than 8–12 hours (checked 2-hourly), or
• any BGL >15 mmol/L with symptoms/signs of DKA or HHS.

Have a high index of suspicion for euglycaemic DKA in SGLT2-inhibitor users — ketoacidosis with normal or only mildly raised glucose. Other high-risk groups: insulin-pump users, previous DKA, pregnancy, the elderly, corticosteroid or atypical-antipsychotic use, and acute infection/sepsis/MI/pancreatitis/trauma.

Diabetic ketoacidosis (DKA)

Absolute insulin deficiency → lipolysis, ketogenesis and metabolic acidosis. Typically type 1 (first presentation or missed insulin/pump failure), but also type 2 under severe stress and in SGLT2i users.

Biochemical criteria:

• Serum glucose >11 mmol/L (or known diabetes)
• Venous pH <7.3 or bicarbonate <15 mmol/L
• Ketonaemia (blood ketones ≥3.0 mmol/L) or significant ketonuria

Severity (by the worst parameter):

Severity	Venous pH	Bicarbonate (mmol/L)
Mild	<7.3	<15
Moderate	<7.2	<10
Severe	<7.1	<5

Key principles of management (hospital-based; GPs need the first few hours if rural):

1. Correct dehydration — IV fluids. Note the degree of dehydration is often over-estimated in DKA (acidosis causes peripheral shutdown); excessive fluid increases the risk of cerebral oedema.
2. Reverse ketosis / correct acidosis and glucose — fixed-rate IV insulin infusion; add dextrose once glucose falls to keep the insulin running.
3. Replace potassium — total body potassium is depleted regardless of the initial serum level; replace early once passing urine.
4. Monitor for complications — cerebral oedema (the key life-threatening complication, especially in children), hypo/hyperkalaemia, hypoglycaemia. Corrected sodium may be falsely low from osmotic dilution by glucose.
5. Identify and treat the precipitant — infection, missed insulin, new diagnosis.

For a first presentation of type 1, collect the diagnostic work-up with the initial bloods where practical: insulin/GAD/ZnT8 antibodies, coeliac screen (total IgA, tTG), TSH and fT4.

Hyperosmolar hyperglycaemic state (HHS)

Profound hyperglycaemia and hyperosmolar dehydration without significant ketoacidosis, evolving over days to weeks (contrast DKA’s onset over hours). Typically older people with type 2 — but increasingly younger adults, sometimes as the first presentation of type 2. Higher mortality than DKA. (Formerly “HONK” — renamed because patients may be severely ill without coma and may be mildly ketotic/acidotic.)

Precipitants: infection/sepsis; insulin omission or inadequate dosing; acute illness (pancreatitis, MI, stroke); drugs affecting carbohydrate metabolism (glucocorticoids, high-dose thiazides, sympathomimetics, second-generation antipsychotics); and any illness compromising access to water in a person who cannot recognise or respond to thirst.

Clinical features: polyuria, polydipsia and weight loss preceding vomiting, dehydration and weakness; severe hypovolaemia (tachycardia >100, SBP <100); altered mental status; focal neurological signs (hemianopia, hemiparesis) and seizures. Severe hypothermia is a poor prognostic sign. Vascular complications (MI, stroke, arterial thrombosis) and, uncommonly, cerebral oedema and central pontine myelinolysis may occur.

Management is hospital-based: cautious IV rehydration (slower than DKA given the higher osmolar load and thrombosis/CPM risk), careful correction of glucose and sodium, VTE prophylaxis, potassium replacement, and low-rate insulin once fluid resuscitation is under way.