General MedicineTier 1Disease (DEADMAN)

Metabolic emergencies - hypo- and hyperglycaemia

Description

Hypoglycaemia: glucose <3.9 mmol/L (treatment threshold), severity by need for third-party assistance/neuroglycopenia
DKA: glucose usually >11 (can be euglycaemic with SGLT2i), ketosis, metabolic acidosis
HHS: profound hyperglycaemia (often >30), hyperosmolality, minimal ketosis, altered consciousness - typically T2DM, older patients

DKA - more common in T1DM but occurs in T2DM (esp. with SGLT2 inhibitor use, or severe illness)
HHS - typically elderly T2DM, often undiagnosed diabetes, precipitated by infection/dehydration/non-adherence
Severe hypoglycaemia - insulin/sulfonylurea therapy, renal impairment, missed meals, alcohol

DKA: absolute/relative insulin deficiency -> unrestrained lipolysis -> ketogenesis -> anion gap metabolic acidosis; osmotic diuresis -> dehydration, electrolyte loss (esp. total body potassium depletion despite normal/high serum level at presentation)
HHS: enough residual insulin to suppress ketogenesis but not hyperglycaemia -> profound osmotic diuresis -> severe dehydration and hyperosmolality
Euglycaemic DKA: SGLT2 inhibitors promote glucosuria masking hyperglycaemia while ketogenesis proceeds unchecked (esp. with fasting, illness, low carbohydrate intake)
Hypoglycaemia: excess exogenous insulin/sulfonylurea relative to intake/activity; impaired counter-regulation with autonomic neuropathy or recurrent hypoglycaemia ("hypoglycaemia unawareness")

DKA: glucose (or history of diabetes) + ketones (blood beta-hydroxybutyrate >=3 mmol/L preferred over urine) + venous pH <7.3 or bicarbonate <15
HHS: glucose usually >30, serum osmolality >320 mOsm/kg, minimal ketosis/acidosis
Hypoglycaemia: Whipple's triad - symptoms + low glucose + resolution with correction
Identify the precipitant in all three - infection, non-adherence, new drug (steroids, SGLT2i), MI, pancreatitis

1. DKA

Fixed-rate IV insulin infusion (0.1 unit/kg/h), IV fluid resuscitation, potassium replacement once level known (add to fluids once K+ <5.5, hold insulin if K+ <3.5 until replaced)
Continue long-acting basal insulin throughout to prevent rebound ketosis
Resolve when ketones <0.6, pH >7.3, bicarbonate >18 - then transition to subcutaneous insulin (overlap with IV infusion by 1-2h)
Stop SGLT2 inhibitor if implicated; do not restart during acute illness

2. HHS

Slower, more cautious fluid replacement than DKA (large fluid deficit, risk of rapid osmotic shifts/cerebral oedema)
Lower-dose or delayed insulin until fluid resuscitation underway (glucose often falls with fluids alone)
VTE prophylaxis (hyperviscosity risk)

3. Hypoglycaemia

Conscious, able to swallow: 15-20g fast-acting oral carbohydrate, recheck in 15 min
Reduced consciousness/unable to swallow: IV dextrose or IM glucagon
Sulfonylurea-induced hypoglycaemia needs prolonged observation - duration of action outlasts a single treatment dose
Identify and correct the precipitant, review diabetes regimen before discharge

DKA: cerebral oedema (esp. children - avoid over-rapid correction), ARDS, VTE
HHS: high mortality (higher than DKA), thromboembolism
Recurrent hypoglycaemia: hypoglycaemia unawareness, cardiovascular events, falls, cognitive impact

DKA mortality low with prompt treatment (<1%) but higher in extremes of age/comorbidity
HHS mortality substantially higher (~10-20%) reflecting older, more comorbid population and degree of dehydration
Recurrent severe hypoglycaemia predicts future cardiovascular events and mortality - a sentinel event prompting regimen review

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