Associated with adverse drug interactions - hypo- and hyperglycaemia

Red flags

Hypoglycaemia + beta-blocker use (masks autonomic warning symptoms - tremor, tachycardia)
Recurrent/severe hypoglycaemia on sulfonylurea in renal impairment (prolonged, needs extended observation/dextrose infusion)
New hyperglycaemia/DKA after starting an SGLT2 inhibitor - can be euglycaemic DKA
Antipsychotic-associated new-onset diabetes/DKA, esp. clozapine and olanzapine

Drug-induced hypoglycaemia

Insulin, sulfonylureas (esp. long-acting/renal accumulation), quinine, beta-blockers (mask symptoms, don't usually cause it alone)
Alcohol (inhibits gluconeogenesis)

Drug-induced hyperglycaemia

Corticosteroids - dose-dependent, common, may unmask latent diabetes
Second-generation antipsychotics (clozapine, olanzapine > quetiapine, risperidone) - metabolic syndrome, new-onset diabetes, rare DKA even without prior diagnosis
Thiazides (dose-dependent), protease inhibitors, tacrolimus/ciclosporin, growth hormone
SGLT2 inhibitors - can precipitate euglycaemic DKA (glucose only mildly raised) - classic trigger: dehydration, low-carbohydrate diet, surgery, intercurrent illness

Diabetes medication regimen, recent dose changes, renal function (sulfonylurea accumulation)
New corticosteroid, antipsychotic, or SGLT2 inhibitor
Reduced oral intake, vomiting, surgery, fasting - especially relevant to SGLT2i euglycaemic DKA and sulfonylurea hypoglycaemia
Alcohol intake

Neuroglycopenic/autonomic symptoms of hypoglycaemia (may be blunted on beta-blockers)
Kussmaul breathing, dehydration (DKA)
Antipsychotic metabolic surveillance findings - weight, waist circumference

Bedside glucose, formal glucose, ketones (blood beta-hydroxybutyrate preferred over urine)
VBG for pH/bicarbonate if DKA suspected - check even with only mildly elevated glucose if on an SGLT2 inhibitor
HbA1c for baseline control context
Renal function (sulfonylurea clearance)

Sulfonylurea hypoglycaemia: IV dextrose + prolonged observation/dextrose infusion (duration of action outlasts a single bolus) - admit
Beta-blocker use - counsel patients to monitor glucose rather than rely on symptoms
Corticosteroid hyperglycaemia: monitor glucose, treat as needed, usually reversible on dose reduction/cessation
Antipsychotic metabolic effects: baseline and regular metabolic monitoring (weight, lipids, glucose) on clozapine/olanzapine; switch agent if significant
SGLT2 inhibitor euglycaemic DKA: stop drug, treat DKA per standard protocol (insulin + dextrose even if glucose only mildly elevated), withhold SGLT2i perioperatively and during acute illness/fasting

Euglycaemic DKA on an SGLT2 inhibitor is missed if ketones aren't checked because glucose looks reassuring
Beta-blockers blunt the adrenergic warning signs of hypoglycaemia without preventing the hypoglycaemia itself
Sulfonylurea hypoglycaemia can recur for 24-48h after a single dose in renal impairment - do not discharge after one normal glucose
Clozapine/olanzapine can cause DKA as the presenting feature of new diabetes, even without prior metabolic risk factors

1. Check ketones, not just glucose

"On an SGLT2 inhibitor, a normal glucose doesn't exclude DKA - I check ketones and the gas."

2. Sulfonylurea hypoglycaemia needs time, not just dextrose

"One bolus of dextrose isn't enough - these patients need extended observation, especially with renal impairment."

7 more sections, plus exam facts

Premium unlocks every note across every specialty, and the full exam fact library behind it.