Hypoglycaemia
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Direct answer
Whipple's triad — symptoms consistent with hypoglycaemia, a documented low plasma glucose (usually below 50-55 mg/dL) and relief with glucose — is the entry point to the physiology. The brain stores no glucose and makes none, consuming about 100-120 g daily, so it lives hand-to-mouth on arterial supply. Counter-regulation is layered by glucose level: insulin secretion switches off first at about 80-85 mg/dL, glucagon and adrenaline surge at about 65-70, and cortisol with growth hormone reinforce over hours. Adrenergic symptoms — tremor, palpitations, sweating — surface near 50-60 mg/dL, while neuroglycopenia (confusion, drowsiness, seizures, coma) declares below roughly 50. Treatment follows simple arithmetic: conscious patient, 15 g fast carbohydrate rechecked at 15 minutes; unconscious patient, 25 g intravenous 50% dextrose or 1 mg glucagon intramuscularly, and never anything by mouth.
What you must remember
- Hormonal hierarchy: insulin off at about 80-85 mg/dL, glucagon and adrenaline on at 65-70, cortisol and growth hormone as slow reinforcement — glucagon is the first responder lost early in type 1 diabetes.
- Symptom thresholds: adrenergic symptoms at 50-60 mg/dL, neuroglycopenia below about 50 mg/dL; long-standing type 1 diabetes develops hypoglycaemia unawareness from blunted adrenaline responses.
- C-peptide logic: insulin and C-peptide are co-secreted equimolarly; during true hypoglycaemia, high insulin with high C-peptide means insulinoma, high insulin with low C-peptide means injected insulin or factitious use.
- Drug risk ranking: sulfonylureas (glibenclamide worst) cause prolonged hypoglycaemia in the elderly and renally impaired — a staple of Indian prescriptions warranting overnight admission; insulin has a plasma half-life near 5 minutes.
- Somogyi versus dawn phenomenon: a 3 a.m. glucose measurement separates rebound nocturnal hypoglycaemia (Somogyi — low then morning high) from dawn phenomenon (normal 3 a.m. glucose, morning rise from growth hormone and catecholamine-driven insulin resistance).
- Neonatal numbers: treatment thresholds around 40-45 mg/dL; infants of diabetic mothers are hyperinsulinaemic and crash after clamping the cord.
- Community rule: 15 g of fast carbohydrate every 15 minutes — in Indian practice, three to four teaspoons of sugar in water remains the taught first response for a conscious diabetic.
Working up a spontaneous spell
A non-diabetic adult presents with recurrent early-morning confusion that relatives abort with tea and biscuits. During a spontaneous episode, draw the four-sample set: glucose, insulin, C-peptide, and ketones (with a sulfonylurea screen if assays allow). Glucose 38 mg/dL with inappropriately normal-or-high insulin and raised C-peptide, ketones suppressed, sulfonylurea screen negative — that is endogenous hyperinsulinism, and imaging follows for insulinoma. The same low glucose with low insulin and high ketones argues fasting adaptation or counter-regulatory failure (adrenal insufficiency, alcohol); low glucose with high insulin but flat C-peptide unmasks injected insulin — factitious or iatrogenic. The discipline is everything drawn during the spell, not after recovery, because insulin's short half-life erases the evidence within the hour.
Where students slip
The Somogyi-dawn pair is answered backwards under pressure: the discriminator is the 3 a.m. glucose, low in Somogyi and normal in dawn phenomenon — one value, question closed. Second, the reason sulfonylurea hypoglycaemia outlasts insulin overdose is pharmacokinetic, not pharmacodynamic: the drug keeps stimulating endogenous insulin release, so observation must be prolonged with glucose ready. Third, glucagon is quoted without its limit — it works by mobilising hepatic glycogen, so it fails in exhausted stores (alcohol fasting, severe malnutrition) and in the glycogen-depleted toddler. And the unconscious patient given oral glucose syrup is the classic unsafe answer in orals; airway protection precedes sweetness, always.
Frequently asked questions
What constitutes Whipple's triad?
Symptoms compatible with hypoglycaemia, a measurably low plasma glucose at the time of symptoms, and prompt relief after glucose administration.
In what order do counter-regulatory hormones respond to falling glucose?
Insulin secretion is suppressed first (about 80-85 mg/dL), then glucagon and adrenaline rise (65-70 mg/dL), followed by slower cortisol and growth hormone support.
How does C-peptide distinguish insulinoma from injected insulin overdose?
Both show high insulin during hypoglycaemia, but C-peptide is high with insulinoma (co-secreted) and low with exogenous insulin, which suppresses the beta cell.
Why is sulfonylurea-induced hypoglycaemia prolonged?
The drug drives continuing endogenous insulin release, especially in the elderly and renally impaired, so hypoglycaemia recurs and needs extended monitoring with repeated glucose.
How are the Somogyi phenomenon and dawn phenomenon differentiated?
By a 3 a.m. blood glucose: low in Somogyi phenomenon (rebound after nocturnal hypoglycaemia) and normal in dawn phenomenon (morning insulin resistance from counter-regulatory hormones).