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Approach to hypoglycemia

The same eight steps, every presentation: threats first, then the history and exam that discriminate, one honest sentence, a mechanism-grouped differential, and the tests read in order.

  1. Immediate threats

    • Neuroglycopenia (confusion, seizure, coma) is brain injury in progress: glucose now, by any working route
    • No IV access: intramuscular glucagon does not require one
    • Sulfonylurea and long-acting insulin overdoses RECUR for hours to days: one recovery is not the end
    • The non-diabetic with unexplained hypoglycemia is a diagnosis, not an event: sepsis, adrenal failure, liver failure, insulinoma, factitious

  2. History that discriminates

    • Diabetic pharmacology in detail: agent, dose, timing, recent changes, renal function (insulin and sulfonylureas linger in kidney failure)
    • Missed meals, alcohol (blocks gluconeogenesis), exercise, gastroparesis
    • Awareness: hypoglycemia unawareness after recurrent lows changes targets and driving advice
    • In the non-diabetic: timing versus fasting, weight change, steroid withdrawal, access to hypoglycemic drugs at home or work

  3. Examination

    • Consciousness and focal signs (hypoglycemia mimics stroke); resolve the deficit with the glucose
    • Sweating and tremor may be absent in unawareness and under beta-blockade
    • Signs of the underlying causes: sepsis, chronic liver disease, hyperpigmentation of adrenal failure

  4. Problem representation

    A type 1 diabetic found confused and sweating after increased insulin and a skipped dinner, glucose 1.9, fully clear after treatment (points at insulin excess) versus recurrent fasting neuroglycopenia in a non-diabetic with a critical sample showing endogenous hyperinsulinism (points at insulinoma).

  5. Differential, by mechanism

    Diabetic therapy

    • Insulin excess or mistimed
    • Sulfonylureas
    • Renal failure prolonging both

    Illness

    • Sepsis
    • Liver failure
    • Adrenal insufficiency
    • Severe malnutrition
    • Alcohol

    Endogenous / factitious

    • Insulinoma
    • Factitious insulin or sulfonylurea use
    • Post-bariatric reactive hypoglycemia

  6. Investigations

    • Confirm on a lab or gas glucose when possible, treat on the meter reading regardless
    • Renal and liver panels; 09:00 cortisol or short synacthen where adrenal weight exists
    • The critical sample DURING hypoglycemia in the non-diabetic: insulin, C-peptide, sulfonylurea screen (C-peptide splits endogenous from injected)

  7. Interpretation

    • Whipple's triad keeps the label honest: symptoms, a low measured glucose, and relief with correction
    • Recurrent lows on unchanged doses are a message: falling renal function, failing counter-regulation, or a missed illness
    • High insulin WITH high C-peptide is endogenous or sulfonylurea; high insulin with suppressed C-peptide is injected

  8. Next steps

    • Treat, then feed long-acting carbohydrate, then find the cause: the third step is the one that prevents the next call
    • Sulfonylurea or long-acting insulin excess: admit for observation with repeated glucose; octreotide has a role in refractory sulfonylurea lows
    • Deprescribe and re-educate before discharge; driving guidance documented where the jurisdiction demands it

Connected

ApproachThe confused versionTopicThe frame this hangs onApproachWhen it presents as a fall

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