Hypoglycaemia

Hypoglycaemia causes altered conscious level, seizures and coma. It is potentially life threatening if undiagnosed or untreated. There is individual variation in the BGL required to produce symptoms, but it is generally regarded as <2.5 mmol/L.

Causes

Patients without previously documented DM

Overdose of insulin or oral hypoglycaemics

Drugs—ethanol, MAOIs, haloperidol, sulfonamides, salicylates

Insulinoma or islet cell hyperplasia

Adrenal insufficiency (Addison’s disease)

Hepatic failure, hypothermia and sometimes sepsis.

Patients with documented DM

Excess insulin or oral hypoglycaemic administration

Increased exercise

Decreased calorie intake, or missed meals or snacks.

Manifestations

Adrenergic response: Catecholamines are released secondary to an absolute decrease in blood glucose. The degree of catecholamine response is inversely proportional to the BGL, and not to the rate at which hypoglycaemia develops. Adrenergic symptoms usually precede neuroglycopenic symptoms (see below), and provide an ‘early warning system’ for the patient. They include:

Sweating

Palpitations

Tremulousness

Anxiety

Hunger.

CNS response (neuroglycopenia): Deficient cerebral glucose availability is usually a secondary and slower response than the adrenergic response, and occurs over
1–3 hours:

Headache, diplopia

Difficulty in concentrating, hallucinations

Confusion, irritability

Focal neurological deficits (e.g. hemiplegia or dysphasia—check the BGL before requesting a CT brain scan in a patient with a suspected stroke!)

Seizures

Coma.

Note: The adrenergic response does not always precede the CNS response. Some patients progress directly from confusion or inability to speak to seizure or coma.

Management

Assess the severity

All symptomatic patients with hypoglycaemia require treatment. Symptoms may be precipitated by either a rapid fall in the usual blood glucose or an absolute low level of blood glucose.

Glucose administration

Immediate therapy:

Assess the patient and perform bedside fingerprick BGL.

In a cooperative, awake patient, give oral glucose in the form of sweetened fruit juice.

If patient is unable to take oral fluids or is unconscious, give 50 mL of 50% dextrose (25 g) IV by direct slow injection. Flush the vein with 50 mL normal saline following dextrose administration, because concentrated dextrose is highly irritant to veins.

If there is no IV access and the patient is unable to take oral fluids, give 1 mg glucagon SC or IM.
Remember: Vomiting may occur after glucagon administration, so the patient must be carefully monitored to prevent aspiration.

Ongoing therapy:

Begin a maintenance infusion of 5% dextrose or 10% dextrose IV at a rate of 100 mL/h if persistent hypoglycaemia is anticipated (e.g. hepatic failure, seizure or coma).

Repeat a fingerprick BGL in 1 hour and reassess the patient.

Hypoglycaemia because of an excess dose of oral hypoglycaemics may require repeated doses of 50% dextrose because of the slow metabolism and excretion of these drugs. Octreotide 50–100 micrograms IV or SC can also be used to prevent further hypoglycaemic episodes in these patients and may avoid the need for further boluses of hypertonic glucose.

Further investigations

Send blood samples for insulin and C peptide measurement when the cause of hypoglycaemia is unclear or obscure

Insulin produced endogenously includes the C peptide fragment; commercial preparations of insulin do not.

Thus, a high insulin level associated with a high C peptide level and hypoglycaemia suggests endogenous production of excess insulin (e.g. an insulinoma—rare but exciting diagnosis)

A high insulin level associated with a low C peptide level and hypoglycaemia suggests therapeutic (or surreptitious) administration of exogenous insulin.

Reference: Marks V, Teale JD. Investigation of hypoglycaemia. Clin Endocrinol (Oxf) 1996;44:133-136