SPONTANEOUS HYPOGLYCAEMIA
Hypoglycaemia can be defined as a plasma glucose of <2.5 mmol/L with symptoms of neuroglycopaenia. The mechanisms include excessive or inappropriate insulin, impaired counter-regulatory hormonal response (e.g. GH or cortisol) and impaired hepatic glucose output because of liver disease. The causes of spontaneous hypoglycaemia are broadly categorised into two groups according to whether the symptoms occur in the fasting or postprandial state.
Fasting
hypoglycaemia
The
symptoms of fasting hypoglycaemia occur several hours bafter food (e.g. on waking or at night) or can be
precipitated by exercise (Figure
34.1). Causes include:
• Drugs (insulin, sulphonylureas,
quinine, salicylates, alcohol)
• Organ failure
(liver/renal failure)
• Hormone
deficiency (Addison’s disease, hypopituitarism)
• Insulinoma
(Figure 34.2)
• Non-islet cell
tumours (fibrosarcoma, hepatocellular carcinoma, mesothelioma)
• Autoimmune (insulin
receptor-stimulating antibodies)
• Infection
(septicaemia, malaria)
• Inborn errors of
metabolism (glycogen storage disease, hereditary fructose intolerance, maple syrup disease)
•
Beta cell hyperplasia.
Postprandial
hypoglycaemia
Symptoms
usually occur 2–5 hours after food. Causes include:
•
Post-gastrectomy
•
Alcohol-induced
•
Incipient diabetes mellitus.
Assessment
The
history should look to elucidate adrenergic (pallor, sweating, tachycardia,
tremor) and neuroglycopaenic (impaired concentration, irritability, change in
behaviour, confusion, seizures or coma) symptoms in addition to clarifying
whether they occur in the fasting or postprandial state. A history of relevant drug exposure, known diabetes, renal, liver
or endocrine disease should be sought. Fingerprick capillary glucose readings
(‘BMs’) are unreliable for low glucose concentrations, hence a laboratory
plasma glucose should always be measured to confirm true hypoglycaemia (<2.5
mmol/L). Liver and renal function should be checked, in addition to a septic
screen and ethanol levels if relevant. A Synacthen test should be considered to
exclude adrenal insufficiency.
Further
investigation of fasting hypoglycaemia
Rarer
causes of fasting hypoglycaemia should be considered if the above tests are
normal. Fasting insulin, C-peptide, ketones and glucose should be measured
during a confirmed episode of hypoglycaemia (Table 34.1). This may need to be
undertaken as part of a prolonged (up to 72 hours) supervised fast. In the
presence of hypoglycaemia, inappropriately elevated insulin suggests insulinoma
or exogenous insulin or sulphonylurea therapy.
The C-peptide will be suppressed in patients on exogenous insulin but
inappropriately elevated in insulinoma or sulphonylurea therapy. Ketones will
also be suppressed in the presence of insulin.
Further
investigation of postprandial hypoglycaemia
A
prolonged 75 g OGTT with frequent measurement of glucose for up to 6 hours can
confirm postprandial hypoglycaemia.
Management
The
acute treatment of hypoglycaemia is detailed in Chapter 54. Treatment is
directed at the underlying cause. Insulinomas should undergo surgical resection
if possible, after appropriate localisation. Islet tumours can be difficult to
localise as they are often small. Several tests may be needed including MRI/CT
(first line), endoscopic ultrasound, octreotide scanning and/or selective
venous sampling. Where surgery is not curative or not feasible, symptoms can be
controlled by diazoxide or octreotide. Postprandial hypoglycaemia can be
treated with a low carbohydrate diet
and/or frequent small meals in the first
instance.
