Hypoglycaemia is quite frequently met with in the emergency department (ED). The aetiology of hypoglycaemia is varied in human beings. Iatrogenic hypoglycaemia is one of the commonest causes. The commonest clinical scenario encountered will be a known diabetic patient who had correctly used the dose of insulin or oral hypoglycaemic agents with very little or no oral food intake. However, it is uncommon for a non-diabetic with good oral nutrition to present with hypoglycaemia. It is imperative that the clinician recognizes the condition and provides prompt treatment with blood sampling for the necessary tests. In many cases the exact aetiology may not be arrived at in the ED.

A 70 yr old lady was brought to the emergency department in a drowsy state responding to verbal interaction and moving all her limbs. According to the relatives, the patient fell back on getting up from the bed in the morning. They also stated that her limbs were stiff and that she had frothy secretions in her mouth. There was no history of diabetes, hypertension, epilepsy or asthma. There was a past history of left tuberculous cervical adenitis 40 years ago for which she was treated completely elsewhere.

She was thin built, had skin lesions - vitiligo on the abdomen and neck, tinea unguum on the 2nd and 3rd nails of the right hand and psoriasis on the feet. Her systemic examination revealed no abnormality. Her pulse rate was 86/min and BP was 150/80 mmHg. At the ED an iv access was secured and after sampling blood for sugar 50 ml of 25% Dextrose was given.

The relatives informed that she had complained of giddiness 4 days ago and that she had been prescribed a vestibular sedative elsewhere. Besides that she was on calcium supplements, multivitamins and cetirizine. Her oral food intake was good and she had not fasted prior to the episode. The lady’s husband was a diabetic who was on oral anti-diabetics. The relatives claimed that his medicines were kept in a different box and that their medications were never mixed up.

The patient responded well to the dextrose infusion. She was shifted to the Intensive Care Unit where she was maintained on 10% Dextrose. Her blood sugar taken on admission was found to be 35 mg/dl. This lead to further interrogation and the relatives later found that a strip of semi-daonil (glibenclamide), a sulphonylurea taken by the husband was indeed found in the patient’s drug box, with 4 tablets used, the medication’s packing on the reverse side was similar in appearance to cetirizine that she was taking (Figs. 1a,b).

The patient improved rapidly on maintenance with 10% dextrose. Her blood sugar were on the lower side for a couple of days. All the other investigations including haemogram, urine examination, renal parameters, electrolytes, liver function tests, serum calcium and phosphorus were within normal limits. Her ECG was normal. Her chest and abdominal X-rays revealed no abnormality except for osteoporotic lesions. The results of the other investigations were not indicative of Addison’s disease or other causes of hypoglycaemia. The blood sulphonylurea levels were not done due to technical difficulties. The patient has been regularly followed up and she has been found to be doing well.

Hypoglycaemia is a biochemical abnormality, below 2.2 mmol/l (40 mg/dl), normal being 3.5 to 6.5 mmol/l (60-110 mg/dl). The classic presentation of hypoglycaemia is a diaphoretic patient with a history of diabetes mellitus with an altered mental status who had used insulin or anti-diabetic drugs with little or no oral nutrition. A firm diagnosis of hypoglycaemia is based on Whipple’s triad of:

Figs.1a,b: New strip of the accidentally interchanged medication used by the patient.

1. hypoglycaemic symptoms
2. a low blood glucose demonstrated biochemically
3. symptoms relieved by glucose administration Iatrogenic hypoglycaemia occurs due to ingestion of insulin or ingestion of sulphonylureas. Hypoglycaemia due to sulphonylureas may be severe and longer lasting than episodes secondary to insulin. Sulphonylureas bind to receptors on islet B-cells leading to insulin release. This hyperinsulinaemia suppresses endogenous glucose production leading to fasting hypoglycaemia. Relapse after a satisfactory response to intravenous glucose is recognized. This is because, though the intravenous glucose rapidly corrects the hypoglycaemia it acts as a secretogogue to the sulphonyluera sensitized B-cells which stimulates insulin secretion leading to recurrence of hypoglycaemia. For this reason, patients with sulphonylurea - induced hypoglycaemia may require intravenous glucose for many days. Octreotide can reduce the relapse rate by inhibiting insulin secretion. Treatment with glucose and octreotide may be required for several days. Glucagon is contraindicated in sulphonylurea-induced hypoglycaemia as it stimulates insulin secretion. The blood glucose concentration should be maintained around 5-7 mmol/l (80-120 mg/dl).
   
   In a patient administered insulin, C-peptide levels are low while insulin levels are inappropriately high. Surreptitious use of sulphonylureas increases both insulin and C-peptide concentrations, similar to that seen in a patient with insulinoma. Hence a urine sample or a blood sample can be analysed for sulphonylureas. In case of tolbutamide, a white precipitate, carboxytolbutamide is formed upon acidification of urine. However the newer sulphonylureas like glimepiride and other insulinotropic hypoglycaemic drugs like repaglinide and nateglinide are not detected in the standard assays for sulphonylureas. There are other drugs that can lead to hypoglycaemia like quinine, salicylates, propranolol and pentamidine.
   
   The most frequent situation managed in the emergency department involves a diabetic patient who is on either insulin or oral hypoglycaemic agents (OHA). However, at times a patient without diabetes mellitus, as in this case, will present with hypoglycaemia resulting from an adverse reaction to such medication.
   
   In a non-diabetic it is extremely difficult to discover hypoglycaemia and its cause if unsuspected. Iatrogenic hypoglycaemia should be an early and seriously considered diagnosis for all patients with hypoglycaemia. Individuals with access to insulin or OHA’s, such as medical personnel or relatives of diabetics are especially at risk. These persons may deny self-induced hypoglycaemia. So it is essential that the clinician searches for clues to the aetiology.