Title: Management of Hypoglycaemia

Key words: Diabetes, fasting, post-prandial hypoglycaemia, neuroglycopenia, treatment, amino acid supplementation, chromium, ginseng

Date: March 1999

Category: 13. Specific Conditions

Type: Article

Author: Dr van Rhijn


Management of Hypoglycaemia



Patients presenting with vague complaints of "feeling tired" merit appropriate and thorough investigations, as it is a very general and non-specific symptom of numerous clinical conditions, including hypoglycaemia. Appropriate diagnosis is a prerequisite for proper management, as hypoglycaemia can be life threatening but is readily treatable1.


Proper history taking will elucidate and divide the spontaneous hypoglycaemia into two main categories2:

Fasting hypoglycaemia, which only occurs after several hours without food and always indicates underlying disease, in contrast to

Post-prandial hypoglycaemia which occurs 3-5 hours after meals, usually occurs in the absence of organic disease.

Following some individual variation, the threshold for symptom development is usually below 2.5 mmol/L blood glucose, but there is a poor correlation between symptoms and biochemical hypoglycaemia3. Numerous clinical conditions need to be excluded such as those due to malnutrition, fasting, exercise, dumping syndrome, alcohol abuse, advanced liver disease, infections (malaria)4, endocrine causes (especially the rare insulinomas and insulin-like growth factor II secreting tumours) and various drugs. Poorly managed IDDM is a very common cause of hypoglycaemia5, which may also be Factitious, and induced by insulin or a sulphonylurea drugs. The condition of Non-hypoglycemia following coffee ingestion should form part of the differential diagnosis.


Hypoglycaemia is defined as a fasting arterial blood glucose level of < 2.2 mmol/L6, and a random, venous test is of limited value. If a capillary blood glucose level "during an attack" is positive (< 3 mmol/l), measure pro-insulin, insulin, C-peptide and b -hydroxybutyrate levels for differential diagnosis of the above mentioned causes. It may be useful to admit the patient for 72 hours for a supervised fast as a screening procedure7. The glucose tolerance test (GTT) is of little value for the diagnoses of post-prandial hypoglycaemia due to false positive results, especially if venous blood rather than arterial blood is sampled. Factitious hypoglycaemia, due to insulin, can thus also be identified, and plasma chromatography may detect sulphonylureas.



All hypoglycaemic episodes must be treated without delay8. Acute, spontaneous attacks only require ingestion of snacks from rapidly assimilable carbohydrate (glucose or sweets). Prevention is essential by advising frequent (3-4 hourly) small meals9 consisting of high fibre and rich in poorly absorbed carbohydrates. In severe cases, intravenous dextrose (50%) and glucagon 1mg (i.m.) may be used in the short term. Glucagon10 is only effective in raising insulin levels if the liver contains adequate glycogen stores, which should, therefore, be replenished with oral glucose. Pharmaceutical agents such as guar and acarbose11 slow glucose absorption and decrease insulinaemic response. Treatment may revert to an a -glucosidase inhibitor where the glucose homeostasis is difficult to control. An overdose with sulphonylurea drugs may require treatment with diazoxide, and a referral for psychiatric help may be appropriate in cases of factitious hypoglycaemia, due to the severe denial involved.

Dietary supplementation with aminoacids (glutamine, leucine and isoleucine), the mineral Chromium, herbs (ginseng & licorice) and even parsnips have been found in practice to alleviate hypoglycaemia.


Management is always aimed at normalising the plasma glucose concentration and obtaining proper glucose homeostasis. Brain malfunction (neuroglycopenia) due to hypoglycaemia can have serious consequences and a thorough clinical investigation is required to identify and treat the diverse but rare physical causes.


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