Emergency treatment of hypoglycemia

Glucose should be administered orally (10-20 g in adult patient, 3 times before giving a meal). If oral therapy is not possible the parenteral dose of glucose for adult should be 25-50g as 50-100 mL of 50% dextrose should be given. Failure to respond to glucose, glucagon should be administered intramuscularly or intravenously, steroids (hydrocortisone).

Causes of hypoglycemia:

1.    Medical therapy of diabetes especially insulin administration or oral hypoglycemia drug is the most common cause of fasting hypoglycaemia.

2.   Surreptitious (self-induced) administration of hypoglycemic agents (factitious or felonious hypoglycaemia) like insulin, sulphonylureas, metiglinides, etc.

3.      Insulinoma: Insulin producing islet cell tumors.

4.      Autoimmune hypoglycemia 

In one condition antibodies binds to insulin receptors and mimic the action of insulin. Laboratory finding shows high plasma insulin concentrations but suppressed C-peptide and proinsulin. The other syndrome, autoimmune insulin syndrome, in which antibodies are direction towards insulin. Laboratory finding shows high plasma concentration of insulin and C-peptide (C-peptide level is quiet less than insulin).

1.      Hypoglycaemia associated with renal failure:

Renal impairment leading to hypoglycaemia is the second most common cause of hypoglycaemia, after insulin therapy. The most important factor here is calorie restriction. In normal subjects, the kidney, by gluconeogenesis supply 45% of glucose during prolonged starvation. In uraemic patient this process is impaired. Other mechanisms include increase insulin half-life due to impaired renal clearance and degradation.

2.      Hypoglycemia associated with liver disease:

Liver can maintain glucose homeostasis even functioning liver mass reduces to <20% and hypoglycemia does not occur unless liver is extensively damaged. Conditions like fatty liver, cirrhosis, infective hepatitis, hepatocellular carcinoma are associated with hypoglycaemia.

3.      Alcohol induced hypoglycaemia: 

Alcohol induced fasting hypoglycemia is due to direction inhibition of gluconeogenesis. This is due to accumulation of NADH and increased NADH/NAD⁺ ratio resulting from the oxidation of ethanol. Alcohol induced fasting hypoglycemia usually develops 6-36h after ingestion of alcohol. There is severe metabolic acidosis with high blood lactate. Hyperketonaemia and ketonuria are present predominantly β-OHB, since the accumulation of NADH suppress the conversion of it to acetoacetate. Prompt IV glucose treatment should be done.

Alcohol potentiates the hypoglycemic effect of insulin and sulphonylurea drugs. Alcohol potentiates the insulin-stimulating effect of glucose and thus increase the risk of reactive hypoglycemia. This is seen during consumption of alcohol and sucrose (e.g. in syrup or tonic) in empty stomach and followed by not eating for few hours afterward. This effect is not seen when saccharin or fructose is substituted for sucrose as sweetening agent. Starchy foods like breads increase the risk fro reactive hypoglycaemia, whereas foods providing fat or protein have the reverse effect.

During exercise, during the first 5-10 minutes of severe exercise, muscle glycogen is the source of energy, by 40 min, 75-90% of glucose is supplied by blood, mainly from increased hepatic glucose production (75% from glycogenolysis and 25% from gluconeogenesis).

4.      Reactive (alimentary) or postprandial hypoglycemia

This occur after gastric surgery, antibodies to insulin, inborn error of metabolism. Symptoms occurring 2-4h after food ingestion and last for about 10-20 min. This is also seen in patients with hereditary fructose intolerance after ingestion of fructose.

Hypoglycemia in Diabetes Mellitus

Hypoglycemia occur frequently in both type 1 and 2 diabetes. This occurs in diabetic patients using hypoglycemia drugs or insulin. In many patients with type 1 disease do not experience the neurogenic warning symptoms for years and are prone to severe hypoglycemia this is called hypoglycemia unawareness.