Diabetes

Abstract

Diabetes mellitus is caused by an absolute (type I) or relative (type II) lack of insulin. Treatment was first described by Banting and Best in the form of injectable pancreatic extract (insulin) in 1922. Approximately, 6% of the world's population suffers from diabetes mellitus and this is set to rise to 300 million sufferers by 2025. Ninety seven percent will have type II diabetes. Normal carbohydrate metabolism depends upon the presence of insulin. Both diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic state (HHS) are caused by the reduced effect of insulin with a concomitant rise in counter-regulatory hormones such as glucagon, catecholamines, cortisol and growth hormone. Decreased insulin and increased epinephrine levels activate adipose tissue lipase causing lipolysis of trigylcerides into glycerol and free fatty acids (FFAs) with subsequent promotion of fatty acid transport into mitochondria where ketone body formation occurs. HHS does not have the ketogenic features of DKA and there are reduced levels of FFAs, glucagon, cortisol and growth hormone relative to DKA although this is by no means absolute. Hyperosmolarity is the prominent feature of HHS. The keystone of treatment is fluid replacement and insulin administration. Fluid to replace losses, correct the obvious hypovolaemia and then more slowly allow the patient to correct their intracellular deficit. Insulin is used in moderation. An initial bolus dose of 0.15 U/kg followed by low dose (0.1 U/kg/h) insulin infusions with gradual correction of hyperglycaemia results in a reduced mortality. With this approach there are less therapy-induced episodes of hypoglycaemia and hypokalaemia. In HHS, it is likely that insulin requirements to achieve normo-glycaemia are usually lower than DKA, although insulin resistance can occur due to the presence of counter-regulatory hormones in the acute illness. The main areas of concern in the treatment of acute diabetic hyperglycaemic episodes are: speed of glucose correction, over-aggressive fluid resuscitation and the role of bicarbonate in correcting an acidosis. The latter is a more particular consideration in DKA.