Diabetic Ketoacidosis

Topics: Insulin, Diabetes mellitus, Glucose Pages: 7 (2014 words) Published: August 27, 2013
1. Introduction
People still die from diabetic ketoacidosis. Poor patient education is probably the most important determinant of the incidence of the catastrophe that constitutes "DKA". In several series, only about a fifth of patients with DKA are first-time presenters with recently acquired Type I diabetes mellitus. The remainder are recognised diabetics who are either noncompliant with insulin therapy, or have serious underlying illess that precipitates DKA. Most such patients have type I ("insulin dependent", "juvenile onset") diabetes mellitus, but it has recently been increasingly recognised that patients with type II diabetes mellitus may present with ketoacidosis, and that some such patients present with "typical hyperosmolar nonketotic coma", but on closer inspection have varying degrees of ketoacidosis. 2. Insulin and its antagonists

DKA is best seen as a disorder that follows on an imbalance between insulin levels and levels of counterregulatory hormones. Put simply: |"Diabetic ketoacidosis is due to a marked deficiency of insulin in the face of high levels of hormones | |that oppose the effects of insulin, particularly glucagon. Even small amounts of insulin can turn off | |ketoacid formation". |

Many hormones antagonise the effects of insulin. These include: o glucagon
o cortisol
o oestrogen
o growth hormone
o catecholamines
In addition, several cytokines such as IL1, IL6 and TNF alpha antagonise the effects of insulin. [J Biol Chem 2001 Jul 13;276(28):25889-93] It is thus not surprising that many causes of stress and/or the systemic inflammatory response syndrome, appear to precipitate DKA in patients lacking insulin. Mechanisms by which these hormones and cytokines antagonise insulin are complex, including inhibition of insulin release (catecholamines), antagonistic metabolic effects (decreased glycogen production, inhibition of glycolysis), and promotion of peripheral resistance to the effects of insulin. 3. Triggers of ketoacidosis

Persons presenting with DKA are often seriously ill, not only because DKA itself is a metabolic catastrophe, but also because significant underlying infection or other disorders may be present. Common precipitants of DKA are: o Poor compliance with insulin therapy; or

o Underlying serious infection; or
o Other intercurrent disease (such as acute myocardial infarction, stroke, or gangrenous bowel); o Of interest is the recent observation that 'atypical' antipsychotic agents (clozapine, olanzapine) may precipitate diabetic ketoacidosis. o (In a small proportion, no precipitant will be found); 4. Deficits

Patients with DKA have marked fluid and electrolyte deficits. They commonly have a fluid deficit of nearly 100ml/kg, and need several hundred millimoles of potassium ion (3-5+mmol/kg) and sodium (2-10mmol/kg), as well as being deficient in phosphage (1+ mmol/kg), and magnesium. Replacement of these deficits is made more difficult due to a variety of factors, including the pH derangement that goes with DKA. Mainly in children, an added concern is the uncommon occurrence of cerebral oedema, thought by some to be related to hypotonic fluid replacement. There are several mechanisms for fluid depletion in DKA. These include osmotic diuresis due to hyperglycaemia, the vomiting commonly associated with DKA, and, eventually, inability to take in fluid due to a diminished level of consciousness. Electrolyte depletion is in part related to the osmotic diuresis. Potassium loss is also due to the acidotic state, and the fact that, despite total body potassium depletion, serum potassium levels are often high, predisposing to renal losses....
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