The Laboratory diagnosis and management of diabetic coma

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The Laboratory diagnosis and management of diabetic coma

People with diabetes can suffer several types of comas. One of the most common is insulin shock this develops relatively rapidly and is caused by an excess of injected insulin or other sugar-lowering medication that causes a depletion of blood sugar (hypoglycemia). Other types of diabetic coma result from inadequate insulin, which leads to hyperglycemia as in hyperosmolal non ketotic coma and sometimes the buildup of toxic substances as in diabetic ketoacidosis.

Diabetic ketoacidosis is a potentially fatal complication of diabetes, this occurs when blood glucose levels are high (often above 400 mg/dL) and insulin levels are very low. Insulin is the pivotal hormone of blood glucose regulation, increasing peripheral glucose uptake while stimulating glycogen synthesis and peripheral fat deposition. Insulin deficiency exaggerates the normal response to fasting, which is to increase liver production of glucose by gluconeogenesis from fat and protein together with breakdown of liver glycogen stores by glycogenolysis. The metabolic consequences follows of this is hyperglycemia which further impairs peripheral glucose uptake and inhibits any residual insulin synthesis. Blood glucose levels rise above the renal threshold for glucose reabsorption, causing an osmotic diuresis, this causes large losses of fluid, typically 3-10% of body weight. Most water is lost by osmotic diuresis, with important contributions from hyperventilation and vomiting. The diuresis also leads to considerable urinary losses of potassium, sodium, phosphate, and magnesium ions.

Insulin also has the effect of inhibiting the lipolytic action of cortisol and growth hormone so insulin deficiency has a secondary effect of increases circulating levels of fatty acids. These are oxidized in the liver, producing the acidic ketone bodies beta-hydroxybutyrate and acetoacetate, from which acetone forms. The resulting acidosis primarily is due to circulating ketone bodies, but is also effected by the excess fatty acids and lactic acidosis, this causes poor tissue perfusion. Eventually, hyperventilation no longer can compensate for the metabolic acidosis, which together with dehydration, leads to renal failure and circulatory collapse, followed by coma and death. (Mayne 1994).

         Non ketotic hyperglycemic-hyperosmolar coma  is a complication of type II Diabetes and has a mortality rate of over 50%. It usually develops after a period of symptomatic hyperglycemia in which fluid intake is inadequate to prevent extreme dehydration from the hyperglycemia causing osmotic diuresis. Unlike diabetic ketoacidosis there are no detectable ketoacids this is probably due to small amounts of insulin activity able to suppress lipolysis but insufficient to suppress gluconeogenesis or facilitate glucose transport into cells. (Mayne 1994).

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A precipitating factor may be a coexisting acute infection such as pneumonia  but Non ketotic hyperglycemic-hyperosmolar coma  can also occur when patients with undiagnosed or neglected type II Diabetes receive drugs that impair glucose tolerance (eg, glucocorticoids) or increase fluid loss (diuretics). The consistent and diagnostic features of Non ketotic hyperglycemic-hyperosmolar coma are CNS alterations, extreme hyperglycemia, dehydration and hyperosmolarity, mild metabolic acidosis without marked hyperketonemia, and prerenal azotemia (or pre existing chronic renal failure). The state of consciousness at presentation varies from mental cloudiness to coma. In contrast to diabetic ketoacidosis , focal or generalized seizures may occur. The ...

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