Ketoacidotic coma

If the production of ketone bodies exceeds the demand for them outside the liver, there is an increase in the concentration of ketone bodies in the plasma (ketonemia) and they are also eventually excreted in the urine (ketonu-ria). Both phenomena are observed after prolonged starvation and in inadequately treated diabetes mellitus. Severe ketonuria with ketoacidosis can cause electrolyte shifts and loss of consciousness, and is therefore life-threatening (ketoacidotic coma). 

Hyperosmolar diabetic coma occms chiefly in noninsulin-dependent diabetics who fail to compensate for their continuing, osmotic glucose diuresis. It is characterised by severe dehydration, a very high blood sugar (> 33 mmol/1 600 mg/100 ml) and lack of ketosis and acidosis. Treatment is with isotonic (0.9%) saline, at half the rate recommended for ketoacidotic coma, and with less potassium than in severe ketoacidosis. Insulin requirements are less than in ketoacidosis, where the acidosis causes resistance to the actions of insuhn, and should generally be half those shown in Table 35.2. Patients are more liable to thrombosis and prophylactic heparin is used. 

The reagent carrier should not be used in patients with neonatal hypogly-caemia and in patients suffering from ketoacidotic coma. 

The most dangerous acute symptom of Type-I diabetes is the ketoacidotic coma, which is noted as a first sign in 10% of newly diagnosed patients. 

Di Abietes, a 27-year-old woman with type 1 diabetes mellitus, had been J admitted to the hospital in a ketoacidotic coma a year ago (see Chapter 4). 

The observation that progressive insulin resistance which developed during continuous insulin infusion with bovine regular insulin for ketoacidotic coma disappeared after substitution with MC insulin (IF) was interpreted as a beneficial effect of MC insulin. However, this type of observation (i.e. disappearance of insulin resistance during continued treatment) is not uncommon during treatment of coma with regular insulin. 

Isovaleryl-CoA dehydrogenase (EC 1.3.99.10). Defective conversion of isovaleryl-CoA to methylcro-tonyl-CoA (see Leudne). Elevated isovalerate in plasma and urine also increased urinary isovaleryl-glydne, isovalerylcamitine and sometimes 3-hydro-xyisovalerate. Ketoacidotic crises, sometimes with fatal coma. Slight mental retardation in survivors. Treated with low leucine diet and supplements of glycine and/or carnitine to increase excretion of isovaler-yl conjugates. Peritoneal dialysis in crises. 

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See also in sourсe #XX -- [ ]

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