Diabetic ketoacidosis

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Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state

Jean-Louis Chiasson, Nahla Aris-Jilwan, Raphaël Bélanger, Sylvie Bertrand, Hugues Beauregard, Jean-Marie Ékoé, Hélène Fournier, Jana Havrankova

bstract

DIABETIC KETOACIDOSIS AND THE HYPERGLYCEMIC hyperosmolar state are the most serious complications of diabetic decompensation and remainassociated with excess mortality. Insulin deficiency is the main underlying abnormality. Associated with elevated levels of counterregulatory hormones, insulin deficiency can trigger he- patic glucose production and reduced glucose uptake, resulting in hyperglycemia, and can also stimulate lipolysis and ketogenesis, resulting in ketoacidosis. Both hyperglycemia and hyperketone- mia willinduce osmotic diuresis, which leads to dehydration. Clinical diagnosis is based on the finding of dehydration along with high capillary glucose levels with or without ketones in the urine or plasma. The diagnosis is confirmed by the blood pH, serum bicarbonate level and serum osmolality. Treatment consists of adequate correction of the dehydration, hyperglycemia, ke- toacidosisand electrolyte deficits.

CMAJ 2003;168(7):859-66

iabetic ketoacidosis (DKA) and the hyperglycemic hyperosmolar state (HHS) appear as 2 extremes in
Glucose and lipid metabolism

When insulin is deficient, the elevated levels of glucagon, catecholamines and cortisol will stimulate hepatic glucose production through increased glycogenolysis and enhanced gluconeogenesis4(Fig. 1). Hypercortisolemia will result in increased proteolysis, thus providing amino acid precursors for gluconeogenesis. Low insulin and high catecholamine concentrations will reduce glucose uptake by peripheral tis- sues. The combination of elevated hepatic glucose produc- tion and decreased peripheral glucose use is the main patho- genic disturbance responsible for hyperglycemia inDKA and HHS. The hyperglycemia will lead to glycosuria, os- motic diuresis and dehydration. This will be associated with decreased kidney perfusion, particularly in HHS, that will result in decreased glucose clearance by the kidney and thus further exacerbation of the hyperglycemia.
In DKA, the low insulin levels combined with increased levels of catecholamines, cortisol and growthhormone will activate hormone-sensitive lipase, which will cause the breakdown of triglycerides and release of free fatty acids.
the spectrum of diabetic decompensation.1
They
The free fatty acids are taken up by the liver and converted
remain the most serious acute metabolic complications of diabetes mellitus and are still associated with excess mortal- ity. Because the approachto the diagnosis and treatment of these hyperglycemic crises are similar, we have opted to ad- dress them together.
The incidence of DKA is between 4.6 and 8.0 per 1000 person-years among patients with diabetes, whereas that of HHS is less than 1 per 1000 person-years.2 Based on the es- timated diabetic population in Canada,3 we can anticipate that 5000–10 000 patients will beadmitted to hospital be- cause of DKA every year and 500–1000 patients because of HHS. The estimated mortality rate for DKA is between 4% and 10%, whereas the rate for HHS varies from 10% to
50%, the range most likely owing to underlying illnesses.2

Pathogenesis

In both DKA and HHS, the underlying metabolic ab- normality results from the combination of absolute or rela- tiveinsulin deficiency and increased amounts of counter- regulatory hormones.
to ketone bodies that are released into the circulation. The process of ketogenesis is stimulated by the increase in glucagon levels.5 This hormone will activate carnitine palmitoyltransferase I, an enzyme that allows free fatty acids in the form of coenzyme A to cross mitochondrial membranes after their...
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