diabetic ketoacidosis and the hyperglycemic hyperosmolar state
Cerebral edema in diabetic ketoacidosis and cardiac complications of iatrogenic hypokalemia.
Iatrogenic hypokalaemia is a major and avoidable cause of death in diabetic ketoacidosis. |
DIABETIC KETOACIDOSIS
Hyperglycemic Crises in Patients With Diabetes Mellitus ...
Vasogenic edema
1. Hypoxia induced damage of the blood brain barrier (BBB): Acidosis and dehydration decrease CNS perfusion and induce hypoxia which in turn damages the blood brain barrier. On the background of a damaged less restrictive blood brain barrier, as soon as rehydration is begun and the plasma osmolality falls, there occurs movement of water from the lower osmolal plasma to the higher osmolal interstitial fluid of the brain, thus increasing intracranial pressure. Compare with drug- induced BBB breach.
2. A bolus of saline during initial therapy increases the hydrostatic pressure in the capillaries and forces water out into the interstitium more rapidly.
Cytotoxic edema
1. The formation of osmolytes within the brain cell: During the period of prolonged hyperglycemia prior to the institution of treatment for diabetes or DKA, the plasma and interstitial osmolality rise. The osmolality within the cells is kept up by the formation of osmolytes (formerly called idiogenic osmoles), which are now known to be molecules such as taurine and myoinositol(17). When intravenous fluid therapy is started, even normal saline is hypotonic compared to the plasma osmolality of the patient. Thus, the plasma osmolality is suddenly lowered, whereas due to slow movement of osmolytes intracellular osmolality remains high, forcing water from the low osmolal region (plasma) into the high osmolal region (the astrocyte).
Insulin deficiency is the main underlying abnormality. Associated with elevated levels of counterregulatory hormones, insulin deficiency can trigger hepatic glucose production and reduced glucose uptake, resulting in hyperglycemia, and can also stimulate lipolysis and ketogenesis, resulting in ketoacidosis. Both hyperglycemia and hyperketonemia will induce 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, ketoacidosis and electrolyte deficits.