Treatment

Initial management is the administration of 1 g/kg body weight dextrose, as 50% dextrose in water (D50/W) in adults. This can be followed by the infusion of 10% dextrose at a rate to maintain the serum glucose above 100 mg/dL. Repeat bedside glucose determination should be done every 30 min for the first 2 h, to detect rebound hypoglycemia. The best replacement is oral, however. A total of 300 g (1200 cal) of carbohydrate should be given orally, as sodas, juices, sandwiches, or snacks. A total of 50 mL of 105C W contains only 100 cal. Whereas some suggest that each ampule of glucose (50 g of a 50% dextrose solution) will raise the serum glucose by 60 mg/dL,14 others feel that prediction of posttreatment levels is impossible.15

Glucagon, 1 mg intramuscularly or IV, can be used in diabetics or in those in whom IV access is unobtainable. Response to glucagon therapy is generally slower when compared with IV dextrose, requiring 7 to 10 min prior to normalization of mental status; additionally, the response to glucagon administration may be short-lived. The condition of alcoholics, the elderly, and others with depleted glycogen stores will generally not improve with glucagon. Fructose and other complex carbohydrates should not be used to correct hypoglycemia in that these sugars do not cross the blood-brain barrier effectively or require extensive metabolic conversion.

Persistent hyperglycemia, maintained by slow administration of dextrose, indicates that the infusion may be reduced and eventually withdrawn. Failure to respond to parenteral glucose administration should prompt consideration of other causes of hypoglycemia.

A total of 100 mg parenteral thiamine should be given in conjunction with glucose, because, historically, the administration of glucose without thiamine in severe nutritional deficiency states could precipitate Wernicke's encephalopathy. 16 Today, this is rare. Thiamine acts as a coenzyme in several reactions in intermediary metabolism, specifically in the conversions of pyruvate to acetyl coenzyme A (linking glycolysis to the TCA cycle) and a-ketoglutarate to succinate (a reaction in the TCA cycle). As thiamine reserves disappear, the reactions halt, removing the CNS's main source of ATP and causing the acute development of Wernicke's syndrome.

Steroid administration should be considered for hypoglycemia that is either resistant to aggressive glucose replacement therapy or associated with the signs of adrenal insufficiency (see C.h.a£..2.0.8). The dose is 100 to 200 mg hydrocortisone IV in adults.

Studies in the early 1980s suggested that hyperglycemia at the time of hospital admission is associated with poor neurologic recovery in stroke patients 17 and survivors of out-of-hospital cardiopulmonary arrest.18 More recently, similar concern has been voiced regarding the association of worsened neurologic outcome and hyperglycemia in patients with acute head injury.1920 It is theorized that hyperglycemia accentuates local tissue damage by continued or increased anaerobic metabolism, lactate production, and intracellular acidosis. Acidosis may trigger a cascade that includes calcium entry into cells, lipolysis, and cytotoxic fatty acid release, culminating in neuronal death. The clinical significance has not been demonstrated, and this information should not alter the clinical management of hypoglycemia at this time.

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