Once hypoglycemia is diagnosed, the aim of treatment is to correct it rapidly and maintain a blood glucose level that prevents neuroglycopenia. Uncomplicated hypoglycemia requires a level of 1.1 mmol/l or less to trigger the events that lead to brain damage. Mitochondrial disruption leads to neuronal death with cerebral edema, gliosis, and permanent sequelae as a result. However, hypoxemia, hypotension, and epileptic activity all act synergistically with hypoglycemia to reduce the substrates necessary for neuronal respiration, and will increase the chance of an unfavorable outcome.
Brain damage from hypoglycemia tends to occur in the 'watershed' areas of critical cerebral perfusion. Slowness to recover from the cerebral symptoms of neuroglycopenia is a measure of the degree of the hypoglycemic insult and may reflect cerebral edema.
Therefore it is essential to resuscitate the patient and his or her cellular milieu according to clinical priorities, restoring oxygenation and the circulation before or simultaneously with the correction of the blood glucose. Bedside monitoring should include frequent estimations of blood glucose to prevent a relapse into dangerous hypoglycemia. Treatment may be necessary for several days, particularly in drug-induced hypoglycemia or severe liver disease. Overdose of the long-acting sulfonylurea chlorpropamide (f1/2 = 32 h) commonly requires 5 to Z days of glycemic support. The endpoint of therapy is when the hypoglycemic stimulus diminishes and/or iatrogenic hyperglycemia begins to occur, which is an indication to withdraw treatment over 24 h.
Was this article helpful?