Fasting Hypoglycemia

Management of fasting hypoglycemia requires urgent treatment, diagnosis, and long-term prevention. The short-term treatment of hypoglycemia is the oral or intravenous administration of glucose. If the patient is unable to take carbohydrate by mouth, 25 to 50 g of glucose (in the form of a 50% glucose solution) should be given by intravenous injection immediately after drawing a sample for glucose determination and a sample to be saved for additional diagnostic studies. Glucagon (1.0 mg intramuscularly), which promotes hepatic glucose release, can be used when immediate glucose administration is impractical. However, the effect of glucagon is transient and exogenous glucose administration should be started as soon as possible.

The plasma glucose concentration is followed to ensure that hypoglycemia does not recur; continuous glucose infusions may be required to prevent recurrent hypoglycemia in some disorders.

After initial treatment the mechanism of hypoglycemia should be determined. Drug-induced hypoglycemia can be treated with glucose infusion and drug withdrawal. Documented hormonal deficits can be treated by hormone replacement. Hypoglycemia associated with extrapancreatic tumors may improve with reduction in tumor size achieved through surgery, chemotherapy, or radiotherapy. Hepatic dysfunction extensive enough to cause hypoglycemia is generally fatal unless it is either reversible or treated with hepatic transplantation. Recurrent fasting hypoglycemia associated with inanition, as in chronic renal failure, may respond to a high-caloric intake with frequent feedings.

The primary treatment of fasting hypoglycemia attributable to endogenous hyperinsulinism is surgical excision of the beta-cell abnormality. Solitary pancreatic tumors can be enucleated. Multiple tumors should be resected as much as possible, and sufficient pancreatic tissue to preserve function should be left. Because reduction of total tumor mass, even without cure, may render the patient euglycemic, total pancreatectomy should not be the primary procedure. In a collected series, 95% of patients with benign insulinomas were euglycemic after surgery. Complications include pancreatitis, pancreatic fistulas, and infections. Permanent diabetes may follow extensive pancreatic resection.

Computed tomography of the abdomen should be performed before surgery for insulinoma, since it can locate a minority of beta-cell tumors and can detect hepatic metastases from malignant insulinomas. Many other preoperative localization procedures have been proposed, but none has more than limited sensitivity, in part because insulinomas are usually small (median diameter, 1 to 2 cm). In patients with a clearly established diagnosis of endogenous hyperinsulinism, palpation by an experienced surgeon combined with intraoperative ultrasonographic examination of the pancreas allows successful removal of an insulinoma in the great majority of patients.

This high success rate suggests that invasive preoperative localization studies are not warranted, since negative results do not eliminate the need for surgery and positive results have not been shown to improve the outcome of surgery. If a pancreatic tumor cannot be located at laparotomy, it is preferable to forego extensive resection and pursue further localizing studies.

Medical palliation of hyperinsulinism that is not surgically correctable includes frequent oral feedings. Diazoxide, a drug that suppresses insulin secretion, may ameliorate hypoglycemia. Side effects include edema, nausea, and hypertrichosis. The somatostatin analog octreotide ameliorates hypoglycemia in some patients but is ineffective or worsens hypoglycemia in others. Chemotherapy may palliate symptoms in some patients with metastatic islet cell carcinomas; a combination of streptozocin and doxorubicin appears most effective.

Patients with reactive hypoglycemia attributable to galactosemia or hereditary fructose intolerance should avoid foods containing those sugars.