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HYPOGLYCEMIA, a serum glucose value lower than 60 mg/dL. The diagnosis is generally not pursued when the glucose deficit is minor and lacks symptoms. Serum glucose levels are tightly maintained within a narrow range. Insulin enhances cellular glucose uptake thus lowering serum values. Glucagon, growth hormone, cortisol, and epinephrine all increase glucose production and limit glucose utilization and result in elevated serum values. Symptoms of hypoglycemia may be secondary to cerebral glucose deprivation (altered mental status, headache, lethargy, confusion, motor abnormalities, coma, or even death) or they may be the result of increased sympathoadrenal discharge with resultant adrenergic symptoms (tachycardia, palpitations, anxiety, or diaphoresis). In cases of recurrent symptoms, weight gain may result from overeating in an effort to combat symptoms. Most episodes are secondary to medications or alcohol abuse. Medications of the sulfonylurea class are a common culprit and can result in a prolonged acute episode of several days especially when associated with underlying liver disease or significant renal impairment.
The workup of hypoglycemia begins with ruling out exogenous insulin or OHA use/abuse. Once these medications have been excluded, the workup proceeds by determining the serum values for insulin, proinsulin, C-peptide, and cortisol along with the glucose level during a hypoglycemic episode. Hypoglycemic patients with a low insulin level during a hypoglycemic attack should be worked up for non-beta-cell tumors, particularly hepatocellular carcinoma (HCC) and retroperitoneal tumors after liver failure and alcohol abuse have been excluded. Hypoglycemic patients with a normal or elevated insulin level during a hypoglycemic attack exhibit inappropriately suppressed insulin levels, and diagnostic considerations include insulinoma, anti-insulin antibodies, exogenous insulin administration, or OHA ingestion. At this point, the next step is to determine the source of the excess insulin, either endogenous or exogenous. This is accomplished by determining the C-peptide level. The C-peptide is a byproduct of endogenous insulin production and is not elevated in patients receiving exogenous insulin. An uncommon cause of an elevated insulin out of proportion to the C-peptide is anti-insulin antibodies, which bind to endogenous insulin rendering it inactive only to dissociate at a later time and allow the now functional insulin to induce hypoglycemia. If the C-peptide level is increased, indicating excessive endogenous insulin production, diagnostic considerations include insulinoma or OHA ingestion. OHA ingestion may easily be excluded by urinary screening for these drugs. Insulinomas are solitary, small, usually benign (5-10% are malignant) pancreatic tumors characterized by an inability to convert proinsulin to insulin. Therefore, the serum proinsulin level and serum proinsulin/insulin ratio are increased in these patients. A carefully supervised 72-hour fast is often helpful in establishing the diagnosis. During a prolonged fast, plasma insulin levels should decline in normal individuals; however, in persons suffering from an insulinoma, high insulin levels persist despite hypoglycemia. CT and angiography are useful to help localize the tumor, and surgery may be curative; however, many tumors are minute and localization procedures are ineffective. Low insulin and C-peptide levels with an elevated cortisol level are indicative of increased glucose utilization seen in some malignancies such as large fibromas, sarcomas, renal cell carcinomas, or adrenal cancers. Low levels of insulin, C-peptide, and cortisol suggest adrenal insufficiency as the underlying etiology.
Patients with diabetes mellitus on intensive therapy, who engage in strenuous exercise, or who lose significant amounts of weight without a downward therapeutic titration are at an increased risk of hypoglycemic episodes. Emergency treatment entails intravenous glucose or glucagon therapy (1 mg IM, IV, or SQ). Hypoglycemia secondary to oral sulfonylurea therapy/overdosage/abuse may be recurrent during the acute period (up to 48-72 hours) especially in cases with underlying renal or hepatic disease. These patients will require repeated glucose rescue therapy. If volume overload is a concern or intravenous glucose is not sufficient to correct the hypoglycemia, these patients may respond to octreotide (50 micrograms every 8 hours SQ) or diazoxide therapy which inhibit beta cell insulin secretion. Diazoxide (5-15 mg/kg/day) may also be used in cases of congenital hyperinulinism except in cases where there is the total lack of beta cell potassium channels. Diabetic patients at increased risk for hypoglycemia should be instructed regarding oral therapy when symptomatic and should be given an emergency glucagon self-injection kit. Chronic diabetic therapy should be adjusted especially if the HgbA1c shows overly aggressive management (<7.0 mg.dL) as there is little benefit to be gained from such strict control or in elderly patients with end organ damage who will not gain significant benefit from aggressive therapy..