Hypoglycemia

Hypoglycemia is a common and easily treatable condition in the pre-hospital and Emergency Department settings. Recognition of the varied faces of clinical hypoglycemia, coupled with determination of blood glucose levels and expeditious glucose replacement, can prevent serious morbidity. A directed history, careful physical examination, and appropriate laboratory studies during the Emergency Department visit can uncover the etiology of hypoglycemia in most cases, and in the rest will contribute to any further diagnostic evaluation that may prove necessary.     

Hypoglycemia.

In the present review, we have tried to briefly define the types of hypoglycemia which may be seen most frequently in medicine. Wherever possible, mechanisms and appropriate diagnostic tests have been described. Treatment of hypoglycemia has been purposely avoided, since therapy should be obvious once diagnosis is made and mechanisms are understood. While it is recognized that this review is not exhaustive, it should cover over 95 per cent of the cases of hypoglycemia encountered by the practicing physician.     

Hypoglycemia in diabetes

Iatrogenic hypoglycemia causes recurrent morbidity in most people with type 1 diabetes and many with type 2 diabetes, and it is sometimes fatal. The barrier of hypoglycemia generally precludes maintenance of euglycemia over a lifetime of diabetes and thus precludes full realization of euglycemia's long-term benefits. While the clinical presentation is often characteristic, particularly for the experienced individual with diabetes, the neurogenic and neuroglycopenic symptoms of hypoglycemia are nonspecific and relatively insensitive; therefore, many episodes are not recognized. Hypoglycemia can result from exogenous or endogenous insulin excess alone. However, iatrogenic hypoglycemia is typically the result of the interplay of absolute or relative insulin excess and compromised glucose counterregulation in type 1 and advanced type 2 diabetes. Decrements in insulin, increments in glucagon, and, absent the latter, increments in epinephrine stand high in the hierarchy of redundant glucose counterregulatory factors that normally prevent or rapidly correct hypoglycemia. In insulin-deficient diabetes (exogenous) insulin levels do not decrease as glucose levels fall, and the combination of deficient glucagon and epinephrine responses causes defective glucose counterregulation. Reduced sympathoadrenal responses cause hypoglycemia unawareness. The concept of hypoglycemia-associated autonomic failure in diabetes posits that recent antecedent hypoglycemia causes both defective glucose counterregulation and hypoglycemia unawareness. By shifting glycemic thresholds for the sympathoadrenal (including epinephrine) and the resulting neurogenic responses to lower plasma glucose concentrations, antecedent hypoglycemia leads to a vicious cycle of recurrent hypoglycemia and further impairment of glucose counterregulation. Thus, short-term avoidance of hypoglycemia reverses hypoglycemia unawareness in most affected patients. The clinical approach to minimizing hypoglycemia while improving glycemic control includes 1) addressing the issue, 2) applying the principles of aggressive glycemic therapy, including flexible and individualized drug regimens, and 3) considering the risk factors for iatrogenic hypoglycemia. The latter include factors that result in absolute or relative insulin excess: drug dose, timing, and type; patterns of food ingestion and exercise; interactions with alcohol and other drugs; and altered sensitivity to or clearance of insulin. They also include factors that are clinical surrogates of compromised glucose counterregulation: endogenous insulin deficiency; history of severe hypoglycemia, hypoglycemia unawareness, or both; and aggressive glycemic therapy per se, as evidenced by lower HbA(1c) levels, lower glycemic goals, or both. In a patient with hypoglycemia unawareness (which implies recurrent hypoglycemia) a 2- to 3-week period of scrupulous avoidance of hypoglycemia is advisable. Pending the prevention and cure of diabetes or the development of methods that provide glucose-regulated insulin replacement or secretion, we need to learn to replace insulin in a much more physiological fashion, to prevent, correct, or compensate for compromised glucose counterregulation, or both if we are to achieve near-euglycemia safely in most people with diabetes.     

Hypoglycemia Rebound Migraine

OBJECTIVE: To describe a patient with specific hypoglycemia rebound migraine. BACKGROUND: There is an increased prevalence of headache in persons with diabetes. Although hypoglycemia may precipitate headache in some diabetic (and nondiabetic) patients, it is not a universal pathogenetic mechanism responsible for headache in those individuals or in normal fasting subjects. METHODS: Clinical history, review of past medical records, neurologic examination, follow-up evaluation, electroencephalogram, and computerized tomography of the head. RESULTS: A 56-year-old man with unstable diabetes mellitus had recurrent monthly episodes of profound hypoglycemia for 40 years. These episodes were followed by severe, global, pulsatile headache after glycemia became normal subsequent to intravenous infusion of glucose and the patient was no longer confused and lethargic. He had no headache preceding or throughout the actual hypoglycemic phase. His neurologic examination was normal when asymptomatic. His baseline electroencephalogram was normal, but showed mild slowing of the background in the immediate posthypoglycemic state. Computerized tomography of the head demonstrated mild atrophic changes. His severe bouts of hypoglycemia and migraine were ameliorated by prophylactic treatment with valproic acid. CONCLUSION: Posthypoglycemic migraine may occur exceptionally in patients with unstable diabetes as a rebound phenomenon, caused by an unidentified mechanism.     

Ethanol-associated Hypoglycemia Is Uncommon

Objective: To determine the association of ethanol intoxication with hypoglycemia in ED patients. Methods: Retrospective, laboratory log review of 953 consecutive patients who were evaluated for ethanol intoxication in an urban university hospital ED over a three-month period. Simultaneous serum glucose determination was carried out for each patient and associations between ethanol level and glucose were sought. Results: Glucose concentrations were unavailable for 16 patients (1.7%). Of the remaining patients, 584 patients had detectable ethanol concentrations (ethanol-positive), and 353 had no detectable ethanol (ethanol-negative). Ethanol concentrations (mean ± SD) in the ethanol-positive group were 50.11 ± 24.08 mmol/L (231 ± 111 mg/dL), and glucose concentrations were 5.83 ± 1.94 mmol/L (105 ± 35 mg/dL). Hypoglycemia [glucose <3.72 mmol/L (67 mg/dL)] was observed for five (0.9%) ethanol-positive patients. It was classified as mild-moderate [2.78–3.66 mmol/L (50–66 mg/dL)] for four patients (0.7%) and severe [<2.78 mmol/L (50 mg/dL)] for one (0.2%). Ethanol concentrations ranged from 25.60 to 68.33 mmol/L (118 to 315 mg/ dL). There was no correlation between ethanol and glucose concentrations in any subset of the ethanol-positive patient population. In the ethanol-positive group, patients who had several ethanol-positive visits (56 patients, mean 3.6 visits/patient) accounted for four of the five episodes of hypoglycemia, including the one episode of severe hypoglycemia. The frequency of hypoglycemia in repeat visitors (2.0%) was higher than that in the group of patients without repeat visits (0.2%). In the ethanol-negative group, there were four (1.1%) episodes of mild-moderate hypoglycemia and no severely hypoglycemic patient. Hypoglycemia was not more likely to occur among ethanol-positive patients than it was among ethanol-negative patients. Conclusion: Hypoglycemia was uncommonly associated with ethanol intoxication, and was found almost exclusively among patients with several ethanol-positive visits. Glucose and ethanol concentrations do not show any linear correlation; patients with higher ethanol concentrations are not at higher risk of hypoglycemia. Hypoglycemia is not more likely to occur in ethanol-positive than in ethanol-negative patients. Initial glucose screening does not appear to be necessary for all patients suspected of intoxication; selective screening may be more appropriate.     

Endocrine crises. Hypoglycemia

Hypoglycemia is defined as the occurrence of a wide variety of symptoms in association with a plasma glucose level of 40 mg/dL or less. The conditions associated with hypoglycemia in hospitalized patients include exogenous insulin administration, ethanol, drugs (especially chlorpropamide), renal insufficiency, liver disease, infections, total parenteral nutrition, treatment of hyperkalemia with insulin, extensive burns, neoplasia, pregnancy, and a wide variety of less common causes. Although clinical features are helpful in making a diagnosis, a significant proportion of the patients are either asymptomatic or present with symptoms of altered mental status. The diagnosis of hypoglycemia should be considered in all hospitalized patients presenting with adrenergic or neuroglycopenic symptoms and signs suggestive of hypoglycemia. A detailed history along with a physical examination and appropriate laboratory investigations usually identify the specific cause of the hypoglycemia. An episode of hypoglycemia, especially if severe, should be treated with prolonged intravenous infusion of glucose. Prompt recognition and management of hypoglycemia are necessary to prevent significant morbidity and mortality.