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Hypoglycemia
Counselor,

Hypoglycemia is considered present when serum glucose level is less than 50 mg/dL. An alternative definition is a decrease in the blood glucose level or its tissue utilization that results in demonstrable signs or symptoms. These signs or symptoms usually include altered mental status and/or sympathetic nervous system stimulation. The glucose level at which an individual becomes symptomatic is highly variable.

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Pathophysiology:

The organ systems that manifest the signs and symptoms of hypoglycemia are the central and autonomic nervous systems. Hypoglycemia can be due to alimentary problems, idiopathic causes, fasting, insulinoma, endocrine problems, extrapancreatic causes, hepatic disease, and miscellaneous causes.

Mortality/Morbidity:

Delay in treatment can result in profound sequelae, including death. Acute sequelae include coma, cardiac dysrhythmia, and death. The risk of permanent neurologic deficits increases with prolonged hypoglycemia; such deficits can include hemiparesis, memory impairment, diminished language skills, decreased abstract thinking capabilities, and ataxia. Because the consequences of hypoglycemia can be devastating and an antidote is readily available, diagnosis and treatment must be rapid in any patient with suspected hypoglycemia, regardless of the cause.

History:

Patients often have a history of diabetes mellitus. A history of insulin usage or ingestion of an oral hypoglycemic agent may be known, and possible toxic ingestion should be considered. Obtaining an accurate medical history may be difficult if the patient's mental status is altered.

The medical history may include diabetes mellitus, renal insufficiency/failure, alcoholism, hepatic cirrhosis/failure, other endocrine diseases, or recent surgery. The patient's medication and drug history should be reviewed carefully for potential causes of hypoglycemia. The social history may include ethanol intake and nutritional deficiency both of which can contribute to the development of hypoglycemia.

Central nervous system findings are the most prevalent. These include headache, confusion, personality changes, palpitations, adrenergic symptoms, sweating, anxiety, nervousness and tremulousness. Hunger and nausea are also prevalent findings.


Physical:

Physical findings are nonspecific in hypoglycemia and generally are related to the central and autonomic nervous systems. Vital signs might show hypothermia, tachypnea, tachycardia, hypertension, and bradycardia (neonates).

The head, eyes, ears, nose, and throat (HEENT) examination may indicate blurred vision, pupils normal to fixed and dilated, icterus (usually cholestatic due to hepatic disease), and parotid pain (due to endocrine causes). Cardiovascular disturbances may include tachycardia (bradycardia in neonates), hypertension or hypotension, and dysrhythmias. Respiratory disturbances may include dyspnea, tachypnea, and acute pulmonary edema. GI disturbances may include nausea and vomiting, dyspepsia, and abdominal cramping. Skin may be diaphoretic and warm or show signs of dehydration with decrease in turgor.

Neurologic conditions include coma, confusion, fatigue, loss of coordination, combative or agitated disposition, stroke syndrome, tremors, convulsions, and diplopia.


Causes:

Causes of hypoglycemia are varied, but it is seen most often in diabetic patients. Hypoglycemia may result from medication changes or overdoses, infection, diet changes, metabolic changes over time, or activity changes; however, no acute cause may be found.

Drugs that may be related to hypoglycemia include the following: oral hypoglycemics, sulfonamide, phenylbutazone, insulin, bishydroxy coumarin, salicylates, p-aminobenzoic acid, propoxyphene, haloperidol, stanozolol, ethanol, hypoglycin, carbamate insecticide, disopyramide, isoniazid, methanol, methotrexate, pentamidine, sulfonamide, tricyclic antidepressants, cytotoxic agents, organophosphates, propranolol plus ethanol, didanosine, chlorpromazine, quinine, sulfa drugs, fluoxetine, sertraline, fenfluramine, trimethoprim, 6-mercaptopurine, thiazide diuretics, thioglycolate, tremetol, ritodrine, disodium ethylenediaminetetraacetic acid (EDTA), clofibrate, angiotensin converting enzyme (ACE) inhibitors, and lithium.

Other causes include the following: GI Surgery, hepatic disease, islet cell tumor or extrapancreatic tumors, exercise in diabetic patients, pregnancy, adrenal insufficiency, enzyme deficiencies, hypopituitarism, starvation, and sepsis.


Lab Studies:

Treatment and disposition of hypoglycemia are guided by the history and the clinical picture. Serum glucose should be measured frequently and used to guide treatment, because clinical appearance alone may not reflect the seriousness of the situation.

If the cause of hypoglycemia is other than oral hypoglycemic agents or insulin in a diabetic patient, other lab tests may be necessary. C-peptide is elevated in insulinoma, normal or low with exogenous insulin, and elevated with oral sulfonylureas. Liver function tests, serum insulin, and cortisol and thyroid levels should be checked. A source of infection should be ruled out by utilizing the usual screening tests: complete blood count, urine analysis, chest x-ray and blood cultures.


Imaging Studies:

Performing an abdominal CT scan or an ultrasound to rule out an abdominal tumor may be appropriate in the patient with new-onset hypoglycemia and no clear etiology. In diabetic patients presenting with hypoglycemia a chest x-ray should be performed to rule out infection.

Treatment:

Treatment of hypoglycemia consists of correcting the glucose deficiency with glucose and directing further treatment to the underlying cause.

The initial approach should include the following: ABCs, intravenous (IV) access, oxygen, monitoring, and Accucheck. Administration of glucose as part of the initial evaluation of altered mental status often corrects hypoglycemia.

Treatment should not be withheld while waiting for a laboratory glucose value. Because the brain uses glucose as its primary energy source, neuronal damage may occur if treatment of hypoglycemia is delayed. A hyperglycemic patient with an altered mental status may receive a bolus of glucose. This procedure is unlikely to harm the patient with high glucose; however, the delay in giving glucose to the hypoglycemic patient may be detrimental.

Once the diagnosis of hypoglycemia is made, search carefully for the cause in the previously healthy patient. In the diabetic patient, search diligently for the cause (e.g.: medication changes, dietary changes, new metabolic changes, recent illness, occult infection) of the episode.

Admission is reserved for patients with no known cause or no previous episodes of hypoglycemia, for overdose, accidental ingestion, or therapeutic misadventures with oral hypoglycemics. The length of admission and observation is based on the ingested oral hypoglycemic agent.


Medical/Legal Concerns:

Prolonged hypoglycemia may cause permanent neurologic deficit or death. The standard of care for altered level of consciousness is to immediately assess the blood glucose level. If that cannot be done immediately, all patients should receive oral or intravenous glucose.

Unrecognized infection causing hypoglycemia in diabetic patients may result in recurrent hypoglycemic spells or progression of the infection. Therefore, when hypoglycemia is diagnosed, a search for possible infection should ensue.

Lastly, clinicians make a major mistake when they send home a patient who has become awake and alert after the administration of glucose, when the cause for the hypoglycemia is oral hypoglycemic medications. These patient usually drop their blood glucose again, and can lose consciousness and suffer related complications such as aspiration or fractures and head injury secondary to falling.


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Thank you for your time,


Attorney & Physician Advisory Board
AMFS, Inc.

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