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DESCRIPTION
- The normal body temperature is 35.8° to 37.2°C (96.5°-99°F).
- Elevation of the temperature above 38°C (100.4°F) should be considered hyperthermia.
PATHOPHYSIOLOGY
Hyperthermia occurs when normal thermoregulation mechanisms are overwhelmed by increased motor activity, impairment of normal heat dissipation mechanisms, increased environmental heat, impairment of behavior to avoid increased environmental temperature, or impaired hypothalamic thermoregulation.
EPIDEMIOLOGY
- Hyperthermia related to drug use is common.
- Toxic effects following exposure are typically mild.
- Individuals with severe hyperthermia who do not receive timely supportive care may die.
PREGNANCY AND LACTATION
Hyperthermia in the pregnant patient is associated with an increased risk of congenital anomalies.
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The patient's temperature should be taken rectally to confirm hyperthermia.
DIFFERENTIAL DIAGNOSIS
Further information on each poison is available in SECTION IV, CHEMICAL AND BIOLOGICAL AGENTS.
Toxicologic Causes
- Neuroleptic malignant syndrome (NMS) consists of autonomic dysfunction (fever, tachycardia, hyper- or hypotension), movement disorder (rigidity, tremors, Parkinson-like symptoms, myoclonus), and an altered mental status following the use of neuroleptic drugs.
- Serotonin syndrome (SS) resembles NMS but occurs with use or overdose agents that increase serotonergic activity in the CNS.
- Monoamine oxidase (MAO) inhibitors. Agitation, tachycardia, hyper- and hypotension may accompany an MAO inhibitor overdose; phenelzine and tranylcypromine are included.
- Many drugs or foods interact with MAO inhibitors and produce a syndrome that involves autonomic dysfunction, an altered mental status, and rigidity.
- Malignant hyperthermia is a rare inherited disorder typified by fever, autonomic dysfunction, and severe muscular rigidity in patients undergoing general anesthesia.
- Anticholinergics and antihistamines cause fever in overdose and exacerbate hyperthermia by inhibiting the ability to cool evaporation; antihistamines and plant alkaloids found in jimsonweed and other plants, cyclic antidepressants, atropine, and phenothiazines are included.
- Aspirin and salicylates. Hyperthermia may accompany tachypnea, tinnitus, metabolic acidosis, and an altered mental status.
- Hallucinogens (LSD, PCP, peyote). Agitation associated with hallucinations may cause hyperthermia.
- Sympathomimetic drugs. Agitation, delirium, seizures, diaphoresis, tachycardia, hypertension, mydriasis, and seizure may occur with cocaine, caffeine, theophylline, methylphenidate (Ritalin), and amphetamines, including diet pills such as Fen-Phen (fenfluramine and phentermine), and methamphetamine intoxication.
- Withdrawal from ethanol, benzodiazepines, or barbiturates causes a sympathomimetic surge with delirium, diaphoresis, and agitation, such as that described for sympathomimetic overdose; seizures also may occur and contribute to hyperthermia.
Uncommon Toxicologic Causes
- Arsenic. Hyperthermia may occur with acute arsenic toxicity.
- Isoniazid may cause multiple seizures that contribute to hyperthermia.
- Thyroid hormones may cause agitation associated with hyperthermia as well as tachycardia, hypertension, tremors, goiter, and many other symptoms.
Other Causes
- Seizures, agitation, and inappropriate behavior in response to heat (overexertion, overswaddling of infants, or remaining in hot, unventilated rooms) due to any cause may bring on hyperthermia.
- Heat stroke and heat exhaustion also may present with dehydration, altered mental status, and organ failure, making them difficult to distinguish from drug-induced hyperthermia.
- Infection commonly causes hyperthermia but is usually identifiable.
- Thyroid storm may present with hyperthermia, tachycardia, hypertension, agitation, tremors, and other symptoms.
- Neoplasms, connective tissue disease, and granulomatous disease are associated with hyperthermia, but often have other diagnostic signs.
SIGNS AND SYMPTOMS
- Physical signs may help reveal the poison involved when they occur in the setting of hyperthermia.
- Delirium, agitation, coma, hypotension, seizures, and multiorgan failure may develop in severe cases.
Vital Signs
Extreme hypertension may occur with neuroleptic malignant syndrome, serotonin syndrome, or MAO inhibitor poisoning.
HEENT
- Tinnitus often accompanies salicylate toxicity.
- Dilated pupils are associated with anticholiergic or sympathomimetic toxicity, or hypoxia.
Dermatologic
- Flushed dry skin suggests an anticholinergic agent.
- Pale, sweaty skin may be associated with sympathomimetic drugs, cholinergic agents, or hypotension.
Cardiovascular
- QRS widening or presence of an R wave in the ECG lead aVR suggests tricyclic antidepressant poisoning.
- Severe tachydysrhythmia may indicate theophylline, sympathomimetic agent, NMS, SS, or MAO inhibitor toxicity.
Pulmonary
Tachypnea is produced by salicylates or any cause of metabolic acidosis.
Gastrointestinal
- Nausea and vomiting are common with aspirin and theophylline.
- Bowel sounds are commonly decreased with anticholinergic agents.
Fluids and Electrolytes
Dehydration is common due to increased insensible water losses.
Musculoskeletal
Rigidity, myoclonus, and tremors may indicate development of NMS, SS, or MAO inhibitor toxicity.
Neurologic
- Hallucinations may indicate anticholinergic poisoning or abuse of hallucinogens or stimulants.
- The triad of altered mental status, autonomic dysfunction, and movement disorder may indicate NMS, SS, or MAO inhibitor toxicity.
PROCEDURES AND LABORATORY TESTS
Essential Tests
No tests may be needed for mild hyperthermia (e.g., transient, mild, and environmental) that does not worsen.
Recommended Tests
- Serum electrolytes, glucose, BUN, and creatinine
- Dehydration with hypernatremia is common.
- Hyperkalemia may occur if renal failure or rhabdomyolysis is present. Hyperglycemia may occur. Metabolic acidosis is the rule in severe cases, sometimes preceded by respiratory alkalosis.
- Hypophosphatemia and hypocalcemia may also occur.
- Urinalysis. Blood and protein may be seen with the development of rhabdomyolysis.
- Serum aspartate aminotransferase, alanine aminotransferase, and lactic dehydrogenase in a hepatocellular pattern may occur.
- Creatine kinase may be elevated due to agitation or seizures causing muscle breakdown.
- Prothrombin time, partial thromboplastin time, fibrinogen, and fibrin split products may help to evaluate potential disseminated intravascular coagulation.
- An ECG may reveal various nonspecific findings.
- Arterial blood gases may show respiratory alkalosis followed by respiratory acidosis if the condition worsens.
- Serum acetaminophen and aspirin levels are advised in an overdose setting to detect an occult overdose with analgesic medications.
- A urine toxicology screen is recommended for patients with hyperthermia of unknown cause.
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- Intravenous access should be established, and cooling measures should begin immediately if temperature is above 40°C, particularly in the presence of altered mental status.
- The dose and time of exposure should be determined for all substances involved.
- Specific treatment (e.g., naloxone for mental status depression) should be initiated while continuing supportive care.
DIRECTING PATIENT COURSE
The health-care provider should call the poison control center when:
- cause of hyperthermia could be toxic.
- coingestant, drug interaction, or underlying disease presents unusual problems.
DECONTAMINATION
Out of Hospital
- Induction of emesis is not recommended.
In Hospital
- Gastric lavage should be performed in pediatric (tube size 24-32 French) or adult (36-42 French) patients for large ingestion presenting within 1 hour of ingestion or if serious effects are present.
- One dose of activated charcoal (1-2 g/kg) should be administered without a cathartic if substantial ingestion has occurred within the previous few hours.
ADJUNCTIVE TREATMENT
Aggressive supportive care is vital to avoid sequelae from severe hyperthermia.
- To control agitation, the provider should administer a benzodiazepine with which he has experience, while monitoring the patient's airway closely.
- Diazepam. The adult dose is 5 to 10 mg intravenously; the pediatric dose is 0.2 to 0.5 mg/kg intravenously, with doses repeated at 5-minute intervals, titrating to effect.
- Lorazepam. The adult dose is 1 to 2 mg intravenously; the pediatric dose is 0.05 mg/kg, with doses repeated at 5-minute intervals, titrating to effect.
- To reduce body temperature, all clothing should be removed, intravenous infusion of isotonic crystalloid should begin, and agitation should be controlled.
- Fluid losses may be severe and should be replenished until a urine output of 1 to 2 ml/kg/h is reached.
- Electrolyte abnormalities due to the initial insult or from iatrogenic changes should be corrected.
- Fluid administration should be carefully monitored to avoid fluid overload in predisposed patients, such as those with congestive heart failure, adult respiratory distress syndrome, or renal failure.
- Cooling fans and wet sheets are effective, especially in dry climates. Cooling blankets or application of ice may be needed in severe cases.
- Sedation and neuromuscular paralysis/mechanical ventilation may also assist decrease of temperature in agitated patients.
- Central temperature should be frequently monitored, and cooling should be discontinued when the body temperature decreases to 39°C.
- Tachycardia that persists after treatment of hyperthermia may be due to a toxic agent, hypovolemia, or a myocardial injury.
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PATIENT MONITORING
Temperature, respiratory, and cardiac function should be monitored continuously.
EXPECTED COURSE AND PROGNOSIS
Mild hyperthermia resolves without sequelae, but victims of severe hyperthermia may die immediately from multiorgan failure or survive the initial insult and die days later as a result of complications.
DISCHARGE CRITERIA/INSTRUCTIONS
Asymptomatic patients who experienced only mild hyperthermia may be discharged after monitoring for 6 hours and psychiatric evaluation, if needed.
Section Outline:
ICD-9-CM 780.6General symptoms: pyrexia of unknown origin. Certain adverse effects: hyperthermia following anesthesia.
See Also: SECTION II, NMS and Serotonin Syndrome, and Tachycardia chapters; and SECTION IV for chapters on specific agents.
RECOMMENDED READING
Goldfrank LR, Flomenbaum NE, Weisman RS, Lewin NA. Vital signs and toxic syndromes. In: Goldfrank LR, et al., eds. Goldfrank's toxicologic emergencies, 6th ed. Norwalk, CT: Appleton & Lange, 1998.
Author: Lada Kokan
Reviewer: Richard C. Dart