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DESCRIPTION
Chloral hydrate is an oral sedative-hypnotic agent.
FORMS AND USES
- Chloral hydrate is used for sedation and hypnosis, treatment of insomnia, adjunct to perioperative anesthesia and analgesia, and the treatment of alcohol withdrawal.
- Chloral hydrate is available as syrup (250 mg/5 ml, 500 mg/5 ml), tablet (250 and 500 mg), or suppository (325, 500, and 650 mg).
- Typical adult therapeutic dose for sedation and hypnosis is 0.5 to 1 g orally; pediatric, 25 to 50 mg/kg/day orally up to 1 g in three or four divided doses.
TOXIC DOSE
- Range of toxicity varies widely as for most sedative-hypnotic agents.
- Ingestion of more than the therapeutic dose may cause CNS depression.
PATHOPHYSIOLOGY
- Chloral hydrate is metabolized to trichloro-ethanol (TCE), which is largely responsible for its action and has a half-life of 4 to 12 hours.
- TCE is then metabolized to trichloroacetic acid (TCA), which is highly protein-bound and displaces other drugs (e.g., warfarin) from protein binding sites.
- Concurrent ethanol ingestion potentiates formation of TCE, producing greater toxicity.
- Withdrawal syndrome after cessation of prolonged abuse has been reported.
EPIDEMIOLOGY
- Poisoning is uncommon.
- Toxicity is usually mild.
- Death is rare, occurring in patients in whom the airway is not controlled.
CAUSES
- Toxicity usually results from pediatric accidental ingestion or adult abuse.
- Child neglect or abuse should be considered if the patient is less than 1 year of age, suicide attempt if the patient is over 6 years of age.
DRUG AND DISEASE INTERACTIONS
- Administration with other sedative-hypnotics will produce additive effect.
- Disulfiram-like reaction may occur when ingested with ethanol.
PREGNANCY AND LACTATION
- FDA Pregnancy Category C. The drug exerts animal teratogenic or embryocidal effects, but there are no controlled studies in women, or no studies are available in animals or women.
- Excretion in breast milk has been reported.
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DIFFERENTIAL DIAGNOSIS
Other toxicologic causes of CNS depression are numerous, including all sedative-hypnotic agents, narcotics, alcohols, barbiturates, tricyclic antidepressants, and many others.
SIGNS AND SYMPTOMS
Vital Signs
Bradypnea, hypotension, and hypothermia may occur in severe cases.
HEENT
Symptoms may include miosis, a peculiar and acrid pearlike odor on the breath, mucous membrane irritation, and laryngospasm.
Cardiovascular
Supraventricular and ventricular dysrhythmias, hypotension, and depression of myocardial contractility may occur in severe cases.
Pulmonary
Bradypnea may develop.
Gastrointestinal
Nausea, vomiting, esophageal and abdominal pain are common.
Neurologic
Lightheadedness, headache, ataxia, altered mental status, coma, and decreased deep tendon reflexes may occur.
PROCEDURES AND LABORATORY TESTS
Essential Tests
No tests may be needed in asymptomatic patients.
Recommended Tests
- Serum electrolytes, BUN, and creatinine are used to assess other causes of CNS depression.
- ECG is used to detect dysrhythmia.
- Pulse oximetry is used to assess oxygenation.
- Serum acetaminophen and aspirin levels should be obtained in an overdose setting to detect occult overdose.
- Trichloroethanol and urochloralic acid (metabolite of TCA) levels may help to confirm exposure but are not available rapidly for clinical use.
- Chloral hydrate is radiopaque and may be visible on an abdominal x-ray; however, the absence of radiopacities does not rule out an ingestion.
Not Recommended Tests
Measuring the serum chloral hydrate level is not useful.
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Supportive care and airway management are mainstays of therapy.
DIRECTING PATIENT COURSE
The health-care professional should call the poison control center when:
- Severe or persistent effects develop.
- Coingestant, drug interaction, or underlying disease presents an unusual problem.
The patient should be referred to a health-care facility when:
- Toxic effects develop.
- Coingestant, drug interaction, or underlying disease presents an unusual problem.
Admission Considerations
Inpatient management is warranted for patients with CNS depression, hypotension, or cardiac dysrhythmia.
DECONTAMINATION
Out of Hospital
Ipecac should not be administered because of the potential for CNS depression.
In Hospital
- Emesis should not be induced because of the potential for rapid deterioration.
- Gastric lavage should be performed in pediatric (tube size 24-32 French) or adult (tube size 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 a substantial ingestion has occurred within the previous few hours.
ANTIDOTES
There is no specific antidote for chloral hydrate poisoning.
ADJUNCTIVE TREATMENT
- Cardiac dysrhythmias should be treated according to standard Advanced Cardiac Life Support System protocols.
- Case reports suggest that hemodialysis and charcoal hemoperfusion can improve outcome by removing chloral hydrate and trichloro-ethanol.
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PATIENT MONITORING
ECG should be obtained and respiratory, cardiac, and hemodynamic status monitored continuously.
EXPECTED COURSE AND PROGNOSIS
Toxic effects begin within minutes; recovery occurs over hours unless sequelae of hypoxia intercede.
DISCHARGE CRITERIA/INSTRUCTIONS
- From the emergency department. Asymptomatic patients may be discharged after decontamination, observation for 4 to 6 hours, and psychiatric evaluation, if needed.
- From the hospital. Patients may be discharged when toxic effects have resolved, and following decontamination and psychiatric evaluation, if needed.
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DIAGNOSISClinician should consider all the potential causes of CNS depression, toxicologic and nontoxicologic.
ICD-9-CM 967.1Poisoning by chloral hydrate group.
See Also: SECTION II, Ventricular Dysrhythmia chapter.
RECOMMENDED READING
Ellenhorn MJ. Medical toxicology, 2nd ed. Baltimore: Williams & Wilkins, 1997:695.
Author: Edwin K. Kuffner
Reviewer: Richard C. Dart