Sedative-Hypnotic Toxicity Clinical Presentation

Updated: Oct 11, 2019
  • Author: Jeffrey S Cooper, MD, FAAEM, FACEP; Chief Editor: Asim Tarabar, MD  more...
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Presentation

History

The history should include the following information:

  • Agent(s) ingested
  • Amount of ingestion
  • Time of ingestion
  • Cause and/or reason for ingestion (eg, accidental, intentional, suicide attempt, recreational)
  • Whether ingestion is acute or chronic
  • Past medical history and history of drug abuse
  • Circumstances surrounding the overdose
Next:

Physical Examination

Focus the physical examination on vital signs and neurologic and cardiopulmonary status. Mild toxicity resembles ethanol intoxication. Severe respiratory depression is more likely to occur when the sedative-hypnotic is ingested with other CNS depressants or alcohol. Flexor or extensor posturing can be present in coma resulting from sedative drug ingestion. It does not imply structural damage in this setting.

Barbiturates

Mild intoxication is characterized by ataxia, incoordination, nystagmus, slurred speech, and altered level of consciousness. Moderate poisoning leads to respiratory depression and hyporeflexia. Severe poisoning leads to flaccid areflexic coma, apnea, and hypotension. Generally, 10 times the hypnotic dose produces severe toxicity.

Occasionally, hyperreflexia, rigidity, clonus, and Babinski signs are present. Miosis is common, but mydriasis may be present with certain agents. However, the nonbarbiturates, such as methyprylon and glutethimide, more commonly produce mydriasis. Hypotension is usually secondary to vasodilation and negative cardiac inotropic effects.

Complications include the following:

  • Noncardiogenic pulmonary edema
  • Hypothermia
  • Delayed gastric emptying (therefore, late lavage and multiple charcoal is effective)
  • Skin lesions (clear vesicles and bullae on an erythematous base at contact surfaces) occur in 6% of ingestions and in approximately 50% of lethal ingestions.

Methaqualone (Quaalude)

Methaqualone intoxication resembles barbiturate poisoning but has more pronounced motor problems (eg, ataxia); the drug is known as wallbanger because of this phenomenon. Progression to severe muscular hypertonicity and seizures is possible.

Glutethimide (Doriden)

Signs and symptoms of glutethimide toxicity include the following:

  • Loss of brainstem reflexes
  • Flaccidity
  • Anticholinergic effects
  • Delayed gastric emptying
  • May cause hyperthermia or heatstroke

Ethchlorvynol (Placidyl)

Ethchlorvynol toxicity is characterized by a pungent odor of breath and gastric contents and prolonged coma (up to 2 weeks). Acute respiratory distress syndrome (ARDS) predominates in IV use.

Chloral hydrate

Signs and symptoms of chloral hydrate toxicity include the following:

  • Synergistic with alcohol (knockout drops, Mickey Finn)
  • Cerebellar incoordination
  • Severe gastritis and GI bleeding
  • Multiple dermatologic effects, including purpura, bullae, urticaria, and erythema multiforme (EM)
  • CNS depression with cardiopulmonary collapse
  • Associated with hepatitis, gastritis, proteinuria, and dysrhythmias
  • Odor of pears

Z-drugs (Imidazopyridine)

Sleepwalking or other complex bizarre behaviors have been reported in patients taking z-drugs (ie, zopiclone, zaleplon, zolpidem); prolonged coma and respiratory failure are possible. Chromaturia (blue-green urine discoloration) has been reported with zaleplon (Sonata) overdose.

Meprobamate

Meprobamate toxicity is characterized by hypotension and CNS and respiratory depression. 

Gamma-hydroxybutyrate and gamma-butyrolactone

Mild intoxication includes the following:

  • Slurred speech
  • Disinhibition
  • Euphoria
  • Mild lethargy
  • Moderate intoxication
  • CNS and mild respiratory depression
  • Agitation when stimulated
  • Myoclonus

Severe intoxication includes the following:

  • Unresponsive coma
  • Miosis
  • Bradycardia
  • Mild hypotension
  • Seizures
  • Respiratory depression and apnea

After ingestion, the onset of effects occurs within 15 minutes and peaks in 1.5-2 hours. Elimination of GHB is rapid (elimination half-life 1-2 h). The duration of clinical effects is 2-8 hours.

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