Sedative-Hypnotic Toxicity Clinical Presentation

Updated: Dec 29, 2015
  • 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:

  • Agents 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

Focus the physical examination on vital signs and neurologic and cardiopulmonary status.

General

Mild toxicity resembles ethanol intoxication. Severe respiratory depression is more likely to occur when the sedative-hypnotic is ingested with other CNS depressants.

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.

The nonbarbiturates, such as methyprylon and glutethimide, more commonly present with 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)

See the list below:

  • Resembles barbiturate poisoning
  • Has more pronounced motor problems (eg, ataxia) and is known as wallbanger because of this phenomenon
  • Can lead to severe muscular hypertonicity and seizures

Glutethimide (Doriden)

See the list below:

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

Ethchlorvynol (Placidyl)

See the list below:

  • Pungent odor of breath and gastric contents
  • Prolonged coma (up to 2 wk)
  • Acute respiratory distress syndrome (ARDS) predominates in IV use

Chloral hydrate

See the list below:

  • Synergistic with alcohol (knockout drops, Mickey Finn)
  • Cerebellar incoordination
  • Severe gastritis and GI bleed
  • 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
  • Radiopaque

Imidazopyridine

See the list below:

  • Sleepwalking or other complex bizarre behaviors
  • Chromaturia (blue-green urine discoloration) has been reported with zaleplon (Sonata) overdose.
  • Prolonged coma and respiratory failure

Meprobamate

See the list below:

  • CNS and respiratory depression
  • Hypotension (common)

GHB and GBL

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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