Sarin Poisoning

Sarin is an organophosphate nerve agent and is one of the most toxic chemical warfare agents known. Sarin is absorbed rapidly through the eyes, respiratory tract and skin. Nerve agents irreversibly inactivate acetylcholinesterase, producing an accumulation of acetylcholine at cholinergic receptors. This may then lead to:

• Muscarinic receptors: miosis, increased salivary, bronchial and tear secretion, bronchoconstriction, vomiting, diarrhoea, urinary and faecal incontinence, bradycardia
• Nicotinic receptors: sweating, muscle weakness and flaccid paralysis
• Central nervous system: irritability, giddiness, fatigue, lethargy, amnesia, ataxia, seizures and respiratory depression
• Stimulation of the adrenal medulla causes tachycardia and hypertension

• About 600 people were exposed to sarin released in a residential area of the Japanese city of Matsumoto in June 1994. Fifty-eight residents were admitted to hospital and seven died.¹
• In March 1995 sarin was released into the Tokyo subway system during rush hour. Over 5,000 people sought medical attention. Of these people, 984 were moderately poisoned, 54 were severely poisoned and 12 died. However the vast majority had no signs of organophosphate poisoning.² Many more people presented in the following 24 hours, but none had features of organophosphate poisoning.

• Eyes:
  • Miosis: this may be painful and last for several days. It occurs rapidly following exposure to sarin vapour and is a sensitive index of exposure to sarin vapour.³
  • Impaired accommodation.
  • Conjunctival injection.
• Skin:
  • Liquid sarin may cause localised sweating and fasciculation.
• Inhalation:
  • Chest tightness, rhinorrhoea and increased salivation occur within minutes.
• Ingestion:
  • Ingestion of contaminated food or water may cause abdominal pain, nausea, vomiting, diarrhoea and faecal incontinence.
• Systemic features:
  • May follow contact by vapour, liquid on skin or ingestion. Systemic features follow vapour exposure very rapidly but more slowly following skin contact or ingestion.
  • Abdominal pain, nausea and vomiting, involuntary micturition and defecation, muscle weakness and fasciculation, tremor, restlessness, ataxia and convulsions.
  • Bradycardia, tachycardia and hypotension may occur.

Other organophosphate nerve agents used as chemical warfare agents include tabun, soman and cyclosarin.

• Erythrocyte and plasma cholinesterase activities confirm the diagnosis.
• Monitor blood gases.

• Contact the National Poisons Information Service (0870 600 6266) or access the TOXBASE website (see below) for further advice. See separate article Acute poisoning - general measures.
• Prevention of secondary casualties:
  • Healthcare workers should wear adequate protection when dealing with contaminated casualties, as secondary contamination may occur.⁴
  • Ideally, breathing apparatus should be used in contaminated areas.
  • Contaminated clothing should be carefully sealed in labelled bags in order to prevent further contamination.
• Casualties should be moved to hospital as rapidly as possible.
• Eye exposure:
  • Remove contact lenses.
  • Irrigate the eyes immediately with lukewarm water or sodium chloride solution.
  • Apply local anaesthetic for eye pain.
• Skin exposure:
  • Remove contaminated clothing to reduce further absorption.
• Inhalation:
  • Remove the casualty from further exposure.
  • Establish and maintain a clear airway. Oxygen may be required.
• Further management:
  • Establish intravenous access.
  • Increased bronchial secretions: give intravenous atropine every 10-30 minutes until secretions are minimal and atropine is fully effective (dry skin and sinus tachycardia).
  • Moderately or severely poisoned patients should be given pralidoxime mesilate or chloride 30 mg/kg body weight (2 g in an adult) intravenously over four minutes to reactivate phosphonylated enzyme. In severe cases, pralidoxime mesilate or chloride will be required intravenously every four to six hours, but an infusion of pralidoxime mesilate or chloride 8-10 mg/kg/hr is preferable.²
  • Intravenous diazepam: useful in controlling apprehension, agitation, fasciculation and convulsions.

• Post traumatic stress disorder.⁵ Survivors of large dose exposures may develop insomnia, irritability, difficulty concentrating and depression.²
• Persistent neurological abnormalities, including EEG abnormalities, may occur in severely exposed patients.^{6 7}

• If exposure is substantial death may occur from respiratory failure within minutes.
• Mild or moderately exposed individuals usually recover completely.