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Sarin is one of the most toxic chemicals ever synthesized. It is a nerve gas which makes for easy exposure. EXTREMELY TOXIC by all routes of exposure; emits very toxic fumes of fluoride and phosphorus oxides when heated to decomposition or reacted with steam. Sarin's toxic effects are a result of it preventing the breakdown of acetylcholine by inactivating the enzyme cholinesterase. As acetylcholine builds up, nerve impulses are transmitted too quickly causing muscles and other organs to be overstimulated. The heart beats too fast and erratically causing convulsion and/or death.Substance Characteristics: Pure Form - Colorless liquid and vapor. Odor - Almost none.

Symptoms

Warning: Death may occur within 1 to 10 minutes of inhalation exposure to a minute amount of sarin. Immediate decontamination of the smallest drop is essential. Effects may be delayed with dermal exposure. Extreme caution is advised. The first indication of exposure to sarin may be a reaction at the point of contact: localized sweating, muscular twitching, and pinpoint eye pupils. Rhinorrhea (running nose), tightness of the chest with shortness of breath, and dimness of vision may be noted. In more severe exposure, headache, cramps, nausea, vomiting, involuntary defecation and urination, twitching, jerking, staggering, convulsions, drowsiness, coma, and respiratory arrest may be seen.

Clinical manifestations of excessive cholinergic activity may be divided into muscarinic, nicotinic and central effects. The relative severity of these effects differs between individual cases.

Muscarinic effects are those of parasympathetic overactivity and include bradycardia, pinpoint pupils, sweating, blurred vision, excessive lacrimation, excessive bronchial secretions, wheezing, dyspnoea, coughing, vomiting, abdominal cramping, diarrhoea, and urinary and faecal incontinence.

Nicotinic effects are those of sympathetic overactivity and neuromuscular dysfunction and include tachycardia, hypertension, dilated pupils, muscle fasciculation and muscle weakness. Central effects may include agitation, psychosis, confusion, coma and seizures.

LONG TERM COMPLICATIONS Peripheral neuropathy Neuropsychiatric sequelae

Diagnosis

The full clinical syndrome usually presents no diagnostic dilemma. Where particular manifestations of poisoning predominate, the following conditions may be considered: Bronchial asthma Gastroenteritis Myasthenic crisis Pulmonary oedema Status epilepticus of other aetiology RELEVANT INVESTIGATIONS Arterial blood gases Chest X-ray ECG Electrolytes, urea and creatinine Glucose Oximetry Serum and/or erythrocyte acetylcholine esterase activity. Depression of acetylcholine esterase activity is diagnostic of carbamate or organophosphorus poisoning but is not helpful in the acute management of the cholinergic syndrome.

Treatment

Acute exposure to sarin may require decontamination and life support for the victims. Emergency personnel should wear protective clothing appropriate to the type and degree of contamination. Air-purifying or supplied-air respiratory equipment should also be worn, as necessary. Rescue vehicles should carry supplies such as plastic sheeting and disposable plastic bags to assist in preventing spread of contamination.

Inhalation Exposure

1.Move victims to fresh air. Emergency personnel should avoid self-exposure to sarin. 2. RUSH to a health care facility! 3. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. DO NOT perform mouth-to-mouth resuscitation when facial contamination exists; use forced-oxygen mask. If breathing is labored, administer oxygen or other respiratory support. 4. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures.

Dermal/Eye Exposure

1.Remove victims from exposure. Emergency personnel should avoid self-exposure to sarin. 2. RUSH to a health care facility! 3. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. DO NOT perform mouth-to-mouth resuscitation when facial contamination exists; use forced-oxygen mask. 4. Remove and isolate contaminated clothing as soon as possible. 5. If eye exposure has occurred, eyes must be flushed with lukewarm water for at least 15 minutes. 6. Wash exposed skin areas thoroughly with commercial household liquid bleach and then flush with water. Avoid contacting the eyes or mouth with bleach. 7. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures.

Ingestion Exposure

1. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. DO NOT perform mouth-to-mouth resuscitation when facial contamination exists; use forced-oxygen mask. If breathing is labored, administer oxygen or other respiratory support. 2. RUSH to a health care facility! 3. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures. 4. DO NOT induce vomiting or attempt to neutralize. 5. Activated charcoal may be administered if victims are conscious and alert. Use 15 to 30 g (1/2 to 1 oz) for SARIN children, 50 to 100 g (1-3/4 to 3-1/2 oz) for adults, with 125 to 250 mL (1/2 to 1 cup) of water. 6. Promote excretion by administering a saline cathartic or sorbitol to conscious and alert victims. Children require 15 to 30 g (1/2 to 1 oz) of cathartic; 50 to 100 g (1-3/4 to 3-1/2 oz) is recommended for adults. In severe cases, the initial priority is to secure the airway, maintain ventilation and oxygenation, secure intravenous access and control seizures with intravenous diazepam. Decontamination appropriate to the offending agent and route of exposure should be performed. Atropine is the specific antidote for the muscarinic effects and should be administered as soon as the diagnosis is suspected. It has no effect on nicotinic receptors. The initial dose of 1 to 2 mg (0.05mg/kg in children) intravenously should be repeated every 5 to 10 minutes until drying of respiratory secretions is achieved. In severe cases, very large doses of atropine (up to 100 mg) may be required. Excessive dosing of atropine will manifest itself as agitation and tachycardia. The patient should remain under close observation and further doses of atropine should be given as required. Where intravenous access is not available, atropine may be administered via the intramuscular, subcutaneous, endotracheal or intraosseous (children) routes. In moderate-to-severe cases of cholinergic syndrome due to organophosphorus pesticide or warfare agent poisoning, an acetylcholine esterase reactivator should be administered (if available) following atropine. Either pralidoxime or obidoxime are suitable. The dose of pralidoxime is 30 mg/kg intravenously followed by a continuous infusion of 8 mg/kg/hour until clinical recovery is observed and for at least 24 hours. Alternatively, continued administration of pralidoxime may be by intermittent intravenous or intramuscular doses of 30 mg/kg every 4 hours. The dose of obidoxime is 4 mg/kg intravenously followed by a continuous infusion of 0.5 mg/kg/hour until clinical recovery is observed and at least 24 hours. Alternatively, continued administration of obidoxime may be by intermittent intramuscular or intravenous doses of 2 mg/kg every 4 hours. In severely poisoned patients, doses greater than this may be necessary to achieve enzyme reactivation. Patients should remain under close observation after cessation of oxime therapy. Recurrence of clinical manifestations of toxicity indicates the need for further oxime therapy.