More than 2.4 million cases of accidental or purposeful cases recorded in 2004, with 1,183 deaths and 80,0000 intensive care hospital admissions.
Poison exposure is a common reason for emergency department visits.
Unintentional poisoning was second only to motor vehicle accidents as a cause of accidental injury or death for all ages in 2009.
Unintentional poisoning accounted for more than 830,000 visits to the emergency department in 2010.
Deaths associated with poisoning occurred in 83% of patients over the age of 20 years.
Deaths most common associated with ethanol, aspirin, acetaminophen, street drugs, sedatives, hypnotics, antidepressants and cardiovascular drugs.
Initial evaluation includes assessment of airway, breathing and circulation.
Common complications include respiratory depression, loss of airway reflexes which protect the airway, and aspiration.
Endotracheal intubation may be needed in obtunded patients and those with seizures.
Ventilatory failure may occur due to respiratory depression, muscle paralysis or weakness.
Elevation of Paco2 associated with somnolence or obtundation is an indication for assisted ventilation.
Inhalation injury may cause bronchospasm.
Hypoxemia may result from toxin-associated hypoventilation, pulmonary edema or from aspiration.
Hypoxemia may require oxygen therapy or mechanical ventilation support.
May lead to abnormal cardiac rhythms, hypotension and shock.
Patients are at high risk for acute destabilization, and anticipation of such processes as thermsl dysregulation, blood-pressure extremes, respiratory collapse, arrhythmias, seizures, and other altered mental status states.
Patient should have an intravenous access established, fluid resuscitation with crystalloid fluids.
Advanced cardiac and trauma life-support measures may be necessary.
Specific therapies may be available for certain types of toxin-induced cardiac arrest such as tricyclic antidepressant wide QRS pulseless rhythms by treatment with sodium bicarbonate and hyperkalemia arrest from salicylate poisoning with the same treatment.
The physical examination and history are essential to help identify the offending agent.
Examination may reveal characteristic odors, pupil changes, muscle tone alterations, and skin findings which may help in the elucidation of the poison.
Information from patients may be unreliable, particularly in cases of self poisoning.
May require cardiac monitoring, intravenous fluids, and vasopressors.
All overdoses are to be considered as polysubstance in nature, as ethanol and opiates are common additional components of overdoses.
All patients with altered mental status need to be treated empirically for possible hypoglycemia.
In all such instances serum levels of acetaminophen , urine screen for tricyclic antidepressants, and salicylate serum levels should be done along with a CBC and serum chemistry profile.
Arterial blood gas analysis should be done in the presence of respiratory impairment, altered mental status, lethargy, coma or cyanosis.
EKGs should be done to screen for electrocardiographic abnormalities.
In women of childbearing age a pregnancy test should be obtained.
X-ray studies may identify ingestion of heavy metals, internal concealment of illicit drugs, and the presence of pulmonary edema.
Patient’s with history of exposure to digitalis, lithium, theophylline, phenytoin, and iron should have serum levels of those agents analyzed.
Specific toxidrome findings should be sought to help establish the type of agents that may be responsible for the clinical presentation.
Clinical toxidrome-sympathomimetic-hypertension, tachycardia, tachypnea, hypothermia, mydriasis, agitation, hallucinations and diaphoresis.
Clinical toxidrome-anticholinergic-hypertension, tachycardia, tachypnea, hypothermia, mydriasis, agitation, delirium, hallucinations, dry skin, dry mouth, ileus, urinary retention.
Clinical toxidrome-cholinergic “SLUDGE)-salivation, lacrimation, urination, diarrhea, gastrointestinal distress, emesis: bradycardia, miosis, confusion, coma, bronchorestriction.
Clinical toxidrome-opioid-hypotension, bradycardia, hypoventilation, slowed respiratory rate, hypothermia, miosis, CNS depression, coma, decreased bowel function and pulmonary edema.
Clinical toxidrome-sedative-hypnotic-hypotension, bradycardia, hypoventilation, CNS depression, coma.
Clinical toxidrome-extra pyramidal-rigidity, torticollis, opisthotonos, trismus, oculogyric crisis, and dysphoria.
Agents associated with sympathomimetic syndrome include: cocaine, amphetamines, ephedrine, pseudoepineprine, theophylline and caffeine.
Agents associated with anticholinergic features include: tricyclic antidepressants, antihistamines, atropine, phenothiazines, scopolamine, belladona.
Cholinergic syndrome associated with : organophosphates, physostigmine, pyridostigmine, and edrophonium.
Sedative-hypnotic syndrome associated with benzodiazepines, barbiturates and alcohol.
Extra pyramidal syndrome associated with prochlorperazine, haloperidol, chlorpromazine, and other psychotics.
The presence of anion gap, osmolal gap, and oxygen saturation gap give clues to the diagnosis of ingested toxins.
Presence of an elevated anion gap suggests ingestion of ethylene glycol, methanol or salicylate.
Osmolal gap elevations may be seen with ingestion of alcohols.
A coma cocktail should be administered as a therapeutic and diagnostic test which includes dextrose, oxygen, naloxone and thiamine in patients exposed to unknown poisons.
The use of gastrointestinal decontamination methods such as cathartics, gastric lavage, adminstration of activated charcoal and bowel irrigation are presently controversial.
Activated charcoal may have some benefit within 60 minutes following ingestion of a highly toxic agent.
Patient should be hospitalized in the intensive care unit if there is a partial pressure of arterial carbon dioxide above 45 mg of mercury, requirements for endotracheal intubation, presence of seizures, manifestations of arrhythmias, QRS duration longer than 0.12 seconds, second or third degree AV blocks, blood pressure of 80 mm or less and unresponsiveness to verbal stimuli (Brett AS et al).