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    Acetaminophen is a common analgesic found in many nonprescription and prescription products. After absorption, it is metrabolized mainly by glucuronidation and sulfation, with a small fraction metabolized via the P450 mixed-function oxidase system to a highly toxic reactive intermediate. This toxic intermediate is normally detoxified by cellular glutahione. With acute acetaminophen overdose, hepatocellular glutathione is rapidly depleted and the reactive intermediate attacks other cell proteins, causing necrosis. Patients with enhanced P450 activity, such as chronic alcoholics and patients taking anticonvulsants, are at increased risk of developing hepatotoxicity. Hepatic toxicity may also occur after chronic accidental overuse of acetaminophen - eg, as little as 1 g of acetaminophen every 4 - 6 hours for 1 - 2 days in a patient with chronic accidental overuse of acetaminophen - eg, as little as 1g of acetaminophen every 4 - 6 hours for 1 - 2 days in a patient with chronic excessive alcohol use.

    Clinical Findings

    Shortly after ingestion, patients may have nausea or vomiting, but there are usually no other signs of toxicity until 24 - 48 hours after ingestion, when hepatic aminotransferase levels begin to increase. With severe poisoning, massive hepatic necrosis may occur, resulting in jaundice, hepatic encephalopathy, renal failure, and death.

    The diagnosis of severe poisoning after acute over-dose is based on measurement of the serum acetaminophen level. Plot the serum level versus the time since ingestion on the acetaminophen nomogram. Ingestion of sustained-release produces or coingestion of an anticholinergic agent, salicylate, or opioid drug may cause delayed elevation of serum levels.


    A. Emergency and Supportive Measures :

    Empty the stomach by emesis or gastric lavage. Administer activated Charcoal. Although charcoal may bind the oral antidote aceylecysteine, this is not considered clinically significant.

    B. Specific Treatment

    If the serum acetaminophen level is higher than the upper toxic line on the nomogram, begin treatment with a loading dose of acetylcysteine, 140 mg/kg orally, followed by 70 mg/kg every 4 hours. Dilute the solution to 5% with water, juice, or soda. If vomiting interferes with oral acetylcysteine administration, give the dose by gastric tube and use metoclopramide, 1 - 2 mg/kg intravenously. The most widely used protocol in the USA continues treatment for 72 hours. However, other regimens have demonstrated equivalent success with 20 - 48 hours of treatment. Treatment with acetylcysteine is most effective if started within 8 --10 hours after ingestion. If the precise time of ingestion is unknown or if the patient is at higher risk of hepatotoxicity, then use a lower threshold for initiation of acetylcysteine.

    Acetylcysteine may also be given intravenously; this is the preferred method in Europe and Canada, but there is no approved parenteral formulation or dosing schedule in the United States. If the patient cannot tolerate acetylcysteine despite antiemetics and administration via a gastric tube, the United States formulation may be give intravenously. Call a regional poison control centre or medical toxicologist for assistance.


    The strong mineral acids exert primarily a local corrosive effect on the skin and mucous membranes. Symptoms include severe pain in the throat and upper gastrointestinal tract; bloody vomitus; difficulty in swallowing, breathing, and speaking; discoloration and destruction of skin and mucous membranes in and around the mouth; and shock. Severe systemic metabolic acidosis may occur both as a result of cellular injury and from systemic absorption of the acid.

    Severe deep destructive tissue damage may occur after exposure to hydrofluoric acid because of the penetrating and highly toxic fluoride ion. Systemic hypocalcemia and hyperkalemia also may occur after fluoride absorption, even following skin exposure.

    Inhalation of volatile acids, fumes, or gases such as chlorine, fluorine, bromine, or iodine causes severe irritation of the throat and larynx and may cause upper airway obstruction and noncardiogenic pulmonary edema.


    A. Ingestion

    Do not induce emesis. Dilute immediately by giving a glass of milk or water to drink. Do not give bicarbonate or other neutralizing agents. Some experts recommend immediate gastric lavage.

    Perform flexible endoscopic esophagoscopy promptly to determine the presence and extent of injury. X-rays of the chest and abdomen may reveal the presence of free air in patients with esophageal or gastric perforation. Perforation, peritonitis, and major bleeding are indications for surgery.

    B. Skin Contact :

    Flood with water for 15 minutes. Use no chemical antidotes; the heat of the reduction may cause additional injury.

    For hydrofluoric acid burns, soak the affected area in magnesium sulfate solution or apply 2.5% calcium gluconate gel; then arrange immediate consultation with a plastic surgeon or other specialist. Binding of the fluoride ion may be achieved by injecting 0.5 mL of 5% calcium gluconate per square centimeter under the burned area. (Caution : Do not use calcium chloride).

    C. Eye Contact

    Anesthetize the onjunctiva and corneal surfaces with topical local anesthetic drops. Flood with water for 15 minutes, holding the eyelids open. Check pH with pH 6.0 - 8.0 test paper, and repeat irrigation, using 0.9% saline, pH is near 7.0. Check for corneal damage with fluorescein and slitlamp examination; consult an ophthalmologist about further treatment.

    D. Inhalation

    Remove from further exposure to fumes or gas. Check skin and clothing. Treat pulmonary edema.


    The strong alkalies are common ingredients of some household cleaning compounds and may be suspected by their "soapy" texture. Those with alkalinity above pH 12.0 are particularly corrosive. Clinitest tables and disk batteries are also a source. Alkalies cause liquefactive necrosis, which is deeply penetrating. Symptoms include burning pain in the upper gastrointestinal tract, nausea, vomiting, and difficulty in swallowing and breathing. Examination reveals destruction and edema of the affected skin and mucous membranes and bloody vomitus and stools. X-ray may reveal the presence of disk batteries in the esophagus or lower gastrointestinal tract.


    A. Ingestion

    Do not induce emesis. Dilute immediately with a glass of water. Some gastroenterologists recommend immediate gastric lavage after ingestion of liquid caustic substances to remove residual material.

    Immediate endoscopy is recommended to evaluate the extent of damage. If X-ray reveals the location of ingested disk batteries in the esophagus, immediate endoscopic removal is mandatroy.

    The use of corticosteroids to prevent stricture formation is of no proved benefit and is definitely contraindicated if there is evidence of esophageal perforation.

    B. Skin Contact :

    Wash with running water until the skin no longer feels soapy. Relieve pain and treat shock.

    C. Eye Contact :

    Anesthetize the conjunctival and corneal surfaces with topical anesthetic. Irrigate with water or saline continuously for 20 - 30 minutes, holding the lids open. Check pH with pH test paper, and repeat irrigation, using 0.9% saline, for additional 30 minute periods until the pH is near 7.0. Check for corneal damage with fluorescein and slitlamp examination; consult an ophthalmologist for further treatment.


    Amphetamines and cocaine are widely abused for their euphorigenic and stimulant properties. Both drugs may be smoked, snorted, ingested, or injected. Amphetamines and cocaine produce central nervous system stimulation and a generalized increase in central and peripheral sympathetic activity. The toxic does of each drug is highly variable and depends on the route of administration and individual tolerance. The onset of effects is most rapid after intravenous injection or smoking. Amphetazine derivatives and related drugs include methamphetamine, and methcarthinone. Nonprescription medications and nutritional supplements may contain stimulant or sympathomimetic drugs such as ephedrine or caffeine. Phenylpropanolamine was recently withdrawn from the market because of an increased incidence of hypertensive intracerebral hemorrhage in young women.

    Clinical Findings

    Patients may present with anxiety, tremulousness, tachycardia, hypertension, diaphoresis, dilated pupils, agitation, muscular hyperactivity , and psychosis. Metabolic acidosis may occur. In severe intoxication, seizures and hyperthermia may occur. Sustained or severe hypertension may result in intracranial hemorrhage, aortic dissection, or myocardial infarction. Hyponatremia has been reported after MDMA use; the mechanism is not known but may involve excessive water intake, SIADH, or both.

    The diagnosis is supported by finding amphetamines, cocaine, or the cocainemetabolite benzoylecgonine in the urine. Blood screening is not sensitive enough to detect these drugs.


    A. Emergency and Supportive Measures

    Maintain a patent airway and assist ventilation, if necessary. Treat coma or seizures. Rapidly lower the body temperature in patients who are hyperthermic. Treat agitation or psychosis with a benzodiazeine such as diazepam, 5 - 10 mg intravenously, o rmidazolam, 0.1 - 0.2 mg/kg intramuscularly.

    For poisoning by ingestion, perform gastric lavage and administer activated charcoal, or administer activated charcoal alone without prior gut emptying. Do not induce emesis, because of the risk of seizures.

    B. Specific Treatment

    Treat agitation with a sedative as lorazepam, 2 - 3 mg intravenously. Treat hypertension with a vasodilator drug such as phentolamine or nifedipine or a combined - and - adrenergic blocker such as labetalol. Do not administer a pure beta - blocker such as propranolol alone, as this may result in paradoxic worsening of the hypertension as a result of unopposed - adrenergic effects. Treat tachycardia or tachyarrhythmias with a short-acting beta-blocker such as esmolol.


    Warfarin and related compounds inhibit the clotting mechanism by blocking hepatic synthesis of vitamin K-dependent clotting factors.

    Anticoagulants may cause hemoptysis, gross hematuria, bloody stools, hemorrhages into organs. Wide spread bruising, and bleeding into joint spaces. The prothrombin time is increased within 12 - 24 hours after a single overdose. After ingestion of brodifacoum and indanedione rodenticides, inhibition of clotting factor synthesis may persist for several weeks or even months after a single dose.


    A. Emergency and Supportive Measures:

    Discontinue the drug at the first sign of gross bleeding, and determine the prothrombin time. If the patient has ingested an acute overdose, empty the stomach by emesis or lavage and administer activated charcoal.

    B. Specific Treatment

    Do not treat prophylactically - wait for the evidence of anticoagulation. If the prothrombin time is elevated, give phytonadione, 5 - 10 mg subcutaneously or 10 - 25 mg orally, and additional doses as needed to restore the prothrombin time to normal. Give fresh-frozen plasma as needed to rapidly correct the coagulation factor deficit if there is serious bleeding. If the patient is chronically anticoagulated and has strong medical indications for being maintained in that status, give much smaller doses if vitamin k and flesh - frozen plasma as titrate to the desired prothrombin time.

    If the patient has ingested brodifacoum or a related superwarfarin, prolonged observation and repeated administration of large doses of vitamin k may be required.

    (Carbamazepine, Phenytoin, Valporic Acid)

    There drugs are widely used in the management of seizure disorders. In addition, carbamazepine and valproxic acid are increasingly used for treatment of mood disorders.

    Phenytoin can be given orally or intravenously. Rapid intravenous injections of phenytoin can cause acute myocardial depression and cardiac arrest owing to the solvent propylene glycol; a never form of phenytoin is available that does not contain this diluent. Phenytoin intoxication can occur with only slightly increased doses because of the small toxic- therapeutic window. Phenytoin intoxication can also occur following acute intentional of accidental overdose. The overdose syndrome is usually mild even with high serum levels. The most common manifestations are ataxia, nystagmus, and drowsiness. Choreoathetoid movements have been described.

    Carbamazepine was first used for the treatment of trigeminal neuralgia. It has since become a first-line agent for temporal lobe epilepsy and other seizure disorders. Intoxication causes drowsiness, stupor, and, with high levels, coma and seizures. Dilated pupils and tachycardia are common. Toxicity may be seen with serum levels greater than 20 mg/L, though severe poisoning is usually associated with concentrations greater than 30 - 40 mg/L. Because of erratic and slow absorption, intoxication may progress over several hours to days.

    Valporic acid intoxication produces a unique syndrome consisting of hypernatremia, metabolic acidosis, hypocalcemia, elevated serum ammonia, and mild liver aminotransferase elevation. Hypoglycemia may occur as a result of hepatic metabolic dysfunction, Coma with small pupils may be seen and can mimic opioid poisoning. Encephalopathy and cerebral edema can occur.


    A. Emergency and Supportive Measures :

    For recent ingestion, give activated charcoal orally or by gastric tube. For large ingestions of carbamazepine or valporic acid - especially of sustained-release for mulations - consider whole bowel irrigation. Multiple-dose activated charcoal may be beneficial in ensuring gut decontamination for large ingestions and may enhance elimination of absorbed drugs.

    B. Specific Treatment

    There are no antidotes. Naloxone was reported to have reversed valptoic acid overdose in one anecdotal case. Consider hemodialysis or hemoperfusion for massive intoxication.


    Arsenic is found in pesticides and industrial chemicals. Symptoms of poisoning usually appear within 1 hour after ingestion but may be delayed as long as 12 hours. They include abdominal pain, vomiting, watery diarrhea, and skeletal muscle cramps. Profound dehydration and shock may occur. In chronic poisoning, symptoms can be vague but often include those of peripheral sensory neuropathy. Urinary arsenic levels may be misleading and are falsely elevated after certain meals that contain large quantities of relatively nontoxic organic arsenic.


    A. Emergency Meausres

    Induce vomiting or perform gastric lavage, and administer 60 - 100 g of activated charcoal.

    B. Antibote :

    For symptomatic patients or those with massive overdose, give dimercaprol injection, 10% solution in oil, 3 - 5 mg/kg dimercaprol intramuscularly every 4 - 6 hours for 2 days. The side effects include nausea, vomiting, headache, and hypertension. Follow dimercaprol with oral penicillamine, 100 mg/kg/d in four divided doses, 10 mg/kg every 8 hours, for 1 week. Consult a medical toxicologist or regional poison control centre for advice regarding chelation.


    Atropine, scopolamine, belladonna, diphenoxylate with atropine. Datura stramonium, Hyoscyamus niger, some mushrooms, tricyclic antidepressants, and antihistamines are antimuscarinic agents with variable central nervous system effects. The patient complains of dryness of the mouth, thirst, difficulty in swallowing, and blurring of vision. The physical signs include dilated pupils, flushed skin, tachycardia, fever, delirium, myocolonus, ileus, and flushed appearance. Antidepressants and antihistamines may induce convulsions.

    Antihistamines are commonly available with or without prescription. Diphenhydramine commonly causes delirium, tachycardia, and seizures. Massive overdose may mimic tricyclic antidepressant poisoning. The nonsedating agents terfenadine and astemizole have caused QT interval prolongation and torsade de pointes. Loratidine has not caused this problem.


    A. Emergency and Supportive Measures

    Perform gastric lavage, and administer activated charcoal. Do not induce emesis in patients who have ingested antihistamines or antidepressants, because seizures may occur abruptly. Tepid sponge baths and sedation are indicated to control high temperatures.

    B. Specific Treatment

    For pure atropine or related anticholinergic syndrome, if symptoms are severe, give p hysostigmine salicylate, o.5 - 1 mg slowly intravenously over 5 minutes, with electrocardiographic monitoring, until symptoms are controlled. Bradyarrhythmias and convulsions are a hazard with physostigmine administration, and it should not be used in patients with tricyclic antidepressed overdose.


    There are wide variety of beta-adrenergic blocking drugs, with varying pharmacologic and pharmacokinetic properties. The most commonly used and most toxic beta-blocker is propranolol. Propranolol competitively blocks beta1 and beta2 adrenoceptors and also has direct membrane depressant and central nervous system effects.

    Clinical Findings

    The most common findings with mild or moderate intoxication are hypotension and bradycardia. Cardiac depression from more severe poisoning is often unresponsive no conventional therapy with beta-adrenergic stimulants such as dopamine and norepinephrine. In addition, with propranolol and other lipid - soluble drugs, seizures and coma may occur.

    The diagnosis is based on typical clinical findings. Routine toxicology screening does not usually include beta-blockers.


    A. Emergency and Supportive Measures :

    Initially, treat bradycardia or heart b lock with atropine, isoproterrenol by intravenous infusion, titrated to the desited, or an external transcutaneous cardiac pacemaker. Specific antidotal treatment may be necessary.

    For ingested drugs, empty the stomach by gastric lavage and administer activated charcoal. Do not induce emesis because of the risk of seizures.

    B. Specific Treatment :

    If the above measures are not successful in reversing bradycardia and hypotension, give glucagon, 5 - 10 mg intravenously, followed by an infusion of 1 - 5 mg/h. Glucagon in an inotropic agent that acts as a different receptor site and is therefore not affected by beta-blockade.


    Calcium channel blockers used in the United States include verapamil, diltiazem, nifedipine, nicardipine, amlodipine, felodipine, isradipine, nisoldipine, and nimodipine. These drugs share the ability to cause arteriolar vasodilation and depression of cardiac contractility, especially after acute overdose. Patients may present with bradycardia. AV nodal block, hypotension, or a combination of these effects. With severe poisoning, cardiac arrest may occur.


    A. Emergency and Supportive Measures

    Maintain a patient airway and assist ventilation, if necessary. Treat coma, hypotension, and seizures as described at the beginning of this chapter. Treat bradycardia with atropine, isoproterenol, or a transcutaneous or internal cardiac pacemaker.

    For ingested drugs, perform gastric lavage and administer activated charcoal. In addition, whole bowel irrigation should be initiated as soon as possible if the patient has ingested a sustained - release product. Because of the risk of hypotension and seizures, do not induce emesis.

    B. Specific Treatment :

    If bradycardia and hypotension are not reversed with these measures, administer calcium chloride intravenously. Start with calcium chloride 10%, 10 mL, or calcium gluconate, 20 mL. Repeat the dose every 3 - 5 minutes. The optimum dose has not been established, but there are reports of success after as much as 10 - 12 g of calcium chloride. Calcium is most useful in reversing negative inotropic effects and is less effective for AV nodal blockade and bradycardia. Epinephrine infusion and glucagon, 5 - 10 mg intravenously, have also been recommended.


    Carbon monoxide is a colorless, odorless gas produced by the combustion of carbon-containing materials. Poisoning may occur as a result of suicidal or accidental exposure to automobile exhaust, smoke inhalation in a fire, or accidental exposure to an improperly vented gas heater or other appliance. Carbon monoxide avidly binds to hemoglobin, with an affinity approximately 250 times that of oxygen. This results in reduced oxygen-carrying capacity and altered delivery of oxygen to cells.

    Clinical Findings
    At low carbon monoxide levels, victims may have headache, dizziness, abdominal pain, and nausea. With higher levels, confusion, dyspnea, and syncope may occur. Hypotension, coma, and seizures are common with levels greater than 50 - 60%. Survivors of acute severe poisoning may develop permanent neurologic deficits. The fetus and newborn may be more susceptible because of high carbon monoxide affinity for fetal hemoglobin.

    Carbon monoxide poisoning should be suspected in any person with severe headache or acutely altered mental status, especially in cold weather, when improper heating systems may have been used. Diagnosis depends on specific measurement of the arterial or venous carboxyhemoglobin saturation, although the level may have declined if high-flow oxygen therapy, has already been administered. Routine arterial blood gas testing and pulse oximetry are not useful because they may give fulsely normal oxyhemoglobin saturation determination.


    A. Emergency and Supportive Measures :

    Maintain a patent airway and assist ventilation, if necessary. Remove the victim from exposure. Treat patients with coma. Hypotension, or seizures, as described at the beginning of this chapter.

    B. Specific Treatment :

    The half-life of the carboxyhemoglobin complex is about 4 - 5 hours in room air but is reduced dramatically by high concentration of oxygen. Administer 100% oxygen by tight-fitting high flow reservoir face mask or endotracheal tube. Hyperbaric oxygen can provide 100% oxygen under higher than atmosphere pressures, further shortening the half-life; it may be useful if immediately available for patients with coma or seizures and in pregnant women, though controlled studies have failed to prove that HBO is superior to high - flow oxygen at normal pressure.