poisoning
(poy'zŏn-ing 
)
- Illness caused by a toxic substance introduced into the body.
- Administration of a noxious substance.
SEE: intoxication.
Patient Care: Poisoning should be suspected in many clinical circumstances but esp. when a patient has otherwise unexplained alterations in consciousness. The stand ard care of the poisoned patient begins with immediate stabilization of the patient's airway, breathing, circulation, and neurological status if these are compromised. This may require oximetry, blood gas analysis, electrocardiographic monitoring, airway placement, endotracheal intubation, fluid resuscitation, administration of naloxone and dextrose, or the use of pressors for some severely intoxicated patients. If the poison can be identified, reference texts or local poison control centers should be contacted to determine specific antidotes or treatments. When the poison is unidentified or when rescuers are uncertain about its cause, it is safest to test blood and urine for acetaminophen, aspirin, and commonly abused drugs. Blood testing should also include assessments of electrolytes, kidney function, liver function, and a complete blood count. Women of childbearing age should also be routinely screened for pregnancy.
Many illnesses (such as massive strokes, postictal states, insulin reactions, sepsis, meningitis, uremia) mimic the symptoms of poisoning, esp. when the patient has altered mental status.
Once the patient is stabilized, the cause for the intoxication should be addressed. Patients with substance abuse problems should be referred for detoxification, support, and counseling; suicidal and depressed patients may benefit from counseling or drug therapy. Demented patients who have poisoned themselves because of confusion about their medications should have the administration of their medications supervised. In some cases, poisonings are iatrogenic.
Decontamination of the gastrointestinal (GI) tract includes activated charcoal if the patient has ingested a drug or chemical to which the charcoal can bind; or whole bowel irrigation, which sweeps toxins from the bowel before they are absorbed. Inducing vomiting, formerly relied on in poisonings, is now rarely used because it has not been shown to improve outcome and may cause complications such as aspiration pneumonia. After decontamination procedures, specific antidotes, if available, should be administered. The elimination of many drugs from the body can be enhanced by other means, including the administration of alkaline fluids, hemodialysis, or hemoperfusion.
acetaminophen p.Poisoning from an overdose of acetaminophen, causing injury to or necrosis of the liver or liver failure.
Shortly after ingestion, patients may suffer nausea, vomiting, and malaise.
Because acetaminophen is one of the most commonly used over-the-counter (OTC) pain relievers and prescription drugs, this is one of the most common poisonings encountered in emergency departments and hospitals. If a reliable history of the amount of drug can be obtained, ingestions that exceed 7.5 g in the adult or about 150 mg/kg in children should be considered potentially toxic. In most cases, data about overdoses are not reliable, and plasma levels of acetaminophen concentration are routinely measured and compared with stand ard nomograms to decide whether a patient will need antidotal therapy with N-acetylcysteine.
If appropriate treatment is not instituted, hepatitis develops, with elevated liver enzymes in the first day, and jaundice and coagulation disorders by about 36 hr. Encephalopathy may follow. A prolonged course of recovery or complete liver failure may result, depending on the amount of drug ingested and the severity of the liver injury.
GI decontamination with activated charcoal absorbs toxin from the GI tract, but it should be given within 4 hr of ingestion of the drug. A specific antidote, N-acetylcysteine, is given orally within 8 to 10 hr after ingestion in an initial dose of 140 mg/kg and then in 70 mg/kg doses every 4 hr for 17 doses if acetaminophen levels are toxic. Alternatively, acetylcysteine may be administered intravenously. Blood should be drawn for stat acetaminophen level, complete blood count, electrolyte levels, blood urea nitrogen, serum creatinine, serum glucose, liver function, prothrombin time, and further toxicology screens. Urine should also be analyzed for drug content. If the patient with a suspected overdose is a female of child-bearing age, a pregnancy test should be done as a part of routine laboratory studies. The overdosed patient should be cared for in an intensive care unit until medically and psychiatrically cleared for discharge.
SEE: Rumack nomogram.
Taking more than 4 g of acetaminophen in 1 day (adults) or more than 90 mg/kg (children) can damage the liver and may lead to coma, kidney failure, and death.acetanilid p.Poisoning from ingestion of acetanilid.
Symptoms include cyanosis caused by formation of methemoglobin, cold sweat, irregular pulse, dyspnea, and unconsciousness. Sudden cardiac failure may occur.
Irrigate exposed skin with soap and water, e.g., in the safety shower. Support breathing and oxygenation. Notify the local poison control center.
acetylsalicylic acid p.Aspirin poisoning.
acid p.Poisoning from ingestion of a toxic acid.
Dilute with large volumes of water. Give demulcents and morphine for pain. Treat as a chemical burn.
The use of emetics and stomach tubes is contraindicated.acute cocaine hydrochloride p.Poisoning from an overdose of cocaine that has been eaten, smoked, inhaled, or injected.
An overdose of cocaine is an accelerated version of the classic physiological and psychological responses to cocaine use. Initial euphoria is followed by excitability, delirium, tremors, convulsions, tachycardia, and angina pectoris, all of which are signs of overwhelming sympathetic stimulation of the brain, heart, and lungs. Death is usually caused by a cardiovascular event or to respiratory failure. Plasma and liver pseudocholinesterase detoxify cocaine into water-soluble metabolites that are excreted in urine. Anyone with low plasma cholinesterase activity (such as a fetus, infant, pregnant woman, or someone with liver disease) is very prone to cocaine toxicity. People who congenitally lack pseudocholinesterase are highly sensitive to the effects of any dose of cocaine.
Many chronic cocaine users overdose while taking no more than their usual amount of the drug, when, e.g., the purity (pharmacological strength) of an ingested dose is greater than usual or the drug has been mixed with another psychoactive substance. Lethal overdoses are usually caused by acute coronary syndromes. Some cocaine users may die instead of intracerebral hemorrhage. The presenting findings may include seizures, hemiplegia, aphasia, or coma. Patients admitted for trauma may also be cocaine intoxicated (two thirds of cocaine-related deaths result from traumatic injuries, not drug overdose). Because many signs and symptoms that cocaine produces resemble those from injuries, and because cocaine poisoning is life-threatening, emergency department care providers must quickly distinguish drug-related problems from traumatic injury problems.
Oxygen and aspirin should be given with benzodiazepines to reduce agitation and calcium channel blockers to reduce high blood pressure. Beta blockers should be avoided. If the patient survives the acute poisoning episode, treatment is directed toward helping the patient abstain from drugs and preventing relapses.
Studies support the effectiveness of a 12-step program, such as Cocaine Anonymous, to help build a solid recovery program. Other community resources can also be used for support and to help the patient identify and manage relapse triggers.
Vital signs are checked frequently, the patient is attached to a cardiac monitor, and an intravenous line is initiated. Large volumes of fluids are infused to help remove protein breakdown products from the body (a result of rhabdomyolysis). Bilateral lung sounds are auscultated frequently during fluid resuscitation because aggressive fluid therapy can worsen heart failure. Care providers try to physically control patients to prevent them from injuring themselves. If patients demonstrate violent or aggressive behavior, chemical or physical restraints may be necessary. Calcium channel blockers or a benzodiazepine is administered as prescribed to reduce the patient's blood pressure and heart rate. Seizures, which occur because the seizure threshold is lowered by cocaine, are treated with diazepam. Because cocaine causes hypothalamic thermal regulatory dysfunction, core body temperature must be monitored closely. Elevated temperature is treated with acetaminophen and cooling blankets, cool-air ventilation, and cool saline gastric lavage. Central nervous system (CNS) stimulation may be followed by CNS depression (flaccid paralysis, coma, fixed and dilated pupils, respiratory failure, and cardiovascular collapse).
Cocaine smuggling often involves body packing (swallowing balloons, condoms, or other objects filled with cocaine). If these items leak, the patient becomes intoxicated and is at high risk for death.
acute lead p.Poisoning from ingestion or inhalation of a large amount of lead, causing abdominal pain, metallic taste in mouth, anorexia, vomiting, diarrhea, headache, stupor, renal failure, convulsions, and coma.
Adequate urine flow should be established; convulsions may be controlled with diazepam. Calcium disodium edetate and dimercaprol are administered to remove lead from the body. After acute therapy is completed, penicillamine is given orally for 3 to 6 months for children and up to 2 months for adults. The exposure to lead should be reduced or eliminated.
Patients receiving penicillamine therapy must be monitored weekly for adverse reactions, including diffuse erythematous rashes, angioneurotic edema, proteinuria, and neutropenia. Penicillamine is contraindicated in patients with a history of penicillin sensitivity, renal disease, or both.acute nicotine p.Poisoning from exposure to nicotine, causing excessive stimulation of the autonomic nervous system. Usually nicotine poisoning occurs when young children accidentally consume nicotine chewing gum or patches found in the home.
Nausea, salivation, abdominal pain, vomiting, diarrhea, sweating, dizziness, and mental confusion. If the dose is sufficient, the patient will collapse, develop shock, convulse, and die of respiratory failure caused by paralysis of respiratory muscles.
Activated charcoal may be given to conscious patients who are not vomiting. Unconscious patients should be intubated and supported in an intensive care unit. Anticonvulsants are used to treat seizures.
alkali p.Poisoning from ingestion of an alkali, e.g., lye or caustic potash.
Large amounts of water are given by mouth. Consultation with an ear, nose, and throat specialist is often advisable. Tracheostomy or intubation is performed if necessary to protect the airway.
Emetics, strong acids, and lavage should be avoided. Fluid balance and electrolytes should be carefully monitored.Morphine is useful in allaying pain. Rest, heat, quiet, and adequate fluid intake are necessary.
aluminum p.Poisoning from excessive exposure to aluminum, causing nausea, vomiting, renal dysfunction, and cognitive disorders. Aluminum poisoning with its attendant impaired cognition or dialysis dementia in patients with end-stage renal disease, has been nearly eliminated now that dialysates no longer contain aluminum.
amnesic shellfish p.Poisoning from eating crabs and shellfish contaminated with domoic acid, causing permanent short-term memory loss, brain damage, and , in severe cases, death.
antimony p.Poisoning from ingestion of antimony.
Symptoms include an acrid metallic taste, cardiac failure, sweating, and vomiting about 30 min after ingestion. In large doses, it causes irritation of the lining of the alimentary tract, resembling arsenic poisoning.
Dimercaprol can be used as an antidote.
arsenic p.Poisoning from ingestion of arsenic.
Symptoms include a burning pain throughout the GI tract, vomiting, dehydration, shock, dysrhythmias, coma, convulsions, and paralysis.
The stomach should be lavaged with copious amounts of water. Dimercaprol or other chelators (such as penicillamine) should be given immediately.
Left untreated, arsenic poisoning can cause death.
After first aid, fluid and electrolyte balance must be maintained. Morphine should be given for pain. The patient is treated for shock and pulmonary edema. Blood transfusion may be required.
arum family p.Poisoning from ingestion of plants of the genus Arum, e.g., dieffenbachia, caladium, and philodendron, which contain poisonous calcium oxalate crystals.
Symptoms include irritation, pain, burning, and swelling of the affected areas.
The affected area should be washed with water, and ice should be applied. If pain is severe, corticosteroids are of benefit.
aspirin p.Poisoning from ingestion of an overdose of aspirin.
In acute poisoning, signs vary with increasing doses from mild lethargy and hyperpnea to coma and convulsions. Sweating, dehydration, hyperpnea, hyperthermia, and restlessness may be present with moderate doses. In chronic poisoning, tinnitus, skin rash, bleeding, weight loss, and mental symptoms may be present. Aspirin poisoning in very young infants may produce very few signs and symptoms other than dehydration or hyperpnea.
Activated charcoal is given by mouth. Intravenous (IV) fluids are given for dehydration but must not be overloaded. Enough IV fluids should be given to establish 3 to 4 mL/kg/hr of urine flow. Alkalinization of urine is achieved by administering bicarbonate. The goal is a urine pH of 8 or higher. After urine flow is established, potassium 30 mEq/L of administered fluid should be added. After serum potassium levels reach 5 mEq/L, potassium should be discontinued. If alkalinization of the urine is not attained, hemodialysis may be needed.SYN: acetylsalicylic acid poisoning.
atropine sulfate p.Poisoning from ingestion of atropine, resulting in anticholinergic side effects of restlessness, dry mouth, fever, hot and dry skin, pupillary dilation, tachycardia, hallucinations, delirium, and coma. SYN: atropinism.
Oxygen is given; a cardiac monitor, oximeter, and automated blood pressure cuff are applied; and intravenous fluids are administered. Patients experiencing restlessness may respond to the administration of a benzodiazepine (such as lorazepam or diazepam). If the atropine has been ingested orally, gastric lavage with activated charcoal may absorb some of the toxin from the GI tract. Severe neurological side effects (such as seizures) may be treated with physostigmine.
barbiturate p.Poisoning from an overdose of barbiturates, resulting in excessive sedation, sometimes accompanied by an inability to protect the airway, coma, shock, and hypothermia.
Agents commonly taken in overdose include secobarbital, phenobarbital, or butalbital.
When oxygenation and ventilation are compromised, intubation and mechanical ventilation may be needed. Other supportive treatments include activated charcoal, bicarbonate-containing fluids (to make the urine alkaline and increase barbiturate excretion), rewarming techniques, and fluids or drugs to support blood pressure.
bismuth p.Poisoning from ingestion of bismuth.
Symptoms include metallic taste, foul breath, fever, GI irritation, a bluish line at the gum margin, ulcerative process of the gums and mouth, headache, and renal tubular damage.
The source of bismuth is removed; gastric lavage and /or activated charcoal are given; respiratory support and chelation therapy with dimercaprol are provided.
blood p.An obsolete term for septicemia.
boric acid p.Poisoning from consumption of or exposure to boric acid.
Symptoms include nausea, vomiting, diarrhea, convulsions, weakness, CNS depression, livid skin rash characterized as “boiled lobster rash,” and shock. Acute renal failure and cardiac failure may result from large ingestions.
Activated charcoal may prevent absorption of boric acid from the GI tract. Hemodialysis is sometimes required for severe intoxications.
brass p.Poisoning from the inhalation of fumes of zinc and zinc oxide, causing destruction of tissue in the respiratory passage.
Symptoms include dryness and burning in respiratory tract, coughing, headache, and chills.
Brass poisoning is rarely fatal.
Call the nearest poison control center to determine proper therapy.brodifacoum p.Poisoning from the ingestion of brodifacoum. Brodifacoun, a long-acting derivative of warfarin, is often found in rodenticides.
Hemorrhage is the most common side effect and may occasionally be life-threatening. Bleeding within the kidneys and urinary tract produces acute renal failure.
Because warfarin interferes with the liver's use of vitamin K to produce clotting factors, brodifacoum poisoning is treated with vitamin K, fresh frozen plasma, and supportive therapy.
bromide p.Poisoning caused by an overdose of bromide.
Symptoms include vomiting, abdominal pain, respiratory and eye irritation if inhaled, corrosion of the mouth and intestinal tract if swallowed, cyanosis, tachycardia, and shock.
If bromide is inhaled, oxygen is administered, respiratory support provided, and pulmonary edema treated. If bromide is swallowed, gastric lavage may reduce intestinal absorption.
buckthorn p.Poisoning from consumption of the fruit of the buckthorn (a species of Bumelia), which grows in the southeastern U.S., resulting in motor paralysis.
carbon dioxide p.Poisoning from inhalation of carbon dioxide (CO2). In small quantities (up to approx. 5%) in inspired air, CO2 stimulates respiration in humans; in greater quantities it produces an uncomfortable degree of mental activity with confusion. Although not toxic in low concentrations, CO2 can cause death by suffocation. CO2 poisoning is rarely fatal unless exposure occurs in a closed space.
Symptoms include a sensation of pressure in the head, ringing in the ears, an acid taste in the mouth, and a slight burning in the nose. With massive exposures to very concentrated CO2, respiratory depression and coma may occur.
The patient should be removed to fresh air and given oxygen and , if needed, ventilatory assistance.
carbon monoxide p.Poisoning from inhalation of small amounts of carbon monoxide (CO) over a long period or from large amounts inhaled for a short time.
CO poisoning results from the avid chemical combination of the gas with hemoglobin, forming carboxyhemoglobin (COHb).
Pulse oximetry is not a useful measure in CO intoxication: it cannot differentiate between carboxyhemoglobin and oxyhemoglobin and therefore gives a falsely elevated indication of oxygenation.In the U.S., where exposure to smoke, car exhaust, and other sources of incomplete combustion of carbon fuels is common (particularly during winter), CO poisoning is one of the most frequent, and potentially deadliest, intoxications. About 500 deaths in the U.S. are caused by CO poisoning each year.
The symptoms of CO poisoning vary with the level of exposure and the concentration of COHb in the bloodstream. At levels of less than 10%, patients may be symptom-free or may complain only of headache. (Heavy cigarette smoking may produce levels as high as 7% to 9%.) COHb levels of 30% produce mild neurological impairment (dizziness, fatigue, difficulty concentrating), and levels of 50% may cause seizures or coma. Death is likely when COHb levels exceed 70%.
Home CO monitors can alert people to dangerous levels of carbon monoxide in the home.
Arterial or venous COHb levels should be obtained immediately, and serial levels checked hourly to monitor treatment effectiveness. Blood glucose, ethyl alcohol, acetaminophen, and other drug levels should be measured on all patients who come to the emergency room with altered mental status. Computed tomography or magnetic resonance imaging of the brain may also be necessary. The patient should be removed immediately from exposure to CO. If the patient has severe CO poisoning (indicated by carboxyhemoglobin levels above 25%) or cardiovascular and neurological impairment regardless of levels, hyperbaric oxygen therapy should be employed if available, and the patient admitted to the hospital. One hundred percent oxygen is given with a tight-fitting non-rebreather mask, under pressure (hyperbaric) if possible. Intubation and mechanical ventilation should be used if indicated. A venous access is used to provide saline infusion, and cardiac and hemodynamic monitoring is established. The patient should be kept at bedrest to reduce the body's oxygen requirements.
Potential complications of hyperbaric therapy include sinus and middle ear barotrauma, hyperoxic seizure, anxiety, and oxidative stress. Intubation and mechanical ventilation should be used for patients with diminished level of consciousness or respiratory distress, esp. if hyperbaric treatment is not available. An antiemetic may be prescribed to manage nausea and prevent vomiting. Bedrest limits exertion and tissue oxygen demand , reducing organ ischemia. Patients with cardiac or renal disease are necessarily at increased risk for CO complications. In general, people with more severe initial symptoms are at higher risk for sequelae.
Clinical improvement after treatment is indicated by the presence of hemodynamic stability without IV support, mechanical ventilation, or supplemental oxygen; sufficient urine output; the return of an appetite; and a stable neurological status. A follow-up visit with a health care professional is advisable shortly after discharge. Patients should be taught about the major causes of CO exposure and should not return home until the source of carbon monoxide has been eliminated, e.g., by a certified heating and ventilation specialist. The importance of having the home heating furnace inspected and cleaned annually should be stressed. Patients should also be cautioned about working on an automobile in a garage with the engine running or burning items indoors. The Consumer Product Safety Commission recommends that CO detectors be installed on each level of the home and just outside the sleeping areas. Most are battery operated and easily installed. Patients should be advised to evacuate the home if an alarm sounds, leaving windows or doors open for ventilation, and to call 911. Alarms should never be turned off or ignored, and batteries should be replaced when the clocks are changed in spring and fall, as for smoke alarms.
SEE: table - Toxicity of Carbon Monoxide.
carbon tetrachloride p.Poisoning from prolonged inhalation of carbon tetrachloride.
Symptoms include irritation of the eyes, nose, and throat, headache, confusion, CNS depression, visual disturbances, nausea, anorexia, hepatitis, nephropathy, and cardiac arrhythmias.
Clothes contaminated with carbon tetrachloride are removed. Oxygen, artificial respiration, gastric decontamination, and management of cardiac rhythms are often needed.
chloral hydrate p.Poisoning from ingestion of excessive amounts of chloral hydrate. The drug depresses and eventually paralyzes the CNS and may cause liver toxicity. There may be nausea and vomiting caused by gastric irritation.
An airway must be maintained and a cuffed endotracheal tube used if necessary. Mechanical ventilation may be required. A slurry of activated charcoal is administered. Beta blockers (such as propranolol) are used to manage arrhythmias.
chromium p.Poisoning from excess chromium (as in mining, welding, or pigment manufacturing).
Symptoms include contact dermatitis, skin burns, or lung, liver, or kidney damage.
Treatment after ingestion consists of GI irrigation followed by forced diuresis and alkalinization of urine.
chronic lead p.Poisoning from chronic ingestion or inhalation of lead, which damages the central and peripheral nervous systems, kidneys, the blood-forming organs, and the GI tract.
In 2013, the CDC estimated that 1 in 38 children, about 535,000, had “harmful levels of lead in their bodies.”
Early symptoms include loss of appetite, weight loss, vomiting, fatigue, weakness, headache, lead line on gums, apathy or irritability, and a metallic taste in the mouth. Long-lasting consequences of lead poisoning include cognitive deficits, attention-deficit disorder, and other neuropsychiatric symptoms.
Patients suspected of lead poisoning are often anemic. Laboratory diagnosis is established when a blood lead level is above 5 µg/dL, or when tests detect elevated free erythrocyte protoporphyrin, increased excretion of lead in urine, and characteristic x-ray changes in the ends of growing bones.
Exposure to lead should be eliminated and an adequate diet with added vitamins provided. Chelating agents such as dimercaprol, dimercaptosuccinic acid (succimer), or ethylenediamine tyetracetic acid are given to reduce lead levels to normal.
A history is obtained to determine whether the sources of lead ingestion or inhalation are caused by the environment, work, or folk remedies, and preparations are made for their removal. (In many states, removal of household lead must be done by state-licensed specialists, not homeowners. The CDC and local poison-control centers provide relevant information. A 1-cm square chip of lead-based paint may contain a thousand times the usual safe daily ingestion of lead.) A history is obtained of pica; recent behavioral changes, particularly, in children, a lack of interest in playing; and behavioral problems such as aggression and hyperirritability. The patient is assessed for developmental delays or loss of acquired skills, esp. speech. CNS signs indicative of lead toxicity may be irreversible. The younger child is assessed for at-risk characteristics such as the high level of oral activity in late infancy and toddlerhood; small stature, which enhances inhalation of contaminated dust and dirt in areas heavily contaminated with lead; and nutritional deficiencies of calcium, zinc, and iron, the single most important predisposing factor for increased lead absorption. Older children are assessed for gasoline sniffing, which is esp. prevalent among children in some cultures. The parent-child interaction is assessed for indications of inadequate child care, including poor hygienic practices, insufficient feeding to promote adequate nutrition, infrequent use of medical facilities, insufficient rest, less use of resources for child stimulation, less affection, and immature attitudes toward maintaining discipline. Prescribed chelating agents are administered to mobilize lead from the blood and soft tissues by enhancing its deposition in bones and its excretion in urine. A combination of drugs may result in fewer side effects and better removal of lead from the brain. If encephalopathy is present, fluid volume is restricted to prevent additional cerebral edema. Injections are administered intramuscularly, and injection sites are rotated for painful injections (which may include simultaneous procaine injections for local anesthesia). The child is allowed to express pain and anger, and physical and emotional comfort measures are provided to relieve related distress. If there is no encephalopathy, injections are administered intravenously, and hydration is maintained. The patient is evaluated for desired drug effects measured by blood levels and urinary excretion of lead and for signs of toxicity from the chelating agents. (Special blood collection and urine collection containers are necessary for some of the monitoring tests. The laboratory should be consulted before collection.) Prescribed anticonvulsants are administered as necessary to control seizures (often severe and protracted), an antiemetic for nausea and vomiting, an antispasmodic for muscle cramps, and analgesics and muscle relaxants for muscle and joint pain. Serum electrolytes are monitored daily, and renal function is evaluated frequently. Whole bowel irrigation is used when lead is visible in the GI tract (or for episodes of acute lead ingestion). Adequate nutrition is provided, and nutritional deficiencies are corrected, by administering prescribed supplements, such as iron. An active, active-assisted, or passive range-of-motion exercise program is established to maintain joint mobility and prevent muscle atrophy. Parents are taught and supported to prevent recurrence, and the public is educated about the dangers of lead ingestion, the importance of screening young (esp. preschool) children at risk, the signs and symptoms indicative of toxicity, and the need for treatment.
ciguatera p.Poisoning from eating certain types of bottom-dwelling shore fish, e.g., grouper, red snapper, sea bass, and barracuda.
The toxin, ciguatoxin, is present in fish that feed on dinoflagellates. It acts within 5 hr of ingestion, and symptoms may persist for 8 days or longer. The toxin interferes with nerve impulse transmission by altering cell membrane sodium channel polarization.
Symptoms include tingling of the lips, tongue, and throat, abdominal cramps, nausea, vomiting, diarrhea, paresthesia, hypotension, and respiratory paralysis.
Treatment is supportive; treatment of respiratory paralysis may be required.
SEE: opiate poisoning.
cone shell p.Poisoning from the conotoxins (neurotoxins delivered by the pointed, hollow teeth of the predatory sea snails of the genus Conus).
Intense local pain, swelling, and numbness may last several days. In severe poisoning, muscular incoordination and weakness can progress to respiratory paralysis.
There is no specific therapy, but supportive measures including artificial respiration and supplemental oxygen may be needed.
Death can occur, but recovery within 24 hr is the usual outcome.
copper sulfatep.Poisoning from ingestion of toxic amounts of the pesticide copper sulfate.
Large ingestions may cause liver failure, acute renal failure, and shock.
Penicillamine or dimercaprol should be given. The caregiver should monitor vital signs, treat shock, administer oxygen if needed, control convulsions, and maintain electrolyte balance.
corrosive p.Poisoning from strong acids, alkalies, strong antiseptics and disinfectants including bichloride of mercury, carbolic acid (phenol), cresol compounds, tincture of iodine, and arsenic compounds. These agents cause tissue damage similar to that caused by burns. If the substances have been swallowed, any part of the alimentary canal may be affected. Tissues involved are easily perforated. Death may result from shock or from asphyxiation caused by swelling of the throat and pharynx. Esophageal injury and stricture may be a late complication.
Corrosive poisoning is marked by intense burning of the mouth, throat, pharynx, and abdomen; abdominal cramping, retching, nausea, and vomiting, and , often, collapse. There may be hematemesis and diarrhea; the stools are watery, mucoid, bloody, and possibly stained with the poison or its products, resulting from its action on the contents of the alimentary tract. Stains of the lips, cheeks, tongue, mouth, or pharynx are often a characteristic brown; stains on the mucous membranes may be violet or black. Carbolic acid (phenol) stains are white or gray, resembling boiled meat; hydrochloric acid stains are grayish; nitric acid, yellow; sulfuric acid leaves tan or dark burns.
Immediate treatment in a hospital is mand atory. It is important to try to discover the chemical substance ingested, and all materials such as food, bottles, jars, or containers should be saved. This is essential if the patient is comatose or an infant.
In treating corrosive poisoning, vomiting must not be induced, gastric lavage must not be attempted, and no attempt should be made to neutralize the corrosive substance.Vomiting will increase the severity of damage to the esophagus by renewing contact with the corrosive substance. Gastric lavage may cause the esophagus or stomach to perforate. If the trachea has been damaged, tracheostomy may be needed. Emergency surgery must be considered if there are signs of possible perforation of the esophagus or of the abdominal viscera. Opiates will be needed to control pain. For esophageal burns, broad-spectrum antibiotic and corticosteroid therapy should be started. Intravenous fluids will be required if esophageal or gastric damage prevents ingestion of liquids.
Long-range therapy is directed toward preventing or treating esophageal scars and strictures.
cyanide p.Poisoning from any of several compounds containing cyanide. These compounds are very potent blockers of cellular oxygenation and inhibit respiration by blocking oxidative phosphorylation.
The most common patients are jewelers, metal platers, those who hand le rodenticides, victims of smoke inhalation, and patients treated with very high doses of sodium nitroprusside. Rarely, cyanide poisoning results from the ingestion of certain fruits, e.g., the bitter cassava and some stone fruits.
Palpitations, disorientation, and confusion may be rapidly followed by respiratory failure, seizures, coma, and death in patients who suffer large exposures. Smaller exposures may produce anxiety, dizziness, headache, and shortness of breath. Patients may report that they have detected an odor of bitter almonds at the time of exposure to cyanide.
The patient is immediately treated with gastric lavage, and activated charcoal is given to adsorb whatever toxin may remain in the GI tract. Emesis is contraindicated. Oxygen is immediately provided; intubation and mechanical ventilation may be needed when the patient has suffered respiratory failure. Antidotes to cyanide poisoning include hydroxocobalmin and sodium thiosulfate.
ABBR: DSP
Poisoning from eating shellfish that have ingested okadaic acid and other toxins produced by marine algae (dinoflagellates), resulting in nausea, vomiting, abdominal cramping, and diarrhea. The disease resolves spontaneously from within hours to a few days.digitalis p.Acute or chronic poisoning from the cumulative effect of digitalis. Digitalis poisoning is potentially life threatening and is often a drug-related complication.
Extracardiac signs develop initially in most patients, the first of which is almost always anorexia. Nausea and vomiting, sometimes with abdominal pain and increased salivation, usually appear 1 to 2 days later. Other symptoms include fatigue, drowsiness, general muscle weakness, and visual disturbances such as blurring of vision, yellow-green or white halos around visual images, light flashes, photophobia, and diplopia. Mental disturbances (such as agitation, hallucinations, and disorientation) are very common in older atherosclerotic patients. If the early signs are unheeded, 80% of patients eventually will show more serious cardiac signs. Toxic concentrations of digitalis can cause nearly every known arrhythmia. They can decrease heart rate by slowing conduction and increasing the refractory period at the AV node, or they can increase the rate by creating abnormal pacemaker activity in the conductive tissue.
The distinction between therapeutic and toxic levels of digoxin is narrow; therefore, health care providers must be alert to signs of digitalis poisoning in patients. Older patients and those with liver or kidney disease are at esp. high risk because their absorption, metabolism, and excretion rates are unpredictable. Health care providers should consider health status changes that can alter a patient's response to digitalis, including vomiting, diarrhea, or other GI upset; acid-base or electrolyte disturbances (such as hypokalemia, hypomagnesemia, or hypercalcemia), which alter the heart's sensitivity to digitalis; hypothyroidism, which disrupts the patient's ability to metabolize digitalis; and liver or kidney disease, which modifies metabolism and excretion. Changes in a treatment regimen also can predispose the patient to toxicity, esp. the addition of or increase in dosages of drugs such as antiarrhythmics, calcium channel blockers, or potassium-wasting diuretics. Assessment for digitalis toxicity is necessary if electrical cardioversion is used to restore a patient to sinus rhythm because this procedure increases the heart's sensitivity to digitalis.
Because digitalis toxicity develops quickly and insidiously, the patient is taught early symptoms to report. Extracardiac signs can be missed or mistaken for complications of another condition being treated, such as pneumonia. Health care providers need to compare the patient's current appetite and activity to the patient's previous health status, and carefully monitor the patient for electrolyte imbalances. Significant decreases or increases in heart rate and rhythmic irregularities must be reported because toxic concentrations may lead to ventricular fibrillation and death. If toxicity is suspected, an electrocardiogram is performed. Electrocardiographic signs of digitalis toxicity include first-degree atrioventricular (A-V) block with depressed S-T segments, shortened Q-T intervals, and flattened T waves. In the presence of such changes a serum digoxin level and basic chemistries may be used to confirm toxicity. Because hypokalemia is a major cause of digitalis toxicity, adequate potassium intake in the diet and prescribed supplementations are essential. The patient is advised about conditions such as diarrhea, which may deplete the body of potassium or contribute to dehydration and renal insufficiency. The patient is advised not to take OTC medications without notifying his health care provider because these may alter his sensitivity to digitalis.
Digitalis poisoning may sometimes occur because of accidental or deliberate overdose. Emergency department personnel may sometimes remove the drug from the stomach by lavage or activated charcoal, administer intravenous fluids, provide potassium, monitor cardiac status, and /or treat cardiac arrhythmias as they arise. They may also administer digoxin immune Fab (ovine) to bind serum digoxin, preventing it from binding to cardiac receptors.
ergot p.Poisoning from eating bread made with grain contaminated with the Claviceps purpurea fungus, or from an overdose of ergot. SYN: ergotism.
Within several hours of ingestion, the patient may develop anticholinergic symptoms (such as abdominal cramping, bradycardia, pupillary dilation, urinary retention) and vasoconstriction (with ischemia and gangrene of the extremities).
Sodium nitroprusside may counteract the vascular spasm produced by ergots.
fish p.Poisoning from eating fish that are inherently poisonous or become poisonous from decomposition, infection, or feeding on poisonous foods.
food p.Poisoning from ingestion of foods containing poisonous substances. These include mushrooms; shellfish; foods contaminated with pesticides, lead, or mercury; milk from cows that have fed on poisonous plants; foods that have putrefied or decomposed, or foods in which bacterial toxins have accumulated.
SEE: staphylococcal food poisoning.
formaldehyde p.Poisoning from ingestion of formaldehyde.
Symptoms include local irritation of the eyes, nose, mouth, throat; respiratory and GI tracts; CNS disorders (including vertigo, stupor, convulsions, unconsciousness); and renal damage.
gasoline p.Poisoning from ingested or inhaled gasoline.
The most hazardous symptom of gasoline exposure is a potentially fatal inflammation of the lungs, caused by aspiration of even small quantities of distilled petroleum.
Symptoms of oral ingestion may also include dizziness, disorientation, seizures, and other neurological difficulties; gastric irritation and vomiting; rashes; and cardiac rhythm disturbances.
Patients with evidence of chemical pneumonitis should be treated with oxygen and monitored in a hospital. Patients in full respiratory failure will require mechanical ventilation. Those who have deliberately ingested gasoline may benefit from supportive psychotherapy or psychiatric referral.
The patient should be observed for at least 6 hr. If no evidence of respiratory distress or dysfunction is found, and if a chest x-ray exam shows no signs of chemical pneumonitis, the patient may be safely discharged home.
heavy metal p.Poisoning from ingestion, inhalation, or absorption of a heavy metal, esp. lead or mercury.
Symptoms are determined by the type and duration of exposure and may include pulmonary, neurological, integumentary, or GI disorders.
hemlock p.Poisoning from ingestion of hemlock Conium maculatum.
Symptoms include weakness, drowsiness, nausea, vomiting, difficulty breathing, and paralysis.
Oral activated charcoal may be given to decrease the absorption of the toxin from the GI tract. Respiratory failure should be treated with intubation and mechanical ventilation. The local Poison Control Center should be contacted for additional instructions.
If untreated, hemlock poisoning may cause death.
herbicide p.Poisoning from the use of a toxic herbicide such as 2,4-D.
ink p.Poisoning from contact with ink. Many such poisonings are forms of dermatitis caused by several types of materials. Ordinary ink may cause irritation because of its composition or because of a person's sensitivity to certain ingredients in the ink. Sometimes cleaning materials used to remove ink stains are toxic.
Symptoms include redness, pustule formation, and cracking of the skin.
The area should be washed with alcohol, soap, and water. It then should be rinsed carefully and covered with a bland dressing such as cold cream.
iodine p.Poisoning from accidental ingestion of iodine or its compounds. SYN: tincture of iodine poisoning.
Symptoms include brown stains on the lips and mouth; burning pain in the mouth, throat, and stomach; vomiting (blue vomit if the stomach contained starches, otherwise yellow vomit); bloody diarrhea.
The patient should immediately be given a cornstarch or flour solution by mouth: 15 g in 500 mL (2 cups) of water. Activated charcoal or gastric lavage may also be employed.
iron p.Acute poisoning usually caused by the accidental ingestion (usually by infants or small children) of iron-containing medications intended for use by adults. In the U.S., about 20,000 accidental iron exposures are reported each year.
Symptoms include vomiting, usually within an hour of ingestion of the iron. Vomiting of blood and melena may occur. If untreated, restlessness, hypotension, rapid respirations, and cyanosis may develop, followed within a few hours by coma and death.
Whole bowel irrigation should be used to force ingested iron out of the GI tract. Chelation of iron can be performed with deferoxamine, which binds circulating iron from the bloodstream.
SEE: poison ivy dermatitis.
lead p.Poisoning from ingestion or inhalation of substances containing lead.
Lead has been used worldwide for millennia, and the effects of exposure to it are well known. Environmental lead is ubiquitous, and everyone has some measurable lead in the blood. Lead is one of the largest environmental and medical problems with regard to the number of people exposed, and exposure to lead accounts for approx. 0.2% of all deaths and approx. 0.6% of disability adjusted life years worldwide.
Symptoms of acute poisoning include a metallic taste in the mouth, burns in the throat and pharynx, and later abdominal cramps and prostration. Chronic lead poisoning is characterized by anorexia, nausea, vomiting, excess salivation, anemia, a lead line on the gums, abdominal pains, muscle cramps, kidney failure, encephalopathy, seizures, learning disabilities, and pains in the joints.
Diagnosis includes determining the clinical signs, medical history, and possible routes of exposure. Laboratory analysis of the blood lead level is the main tool in diagnosing and assessing the severity of lead poisoning. Toxicologists may be involved in diagnosis and treatment.
The chief therapies are removal of the patient from the source of lead and , for those with significantly high levels of lead in the blood or symptoms of poisoning, chelation therapy.
Acute poisoning: Seizures are treated with benzodiazepines. Fluid and electrolyte balance is maintained. Cerebral edema is treated with mannitol and dexamethasone. The blood lead level is determined. If it is above 50 to 60 µg/dL, the lead is removed from the body with a chelator, e.g., edetate calcium disodium, dimercaprol, D-penicillamine, or succimer (2,3-dimercaptosuccinic acid). Succimer has the advantage of being orally active and is esp. helpful in treating children. The effect of treatment is monitored; it may have to be continued for a week or longer or repeated if the lead level rebounds. Chronic lead poisoning: A blood lead level ≥10 μg/dL in a child may impair normal development of the CNS. Parents of exposed children should be educated about potential environmental or nutritional sources of lead exposure, and the child should be rechecked in a month. Rising levels, e.g., above 25 μg/dL or higher, may warrant treatment with chelators. Public health officials should be notified when a child's lead level is elevated so that environmental remediation or relocation of the patient and family, as indicated, may be undertaken.
manganese p.An uncommon cause of toxicity in workers regularly exposed to manganese.
Symptoms include muscular weakness, difficulty walking, tremors, CNS disturbances, and salivation.
match p.GI irritation caused by ingesting or sucking on the heads of matches (usually by children).
The child should be treated supportively, e.g., with oral fluids as tolerated and antiemetics if they are needed.
SEE: phosphorus poisoning.
mercuric chloride p.Acute poisoning from salt of mercury ingested, inhaled, or absorbed through the skin.
Symptoms include severe GI irritation with pain, cramping, constriction of the throat, vomiting, and a metallic taste in the mouth. Abdominal pain may be severe. Bloody diarrhea, bloody vomitus, scanty or absent urine output, prostration, convulsions, and unconsciousness may follow. Death from uremia is the usual outcome unless treatment is begun immediately.
Oxygen and intravenous fluids are given. Gastric lavage (not emesis) is used to empty the GI tract. Dimercaprol or d-penicillamine is used for chelation. Similar treatment is given for mercurous chloride poisoning.
mercurous chloride p.Acute poisoning from ingestion or absorption through the skin of mercurous chloride, a mercury salt. Acute poisoning is rare because it is poorly absorbed. Symptoms include increased salivation, abdominal discomfort, and diarrhea.
mercury p.The acute or chronic poisoning from the ingestion or inhalation of mercury.
Symptoms include nausea, vomiting, abdominal pain, renal failure, gingivitis, behavioral and cognitive deficits, seizures, paralysis, and pneumonitis.
Gastric lavage or whole bowel irrigation may be used to empty the GI tract. Hemodialysis or chelation therapy, e.g., with succimer or penicillamine, may also be helpful.
If untreated, mercury poisoning may cause death.
methyl alcohol p.Poisoning from methanol (methyl alcohol).
The initial primary consequences are depression of CNS function (including coma or convulsions), visual disturbances (including permanent blindness) caused by the concentration of the toxin in the vitreous humor and optic nerve, headache, abdominal cramping, nausea, weakness, and an anion-gap metabolic acidosis.
Fluids and electrolyte and acid-base balance should be carefully monitored and adjusted. Methanol may be removed from the bloodstream by hemodialysis.
Variant: methyl mercury poisoning
Minamata disease.morphine p.Acute poisoning from injected, inhaled, or orally consumed morphine sulfate.
SEE: opiate poisoning.
Variant: mushroom and toadstool poisoning
Poisoning from ingestion of mushrooms such as Amanita muscaria, which contains muscarine, or species that contain phalloidin, a component of the amanita toxin.The nearest poison control center should be called for emergency treatment.
SYN: toadstool poisoning.mussel p.Poisoning from eating mussels or clams that have ingested dinoflagellates contaminated with saxitoxin, a neurotoxin that is not destroyed by cooking. Mussel poisoning typically occurs from June to October and is common on the U.S. Pacific Coast.
narcotic p.Poisoning from narcotic or sleep-inducing drugs such as opium or its derivatives.
The patient may experience brief exhilaration followed by drowsiness, respiratory depression, or coma, or, in massive overdoses, death.
An airway should be established and ventilation provided. A narcotic antagonist such as naloxone should be given.
nitric acid p.Poisoning from contact with nitric acid.
Symptoms include pain, burning, vomiting, thirst, and shock.
Emergency measures include oral administration of activated charcoal and large volumes of water. Emetics and stomach tubes should be avoided because they may cause rupture of the esophagus or stomach.
opiate p.Poisoning from opiate or opioid analgesics taken by injection, inhalation, cutaneously, or orally.
Brief exhilaration is typically followed by slowing of the respiratory rate.
An airway should be established and ventilation provided. A narcotic antagonist such as naloxone is given, which may be repeated periodically if symptoms return. Pulmonary edema may be treated with diuretics, nitrates, and /or positive pressure ventilation. SYN: opioid analgesic overdose; codeine poisoning; opium poisoning.
oxalic acid p.Acute poisoning from accidental ingestion of oxalic acid, esp. of foods rich in oxalic acid, e.g., wood sorrel. Ingestion of 5 g of oxalic acid may be fatal. Chronic poisoning may result from inhalation of vapors.
Signs and symptoms include a corrosive action on the mucosa of the mouth, esophagus, and stomach; a sour taste; burning in the mouth, throat, and stomach; great thirst; bloody vomitus; collapse; and , sometimes, convulsions and coma.
Gastric lavage should be used to empty the GI tract. Activated charcoal can be given to bind the acid. Vomiting should not be induced.
paraldehyde p.Poisoning whose symptoms resemble those of chloral hydrate poisoning.
Symptoms include cardiac and respiratory depression, dizziness, and collapse with partial or complete anesthesia; the poisoning may also produce severe lactic acidosis.
There is no specific antidote. Supportive care includes airway management, ventilation, and hemodialysis.
ABBR: PSP
Poisoning from ingestion of shellfish contaminated by toxic marine algae that produce saxitoxin.Symptoms include numbness and tingling, nausea and vomiting, and , in severe intoxications, paralysis and respiratory failure.
Care includes the administration of intravenous fluids, respiratory support, and the oral administration of activated charcoal.
SEE: saxitoxin.
paraquat p.Poisoning from ingestion of the herbicide paraquat. Patients may be treated with oral activated charcoal or, if kidney failure is present, with hemodialysis.
parathion p.Poisoning from inhalation or ingestion of parathion (an agricultural pesticide) or from food products contaminated with it.
Headache, sweating, salivation, lacrimation, vomiting, diarrhea, muscular twitching, convulsions, dyspnea, and blurred vision occur shortly after exposure.
SEE: opiate poisoning.
phenol p.Poisoning or chemical burns of the skin from exposure to compounds containing carbolic acid, e.g., some dyes, deodorizers, and disinfectants. Such substances are corrosive to the skin and mucous membranes.
Symptoms include coagulative necrosis of affected skin or mucous membranes or with evidence of internal organ damage.
Contaminated clothing should be removed immediately. The skin should then be irrigated with copious amounts of water and either isopropyl alcohol or a solution containing polyethylene glycol. Patients who have ingested phenols should be treated with activated charcoal to absorb as much toxin as possible and be given general supportive care. Consultation with specialists in toxicology, otorhinolaryngology, and critical care medicine may be necessary in cases of massive or severe exposure.
phosphorus p.Poisoning from ingestion of substances containing yellow phosphorus, such as rat poison or roach poison. Yellow phosphorus is used in manufacturing fireworks and fertilizers.
Symptoms include profound weakness, hemorrhage, and heart failure. Occasionally, nervous system symptoms predominate. Liver failure may follow acute irritation of the GI tract. There may also be kidney damage.
Gastric lavage is performed if phosphorus was swallowed. The airway is protected by cuffed endotracheal intubation. Charcoal and a cathartic drug are administered. Depending on the length of time since ingestion, intravenous fluids may be used to flush the poison out of the system by diuresis. In some cases, peritoneal or hemodialysis may be needed.
The patient requires close monitoring for delayed effects for at least 24 hr. If the poison was intentionally ingested, the patient is placed on suicide precautions and referred for further psychological counseling.
pokeroot p.Poisoning from ingestion of the herb pokeroot (Phytolacca americana).
Symptoms include nausea, vomiting, drowsiness, vertigo, and possible convulsions and respiratory paralysis.
Treatment includes administration of whole bowel irrigation or gastric lavage.
potassium chlorate p.Poisoning from potassium chlorate (KClO3, used as an oxidizing agent, a disinfectant, and in matches, fireworks, and explosives), large doses of which cause abdominal discomfort, vomiting, diarrhea, hematuria with nephritis, and disturbances of the blood. Gastric lavage should be used to empty the stomach. Other treatment is symptomatic.
Vomiting should not be induced.potassium chromate p.Poisoning from potassium chromate (K2CrO4, a strong oxidant and carcinogen), possibly contracted by inhalation or from touching the nose with contaminated fingers, causing deep indolent ulcers.
When taken by mouth, potassium chromate has a disagreeable taste; it causes cramping, pain, vomiting, diarrhea, slow respiration; and it may affect the liver and kidneys.
Vomiting should not be induced.For poisoning by ingestion, the patient is treated as if poisoned with a strong acid. Gastric lavage is administered through a nasogastric tube. Bronchoalveolar lavage or penicillamine may be used.
potassium hydroxide p.Poisoning from potassium hydroxide (NaOH; caustic potash; lye), characterized by nausea, soapy taste, and burning pain in the mouth; bloody, slimy vomitus; abdominal cramping; bloody purging and prostration.
Vomiting should not be induced.The patient requires hospitalization, morphine for pain, and , often, treatment for shock. If the patient's airway has been burned, topical care is provided; tracheostomy may be required. Corticosterioids and antibiotics may be given.
potato p.Poisoning from ingestion of potatoes containing excess amounts of solanine. Potatoes usually contain about 7 mg of solanine per 100 g; the toxic dose of solanine is about 20 to 25 g. Boiling, but not baking, removes most of the solanine from the potato.
Symptoms include headache, vomiting, abdominal pain, diarrhea, and fever. Neurological disturbances include apathy, restlessness, drowsiness, confusion, stupor, hallucinations, and visual disturbances.
There is no specific therapy. With appropriate supportive and symptomatic therapy, prognosis is good.
SEE: solanine.
quail p.Acute myoglobinuria caused by eating quail (Coturnix coturnix), a game bird. The cause is unknown but is suspected to be toxic rather than genetic (as was once believed).
red kidney bean p.Poisoning from phytohemagglutinin in undercooked red kidney beans (Phaseolus vulgaris).
Shortly after the ingestion of raw beans, nausea and vomiting develop, occasionally resulting in dehydration and the need for hospitalization in order to receive intravenous fluids.
The intoxication usually lasts a few hours and then spontaneously resolves.
SEE: phytohemagglutinin.
risk for p.Susceptible to accidental exposure to, or ingestion of, drugs or dangerous products in sufficient doses that may compromise health [and /or the adverse effects of prescribed medication/drug use].
SEE: Nursing Diagnoses Appendix.
salicylate p.Poisoning from aspirin or one of its derivatives. It causes a metabolic acidosis and respiratory alkalosis in adults.
Ringing in the ears (tinnitus), nausea, vomiting, and diaphoresis are other common symptoms. Severe intoxications produce hyperthermia, changes in mental status, and pulmonary edema.
Patients who have overdosed on aspirin are treated with bicarbonate to increase the systemic pH and enhance excretion of salicylates in the urine. Hemodialysis is used to remove salicylates from the blood in life-threatening intoxications.
SEE: aspirin poisoning.
salt p.Poisoning from by excessive intake of table salt (sodium chloride), which usually occurs in hospitalized patients treated with concentrated sodium solutions. It typically results in acute hypernatremia.
scombroid fish p.Poisoning from eating raw or inadequately cooked fish of the suborder Scombroidea (such as anchovies, tuna, mackerel, or sardines), as well as certain nonscombroid fish (such as amberjack, mahimahi, and bluefish). Certain bacteria act on the fish after they are caught to produce a histamine-like toxin. Therefore, these fish should be either properly cooked and eaten shortly after being caught or refrigerated immediately.
Nausea, vomiting, abdominal cramps, diarrhea, flushing, headache, urticaria, a burning sensation and metallic taste in the mouth, dizziness, periorbital edema, and thirst may develop 30 min after eating the fish and last a few hours.
Antihistamines reverse many of the symptoms of the syndrome.
shellfish p.Poisoning from eating shellfish that have fed on plankton during a red tide. There are several recognized syndromes that may result, including amnesic shellfish poisoning, diarrheal shellfish poisoning, and paralytic shellfish poisoning.
silver nitrate p.Poisoning from repeated exposure to silver compounds, marked by a bluish pigmentation of the skin or occasionally of the eyes. In the past, many medications contained biologically available silver; the incidence of this intoxication nowadays is very low.
SEE: argyria.
sodium fluoride p.Poisoning from exposure to a toxic dose of sodium fluoride, which is normally used in dentistry or in fluoridating water supplies.
Symptoms include conjunctivitis, nausea, vomiting, kidney disturbances, and interference with blood coagulation.
The affected areas of the skin should be washed and the compound precipitated by addition to the wash solution of soluble calcium salts such as lime water, calcium gluconate, or calcium lactate.
staphylococcal food p.Poisoning from food containing any one of several heat-stable enterotoxins produced by certain strains of staphylococci.
Symptoms include nausea, vomiting, diarrhea, intestinal cramps, and , in severe cases, prostration and shock.
Hygienic preparation techniques can prevent this form of food poisoning. Food hand lers must cook all foods thoroughly, refrigerate them during storage, wash their hand s, and clean equipment and surfaces used in food preparation before and after hand ling foods. Certain foods (meat, poultry, fish, and those containing mayonnaise, eggs, or cream) must be refrigerated and used as soon as possible and cooked until their internal temperatures equal or exceed safe limits.
The attack usually lasts less than a day, and fatalities are rare. Patients who contract food poisoning should ingest clear fluids until abdominal pain subsides and then gradually return to a normal diet. Fluid and electrolyte balance is monitored, and supportive therapy is maintained as indicated. Enteric precautions are used until evidence of infection subsides.
stramonium p.Poisoning from the dried leaves of the Jimson weed (Datura stramonium), a powerful anticholinergic agent (containing belladonna alkaloids) that produces atropine-like effects.
SEE: atropine sulfate poisoning.
Symptoms include delirium and hallucinations, tachycardia and hypertension, fever, pupillary dilation, and , sometimes, seizures, coma, cardiac rhythm disturbances, or death.
After the GI tract is decontaminated with activated charcoal, stimulation of the intoxicated person should be minimized. Severely poisoned people (those with seizures, extremely high body temperatures, or cardiac dysrhythmias) may be treated with intravenous physostigmine, given slowly.
strychnine p.Poisoning from ingestion of strychnine.
Overdoses should be treated with gastric decontamination (such as activated charcoal) and drugs (such as diazepam) that limit muscular contraction.
Supportive care includes intravenous hydration with alkalinization of the urine to prevent or treat the consequences of rhabdomyolysis.
sulfuric acid p.Poisoning from contact with or ingestion of sulfuric acid, e.g., in laboratories, agriculture, or weapons manufacturing.
Early local effects of acid injury, e.g., necrosis of the skin or the upper GI tract, result from direct contact of sulfuric acid with the epithelium. The patient may complain of intense pain, e.g., in the mouth or throat. If acid contacts the eye, it may cause pain and corneal injury, sometimes resulting in blindness. Several days to 2 weeks after massive acid ingestion, perforation of internal organs may occur. When the stomach is involved, the perforation may leak acid into the mediastinum or peritoneum, causing pain, dyspnea, hypotension, tachycardia, or shock.
Exposed surfaces should be promptly washed in water to dilute the concentration of acid and minimize the depth of acid penetration. If the airway is compromised, the patient should be immediately intubated and ventilated before undergoing dilutional therapy. Activated charcoal, which is helpful in many other exposures, is not useful. Neutralizing substances such as diluted alkalies are probably not helpful.
Most patients who ingest significant quantities of acid will undergo upper GI endoscopy to evaluate the extent of the acid burn. Strictures (such as esophageal strictures) that develop as a result of scarring from acid burns are treated with dilation. People with ocular exposures need immediate ophthalmological consultation. Immediate surgery is warranted for patients with internal organ perforation.
Blind nasogastric intubation is generally contraindicated because it may damage the upper GI tract. Gastric intubation and lavage should be performed by experienced endoscopists.tellurium p.A rare poisoning from ingestion of tellurium, usually in the workplace.
Symptoms include a strong garlicky odor of the mouth and excreta; dry skin and mouth; anorexia; weakness; and , in severe cases, respiratory or circulatory collapse.
Treatment is supportive.
thallium p.Poisoning from ingestion of thallium, characterized by severe abdominal pain, vomiting, diarrhea, tremors, delirium, convulsions, paralysis, coma, and death. SYN: thallotoxicosis.
theophylline p.Poisoning from excessive levels of compounds containing theophylline in the blood, characterized by nausea, vomiting, agitation, cardiac arrhythmias, and , in some instances, seizures or death.
For young patients with asthma, theophylline levels exceeding 20 mg/dL are typically toxic; even lower levels, e.g., 15 mg/dL, may produce toxic effects in people over 60. Theophylline levels above 30 mg/dL have a high likelihood of adverse effects at any age.
Theophylline toxicity may occur if the patient's symptoms and drug levels are not monitored regularly while he or she takes compounds containing theophylline. Many common drugs (such as cimetidine, ciprofloxacin, erythromycin, and rifampin) alter the metabolism of theophylline and may produce toxic reactions if they are taken during theophylline therapy; these drugs should be avoided. Because of the risk of theophylline poisoning, most patients with reactive airway diseases are treated with inhaled bronchodilators instead of theophylline.
The patient may require monitoring in a critical care unit, where blood pressure and cardiac rhythm can be observed closely and early interventions taken against seizures or potentially fatal arrhythmias. Anticonvulsants are given for seizures (or to prevent seizures when theophylline levels exceed 100 mg/dL); the GI tract should be decontaminated with activated charcoal, and antiarrhythmic drugs are administered, as indicated, for disturbances in cardiac rhythm. Severe overdoses or ones with refractory symptoms should be treated with charcoal hemoperfusion.
SEE: theophylline.
thiram p.Poisoning from exposure to thiram (C6H12N2S4, a parasiticide used to prevent fungal diseases in seeds and crops and also used as an animal repellent to protect fruit trees and ornamentals from damage by rodents and deer). This may occur in those engaged either in manufacturing or applying this compound in agriculture.
tin p.Poisoning from exposure to organic compounds containing tin or tin arsenites.
Most of the symptoms are neurological, e.g., changes in behavior, cognition, or awareness.
Some toxic effects of tin are found on electroencephalographic examination.
tincture of iodine p.Iodine poisoning.
toadstool p.Mushroom poisoning.
turpentine p.Poisoning usually caused by inhalation of turpentine.
Symptoms include a warm or burning sensation in the esophagus and stomach, followed by cramping, vomiting, and diarrhea. Pulse and respiration become weak, slow, and irregular. Irritation of the urinary tract and CNS resembles alcoholic intoxication.
The airway should be secured and breathing assessed. Other therapies are supportive, e.g., intravenous fluids, oxygen.
p. by unknown substances Poisoning in which there is no information concerning the nature of the poison taken, and in which the signs and symptoms are not recognized as being caused by any particular substance, and for which specific antidotes cannot be given in this situation.
Some agents act in a general manner and may be efficacious. One of these is activated charcoal, which binds most organic toxins. Whole bowel irrigation can be used to flush ingested substances from the GI tract. When dermal exposure is suspected, the patient should be showered to remove chemicals from the skin.
verdigris p.Poisoning from ingestion of verdigris. Symptoms are identical to those caused by ingesting copper sulfate.
SEE: verdigris.
warfarin p.Poisoning from administration of an overdose of warfarin, which causes excessive anticoagulation and resulting in bleeding or an increased risk of bleeding.
Many drugs interact with warfarin. To prevent problems with clotting or bleeding, patients taking anticoagulants should consult with health care professionals before adding or deleting medicines from their drug regimens.The patient is instructed to observe for signs of bleeding such as epistaxis, bleeding gums, hematuria, hematochezia, hemetemesis, melena, and bleeding into the skin (ecchymosis, purpura, or petechia). The importance of regular blood tests (to assess the prothrombin time and international normalized ratio [INR]) and medical follow-up is stressed. Maintaining constant intake levels of foods containing vitamin K also is stressed, as intermittent intake can result in widely varied coagulation levels. The patient should wear or carry a medical identification tag listing the prescribed drug, dosage, and frequency of administration. Patients who have mild to moderately elevated INRs should be treated with vitamin K; patients who have serious bleeding and warfarin poisoning should be treated emergently with infusions of prothrombin complex concentrate, factor IX complex concentrate, and recombinant activated factor VII. If these are not readily available, fresh frozen plasma may be used.
SEE: warfarin.
xylene p.Poisoning from a benzene-like compound.
zinc phosphate p.Poisoning from the rodenticide zinc phosphide, which causes fatal lung and cardiac injury.
There is no specific antidote.