Taber’s Medical Dictionary

Medical Emergencies

Poisons and Poisoning

Substance	Pathology	Symptoms	Emergency Measures	Comments
Acetaminophen	Production of toxic intermediate metabolite that cannot be detoxified due to glutathione depletion.	Phase 1 (0-24 hr): Sometimes asymptomatic—anorexia, nausea, vomiting. Phase 2 (24-48 hr): GI a symptoms resolve; hepatotoxicity is subclinical, but liver function tests and coagulation tests are abnormal. If liver damage is significant, patient may progress to phase 3. Phase 3 (48-96 hr): Problems due to severe hepatic compromise—bleeding disorders, hypoglycemia, hepatic encephalopathy. Phase 4 (>96 hr): Recovery period. Laboratory values return to normal and symptoms resolve.	Administer activated charcoal. Toxicity is unlikely at a dose <140 mg/kg. For significant serum levels of acetaminophen, acetylcysteine can be administered orally in a loading dose followed by a maintenance regimen.	Patients with toxic levels of acetaminophen 4 hr after ingestion require hospitalization for observation and supportive measures. Hepatic failure can occur several days after the ingestion, and renal complications or failure can also develop. Most patients recover fully without further sequelae. In some instances, hepatic failure may require transplantation. Check acetaminophen levels routinely in patients with any oral overdose.
Acids - Acetic Hydrochloric Nitric Phosphoric Sulfuric Any other strong acid	Immediate destruction and necrosis with eschar formation of mucous membranes and tissues on contact.	Burning pain on contact with mucous membranes of the mouth and throat, dysphagia, abdominal pain, nausea, hematemesis, thirst, esophageal or gastric perforation, shock, death.	Establishment of airway patency, aggressive volume resuscitation, radiographic evaluation of damage, irrigation of exposed tissues. Surgical intervention may be required.	Permanent damage to the esophagus and stomach can result in chronic dysphagia and stricture formation.
Alkalis	Irreversible destruction and liquefactive tissue necrosis that penetrates beyond surface contact with alkali.	Immediate burning and blistering of tissue on contact; severe pain of mouth, esophagus, and chest; esophageal or gastric perforation; pancreatitis; hematemesis; shock; death.	Establishment of airway patency, aggressive volume resuscitation, radiographic evaluation of damage, irrigation of exposed tissues. Surgical intervention may be required.	Permanent damage to the esophagus and stomach can result in chronic dysphagia, stricture formation, and necrosis of tissue.
Ammonia and ammonium hydroxide	Tissue destruction due to alkaline injury on contact with mucous membranes. Degree of destruction depends on alkalinity of product and amount and length of exposure.	Burning of mouth and throat, chest pain, esophageal and gastric damage, hematemesis. Inhalation of gas can cause coughing, bronchospasm, and pulmonary edema.	Airway protection if needed, supplemental humidified oxygen and bronchodilators for inhalation exposures, moderate amounts of water or milk to dilute ingestion, analgesics for pain. Additional procedures may be required to assess extent of tissue injury.	Most significant damage is seen with intentional massive ingestions or occupational exposures to concentrated strengths of ammonia. Most accidental exposures to household strength products resolve without residual damage.
Amphetamines and amphetamine-like agents	Excessive stimulation of the CNS a and of peripheral alpha and beta receptor sites.	Excitement, restlessness, tremors, hyperactive reflexes, nausea, vomiting, diarrhea, palpitations, arrhythmias, hypertension, hyperthermia, dehydration, mydriasis, agitation, seizures, coma, death.	Supportive care including airway maintenance and cardiac monitoring; administration of activated charcoal and a cathartic; cooling measures for hyperthermia; benzodiazepines for seizures; vasodilators and beta-adrenergic blockers.	Toxicity can occur with slightly higher than therapeutic doses. Tolerance can readily develop with repeated use.
Antidepressants: selective serotonin reuptake inhibitors (SSRI) Fluoxetine Paroxetine Sertraline Bupropion Fluvoxamine	CNS a depression, excessive stimulation of serotonin receptors.	Serotonin syndrome: hypomania, confusion, myoclonus, diaphoresis, hyperreflexia, tremor, hyperthermia, agitation, restlessness, insomnia, nausea, vomiting, drowsiness, ataxia, seizures, coma.	Maintenance of airway, breathing, and circulation; oral administration of activated charcoal to adsorb ingested drug from the gastrointestinal tract. Cooling measures for febrile patients, e.g., those with serotonin excess.	SSRIs are less likely than tricyclic antidepressants to cause airway compromise, cardiac dysrhythmias, coma, ICU admission, or death. Drugs (such as alcohol or sedatives) that are coingested with SSRIs may pose additional health risks.
Antidepressants: cyclic Amitriptyline Amoxapine Clomipramine Desipramine Doxepin Imipramine Nortriptyline Protriptyline	Toxic cardiovascular and CNS a effects secondary to anticholinergic activity, inhibited reuptake of neurotransmitters, peripheral alpha-adrenergic blockade, alteration of cardiac cells resulting in conduction disturbances.	Confusion, dizziness, altered mental status (lethargy to coma), hypotension, tachycardia, hyperthermia, mydriasis, dry mucous membranes, prolonged QRS complex, cardiac dysrhythmias, seizures.	Cardiac monitoring; assessment of width of QRS complex on the 12-lead ECG; gastric decontamination with activated charcoal; alkalinization of the urine with bicarbonate-containing solutions.	Patients with wide QRS complexes (>0.12s) or cardiac dysrhythmias are monitored in the CCU or ICU.
Antihistamines: sedating (major classes) Alkylamines Ethanolamines Ethylenediamines Phenothiazines Piperazines	Excessive central and peripheral anticholinergic effects.	Lethargy, agitation, confusion, miosis, tachycardia, hyperthermia, decreased GI a motility, hypotension, respiratory depression, ataxia, stupor, seizures, dysrhythmias, coma, circulatory collapse, death.	Maintenance of airway, breathing, circulation, and fluids for hypotension; gastric decontamination by activated charcoal. If patient is sedated, intubate the airway. Give IV physostigmine for anticholinergic toxicity, benzodiazepines for seizures.	Most ingestions are complex to manage because many antihistamines are commercially available in combination with various analgesics and decongestants. With early intervention, most overdoses have excellent outcomes without consequences. a
Arsenic and arsenic salts	Disruption of enzymatic reactions that are essential for cellular metabolism; possible phosphate replacement or interaction with sulfhydryl groups.	Nausea, vomiting, hemorrhagic gastritis, severe watery diarrhea, dehydration, pulmonary edema, hypotension, delirium, encephalopathy, arrhythmias, convulsions, shock, death. Symptoms may have delayed onset.	Support of the patient’s airway and breathing, and aggressive fluid replacement to support the circulation; activated charcoal or gastric lavage for larger ingestions, dimercaprol (BAL) a 3-5 mg/kg IM every 4-6 hr for symptomatic patients.	Toxicity depends on the type of arsenic, amount involved, and route of exposure. Systemic toxicity can result from percutaneous absorption. Arsenic is a carcinogen.
Aspirin SEE: salicylates
Atropine and anticholinergic agents	Acetylcholine blockade at muscarinic receptor sites; affects exocrine glands and cardiac tissue.	Dry mouth and burning pain in throat, thirst, blurred vision, mydriasis, dry, hot, flushed skin, hyperpyrexia, tachycardia, palpitations, restlessness, excitement, confusion, convulsions, delirium; rarely, death.	Airway maintenance and ventilation assistance, gastric lavage, activated charcoal and cathartic, diazepam for sedation and control of convulsions, physostigmine 0.5-1 mg IV for life-threatening atropine toxicity, cooling measures for hyperthermia.	Classes of drugs that possess anticholinergic activity include antihistamines, antipsychotics, antispasmodics, cyclic antidepressants, and skeletal muscle relaxants. Atropine in ophthalmic preparations may be toxic to infants/young children.

Substance	Pathology	Symptoms	Emergency Measures	Comments
Barbiturates Amobarbital Aprobarbital Butabarbital Mephobarbital Methohexital Pentobarbital Phenobarbital Secobarbital Talbutal Thiopental	Depressed neuronal activity of the brain, hypotension caused by depression of central sympathetic tone, inhibition of cardiac contractility.	Drowsiness, confusion, ataxia, vertigo, slurred speech, shallow respiration and pulse, headache, stupor, hypotension, areflexia, cyanosis, hypothermia, cardiovascular collapse, respiratory arrest, death.	Airway maintenance and ventilation assistance, treatment of hypotension, activated charcoal and cathartic, alkalinization of urine to enhance phenobarbital elimination, hemoperfusion for severe toxicity.	Severity of toxicity depends on the agent ingested.
Benzene Xylene Toluene	Irritation of mucous membranes and airway caused by agents and their metabolites, CNS a depression, myocardial effects resulting in conduction disturbances.	Burning sensation of mouth and stomach, nausea, vomiting, chest pain, cough, headache, pneumonitis (if inhaled), vertigo, ataxia, confusion, stupor, ventricular dysrhythmias, convulsions, coma, respiratory failure, death.	Airway maintenance and ventilation assistance, activated charcoal and cathartic, therapy for arrhythmias and seizures. Gastric lavage within 30 min is useful for larger ingestions.	Chronic exposure can result in permanent renal damage, bone marrow suppression, and neuropsychological damage.
Benzodiazepines Alprazolam Chlordiazepoxide Clonazepam Clorazepate Diazepam Estazolam Flurazepam Lorazepam Midazolam Oxazepam Prazepam Quazepam Temazepam Triazolam	Generalized CNS a depressant effects caused by enhanced activity of gamma-aminobutyric acid, an inhibitory neurotransmitter.	Confusion, dizziness, somnolence, ataxia, hypotension, coma, respiratory depression, cardiovascular depression.	Airway maintenance and ventilation assistance, if necessary; administration of activated charcoal. For ingestions by patients with no history of chronic use, flumazenil (a benzodiazapine antagonist) can be administered as a specific antidote. Flumazenil should be avoided in chronic users - it may trigger seizures.	Generally considered safe, even in high doses. Fatalities are rare and usually due to coingestions with other CNS a depressants.
Boric acid and borate salts	Exact mechanism of toxicity unknown.	Headache, nausea, vomiting (vomitus may be blue green), fever, oliguria or anuria, diarrhea, stomach pain, lethargy, restlessness, distinctive erythroderma, tremor, convulsions, renal and hepatic injury or failure, cyanosis, coma, shock with vascular collapse, death.	Airway maintenance and ventilatory assistance. Treat convulsions with benzodiazepines. Activated charcoal is not effective. Hemodialysis may sometimes be needed for large ingestions, e.g., more than 12 g.	Reports of toxicity from boric acid ingestions and exposures has declined in recent years due to decreased use as an irrigant and antiseptic agent.
Botulinum toxin	Potent neurotoxicity produced by Clostridium botulinum; prevents release of acetylcholine by irreversibly binding to cholinergic nerve terminals.	Nausea, vomiting, occasional diarrhea, dysphagia, diplopia, loss of visual acuity and pupillary reflexes, profuse sweating, rapid and weak pulse, death usually caused by respiratory failure. Symptoms may present up to a week after ingestion.	Airway maintenance and ventilatory assistance, as needed. Trivalent botulinum antitoxin may be administered in severe overdoses to bind free toxin, although its use often causes hypersensitivity reactions.	Even with excellent supportive care, recovery may take months to years. Common long-term sequelae include dysgeusia, dry mouth, dyspepsia, constipation, tachycardia, arthralgias, and fatigue. Botulinum antitoxin is available from the local health department.

Substance	Pathology	Symptoms	Emergency Measures	Comments
Cadmium salts or fumes	Diverse multisystemic toxicities that are not clearly understood.	Nausea, vomiting, diarrhea, abdominal cramps, salivation, gastritis, headache, vertigo, exhaustion, collapse, acute renal failure, chemical pneumonitis with pulmonary edema on inhalation, death.	Gastric lavage and catharsis, with chelating agents such as EDTA, may be useful in some acute exposures. Inhalation may require ventilatory support.	Long-term effects vary with duration and severity of exposure. Renal function may be affected. Chronic exposures have resulted in osteomalacia, emphysema, and increased risk of lung or prostate cancer.
Calcium channel blockers Myocardial and vascular effects Bepridil Diltiazem Verapamil Primarily vascular effects Amlodipine Felodipine Isradipine Nicardipine Nifedipine	Prevention of calcium entry into cells, resulting in decreased myocardium contractility, blockade of AV aand SA nodes, and peripheral vasodilation.	Nausea, vomiting, dizziness, headache, confusion, stupor, hyperglycemia, hypotension, bradycardia, metabolic acidosis, cardiac conduction disturbances, seizures, coma, death.	Maintenance of airway, breathing, and circulation; fluids and vasopressors for hypotension; multiple-dose activated charcoal; calcium chloride or calcium gluconate for hypotension and bradydysrhythmias, atropine or isoproterenol for bradycardia.	Intentional overdoses of calcium channel blockers are life threatening and often fatal despite aggressive management.
Camphor	CNS a stimulant with toxic effects; underlying mechanism is not known.	Burning of mouth and throat, nausea, vomiting, headache, CNS a hyperactivity followed by CNS a depression, vertigo, liver function abnormalities, delirium, tremor, convulsions, apnea, coma, death from respiratory arrest secondary to status epilepticus.	Airway maintenance, gastric lavage with copious amounts of fluid, activated charcoal and cathartic, benzodiazepines for seizures.	Fatalities have been reported with 1- or 2-g doses; however, most exposures can be effectively managed and resolved without residual complications.
Carbon monoxide	Hemoglobin binding preventing delivery of oxygen to cells; has significantly greater affinity for hemoglobin than oxygen.	Mild headache, dyspnea with moderate exertion, irritability, fatigue, nausea, vomiting, confusion, ataxia, syncope, convulsions, death from respiratory arrest.	100% oxygen by face mask or endotracheal tube, IV fluids, cardiac monitoring, hyperbaric oxygen for significant exposures.	Residual effects can include dementia, psychosis, paralysis, peripheral neuropathy, and parkinsonism. Consider CO toxicity in persons with significant smoke inhalation burns.
Carbon tetrachloride	Metabolites cause renal and hepatic toxicity; potent CNS a depressant effects.	Nausea, vomiting, abdominal pain, headache, confusion, drowsiness, coma, renal and hepatic failure. Death is caused by respiratory arrest, circulatory collapse, or ventricular fibrillation.	Airway maintenance and ventilation assistance, gastric lavage, activated charcoal and cathartic, acetylcysteine to decrease effects of intermediate metabolite.	Toxicity from inhalation can be severe; small ingestions (<10 ml) can be fatal.
Chlorate salts	Potent oxidative properties that destroy red blood cells; toxicity to kidneys are due to direct effects and hemolysis.	Abdominal pain, nausea, vomiting, diarrhea, methemoglobinemia, intravascular hemolysis, delirium, coagulopathy, coma, convulsions, cyanosis, renal failure, death.	Activated charcoal and methylene blue for mild toxicities, hemodialysis to remove toxin. Sodium thiosulfate IV has been used to inactivate the chlorate ion, with inconsistent results.	In some instances, exchange transfusions have been advocated to reverse effects of poisoning.
Chlorinated compounds Chlorine Chlorine gas Sodium hypochlorite	Corrosive effect on contact with mucous membranes.	Immediate burning of mouth and throat, coughing, choking, bronchospasm, chest and abdominal pain, stridor, pulmonary edema, esophageal burns.	For inhalation, humidified supplemental oxygen and bronchodilators; for dilute ingestions, water or milk; for concentrated ingestions, gastric lavage and endoscopic evaluation.	Esophageal damage can result in stricture formation.
Chlorinated hydrocarbon pesticides Aldrin Chlordane DDT (chlorophenothane) Dieldrin Heptachlor Lindane Thiodan Toxaphene	Direct toxicity to neuronal axons, interfering with transmission; affects myocardium stability resulting in arrhythmias.	Vomiting, headache, fatigue, tremors, ataxia, weakness, confusion, seizures, respiratory depression, arrhythmias, coma. In agents other than DDT, seizure may be first sign of toxicity.	Maintenance of airway, breathing, circulation; activated charcoal and cathartic; lavage for large ingestions; multiple-dose activated charcoal and cholestyramine to enhance removal; appropriate therapy for seizures and arrhythmias.	These agents can be absorbed transdermally and by inhalation. Toxicity and outcomes vary.
Cocaine	CNS a stimulation and inhibition of neuronal uptake of catecholamines, depressed conduction, and myocardial contractility.	Anxiety, agitation, delirium, hypertension, tachycardia, hyperthermia, diaphoresis, tremor, mydriasis, flushing, seizures, ECG a abnormalities, stroke, areflexia, coma, death.	Airway maintenance and ventilatory assistance, cardiac monitoring, activated charcoal for ingestion, benzodiazepines, cooling measures.	Overdose can result from inhalation, injection, or absorption of the drug from the gastrointestinal tract (“body packing”).
Copper salts	Mucous membrane irritation, multisystemic toxicities with salts. Elemental copper is poorly absorbed and causes little toxicity.	Pain in mouth, esophagus, and stomach; abdominal pain; vomiting; gastroenteritis; shock; hepatic and renal injury; hemolysis; seizures; coma; death.	Fluid replacement and pressors, whole-bowel irrigation; dimercaprol and penicillamine for large ingestions.	Long-term copper exposures have resulted in liver fibrosis, cirrhosis, and renal dysfunction.
Cyanide	Nonspecific inhibition of enzyme systems; binds to cytochrome oxidase of cells, blocking oxygen use.	Nausea, vomiting, abdominal pain, almond odor of breath, headache, dyspnea, agitation, confusion, syncope, convulsions, lethargy, coma, cardiovascular collapse, death. Onset of symptoms is abrupt.	Oxygen and assisted ventilation, if needed; gastric lavage, activated charcoal, and cathartic; inhalation of amyl nitrite pearls until antidote is available. Antidote kit contains amyl and sodium nitrites and sodium thiosulfate. The administration of vitamin B 12 may be helpful.	Oxygen and assisted ventilation, if needed; activated charcoal by mouth. Antidotes include a vitamin B12 analogue, hydroxocobalamin.
a AV = atrioventricular; BAL = British anti-lewisite; CNS = central nervous system; ECG = electrocardiogram; EDTA = ethylenediamenetetra-acetic acid; GI = gastrointestinal; NMS = neuroleptic malignant syndrome; PT = prothrombin time; SA = sinoatrial.

Substance	Pathology	Symptoms	Emergency Measures	Comments
Digoxin and digitalis	Excessive excitability and automaticity of myocardium resulting in conduction disturbances and dysrhythmias; AV a block.	Anorexia, nausea, vomiting, diarrhea, headache, fatigue, weakness, drowsiness, electrolyte disturbances, confusion, delirium, visual disturbances, dysrhythmias, bradycardia, AV a block, death from ventricular fibrillation.	Cardiac monitoring, activated charcoal, digoxin-specific antibody fragments (Fab) for severe toxicity, lidocaine or phenytoin for ventricular irritability. Correct electrolyte abnormalities, such as hypokalemia, immediately.	Most poisonings result from ingestion of prescribed digoxin, esp. in patients with renal failure, hypokalemia, or advanced age.
Dinitrophenol and pentachlorophenol	Uncoupling of oxidative phosphorylation in mitochondria, hypermetabolic state and lactic acid production. Dinitrophenol oxidizes hemoglobin to methemoglobin.	Fatigue, thirst, nausea, vomiting, abdominal pain, sweating, flushing, restlessness, excitement, hyperthermia, tachycardia, hyperpnea, metabolic acidosis, cyanosis, seizures, coma, death from respiratory or circulatory failure.	Maintenance of airway, breathing, circulation; activated charcoal by mouth; methylene blue IV; fluid replacement; benzodiazepines; cooling measures.	Ingestion of 1-3 g of these agents can be lethal. Many accidental transdermal poisonings have been reported.

Substance	Pathology	Symptoms	Emergency Measures	Comments
Ergotamines or ergot alkaloids	Central sympatholytic effects: serotonin release and interference with neuronal uptake. Peripherally, may act as a partial alpha-adrenergic agonist or an antagonist at adrenergic, dopaminergic, and tryptaminergic receptors.	Nausea, vomiting, dizziness, diarrhea, headache, thirst, weak pulse, tingling and numbness of extremities, dyspnea, hallucinations, blood pressure changes, hemorrhagic vesiculations, paresthesias, peripheral ischemia, convulsions, loss of consciousness, gangrene.	Protect the airway, and provide ventilatory assistance as needed. Give multiple doses of activated charcoal to enhance drug elimination. Provide benzodiazepines to control seizures. Use nitroglycerin, heparin, or thrombolytics for organ ischemia.	Outcome is based on route and amount of ingestion.
Ethanol	CNS a depression; effects can be additive when combined with other CNS a depressants.	Impaired motor coordination, slurred speech, inebriation, ataxia, peripheral vasodilation, rapid pulse, nausea, vomiting, drowsiness, stupor, coma, peripheral vascular collapse, hypotension, tachycardia, hypothermia, death from respiratory or circulatory failure.	Provide intravenous fluids, esp. with dextrose, to prevent hypoglycemia. Give parenteral thiamine. Provide other supportive measures, including airway control and ventilation, external warming, and prophylaxis against alcohol withdrawal symptoms as indicated.	Ethanol is often coingested with other toxic substances in suicide attempts; emergency treatment may vary depending on other substances ingested.
Ethylene glycol	Metabolism to oxalic, glyoxylic, and glycolic acids; conversion to lactate, increasing the lactic acid level; calcium oxalate crystal formation and deposition in tissues; metabolite toxicity to kidneys, CNS, aand lungs.	Nausea, vomiting, excitability, hypotension, abdominal cramps, weakness, metabolic acidosis, ataxia, vertigo, arrhythmias, stupor, coma, death from respiratory or renal failure with uremia.	Maintain airway, breathing, and circulation. Provide ethanol, folic acid, 4-methylpyrazole, pyridoxine, and thiamine. Hemodialysis will remove ethylene glycol from the blood in cases of severe toxicity.	Outcomes vary; in general, comatose patients have a poor prognosis.

Substance	Pathology	Symptoms	Emergency Measures	Comments
Fluoride salts	Direct metabolic and cytotoxic effects; multiple adverse effects from calcium and magnesium binding.	Salivation, thirst, nausea, abdominal pain, vomiting, diarrhea, muscle weakness, hypocalcemia, hyperkalemia, tetanic contractions, death due to vascular collapse and shock.	Maintenance of airway, breathing, circulation; cardiac monitoring; calcium salts; for severe toxicity, IV calcium chloride; therapy for electrolyte disturbances.	Degree of toxicity depends on salt solubility and the amount of elemental fluoride ingested. Pediatric toxicities are often caused by fluorinated toothpaste ingestions.

Substance	Pathology	Symptoms	Emergency Measures	Comments
Hydrogen sulfide gas	Inhibition of oxidative phosphorylation enzymes, potent inhibition of cytochrome oxidase. Exposure results in cellular hypoxia.	Irritated mucous membranes, conjunctivitis, headache, nausea, vomiting, weakness, bradycardia, hypotension, dyspnea, rapid loss of consciousness with larger exposure, pulmonary edema, cyanosis, convulsions, coma, death due to cardiac or respiratory arrest.	High-flow oxygen, advanced cardiac life support as indicated, sodium nitrite, blood pressure monitoring, hyperbaric oxygen if available. Methemoglobin level should be recorded 30 min after sodium nitrate infusion.	If patient is immediately removed from the exposure, recovery may be rapid and complete. More severe exposures have resulted in permanent neurological changes and myocardial ischemia.

Substance	Pathology	Symptoms	Emergency Measures	Comments
Ipecac syrup or fluid extract	Cardiac and neuromuscular toxicity with systemic absorption; toxicities are seen with chronic and prolonged use.	Vomiting, diarrhea, lethargy, irritability, hypothermia, hypotonia, dehydration, gastritis, seizures, cardiac toxicity, neuromuscular toxicity, shock, death.	Activated charcoal may be given if the patient is not vomiting. Supportive care includes fluid replacement, correction of electrolyte abnormalities, cardiac monitoring, and therapy for dysrhythmias.	Chronic exposures are reported in patients with eating disorders; cases of toxicity secondary to Munchausen syndrome by proxy have also been documented.
Iron salts	Several mechanisms: direct corrosive effects on GI a mucosa, hepatocellular toxicity, cardiovascular compromise, metabolic acidosis. Neurological manifestations are caused by hypoperfusion, metabolic acidosis, and hepatic compromise.	Nausea, vomiting, severe gastroenteritis, hematemesis, diarrhea, tachypnea, tachycardia, hypotension, lethargy, cyanosis, convulsions, coma, shock, or death.	Use gastric lavage or whole-bowel irrigation to remove tablets from the gastrointestinal tract. Intravenous deferoxamine is used as an iron-chelating agent.	Patients with systemic complications require hospital admission, constant monitoring, and supportive care until resolution. Late complications (2-8 wk) include GI a stricture and obstruction. Toxicity is unlikely at a dose <20 mg/kg.
Isopropanol Isopropyl alcohol Rubbing alcohol	Potent CNS a depressant metabolized to acetone; may contribute to CNS a depression.	Nausea, vomiting, abdominal pain, hypotension, ataxia, areflexia, inebriation, muscle weakness, ketonemia, ketonuria, respiratory depression, hemorrhagic tracheobronchitis, myocardial depression, coma, death.	Maintain airway and provide ventilatory support when neurological depression is present. Do not induce emesis. Irrigate the GI tract after recent ingestions. Use hemodialysis for near-fatal overdoses.	A majority of cases resolve without consequences.

Substance	Pathology	Symptoms	Emergency Measures	Comments
Lead and lead salts	Heavy metal interaction with sulfhydryl groups and interference with action of numerous enzymes, interference with heme production and survival of red blood cells. Chronic exposure can cause irreversible CNS a and developmental effects.	Abdominal pain, vomiting, lethargy, behavioral changes, ataxia, arthralgias, abdominal or renal colic, anemia, acute encephalopathy, seizures, coma, death.	Use whole-bowel irrigation to empty the GI tract shortly after oral ingestions. Chelating agents that remove lead from the blood include Calcium Disodium Versenate, dimercaprol and related compounds, and d-penicillamine. Seizures are treated with benzodiazepines.	Chronic exposure to lead can produce renal and neuropsychiatric effects, esp. in children. Blood lead levels and erythrocyte protoporphyrin levels are used to gauge the effect of treatment.
Lithium	Lithium often produces cellular disturbances in the central nervous system, kidneys, and gastrointestinal tract. This is probably due to its effects on cell membrane ion transport, as well as its effects on cAMP.	Nausea, vomiting, diarrhea, fine resting tremor, lethargy, confusion, tremors, ataxia, ECG a abnormalities, profound weakness, muscle fasciculations, hyperreflexia, clonus, stupor, seizures, acute renal failure, coma, death.	Maintain the airway and provide assisted ventilation to patients who are comatose or difficult to arouse. For acute ingestions use gastric lavage or whole bowel irrigation. Activated charcoal is ineffective because it does not bind to metals. Hemodialysis is used to clear lithium from the body in life-threatening intoxications.	Chronic or acute-on-chronic overdoses are more life threatening than acute poisonings. Chronic exposure permits intracellular accumulation. In acute poisonings, most lithium remains in the extracellular fluid for many hours, causing toxicity.
Mercuric salts	Reaction with carboxyl, sulfhydryl, phosphoryl, and amide groups; interference with enzyme and cellular functions; toxicity involving multiple organ systems.	Burning of mouth and throat, thirst, abdominal pain, nausea, corrosive gastroenteritis, hematemesis, diarrhea, dehydration, shock, acute tubular necrosis. Neurological symptoms such as tremor, irritability and other personality changes, and depression are common.	The patient should be treated with oxygen and the gastrointestinal tract decontaminated, e.g., with whole-bowel irrigation). Chelating agents such as dimercaprol, dimercaptosuccinic acid, or d-penicillamine, should be given to bind and remove mercury from the body.	Doses of 1-4 g of mercuric chloride can be fatal. Chronic poisonings have resulted in neurological abnormalities, renal dysfunction, and gastrointestinal symptoms.
Methanol	Metabolism to formaldehyde and formic acid.	Latent period (24-72 hr) before development of symptoms, dizziness, inebriation, blurred vision, headache, nausea, vomiting, abdominal pain, delirium, visual disturbances that may progress to blindness, weak and rapid pulse, shallow respirations, cyanosis, coma, metabolic acidosis, respiratory failure, death.	Activated charcoal for recent ingestion, ethanol IV or orally to inhibit toxic metabolites, hemodialysis in severe cases, aggressive management of metabolic acidosis. Folic acid and 4-methylpyrazole can be used as antidotes.	Visual impairment, optic atrophy, and blindness are due to effects of formic acid on the optic nerve.
Mushrooms containing cyclopeptides Amanita phalloides (death cap) Amanita tennifolia Amanita virosa (destroying angels) Galerina autumnalis Galerina marginata Galerina venenata Lepiota helveola Lepiota josserandii	Cytotoxicity of cyclopeptides (phallotoxins, amatoxins, virotoxins), cellular insult causing hepatic, renal, GI a , and CNS a damage.	Phase 1 (6-12 hr): Nausea, abdominal pain, vomiting, watery diarrhea, thirst. Phase 2 (12-24 hr): Symptomatic improvement, elevated hepatic enzymes. Phase 3 (1-6 days): Restlessness, delirium, hallucinations, hematuria, gastroenteritis, pancreatitis, hypoglycemia, shock, acute renal failure, jaundice, hepatic coma, death.	Activated charcoal; fluid and electrolyte resuscitation; hepatic transplantation in fulminant hepatic failure.	Cyclopeptide-containing mushrooms are responsible for most mushroom fatalities in North America. Toxic cyclopeptides are heat stable, insoluble in water, and not affected by drying.
Mushrooms containing muscarine Amanita muscaria (fly agaric) Amanita panterina (panther) Clitocybe dealbata (sweater) Clitocybe dilatata Clitocybe illudens Most Inocybe species	Peripheral cholinergic effect due to muscarine; stimulation of autonomic nervous system.	Lacrimation, diaphoresis, salivation, abdominal cramps, vomiting, loss of bowel and bladder control	Gastric decontamination with activated charcoal may adsorb recently ingested mushroom toxins from the GI tract. Patients with fulminant hepatic failure will need intensive care and possible referral for liver transplantation.	Identification of ingested mushroom may help guide therapy if uneaten mushroom samples are available for analysis. Patients afflicted with fulminant liver failure have a high risk of death if a donor liver is not available.

Substance	Pathology	Symptoms	Emergency Measures	Comments
Naphthalene	Metabolism to numerous by-products including alpha-napthol, a potent hemolytic agent.	Fever, nausea, vomiting, abdominal pain, diarrhea, lethargy, seizures, hemolysis, pallor, jaundice, cyanosis.	Activated charcoal; IV hydration and urinary alkalinization; transfusions for hemolysis.	Hemolysis is acute and severe in patients with glucose-6-phosphate dehydrogenase deficiency. Naphthalene is used in mothballs and toilet bowl cleaners, but less toxic agents are available.
Nicotine	Binding to cholinergic nicotine receptors; toxicity due to sympathetic and parasympathetic stimulation followed by ganglionic and neuromuscular blockade.	Nausea, vomiting, abdominal pain, headache, salivation, diarrhea, hyperpnea, diaphoresis, tachycardia, hypertension, pallor, agitation, tremor, ataxia, confusion, dysrhythmias, hypotension, shock, muscle paralysis, coma, death.	Maintenance of airway, breathing, circulation; activated charcoal; thorough washing of exposed skin; therapy for seizures, hypertension, hypotension, and arrhythmias.	Because most commercial sources of nicotine are not concentrated, a majority of exposures cause mild toxicity and resolve without complications.
Nitroglycerines, nitrates, nitrites	Vasodilation causing hypotension. Nitrites are potent oxidizing agents that cause methemoglobinemia.	Headache, hypotension, syncope, skin flushing, nausea, methemoglobinemia, cyanosis, symptoms of cardiac ischemia or cerebrovascular disease, seizures secondary to hypotension.	Activated charcoal; administration of intravenous fluids, anticonvulsant medication, hemodialysis, or therapies for GI bleeding (if needed).	Most cases can be managed successfully with early, aggressive interventions. Drugs for erectile dysfunction should not be taken by patients being treated with nitrates.
Nonsteroidal anti-inflammatory agents Ibuprofen Ketoprofen Naproxen and many others	Inhibition of prostacyclin and prostaglandin E2 production resulting in acute renal failure.	Nausea, vomiting, gastrointestinal distress and bleeding, tinnitus, metabolic acidosis, CNS a depression, respiratory depression, mild hepatic toxicity, acute renal failure, seizures.	Activated charcoal for recent ingestions; intravenous fluids: administration of gastric protectants, e.g., proton pump inhibitors or H2 receptor antagonists.	Baseline renal and hepatic function should be assessed. Most toxic exposures to this class of agents are successfully treated and resolve fully without residual sequelae.

Substance	Pathology	Symptoms	Emergency Measures	Comments
Opioids and Opiates Codeine Dilaudid Fentanyl Heroin Morphine Methadone Oxycodone Oxycontin and other synthetic opioids	Excessive stimulation of CNS a opiate receptors causing sedation and respiratory failure.	Drowsiness, nausea, dysphoria, bradypnea, miosis, hypothermia, respiratory depression, hypotension, bradycardia, weak pulse, coma, apnea, death.	The airway should be secured and ventilatory assistance provided to comatose or apneic patients. Naloxone, naltrexone, or nalmefene can be given as an antidote. Activated charcoal may adsorb recently ingested pills.	Antidotes are useful in reversing effects of the opiates, but administration may precipitate severe withdrawal symptoms. The effects of naloxone are short-term. The drug may need to be given repeatedly or by intravenous infusion to prevent repeated episodes of respiratory depression or coma.
Oxalic acid and oxalate salts	Corrosion of tissues on contact; precipitation with calcium to form insoluble deposits throughout organs, causing systemic damage.	Irrigation of mouth and esophagus, vomiting, weakness, shock, tetany, convulsions, cardiac arrest, death. Inhalation can cause pneumonitis and pulmonary edema.	Calcium chloride, calcium gluconate, or calcium carbonate to precipitate oxalate; flushing and lavage with copious amounts of water; IV calcium chloride or calcium gluconate for symptomatic hypocalcemia; maintenance of high urine output; therapy for seizures and arrhythmias.	Ingestions of 5-15 g of oxalic acid have resulted in death.

Substance	Pathology	Symptoms	Emergency Measures	Comments
Parathion and other organophosphates	Acetylcholinesterase inhibition, resulting in excessive acetylcholine stimulation of muscarinic and nicotinic receptors.	Nausea, vomiting, diarrhea, abdominal pain, tremor, muscle fasciculations, excessive salivation and sweating, dehydration, bradycardia, weakness, shock, death usually caused by respiratory paralysis.	Maintain airway and clear secretions. Provide assistance with ventilation. Decontaminate exposed skin and remove soaked clothing. Decontaminate the GI tract. Use atropine and/or pralidoxime for anticholinergic crises. Give diazepam or related drugs for seizures, and standard antiarrhythmic protocols for ventricular rhythm disturbances.	Toxicity depends on the relative toxicity of the organophosphate and the quantity involved.
Phenol	Corrosive injury to skin, eyes, and respiratory tract; protein denaturation and coagulation necrosis.	Vomiting, diarrhea, gastrointestinal injury, agitation, confusion, seizures, hypotension, shock, coma, respiratory failure, death.	Multiple-dose activated charcoal and cathartic; washing of exposed areas; benzodiazepines for seizures. Low molecular weight polyethylene glycol has been used for gastric decontamination and topical exposures. If corrosion has occurred, tube passage may cause rupture.	Corrosive burns of the skin and mucous membranes and GI a perforation can occur. Esophageal stricture and renal failure rarely occur.
Phenothiazines and neuroleptics	Prominent cardiovascular and CNS a effects; toxicity due to inhibitory effects of dopaminergic, cholinergic, alpha-adrenergic, histaminic, and serotonergic receptors.	Sedation, somnolence, stupor, dry mouth, tachycardia, labile blood pressure, hypothermia or hyperthermia, dysrhythmias, extrapyramidal symptoms, coma, NMS, aseizures, cardiac arrest, death, akathisias.	Maintain airway and provide ventilatory and circulatory support if necessary. Decontaminate the GI tract. Follow standard ACLS protocols for managing cardiac rhythm disturbances. Give diphenhydramine or benztropine for dystonias. Bromocriptine, benzodiazepines, and/or dantrolene may be helpful in NMS. a	Although death from neuroleptic overdose is rare, NMS may be fatal in 20% or more of affected patients.
Phosphorus and phosphides	Local irritation and tissue burns; direct toxic effect to myocardium and vessels; hepatic, renal, and GI a damage due to latent systemic toxicity.	Painful burns to mucous membranes and skin on contact, nausea, vomitus and diarrhea with garlicky odor, jaundice, metabolic derangements, dysrhythmias, coma, shock, seizures, hepatic or renal failure, cardiac arrest. Inhalation can cause pneumonitis and pulmonary edema.	Maintenance of airway, breathing, circulation; endoscopy to assess GI a burns; cautious gastric lavage with hydrogen peroxide or potassium permanganate, followed by activated charcoal and mineral oil cathartic; fluid replacement and correction of electrolyte imbalance.	After acute effects from ingestion, a symptom-free period of a few weeks may be followed by a stage of systemic toxicity involving the liver, kidneys, heart, CNS, a and GI atract.

Substance	Pathology	Symptoms	Emergency Measures	Comments
Salicylates Aspirin Salicylate salts	Effect on multiple organ systems, uncoupling of oxidative phosphorylation, and interference with the Krebs cycle. Effects are due to stimulation of respiratory center, intracellular uncoupling of oxidative phosphorylation, and alteration of platelet function.	Nausea, vomiting, agitation, hyperthermia, lethargy, hyperglycemia or hypoglycemia, hyperpnea, tachypnea, tinnitus, hemorrhagic gastritis, delirium, stupor, acid-base disturbances, electrolyte imbalance, cerebral edema, convulsions, cardiovascular collapse.	Maintenance of airway, breathing, circulation; lavage; activated charcoal; urinary alkalinization; correction of acid-base and fluid-electrolyte abnormalities; hemodialysis for severe toxicity or deteriorating condition.	The prognosis of patients suffering from an acute toxic ingestion can be assessed on the basis of serum levels obtained within 6 hr of ingestion.
Strychnine	Competitive antagonism of glycine at postsynaptic spinal cord motor neuron.	Muscle twitching, extensor spasm, opisthotonos, trismus or facial grimacing, seizures, medullary paralysis, death. Symptoms occur within 20 min.	Activated charcoal; dark and quiet environment; benzodiazepines or neuromuscular blockade; mechanical ventilation.	Poisonings are rare since commercial use in rodenticides has decreased. Most exposures result in death. The approximate fatal dose for a child is 15 mg; for an adult, 5-10 mg/kg.

Substance	Pathology	Symptoms	Emergency Measures	Comments
Thallium salts	Combination with mitochondrial sulfhydryl groups, interference with oxidative phosphorylation.	Nausea, vomiting, abdominal pain, hematemesis, bloody diarrhea, headache, alopecia, hematuria, proteinuria, elevated hepatic enzymes, lethargy, tremors, ataxia, delirium, seizures, coma, death.	Activated charcoal; fluids and electrolytes intravenously; benzodiazepines for seizures. Hemoperfusion and hemodialysis may be moderately successful.	Alopecia and Mee’s sign, single white transverse lines on the nails 2-3 weeks postexposure, are common diagnostic features. Long-term neurological impairment can occur.
Theophylline SEE: xanthine derivatives

Substance	Pathology	Symptoms	Emergency Measures	Comments
Xanthine derivatives Aminophylline Caffeine Theophylline	Antagonism of adenosine activity and release of catecholamines; in high doses, phosphodiesterase inhibition. Toxic effects are secondary to smooth muscle relaxation, peripheral vasodilation, myocardial stimulation, and CNS a excitation.	Nausea, protracted vomiting, hypotension, respiratory alkalosis, metabolic acidosis, hypokalemia, tachycardia, hypercalcemia, ventricular dysrhythmias, seizures, death due to cardiovascular collapse.	Activated charcoal. For deteriorating conditions, charcoal hemoperfusion. Treat seizures with benzodiazepines or barbiturates, and cardiac rhythm disturbances with standard ACLS protocols. Monitor theophylline levels several times a day.	Eliminate drugs that increase theophylline levels, such as erythromycins or related antibiotics, cimetidine, estrogens, or allopurinol. Consider the use of safer drugs, such as levalbuterol or other inhaled medications.
Warfarin and related anticoagulant compounds	Inhibition of vitamin K 2,3-epoxide reductase and quinone reductase activity (these are necessary to activate vitamin K, which is essential in coagulation).	Fatigue, hematuria, nosebleeds, ecchymoses, GI a hemorrhage, hypotension, intracranial hemorrhage, hemorrhagic shock, death (rare).	Decontaminate the GI tract (for recent ingestions only). Hold warfarin if the protime is slightly elevated and no bleeding is present. Give vitamin K for markedly prolonged protimes with INR greater than 6-9 or fresh frozen plasma for life-threatening bleeding.	Most accidental ingestions resolve without further sequelae. Intentional ingestions or delay in seeking treatment may result in severe coagulopathy. Bleeding patients require hospitalization, frequent monitoring of blood pressure, pulse, hemoglobin levels and the prothrombin time/INR. Cauterization of bleeding lesions may be needed.

Emergency Situations

Medical Emergency	Underlying Causes	Findings	Treatment
Acute myocardial infarction (MI, AMI) Acute coronary syndromes (ACS)	Most heart attacks are caused by the rupture of a plaque in the wall of the coronary artery that results in the blockage of blood flow and the death of myocardial tissue. Risk factors often present include tobacco use, hypertension, hypercholesterolemia, diabetes mellitus, obesity, physical inactivity, or family history of heart disease. Men and postmenopausal women are at greater risk than premenopausal women. Modification of risk factors lowers the risk for disease.	Patients often complain of tightness, heaviness, pressure, pain, or burning in the chest. The symptoms may radiate into the neck, jaw, shoulders, back, or arms. Shortness of breath, nausea and vomiting, or sweating often accompany the chest pain or pressure. Some patients (esp. older individuals, women, or diabetics) may report difficulty breathing, nausea and vomiting, or loss of consciousness as their only symptoms. A 12-lead ECG may show evidence of an MI, although a large percentage of patients may have a nondiagnostic ECG initially. Abnormal levels of cardiac enzymes, e.g., troponins, creatinine kinase, usually appear in the blood about 8 hr after chest pain begins.	Supplemental oxygen, aspirin, other antiplatelet drugs, anticoagulants, beta blockers, and narcotics like morphine should be used acutely to alleviate pain, improve oxygenation and blood flow, and reduce stress. Cardiac monitoring, oximetry, and automatic blood pressure monitors are used to identify changes in heart rhythm, hemodynamics, and breathing. A 12-lead ECG should be completed within 10 min of the patient’s presentation to the hospital, and preferably while the patient is in transit to the hospital. If an ST segment elevation MI is identified, patients should be triaged to percutaneous coronary intervention (PCI) in the first 90 min or, if PCI is not available, to fibrinolytic therapy within 30 min (unless contraindicated). Other treatments depend on the presentation, e.g., the patient in shock may be treated with pressors; a patient with acute pulmonary edema may need diuretics, etc. Nonsteroidal anti-inflammatory drugs (esp. those that are COX-2 selective) should be discontinued. The patient in full cardiac arrest is treated with advanced life support protocols.
Airway obstruction	Complete or partial obstruction of the oropharynx or nasopharynx, larynx, or trachea, with impairment of gas exchange, caused by foreign bodies, anatomical abnormalities, allergic reactions, infection, or trauma.	Signs of respiratory distress, including a rapid respiratory rate, wheezing, stridor, or labored breath are usually present. The patient usually appears agitated. Cyanosis of the fingers or lips may be present when there is inadequate oxygen in the blood. Loss of consciousness may occur if airway obstruction is not effectively relieved.	Foreign body airway obstruction is treated using the Heimlich maneuver in adults and back blows and chest thrusts in infants and children. Endotracheal intubation or cricothyroidotomy, along with mechanical ventilation, may be lifesaving interventions.
Angina pectoris	Inadequate supply of oxygen to the myocardium when oxygen demand exceeds supply. Unstable angina, marked by more frequent attacks, pain with less exertion or at rest, reduced response to nitroglycerin, or more severe episodes may indicate a progression in the patient’s coronary artery disease and a higher risk for MI. Stable angina is discomfort typical of the patient’s usual pattern.	Similar to MI. Chest discomfort typically resolves in less than 15 min, and improves with nitroglycerin and rest. There may be evidence of ischemia on a 12-lead ECG. Cardiac enzymes usually do not show evidence of acute MI on initial testing.	Oxygen, nitroglycerin, and aspirin are given initially, and the patient’s response is noted. Beta blockers, to slow heart rate and lower blood pressure, are used unless there is evidence of heart block, heart failure, or active wheezing. Morphine is used for refractory pain and breathlessness. Heparins are used for pain that does not resolve with initial treatments. Persistent symptoms, ECG changes, or elevated cardiac enzymes suggest an acute coronary syndrome and may require further treatments (see above under Acute Myocardial Infarction). The patient with new or unstable angina is usually admitted to the hospital for further studies and stabilization.
Arterial bleeding	Trauma to blood vessels; surgery; erosion of arteries by ulcers, infection, or cancer.	Blood that spurts out in pulsatile fashion from a vessel is characteristic of bleeding from an artery. (Blood that oozes from a vessel continuously is characteristic of bleeding from a vein.)	Arterial bleeding from a vessel in an arm or leg can often be controlled with pressure applied directly over the bleeding vessel or just proximal to it. Arterial ligation may be performed surgically if direct pressure does not limit blood loss. Arterial bleeding from peptic ulcers is typically controlled with the injection of sclerosing agents during endoscopy or with electrocoagulation or coaption. Bleeding from other internal vessels may also be controlled endoscopically, e.g., bleeding from bronchial arteries during bronchoscopy. In some instances, blood flow through internal arteries can be stopped with therapeutic embolization.
Asthma	Episodic bronchospasm, caused by exposure to allergens (such as pollens), smoke, pollutants, cold air, exercise, or other triggers of airway inflammation.	Difficulty breathing, wheezing, and chest tightness. Patients are often able to identify the triggering event. They may report that their inhalers are not providing adequate relief. Physical findings include tachypnea, tachycardia, and labored breathing, often with a prolonged expiratory phase and wheezing. Cyanosis of the fingers or the lips suggests inadequate oxygenation. Patients may be agitated, frightened, or, in severe attacks, lethargic or comatose.	Supplemental oxygen should be supplied, and the patient should be given inhaled bronchodilators, e.g. beta-2-agonists, such as albuterol. Oral or intravenous steroids are used to reduce airway inflammation. Epinephrine may be injected subcutaneously in severe asthma; antibiotics are used when there is evidence or suspicion of a bacterial infection. Helium-oxygen mixtures may be given for the patient to inhale. Severe asthma may result in respiratory failure and the need for ventilatory support, e.g., noninvasive ventilation or tracheal intubation.

Medical Emergency	Underlying Causes	Findings	Treatment
Chronic Obstructive Pulmonary Disease (COPD), exacerbation of	An acute or gradual worsening of pulmonary function in patients with chronic lung disease, typically brought on by a viral or bacterial infection, or by congestive heart failure, allergies, pulmonary emboli, or the rupture of an emphysematous bleb at the margins of the lung.	Patients typically report increased shortness of breath, cough, sputum production, and fevers, and appear to labor more than usual to breathe. Tachypnea, tachycardia, and hypoxemia or carbon dioxide retention are often present. Breath sounds may be distant, or wheezing may be present.	Oxygen is supplied, and the patient is carefully monitored clinically. Continuous oximetry should be used, and arterial blood gases checked when there is clinical suspicion of impending respiratory failure. Bronchodilators (such as albuterol and ipratropium) are given by inhalation. Corticosteroids are used to reduce airway inflammation. Antibiotics are used when there is evidence or suspicion of a bacterial infection. Severe exacerbations may result in respiratory failure and the need for ventilatory support, e.g., noninvasive ventilation or tracheal intubation.
Cold-induced soft tissue injury (frostnip, chilblain, frostbite)	Frostnip: superficial, reversible injury caused by ice crystal formation on the surface of the skin. Chilblain: superficial injury caused by exposure to cold, humid air. Tissue does not freeze. Frostbite: destruction of tissue by freezing. The extent of tissue loss reflects the duration of cold exposure and the magnitude of temperature depression.	Frostnip: usually, paresthesias, pain, and numbness. Chilblain: redness, itching, numbness, burning, and pain. Frostbite: similar to chilblain. Frostbitten skin may be waxy and white or mottled and cyanotic. The frozen part will have no sensation. Surrounding tissue may be painful and tender. As the tissue thaws its appearance changes. In partial-thickness frostbite the skin becomes red and warm. Blisters containing clear fluid may appear. In full-thickness frostbite the blisters contain a bloody fluid. There is no sensation in full-thickness frostbite.	Initial treatment involves removing the patient from the cold environment. Concomitant hypothermia is a hazard. The frozen parts should not be rewarmed if there is danger of refreezing. Rapid rewarming should be performed by soaking the injured part in warm water (42°C). Rubbing or other manipulation of frozen tissue may worsen the injury. Further treatment may be needed for more serious injuries.
Congestive heart failure (CHF)	An impairment in the ability of the heart to move blood into the systemic circulation, either because of damage to heart muscle, e.g., after a heart attack, failure of the heart muscle to relax properly, pericardial restriction, valvular heart disease, or other causes.	Most patients are winded with exertion, and some are short of breath at rest. Many cannot lie flat in bed at night because the supine position makes them breathless. Lower extremity and sacral swelling are common physical findings, along with ascites, liver enlargement, and elevated jugular veins. Crackles or wheezes may be heard in the lung bases or throughout the lungs in left ventricular CHF. The patient is often hypoxemic. Chest x-rays may show an enlarged heart with fluffy infiltrates near the hila.	Oxygen, potent diuretics, morphine sulfate, nitroglycerin, nesiritide, and ACE inhibitors may be used to manage CHF or acute pulmonary edema as long as the patient is not hypotensive. Noninvasive positive pressure ventilation, or intubation and mechanical ventilation may be needed to support respiration. Hypotensive patients may be treated with dobutamine, combinations of dopamine and nitroprusside, or other drugs and interventions.

Medical Emergency	Underlying Causes	Findings	Treatment
Fractures and Dislocations	Most fractures and dislocations are caused by significant trauma, e.g., automobile collisions, falls, or sports injuries. Fractures that occur without a powerful mechanism of injury are termed “pathological.” They may occur in patients with underlying malignancies that have spread to bone or in patients with osteoporosis.	Limb fractures or joint dislocations are often clinically obvious. The affected limbs are usually swollen, visibly deformed or rotated, and exquisitely painful to gentle touch or any movement. Patients with rib fractures may complain of pain on breathing or coughing. The injured chest wall is tender and may be bruised. Patients with fractures of the vertebral bodies (or patients suspected of having vertebral fractures) often complain of neck, thoracic, or lumbar pain after a fall or automobile accident. X-rays of the affected bones confirm the diagnosis.	Primary treatment includes immobilization (splinting) of any affected bones or joints until diagnostic x-rays can be obtained. Analgesics are given as required, and cold packs or ice are applied to limit pain and inflammation. Limb fractures or dislocations are sometimes amenable to immediate treatment with closed reduction, although operative reductions and placement of fasteners may be needed to obtain optimal healing. Patients suspected of having vertebral fractures should be placed in firm cervical collars or restrained on spinal boards until examination and x-rays clearly demonstrate that the spine is stable.

Medical Emergency	Underlying Causes	Findings	Treatment
Gastrointestinal (GI) bleeding	Upper gastrointestinal bleeding often results from esophagitis, esophageal tears, gastritis, peptic ulcer disease, esophageal varices, or vascular malformations. Lower GI bleeding typically is caused by hemorrhoids, anal fissures, diverticula, vascular malformations, or cancers.	The rapidly bleeding patient may present in shock, i.e., dizzy on arising, hypotensive, tachycardic, cool, clammy, diaphoretic, and confused. Bleeding from the upper GI tract often reveals itself when the patient vomits bright red blood or digested blood that resembles coffee grounds. Occasionally, bleeding from the upper tract is so vigorous that it causes the loss of bright red blood from the rectum. Usually, however, this is a finding in lower GI bleeding. Digested blood that is expelled in the feces is typically black and tarry (melenic).	Patients with significant blood loss are treated immediately with intravenous fluids. Blood is obtained for typing and cross-matching, and transfusions are given when indicated. Upper GI bleeding resulting from peptic ulcer disease, esophagitis, or gastritis may respond to treatment with IV or oral proton pump inhibitors. The loss of bright red blood from the upper GI tract should be promptly evaluated with esophagogastroduodenoscopy (EGD). Patients with a bleeding ulcer vessel or esophageal varices may be treated with endoscopic therapies to cauterize or band bleeding vessels or with medical therapies including agents such as octreotide. Patients suspected of having lower GI blood loss are evaluated with colonoscopy, e.g., to identify arteriovenous malformations, cancers, diverticula, or ulcerative colitis.

Medical Emergency	Underlying Causes	Findings	Treatment
Hyperglycemia	Elevated blood glucose levels are usually caused by impairments in glucose metabolism (type 1 or type 2 diabetes mellitus, gestational diabetes mellitus, or drugs or infections that temporarily predispose patients to high blood glucose levels). In diabetics sudden elevations of blood glucose are typically caused by failure to maintain a careful dietary and medical regimen, taking medications such as corticosteroids, or serious illnesses, e.g., infections, heart attack, stroke.	Patients often report thirst, frequent urination, increased appetite, and increased consumption of fluids. Those who become dehydrated may be dizzy when they get up from a bed or chair. Blood chemistries typically reveal a blood glucose of more than 200 mg/dl, and glucose is present in the urine.	Fluids are administered by mouth (if possible) and intravenously. Insulin or oral hypoglycemic agents are given.
Hyperthermia (heat cramps, heat exhaustion, heatstroke)	Inability of the body to cope with heat stress resulting from excessive heat production or decreased heat loss. Heat cramps: muscle cramps and fatigue accompanied by water and mild salt depletion. Heat exhaustion: serious dehydration with water and electrolyte depletion. Patients maintain thermoregulatory control. Heat exhaustion may progress to heatstroke, characterized by thermoregulatory failure and profound dehydration.	The person with heat cramps complains of painful muscle spasms. There is a history of recent exertion in a hot environment. The patient has been sweating profusely with inadequate or hypotonic fluid replacement. The patient with heat exhaustion has also been sweating in a hot environment. Symptoms include thirst, weakness, fatigue, vomiting, and anorexia. The skin is cool and clammy. Body temperature may be normal or subnormal. The heatstroke victim will have an altered mental status and will be tachycardic, hypotensive, hyperthermic, and tachypneic. Signs of dehydration will be present.	First aid begins with removal of the patient from the hot environment. Heat cramp victims are treated with an oral or intravenous fluid and electrolyte solution. Heat exhaustion is treated by intravenous fluids. Patients with severe dehydration may require more than 4 L of IV fluid. Patients with heatstroke require rapid cooling. Many techniques are available, but evaporation with water is practical and effective. The patient may be sprayed with water and fanned until the core temperature is about 38.5°C. Cooling beyond this may cause overshoot hypothermia. IV fluid resuscitation as for heat exhaustion is also needed.
Hypoglycemia	The most frequent causes are an excessive dose of insulin or an oral hypoglycemic agent, or inadequate food intake by a diabetic patient treated with those drugs, e.g., during an illness that causes anorexia, nausea, or vomiting. Low blood sugars deprive the brain and other organs of the glucose they need for normal metabolism.	Mental status may vary from confused to agitated to unconscious. The patient is often sweaty, tremulous, and tachycardic. Occasionally, hypoglycemia may mimic strokes or seizures.	Mild hypoglycemia usually responds to a snack. Glucose or dextrose should be given immediately—intravenously if the patient is unable to safely eat, orally if the patient is conscious and sufficiently oriented. One mg of glucagon, administered by intramuscular injection, is an alternative. Blood sugar levels should be tested with a glucometer. Hospitalization may be necessary if the patient has taken an overdose of long-acting insulin or an oral antihyperglycemic agent.
Hypothermia	Core temperature less than 35°C (95°F), caused by decreased heat production, increased heat loss, or impaired temperature regulation. Exposure to cold or wet conditions, sepsis, or profound hypothyroidism may be predisposing conditions. Central nervous system, cardiovascular, and respiratory systems are impaired when the temperature is below 35°C.	Lethargy, confusion, and fatigue in mild cases. Heart rate and respiratory rate may be increased. As hypothermia worsens, the patient stops shivering. Heart rate, blood pressure, and respirations slow. The patient eventually loses consciousness. Respirations and pulses may be difficult to detect.	Cold or wet clothing should be removed. The patient should be rewarmed. Warm blankets, warm oxygen, and warm IV fluids may be used. An accurate core temperature must be recorded, if possible. Temperatures less than 32°C may require more aggressive rewarming techniques, such as gastric lavage, peritoneal lavage, hemodialysis, or cardiopulmonary bypass. If pulses are absent, cardiopulmonary resuscitation is indicated.

Medical Emergency	Underlying Causes	Findings	Treatment
Seizure	An abnormal electrical discharge by central nervous system neurons that produces autonomic, behavioral, motor, or sensory abnormalities. Seizures may result from structural diseases of the brain, e.g., arteriovenous malformations, strokes, trauma, or tumors, from metabolic disorders, e.g., severe electrolyte disorders, low blood sugars, renal failure, or hypoxia, or from drugs (or drug or alcohol withdrawal).	During a generalized motor seizure, the patient is unconscious and has repetitive back-and-forth movements of the upper and lower extremities. Patients may bite the tongue, lose control of the bowels or bladder, or injure themselves when they fall. After the seizure, there is usually a period of gradual and progressive return to normal consciousness, which may take 30 to 60 min. Some patients may have a brief period of focal paralysis after the event.	During the seizure, the patient should be guarded against injury. This may involve helping the patient to the floor and moving furniture out of the way. Supplemental oxygen should be given. Objects should not be inserted into the patient’s mouth—an obstructed airway may result. Medications such as lorazepam, diazepam, fosphenytoin, or phenobarbital may be used to abort the seizure. Most seizure patients will require some investigation into the cause of the seizure. In patients with a history of prior seizures, this may include checking blood levels of anticonvulsant medications. Patients with first-time seizures may need a more extensive evaluation, including a CT scan, an EEG, MRI, blood work, and a lumbar puncture.
Stroke (cerebrovascular accident)	Inadequate blood flow to an area of the brain causing tissue death. In thrombotic stroke, blood vessels narrowed by atherosclerosis limit delivery of oxygenated blood to the brain or a portion of it. In embolic stroke, clots travel from other areas of the body to block cerebral vessels. Hemorrhagic stroke results from bleeding caused by hypertension or rupture of cerebral aneurysms.	Patients often present with weakness or numbness on one side of the body or the face; with speech disturbances; or with confusion, clumsiness, difficulty walking, loss of consciousness, or coma.	Oxygen is administered and cardiac monitoring is begun. A computed tomographic (CT) scan of the brain is used to rule out a hemorrhage as a cause of new neurological deficits. Tissue plasminogen activator (a thrombolytic, or “clot-busting” drug) may be given to patients who present in the first 4.5 hr of nonhemorrhagic stroke.
Suicidal ideation	Major depression; alcohol abuse; dysphoria; adjustment disorders; borderline personality disorders; psychotic disorders; poor social situations and recent stressful events. Older men living alone are most likely to use lethal means to harm or kill themselves. Younger persons are most likely to come to an emergency department in distress.	Patients may report feelings of hopelessness, misery, anxiety or tension, or may feel that life has lost its meaning or joy. People who have taken medications in an attempt to overdose may have signs and symptoms related to the ingested drug(s) and may need inpatient stabilization. Consult Appendix 9-1.	Hospitalization is indicated for patients who are intoxicated by drug or alcohol overdose or who have a concrete plan to take their own lives. Outpatient therapy may be appropriate for people without the means to use potentially lethal drugs or devices to jeopardize their health and safety. Antidepressant medications, counseling, alcohol and drug rehabilitation, therapies, and psychiatric consultation are used individually or in combination for selected suicidal patients.

Medical Emergency	Underlying Causes	Findings	Treatment
Thermal burns	First- and second-degree burns: partial-thickness injuries involving only the epidermis or the epidermis and dermis. Third-degree burns: full-thickness injuries involving the deeper tissues. Burns impair the skin’s ability to prevent heat and water loss. Burned skin is not an effective barrier to injection. Severity depends on the character and temperature of the agent, the duration of exposure, and the type of skin injured.	First-degree burns: red and painful. Second-degree burns: red, painful, and blistered. These burns heal without scarring. Third-degree burns: may be white or charred. The subcutaneous nerves have been destroyed; thus there is no pain. Surrounding areas are painful. Full-thickness burns heal poorly, leaving a scar.	The first step is to stop the burning process. Oxygen should be administered if there has been smoke inhalation. Jewelry and clothing should be removed in anticipation of swelling. Sterile sheets or dressings should be applied to the burned areas.
Transient ischemic attack (TIA)	See Stroke .	Symptoms and signs are similar to those of a stroke, but usually last less than 1 or 2 hr.	Patients with TIAs are treated with antiplatelet therapies, such as aspirin or clopidogrel, and are evaluated with electrocardiographic monitoring, e.g., to rule out atrial fibrillation, CT scans of the head (to rule out small strokes), and carotid ultrasonography (to determine whether the patient has a surgically correctable stenosis of the carotid arteries).