eMedicine Specialties > Emergency Medicine > Toxicology

Toxicity, Cocaine: Treatment & Medication

Author: Lynn Barkley Burnett, EdD, MS, LLB(c), Medical Advisor, Fresno County Sheriff's Department; Attending Consultant-in-Chief and Chairman, Medical Ethics, Clinical Faculty, Community Medical Centers; Adjunct Professor of Forensic Pathology, National University Master of Forensic Science Program
Coauthor(s): Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Contributor Information and Disclosures

Updated: Nov 10, 2008

Treatment

Prehospital Care

  • Establish the patient's airway, breathing, and circulation (ABCs); provide oxygen; obtain intravenous access; monitor and frequently check vital signs; monitor glucose levels (eg, with the Accu-Chek device) in patients with altered mental status; and carefully use naloxone (Narcan) in patients with altered mental status.
  • Administer benzodiazepines to manage seizures.
  • Patients with cocaine toxicity may be combative, aggressive, and disoriented, and they may have delusions of persecution or hallucinations. Caution is appropriate because the patient may attempt to harm the emergency medical technician (EMT). The patient may have to be restrained, though this should be done with caution and adequate personnel.

Emergency Department Care

Data of DAWN-reporting EDs may provide an impression of the degree of physiologic derangement in cocaine-toxic patients presenting to EDs. Past reports indicated that 52.2% of patients presenting to EDs with cocaine toxicity were treated and released, 44.2% were admitted, and 2.2% left against medical advice. The mortality rate was 0.3%.

General considerations

  • Patients presenting with cocaine toxicity initially receive interventions directed at all patients in potentially unstable condition, including attention to ABCs, oxygen, intravenous access, and monitoring (cardiac monitoring and pulse oximetry).
  • As assessment is accomplished, the temperature of a hyperthermic patient may continue to rise secondary to agitation and their fighting of the restraints. The temperature may reach critical levels; therefore, early consideration should be given to the potential need to treat hyperpyrexia.
  • Remove any residual cocaine from the nasal passages.
  • Protect the patient from hypoglycemia, which may present as any neuropsychiatric abnormality.
  • Never base treatment on the results of a drug screen; rely on clinical findings instead.
  • Reassurance is important if the patient is oriented.
  • Avoid physical or pharmacologic restraints if possible. Benzodiazepines are an effective and safe pharmacologic restraint in these patients if one is needed.
  • Pregnancy cannot be readily diagnosed or excluded on the basis of the patient's history. The prevalence of unrecognized pregnancy is as high as 6% in ED patients. Therefore, perform routine pregnancy testing in patients with overdose because physiologic changes in pregnancy may increase the patient's susceptibility to drug toxicity. Drug poisoning may induce miscarriage, premature labor, or fetal toxicity, and modifications may be necessary for acute management of the overdose.
  • The effects of cocaine are generally short lived. Monitor patients until they are no longer tachycardic and hypertensive (because of the drug) and until they are calm and cooperative. Patients who have normal vital signs and normothermia may be discharged home after observation for 2-6 hours.

Therapeutic dilemmas
 
Medications commonly administered to treat one or more of the pathophysiologic effects of cocaine in emergency cardiovascular care may worsen other adverse effects of cocaine, and therefore raise concerns about their use in treating cocaine poisoning. Conflicting reports and recommendations in the literature compound the controversy surrounding pharmacologic treatment of cocaine toxicity.

As an example, the 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care acknowledge that many toxicologic approaches are not based on high levels of research, but rather on case reports, small case series, and data extrapolated from animal studies. Therefore, although the American Heart Association (AHA) recommendations for treatment of individuals with poisoning are class IIb (interventions considered within the standard of care), many represent only expert consensus.

  • Epinephrine and vasopressin
    • Epinephrine has been the drug of choice for the treatment of cardiac arrest, primarily for its alpha-adrenergic effects. However, epinephrine and cocaine have many similar cardiovascular effects. Furthermore, cocaine prevents the reuptake of exogenously administered epinephrine. Therefore, if epinephrine is used, AHA Guidelines 2005 and the AHA Textbook of Advanced Cardiac Life Support for the Experienced Provider recommend that high-dose epinephrine be avoided and that the interval for its administration be increased (q5-10min).
    • If VF or ventricular tachycardia is recurrent or refractory and epinephrine or excessive levels of endogenous catecholamines are the suspected cause, consider withholding further doses of epinephrine.
    • Because of this similarity in the cardiovascular effects caused by cocaine and epinephrine, the administration of epinephrine to a patient who arrests in a hyperadrenergic state has been likened to "pouring gasoline on a fire."26
    • In theory, vasopressin may offer considerable advantages over epinephrine in cardiac arrest secondary to cocaine toxicity.27,26
        • The hyperadrenergic state caused by cocaine increases myocardial oxygen demand. Epinephrine has the same effect. Vasopressin, on the other hand, increases coronary blood flow, and thereby myocardial oxygen availablity.28
        • Cocaine toxicity frequently causes acidosis: epinephrine loses much of its effectiveness in an acidotic milieu28 , whereas vasopressin demonstrates vasoconstricting efficacy even with severe acidosis; vital considerations given that improved coronary perfusion during CPR improves patient survival.29
  • Lidocaine
    • Lidocaine is one of the primary drugs used to treat ventricular dysrhythmias. Although some animal data indicate that lidocaine can reverse the ECG effects of cocaine and protect against death, others indicate that lidocaine may lower the seizure threshold and potentiate cocaine toxicity.
    • Derlet, Tseng, and Albertson caution that lidocaine potentiates the CNS toxicity of cocaine.30 Noting this small "safety window," Derlet states that lidocaine may be used, but advises precautions, such as double or triple checking the total dose, solution concentration, and any infusion pump.31
    • Cocaine and lidocaine have similar pharmacologic effects. Therefore, the possibility that lidocaine may increase toxicity by potentiating the effects of cocaine on the cardiovascular system has been a concern.
    • The AHA Textbook of Advanced Cardiac Life Support for the Experienced Provider cites this similarity for the therapeutic role that lidocaine may play in competing with cocaine at the sodium channel, thereby decreasing the effects of cocaine.
    • In the setting of cocaine toxicity, the decision as to whether or not to use lidocaine must be carefully considered, weighing its potential benefit on ventricular rhythm disturbances versus the synergistic toxic effects of lidocaine on seizure risk.
  • Beta-blockers
    • Strong evidence supports avoidance of nonselective beta-blockers for cocaine-induced ischemia. Echocardiographic data suggest that the antihypertensive effect of propranolol results from depression of cardiac output rather than relief of systemic vascular resistance. Propranolol exacerbates the depression of coronary blood flow induced by cocaine because of unopposed alpha stimulation after beta-blockade. Just before death, cocaine toxicity usually results in hypotension, a condition that use of a beta-blocker further compounds.
    • Malbrain et al recommended esmolol for "save use" in managing life-threatening hypertension and tachycardia.32 Esmolol is a selective beta1-adrenergic blocker with rapid onset and short duration of action (elimination half-life, 9 min). They advise that the coadministration of esmolol and sodium nitroprusside should be reserved for severe hypertension that is unresponsive to other treatment and/or complicated by aortic dissection.
    • Guidelines 2005 does discuss use of carefully titrated doses of labetalol as a third-line agent for drug-induced hypertensive emergencies.33 However, labetalol, a combined alpha- and beta-blocking agent, has an alpha-to-beta blockade ratio of 1:7. Therefore, it may not provide enough protection for cocaine-toxic patients from (relatively) unopposed alpha stimulation. Its risk of exacerbating myocardial ischemia parallels the risk of beta-blockers. Labetalol also increased seizures and mortality in animal models; therefore, its use cannot be promoted.

Cardiovascular concerns

  • Cocaine-associated VF: Prolonged resuscitative efforts are recommended in AHA Guidelines 2005 for patients with cardiopulmonary arrest in a setting of drug intoxication.34
    • Hypotheses about the causes of cocaine-associated VF, if confirmed, have treatment implications. In one study, when the heart rate is held constant, alpha-adrenergic but not beta-adrenergic receptor antagonists prevented cocaine-induced VF. Cocaine activation of myocardial alpha-adrenergic receptors, specifically alpha1A-adrenergic receptors, may substantially contribute to VF during myocardial ischemia. Activation of these receptors elevates cytosolic calcium levels and provokes delayed after-depolarizations. Therefore, calcium overload may be the final common pathway linking enhanced adrenergic activity to cocaine-induced VF.
    • This observation raises a question as to the role, if any, of calcium antagonists in cocaine toxicity. Studies supporting the use of calcium channel blockers have been performed only in animal models. Consistent with a local anesthetic mechanism of its toxic effects, calcium channel blockers have not been shown to reduce cocaine toxicity in humans. Furthermore, they increase the lethality of cocaine. This additive lethality may result from the negative inotropic effects shared by these agents. 
  • Cocaine-associated cardiac dysrhythmias: Ventricular ectopy is usually transient and is managed with careful observation and escalating doses of benzodiazepine to blunt the hypersympathetic state by modulating cocaine-induced CNS stimulation. Treat malignant ventricular ectopy and perfusing VT by ensuring good oxygenation, by treating the hyperadrenergic state with escalating doses of benzodiazepine, and by administering appropriate antidysrhythmic medications if ventricular arrhythmias persist. Ensure that a defibrillator is readily available.
    • Malbrain recommends the use of an antidysrhythmic agent, such as bretylium (though now rarely found on code carts).32 Another pharmacologic option is magnesium sulfate, though caution is necessary because it may cause hypotension.
    • Consider sodium bicarbonate for treating dysrhythmias resulting from the direct toxic effects of cocaine,35 such as when sodium channel blockade causes a QRS >100 milliseconds. Dual mechanisms of action have been proposed for its therapeutic effects: (1) Alterations in pH may change the conformation of the sodium channel, and (2) increased extracellular sodium concentrations may override sodium channel blockade. Hourly measurements of blood pH are indicated, with appropriate adjustments until the blood pH is properly controlled. End points of bicarbonate therapy are a serum pH of 7.50-7.55.
    • Paroxysmal SVT (PSVT), atrial flutter, and rapid atrial fibrillation are generally short-lived and do not require immediate treatment. Use escalating doses of benzodiazepine to treat hemodynamically stable patients with persistent supraventricular arrhythmias to blunt the hypersympathetic state by modulating cocaine-induced stimulation of the CNS, taking caution not to depress consciousness and create a need for respiratory assistance. In drug-induced hemodynamically significant tachycardia, the pathophysiologic mechanism responsible may be increased automaticity, triggered activity, or reentry phenomenon. Tachycardia caused by increased automaticity will not be responsive to interventions such as adenosine and synchronized cardioversion. Benzodiazepines are generally safe and effective in drug-induced hemodynamically significant tachycardia (HST). 
  • Cocaine-associated chest pain and MI: Chest pain may result from musculoskeletal, cardiovascular, pulmonary, or other causes. In patients with cocaine-related chest pain, assume that cardiac ischemia is present until this is proven otherwise. Accordingly, the ED approach to such patients, in addition to oxygen, intravenous access, and monitoring, includes the following steps:
    • Perform 12-lead ECG.
    • Obtain chest imaging.
    • Direct the initial pharmacologic approach to suspected cocaine-related myocardial ischemia at increasing coronary blood flow and decreasing sympathetic output.
    • Nitroglycerin (NTG) is appropriate in managing cocaine-associated infarction or ischemia because it reduces cocaine-induced vasoconstriction in healthy and atherosclerotic segments of the coronary arteries.
    • Small, incremental doses of benzodiazepines decrease norepinephrine release by the CNS, thereby counteracting the sympathomimetic effects of cocaine on the heart. Similar doses of morphine sulfate (MS) also alter hemodynamics and blood flow dramatically in patients with heightened sympathetic activity. Limiting factors for morphine and benzodiazepines include hypotension, somnolence, and respiratory depression. Kercher cautions that short-acting benzodiazepines (eg, lorazepam) should be prescribed at low doses for patients with hepatic disease, organic brain syndrome, and those taking medications inhibiting the metabolism and clearance of benzodiazepines (eg, those using nicotine or cimetidine [Tagamet]).36
    • Although benzodiazepines and NTG are first-line agents in drug-induced acute coronary syndromes, cocaine-induced vasoconstriction also is reversed by phentolamine. Therefore, AHA 2005 Guidelines recommends phentolamine as a second-line agent.33
    • AHA 2005 Guidelines further state that coronary vasodilators administered via the intracoronary route are preferable to peripheral administration, a factor favoring cardiac catheterization, as further addressed below. 
    • In a study of MI in the setting of cocaine use, Hollander reports on 246 patients enrolled over 46 months at 6 hospitals. Of patients presenting with cocaine-associated chest pain, 5.7% had MI; other studies have reported rates of 19% and 31% for acute MI in patients admitted with chest pain and cocaine use. Route, length, and frequency of use and interval from last use did not differ between patients with MI and those without MI. Of interest, a history of chest pain was less common in patients with MI than in others.7
    • In patients with prolonged unexplained chest pain, perform serial ECGs and cardiac-marker measurements to rule out MI. However, in one study, Hollander reports that patients with MI were as likely to present with normal or nonspecific ECG findings as with ischemic ECG findings. The sensitivity of the ECG in predicting MI was only 35.7%; therefore, ECG appears to be less sensitive in patients with cocaine-induced myocardial ischemia than in other patients presenting with ischemic chest pain. Interpretation of cardiac markers in patients with cocaine-induced symptoms may be difficult since levels of creatine kinase (CK) and CK MB-isoform (CK-MB) may be elevated in cocaine users who do not have an MI.
    • Be mindful that as many as 43% of patients with cocaine-related chest pain meet standard ECG criteria for fibrinolysis despite being cardiac marker negative for infarction; a high percentage of such patients have early repolarization.
    • Of additional importance, an increased incidence of mycotic aneurysms and CNS mass lesions may lead to an increased incidence of hemorrhagic complications in these patients. When evaluating patients for fibrinolytic therapy, remember that a history of intravenous drug use poses a relatively high risk for the possibility of coexisting vascular pathology.35 Obtain a detailed history and perform physical and ancillary testing, as appropriate, directed at identifying endocarditis, septic pulmonary emboli, and pseudoaneurysm.
    • AHA 2005 Guidelines state that intracoronary administration of fibrinolytics is preferred to blind peripheral administration in patients with drug-induced acute coronary syndrome. Fibrinolysis in the presence of hypertension or CNS vasculitis may be dangerous, and percutaneous transluminal coronary angioplasty (PTCA) may be a safer alternative when revascularization is indicated.
    • In light of the above confounding factors, the AHA Textbook of Advanced Cardiac Life Support for the Experienced Provider indicates that cardiac catheterization is recommended by many experts. 
    • Fibrinolysis should thus be reserved for patients who cannot receive percutaneous coronary intervention within the requisite time and who have low risk for cerebrovascular bleeding and other hemorrhagic complications of fibrinolytic therapy.
    • Patients may develop chest pain several hours after cocaine use.17 Recurrent coronary vasoconstriction associated with increased levels of benzoylecgonine and ethyl-methyl ecgonine may be responsible. Furthermore, patients with cocaine withdrawal may have dopamine depletion, resulting in intermittent coronary spasm.24 MI has been attributed to cocaine use several days earlier, and Holter monitoring has documented cocaine-induced ischemia for several weeks after cocaine use.17 Recurrent ischemic chest pain is reported in patients who do and in patients who do not continue to abuse cocaine.17 Ischemia may persist for up to 2 weeks after the cessation of cocaine use; therefore, avoiding the use of beta-adrenergic blockade for as long as 2 weeks after withdrawal of the toxin may be prudent.
    • Objective assessment may aid decision-making when the patient's treatment or disposition may be altered in the presence of cocaine.14 For example, beta-blockers are relatively contraindicated in cocaine use, but they are commonly given when cocaine is not considered a factor in myocardial injury or ischemia. However, in one study, 28% of patients with chest discomfort who tested positive for cocaine had denied using it. When beta-adrenergic blockade is being considered, even if cocaine toxicity is not suspected, a rapid bedside test for cocaine use may be appropriate because of its prevalence and the substantial rate of false-negative findings in the history of present illness.
  • Hypertension
    • Cocaine may cause a hypertensive emergency because of CNS stimulation and its peripheral alpha-agonist effects. Cocaine toxicity may also be superimposed on preexisting hypertension in patients who have become dependent on elevated BP to maintain cerebral perfusion. Carefully consider the patient's clinical status and history when deciding to treat hypertension.
    • Hypertension secondary to cocaine is commonly responsive to intravenous benzodiazepines because benzodiazepines minimize the stimulant effects of cocaine on the CNS.
    • A vasodilator, such as NTG or nitroprusside, may be titrated to effect if further therapy is indicated. NTG is the drug of choice in patients with chest pain. The use of nitroprusside to control hypertension has the additional advantage of aiding heat loss by peripheral vasodilatation.
  • Hypotension: Hypotension may be treated with parenteral fluids and, if refractory to fluids, norepinephrine, a direct-acting pressor, is preferred over indirect agents like epinephrine.
  • Aortic dissection: Include type A aortic dissection in the differential diagnosis of cocaine abuse with chest pain. ED care entails close cardiac and hemodynamic monitoring, treatment to reduce the progression of dissection, and administration of narcotics as needed for pain. Sodium nitroprusside should be used to control BP, but it may cause tachycardia, for which esmolol may be considered. Although the goals of therapy are to decrease the heart rate to 60-80 bpm and BP to 100-120 mm Hg, the therapeutic endpoint is the lowest level that permits continued end-organ perfusion.

Pulmonary concerns

  • Cocaine affects pulmonary dynamics and may cause pulmonary edema. Other causes of pulmonary edema in the setting of cocaine use include CHF (with or without MI) and subarachnoid hemorrhage or concomitant use of other drugs (eg, heroin). Most patients with cocaine-associated pulmonary edema respond to standard medical treatment. 
  • For resistant hypoxemia, positive-pressure ventilation with continuous positive airway pressure (CPAP) or intubation supplemented with positive end-expiratory pressure (PEEP) is usually effective. For patients with respiratory depression intubation may be indicated, as it is for those with apnea.
  • Administration of naloxone to a patient who has been speedballing may negate the sedative effect of the opioid and leave the stimulant effect of the cocaine unopposed, precipitating or worsening cocaine toxicity. Naloxone is still indicated in respiratory depression but should be used with caution (ie, slowed rate of administration, lowered doses).
  • Administration of flumazenil to patients with benzodiazepine use (eg, to blunt the effects of cocaine) may be dangerous. Cocaine is a gamma-aminobutyric acid (GABA) antagonist that may be blocked by benzodiazepines and potentiated by flumazenil. Use of flumazenil in the cocaine-intoxicated patient may induce seizures.

Neurologic concerns

  • Seizures are a concern.
  • Cocaine is one of the most common causes of drug- and toxin-associated seizures. Seizures may be a dire sign of toxicity that heralds life-threatening physiologic instability. Cocaine-associated seizures are usually generalized, but they may be partial. They may result directly from toxicity of the CNS or indirectly from hypoxemia, stroke, or other conditions. They may occur after recreational use, long-term abuse, or cocaine overdose. Seizures also occur in people who pack or stuff cocaine in their body, affecting 4% of patients who are body stuffers, with seizures expected in the first 2 hours.
  • Seizures occurring from cocaine toxicity are managed as part of comprehensive patient treatment. Seizures and severe agitation require prompt attention to protect the airway and prevent hyperthermia. Although patients with serious compromise may require paralysis and mechanical ventilation, benzodiazepines are first-line therapy. Benzodiazepines directly enhance GABA-mediated neuronal inhibition, affecting the clinical and electrical manifestations. Their overall effectiveness in terminating cocaine-induced seizures is 75-90%.
  • Although Perrone and Hoffman recommend head CT in all cases of cocaine-associated seizures because of the risk of associated intracranial lesions,24 Renzi believes that a brief seizure, clearly temporally related to cocaine use, requires no further workup if the patient is otherwise healthy, alert, coherent, without headache, and neurologically intact.25 If patients are not admitted, monitor them in the ED for several hours.

Dystonic reactions

  • Emotional distress can exacerbate dystonic reactions, whereas relaxation may reduce the intensity of such attacks. Using a calm reasoned approach in a quiet room markedly complements the effectiveness of pharmacologic interventions.
  • Dopamine and acetylcholine have mutually antagonistic functions in the nigrostriatal system. Although diphenhydramine, with its anticholinergic properties, is the drug of choice for most dystonic reactions, it should be used with caution in cocaine toxicity. Antihistamines cause hyperthermia by central (eg, hypothalamic) and peripheral (inhibition of sweating and muscular rigidity) effects; cocaine also causes hyperthermia. Antihistamines and cocaine are sodium channel blockers. Therefore, coadministration of an antihistamine in the setting of cocaine use may potentiate a molecular pathophysiological cascade that exacerbates end-organ dysfunction.
  • Benzodiazepines, with their anxiolytic and muscle relaxant properties, are alternative drugs for the treatment of dystonia. Although they only treat the manifestations of dystonias and not the pathophysiology underlying their development; the advantage of using benzodiazepines lies in their safety.

Metabolic concerns

  • Hypoglycemia may present as any neuropsychiatric syndrome and is always a consideration in patients who present with altered mental status or convulsions. Rapid diagnosis by meter or Dextrostix prevents the deleterious effects reported for the administration of dextrose in the absence of hypoglycemia. If the adult patient is hypoglycemic, administer thiamine 100 mg followed by 50 mL of 50% dextrose (D50W).
  • Acidosis has a profoundly adverse effect on myocardial contractility and may potentiate the effect of catecholamines. The correction of arterial pH, through ventilatory assistance and appropriate use of sodium bicarbonate, may be effective in terminating cocaine-induced dysrhythmias with resulting improvement of hemodynamics.

Hyperthermia

  • Recognize and treat hyperthermia as a distinct entity. If psychostimulant-intoxicated patients do not die as a result of cardiac or cerebrovascular complications, the next most important steps in preventing further morbidity are control of hyperthermia and treatment of rhabdomyolysis. Assess the patient's core body temperature and maintain a high index of suspicion for hyperthermia. In the setting of serious hyperthermia, continuously monitor the core body temperature.
  • Hyperthermia may be treated with convection cooling, which involves spraying the patient's exposed body with tepid water as fans circulate air. Tepid water prevents maladaptive shivering that may be induced by conduction cooling methods, although ice packs, ice water gastric lavage, or cooling blankets may also be used. Direct efforts at reducing body temperature to 101°F in 30-45 minutes.
  • Do not use restraints (physical or pharmacologic) that interfere with dissolution of heat. If necessary, use light hand and foot restraints. Ensure adequacy of hydration and electrolytes. Benzodiazepines are an effective and safe pharmacologic restraint in these patients. Given parenterally, with the usual precautions, they rapidly calm hyperactive patients.
  • Do not administer phenothiazines. Goldfrank, Flomenbaum, Lewin, and Weisman apply this injunction to butyrophenones as well.37 Contrary views are, however, expressed in the literature. Callaway and Clark maintain that concerns about the potentiation of drug-induced seizures by butyrophenone neuroleptics (eg, haloperidol) may be exaggerated because such drugs have less effect on human seizure threshold than phenothiazines, and they interfere less with sweat-mediated evaporative cooling in drug-induced hyperthermia.10 Although Callaway and Clark believe that further studies are necessary to assess the efficacy of butyrophenones in the treatment of psychostimulant overdose,10 Colucciello and Tomaszewski indicate that haloperidol is effective in treating cocaine-related agitation and that no clinical data proscribe its use, theoretic concerns notwithstanding.38
  • Monitor patients with hyperthermia in the ED for several hours if they are not being admitted.

Cocaine-induced rhabdomyolysis

  • The reported incidence of rhabdomyolysis in ED patients who use cocaine is 5-30%. Pathophysiologic hypotheses include placement of excessive demands on healthy muscle cells that cannot be met by available energy supplies, direct toxicity of cocaine upon the muscle membrane, cocaine-induced seizures, and the potential concomitant use of other drugs (eg, PCP, amphetamines) that are known to cause this syndrome.
  • Risk factors for rhabdomyolysis include altered mental status, hyperactivity, fever, seizures, hypotension, dysrhythmias, and cardiac arrest. Rhabdomyolysis may be associated with hyperphosphatemia, myoglobinuria, nephrotoxicity, hyperkalemia, hypocalcemia, compartment syndromes, or disseminated intravascular coagulation (DIC). The most critical sequelae of rhabdomyolysis are shock and renal failure.
  • Rapid fluid resuscitation promotes urine output and alleviates the effect of myoglobin on the kidneys. Generous amounts of intravenous fluids with close monitoring of urine output and pH are indicated for rhabdomyolysis associated with severe psychostimulant toxicity. Fluid resuscitation should maintain urine output of 1-3 mL/kg/h to minimize renal damage from rhabdomyolysis. Patients with rhabdomyolysis may require up to 20 L of fluid in the first 24 hours to achieve these urinary flow rates, and close monitoring of cardiac status and electrolytes is necessary.
  • In acid urine, myoglobin is essentially a toxin, and uric acid tends to crystallize at low pH; sodium bicarbonate may be used to alkalinize the urine of patents with rhabdomyolysis. However, without prospective randomized studies to differentiate the role played by volume versus alkalinization, it is possible that volume alone represents maximally effective therapy. This is important because cocaine metabolites are best excreted in acid urine, and it calls into question the role of urinary alkalinization.
  • GI concerns: When cocaine has been ingested (not as part of body packing or body stuffing), the patient without altered mental status may be treated by administration of activated aqueous charcoal. Gastric lavage and induction of vomiting via ipecac syrup is not recommended because of the risk of seizure, with the potential for airway compromise and aspiration of vomitus.

Body packing and body stuffing

  • In body packers, although a risk for toxicity exists, the drugs are often carefully packaged to prevent rupture or leakage. Carriers often purge the GI tract with a laxative before they ingest the drug packages and then consume only clear liquids until the drugs are delivered. If a constipating agent was used, they ingest a laxative to enhance evacuation when arriving at their destination.
  • Conversely, body stuffers quickly ingest drug packages to avoid arrest. Therefore, body stuffers are at increased risk for aspiration because of the rapidity with which they attempt to remove the evidence from police accessibility. Bronchoscopy has been used to successfully remove a drug packet aspirated into the lung.
  • Body stuffers have other risks as well. Because they were not planning to ingest the packet (as opposed to the body packer) and because they took no precautions selecting the drug container, the wrapping material often acts as a semipermeable membrane. The hypertonic content of the drug packet attracts water, making the ingested packages especially prone to rupture or leakage resulting in toxicity.
  • Potent polypharmaceutic overdose is also common, resulting from an attempt to swallow all of the illegal drugs on site.
  • The administration of activated charcoal has been recommended to adsorb any toxins from leaking bags, from ruptured bags, or that were liberated during enhancement of bowel transit (eg, whole-bowel irrigation). Treatment of asymptomatic patients should include laxatives (eg, sodium sulfate, magnesium sulfate, magnesium citrate, psyllium hydrophilic mucilage) or whole-bowel irrigation, several doses of activated charcoal, and close observation.
  • If a polyethylene glycol electrolyte lavage solution (eg, GoLYTELY, Colyte) is to be used for whole-bowel irrigation, Malbrain cautions that it must follow the administration of activated charcoal because the maximal adsorptive capacity of activated charcoal is at pH 7 and the polyethylene glycol electrolyte lavage solution has a pH of 8.32 Do not use paraffin-containing laxatives (eg, Lansoyl) because they degrade latex. Avoid endoscopic manipulation and enemas because the drug packet may be ruptured. Contraindications to whole-bowel irrigation include ileus, GI hemorrhage, or bowel perforation.
  • Monitor body stuffers for several hours. Body packers may require hours to days of hospitalization until all the packets have been passed. Surgical intervention is needed if patients present with serious signs or symptoms or intestinal obstruction.

Psychiatric concerns

  • Individuals using cocaine expect to become euphoric, energetic, and confident. However, with large doses or prolonged use, they may become agitated, anxious, or panicky. A wild, combative patient intoxicated with cocaine may be sedated with lorazepam or midazolam, both of which can be adequately absorbed via the intramuscular route if intravenous access is unobtainable.
  • Given the contradictory literature about butyrophenones that was previously addressed, attempt to avoid use of antipsychotics because they may confuse the clinical picture, exacerbate anticholinergic crisis, lower the seizure threshold, or cause a dystonic reaction.

Other considerations

  • When treating a traveler who presents with fever, bizarre mental state, or coma, especially if the person has come from West Africa or South America, consider cerebral malaria, treated with intravenous quinine.
  • Test patients who inject drugs for HIV and hepatitis (with their permission, if required by state law).
  • If a patient with cocaine toxicity is being considered as an organ donor, remember that cocaine preferentially accumulates in the liver and kidney. Therefore, use of these organs may result in the transplantation of a substantial reservoir of the toxin.

Consultations

Consultation with a regional poison control center or a medical toxicologist may be appropriate in complicated cases.

Medication

The general objectives of pharmacotherapeutic intervention in cocaine toxicity are to reduce the CNS and cardiovascular effects of the drug by using benzodiazepines initially and then control clinically significant tachycardia and hypertension while simultaneously attempting to limit deleterious drug interactions.

In a cardiac arrest, vasopressin may offer considerable advantage over epinephrine.

Some patients who abuse cocaine have enhanced sensitivity to benzodiazepines despite a significantly decreased plasma concentration. Be alert to the extreme sedative effects that have been noted after the administration of lorazepam to some patients who used cocaine.

NTG or nitroprusside may be needed to treat severe hypertension. For both of these drugs, an infusion system that ensures a precise rate of flow is needed. Closely monitor the patient's vital signs when vasoactive and antihypertensive medications are used. When vasoactive agents are discontinued, taper them slowly.

Hypotension may compound the patient's status; if present, norepinephrine may be required.

Hypoglycemia is always a possibility in patients presenting with neuropsychiatric syndromes. If bedside glucose results confirm the need, administer thiamine and glucose. Thiamine should be administered before dextrose. Before the intravenous administration of thiamine, administer an intradermal test dose to patients in whom thiamine sensitivity is suspected.

Benzodiazepines

By increasing the action of GABA, a major inhibitory neurotransmitter in the brain, these drugs may depress all levels of the CNS, including the limbic system and reticular formation.


Lorazepam (Ativan)

DOC for status epilepticus because it persists in CNS longer than diazepam. Rate of injection should not exceed 2 mg/min. May be administered IM if unable to obtain vascular access.

Adult

0.044 mg/kg (2-4 mg) IV; titrate to effect; single dose not to exceed 4 mg
Status epilepticus: 4 mg IV over 2-5 min; may repeat in 10-15 min prn; not to exceed 8 mg in 12 h

Pediatric

Children: 0.05 mg/kg IV (0.02-0.1 mg/kg); single dose not to exceed 4 mg
Adolescents: Administer as in adults
Status epilepticus:
Neonates: 0.05 mg/kg IV over 2-5 min; may repeat in 10-15 min prn
Infants and children: 0.1 mg/kg IV over 2-5 min; second dose of 0.05 mg/kg IV in 10-15 min prn; not to exceed 4 mg
Adolescents: 0.7 mg/kg IV slowly over 2-5 min; not to exceed 4 mg; second dose in 10-15 min prn

Toxicity of benzodiazepines in CNS increases with concurrent alcohol and other CNS depressants

Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Monitor for respiratory depression with high or repeated doses; contains benzyl alcohol, which may be toxic to infants at high doses; caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, Parkinson disease, or inhibited benzodiazepine metabolism and clearance (eg, those using nicotine or cimetidine)


Midazolam (Versed)

Alternative for termination of refractory status epilepticus. Because water soluble, takes approximately 3 times longer than diazepam to peak EEG effects; therefore, clinician must wait 2-3 min to fully evaluate sedative effects before initiating procedure or repeating dose. Has twice the affinity for benzodiazepine receptors as diazepam. May be administered IM if unable to obtain vascular access.

Adult

0.01-0.05 mg/kg (usually 0.5-4 mg, up to 10 mg) IV slowly over several min; may repeat q10-15min until adequate response achieved

Pediatric

<32 weeks: 0.5 mcg/kg/min IV infusion; titrate to effect
>32 weeks: 1 mcg/kg/min IV infusion; titrate to effect
Children: 0.05-0.2 mg/kg IV over 2-3 min then continuous infusion of 1-2 mcg/kg/min; titrate to effect; not to exceed 4 mg per dose
Status epilepticus (refractory to standard therapy), >2 months and children: 0.15 mg/kg IV then continuous infusion 1 mcg/kg/min IV, titrate upward q5min until seizures controlled

Theophylline may antagonize sedative effects; narcotics, cimetidine, ethanol, and erythromycin may accentuate sedative effects because of decreased clearance; reduce dose of thiopental by 15% when used together; effects exacerbated by other CNS depressants

Documented hypersensitivity; preexisting hypotension, narrow-angle glaucoma, and sensitivity to propylene glycol (diluent) are main contraindications

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in CHF, pulmonary disease, renal impairment, hepatic failure, neuromuscular disease, hypotension, and patients >60 y; monitor for respiratory depression with high or repeated doses; consider lowering dosages in patients with organic brain syndrome or inhibited benzodiazepine metabolism and clearance (eg, those using nicotine or cimetidine)


Diazepam (Valium)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing GABA activity. Third-line agent for agitation or seizures because of shortened duration of anticonvulsive effects and accumulation of active metabolites that may prolong sedation.

Adult

5-10 mg IV q10-15min until symptoms resolve; not to exceed 30 mg

Pediatric

30 days to 5 years: 0.2-0.5 mg IV slowly q2-5min until symptoms resolve; not to exceed 5 mg total dose
>5 years: 1 mg IV slowly q2-5min until symptoms resolve; not to exceed 10 mg total dose

Increased toxicity with coadministration of phenothiazines, H1 blockers, barbiturates, alcohols, and MAOIs

Documented hypersensitivity; hypotension; acute narrow-angle glaucoma

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution with other CNS depressants, low albumin levels, or renal and hepatic disease (may increase toxicity)

Cardiovascular agents

Alkalinization may benefit cardiac conduction if a wide QRS is noted. Other treatment for cardiac arrest, dysrhythmias, or acute hypertension may also be required.


Sodium bicarbonate (Neut)

Useful for alkalization of urine in patients with rhabdomyolysis.
Appropriate for dysrhythmias from direct toxic effects of cocaine (ie, QRS >100 ms due to sodium channel blockade).

Adult

1 mEq/kg IV bolus; pH (goal, 7.50-7.55) and clinical response guide subsequent doses

Pediatric

Administer as in adults

Urinary alkalinization, induced by increased sodium bicarbonate concentrations, may decrease levels of lithium, tetracyclines, chlorpropamide, methotrexate, and salicylates; increases levels of amphetamines pseudoephedrine, flecainide, anorexiants, mecamylamine, ephedrine, quinidine, and quinine

Documented hypersensitivity; alkalosis; hypernatremia; hypocalcemia; severe pulmonary edema; unknown abdominal pain

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Alkalosis, decreased plasma potassium, hypocalcemia, and hypernatremia; caution in electrolyte imbalances (eg, in CHF, cirrhosis, edema, corticosteroid use, or renal failure); avoid extravasation (can cause tissue necrosis); caution in patients <2 y


Lidocaine (Anestacon, Dilocaine, Xylocaine, Zilactin-L, Dermaflex)

Class IB antiarrhythmic that increases electrical stimulation threshold of ventricle, suppresses automaticity, and slows conduction velocity through ischemic tissue. Indicated for cocaine-induced VF and VT.

Adult

1-1.5 mg/kg IV bolus over 2-3 min
VF or pulseless VT: May repeat in 3-5 min
Perfusing VT: Repeat doses of 0.5-0.75 mg/kg in 5-10 min
Not to exceed 3 mg/kg total

Pediatric

Loading dose: 1 mg/kg IV; may repeat in 5-10 min twice
For perfusing VT: 1 mg/kg IV bolus; then may use continuous infusion of 20-50 mcg/kg/min IV

Coadministration with cimetidine or beta-blockers increases toxicity; coadministration with procainamide and tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine

Documented hypersensitivity; Adams-Stokes syndrome and Wolf-Parkinson-White syndrome; severe sinoatrial (SA), atrioventricular (AV), or intraventricular block if artificial pacemaker not in place

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Use a solution without preservatives; caution in heart failure, hepatic disease, hypoxia, hypovolemia or shock, respiratory-depression, and bradycardia; may increase risk of CNS and cardiac adverse effects in elderly persons; high plasma concentrations can cause seizures, heart block, and AV conduction abnormalities


Bretylium

Class III antiarrhythmic agent for treatment of PVCs. Has catecholamine-releasing properties and adverse effects. Should not be used as initial treatment.

Adult

5 mg/kg IV push; may increase to 10 mg/kg IV bolus and repeat q5min; maximum dose 30-35 mg/kg

Pediatric

5 mg/kg IV push; may repeat with second dose of 10 mg/kg IV push

Pressor catecholamines and digitalis may increase toxicity; coadministration with ofloxacin may increase risk of cardiotoxicity

Documented hypersensitivity; systemic lupus erythematosus, digitalis-induced arrhythmias, complete heart block or second- or third-degree heart block if pacemaker is not in place; torsade de pointes

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause hypotension especially in fixed cardiac output (eg, aortic stenosis); caution in renal insufficiency, severe pulmonary hypertension, and aortic stenosis; half-life increased in elderly person; with renal clearance of 10-50 mL/min, administer 25-50% of dose; rapid IV injections may cause transient hypertension, nausea, and vomiting; limit injection to 5 mL (undiluted) at each injection site; may exacerbate digitalis toxicity


Esmolol (Brevibloc)

Beta-blockers are generally contraindicated in cocaine toxicity. Some recommend to "save use" together with a vasodilator, only to manage life-threatening hypertension, tachycardia, and aortic dissection unresponsive to other therapeutic interventions. Short half-life of 8 min allows for titration to desired effect and quick discontinuation if needed.

Adult

250-500 mcg/kg/min IV loading dose for 1 min; followed by 50 mcg/kg/min maintenance infusion for 4 min; if adequate therapeutic effect not observed within 5 min, repeat loading dose and follow with maintenance infusion by using increments of 50 mcg/kg/min IV for 4 min; sequence may be repeated as many as 4 times prn; as desired BP approached, omit loading infusion and reduce incremental dose of maintenance infusion from 50 to 25 mcg/kg/min or less; interval between titration steps may be increased 5-10 min prn

Pediatric

Not established; suggested dose is 100-500 mcg/kg IV over 1 min

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity may increase when administered with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity increases when administered with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents

Documented hypersensitivity; uncompensated CHF; bradycardia; cardiogenic shock; AV conduction abnormalities

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm may worsen when abruptly withdrawn; withdraw slowly and monitor patient closely


NTG (Deponit, Nitrostat)

Used to treat acute hypertension and cardiac chest pain. Relaxes vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production, decreasing BP. Selection of NTG or sodium nitroprusside based on clinician's preference.

Adult

IV: May administer bolus of 12.5-25 mcg IV before continuous infusion; initial infusion rate of 10-20 mcg/min IV may be increased 5-10 mcg/min q5-10min until desired clinical or hemodynamic response achieved; rates of 500 mcg/min IV may be required
SL: 400 mcg; may repeat as needed until therapeutic goal achieved

Pediatric

Not established

Aspirin and indomethacin may increase nitrate serum concentrations; marked symptomatic orthostatic hypotension may occur with coadministered calcium channel blockers (may need to adjust dose of either agent); increased bioavailability of dihydroergotamine (DHE) and decreased coronary vasodilation of NTG may occur when these agents are used concurrently

Documented hypersensitivity; severe anemia, shock, postural hypotension, head trauma, closed-angle glaucoma, cerebral hemorrhage, hypovolemia, constrictive pericarditis or pericardial effusion, hypertrophic cardiomyopathy, and sildenafil (Viagra) use within previous 24 h

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in coronary artery disease, low systolic BP, glaucoma, hepatic disease, or hyperthyroidism


Phentolamine (Regitine)

Alpha1- and alpha2-adrenergic blocking agent that blocks circulating epinephrine and norepinephrine action, reducing hypertension due to catecholamine effects on alpha-receptors.

Adult

5-20 mg IV/IM

Pediatric

0.05-0.1 mg/kg/dose IV/IM; repeat prn q2-4h until hypertension controlled

Concurrent epinephrine or ephedrine use may decrease effects; ethanol increases toxicity

Documented hypersensitivity; coronary or cerebral arteriosclerosis and renal impairment

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in tachycardia, peptic ulcer, and gastritis; cerebrovascular occlusions, MIs


Nitroprusside (Nitropress)

Used to treat acute hypertension. Produces vasodilation and increases cardiac inotropic activity. At high dosages, may exacerbate myocardial ischemia by increasing heart rate. Selection of NTG or sodium nitroprusside based on clinician's preference.

Adult

0.1 mcg/kg/min IV initially; titrate up q3-5min to effect (up to 5 mcg/kg/min)

Pediatric

1 mcg/kg/min IV initially; uptitrate prn to 8 mcg/kg/min IV infusion

Aspirin and indomethacin may increase nitrate serum concentrations; marked symptomatic orthostatic hypotension may occur with coadministered calcium channel blockers (may need to adjust dose of either agent); increased bioavailability of DHE and decreased coronary vasodilation of NTG may occur when used concurrently

Documented hypersensitivity; subaortic stenosis, idiopathic hypertrophic, and atrial fibrillation or flutter; sildenafil (Viagra) use within previous 24 h

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution with increased intracranial pressure, hepatic failure, severe renal impairment, and hypothyroidism; can lower BP and therefore should be used only when mean arterial pressures >70 mm Hg; not first-line drug in pregnant women unless hypertensive emergency; with renal or hepatic insufficiency levels may increase and can cause cyanide toxicity; monitor for thiocyanate and cyanide or to limit use to <24 h; risk of cyanide toxicity increased with infusions >2 mcg/kg/min


Norepinephrine (Levophed)

Stimulates alpha and beta1-adrenergic receptors with alpha-adrenergic predominance which increases cardiac muscle contractility, heart rate, and vasoconstriction; results are increased systemic BP and coronary blood flow. As a vasopressor, useful in hypotension not responsive to IV fluids alone.

Adult

0.5-30 mcg/min IV; titrate to effect

Pediatric

0.1-2 mcg/kg/min IV initial; begin low and titrate to effect

Chlorpromazine enhances pressor response by blocking bradycardia

Documented hypersensitivity; peripheral or mesenteric vascular thrombosis (may increase ischemia and extend area of infarct)

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

If possible, correct blood-volume depletion before therapy; extravasation may cause severe tissue necrosis (should be administered into large vein); caution in occlusive vascular disease


Epinephrine

Considered the single most useful drug in cardiac arrest. Increases coronary perfusion pressure.

Adult

1 mg (10 mL of 1:10,000 solution) IVP q3-5min or 0.1 mg/kg IVP q3-5 min during resuscitation; follow each dose with 20 mL flush, elevate arm for 10-20s after dose
Higher doses do not improve survival or neurologic outcome
Endotracheal administration requires 2-2.5 times IV dose

Pediatric

0.01 mg/kg IV/IO (0.1 mL/kg of 1:10,000 standard concentration); administer q3-5min during arrest (maximum dose 1 mg)
0.1 mg/kg ET (0.1 mL/kg of 1:1000 HIGH concentration) administered during arrest q3-5min until IV/IO access achieved; then begin with first IV dose)

Increases toxicity of beta- and alpha-blocking agents and that of halogenated inhalational anesthetics

Documented hypersensitivity; cardiac arrhythmias, angle-closure glaucoma; local anesthesia in areas such as fingers or toes because vasoconstriction may produce sloughing of tissue; during labor (may delay second stage of labor)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in elderly, prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias


Vasopressin

May improve vital organ blood flow, cerebral oxygen delivery, ability to be resuscitated, and neurologic recovery.

Adult

40 Units IV single dose

Pediatric

Not established

Lithium, epinephrine, demeclocycline, heparin, and alcohol may decrease effects; chlorpropamide, urea, fludrocortisone, and carbamazepine may potentiate effects

Documented hypersensitivity; coronary artery disease

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cardiovascular disease, seizure disorders, nitrogen retention, asthma, or migraine; excessive doses may result in hyponatremia

GI agents

Whole-bowel irrigation with polyethylene glycol promotes the passage of cocaine packets through the GI tract. Activated charcoal may be empirically used to minimize systemic absorption of the toxin.


Polyethylene glycol (Colovage, CoLyte, GoLYTELY, NuLytely)

Laxative with strong electrolyte and osmotic effects. Cathartic actions in GI tract. May be indicated in treatment of cocaine ingestion in people who carry cocaine packages in their body. Must administer after activated charcoal. Liquid reconstituted per package instructions.

Adult

240 mL (8 oz) PO/NG q10min, to 4 L total or until rectal effluent clear and packets removed

Pediatric

Not established; recommended dose 25-40 mL/kg/h PO/NG for 4-10 h or until rectal effluent clear and packets removed

Reduces effectiveness and absorption of oral medications

Documented hypersensitivity; colitis; megacolon; bowel perforation; gastric retention; GI obstruction

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in ulcerative colitis and hot-loop polypectomy; adverse events (eg, fluid and sodium retention) rare


Activated charcoal (Liqui-Char)

Emergency treatment for absorption of drugs or chemicals. Network of pores adsorbs 100-1000 mg of drug per gram of charcoal. Does not dissolve in water. Some formulations also contain a cathartic.
For maximum effect, administer within 30 min of poison ingestion. Although value of multiple doses to treat acute drug ingestion not established, in some carefully considered situations, dose may be repeated at half original dose q2-6h until symptoms of toxicity subside, serum drug concentrations return to reference range (if initially elevated) or drug packets eliminated. Repeat doses should not contain cathartic.

Adult

5-10 times estimated weight of drug ingested or 1 g/kg body weight PO as single dose

Pediatric

<1 year: 1 g/kg PO without cathartic
1-12 years: 1-2 g/kg or 15-30 g PO without cathartic
>12 years: Administer as in adults

May inactivate ipecac syrup if used concomitantly; effectiveness of other medications may decrease if coadministered; do not mix with sherbet, milk, or ice cream (decreases adsorptive properties)

Documented hypersensitivity; poisoning or overdose of mineral acids and alkalies; unprotected airway with absent gag reflex

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Protect airway before administration if gag reflex is absent or if development of a decreased level of consciousness, seizures, or other airway risks is a concern
If formulation used contains cathartic, electrolyte abnormalities may occur, particularly in children and with repeated doses.
Can administer in early stages of gastric lavage; gastric lavage returns are black
Monitor bowel sounds and bowel function if repeat administration is considered since repeat administration is contraindicated with ileus; not effective for poisoning with ethanol, methanol, iron-salt poisoning and other nonadsorbed toxins; after emesis induced by ipecac syrup, patient may not tolerate activated charcoal for 1-2 h

Nutrients

Thiamine should be administered before glucose to prevent Wernicke encephalopathy.


Thiamine (Vitamin B1)

Administered before glucose to prevent Wernicke encephalopathy.

Adult

100 mg IV over 5 min

Pediatric

10-25 mg IV over 5 min

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Sensitivity reactions; intradermal test dose recommended in suspected sensitivity as anaphylactic deaths due to allergic reactions have resulted from IV use.
Sudden onset or worsening of Wernicke encephalopathy after administration of glucose may occur in thiamine-deficient patients, therefore, administer before or together with dextrose-containing fluids in suspected thiamine deficiency.


Dextrose (D-glucose)

Monosaccharide absorbed from intestine and distributed, stored, and used by tissues. Parenteral injection used in patients unable to sustain adequate oral intake. Direct oral absorption rapidly increases blood glucose concentrations. Effective in small doses and no evidence suggests toxicity. Concentrated infusions provide increased amounts of glucose and increased caloric intake in small volume of fluid.

Adult

50 mL D50W (25 g dextrose) IV

Pediatric

0.5-1 g/kg per PALS protocol
Infants: 5-10 mL/kg D10W
Children: 2-4 mL/kg D25W

In patients who may have decreased thiamine stores (eg, alcoholics, starvation) administer thiamine before or concomitantly with glucose to avoid precipitation of Wernicke syndrome

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

May cause nausea, which also may occur with hypoglycemia; IV solutions may dilute serum electrolyte concentrations or overhydration in fluid overload; caution in congestion or pulmonary edema; hypertonic dextrose given peripherally may cause thrombosis (use central venous catheter); caution in subclinical diabetes mellitus or carbohydrate intolerance; increased risk of significant hyperglycemia or hyperosmolar syndrome if administered rapidly, especially in chronic uremia or carbohydrate intolerance; do not administer concentrated solutions SC or IM; infusion >0.5 g/kg/h IV may produce glycosuria; at infusion 0.8 g/kg/h IV, incidence of glycosuria is 5%; closely monitor fluid balance, electrolyte concentrations, and acid-base balance; may produce vitamin B-complex deficiency; perform bedside glucose tests to reduce potential for neurologic complications due to inappropriate use of glucose; thiamine should be administered before dextrose

More on Toxicity, Cocaine

Overview: Toxicity, Cocaine
Differential Diagnoses & Workup: Toxicity, Cocaine
Treatment & Medication: Toxicity, Cocaine
Follow-up: Toxicity, Cocaine
References
[ CLOSE WINDOW ]

References

  1. Gold MS. Cocaine (and crack): clinical aspects. In: Lowinson JH, et al, eds. Substance Abuse: A Comprehensive Text. 2nd ed. Lippincott Williams & Wilkins: Baltimore, Md; 1992.

  2. Rose JS. Cocaethylene: a current understanding of the active metabolite of cocaine and ethanol. Am J Emerg Med. Jul 1994;12(4):489-90. [Medline].

  3. Signs SA, Dickey-White HI, Vanek VW, et al. The formation of cocaethylene and clinical presentation of ED patients testing positive for the use of cocaine and ethanol. Am J Emerg Med. Nov 1996;14(7):665-70. [Medline].

  4. Karch SB. Cardiac arrest in cocaine users. Am J Emerg Med. Jan 1996;14(1):79-81. [Medline].

  5. Darke S, Kaye S, Duflou J. Comparative cardiac pathology among deaths due to cocaine toxicity, opioid toxicity and non-drug-related causes. Addiction. Dec 2006;101(12):1771-7. [Medline].

  6. Qureshi AI, Suri MF, Guterman LR, et al. Cocaine use and the likelihood of nonfatal myocardial infarction and stroke: data from the Third National Health and Nutrition Examination Survey. Circulation. Jan 30 2001;103(4):502-6. [Medline].

  7. Hollander JE, Hoffman RS, Gennis P, et al. Prospective multicenter evaluation of cocaine-associated chest pain. Cocaine Associated Chest Pain (COCHPA) Study Group. Acad Emerg Med. Jul-Aug 1994;1(4):330-9. [Medline].

  8. Jouriles NJ. Pericardial and myocardial disease. In: Rosen P, ed. Emergency Medicine: Concepts and Clinical Practice. 5th ed. St Louis, Mo: Mosby; 2002.

  9. Ruttenber AJ, Lawler-Heavner J, Yin M, et al. Fatal excited delirium following cocaine use: epidemiologic findings provide new evidence for mechanisms of cocaine toxicity. J Forensic Sci. Jan 1997;42(1):25-31. [Medline].

  10. Callaway CW, Clark RF. Hyperthermia in psychostimulant overdose. Ann Emerg Med. Jul 1994;24(1):68-76. [Medline].

  11. 2006 National Survey on Drug Use and Health. SAMHSA; 2006. [Full Text].

  12. Drug Abuse Warning Network, 2005:National Estimates of Drug-RelatedEmergency Department Visits. SAMHSA; 2006. 23.

  13. Drug Abuse Warning Network, 2003. Area Profiles of Drug-Related Mortality. Available at: http://dawninfo.samhsa.gov/files/ME_report_2003_Front.pdf. [Full Text].

  14. Hollander JE, Todd KH, Green G, et al. Chest pain associated with cocaine: an assessment of prevalence in suburban and urban emergency departments. Ann Emerg Med. Dec 1995;26(6):671-6. [Medline].

  15. California. Turner died of overdose. The New York Times. January 17, 2008;p A23.

  16. US Department of Health and Human Services, Substance Abuse and Mental Health Services Administration. Drug Abuse Warning Network, 2004: National Estimates of Drug-Related Emergency Department Visits. Available at http://dawninfo.samhsa.gov/files/DAWN2k4ED.htm#Dred2.

  17. Hollander JE, Hoffman RS. Cocaine-induced myocardial infarction: an analysis and review of the literature. J Emerg Med. Mar-Apr 1992;10(2):169-77. [Medline].

  18. Shanti CM, Lucas CE. Cocaine and the critical care challenge. Crit Care Med. Jun 2003;31(6):1851-9. [Medline].

  19. Hoffman RS, Reimer BI. "Crack" cocaine-induced bilateral amblyopia. Am J Emerg Med. Jan 1993;11(1):35-7. [Medline].

  20. Ball SA, Carroll KM, Babor TF, et al. Subtypes of cocaine abusers: support for a type A-type B distinction. J Consult Clin Psychol. Feb 1995;63(1):115-24. [Medline].

  21. Rivara FP, Mueller BA, Somes G, et al. Alcohol and illicit drug abuse and the risk of violent death in the home. JAMA. Aug 20 1997;278(7):569-75. [Medline].

  22. Lewin NA, Goldfrank LR, Weisman RS. Cocaine. In: Goldfrank LR, et al, eds. Goldfrank's Toxicologic Emergencies. 3rd ed. Appleton Century Crofts: Norwalk, Conn; 1986.

  23. McCarron MM, Wood JD. The cocaine 'body packer' syndrome. Diagnosis and treatment. JAMA. Sep 16 1983;250(11):1417-20. [Medline].

  24. Perrone J, Hoffman RS. Cocaine. In: Tintinalli JE, ed. Emergency Medicine: A Comprehensive Study Guide. 4th ed. NY: McGraw-Hill; 1996.

  25. Renzi FP. Cocaine poisoning. In: Harwood-Nuss AL, ed. The Clinical Practice of Emergency Medicine. 2nd ed. Philadelphia, Pa: Lippincott Raven Publishers; 1996.

  26. DiMaio TG, DiMaio VJM. Excited Delirium Syndrome: Cause of Death and Prevention. New York: CRC Taylor and Francis Group; 2006.

  27. American Heart Association. Toxicology in Emergency Cardiovascular Care. In: Field JM. Advanced Cardiovascular Life Support Resource Text for Instructors and Experienced Providers. 2008:259-287.

  28. McIntyre KM. Vasopressin in asystolic cardiac arrest. N Engl J Med. Jan 8 2004;350(2):179-81. [Medline].

  29. Wenzel V, Krismer AC, Arntz HR, Sitter H, Stadlbauer KH, Lindner KH. A comparison of vasopressin and epinephrine for out-of-hospital cardiopulmonary resuscitation. N Engl J Med. Jan 8 2004;350(2):105-13. [Medline].

  30. Derlet RW, Tseng CC, Albertson TE. Cocaine toxicity and the calcium channel blockers nifedipine and nimodipine in rats. J Emerg Med. Jan-Feb 1994;12(1):1-4. [Medline].

  31. Derlet RW. More on lidocaine use in cocaine toxicity. J Emerg Nurs. Aug 1998;24(4):303. [Medline].

  32. Malbrain ML, Neels H, Vissers K, et al. A massive, near-fatal cocaine intoxication in a body-stuffer. Case report and review of the literature. Acta Clin Belg. 1994;49(1):12-8. [Medline].

  33. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Toxicology in ECC. Circulation. 2005;112:IV-126-IV-132.

  34. Committee on Child Abuse and Neglect. Distinguishing sudden infant death syndrome from child abuse fatalities. Committee on Child Abuse and Neglect. American Academy of Pediatrics. Pediatrics. Jul 1994;94(1):124-6. [Medline].

  35. Aufderheide TP, Gibler WB. Acute ischemic coronary syndrome. In: Rosen P, ed. Emergency Medicine: Concepts and Clinical Practice. 4th ed. St Louis, Mo: Mosby; 1998.

  36. Kercher EE. Anxiety disorders. In: Rosen P, ed. Emergency Medicine: Concepts and Clinical Practice. 4th ed. St Louis, Mo: Mosby; 1998.

  37. Goldfrank LR, Flomenbaum NE, Lewin NA, Weisman RS. Nonseasonal heatstroke. In: Goldfrank LR, et al, eds. Goldfrank's Toxicologic Emergencies. 3rd ed. Appleton Century Crofts: Norwalk, Conn; 1986.

  38. Colucciello SA, Tomaszewski C. Substance abuse. In: Rosen P, ed. Emergency Medicine: Concepts and Clinical Practice. 4th ed. St Louis, Mo: Mosby; 1998.

  39. Marzuk PM, Tardiff K, Leon AC, et al. Fatal injuries after cocaine use as a leading cause of death among young adults in New York City. N Engl J Med. Jun 29 1995;332(26):1753-7. [Medline].

  40. Brookoff D, O'Brien KK, Cook CS, et al. Characteristics of participants in domestic violence. Assessment at the scene of domestic assault. JAMA. May 7 1997;277(17):1369-73. [Medline].

  41. Ostrea EM Jr, Ostrea AR, Simpson PM. Mortality within the first 2 years in infants exposed to cocaine, opiate, or cannabinoid during gestation. Pediatrics. Jul 1997;100(1):79-83. [Medline].

  42. Reece RM. Fatal child abuse and sudden infant death syndrome: a critical diagnostic decision. Pediatrics. Feb 1993;91(2):423-9. [Medline].

  43. 2006 National Survey on Drug Abuse and Health: National Results. SAMHSA; 2007.

  44. ACEP Clinical Policies Committee; Clinical Policies Subcommittee on Seizures. Clinical Policy: Critical issues in the evaluation and management of adult patients presenting to the emergency department with seizures. Ann Emerg Med. May 2004;43(5):605-25. [Medline].

  45. Toxicology in Emergency Cardiovascular Care. In: Cummins RO, Fields JM, & Hazinski MF. ACLS for Experienced Providers. Dallas TX: American Heart Association; 2003:Chapter 3.

  46. Albertson TE, Derlet RW, Van Hoozen BE. Methamphetamine and the expanding complications of amphetamines. West J Med. Apr 1999;170(4):214-9. [Medline].

  47. American Heart Association in Collaboration with ILCOR. Toxicology in ECC. In: Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. American Heart Association. 2000;I-223-I-228.

  48. Bailey DN. Cocaethylene: a novel cocaine homolog. West J Med. Jul 1997;167(1):38-9. [Medline].

  49. Bandi V. Recognizing drug-induced hyperthermia syndrome: how to distinguish between the possible toxicities. J Crit Illn. Dec 2002.

  50. Billman GE. The effect of adrenergic receptor antagonists on cocaine-induced ventricular fibrillation: alpha but not beta adrenergic receptor antagonists prevent malignant arrhythmias independent of heart rate. J Pharmacol Exp Ther. Apr 1994;269(1):409-16. [Medline].

  51. Bontempo LJ. Rhabdomyolysis. In: Rosen P, ed. Emergency Medicine: Concepts and Clinical Practice. 5th ed. St Louis, Mo: Mosby; 2002.

  52. Brady WJ, Ferguson JD, Ullman EA, et al. Myocarditis: emergency department recognition and management. Emerg Med Clin North Am. Nov 2004;22(4):865-85. [Medline].

  53. Brookoff D, Rotondo MF, Shaw LM, et al. Coacaethylene levels in patients who test positive for cocaine. Ann Emerg Med. Mar 1996;27(3):316-20. [Medline].

  54. Bruce CJ, Livingston DH, Schneider CA, et al. The effect of cocaine on the physiologic response to hemorrhagic shock. Surgery. Aug 1993;114(2):429-34; discussion 434-5. [Medline].

  55. Calder KK, Severyn FA. Surgical emergencies in the intravenous drug user. Emerg Med Clin North Am. Nov 2003;21(4):1089-116. [Medline].

  56. Camus P, Bonniaud P, Fanton A, et al. Drug-induced and iatrogenic infiltrative lung disease. Clin Chest Med. Sep 2004;25(3):479-519, vi. [Medline].

  57. Cobaugh DJ, Schneider SM, Benitez JG, et al. Cocaine balloon aspiration: successful removal with bronchoscopy. Am J Emerg Med. Sep 1997;15(5):544-6. [Medline].

  58. Coluciello SA, Hockburger RS. Suicide. In: Rosen P, ed. Emergency Medicine: Concepts and Clinical Practice. 4th ed. Mosby: St Louis, Mo; 1998.

  59. Cregler LL, Mark H. Medical complications of cocaine abuse. N Engl J Med. Dec 4 1986;315(23):1495-500. [Medline].

  60. Cummins RO, ed. Toxicology in emergency cardiovascular care. In: ACLS for Experienced Providers. American Heart Association; 2003.

  61. Edell DS, McSwain M. Cocaine poisoning: an easily missed diagnosis in an infant. Clin Pediatr (Phila). Dec 1993;32(12):746-7. [Medline].

  62. Falk JL, O'Brien JF, Shesser R. Heart Failure. In: Rosen P, ed. Emergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002.

  63. Feldman JA, Fish SS, Beshansky JR, et al. Acute cardiac ischemia in patients with cocaine-associated complaints: results of a multicenter trial. Ann Emerg Med. Nov 2000;36(5):469-76. [Medline].

  64. Field JM, Hazinski MF, Gilmore D, eds. Handbook of Emergency Cardiovascular Care for Healthcare Providers. American Heart Association; 2005.

  65. Fines RE, Brady WJ, DeBehnke DJ. Cocaine-associated dystonic reaction. Am J Emerg Med. Sep 1997;15(5):513-5. [Medline].

  66. Gallagher EJ. Neurologic principles. In: Goldfrank LR, et al, eds. Goldfrank's Toxicologic Emergencies. 7th ed. New York: McGraw-Hill; 2002.

  67. Gatof D, Albert RK. Bilateral thumb burns leading to the diagnosis of crack lung. Chest. Jan 2002;121(1):289-91. [Medline].

  68. Gold MS, Miller MS, Jonas JM. Cocaine (and crack): neurobiology. In: Lowinson JH, Ruiz P, Millman RB, eds. Substance Abuse: A Comprehensive Text. 2nd ed. Lippincott Williams & Wilkins: Baltimore, Md; 1992.

  69. Goldfrank LR. Toxicologic radiology. In: Goldfrank LR, et al, eds. Goldfrank's Toxicologic Emergencies. 3rd ed. Appleton Century Crofts: Norwalk, Conn; 1986.

  70. Goldfrank LR, Flomenbaum NE, Lewin NA, et al. Principles of managing the poisoned or overdosed patient: An overview. In: Goldfrank LR, et al, eds. Goldfrank's Toxicologic Emergencies. 7th ed. 2002.

  71. Goldfrank LR, Flomenbaum NE, Lewin NA, Weisman RS. Withdrawal. In: Goldfrank LR, et al, eds. Goldfrank's Toxicologic Emergencies. 3rd ed. Appleton Century Crofts: Norwalk, Conn; 1986.

  72. Gumpeni R. Finding the cause of wheezing. (Diagnostic puzzlers: challenging cases to test your clinical skills). Journal of Respiratory Diseases;. July 1, 2003.

  73. Hamid H, El-Mallakh RS, Vandeveir K. Substance abuse: medical and slang terminology. South Med J. Mar 2005;98(3):350-62. [Medline].

  74. Heilig S, Rodriguez M, Martin S, Louie D, eds. Domestic violence: A practical approach for clinicians. San Francisco Medical Society:Available at: http://www.sfms.org/domestic.html. [Full Text].

  75. Hoffman RS. Respiratory principles. In: Goldfrank LR, et al, eds. Goldfrank's Toxicologic Emergencies. 7th ed. New York: McGraw-Hill; 2002.

  76. Hollander JE, Hoffman RS. Cocaine. In: Goldfrank LR, et al, eds. Goldfrank's Toxicologic Emergencies. 7th ed. 2002.

  77. Jones JS, Dickson K, Carlson S. Unrecognized pregnancy in the overdosed or poisoned patient. Am J Emerg Med. Sep 1997;15(5):538-41. [Medline].

  78. Karch SB. Karch's Pathology of Drug Abuse. In: Cocaine. 3rd ed. Boca Raton FL: CRC Press; 2002.

  79. Katz AA, Hoffman RS, Silverman RA. Phenytoin toxicity from smoking crack cocaine adulterated with phenytoin. Ann Emerg Med. Sep 1993;22(9):1485-7. [Medline].

  80. Keller KB, Lemberg L. The cocaine-abused heart. Am J Crit Care. Nov 2003;12(6):562-6. [Medline].

  81. Kleerup EC, Koyal SN, Marques-Magallanes JA, et al. Chronic and acute effects of "crack" cocaine on diffusing capacity, membrane diffusion, and pulmonary capillary blood volume in the lung. Chest. Aug 2002;122(2):629-38. [Medline].

  82. Kothari R, Barsan WG. Stroke. In: Rosen P, ed. Emergency Medicine: Concepts and Clinical Practice. 5th ed. St Louis, Mo: Mosby; 2002.

  83. Kulig K. General management principles. In: Rosen P, ed. Emergency Medicine: Concepts and Clinical Practice. 4th ed. Mosby: St Louis, Mo; 1998.

  84. Leikin JB, Heyn-Lamb R, Aks S, et al. The toxic patient as a potential organ donor. Am J Emerg Med. Mar 1994;12(2):151-4. [Medline].

  85. Littmann L, Monroe MH, Kerns WP 2nd, et al. Brugada syndrome and "Brugada sign": clinical spectrum with a guide for the clinician. Am Heart J. May 2003;145(5):768-78. [Medline].

  86. Lukas SE, Sholar M, Lundahl LH, et al. Sex differences in plasma cocaine levels and subjective effects after acute cocaine administration in human volunteers. Psychopharmacology (Berl). Jun 1996;125(4):346-54. [Medline].

  87. Marik PE, Varon J. The management of status epilepticus. Chest. Aug 2004;126(2):582-91. [Medline].

  88. McKay CA. Can the Laboratory Help Me? Toxicology Laboratory Testing in the Possibly Poisoned Pediatric Patient. CPEM. Jun 2005;6(2):116-122.

  89. McMullen MJ. Cocaine, amphetamines, and other stimulants. In: Rosen P, ed. Emergency Medicine: Concepts and Clinical Practice. 4th ed. Mosby: St Louis, Mo; 1998.

  90. Meraputi. Chronology of diseases and death from illicit recreational drug use in the US. Available at: http://www.meraputi.com.

  91. Miller MB. Arrhythmias associated with drug toxicity. Emerg Med Clin North Am. May 1998;16(2):405-17. [Medline].

  92. Minor RL Jr, Scott BD, Brown DD, et al. Cocaine-induced myocardial infarction in patients with normal coronary arteries. Ann Intern Med. Nov 15 1991;115(10):797-806. [Medline].

  93. Mokhlesi B, Corbridge T. Toxicology in the critically ill patient. Clin Chest Med. Dec 2003;24(4):689-711. [Medline].

  94. Mokhlesi B, Leiken JB, Murray P, et al. Adult toxicology in critical care: part I: general approach to the intoxicated patient. Chest. Feb 2003;123(2):577-92. [Medline].

  95. Mokhlesi B, Leikin JB, Murray P, et al. Adult toxicology in critical care: Part II: specific poisonings. Chest. Mar 2003;123(3):897-922. [Medline].

  96. Mone SM, Gillman MW, Miller TL, et al. Effects of environmental exposures on the cardiovascular system: prenatal period through adolescence. Pediatrics. Apr 2004;113(4 Suppl):1058-69. [Medline].

  97. National Institute on Drug Abuse. Current trends in drug use worldwide. NIDA Notes. 1998;Vol 13:9.

  98. National Institute on Drug Abuse. NIDA InfoFacts: Crack and Cocaine. Available at: http://www.nida.nih.gov/Infofacts/cocaine.html. 2005;[Full Text].

  99. National Institute on Drug Abuse. NIDA InfoFacts: Crack and Cocaine. Available at: http://www.nida.nih.gov/Infofacts/cocaine.html. Revised 3/05. [Full Text].

  100. National Institute on Drug Abuse. NIDA InfoFacts: Hospital Visits. Available at: http://www.drugabuse.gov/infofacts/HospitalVisits.html. 2005;[Full Text].

  101. National Institute on Drug Abuse. NIDA InfoFacts: Hospital Visits. Available at: http://www.drugabuse.gov/infofacts/HospitalVisits.html. [Full Text].

  102. National Institute on Drug Abuse. Research Report Series - Cocaine Abuse and Addiction. Available at: http://www.nida.nih.gov/ResearchReports/Cocaine/cocaine2.html#scope. 2005;[Full Text].

  103. National Institute on Drug Abuse. Research Report Series - Cocaine Abuse and Addiction. What is cocaine? Available at: http://www.nida.nih.gov/ResearchReports/Cocaine/cocaine2.html#scope. [Full Text].

  104. O'Halloran RL, Lewman LV. Restraint asphyxiation in excited delirium. Am J Forensic Med Pathol. Dec 1993;14(4):289-95. [Medline].

  105. Office of Applied Statistics, SAMHSA. Cocaine abuse. Available at: http://www.health.org/govpubs/rpo926/#Coca. [Full Text].

  106. Office of Applied Statistics, SAMHSA. Drug Abuse Warning Network (DAWN) Annual Medical Examiner Data 1999. Available at: http://www.samhsa.gov/oas/dawn.htm#MEcomp. [Full Text].

  107. Office of Applied Statistics, SAMHSA. Drug Abuse Warning Network (DAWN) Detailed Emergency Department Tables 1999. Available at: http://www.samhsa.gov/oas/dawn.htm. [Full Text].

  108. Office of Applied Statistics, SAMHSA. Drug-Related Emergency Room Cases Decline Nationally. 1997;Available at: http://www.samhsa.gov/press/97/971230o.htm. [Full Text].

  109. Office of Applied Studies, SAMHSA. Summary of Findings from the 1998 National Household Survey on Drug Abuse. Available at: http://www.samhsa.gov/oas/nhsda/98SummHtml/TOC.htm. [Full Text].

  110. Office of National Drug Control Policy, ONDCP. Drug Policy Information Clearinghouse Factsheet. Cocaine November 2003. Available at: http://www.whitehousedrugpolicy.gov/publications/factsht/cocaine/. [Full Text].

  111. Perron AD, Gibbs M. Thoracic aortic dissection secondary to crack cocaine ingestion. Am J Emerg Med. Sep 1997;15(5):507-9. [Medline].

  112. Pollack CV, Pollack ES. Seizures. In: Rosen P, ed. Emergency Medicine: Concepts and Clinical Practice. 5th ed. St Louis, Mo: Mosby; 2002.

  113. Pulse Check National Trends in Drug Abuse. Trends in drug use: Spring-Fall. In: Part II: Cocaine. 1996:Available at: http://ncjrs.org/pctrend2.html. [Full Text].

  114. Ramrakha PS, Barton I. Drug smuggler's delirium. BMJ. Feb 20 1993;306(6876):470-1. [Medline].

  115. Review of Optometry. Talc retinopathy. (Vitreous and retina). March 15, 2005.

  116. Saguil A. Evaluation of the patient with muscle weakness. Am Fam Physician. Apr 1 2005;71(7):1327-36. [Medline].

  117. Sauter D, Habal R. Drug therapy and substance abuse. In: Rosen P, ed. Emergency Medicine: Concepts and Clinical Practice. 5th ed. Mosby: St Louis, Mo; 2002.

  118. Savitt DL, Roberts JR, Merigian KS. Psychoactive drug abuse. In: Rosen P, ed. Emergency Medicine Concepts and Clinical Practice. 3rd ed. St Louis, Mo: Mosby; 1992.

  119. Schwartz DT. Diagnostic imaging in toxicology. In: Goldfrank LR, et al, eds. Goldfrank's Toxicologic Emergencies. 7th ed. 2002.

  120. Seymour A. Drug smuggler's delirium. BMJ. Apr 10 1993;306(6883):1002. [Medline].

  121. Substance Abuse and Mental Health Services Administration, Office of Applied Studies. Drug Abuse Warning Network, 2003. Interim National Estimates of Drug-Related Emergency Department Visits. DAWN Series D-26, DHHS Publication No. (SMA) 04-3972. Rockville, MD, 2004. Available at: http://dawninfo.samhsa.gov/files/DAWN_ED_Interim2003.pdf. [Full Text].

  122. Sudhakar CB, Al-Hakeem M, MacArthur JD, et al. Mesenteric ischemia secondary to cocaine abuse: case reports and literature review. Am J Gastroenterol. Jun 1997;92(6):1053-4. [Medline].

  123. Tazelaar HD, Karch SB, Stephens BG, et al. Cocaine and the heart. Hum Pathol. Feb 1987;18(2):195-9. [Medline].

  124. Ungar JR, Schwartz GR, Levine DG. Drug and substance abuse emergencies. In: Schwartz GR, ed. Principles and Practice of Emergency Medicine. 2nd ed. Philadelphia, Pa: Lea & Febiger; 1992.

  125. Van Mieghem C, Sabbe M, Knockaert D. The clinical value of the ECG in noncardiac conditions. Chest. Apr 2004;125(4):1561-76. [Medline].

  126. Vassallo SU, Delaney KA. Thermoregulatory principles. In: Goldfrank LR, et al, eds. Goldfrank's Toxicologic Emergencies. 7th ed. 2002.

  127. Volkow ND, Wang GJ, Fowler JS, et al. Enhanced sensitivity to benzodiazepines in active cocaine-abusing subjects: a PET study. Am J Psychiatry. Feb 1998;155(2):200-6. [Medline].

  128. Wang RY. pH-dependent cocaine-induced cardiotoxicity. Am J Emerg Med. Jul 1999;17(4):364-9. [Medline].

  129. Watson WA, Litovitz TL, Klein-Schwartz W, et al. 2003 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 2004;22(5):335-404. [Medline].

  130. Weiner AL, Bayer MJ, McKay CA Jr, et al. Anticholinergic poisoning with adulterated intranasal cocaine. Am J Emerg Med. Sep 1998;16(5):517-20. [Medline].

  131. Wilson LD. Rapid progression of coronary artery disease in the setting of chronic cocaine abuse. J Emerg Med. Jul-Aug 1998;16(4):631-4. [Medline].

  132. Winbery S, Blaho K, Logan B, et al. Multiple cocaine-induced seizures and corresponding cocaine and metabolite concentrations. Am J Emerg Med. Sep 1998;16(5):529-33. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

cocaine toxicity, cocaine ingestion, cocaine poisoning, benzoylmethylecgonine, blow, coke, crack, snow, toot, nose candy, freebase, club drug, rock, Erythroxylon coca, ecgonine, norcocaine, ethylbenzoylecgonine, cocaethylene, cocaine-induced myocardial infarction, cocaine-induced MI, speedball, ischemic stroke, hemorrhagic stroke, subarachnoid hemorrhage, hyperthermia, agitated delirium, excited delirium, acute coronary syndromes, cocaine-associated rhabdomyolysis, hyperthermia, ventricular dysrhythmias, myocarditis, microfocal fibrosis, contraction band necrosis, tachydysrhythmias, cardiac arrest, coronary atherosclerosis, dilated cardiomyopathy, cocaine-induced seizures, cocaine-associated seizures, neuroleptic malignant syndrome, NMS, dystonic reactions, bradykinesia, akinesia, akathisia, pseudoparkinsonism, catalepsy, neuroleptic-induced dystonias, sudden death, psychostimulant-induced hyperthermia, myoglobinuria, acute tubular necrosis, acidemia, aortic dissection, pneumothorax, pneumopericardium, pneumomediastinum, pulmonary hemorrhage, pulmonary infarction, diffuse alveolar hemorrhage, neurogenic pulmonary edema, exacerbation of asthma, eosinophilic lung disease, chronic diffuse interstitial pneumonia, sudden infant death syndrome, SIDS, pulmonary hypertension, transient pulmonary infiltrates, crack lung, nasal septum perforation, bronchiolitis obliterans organizing pneumonia, granulomatosis, sinusitis, epiglottitis, bronchitis, cellulose granulomas in lung, panlobular emphysema, alveolar accumulation of carbonaceous material, airway burns, tracheal stenosis, hypersensitivity pneumonitis, toxic encephalopathy, neurogenic syncope, movement disorders, cocaine-induced hypertension, crack dancing, mesenteric ischemia, renal infarction, cocaine-associated cerebral vasculitis, central retinal artery occlusion, blurring of vision, endophthalmitis, optic neuropathy, corneal ulcerations, hallucinations, anxiety, depression, delirium, paranoia, toxic psychosis, cocaine bingeing, pocket shot, necrotizing angiitis, acquired immunodeficiency syndrome, AIDS, thrombophlebitis, cellulitis, talc-induced hepatitis, subacute bacterial endocarditis, SBE, foreign-particle pulmonary emboli, tetanus, cotton fever, malaria

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Lynn Barkley Burnett, EdD, MS, LLB(c), Medical Advisor, Fresno County Sheriff's Department; Attending Consultant-in-Chief and Chairman, Medical Ethics, Clinical Faculty, Community Medical Centers; Adjunct Professor of Forensic Pathology, National University Master of Forensic Science Program
Lynn Barkley Burnett, EdD, MS, LLB(c) is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Association for the Advancement of Science, American Association of Suicidology, American Cancer Society, American College of Sports Medicine, American Heart Association, American Professional Society on the Abuse of Children, American Public Health Association, American Society for Bioethics and Humanities, American Society of Law Medicine and Ethics, American Stroke Association, Association of Military Surgeons of the US, Christian Medical & Dental Society, European Society for Trauma and Emergency Surgery, European Society of Cardiology, European Society of Intensive Care Medicine, European Society of Paediatric and Neonatal Intensive Care, Faculty of Forensic and Legal Medicine of the Royal College of Physicians of London, International Homicide Investigators Association, New York Academy of Sciences, Royal College of Surgeons of Edinburgh, Royal Society of Medicine, Society for Academic Emergency Medicine, Society of Critical Care Medicine, and World Association for Disaster and Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: eMedicine.com, Inc. Consulting fee Consulting

Medical Editor

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, Associate Clinical Professor; Medical and Managing Director, South Texas Poison Center, Department of Surgery/Emergency Medicine and Toxicology, University of Texas Health Science Center at San Antonio
Miguel C Fernandez, MD, FAAEM, FACEP, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine, and Texas Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, ABAT, Director of Pharmacy, Sacred Heart Hospital
John T VanDeVoort, PharmD, ABAT is a member of the following medical societies: American Academy of Clinical Toxicology and American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

John G Benitez, MD, MPH, FACMT, FACPM, FAAEM, Associate Professor, Department of Medicine, Clinical Pharmacology Division, Vanderbilt University; Managing Director, Tennessee Poison Center
John G Benitez, MD, MPH, FACMT, FACPM, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, and Wilderness Medical Society
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.