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Cocaine Toxicity Clinical Presentation

  • Author: Lynn Barkley Burnett, MD, EdD; Chief Editor: Asim Tarabar, MD  more...
 
Updated: Jun 30, 2016
 

History

The factors addressed below focus on drug use, and supplement elements of the standard medical-history interview. A drug history is indicated in all patients, although it is all too often not obtained;[24] it should be particularly complete in those presenting with drug reactions, acute anxiety, or other psychological problems, as well as in those with acute cardiovascular, pulmonary, or neurologic symptoms. If the patient is confused or unresponsive, query relatives, friends, or witnesses about antecedent activities, and seizures or syncope. This is crucial, especially if patients are carrying cocaine in their body, because they often have no stigmata of drug abuse.

History of present illness can be determined as follows:

  • What drug was used?
  • When was the substance used and for how long was it used? What is the patient's tolerance, cross-tolerance, and reverse tolerance? Is evidence of a withdrawal syndrome present?
  • What was the total amount of cocaine used? How does this compare with the amount generally used? How long after cocaine use were symptoms noted?
  • By what route was it taken? For how long has this route been used?
  • Does the patient have symptoms such as pain (eg, chest, abdominal), dyspnea, altered tactile sensation (eg, cocaine bugs, Magnan sign), or hallucinations (eg, lilliputian hallucination, halo lights around objects)? Was altered mental status or seizure reported?
  • Is the patient pregnant (eg, decreased plasma cholinesterase)?
  • Is the patient a victim of domestic violence? (Substance abuse may develop or worsen as a result of domestic violence. Accordingly, it is appropriate to consider domestic violence when evaluating a patient for alcohol intoxication or drug toxicity and overdose.)

Review of systems is as follows:

  • Is the effect of cocaine increased secondary to liver disease or CHF? Is evidence of MI or coronary artery disease present? Is evidence of a dysrhythmogenic substrate (eg, myocarditis, cardiomyopathy, WPW) present?
  • When considering the extent of the review of systems (ROS), be mindful of the wide range of organ systems that cocaine and its routes of administration can affect.

Medication and drug use history can be determined as follows:

  • What is the patient's average daily use? What is his or her history of cocaine and other drug use? (The mechanism of fatality differs for long-term cocaine users.)
  • Does the patient use tobacco (ie, does he or she have increased risk for atherosclerosis and coronary vasospasm)? How many packs does the patient smoke per day?
  • Does the patient use alcohol (ie, is cocaethylene formation possible)? If so, did the patient drink before or during cocaine uses? How much alcohol was consumed?
  • What other substances were used? How much was consumed? What route of intake was used?
  • Does the patient have any other drug addictions? Were any drug combinations taken or were drugs taken to increase, prolong, or decrease the effects of cocaine?
  • Could medications taken by the patient potentiate the effects of cocaine? Is the patient in withdrawal?
  • What prompted the visit to the ED? DAWN data for 1998 reflect the reasons for cocaine-related ED visits: unexpected reaction (21.9%), overdose (15.1%), chronic effects (13.8%), accidental injury (4.9%), withdrawal (3.2%)
  • Does the patient want help in coping with cocaine use? DAWN data from 2004 reported that 46% of patients presenting to EDs did so for detoxification. [25]
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Physical

Multisystem effects of cocaine

Suspect cocaine use in patients, especially young patients, with altered mental status, new-onset seizure, hypertension, chest pain, myocardial ischemia or infarction, dyspnea, intracranial hemorrhage, epistaxis, or psychiatric illness. Pay particular attention to the assessment of vital signs and to a detailed examination of the cardiac, pulmonary, and neurologic systems, as listed below.

Association with trauma

Trauma is associated with use of cocaine. Cocaine can cause agitation, paranoia, distractibility, distorted perception, and depression. All of these may increase the likelihood of violence, suicide, or accidental injury. When cocaine is combined with alcohol, the frequency of ED presentations is substantially greater than when cocaine is used alone.

Differential diagnosis

Cocaine overdose may resemble serotonin syndrome, lithium toxicity, cyclic antidepressants toxicity, neuroleptic malignant syndrome (NMS), thyroid storm, and other hyperadrenergic states.

Consider the diagnosis of phenytoin toxicity in cocaine users who present with lethargy or cerebellar findings. Signs of phenytoin toxicity are correlated with serum levels and include nystagmus, ataxia, dysarthria, lethargy, hypotension, and coma.

Vital signs and general presentation

Although bradycardia is reported as an initial effect, the classic presentation of a patient under the influence of cocaine is tachycardia and hypertension. Although the initial increase in heart rate and blood pressure (BP) are dose dependent, plateau of heart rate and BP may occur secondary to an acute tachyphylaxis, even with increasing concentrations of serum cocaine.[26]

When Hollander and Hoffman reviewed the literature concerning 91 patients with cocaine-induced MI, they found that as many patients were bradycardic as tachycardic, and one third were hypertensive.[27] As a result of pathologic vasoconstriction, a patient with hemorrhagic trauma may present with a normal mean arterial pressure. Cocaine causes pathologic vasoconstriction, thus hypovolemia secondary to hemorrhage may be delayed in recognition because the patient maintains a normal mean arterial pressure. This combination of pathophysiologic factors, coupled with delayed recognition, increases the potential for cerebral insult.[28]

Chronic cocaine use downregulates adrenergic receptors and decreases endogenous catecholamine stores in the heart. This may affect the patient's presentation, as was observed in a study of patients admitted to a trauma service. Of 84 patients with a systolic BP less than 100 mm Hg, 45% had relative bradycardia (heart rate < 100 bpm). Toxicology data were obtained infrequently, but when determined, they demonstrated that cocaine was more frequently reported in patients with bradycardia (76%) than in those with tachycardia (26%).

The patient's skin may be cool and clammy though the patient is hyperthermic; therefore, obtaining a rectal temperature is advisable.

Cardiovascular findings

Cardiopulmonary complaints are the most common presenting manifestations of cocaine abuse and include chest pain (frequently observed in long-term use or overdose), MI, arrhythmia, and cardiomyopathy.

In individuals with cocaine-associated MI, median times to the onset of chest pain vary with the route or form of cocaine use: 30 minutes for intravenous use, 90 minutes for crack, and 135 minutes for intranasal use.

Chest pain may be observed in as many as 40% of patients presenting to the ED after admitting to cocaine use. In a study of urban and suburban EDs, cocaine or its metabolites were found in 17% of patients presenting with chest pain. This starkly contrasts with the pretest estimated prevalences of 2-4% for the suburban study site and 10% for the urban sites. The mean age of patients with chest discomfort and positive assays for cocaine was 36 years.

Cocaine and other stimulant use should be included in the differential diagnosis of any acute vascular problem. The long-term outcome of patients presenting with chest pain associated with cocaine use is comparable to patients presenting with “conventional” chest pain.[24]

Vascular spasm may cause blindness, renal infarction, limb ischemia, and intestinal ischemia. Accelerated atherogenesis and thrombosis of the superior mesenteric artery have been reported with chronic cocaine use.[29] Limb ischemia may occur after intra-arterial injection. This may be accidental, or intentional due to the unavailability of veins because of sclerosis secondary to repetitive puncture, or due to the desired effects from arterial injection.

Include cocaine use in the differential diagnosis of any acute vascular problem.

Vascular spasm may cause blindness, renal infarction, limb ischemia, and intestinal ischemia. Limb ischemia may occur after intra-arterial injection. This may be accidental, or intentional due to the unavailability of veins because of sclerosis secondary to repetitive puncture, or due to the desired effects from arterial injection.

Aortic dissection may also be associated with cocaine use.

Hypertension occurs frequently.

Other cardiovascular findings include the following:

  • Dysrhythmia (premature ventricular contractions [PVCs], supraventricular tachycardia [SVT], ventricular tachycardia [VT], and ventricular fibrillation [VF])
  • Vasomotor collapse
  • High-output heart failure

Respiratory findings

As reported in the literature, the primary acute pulmonary complaint associated with cocaine use is cough with black sputum (44% of patients). Chest pain is secondary, affecting 38% (pleurisy in 64% of patients with pain). Of patients with new-onset asthma who present to large urban EDs, 36.4% have a urine screen positive for cocaine (compared with 13.6% of control patients without asthma). Hemoptysis accounts for 25% of pulmonary complaints, the result of pulmonary and bronchial constriction and ischemia resulting in interstitial and alveolar hemorrhage.

"Crack lung," a syndrome usually occurring 1-48 hours after cocaine smoking, is a hypersensitivity pneumonitis. It consists of the constellation of chest pain, cough with hemoptysis, dyspnea, bronchospasm, pruritus, fever, diffuse alveolar infiltrates without effusions, and pulmonary and systemic eosinophilia.

Barotrauma, such as pneumothorax and pneumomediastinum, may result from smoking or snorting cocaine and then performing a prolonged Valsalva maneuver to increase the effect of the drug, or from coughing against a closed glottis. The increased airway pressure ruptures an alveolar bleb, and free air dissects along peribronchial paths into the mediastinum and pleural cavities.

The incidence of respiratory complaints in people who use cocaine is not known. The following respiratory toxic reactions are reported in association with cocaine use:

  • Barotrauma (eg, pneumothorax, pneumopericardium, pneumomediastinum)
  • Pulmonary hemorrhage or infarction
  • Diffuse alveolar hemorrhage
  • Pulmonary edema
  • Wheezing secondary to bronchial muscle constriction
  • Airway irritation via damage to bronchial epithelial cells, and stimulation of vagal receptors, inducing bronchospasm, exacerbating asthma
  • Eosinophilic lung disease
  • Recurrent transient pulmonary infiltrates with peripheral eosinophilia
  • Chronic diffuse interstitial pneumonia with mild fibrosis
  • CNS stimulant effects (eg, neurogenic pulmonary edema, respiratory depression in overdose or postictal state, abnormal hypoxic response in infants of cocaine-abusing mothers, sudden infant death syndrome (SIDS), and pulmonary hypertension)
  • Crack lung or transient pulmonary infiltrates
  • Nasal septum perforation and/or aspiration
  • Bronchiolitis obliterans organizing pneumonia
  • Granulomatosis
  • Sinusitis
  • Epiglottitis
  • Bronchitis
  • Cellulose granulomas in lung
  • Panlobular emphysema
  • Needle or other foreign body aspiration
  • Alveolar accumulation of carbonaceous material
  • Airway burns or tracheal stenosis
  • Tachypnea, irregular breathing
  • Respiratory arrest
  • Acute lung injury (noncardiogenic [increased permeability] pulmonary edema)

Eyes, nose, mouth, and throat findings

Signs include reactive mydriasis, nystagmus (generally vertical but may be bidirectional), epistaxis, atrophic mucosa, ulcerated nasal septa, perforations, acute inflammation or scarring of the tongue, epiglottis, vocal cords, and trachea.

Hoffman and Reimer list a variety of ophthalmologic complications from cocaine use[30] :

  • Cocaine-associated cerebral vasculitis, which may produce gradual decrease in visual acuity or acute blindness
  • Blurring of vision
  • Foreign-body granuloma
  • Foreign-body embolization
  • Optic neuropathy, resulting from chronic sinusitis due to intranasal cocaine use and manifesting as decreased visual acuity
  • Corneal ulcerations secondary to direct instillation of cocaine into the conjunctival fornix and vision loss caused by crack-induced corneal ulceration from direct irritation of the smoke, cocaine-induced epithelial disruption, and repeated mechanical disruption from rubbing
  • Torticollis, trismus, and laryngospasm may endanger the airway.

GI findings

Vomiting, diarrhea, and hyperactive bowel sounds may be present. When evaluating a patient with a history of cocaine use and a complaint of abdominal pain, consider mesenteric ischemia in the differential diagnosis. Patients with abdominal pain must also be evaluated for renal infarction.

The vascular supply to the intestine has many alpha-adrenergic receptors, and their stimulation may cause mesenteric ischemia. The clinical presentation of mesenteric ischemia includes abdominal pain and possibly tenderness, nausea, vomiting, and bloody diarrhea. Muscarinic receptor blockade results from high concentrations of cocaine, with anticholinergic effects on gastric motility that predisposes the person to ulceration from prolonged exposure to acid.

Skin, thermoregulatory, and renal findings

Patients may have sores or linear excoriations; crack pipe burns of the fingers or thumbs; thermal burns of the face and upper airway; and redness, swelling, and tenderness (secondary to phlebitis, vasculitis, cellulitis, and abscess formation).

Search for track marks in the usual sites, such as the antecubital fossae, and unusual sites, such as under the tongue and on top of the feet.

Excoriations from pruritus or hallucinations of crawling insects associated with cocaine use may also be found.

Cocaine affects the anterior hypothalamus, which increases the thermoset point. Agitation secondary to intoxication or withdrawal results in increased motor activity, which causes increased heat production.

Rule out occult infections in patients with fever.

Evaluate patients with abdominal or back pain for renal infarction.

Neurologic and psychiatric findings

Altered sensorium and acute seizures are the most common cocaine-associated neurologic syndromes observed in the ED, accounting for 52% of related presentations. Other cocaine-related neurologic processes are toxic encephalopathy, ischemic and hemorrhagic stroke, neurogenic syncope, and movement disorders. Use of cocaine also decreases rapid eye movement (REM) sleep.

Seizures, which can produce hyperthermia and lactic acidosis, are a major determinant of lethality.

About 3-4% of all strokes occur in patients aged 15-45 years. Cocaine is a common cause of stroke in young patients. Cocaine-induced hypertension may lead to hemorrhage from a cerebral aneurysm or ruptured arteriovenous malformation (AVM).

Extrapyramidal phenomena and other movement disorders, though uncommon, are reported in association with cocaine use. These effects are collectively referred to as "crack dancing." In a patient without a history of neuroleptic use such a presentation may be confusing to the ED physician.

Headaches, some potentially resulting from inhibited serotonin reuptake, are common in people who use cocaine, whereas cerebral vasculitis is rare.

Approximately 60% of people who regularly use cocaine report psychiatric complications of their drug use, and 18% have had visual or tactile hallucinations; a sensation of something crawling on the skin is most common.

Psychiatric complications commonly associated with cocaine use include anxiety, depression, paranoia, delirium, psychosis, and suicide. Toxic psychosis might be misdiagnosed as paranoid schizophrenia.

A crash follows cocaine binging and may result in extreme exhaustion (may be severe enough that the patient appears unresponsive), anxiety, psychomotor retardation, and increased appetite. Of note, the most common problem during a crash is depression that may reach suicidal proportions.

In withdrawal, depletion of dopamine and norepinephrine leads to dysphoria, depression, and drug craving.

In short, neurologic and psychiatric findings may include the following:

  • Normal sensorium
  • Altered mental status (a change in the level of consciousness or the content of consciousness)
  • Confusion
  • Restlessness
  • Severe agitation
  • An increase in purposeless psychomotor activity that may be exacerbated by nonspecific stimulation in the setting of cocaine use (commonly called cocaine leaps)
  • "Overamped" or "wired" behavior
  • Paranoia
  • Delirium (a florid abnormal mental state characterized by disorientation, fear, and irritability with misperception of sensory stimuli)
  • Headache
  • Tremor
  • Depression and extreme exhaustion associated with withdrawal following a binge

Renal findings

Vascular spasm may cause renal infarction. Cocaine may also exacerbate renal susceptibility to rhabdomyolysis by causing hyperthermia, vasoconstriction, and/or hypotension secondary to hypovolemia or MI.

Endocrine and metabolic findings

Acute toxic effects of cocaine may include acidosis, hyperkalemia, and hyperglycemia. Prolonged use of sympathomimetics, such as in a cocaine binge, may result in hypoglycemia.

Musculoskeletal findings

Cocaine use is among the drug-related causes of intrinsic muscle weakness. Wilson and Hobbs report a patient with Cori disease in whom cocaine unmasked subclinical skeletal muscle weakness, causing prolonged respiratory muscle insufficiency. Cocaine has also been implicated as a cause of impairment of neuromuscular transmission in a patient with myasthenia gravis.

Body cavity search

Packets of illicit drugs may be ingested or inserted into body cavities by "swallowers," "internal carriers," "couriers," or "mules" to intentionally transport drug, a practice called body packing. Another practice, body stuffing, involves swallowing relatively small amounts of loosely wrapped drug, or secreting packets in body cavities because of the fear of arrest. With suspicion of body packing or body stuffing, perform careful cavity searches of the rectum and vagina. Continued drug absorption is likely if toxicity continues for more than 4 hours.

Altered mental status

A number of etiologic possibilities are possible, including toxic (eg, drug intoxication, withdrawal), metabolic, structural or traumatic, infectious, epileptic, or psychogenic causes.

A simple toxicologic presentation is rare. Therefore, it is frequently necessary to differentiate agitation secondary to various intoxicants, withdrawal, or possibly both. In the agitated patient with extreme irritability, irrationality, and destructiveness, intoxication or withdrawal should be considered.

Cocaine causes a sympathomimetic toxidrome, as do amphetamines, hallucinogens, and PCP; PCP causes the most persistent psychophysiologic reactions. Withdrawal from alcohol or sedative-hypnotics may cause the triad of hyperthermia, agitated delirium, and seizures.

Phases of acute cocaine toxicity

Three phases are reported. In fatal cases, the onset and progression are accelerated, with convulsions and death frequently occurring in 2-3 minutes, though sometimes in 30 minutes. Cocaine stimulates the CNS in rostral-to-caudal fashion, with findings varying with the time since drug use.

Phase I (early stimulation) is as follows:

  • CNS findings - Mydriasis, headache, bruxism, nausea, vomiting, vertigo, nonintentional tremor (eg, twitching of small muscles, especially facial and finger), tics, preconvulsive movements, and pseudohallucinations (eg, cocaine bugs)
  • Circulatory findings - Possible increase in BP, slowed or increased pulse rate (possibly with ventricular ectopy), and pallor
  • Respiratory findings - Increase in rate and depth
  • Temperature findings - Elevated body temperature
  • Behavioral findings - Euphoria, elation, garrulous talk, agitation, apprehension, excitation, restlessness, verbalization of impending doom, and emotional lability

Phase II (advanced stimulation) is as follows:

  • CNS findings - Malignant encephalopathy, generalized seizures and status epilepticus, decreased responsiveness to all stimuli, greatly increased deep tendon reflexes, and incontinence
  • Circulatory findings - Hypertension; tachycardia; and ventricular dysrhythmias (possible), which then result in weak, rapid, irregular pulse and hypotension; and peripheral cyanosis
  • Respiratory findings - Tachypnea, dyspnea, gasping, and irregular breathing pattern
  • Temperature - Severe hyperthermia (possible)

Phase III (depression and premorbid state) is as follows:

  • CNS - Coma, areflexia, pupils fixed and dilated, flaccid paralysis, and loss of vital support functions
  • Circulatory - Circulatory failure and cardiac arrest (VF or asystole)
  • Respiratory - Respiratory failure, gross pulmonary edema, cyanosis, agonal respirations, and paralysis of respiration
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Causes

The National Institute on Drug Abuse (NIDA) estimates that 10% of individuals who begin using cocaine progress to serious, heavy use. After having tried cocaine, people cannot predict the extent to which they continue using the drug. According to 1999 DAWN data, patients visiting EDs for a drug-related cause provide the following reasons for using cocaine:

  • Dependence (49%)
  • Recreational use (37.6%)
  • Other psychic effects (19.7%)
  • Suicide (8.7%)

A positive family history of substance abuse is related to the speed of developing dependence on cocaine and an earlier age of onset.

Type A and type B dependency

Evidence suggests that cocaine dependence, similar to alcoholism, may have 2 subtypes, A and B (ie, type I and type II in the literature on alcoholism typology). Type A persons may develop cocaine dependence as a function of environmental influences, whereas type B persons may have certain premorbid risk factors that predispose them to a virulent form of cocaine abuse. Ball et al studied 399 patients with cocaine abuse or dependence in the first multidimensional subtyping study of cocaine users.[31] The most common presentation, observed in 67%, was type A. Women and African Americans most commonly had type A dependency, whereas men and whites most commonly had type B dependency.

Compared with persons with type A dependency, those with type B dependency had more severe abuse of alcohol and other drugs, addiction-related psychological impairment, antisocial behavior, and comorbid psychiatric problems.

Persons with type B dependency were more likely to be separated or divorced, to live alone or in an unstable situation, to have a family history of substance abuse, and to have had greater severity of childhood disorder than individuals with type A dependency. They also scored higher than those with type A dependency in assessments of sensation seeking, aggression, criminality, and violence.

Those with type B dependency had an early age of onset for antisocial personality disorder and early age of first use, first binge, first regular use, and first daily use of cocaine and alcohol. The quantity, frequency, duration, and severity of cocaine abuse and adverse effects (eg, loss of consciousness, chest pain, misperceived reality, violence, and use to relieve to stress) are greater with type B than with type A.

Although the groups do not differ in family history for psychiatric disorders, people with type B dependency had lifetime histories of major depression, suicide attempts, and total treatment episodes for psychiatric disorders as well as for abuse of alcohol and other drugs that were significantly greater than those with type A dependency.

No significant differences were found between the subtypes in terms of employment, education, referral source, number of close friends, age, time between the first use and the onset of symptoms of dependence, route of use, previous periods of abstinence from alcohol or other drugs, or the number of strategies used to control use.

Mental disorders

Rivara et al maintain that one half of those who abuse illicit drugs also have a mental disorder. Indeed, cocaine users, along with persons with alcoholism and those who abuse opiates, have elevated rates of antisocial personality, depression, anxiety, and polysubstance abuse. These traits also have been found in their first-degree relatives.[32]

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Contributor Information and Disclosures
Author

Lynn Barkley Burnett, MD, EdD LLB(c), Medical Advisor, Fresno County Sheriff's Office; Attending Consultant-in-Chief and Chairman, Medical Ethics, Community Medical Centers; Adjunct Assistant Clinical Professor of Emergency Medicine and Forensic Pathology, Touro University College of Osteopathic Medicine, California; Core Graduate Adjunct Professor of Forensic Pathology, National University Master of Forensic Science Program; Core Graduate Adjunct Professor of Leadership in Healthcare, Health Law and Healthcare Ethics, Kaplan University Graduate School of Healthcare Administration

Lynn Barkley Burnett, MD, EdD 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 Public Health Association, American Society for Bioethics and Humanities, American Society of Law, Medicine & Ethics, Association of Military Surgeons of the US, Christian Medical and Dental Associations, European Society of Cardiology, New York Academy of Sciences, Royal Society of Medicine, Society for Academic Emergency Medicine, Society of Critical Care Medicine, American Professional Society on the Abuse of Children, American Stroke Association, Royal College of Surgeons of Edinburgh, World Association for Disaster and Emergency Medicine, European Society of Intensive Care Medicine, European Society of Paediatric and Neonatal Intensive Care, European Society for Trauma and Emergency Surgery, International Homicide Investigators Association

Disclosure: Nothing to disclose.

Coauthor(s)

Jonathan Adler, MD, MS Instructor, Department of Emergency Medicine, Harvard Medical School, Massachusetts General Hospital

Jonathan Adler, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Carlos J Roldan, MD, FAAEM, FACEP Associate Professor, Department of Emergency Medicine, University of Texas Health Science Center at Houston Medical School; Consulting Staff, Department of Emergency Medicine, Memorial Hermann Hospital Lyndon Baines General Hospital and MD Anderson Cancer Center

Carlos J Roldan, MD, FAAEM, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Pain Society, American Society of Regional Anesthesia and Pain Medicine, International Association for the Study of Pain, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

John G Benitez, MD, MPH Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Undersea and Hyperbaric Medical Society, Wilderness Medical Society, American College of Occupational and Environmental Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT Associate Clinical Professor, Department of Surgery/Emergency Medicine and Toxicology, University of Texas School of Medicine at San Antonio; Medical and Managing Director, South Texas Poison Center

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine, Texas Medical Association, American College of Occupational and Environmental Medicine

Disclosure: Nothing to disclose.

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

  2. Paczynski RP, Gold MS. Cocaine and Crack. Ruiz P, Strain EC. Lowinson and Ruiz's Substance Abuse: A Comprehensive Text. 5th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2011. 191-213.

  3. The Drug Abuse Warning Network. Highlights of the 2010 Drug AbuseWarning Network (DAWN) Findings onDrug-Related Emergency Department Visits. Substance Abuse and Mental Health Services Administration. Available at http://www.samhsa.gov/data/2k12/DAWN096/SR096EDHighlights2010.pdf. Accessed: September 2012.

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

  5. Signs SA, Dickey-White HI, Vanek VW, Perch S, Schechter MD, Kulics AT. The formation of cocaethylene and clinical presentation of ED patients testing positive for the use of cocaine and ethanol. Am J Emerg Med. 1996 Nov. 14(7):665-70. [Medline].

  6. Zhu NY, Legatt DF, Turner AR. Agranulocytosis after consumption of cocaine adulterated with levamisole. Ann Intern Med. 2009 Feb 17. 150(4):287-9. [Medline].

  7. Liu YW, Mutnuri S, Siddiqui SB, Weikle GR, Oladipo O, Ganti N, et al. Levamisole-Adulterated Cocaine Nephrotoxicity:  Ultrastructural Features. Am J Clin Pathol. 2016 May. 145 (5):720-6. [Medline].

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

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

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

  11. 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. 1994 Jul-Aug. 1(4):330-9. [Medline].

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

  13. Ruttenber AJ, Lawler-Heavner J, Yin M, Wetli CV, Hearn WL, Mash DC. Fatal excited delirium following cocaine use: epidemiologic findings provide new evidence for mechanisms of cocaine toxicity. J Forensic Sci. 1997 Jan. 42(1):25-31. [Medline].

  14. Vilke GM, Bozeman WP, Dawes DM, Demers G, Wilson MP. Excited delirium syndrome (ExDS): treatment options and considerations. J Forensic Leg Med. 2012 Apr. 19(3):117-21. [Medline].

  15. Vilke GM, Payne-James J, Karch SB. Excited delirium syndrome (ExDS): redefining an old diagnosis. J Forensic Leg Med. 2012 Jan. 19(1):7-11. [Medline].

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

  17. Center for Behavioral Health Statistics and Quality. Behavioral health trends in the United States: Results from the 2014 National Survey on Drug Use and Health. 2015. Available at http://www.samhsa.gov/data/sites/default/files/NSDUH-FRR1-2014/NSDUH-FRR1-2014.pdf.

  18. Substance Abuse and Mental Health Services Administration. Drug Abuse Warning Network, 2011: National Estimates of Drug-Related Emergency Department Visits. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2013. HHS Publication No. (SMA) 13-4760, DAWN Series D-39: [Full Text].

  19. Liakoni E, Dolder PC, Rentsch KM, Liechti ME. Presentations due to acute toxicity of psychoactive substances in an urban emergency department in Switzerland: a case series. BMC Pharmacol Toxicol. 2016 May 26. 17 (1):25. [Medline].

  20. Substance Abuse and Mental Health Services Administration. Drug Abuse Warning Network, 2010: Area Profiles of Drug-Related Mortality. HHS Publication No. (SMA) 12-4699, DAWN Series D-36. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2012. [Full Text].

  21. 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). 1996 Jun. 125(4):346-54. [Medline].

  22. 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. 1995 Dec. 26(6):671-6. [Medline].

  23. California. Turner died of overdose. The New York Times. January 17, 2008. A23.

  24. Hiestand BC, Smith SW. Cocaine chest pain: between a (crack) rock and a hard place... Acad Emerg Med. 2011 Jan. 18(1):68-71. [Medline].

  25. 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://www.cocainehelp.org/upload/dl/Crack_Cocaine_and_General_Addiction_Research/DAWN2k4ED.pdf.

  26. Finkel JB, Marhefka GD. Rethinking cocaine-associated chest pain and acute coronary syndromes. Mayo Clin Proc. 2011 Dec. 86(12):1198-207. [Medline].

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

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

  29. Byard RW. Acute mesenteric ischaemia and unexpected death. J Forensic Leg Med. 2012 May. 19(4):185-90. [Medline].

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

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

  32. Rivara FP, Mueller BA, Somes G, Mendoza CT, Rushforth NB, Kellermann AL. Alcohol and illicit drug abuse and the risk of violent death in the home. JAMA. 1997 Aug 20. 278(7):569-75. [Medline].

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

  34. Meehan TJ, Bryant SM, Aks SE. Drugs of abuse: the highs and lows of altered mental states in the emergency department. Emerg Med Clin North Am. 2010 Aug. 28(3):663-82. [Medline].

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

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

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

  38. [Guideline] Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, et al. 2012 ACCF/AHA focused update incorporated into the ACCF/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013 Jun 11. 61 (23):e179-347. [Medline]. [Full Text].

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

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

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

  42. 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. 2004 Jan 8. 350(2):105-13. [Medline].

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

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

  45. Richards JR, Garber D, Laurin EG, Albertson TE, Derlet RW, Amsterdam EA, et al. Treatment of cocaine cardiovascular toxicity: a systematic review. Clin Toxicol (Phila). 2016 Jun. 54 (5):345-64. [Medline].

  46. [Guideline] American Heart Association. Part 10: Special Circumstances of Resuscitation. Web-based Integrated 2010 & 2015 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Available at https://eccguidelines.heart.org/index.php/circulation/cpr-ecc-guidelines-2/part-10-special-circumstances-of-resuscitation/. October 2010; Accessed: June 30, 2016.

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

  48. Chang AM, Walsh KM, Shofer FS, et al. Relationship between cocaine use and coronary artery disease in patients with symptoms consistent with an acute coronary syndrome. Acad Emerg Med. 2011 Jan. 18(1):1-9. [Medline].

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

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

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

  52. 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].

  53. Moreira M, Buchanan J, Heard K. Validation of a 6-hour observation period for cocaine body stuffers. Am J Emerg Med. 2011 Mar. 29(3):299-303. [Medline]. [Full Text].

  54. Brooks M. Anticonvulsant May Help Treat Cocaine Addiction. Medscape Medical News. Oct 28 2013. Available at http://www.medscape.com/viewarticle/813313. Accessed: Nov 5 2013.

  55. Johnson BA, Ait-Daoud N, Wang XQ, Penberthy JK, Javors MA, Seneviratne C, et al. Topiramate for the Treatment of Cocaine Addiction: A Randomized Clinical Trial. JAMA Psychiatry. 2013 Oct 16. [Medline].

  56. Martell BA, Orson FM, Poling J, et al. Cocaine vaccine for the treatment of cocaine dependence in methadone-maintained patients: a randomized, double-blind, placebo-controlled efficacy trial. Arch Gen Psychiatry. 2009 Oct. 66(10):1116-23. [Medline].

  57. 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. 1995 Jun 29. 332(26):1753-7. [Medline].

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

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

 
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Patient transporting cocaine packets seen on KUB and lateral radiographs (mostly on left side). The patient was admitted, and a large number of packets was later obtained without procedural intervention or complication.
Patient transporting cocaine packets seen on KUB and lateral radiographs (mostly on left side). The patient was admitted, and a large number of packets was later obtained without procedural intervention or complication.
CT scan of patient transporting cocaine packets.
Schematics show the 3 types of action potentials in the right ventricle: endocardial (End), mid myocardial (M), and epicardial (Epi). A, Normal situation on V2 ECG generated by transmural voltage gradients during the depolarization and repolarization phases of the action potentials. B-E, Different alterations of the epicardial action potential that produce the ECGs changes observed in patients with Brugada syndrome. Adapted from Antzelevitch, 2005.
Three types of ST-segment elevation in Brugada syndrome, as shown in the precordial leads on ECG in the same patient at different times. Left panel shows a type 1 ECG pattern with pronounced elevation of the J point (arrow), a coved-type ST segment, and an inverted T wave in V1 and V2. The middle panel illustrates a type 2 pattern with a saddleback ST-segment elevated by >1 mm. The right panel shows a type 3 pattern in which the ST segment is elevated &lt; 1 mm. According to a consensus report (Antzelevitch, 2005), the type 1 ECG pattern is diagnostic of Brugada syndrome. Modified from Wilde, 2002.
Table 1. Onset of Effects, Peak Effects, Duration of Euphoria, and Plasma Half-Life by Routes of Administration
Route Onset Peak Effect (min) Duration (min) Half-Life (min)
Inhalation 7 s 1-5 20 40-60
Intravenous 15 s 3-5 20-30 40-60
Nasal 3 min 15 45-90 60-90
Oral 10 min 60 60 60-90
Table 2. DAWN Data, 2011
Total ED Visits for Cocaine in US 505,224
White 185,748
Black 236,089
Hispanic 49,810
Other/2+ Race/Ethnicities 5086
Unknown 28,490
Table 3. Current Cocaine Use by Age: 2011
Age Range (y) Cocaine Use, Any Form, Past Month (Percentage of Same-age Population) Crack Cocaine Use, Past Month (Percentage of Same-age Population)
Total 1.5 million (0.6%) 354,000 (0.1%)
12-17 39,000 (0.2%) 8000 (<0.1%)
18-25 473,000 (1.4%) 29,000 (0.1%)
≥26 1.0 million (0.5%) 317,000 (0.2%)
Table 4. 2011 DAWN Data on Emergency Department Visits for Cocaine, by Age
Age, y Number of Visits
0-11 ...
12-17 5904
18-20 15,198
21-24 37,643
25-29 57,398
30-34 55,247
35-44 127,405
45-54 154,101
55-64 47,064
≥65 4887
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