Cocaine Toxicity 

Updated: Dec 31, 2020
Author: Lynn Barkley Burnett, MD, EdD, JD; Chief Editor: Sage W Wiener, MD 


Practice Essentials

Despite being overshadowed by opioids in recent years, cocaine remains one of the most common causes of drug-related emergency department (ED) visits in the United States.[1] Although nearly every organ system can be affected by cocaine toxicity, most patients present with cardiovascular complaints.[2]

In addition to adverse effects experienced by cocaine users, body packers—people who swallow bags of cocaine in order to smuggle the drug from one country to another—may experience acute toxicity if any of the bags rupture. See the image below.

CT scan of patient transporting cocaine packets. CT scan of patient transporting cocaine packets.

See Can't-Miss Gastrointestinal Diagnoses, a Critical Images slideshow, to help diagnose the potentially life-threatening conditions that present with gastrointestinal symptoms.

Signs and symptoms

Acute cocaine toxicity has three reported phases. In fatal cases, the onset and progression are accelerated, with convulsions and death frequently occurring in 2-3 minutes, though sometimes in 30 minutes.

Phase I (early stimulation) is as follows:

  • Central nervous system (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 blood pressure (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 (ventricular fibrillation [VF] or asystole)

  • Respiratory: Respiratory failure, gross pulmonary edema, cyanosis, agonal respirations, and paralysis of respiration

See Presentation for more detail.


Lab studies

If history is absent or if the patient has moderate to severe toxicity, appropriate laboratory tests may be ordered, including the following:

  • Complete blood count (CBC)
  • Electrolytes, blood urea nitrogen (BUN), creatinine, glucose (Chem-7)
  • Glucose
  • Pregnancy test
  • Calcium
  • Arterial blood gases (ABG) analysis
  • Creatine kinase (CK) level
  • Troponin (in patients complaining of chest pain)
  • Urinalysis (UA): Can aid in finding cocaine-induced rhabdomyolysis, the reported incidence of which is 5-30% in ED patients who use cocaine
  • Toxicology evaluations: Including for urine, blood, gastric contents, and unknown substances clinging to the patient’s body

See Workup for more detail.


Chest radiographs, which should be obtained in patients with chest pain, hypoxia, or moderate to severe cocaine toxicity, may reveal the following:

  • Diffuse granulomatous changes: In cases of chronic parenteral cocaine use, due to the injection of inert insoluble ingredients of oral preparations or insolubles used to cut cocaine (eg, talc)

  • Septic pulmonary emboli: Appear round or wedge shaped; they may clear rapidly or cavitate

  • Aspiration pneumonitis and noncardiogenic pulmonary edema

  • Pulmonary abscess: May become evident after aspiration pneumonitis or after an intravenous injection of bacteria or toxic organic or inorganic materials

  • Aneurysm or pseudoaneurysm: May be noted with mainlining (ie, directly injecting into a central artery or vein); this finding is an indication for further imaging studies

In addition, radiography may be useful for evaluating cellulitis, an abscess, or a nonhealing wound in an intravenous drug user; it may  reveal a foreign body or subcutaneous emphysema produced by gas-forming organisms in an anaerobic infection. Ultrasonography may identify a foreign body or abscess.

Skeletal images can reveal osteomyelitis or fractures. However, because osteomyelitis may not be demonstrable on plain images for 1-2 weeks, other imaging studies should be performed if such a diagnosis is considered.


Obtain a 12-lead electrocardiogram (ECG) in patients with any of the following:

  • Chest pain
  • Hypoxia
  • Dyspnea
  • An irregular, rapid, or slow pulse
  • Altered mental status
  • Moderate to severe toxicity


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

Hyperthermia and rhabdomyolysis

If psychostimulant-intoxicated patients do not die as a result of cardiac or cerebrovascular complications, it is essential to prevent further morbidity by controlling hyperthermia and treating rhabdomyolysis.

Hyperthermia is best treated by submersion in an ice bath, but may also be treated with convection cooling, which involves spraying the patient's exposed body with tepid water as fans circulate air.

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.

See Treatment and Medication for more detail.


The ancient Incas of Peru believed the coca plant to be a gift from the gods. However, cocaine, derived from coca leaves, is a modern-day curse to the emergency physician.[3] Aside from alcohol (and not including tobacco-related illnesses), cocaine has been the most common cause of drug-related ED visits in the United States, accounting for 505,224 ED visits in 2011, according to the Drug Abuse Warning Network (DAWN).[4] Marijuana or hashish constituted the second leading cause at 455,668 visits. Heroin-related visits accounted for 258,482 visits.

Patients who present to the ED with cocaine toxicity often have also taken other drugs; in fact, the combined use of alcohol and cocaine may be the major cause of drug-related deaths.

Across the spectrum of acute and chronic effects, nearly every organ system can be affected. Trauma is often associated with cocaine use. Even the absence of cocaine, after a cocaine binge, may precipitate an ED visit due to withdrawal symptoms.

History of use and abuse

Use of cocaine spans thousands of years, with a duality of effects noted throughout history. Knowledge of its mind-altering function dates to at least 2000 BC. For centuries, indigenous mineworkers in Andean countries have used cocaine derived from the chewing of coca leaves as an endurance-enhancement agent. Spanish physicians reported the first European use of coca for medicinal purposes in 1596. Cocaine was not isolated from coca leaves until 1859. Nevertheless, by 1863, Vin Mariani, a wine fortified with 6 mg of cocaine alkaloid extract per ounce, was marketed in France. By 1880, the US pharmaceutical company Parke-Davis sold a fluid extract containing 0.5 mg/mL of crude cocaine.

In 1884, William Stewart Halsted performed the first nerve block using cocaine as the anesthetic. Halsted subsequently became the first cocaine-impaired physician on record. That same year, Sigmund Freud published the essay "Uber Coca," in which he advocated the use of cocaine in the treatment of asthma, wasting diseases, and syphilis. As with Halsted, Freud also became dependent on cocaine. In 1885, John Styth Pemberton registered French Wine Cola in the United States. The popular product, which contained 60 mg of cocaine per 8-oz serving, was later renamed Coca-Cola.

By 1893, occasional reports of fatality were associated with cocaine use, and in 1895, The Lancet reported a series of 6 deaths. By 1909, more than 10 tons of cocaine was being imported into the United States each year. Many over-the-counter medical products and elixirs had been created. One product for nasal application, called Dr. Tucker's Asthma Specific, contained 420 mg of cocaine per ounce.

The Harrison Narcotics Act of 1914 banned nonprescription use of cocaine-containing products. The resulting reduction in the use of cocaine marked the end of the first American cocaine epidemic. In the 1950s, amphetamine gradually replaced cocaine as the most common stimulant of abuse. However, this trend reversed in the 1970s, with crack ushering in the second epidemic of US cocaine use in 1985.

Crack (cocaine free base), which is generally sold in the form of "rocks," may also be sold in large pieces called slabs. These are approximately the size and shape of a stick of chewing gum and are sometimes scored to form smaller pieces. Crack cocaine differs from cocaine salt in that it is stable to pyrolysis and can be smoked. Users of cocaine in its crack form tend to be young adults aged 18-30 years who live in the central city and who are from low socioeconomic backgrounds. However, in 1986, the National Office of Drug Control Policy reported that young inner-city drug users were beginning to disdain crack as a ghetto drug. In Miami, for example, crack use had become unfashionable, and individuals continuing to use it, particularly blacks, were trying to hide it from their peers.

In 2016, crack use was estimated to constitute less than a quarter of overall cocaine use. This is similar to the estimates for most years from 2008 to 2015.[1]

Cocaine powder (cocaine salt) is currently marketed to adults from all ethnic backgrounds and socioeconomic groups, predominantly  white men older than 30 years who live in the central city. In several locales, cocaine is mentioned as a club drug, but it is not as prominent as methamphetamine and some hallucinogens in the club environment. It cannot be smoked, but is well absorbed transmucosally.

The Drug Enforcement Administration’s 2019 National Drug Threat Assessment notes that while opioid use (the combination of controlled prescription drugs, synthetic opioids, and heroin) remained the principal threat, having reached epidemic levels over the past decade, methamphetamine abuse has remained prevalent and the cocaine threat appears to be rebounding. Cocaine availability and use increased between 2015 and 2016 in the United States, with past-year cocaine initiates and cocaine-involved poisoning deaths reaching levels equal to or greater than those of 2007.[5]

 According to the Drug Enforcement Administration’s Cocaine Signature Program, which studies cocaine seized in the US, in 2018 approximately 90% of cocaine samples tested were of Colombian origin, 6% were of Peruvian origin, and 4% were of unknown origin. Of all cocaine bricks tested, 80% contained no adulterants or diluents; the percentage of uncut bricks was the highest since at least the year 2000 and was a marked increase from the 59% rate in 2017. The rest of the bricks analyzed were cut with various diluents, with 17% containing levamisole and/or levamisole mixtures with dexamisole and 3% containing various other substances.[5]

From January 2013 and December 2017, the average retail price per pure gram of cocaine decreased while the average purity increased. The price decreased 28.2%, from $213 to $153, while purity increased 38.6%, from 46.4% to 64.3%.[5]


The chemical name for cocaine is benzoylmethylecgonine. It is derived from the leaves of Erythroxylon coca, a shrub indigenous to Peru, Bolivia, Mexico, the West Indies, and Indonesia. Cocaine is a bitter crystalline alkaloid with the molecular formula of C17 H21 NO4. Ecgonine, an important part of the cocaine molecule, is an ester-type local anesthetic that belongs to the tropane family, which also includes atropine and scopolamine.

The primary effect of cocaine is blockade of norepinephrine reuptake; its secondary effect is marked release of norepinephrine. These effects act synergistically to increase norepinephrine levels at the nerve terminal. Cocaine also causes moderate release and reuptake-blockade of serotonin and dopamine. Its marked local anesthetic effects are caused by sodium channel blockade, which inhibits the conduction of nerve impulses, decreasing the resting membrane potential and the amplitude of the action potential while simultaneously prolonging the duration of the action potential. In the heart, cocaine acts as a Vaughan Willaims IC sodium channel blocker.

Cocaine also blocks potassium channels. In some cellular membranes, it may block sodium-calcium exchange. The drug is fat soluble and freely crosses the blood-brain barrier. Cocaine appears to stimulate the CNS, with particular activity in the limbic system. There, it potentiates dopaminergic transmission in the ventral basal nuclei, producing the pleasurable behavioral effects that result in its widespread use.

Cocaine enters the United States in the form of a hydrochloride salt, having undergone numerous steps in refinement from the original coca leaf. In its hydrochloride form, cocaine may be absorbed topically across all mucosal membranes, including the oral, nasal, GI, rectal, urethral, and vaginal membranes. It may also be injected intravenously or ingested. Ingested cocaine is poorly absorbed from the stomach because it is a weak base with a pKa of 8.6, but it is readily absorbed from the duodenum. Cocaine may be inhaled through a straw or rolled-up paper currency, or snorted from a coke spoon, typically containing 5-20 mg of the drug. A 1-inch line typically contains 25-100 mg of the drug.

Crack is produced when the hydrochloride molecule is removed by ether extraction, which frees the basic cocaine molecule, or "freebase". Heating does not destroy freebase, rather it melts at 98°C and vaporizes at higher temperatures. These physical properties allow it to be smoked.

Crack is lipid soluble and therefore rapidly absorbed in the pulmonary capillaries. The term crack describes the crackling sound heard when cocaine freebase is smoked. Crack may be smoked in a pipe bowl containing 50-100 mg or in a cigarette with as much as 300 mg. Smoking crack bypasses the vasoconstriction that results when cocaine is snorted; therefore, the effects are similar to taking cocaine intravenously. Crack smokers may aggressively inhale against a small pipe and then perform a Valsalva maneuver before exhaling against pursed lips or forcefully blow the drug into a partner's mouth. These techniques are reputed to enhance the euphoria of cocaine.

Table 1. Onset of Effects, Peak Effects, Duration of Euphoria, and Plasma Half-Life by Routes of Administration (Open Table in a new window)



Peak Effect (min)

Duration (min)

Half-Life (min)


7 s





15 s





3 min





10 min




All of the cocaine injected intravenously is delivered to the circulatory system, versus 20-30% of cocaine that is ingested or inhaled. With repeated use, tolerance develops so that the intensity and duration of effect decrease. People who use cocaine long term may dose themselves as frequently as every 10 minutes, binge as long as 7 days at a time and use as much as 10 g/d. Reverse tolerance, with onset of seizures and paranoid ideation at decreased doses, has been observed in animals and is thought to occur in humans as well.

Approximately 30-50% of cocaine is metabolized by hepatic esterases and plasma pseudocholinesterase, resulting in the formation of ecgonine methyl ester. Spontaneous nonenzymatic hydrolysis of another 30-40% results in benzoylecgonine. Both products are water-soluble, metabolically active, and capable of increasing blood pressure (BP). Benzoylecgonine, which has a half-life of 7.5 hours, can induce seizures, perhaps even hours to days after the last use.

Approximately 80-90% of injected cocaine is rapidly metabolized. Decreased hepatic perfusion, secondary to conditions such as hypotension or low-output congestive heart failure (CHF), results in prolonged elevation of cocaine levels. A similar result may be observed in pregnant women, fetuses, infants, patients with liver disease, and elderly men, because their plasma cholinesterase activity is decreased. In addition, some people have a genetic deficiency of plasma pseudocholinesterase or a nutritional predisposition to abnormally low pseudocholinesterase levels. Some have postulated that these patients may metabolize cocaine slowly and have increased sensitivity to small doses of cocaine, which places them at risk for increased toxicity and sudden death. Evidence supporting this postulate is scant.

Most of the remaining amount of cocaine is metabolized by hepatic N-demethylation into norcocaine, which is metabolically active. Pregnancy, during which circulating progesterone levels are high, or the exogenous administration of progesterone increase the activity of hepatic N -demethylation. This increased formation of norcocaine, which is more vasoconstrictive than cocaine, may result in women being more sensitive to the cardiotoxic effects of cocaine than men as a result of hormonal potentiation.

Approximately 1-5% of cocaine is excreted, unaltered, through the kidneys within 6 hours of use.

With the multiplicity of physiologic and pharmacologic modifiers cited above, the literature reflects tremendous variability in the reported lethal dose of cocaine in humans. The range is as little as 20 mg IV, to a mean of 500 mg ingested orally, to 1.4 g.

Drug interactions and polypharmacy

More than 38 pharmacologically active substances have reportedly been used with cocaine; alcohol and nicotine are the most common. Although alcohol and nicotine are individually well known for their potential sequelae, their use with cocaine may acutely increase morbidity and mortality risks.

Between 30% and 60% of individuals who take cocaine combine it with alcohol. Clinical data indicate that the concurrent use of alcohol and cocaine is associated with increased mortality and morbidity from cardiovascular complications, hepatotoxicity, and behaviors leading to personal injury. In 74% of cocaine-related fatalities in the United States, another drug, usually ethanol, had been co-ingested. The addition of alcohol to cocaine increases the risk of sudden death 25-fold.

The increased risk from the concomitant alcohol use is enhanced by the formation of a third active compound of toxicologic importance, namely, ethylbenzoylecgonine, commonly known as cocaethylene. Although its behavioral pharmacology and psychomotor stimulant effects are similar to those of cocaine, its toxicity is greater. The plasma half-life of cocaethylene is longer than that of cocaine, and inferential evidence suggests that the lethal dose to kill 50% of subjects (LD50) is lower.

Although most cocaine metabolism involves serum cholinesterase, some of the drug is metabolized in the liver by carboxylesterases. In the presence of alcohol, a nonspecific carboxylesterase catalyzes ethyl transesterification of cocaine to cocaethylene. Cocaine is the rate-limiting substrate in this reaction. Cocaethylene can be detected in urine and blood within 100 minutes after a person uses alcohol and intranasal cocaine. Whereas the half-life of cocaine is approximately 40 minutes, the half-life of cocaethylene is 2.5 hours, which may explain why cocaine-related symptoms can continue for some time after cocaine is last used.

The human brain, heart, liver, and placenta bind cocaine and cocaethylene. As with cocaine, cocaethylene binds to dopamine and norepinephrine transporters and inhibits catecholamine reuptake (primarily norepinephrine) into nerve terminals. The increased "high" reported with the concurrent use of alcohol and cocaine may be the result of the additive effect of cocaine and cocaethylene. Yet another reason may be the relationship between these substances and serotonin. The binding of serotonin by cocaine may modulate the high and may be the cause of the dysphoric effects of cocaine. Cocaethylene, which is 40 times less potent than cocaine in binding to the serotonin receptor, does not share this negative property.

In dog studies, cocaethylene was a more potent precipitant of convulsions and cause of lethality than cocaine. This is probably because cocaethylene blocks sodium channels more potently than cocaine. Although the toxic level of cocaethylene in humans is not known, the LD50 in mice was 93 mg/kg for cocaine versus 60 mg/kg for cocaethylene. The process of cocaethylene formation continues for several hours, which may explain why sudden deaths may occur 6-12 hours after cocaine ingestion.

Cocaethylene, which is ultimately metabolized to benzoylecgonine, is not the only factor augmenting the effects of cocaine with ethanol.[6] Consumption of ethanol before cocaine use also increases the bioavailability of cocaine.

Signs et al present an exception to the weight of the literature in a study based on 57 ED patients who tested positive for both alcohol and cocaine. In these patients, systolic and diastolic BP, heart rate, and body temperature did not significantly differ between those testing positive for both alcohol and cocaine and drug-free control subjects.[7] This may be because long-term cocaine users reportedly develop tolerance to the cardiovascular effects of the drug. Signs et al concluded that the incidence of serious cardiovascular complications resulting from simultaneous use of cocaine and ethanol does not appear to be significantly higher than that observed in patients using only cocaine, only ethanol, or no drug.[7]

Nicotine is the second drug most commonly combined with cocaine. Many of the physiologic effects of nicotine are identical to those of cocaine. Nicotine produces a hypertensive and tachycardic response that is mediated by stimulation of the sympathetic ganglia and the adrenergic medulla. This response is coupled with the discharge of catecholamines from sympathetic nerve endings.

Cigarette smoking also causes arterial endothelial desquamation and ultrastructural changes, a reduction of endothelial-cell prostacyclin production, increased serum fibrinogen levels, activation of platelets with enhancement of adhesiveness and aggregability, diminished coronary flow reserve, and an alpha-adrenergically mediated increase in coronary artery tone in patients with coronary atherosclerosis.

Most patients with cocaine-induced myocardial infarction (MI) also smoke cigarettes, a finding which suggests that simultaneous use of cocaine and tobacco may enhance coronary vasoconstriction. Of patients with cocaine-induced MI, 38% had normal coronary arteries; 77% of this group (average age, 32 y) had an anterior-wall MI. More than two thirds were moderate-to-heavy cigarette smokers (>1-2 packs daily). The average number of additional coronary risk factors, however, was less than 1.

Combining cocaine and heroin into a "speedball" causes frequent complications, as evidenced by the high-profile cases of actors John Belushi, River Phoenix, and Chris Farley in the 1980s and 1990s. Speedballing accounts for 12-15% of cocaine-related episodes in patients presenting to EDs in the United States. In speedballing, heroin is injected or snorted, followed immediately by smoking of cocaine. Cocaine is harder to purchase during the summer months than at other times, thus heroin users may speedball with crack in the summer. The effects of heroin last longer than do those of crack, and it modulates symptoms secondary to withdrawal from crack. In both cases, the second drug is used to supplement, rather than substitute, the primary drug.

Persons addicted to crack may also use heroin to dampen the agitation produced by extended crack use. Body packers—smugglers who use their GI tract as a hiding place for large quantities of carefully wrapped packages of cocaine—often use a similar approach. They may take benzodiazepines to prevent becoming too high should a package rupture. Some premedicate themselves with a constipating agent, such as diphenoxylate with atropine, to prevent themselves from having a bowel movement before they arrive at their destination.

Dissolving and injecting crack is less expensive than purchasing enough cocaine powder to produce the same effect. Some users dissolve crack in lemon juice or vinegar before injecting it intravenously, a practice that reportedly produces a more intense rush than smoking the same amount of crack. If the vein is missed, the result is pain and potential abscess formation.

Various agents can heighten the effects of cocaine and contribute to complications. Organophosphates may be taken to inhibit pseudocholinesterase, prolonging the effects of cocaine. However, because it produces organophosphate toxicity, the risk of fatality is increased. Cholinesterase inhibitors, such as carbamates, have a similar effect. Another practice involves coabusing crack cocaine and phenytoin to enhance the intoxication. In this practice, unbound phenytoin causes persons with hypoalbuminemia to become symptomatic at lowered drug levels; if death occurs, it usually is the result of respiratory and subsequent circulatory collapse.

The risk of severe effects is increased when cocaine is combined with drugs such as monoamine oxidase inhibitors, tricyclic antidepressants (TCAs), alpha-methyldopa, and reserpine. These drugs alter the metabolism of epinephrine and norepinephrine, potentiating their effects and, in the presence of cocaine, inducing an adrenergic crisis. Serotonin syndrome may result when serotonin selective reuptake inhibitors (SSRIs), such as fluoxetine (Prozac), are taken concurrently with sympathomimetics.

Illicit drugs are frequently admixed with additional chemicals either to increase the apparent quantity of the street drug or to enhance its effect. For example, 8-20% of stimulants available on the street contain cocaine and methamphetamine hydrochloride.

Adulterants are added to cocaine intentionally or are left over from the manufacturing process. Substitutes are compounds that have pharmacologic properties similar to those of cocaine and that are used in its place. Many of these substances cause pulmonary and systemic reactions when taken intravenously, by insufflation, or by smoking; they may, therefore, substantially contribute to the toxicity of cocaine use.

Among the substances used to cut cocaine are the following:

  • Local anesthetics (eg, procaine, lidocaine, tetracaine)
  • Other stimulants (eg, amphetamine, caffeine, methylphenidate, strychnine)
  • Lysergic acid diethylamide (LSD)
  • Phencyclidine (PCP)
  • Phenytoin
  • Heroin
  • Marijuana
  • Hashish

The veterinary antihelminthic levamisole has been found as an adulterant in 69%-93% of the cocaine in the United States.[8, 5] Levamisole increases dopamine levels in the same areas of the brain as does cocaine, possibly accounting for its current ubiquity.[9] Neutropenia, agranulocytosis, leukoencephalopathy, and cutaneous vasculitis have been reported following use of cocaine contaminated with levamisole.[9, 8]

Other adulterants may include the following:

  • Quinine
  • Talc (ie, magnesium silicate)
  • Ascorbic acid
  • Boric acid
  • Chalk
  • Laundry detergent
  • Meat tenderizer
  • Laxatives
  • Plaster of Paris
  • Cornstarch
  • Lactose


Tachydysrhythmias cause most acute cocaine-related nontraumatic deaths. Other causes of sudden death include stroke, subarachnoid hemorrhage, hyperthermia, and the consequences of agitated delirium. Myocardial infarction (MI) can result from acute vasospasm, dysrhythmia, or chronic accelerated atherogenic disease.


Cardiovascular effects result primarily from direct actions on the heart and secondarily from effects on the CNS. Central and peripheral adrenergic stimulation results from inhibition of norepinephrine and dopamine reuptake at preganglionic sympathetic nerve endings. By preventing catecholamine reuptake at presynaptic terminals, cocaine causes catecholamine to accumulate at the postsynaptic membranes.

Without presynaptic reuptake, the action of a neurotransmitter on its receptors becomes sustained. Effects of endogenous catecholamines are thereby potentiated, resulting in tachycardia, hypertension, vasoconstriction, and increased myocardial oxygen consumption. Although cocaine-related tachydysrhythmias result primarily from increases in catecholamine levels, the local anesthetic properties of cocaine can impair impulse conduction in the ventricle, providing a substrate for reentrant ventricular dysrhythmias.

People who abuse cocaine may be exposed to toxic levels of circulating catecholamines. In one study, 48 mg of cocaine more than doubled circulating levels of norepinephrine (420 pg/mL increased to 900 pg/mL).[10] However, most cocaine-related dysrhythmic fatalities occur in patients with low or modest levels of cocaine use. This finding suggests that the mechanism of death may be different in long-term cocaine users, in whom sudden death is most likely the consequence of adrenergic effects and long-term catecholamine toxicity.

In rat studies, long-term use markedly increased norepinephrine content of the left ventricle. This theoretically suggests that long-term cocaine users could be at increased risk of malignant arrhythmia if excess norepinephrine also accumulates in the human left ventricle. Of note, coincident with the increase in ventricular catecholamine concentration, the rate of catecholamine synthesis was reduced, reflecting physiologic attempts to decrease sympathetic tone secondary to chronic cocaine stimulation.

Alterations in cardiac histology may produce an arrhythmogenic anatomic substrate. Independent of coronary artery disease or clinically documented MI, cocaine use may induce scattered foci of myocarditis, microfocal fibrosis, and contraction band necrosis, the severity of which is correlated with serum and urine concentrations of cocaine. Although common in the hearts of cocaine and other stimulant abusers, such findings are found in only a minority of hearts examined.

Other conditions providing an anatomic arrhythmogenic substrate include the accessory pathways resulting in Wolff-Parkinson-White (WPW) syndrome, and left ventricular enlargement.

In patients with an arrhythmogenic anatomic substrate, even low levels of cocaine can cause tachydysrhythmias. In a study of 19 people who had survived cocaine-related cardiac arrest, 8 had asystolic arrest (5 because of massive overdose) and the remaining 11 had arrest resulting from ventricular fibrillation (VF). Of the latter group, all had an anatomic substrate for the dysrhythmia: 2 patients had an MI, 3 had WPW, and 6 had left ventricular hypertrophy or cardiomyopathy. On subsequent electrophysiologic testing, several patients had dysrhythmias, which were induced only after they had been given cocaine.[10]

Normal electrical conduction may become disrupted in cardiomegaly, which can be observed with chronic cocaine use. Rat studies have demonstrated that cocaine causes genetic changes in cardiac myocytes. Hemodynamic overload results in the production of high levels of atrial natriuretic factor (ANF). Increased levels of mRNA coding for ANF were measurable within 4 hours after rats were injected with 40 mg/kg of cocaine. When that same dose was administered to rats over 28 days, levels of mRNA coding for collagen and heavy-chain myosin increased, and left ventricular mass increased by 20%. Increased collagen production and increased left ventricular mass are independent risk factors for sudden death.

Similar findings also are observed in humans. The hearts of cocaine users are 10% heavier than those of nonusers. In a study of 200 asymptomatic patients in a rehabilitation program who had used cocaine long term, one third had increased QRS voltage, indicative of left ventricular enlargement. Another study of asymptomatic patients in rehabilitation revealed that more than 40% had an echocardiographically demonstrable increased left ventricular mass.[10]

An autopsy study conducted by Darke, Kay, and Duflou compared cardiovascular and cerebrovascular pathology in decedents dying of cocaine toxicity, opioid toxicity, and those dying of hanging who were toxicologically negative for cocaine or opioids.[11] With gender, effects of age, and body mass index (BMI) having been controlled for, 1 in 7 cocaine users were found to have left ventricular hypertrophy, two and one-half times the odds of such a pathologic diagnosis being made in either comparison group. In patients with enlarged hearts due to long-term exposure to high levels of cocaine, even low cocaine levels can be lethal.

Cocaine also has quinidinelike (IC) direct cardiotoxic effects, causing intraventricular conduction delay, as reflected by widening of the QRS and prolongation of the QT segment. In large doses, blockade of the fast sodium channels prolongs the slope of phase 0 of the cardiac action potential, which may result in a negative inotropic response, bradycardia, and, often as a precursor to death, hypotension from decreased contractility and dysrhythmia.

With high blood levels of cocaine, such as those observed in a body packer or body stuffer when a cocaine packet ruptures, or in a binge user with large cocaine supply, the membrane-stabilizing effects of cocaine may cause cardiac arrest from asystole. In such cases, blood levels may exceed 50,000 ng/mL. Cardiac arrest is even more likely if the patient also has been consuming alcohol, with resultant production of cocaethylene. Tolerance rapidly develops to the euphoriant effects of cocaine but not to its local anesthetic effects of membrane stabilization.

MI and acute coronary syndromes

A nationally representative study of 10,085 US adults aged 18-45 years found that regular use of cocaine was associated with an increased likelihood of MI. Approximately 1 of every 4 nonfatal MIs was attributable to frequent use of cocaine (defined in this study as >10 uses in a lifetime).[12]

Patients with cocaine-related MI often have fixed atherosclerotic lesions. Cocaine can induce increased heart rate and BP, resulting in increased myocardial oxygen demand. The additional metabolic requirements may convert an asymptomatic obstruction into one of clinical significance.

Substantial evidence indicates that cocaine use causes accelerated coronary atherosclerosis. According to a 1995 study of trauma fatalities among men with a mean age of 34 years and an incidental finding of cocaine metabolites, 25% had lesions in 2 or more vessels, and 19% had disease in 3-4 vessels. Of the control subjects, only 6% had 2-vessel disease, and none had 3- or 4-vessel disease. In another study of 22 long-term cocaine users with a mean age of 32 years, all of whom died suddenly with detectable serum cocaine levels, severe narrowing of more than 75% cross-sectional area was found in 1 or more coronary arteries in 36% of patients.[10]

Hollander and Hoffman reviewed and analyzed the literature of 91 patients with cocaine-induced MI. Cardiac catheterization in 54 patients demonstrated that 31% had significant coronary atherosclerosis. Autopsy studies of patients with cocaine-related MI revealed atherosclerotic lesions in more than one half of patients.[13]

In another review of medical examiners' records, 495 deceased patients had positive toxicologic findings of cocaine; 6 of them, whose mean age was 29 years, had MI with total thrombotic occlusion primarily involving the left anterior descending coronary artery. All of the patients had significant coronary atherosclerosis, with 83% having lesions that caused luminal stenosis of more than 75% cross-sectional area in 1 or more vessels.

Of the patients reviewed by Hollander and Hoffman, 24% had a thrombotic occlusion in the absence of clinically significant coronary disease.[13] Cocaine's effect of increasing levels of plasma plasminogen activator enhances clot formation. In addition, cocaine activates platelets both directly and indirectly by means of an alpha-adrenergic–mediated increase in platelet aggregation.

Cocaine increases production of the potent vasoconstrictor endothelin, and simultaneously decreases production of nitrous oxide, a powerful vasodilator. As a result of alpha-adrenergic stimulation, cocaine may exert a direct vasoconstrictive effect by increasing the influx of calcium across endothelial cell membranes. These factors may produce coronary artery spasm. Although this may occur even in patients who do not have significant coronary artery disease, spasm is most pronounced in portions of the coronary artery that are already narrowed. Therefore, in patients who do have high-grade obstruction, including patients whose stenoses were previously asymptomatic, coronary artery spasm of even modest degree can have devastating consequences.

In healthy coronary arteries, endothelial cells release endothelium-derived relaxing factor (EDRF) and prostacyclin, which interact synergistically to relax vascular smooth muscle and inhibit platelet adhesion and aggregation. Mild atherosclerosis and hypercholesterolemia impair endothelium-mediated vasodilation in coronary arteries, and animal studies suggest that endothelial dysfunction predisposes a person to vasoconstriction and arterial spasm. Hypersensitivity to the vasoconstrictor effects of catecholamines has also been demonstrated in humans with endothelial dysfunction. Therefore, individuals with mild coronary disease who use cocaine may be predisposed to occlusive vascular spasm at the site of early atherosclerotic lesions.

The combination of intimal hyperplasia, accelerated atherosclerosis, and endothelial dysfunction create a prothrombotic milieu.

Cocaine also potentiates platelet thromboxane production and decreases protein C and antithrombin III production, as well as the production and release of prostacyclin. Aggregating platelets are an important source of serotonin. In patients with dysfunctional endothelium, serotonin causes intense vasoconstriction because of its unopposed effects on vascular smooth muscle.

Chronic use appears to deplete stores of dopamine in peripheral nerve terminals. In patients undergoing cocaine withdrawal, more than one third have frequent episodes of ST-segment elevation (similar to variant angina), as documented on Holter monitoring. Inhibition of dopamine-mediated coronary vasodilatation secondary to dopamine depletion has been advanced as the hypothetical cause.

Patients with cocaine-related ischemic chest pain, even those who have had MIs, tend to do well after they stop using cocaine.

The effects of cocaine on the heart also include myocarditis and dilated cardiomyopathy. Myocarditis may be 5 times more common among cocaine users than in control subjects. Myocarditis may be the result of microvascular injury, and it is a common autopsy finding in patients dying from cocaine toxicity. The mechanisms producing these effects are unknown, but hypotheses include a direct effect on lymphocyte activity, myocardial cell cytotoxicity secondary to an increase in the activity of natural killer cells, hypersensitivity reactions (suggested by eosinophilic infiltrate), and induction of focal myocarditis from catecholamine administration.

Cocaine causes a direct negative inotropic effect on cardiac muscle, resulting in transient toxic cardiomyopathy. In one small series, 8 of 10 subjects who used cocaine long term had chest pain without MI but left ventricular ejection fractions less than 50%. In a case report, Jouriles describes a 35-year-old woman with hypotension, seizures, and hypoxemia who had an ejection fraction of 10% after smoking crack cocaine.[14]

Neurologic effects

Cocaine users have a 14-fold increase in risk of ischemic or hemorrhagic stroke compared to matched controls. In the study of Darke, Kaye, and Duflou, atherosclerosis of the basal vasculature of the brain was noted in approximately 10% of the cocaine toxicity cases autopsied versus less than 1% noted in either of the comparison groups.[11]

Cocaine acts as a CNS stimulant by inhibiting presynaptic reuptake of norepinephrine, dopamine, and serotonin. It also causes release of epinephrine by the adrenal glands. The intensity and duration of the stimulant effects of cocaine are mediated by the rate at which blood levels of cocaine rise (a function of the route of administration) (see Table 1) and the peak of blood levels.

Cocaine may cause generalized tonic and clonic convulsions as well as focal seizures. Intense stimulation of sigma and muscarinic receptors by cocaine and increased synaptic concentration of serotonin have been proposed as causal. Cocaine lowers the threshold for seizures and may produce a kindling effect on neurons that promotes convulsions.

Seizure frequency ranges from 1-29%–perhaps reflecting variations in use and concurrent use of other drugs. Of 474 patients with medical complications of cocaine abuse, 8% experienced first-time seizures and, of these, 85% had seizures during administration of the drug.

Cocaine-associated seizures occur in naive users and among long-term users. Seizures are most frequently single tonic-clonic and resolve without intervention. However, status epilepticus may occur. The first stage of status epilepticus is manifested by generalized tonic-clonic seizures associated with hypertension, hyperpyrexia, and diaphoresis. After approximately 30 minutes, the second stage may occur, in which cerebral autoregulation fails, cerebral blood flow diminishes, and systemic hypotension occurs. During this phase, the only clinical manifestations may be minor twitching, though cerebral electrical seizure activity continues.

Drugs that increase intrasynaptic dopamine change the density and sensitivity of dopamine receptors, with different effects on different receptor subtypes in different areas of the brain.[15] Excited delirium, cocaine-associated rhabdomyolysis (CAR), and neuroleptic malignant syndrome (NMS) share many common features that can be explained by aberrant dopaminergic function.

Long-term cocaine use decreases the density of dopamine-1 (D1) receptors throughout the striatal reward centers, but it does not affect the number of dopamine-2 (D2) receptors. Antagonism of nigrostriatal dopamine function may cause extrapyramidal motor dysfunction, including dystonic reactions, bradykinesia, akinesia, akathisia, pseudoparkinsonism, and catalepsy. Neuroleptic agents are the principal medications that cause dystonic reactions by means of their blockade of dopamine receptors in the nigrostriatal pathways. Cocaine may increase the risk of neuroleptic-induced dystonias, a problem compounded by the street marketing of substances, such as haloperidol, sold as cocaine.

Over time, continued use may result in depletion of dopamine. Therefore, cocaine may be an independent cause of dystonic reactions. Two biochemical events, dopamine receptor blockade by neuroleptics and dopamine depletion by cocaine, result in the same effect, namely, the absence of physiologic dopamine in the nigrostriatal area of the brain. These events may represent the pathophysiologic basis for cocaine-associated dystonias. Intrauterine exposure to cocaine has been suggested as a cause of dystonia in infants.

Agitated (excited) delirium

Patients presenting with agitated delirium, also known as excited delirium, are at high risk for sudden death, with a fatality rate of approximately 10%.[16] Agitated delirium is a common presentation in patients dying from cocaine toxicity. Of cocaine-associated deaths investigated by the Medical Examiner's Department of Metropolitan Dade County, Florida, between 1979 and 1990, excited delirium was the terminal event in approximately 1 of every 6 fatalities. Patients with excited delirium had an immediate onset of bizarre and violent behavior, which included aggression, combativeness, hyperactivity, hyperthermia, extreme paranoia, unexpected strength, and/or incoherent shouting. All of these were followed by cardiorespiratory arrest.[15]

Although heart weight, ventricular hypertrophy, and past MI are not risk factors, repeated binges of cocaine use are associated with fatal excited delirium, with a kindling effect proposed as a mechanism.[17] The frequency of use that increases risk has, however, not been determined.

Individuals with excited delirium may be more sensitive to the life-threatening effects of catecholamine surges than other cocaine users. Excited delirium appears to be generated by increased intrasynaptic dopamine concentrations resulting from a defect in the regulation of the dopamine transporter. Cocaine recognition sites on the striatal dopamine transporter are increased in users without excited delirium compared with drug-free controls. Persons dying from excited delirium have no such increase; therefore, they may have problems in clearing dopamine from the synapses, a condition that can easily result in agitation and delirium.

Hyperthermia, which may also be caused by downregulation of dopamine receptors, increases the incidence of fatal excited delirium. Death from excited delirium is more common in the summer months than at other times (55% vs 33% for other accidental cocaine toxicity deaths); therefore, high ambient temperature and humidity may play roles in the development of hyperthermia. An independent risk factor for fatal excited delirium is a body mass index (weight in kilograms/height in square meters) in the upper 3 quartiles, with the risk appearing to increase after a threshold is exceeded rather than in a dose-response fashion.

Restraints have also been implicated as a contributing factor, particularly when the patient is prone. Sudden death occurring during prone restraint of a person in excited delirium appears to be induced by a combination of at least 3 factors that increase oxygen demand and decrease oxygen delivery:

  1. The psychiatric or drug-induced state of agitated delirium coupled with police confrontation places catecholamine stress on the heart.

  2. The hyperactivity associated with excited delirium coupled with struggling against the police and/or restraints increases oxygen demands on the heart and lungs.

  3. A hogtied position impairs breathing by inhibiting chest-wall and diaphragmatic movement.


Temperature dysregulation is also a problem with cocaine intoxication, as demonstrated by Callaway and Clark, who reported that patients presented with rectal temperatures as high as 45.6°C.[18] Hyperthermia is a marker for severe toxicity, and it is associated with a number of complications, including renal failure, disseminated intravascular coagulation, acidosis, hepatic injury, and rhabdomyolysis.

Because dopamine plays a role in the regulation of core body temperature, increased dopaminergic neurotransmission may contribute to psychostimulant-induced hyperthermia in cocaine users, including those with excited delirium.

D2 receptors are involved with processes that decrease core temperature. The number of D2 receptors in the temperature regulatory centers of the hypothalamus is substantially reduced in persons with excited delirium. These decreases in D2 receptors lead to unopposed increases in temperature mediated through D1 receptors, which are not affected in individuals who die from excited delirium.

Ruttenber et al hypothesize that hyperthermia may result from extensive muscular activity in the setting of warm ambient temperature and, perhaps, humidity in combination with aberrant thermoregulation in the hypothalamus and mesolimbic system.[15] Antagonism of both central and peripheral catecholamine receptors may be required to protect against psychostimulant-induced hyperthermia because peripherally released catecholamines may directly stimulate muscle or other thermogenic tissue.

Cocaine-induced seizures can also contribute to hyperthermia, though cocaine can induce hyperthermia in the absence of seizures. In animal studies, hyperthermia was the most significant parameter in the lethality of continuous cocaine infusion.

Agitation secondary to intoxication or withdrawal increases motor activity, which increases heat production. The patient's volume needs are thereby increased, and, when not met, they lead to decreased renal perfusion. Heat production may also contribute to increased muscle breakdown, resulting in myoglobinuria. Myoglobinuria, in conjunction with decreased renal perfusion, causes acute tubular necrosis.

Cocaine-associated rhabdomyolysis (CAR)

Excitement, delirium, and hyperthermia frequently precede the onset of CAR. If excited delirium and CAR have a similar cause, the spectrum of severity ranges from rhabdomyolysis with no excited delirium or hyperthermia to various combinations of these 3 conditions.

Long-term, rather than short-term, cocaine use is responsible for persistent changes in dopaminergic function that place users at risk for excited delirium and CAR. Elevations in muscle-enzyme levels are observed in asymptomatic people who use cocaine long term and in untreated persons with schizophrenia. This evidence lends support to the hypothesis that chronic alterations in dopaminergic function can affect the physiology of skeletal muscle.


Acidemia is seen in clinically significant toxicity and may play an important role in cocaine-related death. In experimental studies, calcium delivery to myofilaments is decreased and contractile proteins become less responsive in the presence of lowered intracellular pH, resulting in depression of myocardial contractility.

Acidosis also potentiates dysrhythmias by repolarization and depolarization abnormalities that lead to reexcitation states. As pH decreases, calcium is spontaneously released from the sarcoplasmic reticulum, resulting in a transient depolarizing current that can precipitate dysrhythmias during diastole. In addition, acidosis decreases conductance between the gap junctions of cardiac cells, which slows propagation of the action potential. In the presence of cocaine, which diminishes sodium conductance, a severe reduction in conduction velocity may occur, increasing the likelihood of dysrhythmia production by means of reentry excitation.



United States

The 2019 Annual Surveillance Report of Drug-Related Risks and Outcomes by the Centers for Disease Control and Prevention found that in 2018, an estimated 5,529,000 persons aged 12 years and older (2.0% of the population) reported cocaine use in the past year, including 757,000 persons (0.3% cent of the population) who used crack cocaine.  In 2018, an estimated 977,000 (0.4%) persons aged 12 years and older reported a substance use disorder in the past year involving cocaine.[1]

The Annual Report of the American Association of Poison Control Centers' National Poison Data System reported 1264 single exposures to cocaine in 2019. Major outcomes occurred in 167 cases and 11 deaths were reported.[19]

From the early 1970s until its discontinuation in 2011, the Drug Abuse Awareness Network (DAWN), a national survey of approximately 600 hospital EDs, reported the number of episodes of patients seeking treatment related to their use of an illegal drug or their nonmedical use of a legal drug. According to DAWN, in 2011, cocaine accounted for 505,224 (40.3%) of the approximately 1,252,500 ED visits that involved illicit drugs. The rate of involvement was higher for cocaine, at 162 ED visits per 100,000 population, than for any other illicit drug.[20]


The United Nations Office on Drugs and Crime (UNODC) estimates that worldwide, there were 19 million past-year users of cocaine in 2018. The UNODC found indications of increasing cocaine use in Western and Central Europe, stabilization in North America, and mixed trends in South America.[21]

Wastewater analysis from selected European cities has shown an increase of 30% or more during the period 2011-2016.[21]  Wastewater analyses from Australia showed an increase in cocaine consumption of 50% form 2016/17 to 2019.[21] A study of patients presenting with acute toxicity from psychoactive drugs in an urban emergency department in Switzerland from 2014 to 2015 found that cocaine accounted for 33% of the 50,624 cases.[22]


DAWN monitored fatalities reported by Medical Examiners/Coroners (ME/C) in 40 metropolitan areas in the United States. In most areas, cocaine was among the top five drugs involved in drug-related deaths in the DAWN ME/C data for 2010.[23]

Data on drug overdose deaths in the United States show that cocaine-related overdose deaths involving opioids increased from 0.37 to 0.91 per 100,000 population from 2000 to 2006, declined to 0.57 per 100,000 population in 2010, and then increased to 1.36 per 100,000 population in 2015. In contrast, cocaine-related overdose deaths not involving opioids increased from 0.89 to 1.59 per 100,000 population from 2000-2006 and then declined to 0.78 per 100,000 population in 2015.[24]

Sequelae of intravenous injection may cause morbidity. A "pocket shot" is an attempted injection of the internal jugular vein by directing the needle into the depression in the neck superior to the clavicle and lateral to the sternocleidomastoid (the same approach as the supraclavicular approach for subclavian central venous catheter insertion). Such attempts can lacerate the apical pleura and/or vasculature resulting in pneumothorax, hemothorax, or hydropneumothorax. This is usually observed in the left side because most people have right-hand dominance, and it is easiest for them to attempt injection into the left side of the neck.

Intravenous injection may cause aneurysm or pseudoaneurysm of central veins or arteries, and rupture may result in intrathoracic or intra-abdominal hemorrhage, vascular obstruction, and arteriovenous fistulae. A necrotizing angiitis similar to periarteritis nodosa may develop, frequently with severe effects upon the kidneys, such as microaneurysm formation, segmental stenoses, and thromboses. The result is severe hypertension and oliguric renal failure. Similar lesions may occur in the small bowel, liver, and/or pancreas.

Other sequelae that may be observed with intravenous drug use include the following:

  • HIV infection
  • Thrombophlebitis
  • Cellulitis
  • Abscesses
  • Viral and talc-induced hepatitis
  • Subacute bacterial endocarditis (SBE)
  • Foreign-particle pulmonary emboli
  • Tetanus
  • Malaria
  • Cotton fever


Racial breakdown of DAWN data on ED visits in 2011 is shown in Table 2, below.

Table 2. DAWN Data, 2011 (Open Table in a new window)

Total ED Visits for Cocaine in US








Other/2+ Race/Ethnicities




The CDC reported that reported past-year cocaine use in 2018 by race/ethnicity, as a percentage of the population, to be as follows[1] :

  • White - 2.1%
  • Black - 1.8%
  • Hispanic - 1.9%
  • American Indian or Alaska Native - 1.9%
  • Native Hawaiian or other Pacific Islander - 1.6%
  • Asian - 1.4%


In DAWN reports for 2011, men accounted for 325,396 cocaine-related ED visits, and women, 179,520.[1] This disparity may have a physiologic basis.

On a milligram-per-kilogram basis, women who use cocaine intranasally have significantly lower plasma cocaine levels than men. Women using cocaine in the luteal phase of their menstrual cycle have peak plasma levels lower than those observed during the follicular phase of the cycle.[25] Notwithstanding these differences, be mindful of the potential for increased cocaine cardiotoxicity in women previously discussed (see the Pharmacology section in Background).

Men detect the effects of cocaine faster and report more episodes of euphoria and of dysphoria than women.


Age-related breakdown of data on cocaine use and cocaine-related ED visits are shown in Table 3 and Table 4, below.[1]

Table 3. Current Cocaine Use by Age: 2016 (Open Table in a new window)

Age Range (y)

Cocaine Use, Any Form, Past Month (Percentage of Same-age Population)

Crack Cocaine Use, Past Month (Percentage of Same-age Population)


1.9 million (0.7%)

432,000 (0.2%)


28,000 (0.2%)

3000 (< 0.1%)


552,000 (1.4%)

15,000 (< 0.1%)


1.3 million (0.5%)

414,000 (0.2%)

Table 4. 2011 DAWN Data on Emergency Department Visits for Cocaine, by Age (Open Table in a new window)

Age, y

Number of Visits





















A review by Yarnell concluded that cocaine abuse in the older and geriatric age group is on the rise, but remains underdiagnosed and undertreated. In older individuals, cocaine use is associated with a number of adverse medical consequences, including higher rates of hypertension, pulmonary problems, myocardial infarction or coronary artery spasm, stroke, and cognitive impairment.[26]


The principal effect of cocaine, like ethanol, on mortality may be its association with homicide, suicide, and motor vehicle collisions.[27]  In a study of 14,843 persons who were fatally injured in New York City over 3 years, fatal injury after cocaine use exceeded all deaths associated with other causes in persons aged 15-24 years. Although approximately one third of deaths associated with cocaine use were the result of its direct pharmacologic effects, two thirds were the result of traumatic injuries.

Cocaine use, determined by detection of its metabolite benzoylecgonine in urine or blood, was found in 26.7% of the above-mentioned patients, with free cocaine, indicating recent use, detected in 18.3%. Ethanol was detected in 28.1% of those who died. For comparison, household surveys of the general population of New York City showed that the estimated frequency of cocaine use in the preceding 30 days was less than 1.3% overall; demographic groups with the highest rates of use were Hispanics and black men, whose rates were 3-4.1%.

In this study, cocaine use was detected in 69.7% of all cases of accidental poisonings, 29.2% of homicides, 15.3% of suicides, and 9.3% of accidents.


The use of alcohol and illicit drugs increases the risk of suicide 16-fold, which is substantially higher than the rate observed with either substance alone. A study of suicide cases in New York City demonstrated that 20% of individuals younger than 61 years had used cocaine within days of their death. Nearly one half of Hispanic men who commit suicide have toxicologic screens positive for cocaine. Cocaine users typically choose violent means for self-destruction, especially the use of firearms.

Domestic violence

Illicit use of drugs by members of the household increases a woman's risk of death at the hands of a spouse, lover, or close relative 28-fold.

According to Brookoff, approximately 45% of assailants in domestic violence had used alcohol or other drugs to the point of intoxication on a daily basis for the previous month.[28]  Approximately 12% were addicted to drugs, and 14% were addicted to alcohol and drugs. On the day of the assault, the most common intoxicant was cocaine. About 30% of assailants had used cocaine and alcohol, and 13% had used alcohol, marijuana, and cocaine.

In another study of domestic violence, two thirds of assailants had used the combination of alcohol and cocaine on the day of the assault. The active metabolite of this drug combination, cocaethylene, is more intoxicating, longer lived, and possibly more potent in its ability to kindle violent behavior than the parent drugs.

Other concerns

For individuals with one addictive disorder, the risk of having a second addictive disorder is increased 7-fold.

People who use cocaine have an increased incidence of acquiring HIV and other sexually transmitted infections.

Crack cocaine use during pregnancy has been associated with adverse perinatal outcomes. A systematic review and meta-analysis found significantly increased risk of preterm delivery, placental displacement, reduced head circumference, and low birth weight.[29]

Patient Education

The event that prompted the ED visit may provide an opportunity to strongly caution the patient about future use of cocaine and to encourage the patient to seek treatment for drug abuse.

For patient education resources, see the First Aid and Injuries Center and the Mental Health Center. Also, see the patient education articles Cocaine Abuse, Drug Dependence & Abuse, Substance Abuse, Club Drugs, and Poisoning.




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;[30] 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? Note that the use of “speedballs” (cocaine and heroin) and “super speedballs” (cocaine, heroin, and fentanyl) continue to increase; however, cocaine and fentanyl packaged together may be sold as cocaine on the street.[5]

  • 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 heart failure? Is evidence of myocardial infarction or coronary artery disease present? Is the patient showing evidence of a dysrhythmogenic substrate (eg, myocarditis, cardiomyopathy, Wolff-Parkinson-White syndrome)?

  • 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? Possible reasons for cocaine-related ED visits include unexpected reactions, overdose, chronic effects, accidental injury, and withdrawal[31]

  • Does the patient want help in coping with cocaine use?


Multisystem effects of cocaine

Suspect cocaine use in patients, especially young patients, with any of the following:

  • Altered mental status—particularly agitated delirium, though depressed mental status may occur in cocaine washout syndrome (cocaine withdrawal)
  • New-onset seizure
  • Hypertension
  • Chest pain
  • Myocardial ischemia or infarction
  • Dyspnea
  • Signs of intracranial hemorrhage
  • Epistaxis
  • Psychiatric illness

Pay particular attention to the assessment of vital signs. Perform 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, and patients are more likely to require intensive care.[32]

Differential diagnosis

Cocaine overdose may resemble the following:

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. The initial increase in heart rate and blood pressure (BP) are dose dependent but heart rate and BP may plateau because of acute tachyphylaxis, even with increasing concentrations of serum cocaine.[33]

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.[34]  Cocaine causes pathologic vasoconstriction, so a patient with hemorrhagic trauma may present with a normal mean arterial pressure; thus, recognition of hypovolemia secondary to hemorrhage may be delayed. This combination of pathophysiologic factors, coupled with delayed recognition, increases the potential for cerebral insult.[35]

Chronic cocaine use downregulates adrenergic receptors and decreases endogenous catecholamine stores in the heart. This may affect the patient's presentation. Franklin et al observed sinus bradycardia (< 60 beats/min) in 43 of 162 (27%) habitual cocaine users. The bradycardia in these patients was asymptomatic.[36]

The patient's skin may be cool and clammy even if 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.[30]

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.[37] Limb ischemia may occur after intra-arterial injection, which may be done inadvertently, or be intentional due to the unavailability of veins because of sclerosis secondary to repetitive puncture, or due to the desired effects from arterial injection.

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

  • Aortic dissection 

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 the following:

  • Chest pain
  • Cough with hemoptysis
  • Dyspnea
  • Bronchospasm
  • Pruritus
  • Fever
  • Diffuse alveolar infiltrates without effusions
  • 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)

  • Torticollis, trismus, and laryngospasm may endanger the airway.

Eyes, nose, mouth, and throat findings

Signs include reactive mydriasis, nystagmus (generally horizontal and 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[38] :

  • Cocaine-associated cerebral vasculitis, which may produce a gradual decrease in visual acuity or acute blindness

  • Central retinal artery occlusion

  • Blurring of vision

  • Endophthalmitis from systemic or local infection

  • 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

  • Vision loss caused by crack-induced corneal ulceration from direct irritation of the smoke, cocaine-induced epithelial disruption, and repeated mechanical disruption from rubbing

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 scratching in response to 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 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 aassociated with increased risk 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 (which 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 (agitation)

  • 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 stuffing, perform careful cavity searches of the rectum and vagina after obtaining patient consent. 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


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.[39] 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.[40]



Diagnostic Considerations

Other problems to consider in the differential diagnosis of cocaine toxicity include the following:

  • CNS structural disorders (eg, hematoma, subarachnoid hemorrhage, other intracranial hemorrhage, tumor, embolus, abscess, contusion)
  • Drug withdrawal
  • Hypoxemia
  • Mania
  • Thiamine deficiency
  • Xanthine toxicity
  • Water and electrolyte imbalance

Differential Diagnoses



Laboratory Studies

No laboratory studies are indicated if the patient has a clear history and mild symptoms.

If history is absent or if the patient has moderate-to-severe toxicity, appropriate laboratory tests may include the following:

  • Complete blood cell (CBC) count
  • Electrolytes, BUN, creatinine, glucose (basic metabolic panel)
  • Glucose
  • Pregnancy test
  • Calcium
  • Creatine kinase (CK) 
  • Troponin
  • Urinalysis
  • Toxicology screens

A normal CK concentration may be used to help rule out rhabdomyolysis. An elevated concentration is nonspecific, with possible causes ranging from local trauma due to intramuscular injection, to myocardial infarction.

Urinalysis should include inspection to detect myoglobinuria. In cocaine-induced rhabdomyolysis, a dipstick urinalysis reveals an orthotoluidine reaction positive for heme in 75% of patients, findings positive for protein in 67%, and microscopic hematuria in some.

On a urine drug screen, drain cleaner or bleach added to urine can mask cocaine; alkaline urine may raise this suspicion. Desipramine and amantadine, prescribed to reduce cravings for cocaine, may cause false-positive results on urine tests for amphetamines. No substances result in a false-positive urine drug screen for cocaine, though false positives may still occur from switched or mislabeled specimens.

Urine, blood, gastric contents, and unknown substances found on patients, such as on a mustache, may be sent for toxicologic evaluation. Include the patient's clinical history and differential diagnosis of the toxins in question to guide the laboratory evaluations. High plasma cocaine concentrations are rarely observed because cocaine has a short half-life of 30-45 minutes. Furthermore, numerous studies have demonstrated that toxicology screening rarely changes the clinical treatment of patients. Although concentrations higher than 1 mg/L are generally associated with toxicity, deaths have been reported with blood levels of 0.1-20.9 mg/L. Because of this wide range of toxicity, quantitative blood levels of cocaine or metabolites are generally not clinically useful.

Cocaine exhibits first-order kinetics over a wide dose range; therefore, after 5 half-lives (approximately 4 h), virtually all of the cocaine taken should have been converted to its metabolites. Hollander et al concur, indicating that urinary cocaine may be detected for 4-8 hours after a single intranasal dose. However, Lewin, Goldfrank, and Weisman maintain that most cocaine is excreted in the urine within 24 hours of ingestion.[41]

Benzoylecgonine, which may induce neurotoxicity, ischemia, and arrhythmias,[42] may be present in urine for as long as 60 hours after single use and for as long as 22 days after the cessation of heavy cocaine use. If the ratio of benzoylecgonine to cocaine found in the urine is less than 100:1, either the cocaine was ingested less than 10 hours before collection of the sample or ongoing liberation of cocaine is occurring from a body package. The “cocaine” assay on most clinical urine drug screens are for benzoylecgonine and not cocaine itself.

Also consider tests of the following:

  • Cardiac markers in patients with chest pain; cocaine use does not affect the specificity of troponin assays[33]

  • Lactate dehydrogenase (LDH) level, aspartate aminotransferase (AST), prothrombin time (PT), activated partial thromboplastin time (aPTT), and cultures of blood and urine in patients with elevated temperatures

  • Evaluation of cerebrospinal fluid (CSF) for patients with altered sensorium and fever in whom meningitis is being considered

  • Serum osmolality and ketones in patients with altered mental status

Imaging Studies

Obtain a chest radiograph in patients with chest pain, hypoxia, or moderate-to-severe toxicity. The chest radiograph may reveal diffuse granulomatous changes resulting from chronic parenteral use due to the injection of inert insoluble ingredients of oral preparations or insolubles used to cut cocaine (eg, talc). Septic pulmonary emboli appear round or wedge shaped; they may clear rapidly or cavitate. Aspiration pneumonitis and noncardiogenic pulmonary edema may also be demonstrated. Pulmonary abscess may become evident after aspiration pneumonitis or after an intravenous injection of bacteria or toxic organic or inorganic materials.

The chest radiograph may reveal a needle that was lost during drug injection. An aneurysm or pseudoaneurysm may be noted with mainlining (directly injecting into a central artery or vein); this finding is an indication for further imaging studies.

Radiographs may be useful to evaluate cellulitis, abscess, or nonhealing wound in an intravenous drug user, and may reveal a foreign body or subcutaneous emphysema produced by gas-forming organisms in an anaerobic infection. Ultrasonography may identify foreign body or abscess.

Skeletal images can reveal osteomyelitis or fractures. However, osteomyelitis may not be demonstrable on plain images for 1-2 weeks, and other imaging studies should be performed if such a diagnosis is considered.

Radiography to investigate body packing

Swallowed packets of cocaine may rupture, resulting in acute cocaine poisoning. They may also critically obstruct the esophagus or small bowel, typically at the ileocecal valve, or may cause bowel ischemia. Drug packets typically weigh 1-12 g each.

Begin with plain images of the abdomen to search for packets. However, the rate of false-negative results is 1.2-33%. Radiographs depicting packets are shown below.

Patient transporting cocaine packets seen on KUB a 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 a 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.

Results from ultrasonography are occasionally useful for identifying packets, but not sensitive enough to exclude their presence. Contrast-enhanced study of the bowel or abdominal CT may be the only way of identifying the packages. This is shown in the image below.

CT scan of patient transporting cocaine packets. CT scan of patient transporting cocaine packets.

Regular radiologic examination is imperative to confirm successful transit of packages through the GI tract.

McCarron and Wood reported a series of 75 patients with suspected cocaine body packing evaluated with kidneys, ureters, and bladder (KUB) radiography. Cocaine packages (15-175 per individual) were retrieved from 48 patients. In 73%, the KUB images showed foreign bodies. KUB findings were negative in 3% of patients with cocaine packages in the rectum and in another 16% who subsequently passed 15-135 packages.[43]

McCarron and Wood identified 3 types of packages, with the following physical and radiographic characteristics and risk for rupture:[43]

  • Type 1: Condoms, toy balloons, or fingers of latex gloves contained cocaine in loose white powder form. Typically, the package material was stuffed with cocaine, tied, folded back on itself, and tied again at the opposite end. A variation involved wrapping a package with masking tape to make a small bundle, then covering it with 2 more condoms tied with fishing line. Type 1 packages radiographically appeared as well-defined circular or cigar-shaped white opacities. Ties, if radiographically apparent, had a rosette appearance. If gas halos were observed, they were irregular. This type of cocaine package posed the highest risk for breakage or leaching.

  • Type 2: About 5-7 layers of tubular latex, with a smooth tie on each end, covered white or light yellow matted cocaine powder. On direct inspection of the bundles, they appeared light yellow and were relatively large and uniform in size. These radiopaque bundles were oblong. When viewed radiographically, gas halos were present and regular, but no ties were apparent. Type 2 packages were less susceptible to breaking than type 1 packages.

  • Type 3: Yellow, hardened cocaine paste wrapped in aluminum foil, then wrapped again with 3-5 layers of tubular latex and securely tied at both ends. These packages were hard, smaller than type 1 and type 2 packages, and irregularly sized. They did not appear as foreign bodies on abdominal images. No breakage or leaching of cocaine was reported with this type of package.

The risk of bag rupture or leaching increases with dwell time. In one series, 2 patients had sloughed pieces of wrapping, and 1 had evidence of leaching. After the container believed to be the last has passed, Perrone and Hoffman recommend imaging (eg, Gastrografin upper-GI series with small-bowel follow-through or CT of the abdomen and pelvis) to ensure that the GI tract has been fully purged of all packets.[44]

American College of Emergency Physicians guidelines recommend brain CT for a patient presenting with first-time seizure. Perrone and Hoffman recommend CT scan of the head in all patients with cocaine-associated seizures, as intracranial pathology is often identified.[44]

Other Tests

Obtain a 12-lead electrocardiogram (ECG) in patients with any of the following:

  • Chest pain
  • Hypoxia
  • Dyspnea
  • An irregular, rapid, or slow pulse
  • Altered mental status
  • Moderate-to-severe toxicity

Of 48 patients admitted to an intensive care unit with cocaine-induced chest pain, 86% had abnormal ECG findings, but only 6% were found to have sustained a nyocardial infarction.

The Brugada sign has been noted in cocaine users. This finding should prompt consideration of its implications for sudden cardiac death. Note the images below.

Schematics show the 3 types of action potentials i 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 syn 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.

Coma has several possible etiologies in the cocaine-toxic patient, including the second (nonconvulsive) stage of status epilepticus. Therefore, immediate electroencephalography (EEG) is indicated in patients presenting with unexplained coma in whom this is thought to be a possibility.


Renzi recommends lumbar puncture (LP) to rule out intracranial hemorrhage in patients with persistent headache after the patient's BP is normalized and contraindications are ruled out on head CT.[45] When LP is considered for this possible indication, remember that headaches are common in cocaine users secondary to decreased uptake of serotonin. Consider LP in all patients with hyperthermia or altered mental status.



Prehospital Care

Prehospital care includes the following:

  • Assess the patient's airway, breathing, and circulation (ABCs); intervene if necessary
  • Provide oxygen
  • Obtain intravenous access
  • Closely monitor vital signs, including temperature
  • Monitor glucose levels for patients with altered mental status
  • Carefully use naloxone for patients with depressed mental status, if opioid use cannot be excluded
  • Administer benzodiazepines to manage agitation or seizures

Patients with cocaine toxicity may be combative, aggressive, and disoriented, and have delusions of persecution or hallucinations. Caution is appropriate because the patient may attempt to harm care providers. Physical restraint should be avoided if possible due to risks of rhabdomyolysis and hyperthermia. When physical restraint is required it should be used only with caution and adequate personnel.

Emergency Department Care

Note the following:

  • Patients with cocaine toxicity should receive initial evaluation and stabilization, including attention to ABCs, oxygen, intravenous access, and cardiac and pulse oximetry monitoring.
  • In hyperthermic patients, temperature may continue to rise due to agitation and potentially to fighting of restraints. Temperature may reach critical levels; thus, close monitoring and early intervention is indicated.
  • Check the nares for residual cocaine, and remove if present.
  • Monitor for hypoglycemia, which may present as any neuropsychiatric abnormality
  • Never base treatment on the results of a drug screen; rely on clinical findings instead.
  • Avoid physical restraints if possible. Benzodiazepines are effective and safe if sedation is required.
  • The prevalence of unrecognized pregnancy is up to 6% in ED patients. Perform routine pregnancy testing for appropriate patients as physiologic changes in pregnancy may increase cocaine toxicity. Cocaine may induce miscarriage, premature labor, placental abruption, or fetal toxicity, and modifications may be necessary for acute management.
  • Provide reassurance. The effects of cocaine are generally short lived. Monitor patients until they are no longer tachycardic and hypertensive and until they are calm and cooperative.

Therapeutic Dilemmas

Medications commonly administered to treat pathophysiologic effects of cocaine may worsen other adverse effects of cocaine. Thus, there is concern primarily about use of epinephrine, lidocaine, and beta-blockers in the setting of acute cocaine toxicity. Conflicting reports and recommendations in the literature compound the controversy.

As an example, the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care acknowledge that many toxicologic approaches are not based on high-quality research, but rather on case reports, small case series, and data extrapolated from animal studies.[46] The American College of Cardiology Foundation/American Heart Association (ACCF/AHA) 2014 recommendations for treatment of patients with cocaine toxicity are based on class C evidence  (ie, consensus opinion of experts, case studies, or standard of care).[47]

Epinephrine and vasopressin

Vasopressin offers considerable theoretical advantage over epinephrine in cardiac arrest due to cocaine toxicity.[48, 49] 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 myocardial oxygen availability.[50] Cocaine toxicity frequently causes acidosis: epinephrine loses much of its effectiveness in an acidotic milieu[50] , whereas vasopressin demonstrates vasoconstricting efficacy even with severe acidosis.[51]

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, the AHA Textbook of Advanced Cardiac Life Support for the Experienced Provider recommends that high-dose epinephrine be avoided and that the interval for its administration be increased (q5-10 min).

If ventricular fibrillation 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 similarity in cardiovascular effects caused by cocaine and epinephrine, administration of epinephrine to a patient who arrests in a hyperadrenergic state has been likened to "pouring gasoline on a fire."[49]


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.[52] 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.[53]

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, as a IB sodium channel blocker, may play in competing with cocaine, which is a (more dangerous) IC sodium channel blocker, thereby decreasing the effects of cocaine that are mediated through the sodium channel.

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.


The 2014 ACCF/AHA guidelines on unstable angina and non–ST-segment elevation myocardial infarction advise that the use of beta-blockers within 4 to 6 hours after cocaine exposure is controversial, with some evidence for harm. Instead, the guidelines recommend that a combined alpha- and beta-blocking agent (eg, labetalol) may be a reasonable treatment choice for cocaine-related hypertension (systolic blood pressure > 150 mm Hg) or sinus tachycardia (pulse > 100 beats per min), provided that the patient has received a vasodilator, such as nitroglycerin or a calcium channel blocker, within the past hour.[47]

However, labetalol has an alpha-to-beta blockade ratio of 1:7. Therefore, it may not provide cocaine-toxic patients with enough protection 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. Nevertheless, a systematic review of cocaine-related cardiovascular toxicity found that combined alpha/beta-blockers such as labetalol and carvedilol were effective in attenuating both hypertension and tachycardia, with no adverse events reported.[54]

AHA guidelines for cardiopulmonary resuscitation and emergency cardiovascular care advise that pure beta-blockers are not indicated for the treatment of cocaine-related cardiac toxicity.[46]



Cardiovascular Concerns

Cocaine-associated cardiac arrest

Current American Heart Association (AHA) guidelines note that no data exist to support the use of cocaine-specific interventions in cardiac arrest due to cocaine overdose. Instead, resuscitation should follow standard Basic Life Support and Advanced Cardiac Life Support (ACLS) algorithms.[46]

Cocaine-associated acute coronary syndrome

The AHA guidelines note that clear evidence exists that cocaine can precipitate acute coronary syndrome (ACS), and it may be reasonable to try agents that have shown efficacy in the management of ACS in patients with severe cardiovascular toxicity. Agents that may be used as needed to control hypertension, tachycardia, and agitation include the following[46] :

  • Alpha-blockers (phentolamine)
  • Benzodiazepines (lorazepam, diazepam)
  • Calcium channel blockers (verapamil)
  • Morphine
  • Sublingual nitroglycerin (NTG)

The AHA does not recommend any one of those agents over another in the treatment of cardiovascular toxicity due to cocaine, but benzodiazepines should usually be first line.

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 ventricular tachycardia (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.

Consider sodium bicarbonate for treating dysrhythmias resulting from the direct toxic effects of cocaine,[55] 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 supraventricular tachycardia (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

Cocaine-associated chest pain and MI

Chest pain may result from musculoskeletal, cardiovascular, pulmonary, or other causes. Risk of myocardial infarction is highest within the first hour following cocaine use.[56] 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 steps outlined below.

  • 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.

The American College of Cardiology Foundation/American Heart Association (ACCF/AHA) 2014 guidelines on unstable angina and non–ST-segment elevation myocardial infarction include the following class I recommendations for treatment of patients with ischemic chest discomfort and ST-segment elevation or depression after cocaine use[47] :

  • Administer sublingual or intravenous (IV) NTG and IV or oral calcium channel blockers (eg, diltiazem, 20 mg IV)
  • In patients whose ST segments remain elevated after NTG and calcium channel blockers, perform immediate coronary angiography, if possible; if occlusive thrombus is detected, percutaneous coronary intervention is recommended
  • Fibrinolytic therapy is useful in patients with ischemic chest discomfort after cocaine use if ST segments remain elevated despite NTG and calcium channel blockers and coronary angiography is not possible; however, fibrinolysis is often contraindicated

AHA guidelines note that patients with cocaine-induced hypertension or chest discomfort may also benefit from benzodiazepines and/or morphine, in addition to NTG.[46]

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).[57]

In patients with ST-elevation MI (STEMI) or with cocaine-associated chest pain refractory to benzodiazepines, treatment with phentolamine, an alpha antagonist, may also be considered. Phentolamine has been reported to reverse ST elevations in cocaine-associated STEMI, though it has not been studied systematically.

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. However, the specificity of troponin assays is not affected by cocaine use.[33]

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.[55] Obtain a detailed history and perform physical and ancillary testing, as appropriate, directed at identifying endocarditis, septic pulmonary emboli, and pseudoaneurysm.

AHA 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.[34] 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.[44] MI has been attributed to cocaine use several days earlier, and Holter monitoring has documented cocaine-induced ischemia for several weeks after cocaine use.[34] Recurrent ischemic chest pain is reported in patients who do and in patients who do not continue to abuse cocaine.[34] 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.[58] 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.


Cocaine may precipitate hypertensive emergency due to CNS stimulation and peripheral alpha-agonist effects. Toxicity may 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, and phentolamine may be considered. 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 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.


A brief observation period with 2 blood samples sent for troponin measurement within 9-12 hours is a reasonable approach for low-risk patients with cocaine-related chest pain. Admission is indicated for patients whose chest pain has any of the following characteristics:

  • Severe, sustained, or recurrent
  • Associated with significant cardiac risk factors
  • Associated with any acute cardiopulmonary symptoms
  • Accompanied by positive cardiac markers or ECG changes suggestive of ischemia

Other indications for admission to a critical care unit may include unresolved moderate-to-severe signs and symptoms, including seizures and focal neurologic deficits, and suspected ingestion of packages of cocaine.

If critical care is not available, transfer patients requiring such care to an appropriate facility, preferably in an advanced life support unit.

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%.

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.[45]  In contrast, Perrone and Hoffman recommend head CT in all cases of cocaine-associated seizures because of the risk of associated intracranial lesions,[44]  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. Diphenhydramine 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 fingerstick testing 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.


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 early in the evaluation and maintain a high index of suspicion for hyperthermia. In the setting of serious hyperthermia, continuously monitor the core body temperature.

Immersion of the patient in an ice bath is the best way to rapidly lower the body temperature in severe hyperthermia. Hyperthermia may also 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 101ºF 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.[59] 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.[18] Although Callaway and Clark believe that further studies are necessary to assess the efficacy of butyrophenones in the treatment of psychostimulant overdose,[18] Colucciello and Tomaszewski claim that haloperidol is effective in treating cocaine-related agitation and that no clinical data proscribe its use, theoretic concerns notwithstanding.[60]

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 mitigates 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 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 are 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.[61] 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.

Body stuffers should be observed, including cardiac monitoring, for 6 or more hours.[62] 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 toxicity or signs or symptoms of intestinal obstruction or ischemia.

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, which is 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.


In a 12-week, double-blind, randomized study involving 142 cocaine-dependent adults, treatment with the anticonvulsant topiramate was found to be significantly more effective than placebo in improving abstinence from cocaine use, reducing the intensity and frequency of cravings for cocaine in a 24-hour period, and improving observer-rated global functioning.[63, 64]

From weeks 6-12, half of the study’s patients received escalating doses of topiramate, starting at 50 mg daily and increasing to the target maintenance dose of 300 mg/day. The reduction from baseline in the number of days per week in which patients did not use cocaine was 13.3% with topiramate, compared with 5.3% with placebo. In addition, the likelihood of achieving urinary cocaine–free weeks increased by 16.6% with topiramate, versus 5.8% with placebo.


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

Refer the patient for drug abuse counseling and treatment.

If domestic violence is identified from the history or physical examination, refer the patient to an appropriate agency that makes referrals for physical and psychological problems and provides safety, treatment, advocacy, and support.

Provide referral for counseling or testing for HIV and other sexually transmitted disease (STD), as appropriate.


Experimental studies in animals indicate that circulating cocaine can be sequestered by high levels of anticocaine antibodies, thereby facilitating inactivation of the cocaine prior to its entry into the brain, via the action of natural plasma cholinesterase. While the US Food and Drug Administration has not approved any prophylactic pharmacotherapies for cocaine abuse, research using a cocaine-specific vaccine is in the early stages. Using succinylnorcocaine covalently linked with an immunogenic carrier, changes in IgG anticocaine antibody levels have demonstrated response kinetics similar to those of the human conjugate vaccine for nicotine.[65]



Medication Summary

The general objectives of pharmacotherapeutic intervention in cocaine toxicity are to reduce the central nervous system and cardiovascular effects of the drug by using benzodiazepines initially and then to 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.

Nitroglycerin 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 in patients with signs of Wernicke encephalopathy.


Class Summary

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.

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.

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. Diazepam should not be administered intramuscularly, because absorption is unreliable.

Cardiovascular agents

Class Summary

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)

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

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

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

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.

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.

Phentolamine (Regitine)

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

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.

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.


Useful for achieving return of spontaneous circulation, but may not improve the chances of recovery with a good neurologic outcome. Increases coronary perfusion pressure.


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

GI agents

Class Summary

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.

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.


Class Summary

Thiamine should be administered before glucose to prevent Wernicke encephalopathy.

Thiamine (Vitamin B1)

Administered to prevent Wernicke encephalopathy. If the patient is already showing signs of Wernicke encephalopathy, thiamine should be administered before glucose.

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.


Questions & Answers


What is cocaine toxicity?

How does cocaine toxicity progress?

What are the signs and symptoms of phase I (early stimulation) cocaine toxicity?

What are the signs and symptoms of phase II (advanced stimulation) cocaine toxicity?

What are the signs and symptoms of phase III (depression and premorbid) cocaine toxicity?

Which lab tests are performed in the diagnosis evaluation of cocaine toxicity?

What is the role of radiography in the diagnosis of cocaine toxicity?

When is electrocardiography indicated in the workup of cocaine toxicity?

How is cocaine toxicity treated?

How are hyperthermia and rhabdomyolysis treated in cocaine toxicity?

What is the effect of cocaine availability on the incidence of cocaine toxicity?

How common is cocaine toxicity in the US?

What is the historical background of cocaine use, abuse and toxicity?

What are the forms of cocaine that can lead to toxicity?

What is the pharmacology of cocaine toxicity?

How does the route of administration affect cocaine toxicity?

How is cocaine metabolized during the development of cocaine toxicity?

How does alcohol affect cocaine toxicity?

How does nicotine affect cocaine toxicity?

How does heroin affect cocaine toxicity?

How do agents used to enhance effect of cocaine contribute to toxicity?

Which drug interactions increase the severity of cocaine toxicity?

What is the role of adulterants in the development of cocaine toxicity?

What is the role of levamisole in the development of cocaine toxicity?

Which non-pharmacologic adulterants may affect cocaine toxicity?

What is the pathophysiology of cocaine toxicity?

What is the role of dysrhythmia in the pathophysiology of cocaine toxicity?

What are additional findings on the pathophysiology of cocaine toxicity in rat studies?

What is the pathophysiology of cocaine-induced MI?

What is the role of endothelial cells in cocaine-induced vasoconstriction?

What is the role of dopamine in the pathophysiology of cocaine-induced MI?

What types of cardiomyopathy are caused by cocaine toxicity?

What are the neurologic complications of cocaine toxicity?

What is the role of dopamine in cocaine-induced neurologic syndromes?

What is the pathophysiology of delirium in cocaine toxicity?

How do restraints increase the risk for sudden death from cocaine toxicity?

What is the pathophysiology of hyperthermia in cocaine toxicity?

What is the pathophysiology of cocaine-associated rhabdomyolysis (CAR)?

How does acidemia increase the risk for death from cocaine toxicity?

What is the prevalence of cocaine toxicity in the US?

What is the global prevalence of cocaine toxicity?

What is the mortality and morbidity associated with cocaine toxicity?

What are the sequelae of IV cocaine use?

What are the racial predilections of cocaine toxicity?

What are the sexual predispositions of cocaine toxicity?

How does the prevalence of cocaine toxicity vary by age?

What are the possible complications of cocaine toxicity?

What is the prevalence of suicide among cocaine users?

What is the prevalence of domestic violence in patients affected with cocaine toxicity?

What are the health risks of cocaine toxicity?

What is included in patient education about cocaine toxicity?


What is included in the clinical history of suspected cocaine toxicity?

What is the focus of present illness history in suspected cocaine toxicity?

How extensive is the review of systems for the evaluation of suspected cocaine toxicity?

What is the focus of medication and drug use history in the evaluation of suspected cocaine toxicity?

What are the signs and symptoms of "crack lung" in cocaine toxicity?

Which physical findings are characteristic of cocaine toxicity?

What is the association of cocaine toxicity with trauma?

Which conditions should be included in the differential diagnoses of cocaine toxicity?

Which vital sign findings suggest cocaine toxicity?

Which cardiovascular findings are characteristic of cocaine toxicity?

What is the prevalence of respiratory findings in cocaine toxicity?

Which respiratory findings are characteristic of cocaine toxicity?

What are the ENT signs and symptoms of cocaine toxicity?

What are ophthalmologic complications of cocaine toxicity?

Which GI findings are characteristic of cocaine toxicity?

Which cutaneous findings are characteristic of cocaine toxicity?

What causes increased heat production in cocaine toxicity?

Which neurologic and psychiatric findings suggest cocaine toxicity?

What are possible psychiatric complications of cocaine toxicity?

What are the neurologic and psychiatric signs and symptoms of cocaine toxicity?

Which renal findings are characteristic of cocaine toxicity?

Which endocrine and metabolic findings are characteristic of cocaine toxicity?

Which musculoskeletal findings are characteristic of cocaine toxicity?

What is included in the physical exam for cocaine toxicity when body stuffing is suspected?

How is the cause of an altered mental status differentiated in cocaine toxicity?

What are phases of acute cocaine toxicity?

What is the clinical presentation of phase I (early stimulation) cocaine toxicity?

What is the clinical presentation of phase II (advanced stimulation) cocaine toxicity?

What is the clinical presentation of phase III (depression and premorbid) cocaine toxicity?

What are the risk factors for cocaine toxicity?

What are the types of cocaine dependency?

What are the differences between type A and type B cocaine dependency?

Which mental disorders are comorbid with cocaine toxicity?


Which conditions should be included in the differential diagnoses of cocaine toxicity?

What are the differential diagnoses for Cocaine Toxicity?


What is the role of lab testing in the evaluation of cocaine toxicity?

How is toxicology screening performed in the evaluation of cocaine toxicity?

Which lab tests may be performed based on clinical presentation of cocaine toxicity?

What is the role of imaging studies in the workup of cocaine toxicity?

What is the role of radiography in the evaluation of body packing in cocaine toxicity?

What are the types of body packing in cocaine toxicity?

What is the risk of bag rupture or leaching in individuals with body-packed cocaine?

What is the role of CT scanning in the evaluation of cocaine toxicity?

What is the role of ECG in the evaluation of cocaine toxicity?

What is the role of EEG in the evaluation of cocaine toxicity?

What is the role of lumbar puncture in the workup of cocaine toxicity?


What is included in prehospital care for cocaine toxicity?

What is included in emergency department (ED) care for cocaine toxicity?

Which medications may worsen the adverse effects of cocaine toxicity?

What is the role of epinephrine and vasopressin in the treatment of cocaine toxicity?

What is the role of lidocaine in the treatment of cocaine toxicity?

What is the role of beta-blockers in the treatment of cocaine toxicity?

How is cardiac arrest treated in cocaine toxicity?

How is acute coronary syndrome (ACS) treated in cocaine toxicity?

How are cardiac dysrhythmias treated in cocaine toxicity?

How is myocardial infarction (MI) treated in cocaine toxicity?

How is ST-segment elevation or depression treated in cocaine toxicity?

What is the role of fibrinolysis in the treatment of cocaine toxicity?

What cardiac monitoring should be performed during the treatment of cocaine toxicity?

Why is a rapid bedside test for cocaine required prior to administering beta-blocker therapy for MI?

How is hypertension treatment in cocaine toxicity?

How is hypotension treated in cocaine toxicity?

How is aortic dissection treated in cocaine toxicity?

When is inpatient care for cocaine toxicity indicated?

How is pulmonary edema treated in cocaine toxicity?

How is hypoxia treated in cocaine toxicity?

What is the role of naloxone in the treatment of cocaine toxicity?

What is the role of flumazenil in the treatment of cocaine toxicity?

How are seizures treated in cocaine toxicity?

How are dystonic reactions treated in cocaine toxicity?

How is hypoglycemia treated in cocaine toxicity?

How is acidosis treated in cocaine toxicity?

How is hyperthermia treated in cocaine toxicity?

How is rhabdomyolysis treated in cocaine toxicity?

What are GI concerns in the treatment of cocaine toxicity?

How is body packing managed in cocaine toxicity?

How are the psychiatric manifestations of cocaine toxicity treated?

When should cerebral malaria be considered in the differential diagnosis of cocaine toxicity?

Which patients with cocaine toxicity should be screened for HIV and hepatitis?

What are the risks of organ donation following treatment for cocaine toxicity?

What is the role of topiramate in the treatment of cocaine toxicity?

Which specialist consultations are beneficial in the treatment of cocaine toxicity?

How is cocaine toxicity prevented?


What is the role of pharmacotherapeutic intervention in cocaine toxicity?

Which medications in the drug class Nutrients are used in the treatment of Cocaine Toxicity?

Which medications in the drug class GI agents are used in the treatment of Cocaine Toxicity?

Which medications in the drug class Cardiovascular agents are used in the treatment of Cocaine Toxicity?

Which medications in the drug class Benzodiazepines are used in the treatment of Cocaine Toxicity?