AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Cocaine is derived from Erythroxylon coca, a shrub endemic to the Andes, Mexico, West Indies, and Indonesia. The people of the Andes held the shrub in religious reverence and buried their dead with bags of coca leaves. The stimulant effects of the coca leaves are believed to have played a major role in the advancement of the Inca civilization, providing the Incas with the energy and motivation to realize dramatic architectural and social achievements despite the barren, icy, cold, and oxygen-poor environment they inhabited. The Spanish conquistadors quickly became enamored of the euphoric effects of the plant and introduced the shrub to the Europeans, who developed a fondness for the taste and sensations it generated.

Spanish physicians described the first medicinal use of coca compounds as early as 1596, but the use of cocaine did not become more widespread until 1859, when Albert Niemann isolated the drug. Following the isolation of the drug, pharmacists began to concentrate large amounts of cocaine for use. Cocaine is not just a new Hollywood trend. In 1863, Marielli made cocaine-containing wine, which received widespread praise throughout Europe and was endorsed by the Pope. In the late 1800s, William Stewart Halsted, an American physician, self-experimented with cocaine and, in 1885, discovered nerve-block anesthesia. Halsted fell prey to cocaine addiction, which took 2 years to control. Similarly, Freud self-experimented with cocaine and became very addicted. He praised it as a cure for depression and used it extensively to facilitate psychotherapy.

In 1886, John Stith Pemberton, an Atlanta pharmacist, manufactured cocaine-containing syrup to be mixed with carbonated water and called it Coca-Cola (60mg/8 oz serving). Coca-Cola was sold as a tonic and contained cocaine until 1906, when the government passed the Pure Food and Drug Act, which required that medicines and elixirs list the ingredients on the label. Cocaine addiction became an increasingly important public health threat, and, in 1914, the Harrison Narcotics Act banned the nonprescription use of cocaine products and labeled cocaine as a narcotic because of its addictive properties. By 1920 it became the most feared illicit drug in the United States.

The passage of the Harrison Narcotics Act drove recreational cocaine use underground. In the late 1960s, cocaine use was preempted by amphetamine use. In the 1970s, cocaine use became increasingly popular. In the 1980s, crack (an impure freebase form), a much cheaper and easier-to-use form of cocaine, became the stimulant of choice for people younger than 18 years and for poor people.

Currently, the medicinal use of cocaine is limited to topical anesthesia of the upper respiratory tract and eye because the vasoconstrictive properties of cocaine are desirable during these procedures.

Cocaine (benzoylmethylecgonine) is an ester that belongs to the tropane family of natural alkaloids, which also includes scopolamine and atropine. Cocaine is an extremely powerful reinforcing psychostimulant with highly addictive properties that produces many pharmacological effects in humans and results in a spectrum of clinical presentations.

Pathophysiology

Cocaine is a local anesthetic, and, like other local anesthetics, it blocks the generation and conduction of electrical impulses in excitable tissues such as neurons and cardiac muscle. The primary site of action of cocaine is the cell membrane, where it blocks the voltage-gated fast sodium channels, thereby reducing the permeability of the membrane to sodium. As the effects of cocaine gradually increase, the threshold for excitation also increases, the rise rate of the action potential declines, impulse conduction slows, and the probability of propagation of the action potential decreases. Ultimately, the ability of the tissue to generate an action potential is abolished. In nerve cells, these effects are manifested by anesthesia. In myocardial conduction tissue, these effects are manifested by type I antidysrhythmic-like activity.

Cocaine may also interfere with other membrane channels, particularly the potassium channels, thus decreasing the resting membrane potential.

Cocaine differs from other local anesthetics in that it also binds to monoamine transporters and blocks the reuptake of catecholamines and dopamine into the presynaptic nerve terminals. This results in a high degree of adrenergic and dopamine activity with a widespread toxicity. Alpha-adrenergic stimulation, which is largely due to norepinephrine, induces hypertension, whereas beta-receptor stimulation, which is largely due to epinephrine, commonly results in tachycardia (beta-1 effect) and hypotension (beta-2 vasodilation). Other factors, such as the generation of CNS-excitatory amino acids (glutamate and aspartate), may play a role in CNS hyperactivity and cardiovascular pathology.

In the central ventral nuclei of the limbic system and the basal forebrain, the effect of cocaine on dopamine and serotonin reuptake generates the sensation of pleasure and presumably reinforces the use and addiction of cocaine.

Repeated drug abuse produces enduring changes in brain circuits that subserve incentive motivation and stimulus-response learning, this is suggested by the relapsing to addiction in 80-90% of regular cocaine abusers even after prolonged periods of abstinence.

Cocaine is rapidly and well absorbed from all mucous membranes, including oropharyngeal, nasopharyngeal, pulmonary, gastrointestinal, and genitourinary mucosae. The onset of action, peak effects, duration of action, and the plasma half-life of cocaine depend on the dose and the route of administration. When used intravenously, the onset of action of cocaine is immediate and the peak effect occurs 3-5 minutes after the bolus. The effect lasts for 20-30 minutes after injection, and the half-life is 40-60 minutes. Smoking crack has a similar time of onset and peak effect as an intravenous injection.

With insufflation, the onset of action occurs 1-3 minutes after use and peaks 20-30 minutes later. The effect lasts 45-90 minutes, and the half-life is 60-90 minutes. Inhalation of cocaine results in immediate effects that peak 1-5 minutes after inhalation and last for 20 minutes after inhalation. The half-life is 40-60 minutes. Oral use of cocaine results in an onset of effects 10 minutes after use. The effects peak 60 minutes after use and last for 60-90 minutes.

Cocaine is metabolized mainly by the liver via a number of pathways and by plasma cholinesterases. More than 10 metabolites have been discovered; many retain some of the activity of the parent compound, such as vasoconstriction, proconvulsant activity, and sodium channel blockade, thereby increasing the toxicity of cocaine. The presence of alcohol results in an additional metabolite called cocaethylene, which is more toxic than either of the parent compounds and has been associated with an increased mortality in patients intoxicated with cocaine.

The best-described cocaine metabolites include norcocaine, benzoylecgonine (BE), ecgonine, and ecgonine methylester (EME). EME is the least toxic of the cocaine metabolites because it does not have vasoconstrictive properties and does not block the sodium channels. EME is generated by deesterification of cocaine by the liver and plasma pseudocholinesterases and accounts for 30-50% of cocaine metabolism. Nonenzymatic hydrolysis, which generates benzoylecgonine, accounts for 40% of cocaine metabolism. Demethylation, which generates norcocaine, accounts for the remainder of the metabolism of cocaine. Norcocaine is the most toxic of the metabolites because it has many of the same effects as cocaine and, perhaps, a stronger vasoconstrictive effect than the parent compound.

The activity of plasma cholinesterases determines the relative concentration of cocaine metabolites. Reduced plasma-cholinesterase activity shifts the metabolism of cocaine toward the pathways that produce toxic metabolites. Factors or drugs that decrease the activity of pseudocholinesterases include extremes of age, the presence of atypical cholinesterase, organophosphates (found in insecticides, anti–myasthenia gravis agents, and some eye drops), and carbamates (found in insecticides).

Patients who have these drugs in their systems or who have these characteristics have an increase in the incidence of ischemic chest pain, convulsions, and cardiac arrest. Extremes of plasma cholinesterase levels manipulation have been reported in some individuals by injecting insecticides in order to prolong their high. Similarly, factors that increase hepatic N-demethylation, such as pregnancy and progesterone ingestion, increase cocaine toxicity because more toxic metabolites are formed.

Street cocaine may be accidentally contaminated during the preparation process or may be intentionally adulterated by a number of compounds in order to dilute the amount of cocaine used and to increase profits. Commonly used cocaine adulterants include any of the local anesthetics, phenytoin, sugars, amphetamines, phencyclidine, quinine, talc, and others.

The concomitant use of other drugs poses additional risks for the person using cocaine. As noted above, the combination of cocaine with alcohol (some studies report up to 70% of cocaine consumers) produces cocaethylene (ethylbenzoylecgonine), which has more potent proconvulsant and cardiotoxic properties than cocaine itself, coupled with a longer half-life. Heroin is also commonly used with cocaine as a "speedball" in an effort to combine a cocaine high (initial phase) with a heroin high (latter phase) of intoxication. Furthermore, nicotine dependence is reported in up to 88% of patients who use cocaine, thus adding to cocaine cardiovascular risk factors.

Physiologic and psychologic tolerance to cocaine emerges between the first and second dose. In other words, the psychologic high and the physiologic body response (eg, pulse, blood pressure) do not increase with additional doses of cocaine once the initial effect is reached.

Cardiovascular effects

Cocaine causes vasoconstriction by preventing the reuptake of catecholamines in the central nervous system and stimulating the release of norepinephrine from adrenergic nerve terminals. These effects result in increased myocardial oxygen demand and coronary artery spasm. This causes roughly a 10% decrease in the caliber of large epicardial vessels and may progress to myocardial infarction, especially in territories of diminished coronary reserve and narrowed arteries. This effect is of increased importance in the chronic user because the repeated use of cocaine results in accelerated coronary atherosclerosis and increased platelet aggregation. With chronic use, dopamine stores in peripheral nerve terminals are depleted. When this store depletion is coupled with cardiovascular sensitivity to catecholamines, a variant anginalike syndrome with ST elevations may develop during cocaine withdrawal.

The chronic use of cocaine is also associated with multiple foci of myocarditis, fibrosis, contraction band necrosis, sarcoplasmic vacuolization, myofibrillar loss, hypertrophy with inefficient oxygen use, and alterations in the genetic material of the myocytes.

Dysrhythmias are the most common cause of death in patients who are acutely intoxicated. The type of arrhythmia that develops depends on numerous factors, but overall cocaine reduces the ventricular fibrillation threshold. Bradycardia may be secondary to stimulation of vagal nuclei of the brain, myocardial infarction, and acidosis. Tachycardia may be secondary to the ability of cocaine to stimulate central and peripheral sympathetic systems, hypoxia, acidosis, and other factors. The quinidine-like effects of cocaine result in a number of intraventricular conduction abnormalities, including widening of the electrocardiographic wave (QRS) and QTc, as well as negative inotropic and chronotropic effects.

A Brugada pattern (right bundle branch block with ST elevation in leads V1, V2, V3) has been reported as associated with cocaine use and appears to occur due to modulation or unmasking of the sodium channels.

Aortic dissection is a known complication of cocaine use and is presumably due to the increases in shear forces on the vascular wall produced by the drug.

Acidemia, which is a common complication of acute toxicity, may also cause conduction delays and depress myocardial contractility.

Neurological effects

Cocaine blocks the reuptake of catecholamines in the brain and stimulates areas that are catecholamine dependent. In the cortex, this blocking leads to increased vigilance, and, with higher doses, cocaine use results in anxiety, psychoses, and excited delirium. Catecholamine release in the CNS also increases motor activity, which may be manifested by abnormal involuntary movements and convulsions, resulting in acidosis, rhabdomyolysis, and hyperthermia.

Similar to alcohol abuse, once seizures develop, a kindling effect occurs and patients develop more severe seizures at smaller doses of cocaine. The vasoconstrictive properties of cocaine may also result in widespread cerebral vasoconstriction and cause ischemia and necrosis of brain tissue. Chronic cocaine use decreases dopamine receptor density in the brain.

In the hypothalamus, this results in abnormalities in temperature control, and, in the nigrostriatal system, it results in a number of extrapyramidal reactions such as bradykinesis, akinesis, akathisia, pseudoparkinsonism, and catalepsy. Furthermore, the effects of cocaine on the dopaminergic system may play a role in the development of asymptomatic rhabdomyolysis observed with chronic cocaine use.

Rhabdomyolysis

Rhabdomyolysis may be the result of insufficient energy supply in the setting of the increased demands of psychomotor agitation. Other factors that contribute to the development of rhabdomyolysis include compartment syndrome, hypocalcemia, hypokalemia, hypomagnesemia, hypophosphatemia, and uncontrolled seizures. No correlation exists between muscular symptoms and the development of rhabdomyolysis. No correlation exists between the amount of damaged muscular mass and the extent of renal impairment.

Frequency

United States

In 1997, an estimated 682,000 people (0.3% of the population) frequently used cocaine (more than 51 days of the year); this statistic is similar to that found in 1985.

The estimated number of people occasionally using cocaine (people who used in the past year for fewer than 12 days) was 2.6 million in 1997, which is a large decrease from 1985, when it was 7.1 million.

The estimated number of people using crack was about 604,000 in 1997; this estimate has not changed since 1988.

In 2003 alone, 34.9 million Americans older than 12 years of age reported using cocaine at least once. As of 2005, according to the Office of National Drug Control Policy, more than 3 million people in the United States are considered long-term cocaine users.

Currently, cocaine is reported as the most commonly abused drug in patients presenting to the emergency departments.

International

Cocaine abuse is widespread in the world and is becoming a major public health issue in a number of Canadian and European cities. Data suggest that the prevalence of cocaine use in the world is approximately 13 million people, or 0.23% of the global population. Cocaine use is also increasing in a number of Latin American countries, including the countries that are the main producers of cocaine.

Mortality/Morbidity

According to data from the Drug Abuse Warning Network (DAWN), in 2000, the DAWN survey of medical examiners reported 4043 cocaine-related deaths. Cocaine intoxication is implicated in most fatal injuries in New York City, where it is the leading cause of death among young adults.

• Cocaine-related deaths are not dose related, and isolated blood levels do not predict toxicity. Fatalities are multifactorial, and, often times, the cause is difficult to determine. Death from acute cocaine toxicity is a rare event, unless a massive exposure is present (body packers and body stuffers). Otherwise, the cocaine users who are prone to serious illnesses and complications are the chronic users. A list of cocaine-related complications include status epilepticus, ventricular dysrhythmia, myocardial infarction, malignant hyperthermia, aortic dissection, eosinophilic lung disease or "crack lung", pulmonary edema, alveolar hemorrhage, stroke, central retinal artery occlusion, hepatic necrosis, intestinal ischemia, renal infarction, and rhabdomyolysis.
• High mortality rate seems to be associated with rhabdomyolysis, acute renal failure, liver dysfunction, and disseminated intravascular coagulation. An accelerated death has been noted in some patients who develop convulsions within 3-30 minutes of cocaine use. This syndrome is characteristically described in 3 phases. Phase I is characterized by pseudohallucinations ("crawling bugs"), agitation, hyperthermia, and emotional lability. Phase II is characterized by severe hyperthermia, encephalopathy, and seizures associated with ventricular dysrhythmias. Phase III is characterized by coma, fixed dilated pupils, pulmonary edema, and agonal respiration, culminating in death.
• The lethal dose of cocaine is undetermined; clinical toxicity seems to be unrelated to measured plasma concentration levels. A concentration that was once considered close to fatal has been found in barely symptomatic patients. Conversely, fatalities have been documented with cocaine levels below threshold to induce measurable alteration in pulse or blood pressure.

Race

Rates of illicit cocaine use vary by ethnicity and race. While most current recreational cocaine users are white and non-Hispanic, the rates of cocaine use were 1.4% for blacks, 0.8% for Hispanic whites, and 0.6% for non-Hispanic whites. Crack is more commonly used by people who are underprivileged.

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Sex

Rates of illicit drug use vary by gender. As is the case with other drugs, cocaine use among men is almost twice that of women. In terms of emergency department visits, men accounted for 61% and women accounted for 30% of cocaine-related emergency department visits

Age

The rate of current cocaine use is generally highest among people aged 18-25 years, followed by people aged 12-17 years, and people aged 26-34 years (0.9%). The rates of cocaine use in adults older than 35 years dropped to 0.5%. In terms of emergency department visits, the highest peak was found in patients older than 35 years (43% of cases). Forty-one percent of cases involved patients aged 26-34 years, followed by 15% and 1.4% for patients aged 18-25 years and 6-17 years, respectively.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

In general, the clinical presentation of cocaine intoxication is that of a sympathomimetic toxidrome. Virtually any organ system may be affected, and patients may present with a myriad of conditions and symptoms. The lethal effects of cocaine relate to its stimulation of the CNS and the cardiovascular systems. Stimulation of the CNS results in symptoms such as excited delirium, combativeness, hyperactivity, paranoia, violence, involuntary movements, convulsions, severe hyperthermia, intracerebral hemorrhage, and ischemic stroke. Stimulation of the cardiovascular system results in dysrhythmias, myocardial ischemia and infarction, congestive heart failure, hypertensive crisis, and aortic dissection. Other conditions associated with cocaine toxicity include rhabdomyolysis, retinal artery occlusion, renal failure, and infarction of any organ system of the body.

• Because of the widespread effects of cocaine, the review of history and systems should be detailed and extensive.
• • In the alert patient with symptoms, obtain a history of present illness, including the type, amount, and route of administration of cocaine; the time of cocaine use; and the circumstances surrounding and following the ingestion of cocaine. Always be aware of the possibility of toxicity or side effects related to cocaine contaminants added for bulk or profit.
  • Obtain the patient's prior medical history, including the presence or absence of comorbid conditions, such as coronary artery disease, congestive heart failure, seizure disorder, and liver disease.
  • Obtain history of prior drug use.
  • Also obtain history regarding co-ingestions and medications used because they may alter the pharmacokinetics, symptomatology, and outcome of patients with cocaine intoxication.
  • In a patient with an altered mental status, search for corroborating evidence, eg, empty crack vials and drug paraphernalia.
  • Emergency Medical Services (EMS) personnel, police, and bystanders may assist in identifying signs and symptoms that immediately precede the present illness and may assist in the diagnosis.
  • Question the patient's family regarding the patient's immediate history of present illness such as the timing of drug use, co-ingestions, and any history of recent trauma. Also question the family regarding the presence of chronic medical conditions; use of other medications, including prescription and nonprescription medications (eg, aspirin); use of alcohol; use of other drugs; and allergies.
• Body packers and body stuffers may be asymptomatic when brought in by police.
• • The body packers, also called mules, pack their gastrointestinal tract with bags of cocaine (or other illicit drugs) in order to smuggle the drug from one country to another.
  • In contrast, body stuffers hastily insert packages into the mouth, rectum, or vagina in order to conceal the evidence from police at the time of their arrest.
• Central nervous system and neuromuscular system
• • Headache: Cocaine use commonly results in headaches. Cocaine may trigger migraine headaches, but, most importantly, the headache may be secondary to complications of cocaine use such as stroke, subarachnoid hemorrhage, meningitis, brain abscess, and vasculitis. In the presence of trauma, headache may be secondary to a skull fracture and/or epidural or subdural hematoma. Withdrawal from cocaine may also result in headaches that are commonly relieved by the additional administration of cocaine.
  • Seizures: Cocaine-related seizures are usually due to a hyperadrenergic state and usually occur within 90 minutes of drug use but have been delayed for as long as 12 hours. They usually are single, generalized, tonic-clonic seizures that are self-limited and usually follow the intravenous injection of cocaine or the smoking of crack. These patients recover without neurologic deficits and have negative cranial computed tomography (CT) scan and electroencephalogram. The presence of multiple seizures or status epilepticus may be observed in patients with a history of seizure disorder and patients who concomitantly use other drugs, eg, adulterants such as lidocaine, amphetamines, and quinine. Seizures may also be a manifestation of an underlying central nervous system injury such as a stroke, intracerebral and subarachnoid hemorrhages, and vasculitis.
  • Abnormal movements: A variety of abnormal movement disorders have been observed with cocaine use. Patients may present with torticollis, trismus, dystonic reactions, and choreiform movements ("crack dancing"). While most of these are benign, abnormal contractions of the vocal cords and larynx result in laryngospasm, which may be severe enough to cause airway obstruction and suffocation.
  • Nausea and vomiting: Nausea and vomiting are commonly due to stimulation of the vomiting center of the brain and are usually self-limited.
  • Anxiety: Anxiety and restlessness are common manifestations of cocaine toxicity and are due to the sympathomimetic effect of cocaine on the brain.
• Cardiac
• • Chest pain: Chest pain is the most frequent cocaine-related symptom and constitutes approximately 40% of cocaine-related emergency department visits. The etiology of the chest pain following cocaine use remains largely obscure and poorly understood in most patients, but a number of causes may be evident, including myocardial infarction and aortic dissection; other causes of chest pain can be related to the route of administration, including pneumomediastinum and pneumothorax when sniffed, or septic emboli if the intravenous route is used.¹
  • The incidence of cocaine-associated myocardial infarction has been found to range from 0-31% in retrospective studies of patients who present to the emergency department with chest pain following cocaine use. The Cocaine Associated Chest Pain (COCHPA) trial has been the largest prospective multicenter study. That study determined the incidence to be 6%. The pain is frequently described as substernal pressurelike discomfort and is associated with shortness of breath and diaphoresis. Patients who are affected are usually young males (aged 19-40 y) who smoke cigarettes and repetitively use cocaine. Most commonly, the chest pain occurs within 60-120 minutes after use when blood concentration of cocaine is highest, but the period of cocaine metabolites-ischemia may persist for as long as 2 weeks following use. Atypical presentations of myocardial infarction are also very common in the cocaine-using population.
• Respiratory: Shortness of breath, like chest pain, is a frequent symptom that brings patients who use cocaine to the emergency department and may be due to a number of cardiopulmonary processes. Cocaine smoking is associated with acute exacerbations of asthma, bronchiolitis obliterans, cardiogenic and noncardiogenic pulmonary edema, interstitial pneumonitis, pulmonary vascular hypertension, pulmonary hemorrhage, thermal injury to the airway, pneumothorax, and significant impairment of the diffusing capacity of the lung. Shortness of breath may also be due to cocaine-induced laryngospasm. Inhalation of cocaine may result in pneumomediastinum and pneumothorax.
• Gastrointestinal: Abdominal pain following cocaine use should raise suspicion of ischemic bowel; bowel perforation; and, in the smuggler, bowel obstruction. Abdominal pain may also be caused by hepatic necrosis due to cocaine use, which is similar to the necrosis commonly observed with acetaminophen. Renal infarction may also manifest as abdominal pain.
• Skeletal muscle: Cocaine use can lead to rhabdomyolysis, which may be associated with hyperthermia, seizures, or agitation. Rhabdomyolysis associated with cocaine use is usually severe, leading to renal failure and acidosis. Asymptomatic rhabdomyolysis may be observed in patients who chronically use cocaine and may be attributed to the effects of cocaine on the dopaminergic system.
• Back pain may be a symptom of rhabdomyolysis, renal infarction, or aortic dissection.

Physical

• Vital signs
• • Pulse: Cocaine affects the pulse rate and the heart rhythm in numerous ways. The initial effect of cocaine on the pulse is a reduction of the rate, presumably because of stimulation of the vagal centers in the medulla. Subsequently, when epinephrine is released from the adrenal gland, tachycardia ensues. This may be offset by the reflex of the carotid body to hypertension, which results in bradycardia. Pulse rates may be altered by any complication of cocaine use, concomitant disease, or co-ingestants. Cocaine use may result in any arrhythmia, benign or malignant, including life-threatening supraventricular and ventricular tachycardias, atrial and ventricular fibrillation, disorders of atrioventricular (AV) nodal conduction, disorders of the His bundle conduction, and abnormalities in the fascicles and myocytes.
  • Respirations: The initial effect of cocaine on the medulla results in an increase in the respiratory rate. Dyspnea, labored breathing, or irregular breathing may herald demise or may be a sign of developing complications. Massive overdoses may result in shutdown of the medulla and respiratory failure. Respirations may be altered by any complication of cocaine use, concomitant disease, or co-ingestants.
  • Blood pressure: Hypertension is commonly observed in patients with cocaine intoxication and is due to the persistence of adrenergic activity, namely that of norepinephrine at the neurovascular receptor terminals. The blood pressure may be altered by any complication of cocaine use, concomitant disease, or co-ingestants.
  • Temperature: Cocaine causes hyperthermia by increasing motor activity, thereby increasing heat production and reducing heat dissipation by constricting vessels.
• Central nervous system
• • Agitation, delirium, coma, convulsions, and focal neurologic findings may all be a sign of neurologic catastrophe. Agitated delirium characterized by severe hyperthermia and associated with incoherence, hyperactivity, agitation, paranoia, and combativeness is a preterminal event commonly followed by cardiac arrest.
  • Involuntary movements, such as nonintentional tremors, chorea, and dystonic reactions, as well as stereotyped movements, such as scratching, picking, and bruxism, are commonly observed with cocaine use and are referred to as "crack dancing". Tourette syndrome has also been described with cocaine use.
• Head, ears, eyes, nose, and throat
• • Head: The general examination of the head may reveal evidence of trauma.
  • Eyes: Examination of pupils reveals dilation, reactivity to light, and nystagmus. Unequal pupils may be secondary to uncal herniation. Funduscopic examination may reveal hemorrhages associated with subarachnoid hemorrhage and disc edema associated with brain edema.
  • Nose: Cerebrospinal fluid rhinorrhea due to cribriform plate damage secondary to chronic ischemia and necrosis of the nasal septum with chronic intranasal use of cocaine; nasal septum perforation; sinusitis; and epistaxis may be present.
• Neck: Examination of the neck may reveal subcutaneous emphysema associated with pneumomediastinum. Barotrauma may result from smoking and snorting when performing a Valsalva maneuver to increase the penetration of the drug to the alveolar spaces. Deviation of the trachea may be secondary to a tension pneumothorax
• Lungs: Unequal breath sounds may be secondary to pneumothorax. Bilateral wheezing secondary to asthma, eosinophilic lung disease, and thermal lung injury may be present. Bilateral rales may indicate the presence of pulmonary edema, eosinophilic lung disease, and angiitis obliterans. Unilateral wheezing or rales may be secondary to pulmonary infarction.
• Cardiac: Tachycardia, bradycardia, flow murmurs, and the pathologic murmurs may all be encountered with cocaine toxicity due to valvular disease. Typical signs of congestive heart disease can also be the result of cocaine-related cardiomyopathy.
• Abdomen: Absent bowel sounds may be noted in cases of mesenteric ischemia, and right upper quadrant tenderness may occur in cases of hepatic necrosis.
• Vascular: Differences in pulses between upper and lower extremities and right and left extremities may be noted with vascular dissections. Bruits may be notes in areas of dissection and partial obstructions. Absent pulses may be noted in totally occluded vessels.
• Dermatologic: The skin may be pale and diaphoretic due to vasoconstriction. Linear excoriations and ulcers are due to intensive scratching associated with imaginary cocaine bugs. Signs of skin and soft-tissue necrosis may be evident in massive overdoses.

Causes

• Cocaine is an addictive psychostimulant with euphoric effects that may be used occasionally by the casual user and frequently by people who are dependent on cocaine. The addictive properties of cocaine are thought to be due to brain dopamine D2-receptor stimulation. Patient dependence depends on a number of different factors, including the following: genetics, social and environmental factors, and preexisting medical and mental conditions.
• New research in mice suggests that the extent of some organ damage may be influenced by gender and sex hormones, particularly testosterone.
• Poisoning may occur with a single dose of recreational use or after an overdose.
• Poisoning may also occur in body stuffers and body packers when one of the ingested packets ruptures or leaks.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Head trauma with resultant brain injury
Stroke
Subarachnoid hemorrhage
Intracerebral hemorrhage
Status epilepticus
Cerebritis
Meningoencephalitis
Alcohol withdrawal
Wernicke encephalopathy
Serotonin syndrome
Phencyclidine toxicity
Amphetamine toxicity
Appetite suppressants
Monoamine-oxidase inhibitor use
Tricyclic antidepressants
Carbon monoxide poisoning
Thyroid storm
Pheochromocytoma
Hypoglycemia
Hypoxia-anoxia
Acidosis
Hypomagnesemia
Hypophosphatemia
Hypokalemia
Thyrotoxicosis

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• In the unconscious patient, the laboratory examination is an important adjunct to the clinical examination because it may elucidate the differential diagnosis and provide an objective means of monitoring some complications of cocaine use.
• Arterial blood gas analysis: Cocaine toxicity may result in metabolic and respiratory acid-base abnormalities noted by arterial blood gas analysis. Severe agitation, seizures, and hyperthermia can lead to hypoxia, respiratory acidosis (secondary to CNS depression), respiratory alkalosis, and metabolic acidosis. Respiratory alkalosis, observed in about 15% of patients, is secondary to hyperventilation.
• Glucose: Abnormalities of glucose may present with signs of adrenergic hyperactivity similar to that observed with cocaine intoxication.
• Sodium: Sodium abnormalities may mimic cocaine toxicity and may present with altered sensorium and seizures. Hypernatremia may be observed with cocaine-induced brain injury when diabetes insipidus occurs.
• Potassium: Hypokalemia may result in cardiac dysrhythmias and mimic the dysrhythmic effects of cocaine. Severe hypokalemia may also contribute to the development of rhabdomyolysis. Hyperkalemia may be a reflection of muscle breakdown in rhabdomyolysis or renal failure.
• Magnesium: Hypomagnesemia, when severe, may mimic cocaine and may cause torsade de pointes, hypertension, neurologic instability, seizures, and coma.
• Phosphorous: Severe depletion causes muscle breakdown and rhabdomyolysis. Severe depletion is also associated with cardiogenic pulmonary edema and renal failure. During muscle breakdown, phosphorus is released from muscle, resulting in hyperphosphatemia.
• BUN and creatinine: Renal function may be affected by renal infarction, hypertensive nephropathy, and rhabdomyolysis.
• Total creatine kinase: Creatinine kinase (CK) may be the most sensitive and important test in the diagnosis of rhabdomyolysis because clinical signs and symptoms of this complication are sparse. Rhabdomyolysis is defined as a CK level higher than 1000 U/L, or more than 5-fold that of the normal level. Suspect rhabdomyolysis in any patient with hyperthermia, agitation, coma, seizures, or hypotension. Most significant cocaine exposures are associated with some degree of rhabdomyolysis, and as many as 50% of patients who casually use cocaine show elevations of CK levels. CK levels in the 100,000-200,000 range are not rare for cocaine-induced rhabdomyolysis.
• Cardiac enzymes: An abnormally elevated isoenzyme of creatine kinase (CK-MB) fraction suggests cardiac infarction, even in the absence of electrocardiographic abnormalities. Because an isolated normal CK-MB level does not rule out infarction, serial values may aid clinical decision-making in the management of patients who present with chest pain after cocaine use. The value of newer serum markers of cardiac ischemia, such as cardiac troponins, has not yet been determined for cocaine-associated chest pain.
• Complete blood count: Serial hemoglobin and hematocrit levels may be important in patients with trauma and in patients with ongoing hemorrhage. WBC counts may be elevated from cocaine use but should also prompt a search for infectious processes.
• Liver function tests: Liver necrosis is characterized by a rapid rise in serum transaminase levels and prolongation of the prothrombin time, which develops within a few hours of intravenous cocaine injection.
• Urinalysis: The urine dipstick, which uses the orthotoluidine reaction to detect heme, may be used to detect myoglobin as it cross-reacts with orthotoluidine. Cocaine-induced rhabdomyolysis may be detected by urine dipstick as much as 75% of the time. The presence of blood on urinalysis should prompt a workup for renal infarction.
• Toxicology laboratory
• • Serum cocaine levels are not helpful and not clinically relevant because of the short half-life of the drug. The ratio of benzoylecgonine to cocaine, however, may be used to determine the approximate time of cocaine use. With recent use, the ratio of metabolite-to-parent drug is less than 100. This ratio may also be used to determine ongoing absorption of cocaine, which may be especially important in body packers and body stuffers with a ruptured bag.
  • Cocaine may be detected in the urine as long as 24 hours after use, and the metabolite of cocaine, benzoylecgonine, may be detected as long as 60 hours after a single use, which may increase to 22 days in patients who use cocaine chronically. Urine toxicology screens for benzoylecgonine are about 95% sensitive at detecting levels greater than 300 ng/mL.
  • The toxicology laboratory may also be helpful in determining adulterants such as phencyclidine, methamphetamine, and phenytoin.

Imaging Studies

• Roentgenography
• • Plain films of the abdomen with the patient in the supine and upright positions may be useful in the diagnosis of body packing, but false-negative results may occur. Serial abdominal roentgenograms may be useful in detecting the passage of drug packages.
  • A chest x-ray may be helpful in diagnosing pulmonary edema, aortic dissection, alveolitis, pneumonia, pulmonary infarction, septic emboli, pneumomediastinum, pneumothorax, and a ruptured viscus with air under the diaphragm.
• Computed tomographies
• • A noncontrast CT scan of the head may be helpful in diagnosing intracerebral hemorrhages; epidural, subdural, and subarachnoid hemorrhages; skull fractures; and ischemic cerebrovascular disease. Consider noncontrast head CT scan in all patients with change in mental status, seizures, and focal deficits and in patients with persistent headache.
  • A CT scan of the brain with contrast may be necessary to diagnose brain abscesses.

Other Tests

• Electrocardiogram: While the electrocardiogram may be important in determining the type of conduction abnormality, it is not a sensitive method for diagnosing myocardial infarction after cocaine use. Current data may be conflicting and report only a 35.7% sensitivity in predicting myocardial infarction.

  In the Cocaine Associated Chest Pain (COCHPA) trial, the most common ECG findings (50%) were nonspecific changes; of those, 34% showed early repolarization changes, 13% were abnormal but nondiagnostic, 4% showed new ischemic changes, and only 4% had ECG findings suggestive of acute myocardial infarction (AMI).

• • Normal or nondiagnostic results of electrocardiograms do not rule out myocardial injury. When electrocardiographic signs of myocardial infarction are present, they usually mimic the ST-segment and T-wave abnormalities observed with non–cocaine-related acute myocardial injury. These abnormalities may persist throughout the hospital stay even in the absence of chest pain.
  • The electrocardiogram may also help identify cocaine-associated dysrhythmia. Most cocaine-induced dysrhythmias are supraventricular and include atrial fibrillation with fast ventricular response, atrial flutter, and paroxysmal supraventricular tachycardia.
  • Cocaine-associated ventricular arrhythmias include ventricular ectopy. Type I antidysrhythmic properties of cocaine may result in prolongation of the QRS, PR, and QT intervals. Cocaine-induced QRS prolongation (>100 ms) is similar to that noted with tricyclic antidepressants. The presence of deep-inverted T waves in the anterior leads in patients with seizures may be observed in intracerebral hemorrhages.

Procedures

• Consider lumbar puncture in patients with suspected CNS infection and in patients with suspected subarachnoid hemorrhage and absent CT scan findings.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

Patients with cocaine poisoning may exhibit severe CNS and cardiovascular dysfunction, leading to a loss of airway protective reflexes, cardiovascular collapse, and mortality.

Admit all patients with major adrenergic symptoms, severe hyperthermia, severe agitation, recurrent convulsions, persistent arrhythmias and dysrhythmias, severe hypertension, and complications (eg, respiratory failure, cardiogenic and noncardiogenic pulmonary edema, altered mental status, myocardial ischemia and infarction, hypotension and shock, severe rhabdomyolysis, severe acidosis) to the intensive care unit. Complications such as aortic dissection, intracerebral bleeding, and subarachnoid bleeding require surgical intensive care. Also, admit asymptomatic body packers and body stuffers to the ICU.

• Initial assessment: Assessment and stabilization of the airway must be performed early in the course of poisoning, and mechanical ventilation with oxygenation must be provided immediately when the airway is threatened. The infusion of dextrose 50% in water (D50W) and thiamine as part of the advanced cardiac life support (ACLS) protocol are also appropriate first steps of resuscitation if unresponsiveness is the initial mental status presentation.
• Elimination: Administer activated charcoal to patients with oral ingestions of cocaine, ie, body stuffers and body packers, in order to reduce absorption. Whole bowel irrigation may be used to reduce transit time in these patients.
• Hyperthermia: Hyperthermia and severe psychomotor agitation are the most immediately life-threatening complications of cocaine poisoning. Temperatures as high as 114°F have been recorded. In these patients, rapid cooling is the most important therapeutic step. Rapid cooling may be achieved encouraging heat dissipation through conduction and evaporation. Also, accomplish reduction in heat production. Benzodiazepines may be used generously in order to control psychomotor agitation and shivering. While no evidence for the efficacy of dantrolene in cocaine-induced hyperthermia exists, dantrolene may be considered in patients with temperatures higher than 108°F who do not respond to vigorous cooling techniques.
• Psychomotor agitation: The immediate control of psychomotor agitation is critical in preventing the lethality of cocaine poisoning. Psychomotor agitation is managed in the standard fashion. Benzodiazepines, such as diazepam and lorazepam, are the mainstay of therapy and may be used generously until sedation is accomplished. Avoid physical restraints in patients with psychomotor agitation because they may interfere with heat dissipation. Likewise, avoid neuroleptic agents because they interfere with heat dissipation and, perhaps, lower the seizure threshold.
• Convulsions: Aggressively treat recurrent seizures because they may worsen hyperthermia, rhabdomyolysis, hypoxia, and acidosis. Seizures may also be a manifestation of an acute intracerebral complication. Imaging studies and, when indicated, cerebrospinal fluid (CSF) analysis should follow immediate seizure control.
  • In the setting of cocaine toxicity, seizures are treated in the standard manner, except that phenytoin may be ineffective in this circumstance and may be part of the street additives to cocaine bulk. Incremental doses of benzodiazepines, such as diazepam (0.1-0.3 mg/kg, intravenously) and lorazepam, are the preferred initial anticonvulsants because they are quick acting, effective, and titratable. When a total dose of 8 mg of lorazepam fails to control seizures, barbiturates, which have traditionally been effective anticonvulsants in toxic ingestions, may be effective in controlling seizures because they may act synergistically with the benzodiazepines.
  • Because phenobarbital acts slowly, a short-acting barbiturate, such as pentobarbital or amobarbital, may be considered. If these agents are not rapidly effective in controlling the seizures, consider barbiturate anesthesia with ventilatory support and neuromuscular blockade. In these cases, electroencephalographic monitoring is required to monitor the presence or absence of seizure activity.
  • Neuromuscular blockade is indicated to control muscle activity and the subsequent development of acidosis. Neuromuscular blockade may be accomplished with nondepolarizing agents, such as vecuronium. Continue the neuromuscular blockade until the electroencephalogram results are normal for 2 or more hours.
• Hypertension: Hypertension is common in patients intoxicated with cocaine and is due to alpha-mediated vasoconstriction, which is secondary to norepinephrine generated by the CNS. Cocaine-induced hypertension commonly responds to benzodiazepines. Benzodiazepines have been shown to be effective in the treatment of cocaine-induced hypertension, with or without chest pain or tachycardia.
  • When benzodiazepines fail to control hypertension, vasodilators, such as nitroprusside and nitroglycerin, are effective in controlling the blood pressure. If a contraindication to nitrate therapy exists, alpha-blockers, such as phentolamine, which block the vasomotor effect of norepinephrine, may be used.
  • Beta-blockers, in general, are best avoided in the setting of cocaine toxicity because they may result in unopposed alpha effects of cocaine. Beta-blockers have been reported to increase the blood pressure, reduce coronary blood flow, reduce left ventricular function, accentuate vasoconstriction and reduce the cardiac output and tissue perfusion in patients with cocaine toxicity. Furthermore, in animal models of cocaine toxicity, beta-blockers have been associated with an increased risk of seizures and an increased mortality.
  • Beta-blocker toxicity (acute rises in blood pressure) in the setting of cocaine poisoning also extends to the short-acting, beta1 selective antagonists, such as esmolol, and to labetalol, which has both alpha-blockade and beta-blockade activity (in a 1:3 ratio when used intravenously and a 1:7 ratio when used orally).
  • A double-blind, randomized, placebo-controlled trial suggests that B-blockers overall should be avoided since they accentuate cocaine-induced coronary spasm.
  • Nifedipine may potentiate the incidence of seizures and death after cocaine administration and should be avoided in the treatment of cocaine-induced hypertension. In addition, calcium channel blockers are also thought to dilate splanchnic vessels, thereby increasing absorption of ingested cocaine from the gastrointestinal tract, which may become disastrous in body packers and body stuffers.
• Myocardial ischemia and infarction: The administration of oxygen, nitrates, and aspirin are recommended in all patients with cocaine-induced myocardial ischemia. Benzodiazepines (diazepam, lorazepam) may be used to control cocaine-induced sympathetic tone. Phentolamine may relieve cocaine-induced coronary artery vasoconstriction and ameliorate myocardial ischemia. Likewise, verapamil and diltiazem (Cardizem) may ameliorate coronary vasoconstriction.
• In the presence of electrocardiographic signs of myocardial infarction and the absence of any contraindications, the use of thrombolytic therapy is advocated by the American Heart Association and the American College of Cardiology, particularly if immediate coronary angiography and angioplasty are not feasible; however, percutaneous transluminal coronary angioplasty (PTCA) may be as beneficial and safer.
• Supraventricular tachycardias: Consider electrical cardioversion in all unstable patients. Correct hypoxia, acidosis, and myocardial ischemia. Cocaine-induced atrial tachyarrhythmias that are stable commonly respond to benzodiazepines, which reduce CNS sympathetic effects of cocaine. If sedative-hypnotics fail to control the arrhythmia, diltiazem and verapamil may be effective. Adenosine generally is ineffective in cocaine-induced supraventricular tachycardias.
• Ventricular tachycardias: Perform defibrillation in all patients with pulseless ventricular tachycardia. Consider electrical cardioversion in all unstable patients. Theoretically, high-dose epinephrine, which simulates cocaine toxicity, may negatively impact the defibrillation threshold. Consider hypoxia, acidosis, hypovolemia, electrolyte disturbances (eg, hypokalemia, hypomagnesemia), and myocardial ischemia in the differential diagnosis, and immediately correct these conditions if present.
• Ventricular arrhythmias: When ventricular arrhythmias occur shortly after cocaine use, they are thought to be due to the effects of cocaine on the sodium channels. These arrhythmias may respond to sodium bicarbonate, the general antidote for sodium channel blockers. Sodium bicarbonate may be considered in patients with tachycardias associated with QRS durations greater than 100 milliseconds. As in tricyclic antidepressant (TCA) toxicity, maintain the pH at a range of 7.50-7.55.
• • These dysrhythmias also respond to lidocaine, especially when used in combination with benzodiazepines. Initial concerns about the use of lidocaine in the setting of cocaine poisoning have proven unfounded because of major differences in kinetics between the 2 compounds, which actually result in reduced effects of cocaine when lidocaine is present. No adverse effects from the use of lidocaine in the setting of cocaine poisoning have yet been reported.
  • Magnesium may also be considered in the treatment of ventricular dysrhythmias, especially in torsades.
  • Ventricular arrhythmias that occur several hours after cocaine use may be due to myocardial ischemia and, therefore, should be treated accordingly.
• Rhabdomyolysis: Patients with cocaine-induced rhabdomyolysis may develop significant elevations in their CK and significant myoglobinuria. Rhabdomyolysis results in pigment nephropathy, leading to renal failure in as many as one third of patients. Treatment of rhabdomyolysis consists of maintaining urine output at 3 mL/kg/h and preventing the precipitation of myoglobin in the kidneys. Treatment may be accomplished by the infusion of large amounts of intravenous fluids, the alkalinization of the urine, the infusion of mannitol, and hemodialysis if renal failure occurs. Alkalinization of the urine, while effective in promoting myoglobin and uric acid excretion, may slow cocaine excretion and alter the balance of electrolytes.

Surgical Care

Surgical consultation is indicated for patients with aortic dissection and intracranial hemorrhage. Surgical intervention may be required in body packers with gastrointestinal obstruction or a ruptured packet.

Consultations

• Consultation with the poison control center may be beneficial.
• Consultation with a cardiologist may be considered when myocardial infarction, myocarditis, and/or endocarditis are suspected.
• Consultation with a nephrologist may be considered when renal infarction is suspected or renal failure develops.
• Consider consultation with a surgeon when small bowel obstruction, a ruptured packet, intracranial hemorrhage, or aortic dissection is suspected.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The goals of pharmacotherapy are to neutralize toxicity, reduce morbidity, and prevent complications.

Drug Category: Benzodiazepines

These agents are a mainstay of therapy and are effective in reducing the production of catecholamines by the CNS. These agents are uniformly successful in preventing death from cocaine poisoning.

Drug Category: Alkalinizing agents

These agents are mainly indicated to reverse cardiac toxicity type I sodium channel blocker cocaine effect. They are also indicated in cocaine-induced rhabdomyolysis.

Drug Category: Gastrointestinal decontaminants

These agents are used in the prevention of massive absorption of suspected or confirmed cocaine presence in the gastrointestinal tract.

Drug Category: Antiarrhythmics

These agents are used for the management of ventricular arrhythmias, especially uncontrolled ventricular tachycardia.

Drug Category: Osmotic diuretics

These substances are filtered through the glomerulus, resulting in diuresis due to their ability to carry water onto the tubular fluid. These agents are mainly used to treat acute toxic ingestion of substances capable of producing acute renal failure.

Drug Category: Antihypertensives

These agents are used for control of cocaine-induced hypertensive urgencies and emergencies.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Once the acute phase is stabilized, further inpatient care is required for many of the complications of cocaine overdose and chronic use.
• Inpatient antibiotic therapy may be required for infectious complications of intravenous cocaine use, including endocarditis, septic emboli, cellulitis, and osteomyelitis. Empiric antibiotics may be started in the ICU, taking into account the most common pathogens, which include Staphylococcus aureus (61%), streptococci species (16%), pseudomonads species (14%), and polymicrobial species (8%). Necrotizing fasciitis requires early surgical intervention.
• Rehabilitation therapy may be required for all CNS, cardiovascular, and traumatic complications of cocaine use.

Further Outpatient Care

• Chronic outpatient therapy is required for complications of cocaine poisoning, including HIV infection, myocardial infarction, endocarditis, renal failure, and other complications.

Deterrence/Prevention

• Enrollment in deterrence programs, such as Narcotics Anonymous, may be of benefit for some patients. The National Institute on Drug Abuse (NIDA), a component of the National Institute of Health, is responsible for research into causes and treatment for drug addiction. Several medications have been tested and marketed for their potential efficacy to reduce cocaine use. No FDA-approved medications for the treatment of cocaine dependence have shown preliminary evidence of efficacy and are currently included in confirmatory testing in clinical trials or in the planning stages of confirmatory trials. Some of these medications include disulfiram, baclofen, modafinil, and terguride and will soon become part of the new choices to address the growing problem of cocaine addiction.

Complications

• Long-term neurological complications of cocaine use relate to the occurrence of devastating injuries such as anoxic encephalopathy, strokes, and intracerebral hemorrhages. As many as 30% of strokes in young adults are directly related to cocaine consumption.
• Upper respiratory tract complications include cribriform plate damage with chronic CSF rhinorrhea, nasal septum perforation, anosmia, sinusitis, epistaxis, epiglottitis, and bronchitis.
• Lower respiratory tract complications include asthma exacerbation, eosinophilic lung disease, pulmonary edema, septic emboli, pulmonary infraction, pneumonia, alveolar hemorrhage, thermal injury, and pneumothorax. Crack lung syndrome, a hypersensitivity pneumonitis occurring within 1-2 hours of cocaine smoking, presents with chest pain, hemoptysis, cough, palpitations, dyspnea, bronchospasm, fever, alveolar infiltrates, systemic eosinophilia, and significant impairment of diffusing capacity.
• Cardiac complications include cardiogenic shock, valvular heart disease, congestive heart failure, and cardiomyopathy.
• Ophthalmologic complications of cocaine use include central retinal artery occlusion, endophthalmitis, optic neuritis, and corneal ulcerations.
• Complications of intravenous drug use include thrombophlebitis, abscesses, cellulitis, osteomyelitis, retained foreign bodies, endocarditis, septic emboli, tetanus, and AIDS. When incorrectly injected, intravenous drug use may result in pneumothorax, vessel laceration, hemothorax, and chylothorax.
• Cocaine washout syndrome or the cocaine crash syndrome is characterized by severe exhaustion with psychomotor retardation, depression, suicidal ideation, anxiety, and increased appetite, lasting as long as 18 hours after the last consumption. Cocaine washout syndrome is due to catecholamine depletion, is usually self-limited, and only requires supportive therapy.

Prognosis

• The prognosis depends on the severity of cocaine poisoning and on the timely diagnosis and management of its complications.

Patient Education

• For excellent patient education resources, visit eMedicine's Substance Abuse Center, Poisoning - First Aid and Emergency Center, and Mental Health and Behavior Center. Also, see eMedicine's patient education articles Cocaine Abuse, Drug Dependence & Abuse, Club Drugs, Narcotic Abuse, Substance Abuse, and Poisoning.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to diagnose and treat complications of acute cocaine poisoning may lead to disastrous consequences.
• • Failure to institute a vigorous cooling therapy in a patient with severe hyperthermia
  • Failure to adequately sedate patients with psychomotor activity
  • Physically or chemically restraining patients without attention to heat dissipation
  • Failure to consider the diagnosis of rhabdomyolysis
  • Failure to closely monitor potassium levels in patients being alkalinized for rhabdomyolysis
  • Failure to consider myocardial infarction in patients with chest pain in the absence of electrocardiographic findings
  • Failure to consider myocardial ischemia in patients who present with chest pain when cocaine is remote
  • Failure to consider renal infarction in patients with hematuria following cocaine use
  • Failure to consider ischemic bowel in patients with abdominal pain following cocaine use
• Failure to consider the differential diagnosis may lead to devastating consequences.
• • Failure to consider trauma in patients with presumed cocaine poisoning
  • Failure to consider co-intoxications
  • Failure to consider CNS injury as a cause of change in mental status
  • Failure to consider meningoencephalitis as a cause of change in mental status
• Failure to consider potentially lethal drug interactions with cocaine may lead to litigation.

Special Concerns

• Body packers and body stuffers represent a special group of patients who require intensive monitoring and therapy.
• • The