Cocaine intoxication case file

Cocaine intoxication case file

Eugene C. Toy, MD, Barry C. Simon, MD, Terrence H. Liu, MD, MHP, Katrin Y. Takenaka, MD, Adam J. Rosh, MD, MS

Case 39

A 25-year-old woman is brought to the emergency department (ED) by police after attempting to break into a grocery store. When they apprehended her, they noted her pupils were large and that she seemed “high.” The patient states that she has been “smoking” for the past year. She notes that without her “smokes,” she craves the drug, becomes very sleepy, depressed, and has a huge appetite. In the ED, she complains of chest pain. The patient has a temperature of 38°C (100.4°F), heart rate of 120 beats per minute, and blood pressure of 160/90 mm Hg. Her pupils are both 6 mm and reactive. Her thyroid is normal to palpation. The heart and lung examinations reveal tachycardia, but are otherwise normal. Neurologic examination is unremarkable.

⯈ What is the most likely diagnosis?

ANSWER TO CASE: 39

Cocaine Intoxication

Summary: This 25-year-old woman was arrested while attempting to burglarize a grocery store. She lost her job because she was late and stealing, secondary to her desire to “smoke.” She has required more and more of the drug to get high and has been unsuccessful in her attempts to quit “smoking.” She suffers from cravings, sleepiness, depression, and hyperphagia when she is unable to “smoke.” While high, the patient feels euphoric and a sense of heightened energy. Her pupils are widely dilated; she has a low-grade fever, tachycardia, and hypertension. She has unintentionally lost 30 lbs over 6 months.

• Most likely diagnosis: Cocaine intoxication

ANALYSIS

Objectives

1. Recognize the clinical manifestations of cocaine intoxication.
2. Know the treatment for acute cocaine intoxication.

Considerations

This patient has many of the clinical signs and symptoms of cocaine intoxication. Cocaine, a sympathomimetic with local anesthetic characteristics, has potent vasoconstrictive properties. Acute cocaine intoxication can be a medical emergency. Rapidly fatal complications include severe hypertension (with concomitant endorgan damage), hyperthermia, and dysrhythmia. The mainstays of treatment are benzodiazepines (often in large dosages) and supportive measures. β-Blockers are contraindicated due to the risk of unopposed α-adrenergic stimulation. Acute cocaine intoxication may be difficult to distinguish from other conditions such as heat stroke, sedative-hypnotic withdrawal, intoxication with other sympathomimetics/ anticholinergics, thyrotoxicosis, and infections or structural lesions of the central nervous system.

Approach To:

Cocaine Intoxication

CLINICAL APPROACH

Cocaine is the second most commonly used illicit drug, second only to marijuana. With such widespread use, ED visits related to cocaine intoxication and its complications have risen substantially. A recent study shows that 14% of people older than 12 years have tried cocaine. Before the mid 1980s, the main routes of administration were intranasal and intravenous injection of cocaine hydrochloride. During the 1980s, crack cocaine emerged as the form of choice. Frequently, cocaine is combined with other drugs for various effects. Examples include mixing with heroin (“speedball”) or alcohol (“liquid lady”).

Cocaine causes release of norepinephrine, epinephrine, serotonin, and dopamine. This leads to a general stimulatory state including vasoconstriction and increased myocardial contractility. Cocaine also acts as a local anesthetic through sodium channel blockade. This effect is also responsible for many of the dysrhythmias and conduction abnormalities associated with cocaine use.

Symptoms of cocaine intoxication include euphoria, feelings of power or aggression, agitation, anxiety, hallucinations (classically formication, a tactile sensation of insects crawling on the skin), and delusions. Physical examination may reveal mydriasis, tachycardia, hypertension, hyperthermia, diaphoresis, tremors, or seizures. Coingestants or contaminants may result in atypical presentations (eg, cocaine plus heroin: mixed sympathomimetic-opioid presentation).

Table 39–1 lists the acute complications of cocaine intoxication. The effects on the cardiovascular and neurologic systems are of major concern. Severe dysrhythmias, myocardial infarction, seizures, and subarachnoid hemorrhage may result and potentially kill the patient. Body packers, who swallow cocaine wrapped in packets to smuggle it into the country, may die precipitously if a packet ruptures. Patients with seizures, altered mental status, dysrhythmias, or hemodynamic instability are

at increased risk of developing rhabdomyolysis, which may in turn result in renal failure. Half of those who develop acute renal failure die.

Chest pain is a frequent complaint of those who present to the ED after cocaine use. Cocaine causes coronary vasoconstriction while also increasing the myocardial oxygen demand and platelet aggregation. The ED physician must maintain a high index of suspicion for myocardial ischemia and infarction, even with an atypical history and normal initial ECG; between 0.7% and 6% of these patients will have an acute myocardial infarction. These patients are typically younger, nonwhite, cigarette smokers without other risk factors for coronary artery disease. Benzodiazepines, often in large doses, are useful in treating cocaine-induced chest pain. If acute coronary syndrome is suspected, aspirin, nitrates, and morphine are advisable. β-blockers should not be used due to the risk of an unopposed α-adrenergic effect, leading to increased hypertension and coronary vasoconstriction. Thrombolytic therapy of an acute myocardial infarction should be avoided if coronary vasospasm or dissection is suspected or severe, uncontrolled hypertension exists. Emergent coronary artery catheterization may provide the best diagnostic information.

For patient with hyperthermia or agitation, a basic metabolic panel and creatine kinase help rule out renal failure, metabolic acidosis, and rhabdomyolysis. If coronary ischemia or infarction is suspected, ECGs and cardiac enzymes should be obtained. The ECG may reveal conduction abnormalities (including widened QRS complexes), dysrhythmias, or ST-segment or T-wave abnormalities consistent with myocardial ischemia or infarction. Patients with altered mental status or seizures should have a computed tomography of the head performed.

In general, patients with acute cocaine intoxication require only supportive care including monitoring and intravenous fluids. Agitation is best controlled using benzodiazepines such as lorazepam or diazepam. Phenothiazines (such as haloperidol) should be avoided because they may lower the seizure threshold, contribute to hyperthermia, and have dysrhythmic effects. Atrial dysrhythmias may respond to benzodiazepines or other standard therapies (except β-blockers). Intravenous sodium bicarbonate administration may be useful for wide-complex tachycardias (or lidocaine if the dysrhythmia is refractory to bicarbonate). The drug of choice to treat severe hypertension is the α-antagonist phentolamine. Intravenous nitroglycerin or nitroprusside may also be used. Again, β-blocking agents should be avoided. Even labetalol (mixed α- and β-blocker) has been associated with excess morbidity and mortality in animal studies of cocaine toxicity. Seizures are treated with benzodiazepines. Hyperthermia requires continuous monitoring of core temperature and rapid cooling. Patients with rhabdomyolysis require increased fluid resuscitation in order to maintain 1 to 3 mL/kg/h of urine output.

Asymptomatic body packers may be carefully monitored and given activated charcoal and polyethylene glycol to hasten the passage of the packets of cocaine. These packets usually contain ten times the lethal dose of cocaine and are rapidly fatal if ruptured. If the patient becomes hypertensive, hyperthermic, or agitated or manifests other signs of cocaine intoxication, benzodiazepines should be given and surgery should be emergently consulted for operative removal of the packets. Endoscopy is usually avoided due to a risk of packet perforation.

The patient who responds to sedation and has no further complications may be discharged from the emergency department after a period of observation. 

Patients with ongoing chest pain, ECG changes, enzyme elevations or requiring ongoing pharmacologic treatment should be admitted to a monitored bed for further observation. Body packers need to be observed until all packets have passed.

COMPREHENSION QUESTIONS

39.1 A 25-year-old man is brought to the emergency room by police because of suspected cocaine intoxication. He is noted to be very agitated (fighting against five burly policemen) and wild eyed. On examination, his blood pressure is 180/100 mm Hg and heart rate 110 beats per minute. He is noted to have rotatory nystagmus. The neurologic examination reveals no focal abnormalities. Which of the following is the most likely diagnosis?

A. Amphetamine intoxication

B. Cocaine intoxication

C. Opiate intoxication

D. Phencyclidine intoxication

39.2 A 28-year-old man is noted to have extremely elevated blood pressure (210/130 mm Hg) associated with chest pain and dyspnea. His urine drug screen is positive for cocaine metabolites. Which of the following is the best next step?

A. Albuterol intravenously

B. Ephedrine intravenously

C. Labetalol intravenously

D. Lorazepam intravenously

39.3 A 35-year-old man is brought to the ED with altered level of consciousness, drowsiness, and pinpoint pupils. Which of the following is the most appropriate initial therapy for this patient?

A. Activated charcoal

B. Bicarbonate

C. Lorazepam

D. Naloxone

ANSWERS

39.1 D. Phencyclidine intoxication often presents with agitation, superhuman strength, and rotatory or vertical nystagmus.

39.2 D. Benzodiazepines should be used as the first-line agent for nearly all cocaine toxicities. The hypertension is caused by sympathetic stimulation. β-Blockers are contraindicated because they can result in unopposed α-adrenergic stimulation and exacerbation of the chest pain and hypertension. Hypertension not responsive to benzodiazepines may require intravenous phentolamine, an α-adrenergic antagonist.

39.3 D. This patient likely has an opiate intoxication (drowsiness and pinpoint pupils). Cocaine intoxication usually causes agitation and dilated pupils. Naloxone counteracts the effect of opioids.

CLINICAL PEARLS

⯈ The clinical manifestations of cocaine intoxication result from sympathetic overstimulation and vasoconstriction.

⯈ Cocaine intoxication can cause life-threatening complications, such as dysrhythmias, hyperthermia, and hypertensive emergencies.

⯈ Cocaine can cause a quinidine-like effect, prolonging the QT interval and leading to wide-complex dysrhythmias, bradycardia, and hypotension.

⯈ β-Blockers are avoided in patients with cocaine intoxication because of the risk of unopposed α-adrenergic stimulation.

⯈ Benzodiazepines are a mainstay of treatment for cocaine toxicity and many of its complications.

References

Aghababian RV, Allison EJ Jr, Boyer EW, et al, eds. Essentials of Emergency Medicine. Sudbury, MA: Jones and Bartlett; 2006:798-807. 

Marx JA, Hockberger RS, Walls RM, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 7th ed. Philadelphia, PA: Mosby Elsevier; 2009. 

McCord J, Jneid H, Hollander JE, et al. Management of cocaine-associated chest pain and myocardial infarction: a scientific statement from the American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology. Circulation. 2008;117;1897-1907. 

Schaider J, Hayden SR, Wolfe R, Barkin R, Rosen P, eds. Rosen and Barkin’s 5-Minute Emergency Medicine Consult. 3rd ed. Philadelphia, PA: Lippinott Williams & Wilkins; 2007:238-239. 

Tintinalli JE, Kelen GD, Stapczynski JS, eds. Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York, NY: McGraw-Hill; 2011.

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