Cocaine Toxicity: Practice Essentials, Background, Pathophysiology

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. View Media Gallery

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.

Diagnosis

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.

Radiography

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.

Electrocardiography

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

Management

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.