Recreational drug overdose; cocaine abuse

Table I.

Cardiovascular

Myocardial ischemia, infarction

Arrhythmias

Aortic dissection, rupture

Hypertension

Atherosclerosis

Cardiomyopathy

Vasculitis

Central Nervous System

Seizures

Cerebral infarction

Transient ischemic attack

Intracranial hemorrhage (intraparenchymal, intraventricular, subarachnoid)

Agitation, euphoria

Psychosis

Cerebral vasculitis

Cognitive dysfunction

Hyperthermia

Pulmonary

Bronchospasm

Pulmonary edema (noncardiogenic)

Barotrauma

Pulmonary hemorrhage, hemoptysis

Pulmonary hypertension

Renal

Acute kidney injury

Renal infarction

Scleroderma renal crisis

Gastrointestinal

Mesenteric ischemia, infarction

Perforation

Metabolic

Weight loss

Multiple organ failure

Obstetric

Spontaneous abortion

Placental abruption

Intrauterine growth retardation

Premature labor

Other

Rhabdomyolysis

Dystonic reactions

Skin ischemia

4. Initiate specific interventions and supportive care for complications.5. Refer for counseling when stabilized.

2. Emergency Management

1. Assess vital signs, including core temperature and oxygen saturation.

2. Obtain IV access; start IV fluids in patients with agitation, tachycardia, hypotension or hyperthermia or when there is a high suspicion for rhabdomyolysis.

3. Control agitation with benzodiazepines.

4. Stop seizures if present with benzodiazepines.

5. Initiate cooling if core temperature >41 C (105.8 F).

4. Obtain laboratory and radiology tests to assess for organ injury as indicated by initial evaluation (i.e., ECG, CT scan)

Focal neurological deficits and seizures require brain imaging.

An ECG should be obtained in patients with any complaint of chest pain.

Check CK level in all agitated and hyperthermic patients to assess for rhabdomyolysis; a repeat CK level after IV fluids may show a significant increase if the initial level was normal.

Reassessment of the patient is essential during stabilization to determine efficacy of interventions and identify other complications.

3. Diagnosis

Diagnostic criteria

1. Diagnosis of cocaine abuse is made by clinical history with confirmation of cocaine metabolites (benzoylecgonine) by qualitative urine testing. Metabolites are detectable for 1-2 days after acute exposure but prolonged excretion (days to weeks) occurs in chronic high-dose cocaine abusers. Only high doses of prilocaine are known to cause false-positive results. False-negative results can occur if urine testing occurs very soon after cocaine use, before metabolites are formed. A positive result is a marker for recent use rather than diagnostic for acute intoxication.

2. Diagnosis of some complications often requires laboratory and radiologic studies in addition to the clinical examination as outlined below:

Arrhythmias — 12-lead ECG, continuous ECG monitoring

Myocardial ischemia — ECG, cardiac-specific markers (troponin preferred as CK and CK-MB may be affected by rhabdomyolysis). Caution is required in evaluating ST-segment deviations on the ECG as chronic cocaine abusers often have repolarization abnormalities. Myocardial ischemia may be temporally related to cocaine use but may also occur days later.

Intracranial hemorrhage or stroke — CT scan or MRI of brain. These complications may occur at the time of cocaine use or several days later.

Bronchospasm –clinical examination, peak expiratory flow rate, response to bronchodilators

Pulmonary edema, infiltrates, pneumothorax –chest radiograph, arterial blood gas

Rhabdomyolysis — creatine kinase (CK), myoglobin (infrequently evaluated), urinalysis (assess for presence of blood by dipstick, with absent red blood cells suggesting the presence of myoglobin)

Acute kidney injury — BUN, creatinine, urinalysis

Bowel ischemia — angiogram, exploratory surgery

Body packers — plain abdominal radiographs, CT scan

Diagnostic tests

Laboratory findings depend on clinical presentation and presence of complications. WBC count may be elevated in the absence of infection due to catecholamine release. Similarly, glucose may be acutely elevated.

How do I know this is what the patient has?

A history of cocaine use, consistent clinical findings and a urine assay positive for cocaine metabolites are diagnostic for cocaine abuse. However, cocaine abusers may have other conditions (e.g., traumatic injury, infection) that result in complications that mimic cocaine effects. A positive test for cocaine metabolites may be the only clue to cocaine abuse in patients who present without agitation but have a condition that could result from cocaine exposure.

Differential diagnosis

Intoxication with other sympathomimetic drugs such as amphetamine or methamphetamine or hallucinogens such as phencyclidine can mimic the effects of cocaine. Overdose with anticholinergic drugs may also present with similar clinical findings. Acute psychosis, especially mania due to presence of agitation and abnormal vital signs in some patients, may also present with findings similar to acute cocaine intoxication. Less commonly, thyroid storm or severe infection may be considered in patients presenting with fever, tachycardia, agitation and altered mental status.

Confirmatory tests

A urine qualitative assay for cocaine metabolites should be performed to confirm cocaine exposure.

4. Specific Treatment

No antidote exists for cocaine intoxication. Specific treatment for cocaine abuse will depend on the clinical presentation and identification of complications. Management issues are described below for specific conditions but modifications may be needed when multiple problems exist.

Agitation: IV or IM benzodiazepines, usually lorazepam, are first-line drugs for control of agitation. IM midazolam may be an option for immediate sedation when IV access is not available. Haloperidol should not be used initially because of the potential to lower the seizure threshold. It may be considered for treating psychotic symptoms that fail to respond to benzodiazepines.

Chest pain/myocardial ischemia: Cocaine increases platelet aggregation so aspirin should be administered to patients with chest pain thought to be ischemic. Ongoing chest pain can be treated with SL nitroglycerin or benzodiazepines as both have been shown to be effective single agents in small clinical studies. Benzodiazepines should be administered if agitation is present. Although beta-blockers are not appropriate in patients with evidence of an acute sympathomimetic state, beta blockers have been administered safely in patients with chest pain and evidence of cocaine use. Reperfusion should be considered for evidence of ST-elevation MI along with other standard MI management (heparin, clopidogrel, ACE inhibitor, statin, etc). Further cardiac evaluation may be indicated in patients who rule out acutely for myocardial ischemia because of increased risk for atherosclerotic disease.

Arrhythmias: Sinus tachycardia is the most common arrhythmia and usually responds to control of agitation and IV fluids. ACLS protocols for significant tachycardias and bradycardias should be followed. NaHCO₃ has been effective in case reports of wide complex arrhythmias due to cocaine.

Hypotension: Hypotension in a cocaine abuser is most often due to volume depletion. IV fluid resuscitation should be initiated with frequent reassessments.

Hypertension: Elevated blood pressure usually resolves with control of agitation and the rapid decrease of the physiological effects of cocaine. Consider IV nicardipine for severe sustained hypertension.

Seizures: IV lorazepam is the treatment of choice for drug-induced seizures.

Intracranial hemorrhage: Severely elevated blood pressure should be controlled in the setting of intracranial hemorrhage after any agitation is treated. Specialized imaging may be warranted for identification of lesions (AVM, berry aneurysm) that are amenable to surgery or other interventions.

Stroke: Aspirin should be administered if there is no evidence of hemorrhage. Other care is similar to stroke due to other etiologies.

Hyperthermia: Initiate cooling for core temperature >41 C (105.8 F) with evaporative or conductive techniques. Control agitation with IV benzodiazepines and evaluate for rhabdomyolysis.

Pulmonary edema: Administer supplemental oxygen. Noninvasive ventilation may be considered in more severe presentations. Intubation and mechanical ventilation are rarely needed for increased work of breathing, severe hypoxemia or hypercapnia. Diuresis may be considered depending on the intravascular volume status.

Bronchospasm: Administer inhaled beta-agonists. There is no evidence to support the use of systemic corticosteroids unless the patient has a history of bronchospasm.

Rhabdomyolysis: The mainstay of treatment is the administration of IV isotonic fluids (150 -200 mL/h) to ensure adequate urine output. The addition of NaHCO₃ for urinary alkalinization is not needed in most circumstances.

Acute kidney injury: Injury may be multifactorial but IV isotonic fluids are usually indicated for likely hypovolemia. Renal replacement therapy may be indicated for persistent severe dysfunction.

Ischemic bowel: Laparoscopic or open laparotomy may be indicated depending on the clinical examination and imaging studies. Observation with bowel rest and antibiotics may be appropriate in some patients.

Body packers: Surgery is reserved for symptoms/signs of obstruction or packet rupture. Mild laxatives such as polyethylene glycol solution or lactulose may be used to enhance passage of packets.

Benzodiazepines: Lorazepam 1 to 2 mg IV or IM every 5-15 min titrated to control of agitation; midazolam 5 mg IM for control of agitation. Lorazepam 2 mg IV initially up to 0.1 mg/kg for seizures.

Aspirin 325 mg po (chewed)

Haloperidol: 5 mg IV or IM initially

Nicardipine: For control of hypertension, start infusion at 5 mgh and titrate up in 2.5-mg/h increments every 5 to 15 min until desired blood pressure achieved

If agitation is refractory to high doses of IV lorazepam, consider intubation and continuous infusion of lorazepam, midazolam, or propofol.

Follow protocol for refractory status epilepticus.

5. Disease monitoring, follow-up and disposition

Expected response to treatment

Agitation can usually be controlled with benzodiazepines. Prognosis depends on complications associated with cocaine use. Patients may have a prolonged period of sedation once acute agitation is controlled (cocaine washout syndrome).

Incorrect diagnosis

Consider other diagnoses in the following circumstances: failure to arouse after agitation is controlled, persistent fever, and unresolving metabolic acidosis.

Follow-up

Psychiatric evaluation may be warranted for assessment of depression and suicide risk. All patients should be offered drug counseling.

Pathophysiology

Cocaine is rapidly absorbed from all mucosal surfaces. The route of administration plays a significant role in the intensity and duration of the effects. Inhalation of cocaine has the fastest onset and shortest duration of effects, while nasal insufflation has a slower onset and longer duration of effects. Cocaine has local anesthetic effects, vasoconstrictive effects and sympathomimetic effects. Anesthetic effects are due to blockade of voltage-gated sodium channels in the neuronal membrane resulting in blockade of neural conduction. Vasoconstrictive effects are due to stimulation of alpha-receptors in arterial smooth muscle walls.

Sympathomimetic effects are due to central and peripheral inhibition of presynaptic uptake of norepinephrine, dopamine and serotonin. Thrombogenic activity of cocaine may result from increased plasminogen activator inhibitor activity, increased platelet count, and increased platelet activation and aggregation. Adulterants added to cocaine may also cause detrimental effects.

The vasoconstrictive and sympathomimetic effects of cocaine lead to many of the clinical effects directly or indirectly. Myocardial ischemia may result from coronary vasoconstriction, which limits myocardial oxygen demand, coupled with an increase in myocardial oxygen demand due to agitation and tachycardia. Thrombus formation and atherosclerotic disease can also play a role. The euphoria and agitation from cocaine are thought to be due to excessive dopaminergic activity in the central nervous system.

The sudden increase in blood pressure from vasoconstriction may precipitate intracranial hemorrhage. Vasoconstriction and thrombus formation contribute to cocaine-related stroke. Hyperthermia associated with cocaine is thought to be due to dysfunction of the central thermoregulatory centers along with excessive activity. Cocaine has direct myotoxic effects that may contribute to the development of rhabdomyolysis along with muscle ischemia from vasoconstriction.

Epidemiology

Cocaine is abused by more than 6 million Americans age 12 years and older. Although young adult males are the largest group of abusers, cocaine abuse occurs in all age groups.

Cocaine is abused in primarily two forms: water-soluble cocaine hydrochloride (IV, nasal insufflation, ingestion) and alkaloid crack cocaine (inhalation).

Prognosis

Prognosis depends on the type and severity of complications. Intracranial hemorrhage often results in significant disability. Rhabdomyolysis and hypovolemia may lead to permanent renal failure. Severe hyperthermia can be associated with multiorgan failure including disseminated intravascular coagulation that is unresponsive to intensive therapy leading to death. Cocaine addiction frequently leads to repeated episodes of complications requiring medical care.

Special considerations for nursing and allied health professionals.

NA

What's the evidence?

Muniz, AE, Evans, T. “Acute gastrointestinal manifestations associated with use of crack”. Am J Emerg Med. vol. 19. 2001. pp. 61-3. (Report of three cases of ischemic bowel related to cocaine and a brief discussion of GI complications.)

Nzerue, CM, Hewan-Lowe, K, Riley, LJ. “Cocaine and the kidney: a synthesis of pathophysiologic and clinical perspectives”. Am J Kidney Dis. vol. 35. 2000. pp. 783(A good review of the pathophysiologic effects of cocaine on the kidney and specific complications involving the kidneys.)

Knuepfer, MM. “Cardiovascular disorders associated with cocaine use: myths and truths”. Pharmacol Ther. vol. 97. 2003. pp. 181-222. (A review of the various cardiovascular disorders associated with cocaine use.)

Lange, RA, Hillis, LD. “Cardiovascular complications of cocaine use”. N Engl J Med.. vol. 345. 2001. pp. 351-358. (Good overview of potential complications and management.)

Glauser, J, Queen, JR. “An overview of non-cardiac cocaine toxicity”. J Emerg Med. vol. 32. 2007. pp. 181-6. (Review of multiple complications and their management.)

McCord, J, Jneid, H, Hollander, JE. “Management of cocaine-associated chest pain and myocardial infarction. A scientific statement from the American Heart Association Acute Cardiac Care Committee of the Council of Cardiology”. Circulation. vol. 117. 008. pp. 1897-907. (Guidelines for managing myocardial ischemia due to cocaine.)

Goldstein, RA, DesLauriers, C, Burda, AM. “Cocaine: history, social implications, and toxicity–a review”. Dis Mon. vol. 55. 2009. pp. 6-38. (A thorough review of cocaine's history, abuses, pharmacology, drug interactions and toxicities.)

Martin-Schild, S, Albright, KC, Hallevi, H, Barreto, AD, Philip, M, Misra, V, Grotta, JC, Savitz, SI. “Intracerebral hemorrhage in cocaine users”. Stroke. vol. 41. 2010. pp. 680-4. (A large retrospective study addressing the location, pathology, and outcome of patients with cocaine associated intracerebral hemorrhage.)

Haim, DY, Lippmann, ML, Goldberg, SK, Walkenstein, MD. “The pulmonary complications of crack cocaine. A comprehensive review”. Chest. vol. 107. 1995. pp. 233-40. (Older but comprehensive review of pulmonary effects of cocaine.)

Fessler, RD, Esshaki, CM, Stankewitz, RC. “The neurovascular complications of cocaine”. Surg Neurol. vol. 47. 1997. pp. 339-45.

Shanti, CM, Lucas, CE. “Cocaine and the critical care challenge”. Crit Care Med. vol. 31. 2003. pp. 1851

Baumann, BM, Perrone, J, Hornig, SE. “Randomized, double-blind, placebo-controlled trial of diazepam, nitroglycerin, or both for treatment of patients with potential cocaine-associated acute coronary syndromes”. Acad Emerg Med. vol. 7. 2000. pp. 878-85.

Honderick, T, Williams, D, Seaberg, D, Wears, R. “A prospective, randomized, controlled trial of benzodiazepines and nitroglycerine or nitroglycerine alone in the treatment of cocaine-associated acute coronary syndromes”. Am J Emerg Med. vol. 21. 2003. pp. 39-42.

Dattilo, PB, Hailpern, SM, Fearon, K. “Beta-blockers are associated with reduced risk of myocardial infarction after cocaine use”. Ann Emerg Med. vol. 51. 2008. pp. 117-25.

Rangel, C, Shu, RG, Lazar, LD. “Beta-blockers for chest pain associated with recent cocaine use”. Arch Intern Med. vol. 170. 2010. pp. 874-9.

Traub, SJ, Hoffman, RS, Nelson, LS. “Body packing–the internal concealment of illicit drugs”. N Engl J Med. vol. 349. 2003. pp. 2519-26.

Pozner, CN, Levine, M, Zane, R. “The cardiovascular effects of cocaine”. J Emerg Med. vol. 29. 2005. pp. 173-8.

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