Cocaine-Related Psychiatric Disorders Workup
- Author: Christopher P Holstege, MD; Chief Editor: David Bienenfeld, MD more...
When caring for patients with suspected cocaine-induced psychiatric disorders, a number of laboratory studies may be considered. For example, a patient with marked agitation with or without psychotic features may have complications from cocaine intoxication, such as rhabdomyolysis, myocardial infarction, or renal failure. The need for specific laboratory and ancillary tests noted below will vary depending on the clinical scenario.
Typically, hypokalemia occurs in acute cocaine intoxication from intracellular shifts of potassium ions. This corrects as the intoxication resolves. In severe cocaine toxicity, hyperkalemia may develop and lead to cardiac dysrhythmias. The exact etiology of this is unclear, but rhabdomyolysis may be a contributing factor.
Metabolic acidosis (a decreased serum bicarbonate level) also may be observed in acute cocaine intoxication. This also corrects as the toxicity resolves. A progressively worsening metabolic acidosis associated with progressive altered mental status is a poor prognostic sign. Closely monitor these patients.
Urine drug screens: Benzoylecgonine, a metabolite of cocaine, may be present in the urine for 60 hours after a single use of cocaine. In heavy cocaine use, it has been found in the urine as much as 22 days after cessation of cocaine use. Positive screen results are typically verified with gas chromatography with mass spectrometry.
Plasma cocaine levels: Because cocaine has a short half-life of 30-45 minutes and the metabolites are present in the urine for a much longer period, plasma cocaine levels typically are not as helpful as the tests that analyze for cocaine metabolites in the urine.
Cardiac enzymes: Because of the significant prevalence of myocardial infarction associated with cocaine use, patients presenting with chest pain and cocaine abuse should be considered candidates for cardiac enzyme monitoring.
Other lab tests include the following:
Glucose:In any patient presenting with altered mental status, obtain a rapid glucose determination to rule out hypoglycemia.
Renal function tests:Renal failure due to rhabdomyolysis and renal artery thrombosis has been reported with cocaine abuse.
Creatine kinase: This test may help diagnose rhabdomyolysis.
Urinalysis: If an agitated patient shows a urine-dip test result that is positive for blood but microscopic analysis reveals no red blood cells, consider urine myoglobin and rhabdomyolysis as the cause.
Pregnancy test: All women of childbearing age should receive a pregnancy test.
Liver function tests: Hepatic damage may occur in the acutely intoxicated patient. In addition, patients who use cocaine are at risk for infectious hepatitis, which also may result in acute mental status changes.
Complete blood cell count: Anemia, leukocytosis, and leukopenia all may lead the clinician to consider other disease entities.
Chest radiographs should be obtained in patients exhibiting pulmonary signs or symptoms after cocaine use. Pneumomediastinum, pneumothorax, pneumonia, pulmonary embolism, atelectasis, and other air-space diseases have been reported with cocaine use.
Head CT scan
Patients exhibiting acute mental status changes or focal neurological signs and symptoms may require a head CT scan. Cocaine use has been associated with intracranial bleeding and embolic and thrombotic strokes.
Positron emission tomography (PET) imaging
PET imaging studies have shown that cocaine dependence is associated with the dysregulation of striatal dopamine signaling, which is linked to cocaine-seeking behavior. A study by Martinez et al suggests low dopamine transmission is associated with treatment failure. These data suggest that the combination of behavioral treatment with methods that increase striatal dopamine signaling might serve as a therapeutic strategy for cocaine dependence.
Arterial blood gas determination
This test may be useful in patients with either marked tachypnea or a decreased serum bicarbonate level to further delineate the etiology.
An ECG should be obtained if an individual who abuses cocaine reports chest pain, shortness of breath, syncope, or palpitations. Cocaine-induced myocardial ischemia, infarction, and dysrhythmias have been reported.
Cocaine is a known fast sodium channel blocker of cardiac myocytes. This can lead to a delay in the upstroke of phase 1 of depolarization and subsequent widening of the QRS duration.
Cocaine can cause either myocardial ischemia or infarction. This can subsequently lead to ST depression or elevation depending on the ischemia/infarct region. However, many young patients who abuse cocaine have a baseline J-point elevation that may be difficult to differentiate from an infarct pattern. In addition, normal ECG findings do not rule out the possibility of myocardial injury in a patient who abuses cocaine who has chest pain.
Acute cocaine toxicity also may result in hyperkalemia. This can lead to a diffuse peaking of T waves, widening of the QRS, loss of P waves, or, in the most severe cases, a sinusoidal wave pattern.
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