Approach

Cocaine toxicity is primarily a clinical diagnosis. Although laboratory studies may confirm or exclude the diagnosis (as well as check for complications), therapy should not be delayed. Using signs and symptoms alone, it may be impossible to distinguish cocaine toxicity from that of other sympathomimetics, such as methamphetamine. However, because the key management elements of all the sympathomimetics are the same, it is not critical to make this distinction.

History

Cocaine use is greatest in young men ages 18 to 25 years, but occurs in all demographic groups.[2][5][8][9] It is important to ask the patient about recent cocaine use and determine when it was last used. When smoked, insufflated, or injected, the effects of cocaine occur quite rapidly. Patients may present with chest pain, headache, or neurologic deficits. When chest pain is present, the clinician should specifically ask whether the cocaine was smoked.

Because toxicity of other drugs (legal or illicit) may present in a similar way to cocaine toxicity, a history of drug use (or misuse) should be elicited from the patient, including use of (or withdrawal from) anticholinergics, sedatives or hypnotics, alcohol, or other illicit drugs.

If possible, it is important to seek a history of any other medical conditions, focusing particularly on conditions that may present in a similar way to cocaine toxicity (e.g., infections or thyroid storm).

Decreased plasma cholinesterase activity is associated with an increased risk of life-threatening cocaine toxicity.[18]

Examination

Body temperature should be measured promptly to check for hyperthermia. A neurologic examination may identify any deficits. Signs of volume depletion may be present.

Cocaine toxicity presents with a main constellation of signs known as the sympathomimetic toxidrome. This includes tachycardia, hypertension, hyperthermia, mydriasis, diaphoresis, and psychomotor stimulation. The sympathomimetic toxidrome may be difficult to distinguish from the anticholinergic toxidrome (not caused by cocaine but may be caused by coingestants). The anticholinergic syndrome consists of mydriasis, agitation, dry skin, diminished peristalsis, and tachycardia. The presence or absence of dry skin is probably the easiest way to differentiate between the anticholinergic and sympathomimetic toxidrome; however, there are exceptions to this rule.

Initial tests

All patients should have an ECG immediately to identify dysrhythmias or cardiac ischemia.[19]​ ECG may be normal or may show sinus tachycardia, early repolarization pattern, supraventricular tachycardia, prolonged QT interval, ventricular dysrhythmia including asystole, or ischemic changes.[19][20]​ Lengthening of QRS interval is a sign of sodium channel blockade from Vaughan-Williams type IC antidysrhythmic properties of cocaine and norcocaine, a cocaine metabolite.[10]

Serum chemistry, creatinine, BUN, and creatine phosphokinase should be sent in all patients and may identify hyperkalemia, uremia, acidosis, or rhabdomyolysis.[21][22]​​ Bedside serum glucose may identify hypoglycemia.

Cardiac troponin (cTn) measurements are indicated in the presence of chest pain, shortness of breath, or significant vital sign abnormalities regardless of ECG findings.[19][21][22]​​​​​ High-sensitivity cTn (hs-cTn) is the preferred biomarker to rapidly detect or exclude myocardial injury in any patient presenting with chest pain.[23]​ Hs-cTn demonstrates greater sensitivity and negative predictive values than previous generation assays.[23]​ To appropriately interpret a cTn assay, clinicians must be familiar with the assay(s) they use in their practice.[24] Refer to local protocols. Hs-cTn can be elevated as a result of a variety of ischemic, noncoronary cardiac, and noncardiac causes of cardiomyocyte injury, but cocaine use in itself does not elevate hs-cTn.[23][25]​​​ Consideration of the full clinical picture is important when interpreting hs-cTn results. If myocardial injury is present or suspected, see Non-ST-elevation myocardial infarction or ST-elevation myocardial infarction.

Chest x-ray is indicated in the presence of chest pain and may identify pneumothorax, pneumomediastinum or hemorrhagic alveolitis.[22]

Computed tomography (CT) of the brain is indicated for patients with suspected cocaine toxicity who are obtunded, complain of headache, or have seizures in order to identify intracranial hemorrhage or infarction.[22]​ 

Other tests

CT of the abdomen and pelvis to identify packages of cocaine is indicated when body packing is suspected.[21][26]

Urine assays for cocaine metabolites are nearly 100% sensitive and specific for exposure to cocaine in the past 48 to 72 hours. However, the urine cocaine assay does not affect acute management.[27] The cocaine assay may be helpful when child abuse or neglect is suspected or to uncover a substance use history. A negative assay in a body packer or body stuffer indicates only that no packet rupture has occurred. Serum cocaine levels are not widely available. 

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