History and exam
Key diagnostic factors
common
presence of risk factors
Risk factors include history of cocaine use, body packing/stuffing, high ambient temperature, male gender, plasma cholinesterase deficiency, age 20 to 30 years, and concomitant use of other sympathomimetics.
tachycardia
Can be mildly or significantly elevated.
hypertension
Can be mildly or significantly elevated. Hypertensive catastrophes can be associated with cocaine toxicity.[26] See Aortic dissection and Haemorrhagic stroke.
hyperthermia
If hyperthermia is identified, continuous core-temperature monitoring, usually accomplished with a rectal or oesophageal probe, should be initiated.
agitation
Patients often present in an agitated state.
mydriasis
Mydriasis may be absent when cocaine is taken with a co-ingestant that causes miosis, as it occurs with a 'speedball' of cocaine and heroin.
diaphoresis
Diaphoresis can be most easily appreciated in the axillae. Diaphoresis helps to distinguish sympathomimetic toxidrome from the anticholinergic toxidrome.
Other diagnostic factors
uncommon
seizures
Seizures are generally self-limiting and will respond to benzodiazepine therapy. Status epilepticus is rare following cocaine use.
Risk factors
strong
high ambient temperature
Death from cocaine toxicity correlates with high ambient temperature. This relates to the fact that fatal cocaine toxicity is usually caused by hyperthermia, which can be worsened by higher ambient temperatures.[9]
male sex
plasma cholinesterase deficiency
age 18-25 years
Cocaine use is highest among adults aged 18-25 years.[4]
history of cocaine use
The route and time of any exposure to cocaine may help determine whether symptoms observed are a result of cocaine use. Cocaine has the shortest time to effect when smoked, followed by injection and insufflation. All 3 routes produce peak effect within minutes. Ingestion results in the longest time to effect.
concomitant use of other sympathomimetics
Concomitant use of other sympathomimetics may increase the risk of adverse effects.
weak
cocaine body packing
Rupture of cocaine packets in the body is associated with massive release and systemic absorption of the drug. Even if treatment begins immediately after rupture is identified, there is a low likelihood of treatment success. This contrasts to heroin body packing where packet rupture can be managed with naloxone administration or ventilatory support.
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