Cocaine Overdose
Pathophysiology - Sympathomimetic toxidrome associated with following signs and symptoms:
CNS: Cerebral ischemia/infarct, intraparenchymal or subarachnoid hemorrhage, cerebral artery vasospasm, cerebral vasculitis, cerebral atrophy, and cerebral vascular thrombosis.
Cardiac: Myocardial ischemia/infarct, cardiac arrhythmias, dilated cardiomyopathy, infective endocarditis (IVDA), aortic rupture/dissection, acceleration of coronary atherosclerosis.
Pulmonary: Nasal septal perforation, oropharyngeal ulceration, inhalational injuries (smoking crack cocaine), pneumomediastinum, pneumothorax, pulmonary infarct, hypersensitivity pneumonitis.
GI: Gastroduodenal ulceration/perforation, intestinal infarct/perforation, colitis.
Renal: ARF secondary to rhabdomyolysis, renal infarct.
OB: Placental abruption, low birth weight, microcephaly.
Psych: Paranoia, delirium, suicidal ideation
Initial approach and management:
Start with ABCs:
Airway and breathing — O2 as needed.
If RSI intubation is needed avoid succinylcholine - plasma cholinesterase (PChE) metabolizes both succinylcholine and cocaine, and coadministration of succinylcholine can prolong the effects of cocaine and the paralysis from succinylcholine
In the setting of rhabdomyolysis and hyperthermia, succinylcholine may worsen hyperkalemia and cause life-threatening arrhythmias
Use rocuronium as paralytic and benzodiazepines, etomidate, or propofol for induction
Cardiovascular complications result in
Central cardiovascular stimulation responds well to benzodiazepines
Refractory or symptomatic cocaine-induced hypertension can use phentolamine (bolus of 5 to 10 mg intravenously (IV) every 5 to 15 min PRN)
Alternatives nitroglycerin or nitroprusside
Avoid beta-blockers (unopposed α-adrenergic activity)
Avoid calcium channel blockers (may potentiate seizures and death)
Massive cocaine toxicity may result in hypotension due to sodium-channel blockade, cardiac dysrhythmias, or cardiac ischemia
treat with 2 to 3 L of rapidly infused isotonic saline
if no improvement use direct-acting vasopressors such as norepinephrine or phenylephrine
Obtain EKG to evaluate QRS for widening, if present use hypertonic sodium bicarbonate at a dose of 1 to 2 mEq/kg
Psychomotor agitation can be treated with benzodiazepines like diazepam be given in an initial dose of 10 mg IV, then 5 to 10 mg IV every 3 to 5 minutes
Hyperthermia - cool rapidly, optimally in 30 minutes or less, to a goal core body temperature of <102°F.
Gastrointestinal decontamination should be considered especially in cases of body packing but remember that the popular methods of cocaine use are nonenteral
Activated charcoal reduces the lethality of oral cocaine - adminitter at 1 g per kg body weight (up to 50 g) Q4h.
Cocaine abuse + abdominal pain => concern for aortic pathology or intestinal ischemia/infarct or colitis
Specific syndromes:
Chest pain — it causes vasoconstriction and enhances thrombus formation, increasing the risk of myocardial ischemia even in a very young patients.
EKG changes and positive trops consider ASA +/- nitroglycerin, phentolamine (( IV bolus of 1 to 2.5 mg every 5 to 15 minutes PRN) to reverse cocaine-induced vasospasm, cardiology consult for cath
Crack lung — Crack lung is a syndrome of hemorrhagic alveolitis from inhalational cocaine use
Ensure oxygenation, ventilation, and symptomatic care
Early intubation
Disposition:
Severe complications of cocaine abuse - admission
If acute findings from cocaine toxicity resolve - obs 6 to 8 hours and d/c if pt back to baseline.
Pts with cocaine-associated chest pain (CACP) are observed for 8 to 12 hours while two sets of cardiac biomarkers and repeat electrocardiograms (ECGs) are obtained.
Pts with psychomotor agitation, hyperthermia, or other neurological complications consider admission unless pt is back to baseline and symptom free after 6 to 8 hours of observation.
Pearls:
The differential diagnosis of cocaine toxicity should include: methamphetamine abuse, ecstasy abuse, cathinone abuse, and LSD abuse
Smoking and IV injection offer rapid cocaine absorption (< 30 sec), as opposed to snorting (2.5 min) and ingestion (PO 2-5 mins).
Cocaine-induced MIs have been reported as late as 15 hours following substance abuse
References: Uptodate, EMDocs
