Cocaine overdose

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



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.


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

What kind of mood elevator are you on?


Lithium toxicity



Uses: Lithium often prescribed for Bipolar disorder

Has a narrow therapeutic index: therapeutic dose close to a toxic dose

Mechanism of action is still incompletely understood. Lithium increases serotonin release and receptor sensitivity as well as inhibiting release of dopamine and norepinephrine. 

Elimination: Lithium is excreted exclusively by the kidneys. Any insult to kidneys can lead to impaired elimination 



For acute overdose mainly intentional overdose

For chronic Li+ toxicity with present body stores any changes changes in absorption or elimination lead to lithium levels above the narrow therapeutic window like:

  • volume depletion

  • salt restriction

  • advanced age with resultant decrease in GFR, 

  • thiazide diuretics, NSAIDs, ACE inhibitors

  • heart failure



Workup at the ED:

  • Basic labs: CBC, BMP

  • Lithium level

  • Urinalysis

  • thyroid function panel 

  • Co-ingestants: acetaminophen, salicylates if intentional overdose is suspected 


Acute Lithium Toxicity presentation:

  • GI symptoms such as nausea, vomiting, and diarrhea, at times with significant volume loss. 

  • Dry mouth 

  • Lack of coordination

  • systemic and neurologic findings manifest late in acute lithium toxicity because  it takes time for lithium to distribute into tissues and the CNS


Chronic Lithium Toxicity presentation:

  • Potent neurotoxin,altered mental status, seizures, tremor, hyper-reflexia, clonus, fasciculations, and extra-pyramidal symptoms which can persist for month regardless of serum concentration 

  • serotonin syndrome, as well as neuroleptic malignant syndrome. 

  • nephrogenic diabetes insipidus (creates resistance to vasopressin)

  • abnormal ECG findings, including QT prolongation, T-wave inversions across the precordial leads, sinoatrial dysfunction, bradycardia, complete heart block, or unmasking of a Brugada pattern. 

  • Hypothyroidism 

  • hyperthyroidism and thyrotoxicosis

  • hyperparathyroidism and hypercalcemia


Treatment and Disposicion:

  • Supportive care and fluids at the ED

  • Consult Poison control center 

  • Renal service, for hemodialysis in severe intoxications

  • Psychiatric service, for patients with intentional overdose

  • Pt will most likely require admission for monitoring of electrolytes and renal function, hydration, medication adjustment