Cocaine

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Anna Lee & Charles Gomersall

Updated June 2006

Pharmacology

absorbed from all musocal surfaces
most commonly taken IV, by nasal insufflation and by smoking
"crack" is poorly water-soluble alkaloid form of cocaine. Smoked. Onset of action within minutes. Dissipated within 29 mins
metabolism is mainly by plasma and liver cholinesterases
- if ingested with alcohol, cocaine is metbabolized by liver to cocaethylene, which is eliminated more slowly and more cardiotoxic

Mechanism of action

sodium channel blocking effect, has local anaesthetic action on peripheral nerves
blocks noradrenaline uptake a peripheral sympathetic nerve endings and blocks noradrenaline and dopamine re-uptake at central presynaptic sites. Result is increased sympathetic activity.

Poisoning

Presentation

clinical effects due to nervous system stimulation
CNS effects: euphoria, agitation, confusion, seizures, hyperthermia
peripheral vasomotor stimulation by norepinephrine results in tachycardia and hypertension

Complications

CNS complications

acute psychosis
TIA, cerebral haemorrhage, cerebral oedema, cerebral vasculitis and ischaemia

CVS complications

arrhythmias, myocardial ischaemia and infarction, myocarditis
aortic rupture secondary to severe hypertension
sudden death. Due to combination of coronary vasoconstriction causing myocardial ischaemia, VT and increased BP. Can occur irrespective of amount ingested, prior use or route of administration and without underlying heart disease. May be delayed up to 24hr

Pulmonary complications

status asthmaticus
upper airway obstruction
barotrauma
- due to forceful Valsalva manoeuvres that are performed during smoking
pulmonary oedema
- cardiogenic
- negative pressure (during smoking)
- capillary leak due to cocaine induced microangiopathy

Other complications

hyperthermia leading to DIC
rhabdomyolysis with acute renal failure
bowel ischaemia and infarction

Differential diagnosis

other conditions causing hypoxia, fits or both
may mimic neuroleptic malignant syndrome or acute withdrawal from sedatives or ethanol
in pregnant patients: pre-eclampsia/eclampsia

Management

exclude medical causes for agitation
activated charcoal within 1 hour post ingestion
gastric lavage of limited use due to rapid absorption
most important aspect of care is to control psychomotor agitation and hence prevent complications
nurse in single room with close monitoring but minimal intrusions
check SpO2, ECG, core temperature, glucose
IV thiamine
cool by surface cooling if core temperature > 40oC
indications for intubation and ventilation:
- uncontrollable hyperthermia
- extreme agitation with danger of aspiration
- uncontrollable convulsions
- deep coma with danger of aspiration
sedate with diazepam IV until agitation and seizures stop. Exclude intracranial pathology
do not use neuroleptics
SVTs are common and are often caused by hyperthermia and agitation and require no specific antiarrhythmic therapy
VT should be treated with sodium bicarbonate as in tricyclic anti-depressant poisoning
- lignocaine is 2nd line therapy (although the similarity in pharmacological effects of lignocaine and cocaine is a theoretical disadvantage)
severe hypertension not responding to sedation and artificial ventilation should be treated with labetalol or nitroprusside
- avoid beta blockers unless patient heavily sedated as this may lead to unopposed alpha activity and increasing hypertension
treat rhabdomyolysis

Management of body packer

Plain AXR as screening test
For symptomatic patient, immediate surgical removal of the package is indicated. Other treatment as mentioned above

©Charles Gomersall, August, 2008 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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