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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

© Anna Lee & Charles Gomersall, June 2006


©Charles Gomersall, April, 2014 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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