Therapeutic use is as a topical local anaesthetic for mucous membranes in the nose, eye and ear. Cocaine is an ester of benzoic acid. The major clinical effects are due to an increase in catecholamines. Tachycardia and hypertension are characteristic as is vasoconstriction in specific organ beds such as the coronary circulation. Intracerebral haemorrhage and myocardial infarction can occur and chronic use results in accelerated atherosclerosis.
Cocaine has direct membrane (local anaesthetic) stabilising effects. The major clinical effects are due to an increase in synaptic catecholamines (esp. dopamine and noradrenaline) predominantly due to a blockage of reuptake.
Cocaine is well absorbed from all routes of administration (nasal, inhalation, IV, oral, rectal and vaginal). Peak concentrations occur between 30 and 120 minutes following oral or nasal use.
Less than 10% protein binding, with a low volume of distribution (2-3 L/kg).
Predominantly plasma hydrolysis by plasma cholinesterase. Minimal hepatic metabolism. Half-life is 30 to 90 minutes. 10-20% is renally excreted unchanged; metabolites may be detected in urine for up to 6 days. Patients with hereditary or acquired cholinesterase deficiency may have prolonged toxicity.
(from ingestion, injection, or absorption through mucous membranes or skin abrasions)
The initial symptoms are restlessness, excitability, hallucinations, tachycardia, dilated pupils, chills or fever, sensory aberrations, abdominal pain, vomiting, numbness, and muscular spasms. These are followed by irregular respiration, convulsions, coma, and circulatory failure.
Death may occur almost immediately after use of cocaine or may be delayed 1-3 hours.
Hypertension is common and can be complicated by events such as intracerebral haemorrhage and aortic dissection.
Ischaemia of any vascular bed can occur, in particular myocardial and splanchnic ischaemia.
(from ingestion, injection, or absorption through mucous membranes or skin abrasions)
Hallucinations, mental deterioration, weight loss, and change of character. The use of cocaine as snuff can cause perforation of the nasal septum. Chronic use is associated with accelerated atherosclerosis.
Cocaine may produce neurochemical induced behavioural disturbances. Cerebrovascular presentations include both cocaine induced ischaemia and subarachnoid haemorrhage (SAH). In the patients with SAH the aneurysms were noted to be smaller than those seen in SAH patients who do not use cocaine. The onset of symptoms occurs immediately during cocaine use in 60% of patients and within 6 hours of use in a further 33%.
Myocardial ischaemia and infarction are well described. Supraventricular and ventricular arrhythmia can occur. Catecholamine induced cardiomyopathy and myocarditis have been reported. Chest pain during cocaine use may represent significant underlying coronary artery disease.
Blood concentrations are unhelpful in management. Urine screens for cocaine may be helpful diagnostically.
Electrolytes, creatinine, urea, liver function, creatine phosphokinase should be obtained.
Should be performed in all patients.
Patients with neurological symptoms or signs should receive a CT scan or MRI. Patients who have a history of bodypacking should have abdominal X-Ray or CT scan with gastrograffin.
Includes ingestion of other sympathomimetic drugs; in particular amphetamines. Medical differential includes any cause of paroxysmal hypertension. Cocaine use should be considered in young adults who present with organ ischaemia or vascular rupture including cerebrovascular accident.
Maintenance of the airway and ventilation is the first priority in unconscious overdoses. IV access with normal saline infusion should be secured as soon as possible in order to have access for the treatment of seizures or hypertension.
Single dose activated charcoal is the recommended gastrointestinal decontamination procedure, but needs to be given early (within 1 hour) for any expected effect. Asymptomatic body packers should receive whole bowel lavage. Symptomatic body packers should have surgical removal of packages.
There is no evidence of any clinically useful method of enhancing cocaine elimination
The primary treatment of the central nervous system stimulation with hypertension and tachycardia is adequate sedation with benzodiazepine. The dose is titrated against response and should be given intravenously in most cases. We administer diazepam in 5-10 mg aliquots every 2 minutes until the patient is sedated or haemodynamically stable.
Seizures should be treated with intravenous benzodiazepines (in adults: diazepam 5 to 10 mg, repeated if necessary every 15 to 20 minutes). Seizures refractory to diazepam may require phenobarbitone (15 mg/kg).
Cardiac ischaemia should be treated along conventional lines with aspirin and nitrates in addition to benzodiazepines.
Alpha-adrenergic receptor antagonist (e.g. phentolamine) should be considered in patients who do not respond to aspirin, nitrates and benzodiazepines.
Patients with evidence of myocardial infarction should receive conventional treatment. Unselective beta-blockers are considered contraindicated as successful beta-blockade may expose the patient to unopposed alpha mediated vasoconstriction worsening cardiac ischaemia and hypertension. Evidence does not support the use of selective beta-blockers or mixed alpha/beta-blockers such as labetalol.
Patients with broad complex tachyarrhythmia associated with acute cocaine use should be treated in a similar manner to patients with tricyclic antidepressant poisonings. Initial treatment should be aimed at alkalinising the patient with the administration of sodium bicarbonate. Patients refractory to alkalinisation should receive lignocaine.
Patients whose hypertension does not respond to adequate sedation should be considered for intravenous nitroprusside infusion.
Perforation of nasal septum. Accelerated atherosclerosis.
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