Кокаїн

Cocaine use during pregnancy can adversely affect the fetus; the rate of placental abruption and spontaneous abortion is higher.

Effects of cocaine use may differ depending on mode of use. When injected or smoked, cocaine causes hyperstimulation, alertness, euphoria, a sense of increased energy, and feelings of competence and power. The excitation and high are similar to those produced by injecting amphetamines. These feelings are less intense and disruptive in users who snort cocaine powder.

Cocaine can cause damage in any organ system from vasoconstriction, hemorrhage, or enhanced coagulation.

An overdose may cause severe anxiety, panic, agitation, aggression, sleeplessness, hallucinations, paranoid delusions, impaired judgment, tremors, seizures, and delirium. Mydriasis and diaphoresis are apparent, and heart rate and blood pressure are increased. Myocardial ischemia due to cocaine use may also cause chest pain (“cocaine chest pain”), but cocaine can also cause chest pain in the absence of myocardial ischemia; the mechanism is unclear. Arrhythmias and conduction abnormalities may occur. Death may result from myocardial infarction or arrhythmias.

Binges, often over several days, lead to an exhaustion syndrome or "washed out" syndrome, involving intense fatigue and need for sleep.

Severe overdose causes a syndrome of acute psychosis (eg, schizophrenic-like symptoms), hypertension, hyperthermia, rhabdomyolysis, coagulopathy, renal failure, and seizures. Patients with extreme clinical toxicity may, on a genetic basis, have decreased (atypical) serum cholinesterase, an enzyme needed for clearance of cocaine.

People who smoke the drug may develop pneumothorax or pneumomediastinum, causing chest pain, dyspnea, or both. People who inhale or smoke cocaine may develop an acute pulmonary syndrome sometimes called "crack lung," which is a hypersensitivity pneumonitis (which typically includes fever and hemoptysis) that occurs after inhaling cocaine and may progress to respiratory failure. Vasospasm in the pulmonary vasculature may mimic a pulmonary embolism; pulmonary infarction may develop if the spasm is severe.

The concurrent use of cocaine and alcohol produces a condensation product, cocaethylene, which has stimulant properties and may contribute to toxicity.

Severe toxic effects occur in compulsive cocaine users. Myocardial fibrosis, left ventricular hypertrophy, and cardiomyopathy can develop. Rarely, repeated snorting causes cocaine-induced midline destructive lesions such as nasal septal perforation due to local ischemia. Cognitive impairment, including impaired attention and verbal memory, occurs in some heavy users. Users who inject cocaine are subject to the typical infectious complications. When adulterated cocaine is inhaled frequently, interstitial pneumonitis or pulmonary fibrosis may develop.

Because of cocaine's short half-life, the withdrawal symptoms develop quickly after the last dose in habitual users. The main symptoms of cocaine use are depression, difficulty concentrating, and somnolence (cocaine washout syndrome). Appetite is increased. Withdrawal symptoms can last for several weeks to months.

Irrigate to remove cocaine if any powder is left in nares. Body stuffers and body packers may need gastrointestinal decontamination or even surgical removal.

Treatment of mild cocaine intoxication is generally unnecessary because the drug is extremely short-acting. Benzodiazepines are the preferred initial treatment for most toxic effects, including central nervous system excitation and seizures, tachycardia, and hypertension. Lorazepam 2 to 3 mg IV every 5 minutes titrated to effect may be used. High doses and a continuous infusion may be required. When benzodiazepine is inadequate to achieve sedation, barbiturate or propofol may be needed. Occasionally, severely agitated patients must be pharmacologically paralyzed and mechanically ventilated to ameliorate rhabdomyolysis, hyperthermia, and resultant acidosis or multisystem dysfunction.

Hypertension that does not respond to benzodiazepines is treated with IV nitrates (eg, nitroprusside), nicardipine, or alpha-adrenergic antagonist (eg, phentolamine); beta-blockers are not recommended because they allow continued alpha-adrenergic stimulation.

Hyperthermia can be life threatening and should be managed aggressively with sedation plus evaporative cooling, ice packs, and maintenance of intravascular volume and urine flow with IV normal saline solution.

Phenothiazines are not used for sedation because they lower seizure threshold, and their anticholinergic effects can interfere with cooling.

Cocaine-related chest pain is evaluated as for any other patient with potential myocardial ischemia or aortic dissection, with chest x-ray, serial ECG, and serum cardiac markers. As discussed, beta-blockers are contraindicated, and benzodiazepines are a first-line drug. If coronary vasodilation is required after benzodiazepines are given, nitrates are used, or phentolamine 1 to 5 mg IV given slowly can be considered. Beta blockers and type Ia and Ic antiarrhythmics should be avoided for the treatment of cocaine-induced arrhythmias.

Heavy cocaine users and people who inject the drug IV or smoke it are most likely to become dependent. Light users and people who take the drug nasally or orally are at lower risk of becoming dependent. Stopping sustained use requires considerable assistance, and the depression that may result requires close supervision and treatment.

Many outpatient therapies, including support and self-help groups and cocaine hotlines, exist. Inpatient therapy is used primarily when it is required for serious physical or mental comorbidity or when outpatient therapy has repeatedly been unsuccessful.

For treatment of infants born to cocaine-addicted mothers, see Prenatal Drug Exposure.