Cocaine poisoning refers to the immediate and damaging effects of cocaine on the body. Although cocaine poisoning and cocaine dependence may be present in the same individual, this syndrome presents with different symptoms.
Video Cocaine intoxication
Signs and symptoms
Cocaine raises awareness, feelings of well-being, euphoria, energy, competence, sociability, and sexuality. Common side effects include anxiety, elevated temperature, paranoia, anxiety, and tooth rubbing. With long-term use, this drug can cause insomnia, anorexia, tachycardia, hallucinations, and paranoid delusions. Lethal side effects may include rapid heartbeat, abnormal heart rhythm, tremor, seizures, significantly increased core temperature, kidney failure, heart attack, stroke and heart failure.
Depression with the idea of ​​suicide can develop in heavy users. Finally, the loss of vesicular monoamine transporters, neurofilament proteins, and other morphological changes seems to indicate long-term damage to dopamine neurons. Chronic intranasal use may decrease the cartilage separating the nostrils (septum of rice), which can ultimately lead to complete loss.
Studies have shown that cocaine use during pregnancy triggers preterm labor and can cause abruptio placentae.
Overdose
Cocaine can be snorted, swallowed, injected, or smoked. Most of the deaths due to cocaine are unintentional but may also be the result of body packing or stuffing with rupture in the gastrointestinal tract. The use of cocaine causes tachyarrhythmias and marked high blood pressure (hypertension), which can be life-threatening. It can cause death from acute myocardial infarction, respiratory failure, stroke, cerebral hemorrhage, or heart failure. Overdose of cocaine can lead to hyperthermia as stimulation and increased muscle activity leading to greater heat production. Heat loss is also inhibited by the vasoconstriction caused by cocaine. Cocaine and/or associated hyperthermia can cause muscle cell damage (rhabdomyolysis) and myoglobinuria resulting in renal failure. Individuals with cocaine overdose should be immediately transported to the nearest emergency department, preferably by ambulance in the event of a cardiac arrest en route. According to the National Institute on Drug Abuse, about 5000 deaths occur annually in the US due to cocaine overdose.
Withdrawal
Physical withdrawal is not dangerous; However, physiological changes caused by the withdrawal of cocaine include a clear and unpleasant dream, insomnia or hypersomnia, anger, increased appetite and psychomotor retardation or agitation. Cocaine and its metabolites are completely removed from the body for 3 days.
Maps Cocaine intoxication
Pathophysiology
Pharmacokinetics of cocaine involves many complex mechanisms, although the half-life is short (~ 1 hour). These drugs bind and block monoamines (dopamine, epinephrine, norepinephrine, and serotonin) take back transporters with the same affinity. Monoamine accumulates in the synaptic cleft resulting in extended and prolonged sympathetic effects. The acute effect of cocaine on the central nervous system is increasing the amount of dopamine and serotonin in the nucleus accumbens (the center of pleasure in the brain). When this effect stops due to cocaine metabolism, associated neurotransmitter depletion, and down-regulatory receptors (tachyphylaxis), cocaine users may experience dysphoria, or "crash" after the initial height. The main action of cocaine on the cardiovascular system is derived from alpha and beta-1-adrenoceptor stimulation resulting in increased heart rate, systemic arterial pressure, and myocardial contractility, which is a major determinant of myocardial oxygen demand. Cocaine and its metabolites can cause hours of arterial vasoconstriction after use. The epicardial coronary artery is particularly susceptible to this effect, leading to a decrease in myocardial oxygen supply. Cocaine-induced platelet activation and thrombus formation are other damaging effects, caused by increased alpha-adrenergic and adenosine diphosphate additions mediated by platelet aggregation. Plasminogen activator inhibitors also increase after cocaine use, thereby increasing thrombosis. Similar to local anesthetics such as lidocaine, cocaine blocks sodium channels and interferes with potential action propagation. The Vaughn-Williams class IC effect increases the risk of conduction disturbance and tachyarrhythmias. Adding complex toxicity, cocaine targets muscarinic acetylcholine, N-methyl-D-aspartate (NMDA), sigma, and kappa-opioid receptors.
Management
Emergency treatment of cocaine-related hyperthermia consists of administration of a benzodiazepine sedation agent, such as diazepam (Valium) or lorazepam (Ativan) to promote muscle relaxation and reduce sympathetic outflow of the central nervous system. Physical cooling is best accomplished by the evaporation of warm water and cooling with the fan (convection and evaporation), which can be done easily in the field or hospital. There is no specific pharmacologic antidote for cocaine overdose. Chest pain, high blood pressure, and increased heart rate caused by cocaine can also be treated with benzodiazepines. Multiple doses and increased benzodiazepines may be necessary to achieve an effect, which increases the risk of over-sedation and respiratory depression. A comprehensive systematic review of all pharmacological treatments for cardiovascular toxicity of cocaine reveals benzodiazepines may not always reliably lower heart rate and blood pressure.
Vasodilator-mediated nitrogens, such as nitroglycerin and nitroprusside, effectively lower blood pressure and reverse coronary artery vasoconstriction, but not heart rate. Nitroglycerin is useful for cocaine-induced chest pain, but the possibility of reflex tachycardia should be considered. Alpha-blockers such as phentolamine have been recommended and can be used to treat cocaine-induced hypertension and coronary artery vasoconstriction, but these agents do not reduce heart rate. In addition, phentolamine is rarely used, is not available in many emergency departments, and many physicians today are unfamiliar with their use and titratability. Calcium channel blockers can also be used to treat hypertension and coronary artery vasoconstriction, but fail to decrease the tachycardia based on all studies related to cocaine. Non-dihydropyridine calcium channel blockers such as diltiazem and verapamil are preferred, since dihydropyridine agents such as nifedipine have a higher risk of reflex tachycardia.
Restless patients are better treated with benzodiazepines, but antipsychotics such as haloperidol and olanzapine may also be useful. The alpha-2 agonist dexmedetomidine may also be useful for the treatment of agitation, but the effects on heart rate and blood pressure vary based on several studies and case reports. Lidocaine and intravenous lipid emulsions have been used successfully for serious ventricular tachyarrhythmias in some case reports.
The use of beta-blockers for cardiovascular toxicity of cocaine has been subject to relative contraindications by many doctors over the years despite very limited evidence. The phenomenon of "unresponsive alpha stimulation," in which increased blood pressure or coronary artery vasoconstriction worsens after blockade of beta-2 vasodilation in cocaine-abusing patients, is controversial. These rare and unpredictable side effects have led some doctors to advocate absolute contraindications from the use of all beta-blockers, including specific, non-specific, and mixed. Many doctors have ignored this dogma and provided beta-blockers for cocaine-related chest pain and acute coronary syndromes, especially when there is a demand for ischaemia from uncontrolled tachycardia. Of the 1,744 total patients identified in the above-mentioned systematic review, only 7 adverse events resulted from the alleged case of "unresolved alpha stimulation" due to propranolol (n = 3), esmolol (n = 3), and metoprolol (n = 1). Some of the beta-blocker critics for cocaine-induced chest pain have mentioned minimal acute mortality and short half-life of the drug, making it unnecessarily aggressively treating tachycardia and associated hypertension. However, the long-term effects of cocaine use and the development of heart failure, with premature death, high morbidity, and tremendous demand on hospital utilization should be considered.
The beta/alpha blocker labetalol mixture has been shown to be safe and effective for treating cocaine-induced cocaine-induced hypertension and no alpha-stimulated alpha side effects. The use of labetalol was approved by the recent AHA/ACC guidelines for cocaine and methamphetamine patients with unstable/non-STEMI angina.
References
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