Cocaine intoxication
Cocaine intoxication | |
---|---|
Other names | Cocaine toxicity, Cocaine poisoning, Cocaine overdose |
Cocaine | |
Specialty | Toxicology |
Cocaine intoxication refers to the
Adverse effects can develop over time due to repeated use and so become chronic conditions. However, even a one-time intake of the substance can result in severe acute intoxication.
Recurrent cocaine use and dependence to the drug inevitably leads to the reduction of the desired effects perceived by the users, while the occurrence of adverse effects of intoxication increase. The last can sometimes be completely reversed without bearing consequences but they can also potentially kill the users (e.g., in cases of untreated or non-manageable overdoses).
Signs and symptoms
Cocaine increases alertness, feelings of well-being, euphoria, energy, sociability, and sexuality. The former are some of the
Mild
Depression with suicidal ideation may develop in heavy users.[4] Finally, a loss of vesicular monoamine transporters, neurofilament proteins, and other morphological changes appear to indicate a long-term damage to dopamine neurons.[5] Chronic intranasal usage can degrade the cartilage separating the nostrils (the nasal septum), which can eventually lead to its complete disappearance.[6]
Studies have shown that
In cases of severe acute intoxication, potentially lethal adverse effects include prolonged episodes of arrhythmia (i.e., a group of abnormal heart rhythms that also include tachycardia), heavy hypoglycemia, tremors, convulsions, hyperthermia (i.e., markedly increased core temperature), untreated uremia, myocardial infarction, stroke, and sudden cardiac arrest.[9]
Overdose
Cocaine can be snorted, swallowed, injected, or smoked. Most deaths due to cocaine are accidental but may also be the result of
Withdrawal
Cocaine withdrawal is not as severe as the withdrawal from other substances. For example, substances like heroin, alcohol and benzodiazepines can involve severe physical withdrawal symptoms while cocaine results in mostly psychological symptoms. Physiological changes caused by cocaine withdrawal include vivid and unpleasant dreams, insomnia, hypersomnia, anger, increased appetite, weight gain, psychomotor retardation, agitation, depression, and anxiety. According to a study done by Gawin and Kleber in 1986, there are three phases in the withdrawal process. They observed the behavior of 30 cocaine-dependent individuals. Phase one, the crash, is characterized by acute dysphoria, irritability and anxiety, increased desire for sleep, exhaustion, increased appetite, decreased craving to use. Phase two, withdrawal, is characterized by increasing craving to use, poor concentration, some irritability and some lethargy, which persisted for up to 10 weeks. Lastly, phase three is characterized by the intermittent craving to use in the context of external cues.[14] Cocaine and its metabolites are eliminated from the body by 3 days.[15] There are not any FDA-approved medications that specifically help treat cocaine withdrawal, however, there are some useful medications that could possibly help individuals overcome their addiction. One example is propranolol. Propranolol is a beta blocker that has been approved to treat hypertension, angina, anxiety, and other related psychological problems. Buprenorphine and naltrexone are two substances that act as an effective treatment in the earlier stages of withdrawal.
Pathophysiology
Cocaine
Management
There is no specific
The chest pain, high blood pressure, and increased heart rate caused by cocaine may be also treated with benzodiazepines.[28] Multiple and escalating dose of benzodiazepines may be necessary to achieve effect, which increases risk of over-sedation and respiratory depression. A review of cocaine cardiovascular toxicity found benzodiazepines may not always reliably lower heart rate and blood pressure.[29] Lidocaine and intravenous lipid emulsion have been successfully used for serious ventricular tachyarrhythmias in several case reports.
People who are agitated are best treated with benzodiazepines, though antipsychotics such as haloperidol and olanzapine may also be useful.[29] The alpha-2 agonist dexmedetomidine may also be useful for agitation, but effects on heart rate and blood pressure are variable based on several studies and case reports.[29]
Vasodilators
Nitric-oxide mediated vasodilators, such as nitroglycerin and nitroprusside, are effective at lowering blood pressure and reversing coronary arterial vasoconstriction, but not heart rate.[29] Nitroglycerin is useful for cocaine-induced chest pain, but the possibility of reflex tachycardia must be considered.[30]
Alpha blockers
Alpha-blockers such as phentolamine have been recommended[28] and may be used to treat cocaine-induced hypertension and coronary arterial vasoconstriction, but these agents do not reduce heart rate.[29][31] Furthermore, phentolamine is rarely used, not readily available in many emergency departments, and many present-day clinicians are unfamiliar with its use.
Beta blockers
Although the use of
A relative contraindication to the use of beta-blockers is still evident in some guidelines for the treatment of cocaine toxicity despite limited evidence. The phenomenon of "unopposed alpha-stimulation," in which blood pressure increases or coronary artery vasoconstriction worsens after blockade of beta-2 vasodilation in people using cocaine, is controversial.[36][37] This rarely-encountered and unpredictable adverse effect has resulted in some clinicians advocating for an absolute contraindication of all beta-blockers, including specific, non-specific, and mixed.[38] Many clinicians have disregarded this dogma and administer beta-blockers for cocaine-related chest pain and acute coronary syndrome, especially when there is demand ischemia from uncontrolled tachycardia.[39][40][41][42][43] Of the 1,744 people in the aforementioned systematic review,[29] only 7 adverse events were from putative cases of "unopposed alpha-stimulation" due to propranolol (n=3), esmolol (n=3), and metoprolol (n=1).[44][45][46][47][48] Some detractors of beta-blockers for cocaine-induced chest pain have cited minimal acute mortality and the short half-life of the medication, making it unnecessary to aggressively treat any associated tachycardia and hypertension.[38][49] However, the long-term effect of cocaine use and development of heart failure, with early mortality, high morbidity, and tremendous demand on hospital utilization should be taken under consideration.[50][51][52]
Calcium channel blockers
Calcium channel blockers may also be used to treat hypertension and coronary arterial vasoconstriction,[53] but fail to lower tachycardia based on all cocaine-related studies.[29] Non-dihydropyridine calcium channels blockers such as diltiazem and verapamil are preferable, as dihydropyridine agents such as nifedipine have much higher risk of reflex tachycardia (however, clinicians can prevent reflex tachycardia by administering beta-blockers some minutes before using the latter class of CCBs).
See also
- Cocaine Anonymous
- Cocaine dependence
- Crack cocaine § Crack lung
- List of deaths from drug overdose and intoxication
References
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- ^ "Cocaine intoxication: MedlinePlus Medical Encyclopedia". medlineplus.gov. Retrieved 2019-10-21.
- ^ Abuse, National Institute on Drug. "Cocaine". www.drugabuse.gov. Retrieved 2019-10-21.
- ^ "Department of Health | The cocaine withdrawal syndrome". www1.health.gov.au. Archived from the original on 2020-12-03. Retrieved 2019-10-29.
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