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Substance Use Disorders
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
As a hydrochloride, cocaine (also known as Snow) is sold in the form of a powder, or as granules or crystals. Crack, or crack cocaine, is cocaine returned to its pure, alkalinized form by heating it with baking soda and water. The name “Crack” comes from the characteristic sound made during the “cooking” process [115]. This form of cocaine is also called Rock, or Freebase. Cocaine can be injected, snorted, or smoked (in cigarettes or with marijuana). Inhalation is the preferred route of administration by crack users.
Drug abuse in pregnancy: Marijuana, LSD, cocaine, amphetamines, alcohol, and opiates
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Jacquelyn C. Howitt, Anita Bublik-Anderson
Cocaine is a stimulant drug derived from the coca plant, Erythroxylon coca. Cocaine use in pregnancy was widely publicized in the 1980s with reports of the urban phenomenon of “crack babies” flooding maternity wards and burdening society. While harm from cocaine to multiple organ systems is clear, and much of the risk in pregnancy is known, there are numerous confounders that make effects directly attributable to cocaine difficult to isolate; the mania of the media blitz may be unfounded (20,21). A retrospective study of 139 cocaine-abusing women revealed concomitant use of other drugs such as alcohol, tobacco, marijuana, diazepam, heroin, and methadone to occur in 92.8% of users (20). Cocaine use has increased, but its use still pales when compared with that of marijuana and alcohol. In the United States, 1.5million persons over the age of 12 met the criteria for the abuse or dependence of cocaine or crack cocaine over the past year (1).
Inhalational Durg Abuse
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Jacob Loke, Richard Rowley, Herbert D. Kleber, Peter Jatlow
Cocaine is a potent central nervous system stimulant and also causes a significant increase in heart rate, respiratory rate, and blood pressure. The severity of the neuropsychophysiological changes and the sympathomimetic effects will depend on the dose and route of administration of cocaine. Minor neuropsychophysiological changes are usually not seen in the emergency room. Difficulty in breathing, dilated pupils, palpitation, chest pain, cardiac disease, hypertension, and seizures in a person with no prior history of cardiac hisease or seizures should make one suspect cocaine overdose, especially if there are history or stigmata of drug abuse. The patient who presents with chest pain and dyspnea may have cardiac arrhythmia or ischemia in addition to tachycardia and hypertension. The primary concern is to support the cardiopulmonary system (Senay et al, 1982) with maintenance of a patent airway and assessment of the vital signs, level of consciousness, and status of arterial oxygenation. In the advent of significant tachycardia, hypertension, or ventricular ectopy, propranolol (Inderal) 1 mg intravenously may be administered (Gay, 1982; Rappolt et al., 1976). The dose can be repeated. If there is further ventricular ectopy on cardiovascular monitoring, lidocaine can be given in a 50-100 mg bolus intravenously and repeated as needed, or an infusion drip of lidocaine can be started. Acute hypertensive crises with encephalopathy may need aggressive therapy with diazoxide (Hyperstat) or nitroprusside (Nipride).
Pre-bout hypertension in the combat sports athlete: clearance recommendations
Published in The Physician and Sportsmedicine, 2023
Kevin deWeber, Ken S Ota, Cicely Dye
Pre-bout hypertension may also be a sign of drug, exogenous hormone, and/or supplement use. Many prescription medications and illicit drugs can cause elevated BP; common culprits are listed in Table 2. Illicit drug users have a 6.5-times increased risk of hemorrhagic and ischemic stroke; cocaine, amphetamines, Ecstasy, ephedrine, phencyclidine, and LSD are known culprits [24]. Hemorrhagic strokes have also been reported after the use of pre-workout supplements [25–27]. Cocaine use can cause sudden cardiac death, life-threatening arrhythmias, myocardial ischemia and infarction, dilated cardiomyopathy, and acute myocarditis [28]. Amphetamines can cause myocardial infarction [29], and energy drinks have been linked to myocardial ischemia [30]. Androgenic anabolic steroid abuse has been linked to arterial hypertension, accelerated progression of coronary artery disease, and increased risk of myocardial infarction [31]. Participating in combat sports, with its vigorous high-static/high-dynamic exercise and repeated head trauma, while these substances are in the body may compound the risk of significant adverse events.
Cocaine exposures reported to United States poison control centers, 2000–2020
Published in Clinical Toxicology, 2022
Sarah Becker, Henry A. Spiller, Jaahnavi Badeti, Alexandra R. Funk, Marcel J. Casavant, Motao Zhu, Nichole L. Michaels, Gary A. Smith
Prevention efforts should target populations especially at risk for cocaine use. In this study, exposure rates were highest among 20–29-year-olds and 30–39-year-olds, followed by 13–19-year-olds; males accounted for 70% of cases. Previously identified risk factors include individuals 18–49 years old, males, individuals with an income <$20,000, psychological distress, and those using other substances such as alcohol, prescription opioids, and heroin [2]. Strategies to reduce cocaine use and associated overdose deaths include improved supply-reduction enforcement strategies, increased public education, greater awareness of the signs and symptoms of overdose, mental health programs, alcohol and other drug addiction services, emergency medical services, and improvements in social determinates of health [21]. Additionally, strategies should reduce co-exposure to opioids and other substances, including expansion of harm reduction programs, such as improved access to naloxone and fentanyl test strips and education about their use [15].
Cocaine induced heart failure: report and literature review
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Sherif Elkattawy, Ramez Alyacoub, Abraham Al-Nassarei, Islam Younes, Sarah Ayad, Mirette Habib
Cocaine is a highly addictive stimulant that alters human behavior through the limbic system’s activity, a structure in the brain involved in motivation, emotion, learning, and memory. The nucleus accumbens (NA) is a specific area within the limbic system that receives connections through dopaminergic neurons. When stimulated, the accumulation of dopamine at the NA causes euphoria, conditioning the brain to establish a reward pathway in association with a stimulant. Cocaine inhibits dopamine transport protein (DAT) embedded within presynaptic neurons of the NA, forming a reward pathway; thus, explaining the drug’s highly addictive nature and potential for abuse [1, 5]. Although the overall incidence of recreational cocaine use has been declining over the years within the United States, the global prevalence of cocaine is still approximately 0.4%. Many studies have provided significant evidence explaining the relationship between cocaine use and the onset of cocaine-induced morbidity (including cardiovascular, neurovascular, psychiatric, and infectious illnesses) and mortality over time.[2,3,4,6,7]