China
Africa
Explore chapters and articles related to this topic
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).
Intoxicants
Published in Michael Y. Wang, Andrea L. Strayer, Odette A. Harris, Cathy M. Rosenberg, Praveen V. Mummaneni, Handbook of Neurosurgery, Neurology, and Spinal Medicine for Nurses and Advanced Practice Health Professionals, 2017
Cocaine blocks reuptake of dopamine, norepinephrine, and serotonin from the synaptic cleft, therefore prolonging their activity on the postsynaptic membrane. Patients under cocaine intoxication present with euphoria, psychomotor agitation, grandiosity, hallucinations (tactile type is formication), and paranoid ideation (Lukas and Renshaw, 1998). The sympathetic system is overstimulated, and as a result pupils dilate, appetite decreases, and heart rate with blood pressure rises. Systemic vasospasm may have end-organ effect causing myocardial infarction, stroke, or placental infarction. Chronic cocaine users may present with nasal septum perforation (Kiesselbach plexus vasospasm) (Businco et al., 2008). Treatment of cocaine overdose is symptomatic with antipsychotics, benzodiazepines, and antihypertensives. Vitamin C promotes excretion of the drug.
Stimulants
Published in G. Hussein Rassool, Alcohol and Drug Misuse, 2017
Hyperthermia (elevated body temperature) and convulsions occur with cocaine overdoses, and if not treated immediately, can result in death. Excessive doses – whether snorted, injected or smoked – can lead to overdose which can lead to sudden death from respiratory or heart failure. Cocaine-related deaths are often a result of cardiac arrest or seizures followed by respiratory arrest. The physical symptoms of cocaine overdose may include chest pain, nausea, blurred vision, fever, muscle spasms, convulsions and coma. Some of the physical and psychological effects of low to moderate dose, excessive dose and chronic use of cocaine are presented in Table 10.3.
The future of neuromodulation: smart neuromodulation
Published in Expert Review of Medical Devices, 2021
Dirk De Ridder, Jarek Maciaczyk, Sven Vanneste
Most of the innovations in deep brain stimulation were not a direct translation of basic neuroscience, for example, deep brain stimulation resulted from a sequence of serendipitous findings. In 1952, Cooper accidentally damages the anterior choroidal artery (AChA) in tumor removal in a patient, and the patient’s co-morbid Parkinson’s disease (PD) improves. Thus, he continues by ligating the AChA in 34 PD patients with success (1954); however, some patients develop a hemiplegia, as the AChA does not always supply the exact same brain territory [17]. In 1976, a 23-year-old chemistry student Barry Kidston synthesizes MPPP (synthetic opioid) and takes it. Within 3 days, he develops Parkinson symptoms due to MPTP impurities in MPPP. He is treated with levodopa but dies 18 months later of cocaine overdose. Autopsy shows destruction of dopaminergic neurons in substantia nigra. This delineates the territory to investigate the deep brain structures involved in PD symptom generation.
Peripheral vascular changes in the lower limbs following cocaine abuse
Published in Journal of Addictive Diseases, 2020
N. Camilleri, A. Mizzi, A. Gatt, N. Papanas, C. Formosa
Habitual consumption of cocaine has been reported to lead to serious health hazards, particularly involving the cardiovascular system. More than 20% of patients who are admitted into emergency rooms because of cocaine overdose had symptoms relating to the cardiovascular system. Cocaine, compared to other illicit drugs is known to be a risk factor for vascular disease5. Although as stated cocaine-induced cardiovascular and cerebrovascular events are well documented, knowledge about the relationship of cocaine use and its effect on arterial perfusion in the lower limbs is scarce6. The consequence of such substance use disorder could aggravate the prevalence of foot complications in this specific population even amongst the younger generation since such abuse usually starts from a very young age.
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
Study findings revealed a concerning increase in clinical severity of cocaine exposures over the study period. In addition to the increased rate of fatal cocaine exposures reported to US PCCs since 2012, increasing severity was also reflected in increasing proportions of serious medical outcomes and cases requiring admission to a health care facility during the study. The observed trend of increasing clinical severity of cocaine exposures during the study period is consistent with the increase in fentanyl involvement in cocaine overdose [8].