Medical consequences of acute and chronic cocaine abuse may be categorized as those caused directly by cocaine, those due to adulterants, and those related to route of administration. The most common direct medical consequences of cocaine use include cardiovascular and CNS difficulties.
Cocaine use may account for up to 25% of cases of acute myocardial infarction among patients 18-45 years of age (Weber, Hollander, Murphy, Braunwald, & Gibson, 2003). Upon acute administration, cocaine increases blood pressure and heart rate, primarily through an action on the sympathetic nervous system. Through its pharmacological effect at alpha- and beta-adrenergic receptors, cocaine may increase oxygen demand of the myocardium by increasing blood pressure and heart rate. Cocaine also suppresses the baroreflex response and vagal tone, further contributing to its effects on heart rate. At the same time that cocaine is increasing the workload on the heart, it induces coronary artery vasoconstriction and platelet aggregation, potentially leading to coronary spasm and/or cardiac ischemia (Schrank, 1993). In addition, cocaine use is also associated with significantly decreased coronary blood flow velocity, leading to increased microvascular resistance. Slow coronary filling may also suggest the possibility of cocaine use in patients in whom it was not otherwise suspected (Kelly, Sompalli, Sattar, & Khankari, 2003). At higher doses, cocaine can depress ventricular function and slow electrical conduction in the heart. Both these effects appear to be mediated by cocaine's local anesthetic action. Cocaine may potentiate catecholamine activity, impacting voltage-dependent sodium ion channels related to local anesthetic properties.
When cocaine is administered repeatedly over a short period of time, acute tolerance can develop to the sympathomimetic effects of cocaine. In contrast, the effects of cocaine mediated by its local anesthetic action do not appear blunted by anesthesia or susceptible to acute tolerance. In addition to the effects of cocaine alone, the metabolites of cocaine may also contribute to cocaine's acute and chronic cardiovascular toxicity, and both licit and illicit drugs used in combination with cocaine might potentially alter its cardiovascular effects (Schindler, 1996).
With chronic administration, higher cocaine doses appear to induce tolerance, while lower doses may induce sensitization to cocaine's sympathomimetic effects. Chronic cocaine use is associated with multiple cardiovascular conditions, including myocardial infarction, aortic dissection, left ventricular hypertrophy, arrhythmias, sudden death, and cardiomyopathy (Frishman, Del Vecchio, Sanal, & Ismail, 2003).
CNS manifestations of cocaine exposure include seizures, status epilep-ticus, cerebral hemorrhage, and transient ischemic attacks. Cocaine may produce hyperpyrexia through direct effects on thermoregulatory centers. Depression of the medullary centers may result in respiratory paralysis, and sudden death may be caused by respiratory arrest, myocardial infarction or arrhythmia, or status epilepticus (Cregler & Mark, 1986). Migraine-like headaches have been associated with cocaine withdrawal and may be linked to serotonin dys-regulation (Satel & Gawin, 1989). Rhabdomyolysis is a complication of cocaine use. When it is accompanied by acute renal failure, severe liver dysfunction, and disseminated intravascular coagulation, the fatality rate is high (Roth, Alarcon, Fernandez, Preston, & Bourgoignie, 1988).
Other difficulties associated with chronic cocaine use include weight loss, dehydration, nutritional deficiencies (particularly of vitamins B6, C, and thia-mine), and endocrine abnormalities. Neglect of self-care may be evident, including dental caries and periodontitis exacerbated by bruxism. Addicts may medicate their pain with cocaine or other mood-altering drugs and seek medical attention only after prolonged existence of their problem(s).
Adulterants also play a role in the development of medical complications. Local anesthetics and stimulants may increase cocaine's inherent toxicity by increasing the risk of hypertension and cardiovascular complications. Sugars, though relatively benign, may encourage development of bacteria that becomes problematic when injected intravenously.
Other complications of cocaine may be due to the route of administration. Intestinal ischemia caused by vasoconstriction and reduced blood flow in the mesenteric vasculature from catecholamine stimulation of alpha receptors has been reported after oral cocaine ingestion (Texter, Chou, Merrill, Laureton, & Frohlich, 1964). Emergency room patients have required surgical correction of their intestinal perforations, after smoking crack cocaine. The chronological relationship between crack consumption and gastrointestinal perforation indi cates that crack may induce ischemic events, causing intestinal ruptures in some people (Muniz & Evans, 2001).
Gastroenterological exposure to cocaine has been studied among drug smugglers, among whom a 58% mortality rate has occurred when swallowed cocaine packets have ruptured (McCarron & Wood, 1983), or among those who swallow cocaine for other reasons. If a packet ruptures, causing severe cocaine intoxication, immediate laparotomy for removal of the packets is the best treatment option (Schaper, Hofmann, Ebbecke, Desel, & Langer, 2003). The treatment for those who swallow cocaine may be less clear, but each group requires medical attention.
Complications of intranasal administration include loss of sense of smell, atrophy and inflammation, and necrosis and perforation of the nasal septum. Snorting cocaine may anesthetize and paralyze the pharynx and larynx, causing hoarseness and predisposing the person to aspiration pneumonia (Estroff & Gold, 1986). Recurrent snorting of cocaine may result in ischemia, necrosis, and infections of the nasal mucosa, sinuses, and adjacent structures.
In terms of pulmonary effects, pneumomediastinum and cervical emphysema have been reported after smoking cocaine due to alveolar rupture with prolonged deep inspiration and Valsalva's maneuver (Aroesty, Stanley, & Crockett, 1986). Other respiratory complications of inhaling or smoking freebase cocaine include abnormal reductions in carbon monoxide diffusing capacity (Itkonen, Schnoll, & Glassroth, 1984), granulomatous pneumonitis (Cooper, Bai, Heyderman, &Lorrin, 1983), pulmonary edema (Allred &Ewer, 1981), thermal airway injury, pulmonary hemorrhage, hypersensitivity reactions, interstitial lung disease, obliterative bronchiolitis, asthma, and persistent gas-exchange abnormalities (Laposata & Mayo, 1993). Respiratory manifestations include shortness of breath, cough, wheezing, hemoptysis, and chest pains. Severe respiratory difficulties have been reported in neonates of abusing mothers. Inhalation of hot cocaine vapors may also result in bilateral loss of eyebrows and eyelashes (Tames & Goldenring, 1986), and preparation of freebase cocaine with solvents such as ether may result in accidental burns and explosions.
Complications of intravenous cocaine use are multiple and include skin abscesses, phlebitis and cellulitis, and septic emboli resulting in pneumonia, pulmonary abscesses, subacute bacterial endocarditis, ophthalmological infections, and fungal cerebritis (Wetti, Weiss, Cleary, &Gyori, 1984). Injected talcandsili-cate may cause granulomatous pneumonitis with pulmonary hypertension, as well as granulomata of the liver, brain, or eyes (Estroff & Gold, 1986). Hepatitis B, hepatitis C, and delta agent are all too frequently by-products of intravenous drug abuse. In the past several years, concomitant with the increase in HIV infection, there has been an increase in pneumonia, endocarditis, tuberculosis, and hepatitis delta and other sexually transmitted diseases in drug users (see Chapter 19 on HIV and addictions for more information on cocaine and HIV/AIDS).
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