Après d'autres recherches, les douleurs thoraciques representent 40% des 500 000 passages aux urgences des usagers de
cocaine (par an aux USA). Au plus 6% de ces patients ont un infarctus du myocarde et 15% un syndrome coronarien aigu mais sans infarctus.
Donc 80% ont d'autres causes mais je n'ai pas trouvé d'explications ou de recherches sur ces causes. Il faut tout de même citer la possibilité de douleurs pulmonaires (pneumothorax, pneumonie) ou digestives (oesophagite qui pourrait justifier la prise d'un anti acide genre maalox) mais cela parait assez marginal.
En conclusion, la majeure partie des douleurs thoraciques liées à la prise de
cocaine ne semblent pas etre dues à un problème sérieux mais il n'y a pas vriament d'explication. Les services d'urgence parlent souvent d'angoisse comme tu le fais, mais cela me parait plus un moyen de cacher l'ignorance.
J'ai mis en copie un article (en anglais vu que nos amis americains connaissent mieux le pb que nous) à l'appui de mes dires.
En conclusion, pour ce qui te concerne il y a de fortes chances que ta douleur thoracique soit "banale" , mais si tu te decides à consulter ton medecin cela permettrait d'en être plus certain. L'usage du
valium (ou autre BZD) au moment de la consommation/douleur est souvent recommandé. Peut etre aussi la prise preventive d'une petite dose d'aspirine (effet antithrombotique qui pourrait attenuer les effets cardiaques de la
coke) pourrait etre utile. Mais il vaut mieux que ntoutes ces prises sient faites napres et en acccord avec une consultation d'un medecin.
Amicalement
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3228621/Cocaine Chest Pain Revised 6/06
Introduction:
Cocaine related myocardial ischemia costs an estimated 80 million dollars per year. 40 % of
cocaine-related emergency department visits are due to chest pain. Incidence MI in
cocaine-related chest pain is thought to be 6%. Given the potential morbidity and mortality in otherwise healthy patients the importance of understanding the presentation and management cannot be underestimated.
Pharmacokinetics:
Cocaine is absorbed from the respiratory tract and gastrointestinal mucosa in both the hydrochloride and
base forms. Peak effect occurs in 1-2 minutes for inhalation and intravenous routes. Peaks occur at about 20 minutes for intranasal and 90 minutes for gastrointestinal routes. After inhalation or intravenous administration half-life is about 60 minutes. When via intranasal route half-life prolonged to approximately 2-3 hours.
Pathophysiology:
Cocaine causes hypertension, tachycardia, and vasoconstriction including locally in the coronary arteries.
Cocaine is also known to cause thrombogenicity and accelerated atherosclerosis. Additionally it increases oxygen demand. All of these can lead to cardiac ischemia. Amount of
cocaine used and the frequency of use are not related to likelihood of MI.
Cocaine has also been associated with dissection of the coronary arteries, which can lead to myocardial ischemia and infarction as well.
Presentation:
Most patients develop chest pain and suffer their MI within 3 hours of use. Almost all patients develop chest pain within the first 24 hours (93%). Symptoms have been attributed to
cocaine up to 4 days from use. The active metabolite norcocaine may be responsible through enterohepatic recirculation. The location and character of the pain are not predictive of MI and in fact atypical presentations predominate. This in combination with the unusual patient population (for MI) and potential delayed presentation make high index of suspicion paramount.
Workup:
Initial management of
cocaine related chest pain should include
benzodiazepines and the usual workup for myocardial ischemia including EKG, cardiac enzymes, and rule out of other etiologies for chest pain (dissection for instance). The EKG can be difficult to interpret in a young population with a high prevalence of early repolarization and left ventricular hypertrophy- changes that can sometimes be difficult to differentiate from acute ischemia. 43% of patients using
cocaine without MI in one study had ST elevation of greater than 1 mm in two contiguous leads. Enzymes may need to be checked depending on the situation. In one study, specificity of myoglobin and CK-MB were decreased and that of troponin was not altered.
Management:
Patients should be monitored, placed on oxygen, and have
IV access established. Pharmacologic therapy includes
benzodiazepines, aspirin, and nitrates.
Benzodiazepines should be first line and will often alleviate symptoms on their own. In addition or in place of nitrates, use a calcium channel blocker or an alpha blocker for coronary vasodilatation. There is theoretical concern over the use of beta blockers because of unopposed alpha blockade. Even with short acting agents such as esmolol, exacerbation of hypertension has been noted previously. In terms of observation for sequelae and development of enzyme elevation indicating MI, the shortest observation period validated for
cocaine-related chest pain is 12 hours. In a study done by Weber et al those patients with a negative workup and negative stress study at 12 hours had a death rate of 0 percent (95% confidence interval 0-0.99%) and a nonfatal myocardial infarction rate of 1.6% (95% confidence interval (1.1 o 3.1%). Other studies have noted low complication rate of those ruled out for MI. Of those that rule in for MI, 36% in one study developed a complication such as heart failure or a tachyarrhythmia. These complications largely developed in the first 12 hours.
In summary,
cocaine-associated chest pain can lead to morbidity and mortality. These patients should be taken seriously, approached aggressively and likely observed for at least 12 hours.
References:
Hollander JE. The management of
cocaine-associated myocardial ischemia. N Engl J Med 1995 Nov 9;333(19):1267-72.
Hollander JE, Hoffman RS, Burstein JL, Shih RD, Thode HC Jr.
Cocaine-associated myocardial infarction. Mortality and complications.
Cocaine-Associated Myocardial Infarction Study Group. Arch Intern Med 1995 May 22;155(10):1081-6.
Hollander JE; Hoffman RS; Gennis P; Fairweather P; DiSano MJ; Schumb DA; Feldman JA; Fish SS; Dyer S;
Wax P; et al. Prospective multicenter evaluation of
cocaine-associated chest pain.
Cocaine Associated Chest Pain (COCHPA) Study Group. Acad Emerg Med 1994 Jul-Aug;1(4):330-9.
Hollander JE; Levitt MA; Young GP; Briglia E; Wetli CV; Gawad Y. Effect of recent
cocaine use on the specificity of cardiac markers for diagnosis of acute myocardial infarction. Am Heart J 1998 Feb;135(2 Pt 1):245-52.
Karch, SB.
Cocaine Cardiovascular Toxicity. Southern Medical Journal. 2005;98(8): 794-803.
Weber JE, Shofer FS, Larkin GL, Kalaria AS, Hollander JE. Validation of a Brief Observation Period for Patients with
Cocaine-Associated Chest Pain. NEJM 2003; 348(6): pp510-517.
Dernière modification par prescripteur (07 octobre 2012 à 12:19)