A reduction in the Dco has been rep...

A reduction in the Dco has been reported among "free-base" cocaine smoker We reviewed the pulmonary histopathology in 20 deaths suitable to cocaine intoxication for either parenchymal or vascular abnormalities which might explain this physiologic finding. Pulmonary artery medial hypertrophy in the absence of foreign particle microembolization was existing in four of 20 cases (20 percent) Hemosiderinladen macrophages were raise in seven of 20 cases (35 percent These abnormalities were not seen in a matched mastery group. We conclude that in the absence of foreign particle microembolization, pulmonary artery medial hypertrophy happens among cocaine users, although the mechanism of these vascular changes is unknown. In addition, secret alveolar hemorrhage occurs more often among cocaine users than is clinically recognized.

The illicit use of cocaine has reached epidemic proportions in this abiding habitation It is currently estimated that 22 million Americans have tried cocaine and that 5 million are regular users of this drug[1] Among cocaine users, there exists a widespread belief that cocaine is a "safe" drug; and indeed, reports of pulmonary complications were relatively noteworthy when cocaine was taken on the intravenous, oral or intranasal ways However, a more powerful form of cocaine, referred to as freebase or "crack", freshly has been introduced and its popularity and abuse have risen dramatically. Freebase is the alkaloid derivative of cocaine hydrochloride. It possesse a lower melting point than the hydrochloride unite and this property allows it to be smok Consequently the lower respiratory tract may directly be expos to inhaled cocaine. Interestingly, 25 to 60 percent of cocaine freebase users complain of respiratory symptoms including cough chest pain, dyspnea and sanguinary or black sputum.[2,3] Other reported pulmonary complications from cocaine freebase inhalation include barotrauma,[4,5] alveolar hemorrhage,[6] bronchiolitis obliterans[7] and "crack lung" a presum hypersensitivity answer to cocaine smoking.[8] Pulmonary edema has been reported following the pair inhalation and intravenous use of cocaine freebase.[9,10]

While physilogic gas exchange abnormalities in put drugs into abusers have been extensively described, in the greatest degree of these studies have focused in succession changes following intravenous use.[11,12] The physiologic consequences of smoking freebase cocaine are popularly under investigation. Two recently published abstracts lay the foundation of normal pulmonary function and gas exchange among freebase cocaine users.[13,14]

upon the other hand, Tashkin and co-workers[15] noted an increased incidence of obstructive faults when freebase smoking was combined with marjuana and tobacco use. pair other recent studies noted a reduction in the lung's Dco in freebase cocaine inhalers.[2,16] This finding was unexpect because merely one of these individuals had a history of intravenous substance abuse. Since this reduction in Dco give an account ofed an isolated defect in the adjoining matter of otherwise normal tests of pulmonary function, and because this abnormality persisted after cocaine use was discontinued, the authors postulated that postponeed cocaine-induced vasoconstriction might be the mechanism for the abnormal diffusing capacity.

Previous autopsy reports of cocaine-related deaths have not focused upon the lung pathology, and the incidence of pulmonary vascular abnormalities among cocaine users is generally unknown.[17] The present investigation was performed to examine the pulmonary histopathology in cocaine-related deaths for evidence of either parenchymal or vascular abnormalities which might explain the reported reduction in diffusing capacity.

MATERIALS AND METHODS

Records from the Maryland Medical Examiner's Office were reviewed to identify all deaths from cocaine intoxication investigated from that office between June 1984 and February 1988 Whenever possible, autopsy reports, associated medical records, deductions of field investigations and toxicology reports were evaluated. We were specifically interested in the general intents of cocaine abuse on the lung Therefore, any cases with either histories of multiple substance abuse or toxicologic evidence of multiple substance abuse were exclud from further subject of attention We also excluded all cases where there was either a history of a primary lung disorder or the nearness of a systemic illness known to possibly involve the lung All of the remaining cases were then sieveed for evidence of embolized foreign particulate matter using a polarizing light microscope. Any case institute to be positive was exclud from further cogitation This screening process left us with a total of 20 cases which fulfilled our pathologic inclusion criteria. Our command group consisted of ten age-and sex-matched individuals who had died unexpectedly as a result of trauma. These cases had negative toxicology protections at the time of death and no evidence of parenchymal foreign material substance microemboli by polarized light microscopy.