Nguyen Hien, Le Connie, Nguyen Hanh
Perm J. 2009 Winter;13(1):53-6. doi: 10.7812/TPP/08-092.
We submit here an unusual case in which a user of crack cocaine presented with progressive dyspnea of subacute duration and was subsequently found to have concurrent pericardial and pleural effusions and pulmonary emboli. To our knowledge, there is only one prior case report that describes a potential causal relationship between crack cocaine and the development of a pleural effusion, via an eosinophilic process. In contrast in our patient, the most probable mechanism is that crack cocaine induced a prothrombotic state that promoted formation of pulmonary emboli, which are known to be directly associated with exudative pleural or pericardial effusions. An alternative hypothesis is that sympathetic activation or neurostimulation, which is mediated through release of adrenergic neurotransmitters by cocaine, may cause inflammatory changes in the pleura or pericardium. Finally, the pericardial effusion, pleural effusion, and pulmonary emboli could be concurrent but independent processes.
我们在此报告一例罕见病例，一名使用快克可卡因的患者出现亚急性进行性呼吸困难，随后被发现同时患有心包积液、胸腔积液和肺栓塞。据我们所知，之前仅有一例病例报告描述了快克可卡因与通过嗜酸性粒细胞过程导致胸腔积液之间的潜在因果关系。相比之下，在我们的患者中，最可能的机制是快克可卡因诱发了促血栓形成状态，促进了肺栓塞的形成，而肺栓塞已知与渗出性胸腔或心包积液直接相关。另一种假设是，由可卡因释放肾上腺素能神经递质介导的交感神经激活或神经刺激可能导致胸膜或心包的炎症变化。最后，心包积液、胸腔积液和肺栓塞可能是并发但独立的过程。
