Abstract

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.

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