Fig 1 CT scan showing pulmonary fibrosis and organizing empyema. (A) At the level of aortic arch; (B) at the level of carina; (C) at the level of left ventricle, and showing extensive fibrotic changes and honeycombing effect in both lower lobes. Pig-tailed drain also shown.
IntroductionIntrapleural fibrinolytic enzyme therapy is a potentially surgery-sparing treatment for poorly resolving parapneumonic effusion and empyema. It is safe in the majority of patients, however the most significant risk associated with this treatment is severe bleeding secondary to pleural hemorrhage. Contraindications for intrapleural enzyme therapy are not widely agreed upon and little is known about how to treat this difficult and potentially lethal hemorrhagic complication.Case presentationAn independent 82-year-old Caucasian man presented to hospital with an empyema complicating community-acquired pneumonia and coincidental pulmonary embolus. He was initially commenced on intravenous antibiotics, pleural drainage and anticoagulation, however failed to improve significantly and was commenced on intrapleural fibrinolytic enzyme therapy. Shortly after, he suffered severe pleural hemorrhage that was uncontrollable despite emergency thoracotomy and washout. Subsequent hemostasis was achieved after re-exploration and application of topical fibrin-thrombin sealant spray. The patient survived and was discharged home.ConclusionsIntrapleural enzyme therapy can be effective in loculated parapneumonic effusion and empyema, but massive pleural hemorrhage can complicate its use. Pleural hemorrhage appears to be associated with anticoagulation or coagulopathy, and can be difficult to manage. This case adds to the body of data on bleeding complications following intrapleural enzyme therapy, and to the best of our knowledge is the first report of fibrin-thrombin sealant use in this setting.
A left thoracotomy for decortication of an infected haemothorax was performed on a 52-year-old man with a partially infarcted left lower lobe that occurred as a rare complication of a pulmonary venous embolus. Before the completion of surgery, after an uncomplicated 40 minutes of one-lung ventilation, the left lung was temporarily re-expanded to assess air leak. On the resumption of one-lung ventilation the SpO 2 fell rapidly to 85%, despite apnoeic oxygenation of the non-ventilated lung. In the absence of evidence of double-lumen tube displacement, intra-pulmonary shunting as a consequence of impaired hypoxic pulmonary vasoconstriction in the newly expanded markedly pathological lung is considered the most likely mechanism.
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