Abstract Background Acute pulmonary embolism leads to pulmonary infarction in only about 8% of the cases, 5% of which can be complicated by the development of pneumonia. The parenchymal necrosis caused by the pulmonary infarction can lead to a cavitary necrotizing pneumonia, a dreaded complication with extremely high mortality rate. Here we present a case of an elderly male with no known risk factors who presented with pulmonary embolism complicated by resistant necrotizing pneumonia. Case Description 85-year-old male with no reported past medical history presented to the hospital complaining of worsening dyspnea on exertion, fatigue, and generalized malaise for two weeks. On presentation, he was febrile with temperature 101.7oF, heart rate 110 beats per minutes, and hypoxic - oxygen saturation of 85% on room air. CT scan of the chest was indicative of a thromboembolus within the distal right main pulmonary artery with extension into the secondary and tertiary branches. Given his advanced age sand lack of right heart strain, the patient was not a candidate for thrombectomy or catheter directed thrombolysis. Therefore, intravenous heparin was initiated. The CT scan also showed a developing right lower lobe pneumonia, warranting initiation of Vancomycin and Cefepime. Unfortunately, the patient’s respiratory status worsened significantly, ultimately requiring intubation and mechanical ventilation. Despite appropriate treatment, his oxygen requirements did not improve, so a repeat CT scan was obtained, which revealed a large cavitary lesion with internal septation, along with moderate volume pleural effusion. Samples from bronchoalveolar lavage grew pseudomonas aeruginosa resistant to cefepime, so Meropenem was initiated. Despite 14 days of treatment, patient’s respiratory status did not improve. Ultimately, family opted for compassionate extubation with comfort measures only. The patient passed away shortly afterward. Discussion This case illustrates the importance of prompt recognition and treatment of acute pulmonary thromboembolism and its complications. The differential diagnosis for a cavitary lung lesion is very broad, including primary lung malignancy, sarcoidosis, granulomatosis with polyangiitis, tuberculosis, bacterial and fungal infections. In our case, there was no cavitation on the initial Chest X-Ray or CT scan. Therefore, our leading explanation is that the infarction caused by the pulmonary embolism led to a cavitation and provided the milieu for a necrotizing infection with pseudomonas. Our patient did not have any discernible risk factors except for his advanced age, which made him more susceptible to developing a complication and less likely to survive it despite aggressive treatment. This abstract is funded by: None
Venkatesan et al. (Fri,) studied this question.