Esophagopericardial fistula is a rare but life-threatening complication of esophageal stenting and malignancy. Although acute purulent pericarditis is a well-recognized consequence, delayed presentation as constrictive pericarditis years after the initial insult is exceptionally uncommon. A 74-year-old woman presented with a two-month history of progressive dyspnea. She had undergone esophageal stent implantation for esophageal cancer two years earlier, followed by chemoradiotherapy. Transthoracic echocardiography demonstrated preserved biventricular systolic function and constrictive physiology without significant pericardial effusion. Chest computed tomography revealed dense pericardial fluid containing air bubbles, raising suspicion of an esophagopericardial communication. However, contrast-enhanced computed tomography with both oral and intravenous contrast failed to demonstrate an active fistulous tract. Cardiac magnetic resonance imaging confirmed constrictive physiology with septal bounce. The patient underwent surgical pericardiectomy, during which a large amount of firm, white, cheese-like purulent material was evacuated. Microbiological culture of the pericardial specimen grew Enterobacter cloacae, susceptible to piperacillin/tazobactam and meropenem. Histopathological examination demonstrated chronic inflammation, extensive fibrosis, and dystrophic calcification, confirming chronic constrictive pericarditis. Following surgical intervention and targeted antimicrobial therapy, inflammatory markers normalized, and the patient's heart failure symptoms resolved. Delayed constrictive pericarditis secondary to a presumed spontaneously sealed esophagopericardial fistula represents an extremely rare late complication of esophageal stenting. The presence of intrapericardial air should prompt suspicion for prior esophagopericardial communication even when contrast imaging fails to demonstrate an active fistula. Early multimodality imaging, surgical pericardiectomy, and targeted antimicrobial therapy are essential for successful management.

We present a case of disseminated Nocardia otitidiscaviarum infection in a 72-year-old male with a history of renal transplantation on chronic immunosuppressive therapy with prednisone, cyclosporine, and mycophenolate mofetil. He presented with pneumonia and was initially treated with ceftriaxone and azithromycin. Bronchoalveolar lavage (BAL) and cultures from a biopsied thigh lesion both grew N. otitidiscaviarum. His hospital course was complicated by visual hallucinations, and brain magnetic resonance imaging (MRI) revealed multiple intracranial abscesses. He initially received meropenem, trimethoprim-sulfamethoxazole (TMP-SMX), and linezolid. His antimicrobial regimen was subsequently modified during the treatment course. Linezolid was discontinued after hematologic abnormalities developed, TMP-SMX was temporarily held because of worsening renal function and later reintroduced, and meropenem was also discontinued. He was discharged on TMP-SMX and minocycline and completed an initial six-week antimicrobial treatment course from the time of diagnosis. He was subsequently maintained on minocycline and moxifloxacin; moxifloxacin was later discontinued because of QT-interval prolongation, while minocycline was continued for slightly longer than one year, with clinical and radiologic resolution.

Community-acquired pneumonia may occasionally be associated with unexpected respiratory deterioration despite apparent clinical, laboratory, and radiological improvement. We report a case of a previously healthy adult male who presented with progressive dyspnea, persistent cough, generalized weakness, malaise, and low-grade fever. Initial chest radiography showed no significant abnormalities despite marked respiratory symptoms, whereas chest computed tomography revealed bilateral bronchopneumonia with multiple centrilobular nodules and patchy ground-glass opacities. The patient was treated with intravenous meropenem, systemic corticosteroids, inhaled therapy, supplemental oxygen, and supportive care, with gradual improvement in inflammatory markers. On hospital day three, however, he developed sudden severe hypoxemic respiratory failure shortly after antimicrobial administration, requiring intensive care unit admission and high-flow nasal cannula oxygen therapy. Urgent CT pulmonary angiography excluded pulmonary embolism, follow-up imaging demonstrated partial regression of the pulmonary infiltrates, and cardiological evaluation showed no evidence of acute cardiac pathology. Meropenem was replaced with levofloxacin because a drug-related reaction could not be completely excluded. The patient's respiratory status subsequently improved rapidly with supportive treatment, and he was discharged without residual respiratory insufficiency. This case demonstrates that severe transient hypoxemic deterioration may occur during apparently successful treatment of bilateral bronchopneumonia and emphasizes the importance of promptly excluding pulmonary embolism, acute cardiac disease, drug-related reactions, and other potentially life-threatening causes of respiratory worsening.