Extracorporeal membrane oxygenation (ECMO) increasingly is being used to support acute respiratory failure and for bridging to lung transplantation. Bleeding and thrombosis are common complications in the acute setting, but the literature describing long-term ECMO complications is limited, and no previous reports have been made of delayed central venous strictures resulting from remote ECMO bridging. Herein, we describe a patient who demonstrated complete inferior vena cava obstruction resulting from venovenous ECMO bridge to lung transplantation 5 years previously. The severe stricture and secondary thrombosis were managed with inferior vena cava angioplasty, stenting, thrombectomy, and thrombolysis, leading to clinical improvement. This case highlights the need for awareness and monitoring for long-term vascular complications in a growing population of patients who have received ECMO support.

A 29-year-old woman without history of cardiac disease or risk factors sought treatment for sudden onset of chest pain radiating down the back, jaw, and arms, complicated by discomfort in the orthostatic position and severe headache. She had a history of epistaxis since childhood as well as familial history of epistaxis via her mother. BMI was 22 kg/m2, and electrocardiography showed ST segment depression in V1V2 precordial leads and T-wave inversion in inferior leads. Troponin was elevated at 3,700 ng/L (normal, < 34 ng/L), with a peak of 11,115 ng/L.

A 70-year-old man was admitted to the hospital for planned chemotherapy for recently diagnosed CNS lymphoma. His medical history included follicular lymphoma (achieved remission 1 year prior with chemotherapy) and tonic-clonic seizure 1 month prior to admission, which led to his eventual biopsy-confirmed diagnosis of CNS lymphoma. Physical examination revealed temperature 36.4 °C, heart rate of 60 beats/min, BP of 160/81 mm Hg, and 98% oxygen saturation on room air. Neurologic condition, including mental status examination, was normal. His cardiac examination revealed regular rate and rhythm with normal first and second heart sounds without murmurs, rubs, or gallops. The remainder of the examination was unremarkable. Review of systems noted progressive and intermittent confusion prior to his seizure. He denied any shortness of breath, dyspnea on exertion, orthopnea, lower extremity edema, palpitations, or syncope. Laboratory data were unremarkable.

A 50-year-old woman with a history of permanent atrial fibrillation (AF) treated with radiofrequency catheter ablation (RFCA) 6 months ago was admitted to the respiratory department of a tertiary hospital because of recurrent episodes of pleuritic chest pain in the preceding 5 months. The patient reported multiple visits to a regional hospital, where she was treated with broad-spectrum antibiotics after discovery of a left alveolar consolidation on chest radiograph (Fig 1), subsequently imaged with CT scan (Fig 2). On treatment failure and appearance of a left-sided pleural effusion during outpatient follow-up, the patient was re-admitted. Pleural fluid was obtained via thoracocentesis characterized by exudative features and lymphocytic predominance. Abdomen CT scan, with IV and per os contrast agent, was devoid of findings consistent with malignancy, and serum autoantibody levels were below positivity cut off values (antinuclear, cyclic citrullinated peptide antibody, rheumatoid factor, and anti-neutrophil cytoplasmic antibodies). The patient underwent flexible bronchoscopy without endobronchial pathology on visual inspection. Microbiologic studies and cytological examination of samples obtained by bronchial washing/aspiration yielded no clinically relevant information. Lung perfusion/ventilation scintigraphy was ordered to exclude chronic thromboembolic pulmonary hypertension; however, a deficit in vascularization for the left inferior lobe was found, prompting further investigation (Fig 3). Progression of left inferior lobe consolidation and the presence of a small pericardial effusion became evident on reimaging after a 2-month interval. The patient was empirically started on corticosteroids. After emergence of left hilar lymphadenopathy (< 1 cm), a PET-CT scan was performed. The left lower inferior lobe consolidation, whose metabolic activity pattern was consistent with that of inflammation (standardized uptake value equal to 4.4) (Fig 4), as well as the left sided-pleural effusion were markedly improved compared with previous imaging 20 days after corticosteroid initiation (Fig 2). On the grounds of recalcitrant pleuritic pain and pleural effusion recurrence during corticosteroid tapering, the patient was referred to the respiratory department of our university hospital to have her condition diagnosed.

A 27-year-old accountant came to the ED with difficulty walking and progressive weakness of both lower limbs for 4 days' duration. He did not report a history of trauma or fall. He demonstrated no vertigo, headache, neck or back pain, disturbed vision, loss of weight, or weakness in upper limbs. He also reported difficulty breathing, fever, severe abdominal pain, and loose stools of 1 day's duration. His recorded maximum temperature at home was 38.3 °C. The fever subsided with oral paracetamol 500 mg. He did not report having weakness in any limb before the current presentation. He did not have comorbid diabetes mellitus or hypertension. Thirty days before presentation, he experienced fever, cough, and rhinorrhea and received a diagnosis of COVID-19 after reverse-transcriptase polymerase chain reaction testing. At that time, symptoms had been minimal, vitals signs and chest radiography findings were normal, and he had undergone home isolation. He had maintained an oxygen saturation of 98% to 99% as measured on pulse oximetry. He had not received any treatment at that time. His symptoms had lasted for 7 days, and he remained asymptomatic up to the current presentation with paraparesis.

A 63-year-old man, who was a current smoker with a 10-pack-year history, was referred to our hospital for nonmassive hemoptysis for a month, and a large mass was observed in the right upper lobe on chest radiography. He lost 3 kg of weight within a few months. He did not have fever, breathlessness, or night sweats, and he denied a history of liver disease, alcohol consumption, or contact with a person infected with TB. He was previously healthy and was not currently taking any medication.

A 51-year-old Puerto Rican woman, with a known but inconclusive diagnosis of interstitial lung disease (ILD) since 2002 and recent moderate COVID-19, is now presenting with subacute worsening dyspnea on exertion. The patient had sporadic medical care over the years for her ILD (Table 1). Prior workup included chest CT imaging with a "crazy-paving" pattern of lung disease, as defined by ground-glass opacity with superimposed interlobular septal thickening and visible intralobular lines. Bronchoscopy showed normal airway examination, and BAL revealed clear fluid with foamy macrophages and negative cultures. Video-assisted thoracoscopic surgery and transbronchial biopsy specimens both showed foamy macrophages. Results of pulmonary function testing (PFT) revealed an isolated gas transfer defect on diffusing capacity of the lungs for carbon monoxide (Dlco). She had lived with mild yet nonprogressive functional impairment and stable exercise intolerance over these years. She was then hospitalized for COVID-19 in August 2020 and for recurrent shortness of breath in September 2020. She now presented 4 months following her September 2020 hospitalization.

A 36-year-old woman with no significant medical history was referred to our institution for evaluation of recurrent pneumothoraces. She had had approximately 16 right-sided pneumothoraces over the prior 3 years. Her pneumothoraces were accompanied by chest pain, and they all presented within 3 days of her menstrual period. She had had three pleurodeses over the prior 3 years. Additionally, she underwent video-assisted thoracic surgery (VATS) exploration, and her diaphragm was reported as normal. She had had a lung biopsy done, which only revealed normal lung parenchyma.