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Is Venous Thromboembolism a Risk Factor for Pulmonary Hypertension in Fibrosing Mediastinitis?
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A7009 - Is Venous Thromboembolism a Risk Factor for Pulmonary Hypertension in Fibrosing Mediastinitis?
Author Block: M. Teixeira1, A. S. Niven2; 1Anesthesiology / Internal Medicine, Mayo Clinic, Rochester, MN, United States, 2Pulmonary / Critical Care Division, Mayo Clinic, Rochester, MN, United States.
INTRODUCTION:
Fibrosing mediastinitis (FM) is a rare disorder characterized by fibrous tissue proliferation within the mediastinum that can be idiopathic or associated with fungal infections, tuberculosis, or sarcoidosis. While most patients are asymptomatic with a favorable prognosis, compression or occlusion of vital mediastinal structures has been associated with significant morbidity and mortality. We describe a case of in situ thromboembolism in a patient with right pulmonary artery compression from FM and review our institutional experience with this rare complication.
CASE DESCRIPTION:
A 76 year old lady from the upper Mid-West on estrogen therapy presented with several weeks of progressive right shoulder pain, dry cough, and progressive dyspnea. CT pulmonary angiogram demonstrated acute venous thromboembolism in the right main pulmonary artery, significant mediastinal lymphadenopathy, and bilateral pulmonary nodules. Anticoagulation was initiated, and age appropriate cancer screening was normal. PET-CT demonstrated diffuse mediastinal uptake, and bronchoscopy with bronchoalveolar lavage (BAL) and ultrasound guided transbronchial needle aspiration of stations 4R and 4L with adequate samples by ROSE demonstrated hyalinized granulomas and inflammation. BAL cultures, QuantiFERON-TB, and fungal serologies were negative. After 6 months the patient’s symptoms had resolved and repeat CT imaging revealed interval improvement of her pulmonary embolism findings but persistent, extrinsic compression of her right main pulmonary artery from adjacent adenopathy. The patient elected to continue indefinite anticoagulation with serial reimaging of this finding.
DISCUSSION:
Pulmonary vascular complications from FM are generally thought to be from extrinsic compression and vessel obliteration. The incidence of in situ thrombosis pulmonary artery thrombosis in FM patients is unknown, and offers an additional mechanism for the development of pulmonary hypertension long term.
We have identified 990 patients seen at the Mayo Clinic between 1999 and 2016 with FM. These patients underwent an extensive, but varied evaluation including CT and MRI imaging, echocardiography, ventilation-perfusion scans, right heart catheterization or angiography. Of the patients with chronic symptoms, 56 patients were found to have pulmonary hypertension, 34 due to pulmonary arterial and 34 with pulmonary venous involvement due to disease. Symptomatic long-term pulmonary hypertension due to acute venous thromboembolism is rare.
We hypothesize that early, aggressive identification and management of these patients with long term anticoagulation may reduce the risk of progressive, symptomatic pulmonary hypertension as well as the need for repeated endovascular interventions along with their complications.
Author Block: M. Teixeira1, A. S. Niven2; 1Anesthesiology / Internal Medicine, Mayo Clinic, Rochester, MN, United States, 2Pulmonary / Critical Care Division, Mayo Clinic, Rochester, MN, United States.
INTRODUCTION:
Fibrosing mediastinitis (FM) is a rare disorder characterized by fibrous tissue proliferation within the mediastinum that can be idiopathic or associated with fungal infections, tuberculosis, or sarcoidosis. While most patients are asymptomatic with a favorable prognosis, compression or occlusion of vital mediastinal structures has been associated with significant morbidity and mortality. We describe a case of in situ thromboembolism in a patient with right pulmonary artery compression from FM and review our institutional experience with this rare complication.
CASE DESCRIPTION:
A 76 year old lady from the upper Mid-West on estrogen therapy presented with several weeks of progressive right shoulder pain, dry cough, and progressive dyspnea. CT pulmonary angiogram demonstrated acute venous thromboembolism in the right main pulmonary artery, significant mediastinal lymphadenopathy, and bilateral pulmonary nodules. Anticoagulation was initiated, and age appropriate cancer screening was normal. PET-CT demonstrated diffuse mediastinal uptake, and bronchoscopy with bronchoalveolar lavage (BAL) and ultrasound guided transbronchial needle aspiration of stations 4R and 4L with adequate samples by ROSE demonstrated hyalinized granulomas and inflammation. BAL cultures, QuantiFERON-TB, and fungal serologies were negative. After 6 months the patient’s symptoms had resolved and repeat CT imaging revealed interval improvement of her pulmonary embolism findings but persistent, extrinsic compression of her right main pulmonary artery from adjacent adenopathy. The patient elected to continue indefinite anticoagulation with serial reimaging of this finding.
DISCUSSION:
Pulmonary vascular complications from FM are generally thought to be from extrinsic compression and vessel obliteration. The incidence of in situ thrombosis pulmonary artery thrombosis in FM patients is unknown, and offers an additional mechanism for the development of pulmonary hypertension long term.
We have identified 990 patients seen at the Mayo Clinic between 1999 and 2016 with FM. These patients underwent an extensive, but varied evaluation including CT and MRI imaging, echocardiography, ventilation-perfusion scans, right heart catheterization or angiography. Of the patients with chronic symptoms, 56 patients were found to have pulmonary hypertension, 34 due to pulmonary arterial and 34 with pulmonary venous involvement due to disease. Symptomatic long-term pulmonary hypertension due to acute venous thromboembolism is rare.
We hypothesize that early, aggressive identification and management of these patients with long term anticoagulation may reduce the risk of progressive, symptomatic pulmonary hypertension as well as the need for repeated endovascular interventions along with their complications.
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