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Critical Care |

Chronic Pulmonary Thromboembolism

Sowmya Korapati, MBBS
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Upstate University Hospital, Syracuse, NY


Chest. 2013;144(4_MeetingAbstracts):312A. doi:10.1378/chest.1705332
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Abstract

SESSION TITLE: Critical Care Global Case Reports

SESSION TYPE: Global Case Report

PRESENTED ON: Tuesday, October 29, 2013 at 01:30 PM - 02:30 PM

INTRODUCTION: Objectives of this case report are To recognize Chronic Pulmonary Thromboembolism To identify the underlying factors for its origin To understand the approach to its management

CASE PRESENTATION: 41 year old male presented to the ER with complaints of increasing lower extremity edema, that has now extended to involve his scrotum, abdominal wall and back. Patient has had bilateral lower extremity edema since 7 months. He was found to have bilateral DVTs and was treated for massive PE three months ago with TPA. He was sent home on anticoagulation and after IVC filter placement. Non resolution and instead increase in edema since discharge brought him back to the ER. Echocardiogram done showed elevated PA pressures at 105 mm of Hg, which is double of the last PA pressure reading, at the time of initial PE. Septal flattening was noted indicating right ventricular strain. CTA revealed interval increase in thrombus burden. INR at the time was noted to be 3.4. Patients oxygen saturations were 94 on room air, tachypnea and tachycardia were present. Polycythemia was recognized as new finding since his discharge which required phlebotomies during the admission. Work up revealed elevated erythropoietin and negative JAK mutation favoring a secondary cause like hypoxia secondary to chronic pulmonary embolism as a cause. CT abdomen was done to rule out malignancy involving the kidney or liver as a cause of the polycythemia. It came back within normal limits. Past medical history is significant for sarcoidosis on treatment with prednisone 15mg daily, methotrexate and bactrim prophylaxis since 1 year, history of exposure to beryllium with two negative blood lymphocyte proliferation tests and one negative BAL lymphocyte proliferation test, cavitary lung lesions with serology positive for aspergillosis on treatment with posaconazole. Social history is significant for traveling 1000 miles a week as part of his job as a salesman. No history of tobacco use. Family history reveals no bleeding or clotting disorders in the family. He is currently being evaluated for possible pulmonary endarterectomy or lung transplantation. Hypercoagulation panel pending.

DISCUSSION: The natural history of acute pulmonary embolism is near-total resolution with minimal residual abnormalities; however, a minority of patients will develop chronic thromboembolic pulmonary hypertension. Several studies suggest that an underlying hypercoagulable state may be responsible in some patients. Diagnostic criteria are that Pulmonary hypertension must be present, defined as a mean pulmonary arterial pressure (PAP) ≥25 mmHg at rest in the absence of an elevated pulmonary capillary wedge pressure (ie, PCWP is ≤15 mmHg) and thromboembolic occlusion of the proximal or distal pulmonary vasculature must exist and be the presumed cause of the pulmonary hypertension. Surgery is the only definitive therapy for CTEPH.

CONCLUSIONS: Chronic pulmonary thromboembolism occurs in about one percent of patients following acute PE. Recognize any underlying hyper coagulable state. Surgery is the only definitive therapy and it should not be delayed.

Reference #1: Chronic thromboembolic pulmonary hypertension, Am J Respir Crit Care Med 2011 uptodate

DISCLOSURE: The following authors have nothing to disclose: Sowmya Korapati

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