Pulmonary Vascular Disease |

Drug Induced Pulmonary Vein Thrombosis FREE TO VIEW

Timmy Cheng, MD; Virginia Chen, MD
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Santa Clara Valley Medical Center, San Jose, CA

Chest. 2015;148(4_MeetingAbstracts):984A. doi:10.1378/chest.2279478
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SESSION TITLE: Pulmonary Vascular Disease Student/Resident Case Report Posters

SESSION TYPE: Student/Resident Case Report Poster

PRESENTED ON: Tuesday, October 27, 2015 at 01:30 PM - 02:30 PM

INTRODUCTION: Pulmonary vein thrombosis is an exceedingly rare diagnosis in non-surgical patients. Due to its rarity, little is known about its risk factors and clinical course. Case reports have implicated genetics, infections, chemotherapy, inflammatory diseases, and hypercoagulable states as causes for pulmonary vein thrombosis. We describe a case in which carbamazepine was the only risk factor for developing a pulmonary vein thrombosis.

CASE PRESENTATION: A 57 year old female with history of seizures is brought to the emergency room for syncope. She has had 3 episodes of syncope in the last 2 months. These episodes are not accompanied by her typical tonic clonic movements or a post-ictal state. Other than syncope, she also had 2 months of chest pressure with some shortness of breath. Her vital signs on presentation are normal. She is not tachycardic and is saturating 100% on room air. Exam is normal. CTA of the chest reveals a right pulmonary vein thrombosis. ECHO does not show evidence of pulmonary hypertension. She is started on rivaroxaban for anticoagulation. Two months later, she is seen in Pulmonary clinic. She reports no further episodes of syncope. Follow up CTA chest shows complete resolution of her venous thrombus. Workup for hypercoagulable state, including malignancy workup, is negative. She has no personal or family history of blood clots. Her only medications are her anti-epileptics, including carbamazepine and phenobarbital. Carbamazepine, which is known to cause blood clots, is implicated for her PVT.

DISCUSSION: Pulmonary vein thrombosis is rarely diagnosed, but is usually found with diffuse clot burden, called pulmonary veno-occlusive disease. In such patients, the presenting symptoms are related to pulmonary hypertension as a result of the extensive clots. Our patient presented with a single clot and but had no evidence radiologic evidence of PAH. In the setting of no other apparent risk factors for thrombosis, it is possible that our patient's carbamazepine is the culprit. In severe occlusive disease, thrombectomy, treatment of PAH, and anticoagulation are recommended. However, given the rarity of the disease, there are no guidelines on duration of anticoagulation. It is also worth noting that patients diagnosed with idiopathic pulmonary arterial hypertension appear to fare better on anticoagulation, suggesting that perhaps pulmonary venous thrombosis is underdiagnosed and often misclassified as IPAH.

CONCLUSIONS: Pulmonary vein thrombosis is a very rare disease that may be misdiagnosed as idiopathic pulmonary arterial hypertension. Thus far, carbamazepine has not been described to be the culprit of a pulmonary vein thrombosis.

Reference #1: Palazzini M, Manes A. Pulmonary veno-occlusive disease misdiagnosed as idiopathic pulmonary arterial hypertension. Eur Respir Rev 2009; 18:177.

Reference #2: Eyries M, Montani D, Girerd B, et al. EIF2AK4 mutations cause pulmonary veno-occlusive disease, a recessive form of pulmonary hypertension. Nat Genet 2014; 46:65.

DISCLOSURE: The following authors have nothing to disclose: Timmy Cheng, Virginia Chen

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