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Genetic and Developmental Disorders: Genetic Disorders |

Incidental Finding of Severe Hypoxia in an Asymptomatic Patient Caused by Pulmonary Arteriovenous Malformations FREE TO VIEW

Asad Omar, MD
Author and Funding Information

St John Providence Hospital, West Bloomfield, MI


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;149(4_S):A251. doi:10.1016/j.chest.2016.02.261
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Published online

SESSION TITLE: Genetic Disorders

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: Pulmonary arteriovenous malformations (AVMs) are a rare clinical entity, especially when found in isolation with no underlying etiology. Extensive literature reviews suggest that pulmonary AVMs are symptomatic in 91% of cases, with dyspnea in 82% and cyanosis in 79% of patients. Furthermore, 70% are also associated with Osler Weber Rendu Syndrome.

METHODS: We report a case of severe asymptomatic hypoxia, discovered incidentally on routine pre-operative evaluation, later found to have isolated multiple large pulmonary AVMs. Workup failed to show any underlying etiology.

RESULTS: The patient is a 54 year old female, with a history of COPD and severe aortic valve insufficiency, diagnosed via an echocardiogram at another facility, referred to cardiovascular surgery at our hospital. During pre-surgical evaluation, she was found to be hypoxic, with oxygen saturation in the 80%s on 2L of oxygen by nasal cannula and was admitted. Upon admission, her oxygen saturation was at 85% on a non re-breather mask. She denied any symptoms. Physical examination was unremarkable. Laboratory values showed hemoglobin of 17.3g/L and hematocrit of 48.9%. Chest X-Ray revealed a mass like density in the right lower lobe (RLL). CT scan of the thorax with contrast was negative for pulmonary embolus but 4 AVMs in RLL and 2 in right upper lobe were identified. Further questioning and workup was negative for Osler-Weber-Rendu syndrome or other underlying etiology. Resting echo showed an EF of 70% and a Bubble Echocardiogram revealed extensive right to left shunting. Bubbles entered from the pulmonary venous drainage into the left atrium consistent with AVMs. She had a pulmonary angiogram and AVMs of the RLL were embolizedx2 and an amplatzer vascular occlusion plug was deployedx2. After embolization, the patient's oxygen saturation was at 95% on 6L of oxygen. A Transesophageal Echo showed moderate aortic insufficiency and she decided to forego cardiac surgery.

CONCLUSIONS: Studies show most cases of pulmonary AVMs have an underlying etiology and are symptomatic in 91% of patients. Our case represents a patient with large asymptomatic pulmonary AVMs with no underlying etiology.

CLINICAL IMPLICATIONS: It shows that in patients presenting with hypoxia with no clear underlying cause, pulmonary AVMs can be considered as a cause and that pulmonary angiogram and embolization of AVMS is the cornerstone of treatment of pulmonary AVMs.

DISCLOSURE: The following authors have nothing to disclose: Asad Omar

No Product/Research Disclosure Information


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