Pulmonary Vascular Disease |

The Prevalence of Pleural and Pericardial Effusions in Pulmonary Hypertension as Described by Ultrasonography FREE TO VIEW

Edward Kilb*, MD; John Huggins, MD; Kristin Highland, MD; Matthew Divietro, DO; Steven Sahn, MD
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MUSC, Charleston, SC

Chest. 2012;142(4_MeetingAbstracts):848A. doi:10.1378/chest.1390343
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SESSION TYPE: DVT/PE/Pulmonary Hypertension Posters II

PRESENTED ON: Wednesday, October 24, 2012 at 01:30 PM - 02:30 PM

PURPOSE: To demonstrate that pleural effusion in the setting of pre-capillary pulmonary hypertension does not occur without evidence of pulmonary venous hypertension or development of ascites with transdiaphragmatic migration of fluid to the pleural space.

METHODS: Bedside ultrasonography was performed on patients immediately prior to undergoing right heart catheterization to look for fluid in three compartments: pleural, pericardial, and peritoneal spaces. Right heart catheterization measurements and diagnoses were subsequently obtained for analysis. Statistical analysis of data was performed using SigmaStat 11.0 or SAS software.

RESULTS: A total of 22 patients were enrolled. Of those, 17 were female and 5 were male, 11 were African American and 11 were Caucasian. Of the 22 patients, 18 met the criteria for pulmonary hypertension with mean PAP greater than 25mmHg. Of those 18 patients, 14 met criteria for pre-capillary pulmonary hypertension with PCWP less than 15mmHg. The mean PAP was 40.8mmHg. The mean PCWP was 12.5mmHg. Nine patients had small pericardial effusions, and none had moderate or large pericardial effusions. Four patients had pleural effusions, with 3 being small and 1 being small-moderate. Of those 4 patients, 3 had PCWP greater than 15mmHg. No patients demonstrated ascites. Diagnoses for pulmonary hypertension listed include: 6 idiopathic, 6 scleroderma, 3 idiopathic pulmonary fibrosis, 3 pulmonary venous hypertension, 2 portal vein thrombosis, 1 mixed connective tissue disease, 1 sickle cell disease.

CONCLUSIONS: In our 14 patients with pre-capillary pulmonary hypertension as described by elevated mean PAP and PCWP less than 15mmHg, 6 patients had small pericardial effusions and 1 had right sided pleural effusion. The patient with the pleural effusion was also on a tyrosine kinase inhibitor which can cause isolated pleural effusion. Overall, our hypothesis has held true that patients with pre-capillary hypertension should not develop pleural effusions without another insult.

CLINICAL IMPLICATIONS: Understanding the true pathogenesis of pleural and pericardial effusion formation in patients with pre-capillary pulmonary hypertension is essential to efficient and effective management.

DISCLOSURE: The following authors have nothing to disclose: Edward Kilb, John Huggins, Kristin Highland, Matthew Divietro, Steven Sahn

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MUSC, Charleston, SC




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