abscessus. In summary, our case suggests that NTM such as M. abscessus is capable of causing empyema and Autophagy inhibitor mouse empyema necessitatis as well as lung parenchymal infection. Physicians should be aware of the possibility of pulmonary infection and empyema associated with empyema necessitatis caused by M. abscessus even in immunocompetent patients. No author has a conflict of interest to disclose. “
“Pulmonary syndromes in the setting of hepatic disease with portal hypertension include portopulmonary hypertension (POPH), hepatopulmonary

syndrome (HPS) and hepatic hydrothorax. POPH is defined as pulmonary arterial hypertension associated with liver disease and portal hypertension in the absence of other causes. HPS is defined as classical triad of presence of chronic liver disease or portal hypertension, arterial deoxygenation and evidence of intrapulmonary vascular dilatations. We present a case of liver cirrhosis where both POPH and HPS were diagnosed simultaneously. A 63-year-old woman came to the emergency department complaining of a one month history of progressive

dyspnea on exertion and leg swelling. She had a past medical history of hepatitis C diagnosed four years ago which was untreated as patient could not tolerate pegylated interferon. On physical examination, she was found to be severely hypoxic. Chest was clear to auscultation. Abdominal examination showed hepato-splenomegaly PLX3397 solubility dmso and ascites. Her chest radiograph revealed mild cardiomegaly without SPTLC1 any evidence of pulmonary edema. High resolution computed

tomography showed a focal area of linear opacities within the right lower lobe in a reticular pattern with honeycombing and associated septal thickening. Laboratory data was indicative of chronic liver disease, including a bilirubin of 2.8, an INR of 1.2, an albumin of 2.8, and a platelet count of 63,000. Arterial blood gas showed PaO2 of 53 mmHg while breathing room air. Abdominal ultrasound showed features suggestive of portal hypertension (ascites, splenomegaly). Transthoracic echocardiogram revealed an elevated right ventricle systolic pressure (49 mmHg) accompanied by a mildly dilated right atrium and right ventricle with normal left ventricular function. A contrast echocardiogram was done showing the appearance of micro bubbles in the left ventricle approximately 6 beats after their appearance in the right ventricle suggestive of hepatopulmonary syndrome (HPS). Right heart catheterization was performed which confirmed pulmonary arterial hypertension (PAH) with a pulmonary artery systolic pressure of 54 mmHg with a mean pulmonary artery pressure of 39 mmHg, a pulmonary vascular resistance of 266 (dyne*sec)/cm5 a wedge pressure of 15 mmHg and a cardiac output of 7.2 L/min. Investigation of other causes of pulmonary hypertension was unrevealing suggesting portopulmonary hypertension (POPH) as a cause of her worsening shortness of breath. Our patient was treated on oxygen with aggressive diuresis.