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Cardiovascular Disease |

Inhaled Nitric Oxide as a Rescue Therapy for Persistent Hepatopulmonary Syndrome Following Liver Transplant

Jasdip Matharu, MD; Lioudmila Karnatovskaia, MD
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University of Florida College of Medicine Jacksonville, Jacksonville, FL


Chest. 2013;144(4_MeetingAbstracts):132A. doi:10.1378/chest.1705067
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Abstract

SESSION TITLE: Cardiovascular Cases II

SESSION TYPE: Affiliate Case Report Slide

PRESENTED ON: Wednesday, October 30, 2013 at 11:30 AM - 12:30 PM

INTRODUCTION: Longstanding hepatopulmonary syndrome (HPS) causes pulmonary vascular remodeling which can result in significant shunting of un-oxygenated blood leading to hypoxemia. Worsening hypoxemia is an indication for liver transplant in selected patients.

CASE PRESENTATION: 57 year old male underwent orthotopic liver transplant for decompensated liver failure secondary to Hepatitis C and Hepatocellular Carcinoma. Pre-transplant, patient had a PaO2 of 434.7mmHg on 100% FiO2 with a shunt fraction of 14.5%; he was able to maintain sats of 94% on 5L O2 and could perform his usual activities of daily living. Post-transplant, PaO2 declined to 50.8mmHg on 85% FiO2 delivered at 14LPM through an Oxymizer device. CTA was negative for pulmonary embolus but demonstrated significant pulmonary vascular remodeling and dilation (Figures 1 and 2). A bubble echocardiogram demonstrated delayed entry into the left side consistent with a large intrapulmonary shunt, findings consistent with prior echo done pre-transplant. Patient experienced progressive worsening in respiratory symptoms over the three weeks following transplant to the point of remaining recumbent at all times. Even in a supine position on high flow oxygen at 15LPM he was barely able to maintain saturations in the high 80’s with PaO2 of 50.8. Follow-up ABG on a 100% FiO2 was notable for a PaO2 of 212.4mmHg and an increase in shunt fraction to 23%. Given increasing oxygen demand, patient was started on inhaled nitric oxide at 40 parts per million improving PaO2 to 82.6mmHg. Within a day patient had less orthodeoxia and was able to sit upright without de-saturating. PaO2 on day 5 of treatment reached 98.2, and he has been able to start exercising with physical therapy while in bed.

DISCUSSION: HPS is a triad of hepatic disease, arterial oxygen defect, and pulmonary vascular dilation. Patients experience orthodeoxia from a decreased PaO2 leading to significant VQ mismatching due to redistributed blood flow where significant vascular dilation exists. Inhaled nitric oxide may selectively vasodilate ventilated areas allowing for modest correction of the VQ mismatch without adversely affecting intrapulmonary shunt as has been demonstrated in our case.

CONCLUSIONS: This case demonstrates potential utility of using inhaled nitric oxide as a rescue therapy to bridge patients with refractory hypoxemia while post-transplant vascular remodeling is taking place.

Reference #1: Michael J. Krowka et al. Hepatopulmonary Syndrome: Current Concepts in Diagnostic and Therapeutic Considerations. Chest 1994;105:1528-37.

Reference #2: John Alexander et al. Nitric Oxide Treatment of Severe Hypoxemia After Liver Transplantation in Hepatopulmonary Syndrome: Case report. Liver Transpl Surg 1997;3(1):54-5.

DISCLOSURE: The following authors have nothing to disclose: Jasdip Matharu, Lioudmila Karnatovskaia

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