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Peritoneal Dialysis May Provide Survival Benefit in LVAD Patents with ESRF: A Case Report
The 20th Annual Scientific Meeting
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HFSA
S131
375 Peritoneal Dialysis May Provide Survival Benefit in LVAD Patents with ESRF: A Case Report Aysha Amjad, Barbara Pisani, Ebere Chukwu; Wake Forest Baptist University Hospital, Winston Salem, NC Introduction: Patients with long-standing advanced heart failure often have renal dysfunction.This may improve,remain unchanged or worsen after the placement of a ventricular assist device (VAD).People who experience worsening renal function post VAD and go on to develop ESRF, are often deemed poor candidates for hemodialysis (HD) due to the inability of the VAD to adjust automatically to rapid shifts in blood volumes and pressures.Moreover, due to lack of VAD expertise and management protocols at most dialysis centres, there is limited availability of outpatient HD centres and trained staff that can accommodate VAD patients. Peritoneal dialysis (PD), however, can be a safe alternative means of renal replacement therapy (RRT) in such patients. With increasing use of VAD, there may be a significant increase in patients requiring long term RRT. We present a case of a VAD patient, who has successfully utilized PD for past 5 years. Case Presentation: A 63 year old African American man with hypertension, DM, CKD, post cadaveric kidney transplant 5 years prior to VAD placement, atrial fibrillation(a fib) and non- ischemic cardiomyopathy, underwent VAD as BTT due to NYHA class 3 B symptoms. His post- op course was complicated by AKI requiring RRT, recurrent G.I. bleeds, fungal UTI, sepsis, pneumothorax, thrombocytopenia and anemia. He had respiratory failure requiring tracheostomy. His pre-op BUN & creatinine were 37 mg/dl and 1.0 mg/dl respectively and GFR > 60 ml/min. With his long and complicated post-op course, his renal function deteriorated. BUN was 96 mg/dl, creatinine 1.4 mg/dl at 6 weeks post-op. Imaging of the transplanted kidney showed normal echogenicity, but resistive indices were difficult to access due to lack of pulsatile flow related to the VAD. Short term RRT was initiated. It was discontinued due to line sepsis, but resumed a week later due to rising BUN and creatinine and oliguria (BUN 83 mg/dl, creatinine 2.7 mg/dl, GFR 31 ml/min). The patient was then started on intermittent HD. As we were unable to locate a HD center willing to accept a VAD patient, he was transitioned to PD. His post hospital discharge course was uneventful. His tracheostomy closed, he completed rehab and returned home on PD. During the subsequent 5 years he has been admitted twice for volume overload, requiring adjustments in PD flows and target dry weight. He has also had admissions for a fib (successfully rate controlled with BB), Proteus driveline infection with bacteremia, G.I. bleed requiring blood transfusions, generalized fatigue, viral bronchitis. He has had no episodes of peritonitis. His pre albumin ranges from 20–30 mg/L. He is currently has NHYA functional class 3 A and is content with his life. Conclusion: PD can be an effective and long term means of outpatient RRT. Thus, CKD might be considered a relative, rather than absolute contraindication to VAD placement. PD may not only improve survival in end-stage renal failure in a VAD population, but may be the only available outpatient means of RRT in many locales.
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376
Primary Malignant Pericardial Mesothelioma Manifesting as Cardiac Tamponade Xin Zhang1, Andrew Rosenbaum1, William Freeman2; 1Mayo Clinic, Rochester, MN; 2 Mayo Clinic, Phoeniz, AZ
Right Ventricular Stress Relief by Intra-Pulmonary Shunting in Portopulmonary Hypertension Shakil Shaikh, Ahmad Turk, Vikram Grewal, Mara Slawsky, Jaime Hernandez-Montfort; Baystate Medical Center, Springfield, MA
Case presentation: 72 year old man with history of Hodgkin’s Lymphoma Stage III treated with mediastinal radiation, radiation-induced valvular disease, coronary artery disease, chronic ischemic cardiomyopathy, and recent hospitalization for pericardial effusion, presented with progressive dyspnea. Transthoracic echocardiogram demonstrated pericardial effusion with evidence of cardiac tamponade. Pericardiocentesis yielded 900 ml sanguineous fluid resulting in immediate symptom improvement. Initial differential of the recurrent pericardial fluid included autoimmune disease, malignancy, infectious, and systemic inflammatory disease. Pericardial fluid showed high total nucleated cell count. Abnormal mesothelial cell clusters consistent with possible malignant mesothelioma were seen on cytology. PET/CT revealed no hypermetabolic lymphadenopathy or focal lesion. Given the high suspicion for malignancy induced pericardial effusion, video-assisted thoracoscopy (VATS) with pericardial biopsy and pericardial window was performed. During the procedure, a malignant soft tissue mass was discovered in pericardial space. Patient was diagnosed with primary malignant pericardial mesothelioma (PMPM) with metastasis involving superior vena cava and aortic root. He elected for hospice and passed away after one month. Discussion: PMPM is a rare disease with incidence of 0.002% based on 500,000 autopsy reports. It constitutes less than 5% of all primary cardiac tumors and less than 1% of all mesotheliomas. Presentations can include constrictive pericarditis, pericardial effusion, cardiac tamponade, and heart failure. Due to the rarity and variety of presentations, a prolonged diagnostic process is not uncommon. Diagnosis is difficult as pericardial fluid cytology is often negative. Furthermore, histopathological distinction between benign mesothelial hyperplasia and malignant mesothelioma is extremely challenging. In one case series of 120 patients, 75% of diagnoses were made postmortem. Unfortunately, diagnosis is often made at advanced stages leading to poor prognosis. Like our patient, regional metastasis is noted in 30–50% of patients at time of diagnosis. Treatment is limited and mostly involves palliative chemotherapy, surgical resection and radiation. Average survival is on 6–10 months post diagnosis. Conclusion: Although uncommon, PMPM may be considered in a patient presenting with recurrent pericardial effusion. Early diagnosis may prolong survival and improve quality of life. Future studies are necessary to treat this rapidly fatal disease.
Case Presentation: A 74-year old with a history of coronary artery disease, cirrhosis, and diastolic congestive heart failure (NYHA class III) with evidence of increased bi-atrial filling pressures, along with right ventricular systolic dysfunction and pulmonary hypertension presented to our institution with refractory volume overload in the setting of orthopnea and dyspnea on exertion. Right heart catheterization was notable for a right atrial pressure of 17 mmHg, right ventricular pressure of 69 mmHg, pulmonary artery pressure of 76/32 and a pulmonary capillary wedge pressure of 19. A transthoracic echocardiogram was notable for flattening of the inter-ventricular septum during systole and diastole consistent with right ventricular pressure and volume overload, and evidence of left ventricle diastolic dysfunction. Both left and right atria were severely dilated, and a bubble study was notable for significant right to left shunting. Nuclear perfusion and ventilation imaging showed multiple perfusion defects. Given aforementioned imaging, it was determined that the right ventricular failure was secondary to the patients’ pulmonary hypertension, which was begot by the underlying portal hypertension. Coincidentally, the patient developed an arterio-venous shunt in order to offload his right ventricle. The mainstay of therapy was then focused on reducing his pulmonary artery pressures, in an attempt to reduce the workload of his right ventricle. Discussion: Porto-pulmonary hypertension (PoPH) is a serious complication in patients with end stage liver disease. Portopulmonary hypertension has been classified by the WHO, class I subset of pulmonary hypertension. In order to diagnose PoPH, the patient must have a clinical diagnosis of portal hypertension (with or without cirrhosis). The mean pulmonary artery pressure should be greater than 25 mmHg at rest with a mean pulmonary artery occlusion pressure less than 15 mmHg. Overtime, the underlying liver disease results in a hyperdynamic circulatory state. Luo et. al. describes two endothelin receptors in the pulmonary vasculature; ET-A for vasoconstriction, and ET-B mediating vasodilation. Research has demonstrated rat models, which decrease the ET-B receptor expression in pulmonary arteries amongst animals with portal hypertension, thereby allowing unopposed endothelin to act on ET-A receptors causing pulmonary hypertension. Offloading the ventricle involves reducing the pulmonary artery pressures via prostanoids, endothelin receptor antagonists, or phosphodiesterase-5 inhibitors. Interestingly, our patient developed in situ
•
HFSA
S131
375 Peritoneal Dialysis May Provide Survival Benefit in LVAD Patents with ESRF: A Case Report Aysha Amjad, Barbara Pisani, Ebere Chukwu; Wake Forest Baptist University Hospital, Winston Salem, NC Introduction: Patients with long-standing advanced heart failure often have renal dysfunction.This may improve,remain unchanged or worsen after the placement of a ventricular assist device (VAD).People who experience worsening renal function post VAD and go on to develop ESRF, are often deemed poor candidates for hemodialysis (HD) due to the inability of the VAD to adjust automatically to rapid shifts in blood volumes and pressures.Moreover, due to lack of VAD expertise and management protocols at most dialysis centres, there is limited availability of outpatient HD centres and trained staff that can accommodate VAD patients. Peritoneal dialysis (PD), however, can be a safe alternative means of renal replacement therapy (RRT) in such patients. With increasing use of VAD, there may be a significant increase in patients requiring long term RRT. We present a case of a VAD patient, who has successfully utilized PD for past 5 years. Case Presentation: A 63 year old African American man with hypertension, DM, CKD, post cadaveric kidney transplant 5 years prior to VAD placement, atrial fibrillation(a fib) and non- ischemic cardiomyopathy, underwent VAD as BTT due to NYHA class 3 B symptoms. His post- op course was complicated by AKI requiring RRT, recurrent G.I. bleeds, fungal UTI, sepsis, pneumothorax, thrombocytopenia and anemia. He had respiratory failure requiring tracheostomy. His pre-op BUN & creatinine were 37 mg/dl and 1.0 mg/dl respectively and GFR > 60 ml/min. With his long and complicated post-op course, his renal function deteriorated. BUN was 96 mg/dl, creatinine 1.4 mg/dl at 6 weeks post-op. Imaging of the transplanted kidney showed normal echogenicity, but resistive indices were difficult to access due to lack of pulsatile flow related to the VAD. Short term RRT was initiated. It was discontinued due to line sepsis, but resumed a week later due to rising BUN and creatinine and oliguria (BUN 83 mg/dl, creatinine 2.7 mg/dl, GFR 31 ml/min). The patient was then started on intermittent HD. As we were unable to locate a HD center willing to accept a VAD patient, he was transitioned to PD. His post hospital discharge course was uneventful. His tracheostomy closed, he completed rehab and returned home on PD. During the subsequent 5 years he has been admitted twice for volume overload, requiring adjustments in PD flows and target dry weight. He has also had admissions for a fib (successfully rate controlled with BB), Proteus driveline infection with bacteremia, G.I. bleed requiring blood transfusions, generalized fatigue, viral bronchitis. He has had no episodes of peritonitis. His pre albumin ranges from 20–30 mg/L. He is currently has NHYA functional class 3 A and is content with his life. Conclusion: PD can be an effective and long term means of outpatient RRT. Thus, CKD might be considered a relative, rather than absolute contraindication to VAD placement. PD may not only improve survival in end-stage renal failure in a VAD population, but may be the only available outpatient means of RRT in many locales.
374
376
Primary Malignant Pericardial Mesothelioma Manifesting as Cardiac Tamponade Xin Zhang1, Andrew Rosenbaum1, William Freeman2; 1Mayo Clinic, Rochester, MN; 2 Mayo Clinic, Phoeniz, AZ
Right Ventricular Stress Relief by Intra-Pulmonary Shunting in Portopulmonary Hypertension Shakil Shaikh, Ahmad Turk, Vikram Grewal, Mara Slawsky, Jaime Hernandez-Montfort; Baystate Medical Center, Springfield, MA
Case presentation: 72 year old man with history of Hodgkin’s Lymphoma Stage III treated with mediastinal radiation, radiation-induced valvular disease, coronary artery disease, chronic ischemic cardiomyopathy, and recent hospitalization for pericardial effusion, presented with progressive dyspnea. Transthoracic echocardiogram demonstrated pericardial effusion with evidence of cardiac tamponade. Pericardiocentesis yielded 900 ml sanguineous fluid resulting in immediate symptom improvement. Initial differential of the recurrent pericardial fluid included autoimmune disease, malignancy, infectious, and systemic inflammatory disease. Pericardial fluid showed high total nucleated cell count. Abnormal mesothelial cell clusters consistent with possible malignant mesothelioma were seen on cytology. PET/CT revealed no hypermetabolic lymphadenopathy or focal lesion. Given the high suspicion for malignancy induced pericardial effusion, video-assisted thoracoscopy (VATS) with pericardial biopsy and pericardial window was performed. During the procedure, a malignant soft tissue mass was discovered in pericardial space. Patient was diagnosed with primary malignant pericardial mesothelioma (PMPM) with metastasis involving superior vena cava and aortic root. He elected for hospice and passed away after one month. Discussion: PMPM is a rare disease with incidence of 0.002% based on 500,000 autopsy reports. It constitutes less than 5% of all primary cardiac tumors and less than 1% of all mesotheliomas. Presentations can include constrictive pericarditis, pericardial effusion, cardiac tamponade, and heart failure. Due to the rarity and variety of presentations, a prolonged diagnostic process is not uncommon. Diagnosis is difficult as pericardial fluid cytology is often negative. Furthermore, histopathological distinction between benign mesothelial hyperplasia and malignant mesothelioma is extremely challenging. In one case series of 120 patients, 75% of diagnoses were made postmortem. Unfortunately, diagnosis is often made at advanced stages leading to poor prognosis. Like our patient, regional metastasis is noted in 30–50% of patients at time of diagnosis. Treatment is limited and mostly involves palliative chemotherapy, surgical resection and radiation. Average survival is on 6–10 months post diagnosis. Conclusion: Although uncommon, PMPM may be considered in a patient presenting with recurrent pericardial effusion. Early diagnosis may prolong survival and improve quality of life. Future studies are necessary to treat this rapidly fatal disease.
Case Presentation: A 74-year old with a history of coronary artery disease, cirrhosis, and diastolic congestive heart failure (NYHA class III) with evidence of increased bi-atrial filling pressures, along with right ventricular systolic dysfunction and pulmonary hypertension presented to our institution with refractory volume overload in the setting of orthopnea and dyspnea on exertion. Right heart catheterization was notable for a right atrial pressure of 17 mmHg, right ventricular pressure of 69 mmHg, pulmonary artery pressure of 76/32 and a pulmonary capillary wedge pressure of 19. A transthoracic echocardiogram was notable for flattening of the inter-ventricular septum during systole and diastole consistent with right ventricular pressure and volume overload, and evidence of left ventricle diastolic dysfunction. Both left and right atria were severely dilated, and a bubble study was notable for significant right to left shunting. Nuclear perfusion and ventilation imaging showed multiple perfusion defects. Given aforementioned imaging, it was determined that the right ventricular failure was secondary to the patients’ pulmonary hypertension, which was begot by the underlying portal hypertension. Coincidentally, the patient developed an arterio-venous shunt in order to offload his right ventricle. The mainstay of therapy was then focused on reducing his pulmonary artery pressures, in an attempt to reduce the workload of his right ventricle. Discussion: Porto-pulmonary hypertension (PoPH) is a serious complication in patients with end stage liver disease. Portopulmonary hypertension has been classified by the WHO, class I subset of pulmonary hypertension. In order to diagnose PoPH, the patient must have a clinical diagnosis of portal hypertension (with or without cirrhosis). The mean pulmonary artery pressure should be greater than 25 mmHg at rest with a mean pulmonary artery occlusion pressure less than 15 mmHg. Overtime, the underlying liver disease results in a hyperdynamic circulatory state. Luo et. al. describes two endothelin receptors in the pulmonary vasculature; ET-A for vasoconstriction, and ET-B mediating vasodilation. Research has demonstrated rat models, which decrease the ET-B receptor expression in pulmonary arteries amongst animals with portal hypertension, thereby allowing unopposed endothelin to act on ET-A receptors causing pulmonary hypertension. Offloading the ventricle involves reducing the pulmonary artery pressures via prostanoids, endothelin receptor antagonists, or phosphodiesterase-5 inhibitors. Interestingly, our patient developed in situ