Use of macroaggregated albumin lung perfusion scan to diagnose hepatopulmonary syndrome: A new approach

Abrams, Gary A.; Nanda, Navin C.; Dubovsky, Eva V.; Krowka, Michael J.; Fallon, Michael B.

doi:10.1016/s0016-5085(98)70481-0

Cited by 231 publications

(150 citation statements)

References 15 publications

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“…Prior studies have shown that the MAA shunt fraction correlates with the severity of gas exchange abnormalities in HPS. 7,10 Our findings here confirm this result and reveal a strong inverse correlation between the MAA shunt fraction and the PaO 2 on room air (r ϭ Ϫ0.74; Fig. 1) and a strong positive correlation between the MAA and P(A-a)O 2 (r ϭ 0.71; Fig.…”

Section: Resultssupporting

confidence: 82%

“…One hundred percent ABG measurements were obtained while the patient was breathing 100% oxygen through a mouthpiece and wearing a nose clip in the sitting position after a 15-to 20-minute equilibration period. 7 MAA lung perfusion scans were performed as reported previously. 2 The extrapulmonary shunt fraction, assuming that 13% of the cardiac output is delivered to the brain, 8 was calculated with the geometric mean of technetium (GMT) counts around the brain and lung as depicted in the following formula: …”

Section: Methodsmentioning

confidence: 99%

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Prospective evaluation of outcomes and predictors of mortality in patients with hepatopulmonary syndrome undergoing liver transplantation

et al. 2003

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The hepatopulmonary syndrome (HPS) occurs in a subgroup of patients with cirrhosis and results from intrapulmonary vasodilatation, which may cause significant hypoxemia. Liver transplantation has emerged as a therapeutic option for patients with HPS based on retrospective case series and reports. However, morbidity and mortality appear to be increased after transplantation for HPS, and no prospective studies evaluating clinical features that may predict poor surgical outcome are available. Therefore, we prospectively evaluated the utility of the degree of hypoxemia, the arterial oxygen response to 100% oxygen administration, and the macroaggregated albumin (MAA) scan quantification of intrapulmonary shunting as predictors for outcome after liver transplantation. Our cohort consisted of 24 patients with cirrhosis and HPS who underwent liver transplantation over a 5-year period at 2 transplant centers who were followed at least 1 year after transplantation. All patients underwent preoperative evaluation for HPS with standardized methods. Seven patients (29%) died postoperatively, 5 of cardiorespiratory complications. All deaths occurred within 10 weeks after transplantation. A preoperative arterial oxygen tension (PaO 2 ) of < 50 mm Hg alone or in combination with a MAA shunt fraction > 20% were the strongest predictors of postoperative mortality. In conclusion, we found that mortality is increased after liver transplantation for HPS, particularly in patients with more severe hypoxemia and significant intrapulmonary shunting. Preoperative testing for the severity of HPS can be used to stratify patients according to the risk for postoperative mortality. (HEPATOLOGY 2003;37:192-197.)

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Section: Resultssupporting

confidence: 82%

Section: Methodsmentioning

confidence: 99%

Prospective evaluation of outcomes and predictors of mortality in patients with hepatopulmonary syndrome undergoing liver transplantation

et al. 2003

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“…In addition to the oxymetric shunt ratio that is estimated when patients are made to breath 100% O 2 , the pulmonary shunt fraction can be estimated by calculating the ncpgasthep_2007_060f1.eps extra-pulmonary radioactivity to total body radioactivity ratio during the 99m Tc-MAA body scan. 12 The pulmonary shunt fraction is increased when the radioactive pulmonary shunt fraction is >6%. Interestingly, the higher the pulmonary shunt fraction, the more severe the arterial hypoxemia.…”

Section: Pulmonary Vascular Dilatationmentioning

confidence: 99%

“…Interestingly, the higher the pulmonary shunt fraction, the more severe the arterial hypoxemia. 12 Liver disease…”

Section: Pulmonary Vascular Dilatationmentioning

confidence: 99%

Therapy Insight: hepatopulmonary syndrome and orthotopic liver transplantation

Pastor¹,

Schiffer²

2007

Nat Rev Gastroenterol Hepatol

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Hepatopulmonary syndrome (HPS)--a pulmonary complication observed in patients who have chronic liver disease and/or portal hypertension--is attributed to intrapulmonary vascular dilatation and induces severe hypoxemia. HPS is mainly detected when patients are included on the waiting list for orthotopic liver transplantation (OLT) and can be diagnosed by blood gas analysis, transthoracic contrast-enhanced echocardiography or body scan with (99m)Tc-labeled macroaggregated albumin perfusion. When the partial pressure of arterial oxygen (PaO(2)) is >or=80 mmHg, it is unlikely that the patient has HPS. When the PaO(2) is <80 mmHg, imaging techniques should be used to confirm or exclude pulmonary vascular dilatation. When a diagnosis of HPS is confirmed, knowing the degree of hypoxemia is crucial for optimum patient management. Patients who have a PaO(2) >or=50 mmHg but <60 mmHg should be prioritized for OLT. This procedure is not indicated for patients with a PaO(2) between 60 mmHg and 80 mmHg, although follow-up every 3 months is recommended to detect any deterioration of the PaO(2). A PaO(2) of <50 mmHg might preclude OLT, because mortality and morbidity after OLT are greatly increased in these patients

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“…[1][2][3] The current criteria used to infer the existence of pulmonary vascular dilatations include either positive results from a contrast-enhanced transthoracic echocardiography (delayed microbubble opacification in the left atrium greater than three cardiac cycles after right atrial opacification), or abnormal extrapulmonary uptake of technetium-labeled macroaggregated albumin ( 99m TcMAA) after a lung perfusion scan (brain uptake Ͼ5%). 3,4 Chronic liver disease has usually implied cirrhotic or noncirrhotic portal hypertension. 2,3 Complete resolution of HPS after orthotopic liver transplantation (OLT) has been well documented, and some investigators consider this syndrome a valid indication for OLT, [5][6][7] especially in the pediatric age group.…”

Section: H Epatopulmonary Syndrome (Hps) Is Definedmentioning

confidence: 99%

Late recurrence and rapid evolution of severe hepatopulmonary syndrome after liver transplantation

et al. 1999

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Recurrence of hepatopulmonary syndrome (HPS) after orthotopic liver transplantation (OLT) in an adult has never been reported. We describe a 23-year-old woman who initially underwent OLT because of debilitating and severe HPS associated with nonalcoholic steatohepatitis (NASH). Although the clinical resolution of HPS was well documented day 117 post-OLT, the reappearance of NASH was documented by liver biopsy. Severe hypoxemia because of recurrent HPS rapidly evolved beginning approximately day 700 post-OLT. Retransplantation was attempted, but the patient died post-OLT of sepsis and/or multiorgan failure. Copyright 1999 by the American Association for the Study of Liver Diseases H epatopulmonary syndrome (HPS) is defined by the triad of (1) arterial hypoxemia (PaO 2 Ͻ 70 mm Hg or alveolar-arterial oxygen gradient Ͼ 20 mm Hg), (2) intrapulmonary vascular dilatations, and (3) chronic liver disease. 1-3 The current criteria used to infer the existence of pulmonary vascular dilatations include either positive results from a contrast-enhanced transthoracic echocardiography (delayed microbubble opacification in the left atrium greater than three cardiac cycles after right atrial opacification), or abnormal extrapulmonary uptake of technetium-labeled macroaggregated albumin ( 99m TcMAA) after a lung perfusion scan (brain uptake Ͼ5%). 3,4 Chronic liver disease has usually implied cirrhotic or noncirrhotic portal hypertension. 2,3 Complete resolution of HPS after orthotopic liver transplantation (OLT) has been well documented, and some investigators consider this syndrome a valid indication for OLT, 5-7 especially in the pediatric age group. 8 We describe the subsequent recurrence and rapid evolution of severe HPS in a woman approximately 700 days post-OLT who initially underwent transplantation for progressive hypoxemia caused by HPS associated with nonalcoholic steatohepatitis (NASH). Case ReportThe pretransplantation course and posttransplantation clinical resolution of HPS in this patient have been previously reported (Mayo Clinic case no. 3). 5 Briefly, this patient underwent OLT at the age of 23 years because of progressive and severe hypoxemia (PaO 2 , 53 mm Hg standing at rest; 42 mm Hg with exercise, breathing room air) associated with biopsy-proven NASH. Portal hypertension was inferred by the existence of esophageal varices and splenomegly. Delayed, positivecontrast echocardiography and abnormal extrapulmonary (brain) 99m TcMAA uptake after lung perfusion scanning (23%; normal Ͻ5%) were compatible with the existence of intrapulmonary vascular dilatations. The triad of chronic liver disease, arterial hypoxemia, and pulmonary vascular dilatations fulfilled the published criteria for the diagnosis of HPS.By day 117 post-OLT, the patient was asymptomatic, no longer required supplemental oxygen, and had normal oxygenation breathing room air, with a PaO 2 of 76 mm Hg supine and 81 mm Hg standing. The PaO 2 when breathing 100% oxygen was 576 mm Hg supine and 560 mm Hg standing. Brain uptake after a 99m TcMAA lung sc...

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Use of macroaggregated albumin lung perfusion scan to diagnose hepatopulmonary syndrome: A new approach

Cited by 231 publications

References 15 publications

Prospective evaluation of outcomes and predictors of mortality in patients with hepatopulmonary syndrome undergoing liver transplantation

Prospective evaluation of outcomes and predictors of mortality in patients with hepatopulmonary syndrome undergoing liver transplantation

Therapy Insight: hepatopulmonary syndrome and orthotopic liver transplantation

Late recurrence and rapid evolution of severe hepatopulmonary syndrome after liver transplantation

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