Hepatopulmonary Syndrome: An Evolving Perspective in the Era of Liver Transplantation

Krowka, Michael J.; Cortese, Antonio

doi:10.1002/hep.1840110123

Cited by 198 publications

(126 citation statements)

References 22 publications

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“…As observed in our current subject, these patients typically show a substantial increase in Pa,O 2 on breathing 100% oxygen, and measurements of intrapulmonary "anatomical" shunt using the radionuclide macroaggregate technique substantially exceed functional estimates of shunt as measured by the O 2 method [2,7,8]. Taken together, these observations have been interpreted as convincing evidence that diffusion-limitation of O 2 due to alveolar vascular dilatation is a significant contributory mechanism to the arterial hypoxaemia associated with liver disease [2,5,7].…”

Section: Discussionsupporting

confidence: 79%

“…It has been postulated that blood flowing through such dilated interalveolar vessels may not fully equilibrate with alveolar gas because of the increased distance between the alveolar-capillary membrane and red blood cells, resulting in a diffusive impairment to oxygen uptake [4,5]. This mechanism has been proposed to explain why, when such patients breathe 100% oxygen, there is typically both a marked increase in arterial oxygen tension (Pa,O 2 ) and a substantial negative discrepancy between functional and "anatomical" shunt fractions as quantified by the conventional oxygen method and radionuclide macroaggregate technique, respectively [4][5][6][7][8]. These observations, whilst collectively indicative of abnormal interalveolar vascular dilatation, are not sufficiently specific to validate detect both diffusion-limitation for oxygen and the presence of abnormal dilatation of pulmonary vessels exposed to alveolar gas.…”

mentioning

confidence: 99%

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Pulmonary vascular dilatation and diffusion-dependent impairment of gas exchange in liver cirrhosis

Crawford¹,

Regnis²,

Laks³

et al. 1995

Eur Respir J

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the actual presence of diffusion-limitation for oxygen. Thus, significant inequality of alveolar ventilationperfusion ratios (V'A/Q') could equally explain a marked improvement in arterial Pa,O 2 with 100% oxygen breathing. Indeed, recent studies using the multiple inert gas elimination technique (MIGET), an analysis which can indirectly detect oxygen diffusion-limitation, have attributed the arterial hypoxaemia in patients with liver cirrhosis to V'A/Q' inequality and intrapulmonary shunting [9][10][11]. However, none of these MIGET studies has providedany direct evidence of actual pulmonary vascular dilatation; and, hence, they do not, by themselves, invalidate the specific hypothesis that diffusionlimitation for oxygen can occur as a direct consequence of abnormal dilatation of interalveolar vessels.To adequately test the above hypothesis requires an experimental approach that has the power to simultaneously Eur Respir J, 1995, 8, 2015-2021 DOI: 10.1183 ABSTRACT: To test the hypothesis that diffusion-limitation for oxygen is due to abnormal vascular dilatation and significantly contributes to the arterial hypoxaemia of liver cirrhosis requires an experimental approach that detects both diffusion-limitation for oxygen and the presence of abnormal dilatation of pulmonary vessels exposed to alveolar gas. We therefore studied the gas exchange of a 64 year old man with alcoholic liver cirrhosis and severe resting arterial hypoxaemia (arterial oxygen tension (Pa,O 2 ) 7.5 kPa) whilst breathing air and 100% O 2 using conventional blood gas (CBG) analysis, the multiple inert gas elimination technique (MIGET) and whole body scintigraphy (WBS) following the i.v. administration of radiolabelled boli of macroaggregates with a minimum diameter of 15 µM.During air breathing, there was a consistently positive difference between the arterial oxygen tension predicted by MIGET and that actually measured (P-M Pa,O 2 , average 0.9 kPa). During O 2 breathing, P-M Pa,O 2 became negative, (average -12.2 kPa), and shunt estimated by the O 2 method (% of Q') was consistently less than that measured by MIGET. Whereas both O 2 method and MIGET estimates of shunt never exceeded 25%, the WBS shunt was 40%, indicating that a substantial fraction of cardiac output flowed through abnormally dilated pulmonary vessels, some of which were exposed to alveolar gas and, hence, participated in gas exchange.Although our observations pertain to one subject, we believe they provide the most convincing in vivo evidence to date that abnormal dilatation of interalveolar vessels may, per se, result in a significant diffusion impairment for O 2 . Furthermore, in view of the consistently negative P-M Pa,O 2 observed during oxygen breathing, we speculate that such abnormal vascular dilatation may also have produced a significant diffusive impairment of one or more of the less soluble inert gases used in the MIGET analysis. Eur Respir J., 1995Respir J., , 8, 2015Respir J., -2021

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Section: Discussionsupporting

confidence: 79%

mentioning

confidence: 99%

Pulmonary vascular dilatation and diffusion-dependent impairment of gas exchange in liver cirrhosis

Crawford¹,

Regnis²,

Laks³

et al. 1995

Eur Respir J

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“…The postmortem examination confirmed a marked dilatation of the pulmonary alveolar capillaries prominent in the lower zone of the lungs. These findings are consistent with those of hepatopulmonary syndrome (1)(2)(3)(4)(5)(6)(7)9). Patients with hepatopulmonary syndrome often have an accompanying mild to moderate erythrocytosis to compensate for severe hypoxemia (6,7).…”

Section: Introductionsupporting

confidence: 85%

“…The shunt ratio was 69%, as estimated by the quantitative radionuclide method (9). From these findings, a diagnosis of liver cirrhosis associated with hepato pulmonary syndrome was made (1)(2)(3)(4)(5)(6)(7)9). Bone marrow specimens obtained by needle aspira tion disclosed normocellular marrow with pronounced erythroid series hyperplasia, and the myeloid/erythroid ratio was 0.58.…”

Section: Introductionmentioning

confidence: 98%

“…Abnormal pulmonary vascular channels, such as dilated alveolar capillaries and small arteriovenous communications, is thought to be the major cause of severe hypoxemia in these patients (2,3). Recently, the term "hepatopul monary syndrome" has been advocated for these patho physiologic conditions (3)(4)(5). Secondary erythrocytosis has also been noted in many of these patients (6,7).…”

Section: Introductionmentioning

confidence: 99%

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Recurrent Intracranial Hemorrhagic Episodes in Hepatopulmonary Syndrome.

et al. 1992

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A 57-year-old woman with hepatopulmonary syndrome was treated for eight years. Severe hypoxemia continued and her erythrocytosis was slowly progressive. Two episodes of intra cranial hemorrhagic attack had occurred during the follow-up period and the patient died due to multiple organ failure after the second intracranial hemorrhage. Her autopsy findings confirmed not only established liver cirrhosis associated with intracranial hemorrhage but also the marked dilatation of pulmonary capillaries in both lungs. These findings suggest that secondary erythrocytosis in hepatopulmonary syndrome can be contributed to fatal intracranial vascular accidents. The containment of erythrocytosis should be considered in these patients. (Internal Medicine 31: 786-790, 1992)

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2006

Medical Care of the Liver Transplant Patient

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Hepatopulmonary Syndrome: An Evolving Perspective in the Era of Liver Transplantation

Cited by 198 publications

References 22 publications

Pulmonary vascular dilatation and diffusion-dependent impairment of gas exchange in liver cirrhosis

Pulmonary vascular dilatation and diffusion-dependent impairment of gas exchange in liver cirrhosis

Recurrent Intracranial Hemorrhagic Episodes in Hepatopulmonary Syndrome.

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