Arterial Changes in the Lungs in Cirrhosis of the Liver — Lung Spider Nevi

Berthelot, Pièrre; Walker, Josephine G.; Sherlock, Sheila; Reid, Lynne

doi:10.1056/nejm196602102740601

Cited by 326 publications

(151 citation statements)

References 31 publications

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“…The SA are lesions that appear as red spots, shiny, with numerous microvascular radiations wich pales when pressure on a central spot is temporarily applied (2,5,15,23,32,36) . They may be present in physiological situations, as in pregnancy, on children, on women in use of oral contraceptives, but are commonly asso-ciated with chronic liver diseases, its prevalence is variable, ranging from 4 to 47% depending on diagnostic criteria and methods used (23) .…”

mentioning

confidence: 99%

Are the Spider Angiomas Skin Markers of Hepatopulmonary Syndrome?

Silvério

Guimarães

Elias

et al. 2013

Arq. Gastroenterol.

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Context Hepatopathies can significantly influence both veins and arteries, these changes may cause some cutaneous stigmas, such as spider angioma (SA) and some systemic vascular changes, such as those observed in hepatopulmonary syndrome (HPS). Based on this common pathophysiological root we can assume that the SA can be skin markers of HPS. Objective The objective of this study is to assess whether there is a relationship between the presence of SA and HPS. Methods Records of 40 patients with liver cirrhosis who underwent contrast echocardiography were evaluated, in which we researched the description of SA, physical examination, and other clinical and laboratory data. For diagnosis of HPS we use these signs of the disease: presence of liver disease (cirrhosis in the case), abnormalities in gas exchange by arterial blood gases, and evidence of pulmonary vasodilations by the contrast echocardiography. Results The SA were found in 21/40 (52.5%) patients and hepatopulmonary syndrome in 9/40 (22.5%). The HPS was observed in 8/21 (38.1%) of patients with SA and 1/19 (5.3%) patients were without this sign (P<0.01). We found no statistically significant difference between the SA and the presence of HPS with sex or age. Patients with SA had a higher hypoxemia [PaO2 84.8 ± 11.5 mmHg and 19.8 ± 14.7 mmHg alveolar-arterial gradient of oxygen (AAG)] than those without SA (PaO2 90.8 ± 10.7 mmHg and 10.9 ± 11.7 AAG mmHg) (P<0.05). Conclusion Our findings show a correlation between the presence of SA and HPS, suggesting that the SA may be cutaneous markers of HPS.

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confidence: 99%

Are the Spider Angiomas Skin Markers of Hepatopulmonary Syndrome?

Silvério

Guimarães

Elias

et al. 2013

Arq. Gastroenterol.

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“…Moreover, physiological postpulmonary shunting would appear insufficient to account for the observed P-M Pa,O 2 differences, particularly at Pa,O 2 <8.0 kPa. Similarly, portopulmonary anastomosis have only rarely been identified [1] and, when present, carry only small quantities of blood which is relatively O 2 rich [17]. We, therefore, believe that the consistent P-M Pa,O 2 differences obscrved in our subject and those of EDELL et al [10] and CASTAING and MANIER [16] are most likely to represent a significant diffusion impairment for O 2 occurring at the alveolo-capillary level.…”

Section: Discussionmentioning

confidence: 49%

“…Both in vivo angiography and postmortem studies of patients with liver disease and arterial hypoxaemia have consistently documented the presence of extensive pulmonary vascular dilatation, which is limited mainly to those vessels exposed to alveolar gas [1][2][3]7]. 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].…”

Section: Discussionmentioning

confidence: 99%

“…Patients with significant arterial hypoxaemia and liver cirrhosis are known to have extensive pulmonary vascular dilatation, which is largely interalveolar in location [1][2][3]. 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].…”

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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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“…In human cirrhosis, pulmonary vascular dilatation and "spider nevi" have been observed but are not confined to patients with established HPS. 17 The observation that the resolution of HPS after liver transplantation may require prolonged periods of time also indirectly suggests that architectural alterations that take time to resolve are present. 18 Understanding the precise nature of the changes in the pulmonary microvasculature is of significant potential importance for understanding the pathogenesis of and defining effective medical therapies for HPS.…”

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confidence: 99%

Hepatopulmonary syndrome: More than just a matter of tone?

Fallon

2006

Hepatology

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Arterial Changes in the Lungs in Cirrhosis of the Liver — Lung Spider Nevi

Cited by 326 publications

References 31 publications

Are the Spider Angiomas Skin Markers of Hepatopulmonary Syndrome?

Are the Spider Angiomas Skin Markers of Hepatopulmonary Syndrome?

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

Hepatopulmonary syndrome: More than just a matter of tone?

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