Hypoxemia in patients with cirrhosis: relationship with liver failure and hemodynamic alterations

doi:10.1016/S0168-8278(97)80353-4

Journal of Hepatology

Volume 27, Issue 3, September 1997, Pages 492-495

https://doi.org/10.1016/S0168-8278(97)80353-4 Get rights and content

Abstract

Background/Aims: The relationship between hypoxemia, liver failure and the hemodynamic alterations in cirrhosis are unknown. This study examined the relationship between arterial hypoxemia, the severity of liver disease and hyperkinetic circulation in patients with cirrhosis.

Methods: Arterial blood gases, the severity of cirrhosis (Child-Pugh score), and splanchnic and systemic hemodynamics were measured in 120 patients with cirrhosis and without cardiopulmonary disease. Hypoxemia was considered to be present when PaO₂ was ≤70 mmHg.

Results: Seventeen patients had hypoxemia (14%). Hypoxemic patients had significantly lower pulmonary vascular resistance and a significantly higher alveolar-arterial oxygen gradient, Child-Pugh score and hepatic venous pressure gradient than non-hypoxemic patients. Cardiac index and right atrial and pulmonary pressures did not significantly differ between the two groups.

Conclusions: Hypoxemia occurs mainly in patients with severe liver disease and is associated with pulmonary vasodilation.

References (24)

D Roulot et al.
Long-term sympathetic and hemodynamic responses to clonidine in patients with cirrhosis and ascites
Gastroenterology
(1992)
R Brenard et al.
Hemodynamic and sympathetic responses to human atrial natriuretic peptide infusion in patients with cirrhosis
J Hepatol
(1992)
D Lebrec et al.
Transjugular intrahepatic portosystemic shunts: comparison with paracentesis in patients with cirrhosis and refractory ascites: a randomized trial
J Hepatol
(1996)
R Moreau et al.
Abnormal tissue oxygenation in patients with cirrhosis and liver failure
J Hepatol
(1988)
MJ Krowka et al.
Pulmonary aspects of chronic liver disease and liver transplantation
Mayo Clin Proc
(1985)
MJ Krowka et al.
Severe hypoxemia associated with liver disease: Mayo clinic experience and the experimental use of almitrine bismesylate
Mayo Clin Proc
(1987)
J Hourani et al.
Pulmonary dysfunction in advanced liver disease: frequent occurrence of an abnormal diffusing capacity
Am J Med
(1991)
P Andrivet et al.
Mechanisms of impaired arterial oxygenation in patients with liver cirrhosis and severe respiratory insufficiency. Effects of indomethacin
Chest
(1993)
HH Davis et al.
Alveolar-capillar oxygen disequilibrium in hepatic cirrhosis
Chest
(1978)
SJ Schwarzenberg et al.
Resolution of severe intrapulmonary shunting after liver transplantation
Chest
(1993)

MJ Krowka et al.

Hepatopulmonary syndrome. Clinical observations and lack of therapeutic response to somatostatin analogue

Chest

(1993)

P Sogni et al.

Endogenous pulmonary nitric oxide production measured from exhaled air is increased in patients with severe cirrhosis

J Hepatol

(1995)

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HPS can occur in both mild and severe, advanced liver disease. Some studies have suggested a correlation between disease severity and risk for HPS,7 although this correlation is not consistently demonstrated across studies. Recent guidelines from the International Liver Transplant Society define HPS to be characterized by the triad of abnormal arterial oxygenation caused by intrapulmonary vascular dilatations (IPVDs) in the setting of liver disease, portal hypertension, and/or congenital portosystemic shunts.8
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Our study clearly showed a significant association between Child-Pugh and MELD scores. Similar association regarding presence of HPS and liver disease severity was found in many previous studies.10,13,18 Moreover Child-Pugh score has been associated with severity of HPS.13
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Results. 110 patients were included in the study. Twenty-nine patients (26%) had HPS. MELD score was significantly higher (p < 0.01) in patients with HPS (18.93 ± 3.51) as compared to that in patients without HPS (13.52 ± 3.3). Twenty two (75.9%) patients of Child class C, 5 (17.2%) patients of Child class B and 2 (6.9%) patients of Child class A had HPS (P 0.03). The clinical variables associated with presence of HPS were spider nevi, digital clubbing, dyspnea, and platypnea. HPS significantly increased mortality during six month follow up period (HR: 2.47, 95% CI: 1.10-5.55). Child-Pugh and MELD scores were also associated with increased mortality. HPS was no longer associated with mortality when adjustment was done for age, gender, Child-Pugh, and MELD scores (HR: 0.44, 95% CI: 0.14-1.41). Both the Child-Pugh and MELD scores remained significantly associated with mortality in the multivariate survival analysis.
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We consecutively recruited 30 biopsy proven cirrhotic patients equally distributed in the three Child's classes A, B and C (age 54 ± 8 years, mean ± SD). All patients underwent evaluation of chemosensitivity to hypoxia and to hypercapnia and blood sampling for brain natriuretic peptide, norepinephrine and progesterone, besides full clinical characterization. We also recruited 10 age- and gender-matched healthy controls (age 55 ± 7 years).
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Hypoxemia in patients with cirrhosis: relationship with liver failure and hemodynamic alterations

Abstract

Gastroenterology

J Hepatol

J Hepatol

J Hepatol

Mayo Clin Proc

Mayo Clin Proc

Am J Med

Chest

Chest

Chest

Chest

J Hepatol