David T Palma

University of Alabama at Birmingham, Birmingham, Alabama, United States

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Publications (3)21.59 Total impact

  • David T. Palma, Michael B. Fallon
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    ABSTRACT: The hepatopulmonary syndrome (HPS) occurs in as many as 15–20% of patients with cirrhosis; mortality is significantly increased compared to cirrhotic patients without HPS. The only proven effective therapy for HPS is orthotopic liver transplantation (OLT), which should be considered when severe hypoxemia is present. The natural history of HPS without liver transplantation is dismal. While post-OLT mortality is increased in patients with HPS relative to that reported in non-HPS patients, overall outcomes are favorable in properly selected patients. The higher mortality associated with HPS has led to the policy of increasing priority for OLT in selected HPS patients through a Model for End-Stage Liver Disease (MELD) score exception. There is currently no established protocol to screen for HPS in OLT candidates. However, a resting PaO2 < 65–60 mmHg identifies patients who qualify, or who may sufficiently deteriorate over a short time frame to qualify, for MELD exception criteria. In patients with HPS awaiting OLT, no specific therapies are available to improve intrapulmonary vasodilatation. The perioperative management of HPS patients presents particular clinical challenges. Key WordsHepatopulmonary syndrome–Hypoxia–Intrapulmonary shunt–Pulmonary disease
    04/2009: pages 123-133;
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    ABSTRACT: Sleep alters respiratory mechanics and gas exchange, which can adversely affect arterial oxygenation. Whether sleep affects oxygenation in hepatopulmonary syndrome is unknown. The aim of this study was to assess oxygen desaturation during sleep in hepatopulmonary syndrome. Twenty adults with cirrhosis including 10 controls and 10 patients with hepatopulmonary syndrome underwent home pulse-oximetry during sleep. Subjects at high risk for obstructive sleep apnea were excluded through the Berlin questionnaire. Subjects who spent more than 10% of total sleep time with arterial oxygen saturation < 90% were classified as sleep-time oxygen desaturators. Sleep-time desaturation was correlated with clinical variables. The results showed that 7 of 10 hepatopulmonary syndrome subjects and none of the 10 controls had sleep-time oxygen desaturation. The median percentage of total sleep time with arterial oxygen saturation < 90% was significantly higher in hepatopulmonary syndrome subjects than in controls (medians 25% versus 0%, P = 0.005). Hepatopulmonary syndrome subjects had significantly lower wake-time arterial oxygen saturation level (median, 97% versus 95%; P = 0.003) and mean sleep-time arterial oxygen saturation level (median, 96% versus 91%; P = 0.0008) than did the controls. Sleep-time desaturation directly correlated with alveolar-arterial oxygen gradient (P = 0.0007) and inversely correlated with wake-time arterial oxygen tension (P = 0.0007) and oxygen saturation (P < 0.0001). Conclusion: Oxygen desaturation occurred during sleep in 70% of hepatopulmonary syndrome subjects, the degree of which correlated with the severity of hepatopulmonary syndrome. Marked hypoxemia during sleep may occur in hepatopulmonary syndrome patients who, according to wake-time oxygen values, have only mild to moderate hypoxemia.
    Hepatology 04/2008; 47(4):1257-63. DOI:10.1002/hep.22143 · 11.19 Impact Factor
  • David T Palma, Michael B Fallon
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    ABSTRACT: The hepatopulmonary syndrome (HPS) is a pulmonary complication of cirrhosis and/or portal hypertension whereby patients develop hypoxemia as a result of alterations in pulmonary microvascular tone and architecture. HPS occurs in up to 30% of patients with cirrhosis. Although the degree of hypoxemia does not reliably correlate with the severity of liver disease, patients with HPS have a higher mortality than do patients with cirrhosis without the disorder. There has been progress into defining the mechanisms that lead to hypoxemia in HPS, but to date there are no therapeutic options for HPS aside from liver transplantation.
    Journal of Hepatology 11/2006; 45(4):617-25. DOI:10.1016/j.jhep.2006.07.002 · 10.40 Impact Factor

Publication Stats

52 Citations
21.59 Total Impact Points

Top Journals


  • 2006–2008
    • University of Alabama at Birmingham
      • Department of Medicine
      Birmingham, Alabama, United States