Fuhrmann Valentin, Madl Christian, Mueller Christian, Holzinger Ulrike, Kitzberger Reinhard, Funk Georg-Christian, Schenk Peter
Department of Internal Medicine IV, Intensive Care Unit 13H1, Medical University Vienna, Vienna, Austria.
Gastroenterology. 2006 Jul;131(1):69-75. doi: 10.1053/j.gastro.2006.04.014.
BACKGROUND & AIMS: The hepatopulmonary syndrome (HPS) is defined as the triad of liver disease, arterial deoxygenation, and widespread pulmonary vasodilatation. Hypoxic hepatitis, also known as ischemic hepatitis, is the leading cause of acute liver impairment in hospitals. It is unknown whether HPS occurs in hypoxic hepatitis. We assessed the prevalence and clinical consequences of HPS in patients with hypoxic hepatitis.
Forty-four patients with hypoxic hepatitis were screened prospectively for HPS using established criteria: (1) presence of hepatic disease, (2) increased alveolar-arterial difference for the partial pressure of oxygen greater than the age-related threshold, and (3) intrapulmonary vasodilatation detected via contrast-enhanced echocardiography. Sixty-two critically ill patients with different cardiopulmonary diseases but without hepatic disease were screened for prevalence of intrapulmonary vasodilatation as a control group.
Criteria of HPS were fulfilled in 18 patients with hypoxic hepatitis. HPS-positive patients had a significantly decreased partial pressure of arterial oxygen (P = .001) and partial pressure of arterial oxygen/fraction of inspired oxygen ratio (P = .034) at the time of diagnosis of HPS, a significant decreased area under the curve of the partial pressure of arterial oxygen/fraction of inspired oxygen ratio during the first 48 hours after diagnosis of hypoxic hepatitis (P = .009), and a significantly increased peak serum aspartate transaminase level (P = .028), compared with patients without HPS. Complete resolution of intrapulmonary vasodilatation was observed during follow-up evaluation. Contrast-enhanced echocardiography was negative for intrapulmonary vasodilatation in all 62 control patients.
Intrapulmonary vasodilatation indicating HPS frequently occurs in patients with hypoxic hepatitis. It is reversible after normalization of the hepatic dysfunction. Clinicians should consider intrapulmonary vasodilatation and HPS in patients with hypoxic hepatitis.
肝肺综合征（HPS）定义为肝病、动脉血氧合不足及广泛肺血管扩张三联征。缺氧性肝炎，又称缺血性肝炎，是医院急性肝损伤的主要原因。目前尚不清楚HPS是否会在缺氧性肝炎中发生。我们评估了缺氧性肝炎患者中HPS的患病率及临床后果。
采用既定标准对44例缺氧性肝炎患者进行前瞻性HPS筛查：（1）存在肝病；（2）氧分压的肺泡-动脉差值增加超过年龄相关阈值；（3）通过对比增强超声心动图检测到肺内血管扩张。对62例患有不同心肺疾病但无肝病的危重症患者进行肺内血管扩张患病率筛查作为对照组。
18例缺氧性肝炎患者符合HPS标准。与无HPS的患者相比，HPS阳性患者在诊断HPS时动脉血氧分压（P = 0.001）和动脉血氧分压/吸入氧分数比值（P = 0.034）显著降低，在诊断缺氧性肝炎后的头48小时内动脉血氧分压/吸入氧分数比值曲线下面积显著减小（P = 0.009），血清天冬氨酸转氨酶峰值水平显著升高（P = 0.028）。在随访评估中观察到肺内血管扩张完全消退。所有62例对照患者的对比增强超声心动图显示肺内血管扩张为阴性。
提示HPS的肺内血管扩张在缺氧性肝炎患者中经常出现。肝功能恢复正常后可逆转。临床医生应考虑缺氧性肝炎患者存在肺内血管扩张及HPS的情况。
