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19th ISAD

The International Liver Support Meeting Rostock

Pulmonary complications of liver cirrhosis and albumin dialysis

Pulmonary impairment is common in patients with end-stage liver disease ESLD. Formation of ascites results in increased intra-abdominal pressure and decreases the compliance of the respiratory system. Large volume ascites is frequently accompanied by an impaired renal function which finally results in hepato-renal syndrome HRS. As a kind of circulus vitiosus a decreased compliance of the respiratory system impairs respiratory compensation of the metabolic acidosis due to renal failure. Temporary beneficial effects of large volume paracentesis with albumin substitution and trans-jugular porto-systemic stent shunt TIPSS have been shown by several studies. In patients refractory to these approaches liver transplantation and bridging by extracorporeal organ support should be considered.

Tense ascites and renal impairment are common in ESLD. Due to their general impact on outcome they have been included in the majority of scores and staging systems of ESLD including Child-Pugh and MELD. 

By contrast, hepato-pulmonary syndrome HPS and porto-pulmonary hypertension PPS are found in a minority of patients referred for liver transplantation. HPS is characterized by impaired arterial oxygenation due to intrapulmonary vascular dilatations (IPVDs) which are caused by a variety of mediators including nitric oxide, carbon monoxide. Substantial dilatation of the pre- and post-capillary vessels results in a decrease in the ventilation/perfusion-quotient and arterial in hypoxaemia. The clinical symptoms of HPS are dyspnea and platypnea, which is worsening of dyspnea and hypoxaemia when the patient stands up from a lying position. The initial therapy is symptomatic (oxygen therapy). The effects of medical therapy remain to be proven. At present the only effective treatment with evidence for an improved outcome is liver transplantation.

PPS is another potential cause of pulmonary impairment in patients with cirrhosis. Similar to HPS, PPH is found in about 10% of the patients referred for transplantation. While HPS is attributed to an overwhelming effect of vasodilators, PPH is related to vaso-constrictive molecules normally metabolized by the liver. According to the most accepted theory on the pathogenesis of PPH, one or more of these mediators reach the pulmonary vasculature trough porto-systemic collaterals. Per definition these mechanisms result in a mean pulmonary arterial pressure of >25mmHg and a pulmonary arterial wedge pressure of <15mmHg. Therapeutic approaches include epoprostenol, endothelin-antagonists and sildenafil. Similar to HPS liver transplantation is considered as a therapeutic measure. However, the peri-operative mortality of transplantation in patients with PPH is substantially decreased. 

For both HPS and PPH extracorporeal elimination of causative vasoactive substances is an intriguing approach. However, long-term beneficial effects remain to be proven. 

In addition to the above-mentioned specific pathologies, patients with cirrhosis are in general prone to pulmonary impairment resulting in ARDS which has a particularly poor prognosis in these patients. Similar to ARDS-patients without cirrhosis the outcome is substantially related to extra-pulmonary pathologies including circulatory and renal failure. Despite the lack of evidence from a large RCT there is increasing evidence that a multi-targeted extracorporeal organ support including elimination of water-soluble and protein-bound toxins, optimizing the fluid balance and modulating the acid-base balance, eliminating CO2 and thus enabling lung-protective ventilation might be beneficial in these patients.

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