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Pulmonary Complications in Patients with Liver Cirrhosis

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Pulmonary Complications in Patients with Liver Cirrhosis Review Article Pulmonary complications in patients with liver cirrhosis Fabian Benz, Raphael Mohr, Frank Tacke, Christoph Roderburg Charité University Medicine Berlin, Department of Hepatology & Gastroenterology, Campus Virchow Klinikum and Campus Charité Mitte, Berlin, Germany ABSTRACT Patients with advanced chronic liver diseases, particularly with decompensated liver cirrhosis, can develop specific pulmonary complications independently of any pre-existing lung disease. Especially when dyspnea occurs in combination with liver cirrhosis, patients should be evaluated for hepato-pulmonary syndrome (HPS), porto-pulmonary hypertension (PPHT), hepatic hydrothorax and spontaneous bacterial empyema, which represent the clinically most relevant pulmonary complications of liver cirrhosis. Importantly, the pathophysiology, clinical features, diagnosis and the corresponding therapeutic options differ between these entities, highlighting the role of specific diagnostics in patients with liver cirrhosis who present with dyspnea. Liver transplantation may offer a curative therapy, including selected cases of HPS and PPHT. In this review article, we summarize the pathogenesis, clinical features, diagnostic algorithms and treatment options of the 4 specific pulmonary complications in patients with liver cirrhosis. Key words: chronic liver diseases, decompensated liver cirrhosis, dyspnea, hepatopulmonary syndrome (HPS), porto- pulmonary hypertension (PPHT), hepatic hydrothorax, spontaneous bacterial empyema INTRODUCTION degradation of ammonia with development of hepatic encephalopathy), this is called Cirrhotic transformation of the liver is decompensated liver cirrhosis.[2,3] the characteristic outcome in the long run of chronic hepatic inflammation. Liver Pulmonary complications may occur cirrhosis might occur as an end stage in patients either with or without consequence of manifold infectious, toxic, decompensation of liver disease. These metabolic, or autoimmune conditions such specific disorders need to be distinguished as viral hepatitis, alcoholism, non-alcoholic from primary lung diseases, such as chronic steatohepatitis (NASH), autoimmune obstructive pulmonary disease (COPD), which may occur in patients with liver Address for Correspondence: hepatitis (AIH), primary sclerosing Dr. Fabian Benz, Department of diseases as well, but are not pathogenically Hepatology & Gastroenterology, Campus cholangitis (PSC), primary biliary cholangitis Virchow Klinikum and Campus Charité related to the liver cirrhosis. The most Mitte, Charité University Medicine Berlin, (PBC), or a variety of storage disorders like Augustenburger Platz 1, 13353 Berlin, frequent and clinically specific relevant Germany. hemochromatosis, Wilson’s disease and alpha- E-mail: [email protected] [1] pulmonary complications are hepatic 1-antitrypsin deficiency. The functional and hydrothorax, spontaneous pulmonary Access this article online anatomic consequences include: 1) hepatic empyema, hepato-pulmonary syndrome, Website: insufficiency with restricted synthesis www.intern-med.com and portopulmonary hypertension. In and metabolic functions of the liver, 2) the present manuscript, we aimed to give DOI: 10.2478/jtim-2020-0024 portal hypertension, and 3) consecutively an overview of pulmonary complications Quick Response Code: formation of intrahepatic porto-systemic of liver cirrhosis and highlight possible shunts between portal vessels and hepatic treatment strategies. veins.[2,3] If clinically relevant complications and sequelae of portal hypertension occur HEPATIC HYDROTHORAX (e.g., ascites, variceal bleeding, splenomegaly, hepatorenal syndrome) as well as Hepatic hydrothorax (HH) is defined as deteriorating liver function (e.g., limited a pleural transudate in patients with liver formation of coagulation factors, limited cirrhosis and/or portal hypertension, 150 JOURNAL OF TRANSLATIONAL INTERNAL MEDICINE / JUL-SEP 2020 / VOL 8 |ISSUE 3 Benz et al.: Pulmonary complications in patients with liver cirrhosis whenever other etiologies of pleural effusion (e.g., renal increased dyspnea after exertion (7%), non-productive or cardiac decompensation, or primary pulmonal disorder) cough (22%), pleuritic chest pain (8%), or dizziness and have been ruled out (Table 1).[4,5] The presence of an HH fatigue as a consequence of hypoxemia (7%). Respiratory is associated with higher morbidity and mortality when failure and tension hydrothorax with consecutive cardiac compared to ascites alone.[6] A recent study showed that failure have been described.[7,12,13] the appearance of HH is associated with a median survival of 8–12 months.[7] Diagnostic thoracentesis to distinguish between transudate and exudate should be performed at initial diagnosis and if The exact pathophysiological mechanisms involved are recurrent.[7] Complications of diagnostic pleural puncture are yet not completely understood. Since most patients scarce (e.g., pneumothorax < 5%, bleeding <1%, vasovagal have coexisting ascites and hydrothorax, the currently reactions < 1%)[14,15] and can be further diminished by using favored hypothesis is based on a transdiaphragmatic sonographic guided puncture techniques. Prophylactic fluid shift from the peritoneal into the pleural cavity via substitution of blood products (platelet concentrates, diaphragmatic defects. Patients may present microscopic fresh frozen plasma, or coagulation factors) should only be or even macroscopic diaphragmatic lesions,[8] which are considered in patients with grave coagulation disorders (INR observed more frequently in the right hemidiaphragm, > 3, platelets < 25,000/mm³).[16] being thinner and less muscular than the left side. A study including 1038 patients with advanced liver cirrhosis HH is characterized by a total cell count of described the incidence of HH with 5%, mostly right-sided polymorphonuclear cell (PMN) < 250/µL, a total (70%), less frequently left-sided (12%), or bilateral (18%).[9] protein concentration < 2.5 g/dL, an albumin gradient Nevertheless, isolated occurrence of HH without ascites (serum - pleural fluid) > 1.1 g/dL, or an albumin quotient may be conditioned by the negative intrathoracic pressure (pleural fluid/serum) < 0.6. Further optional parameters generated during inspiration, promoting fluid accumulation indicating HH are protein quotient < 0.5 (pleural fluid/ in the pleural space rather than in the abdominal cavity.[10] serum), a LDH gradient < 0.6 (serum - pleural fluid), Ascites is coexisting in 80% of cases with HH but is not and similar pH value as well as glucose concentration in required for diagnosis.[11] serum and pleural fluid.[17,18] As already mentioned above, renal, cardiac, and primary pulmonal causes of pleural Patients may present severe clinical symptoms, even with transudate must been ruled out. Useful tools can be only a little amount of pleural effusion due to the restrictive echocardiography, urine analytics, computed tomography pattern of pulmonary function. Clinical symptoms are not angiography, cytological or microbiological work-up (in very specific and patients may report dyspnea at rest (34%), case of suspected malignancy or tuberculosis, respectively) Table 1: Important clinical, diagnostic and therapeutic options for hepatic hydrothorax and spontaneous bacterial empyema Hepatic hydrothorax Spontaneous bacterial empyema Definition Transudative pleural effusion Spontaneous infection of a preexisting hepatic + liver cirrhosis and/or portal hypertension hydrothorax + exclusion of other reasons of pleural effusion (e.g., primary renal, cardiac and pneumological disease) Prevalence 5% to 15% in patients with cirrhosis In 2% of cirrhotic patients, and 10%-16% among cirrhotic patients with hepatic hydrothorax Diagnostic Sonography, chest X-ray, diagnostic thoracentesis diagnostic thoracentesis Diagnostic criteria 1. a total cell count of PMN < 250/µL Total cell count of PMN of > 250/µL of the pleural 2. a total protein concentration < 2.5 g/dL + a positive pathogen detection effusion 3. an albumin gradient > 1.1 g/dL between serum and pleural or fluid or an albumin quotient (pleura/serum) < 0.6. Total cell count of PMN > 500/µL Optional: a protein quotient < 0.5 (pleura/serum), an LDH + a negative pathogen detection gradient < 0.6 (pleura/serum) and comparable values for pH and glucose in serum and pleural fluid. Clinical features (depending on the amount of pleural effusion) Fever, encephalopathy, hepatorenal dyspnea at rest/after exertion, non-productive cough, pleuritic decompensation chest pain, signs of hypoxemia, respiratory failure and acute tension hydrothorax with cardiac failure Therapy options Sodium restriction, diuretic therapy (furosemide, spironolactone), Intravenous antibiotic and albumin substitution, large-volume paracentesis, thoracentesis, TIPS, liver thoracic drainage transplantation, pleurodesis PMN: polymorphonuclear cell; TIPS: transjugular intrahepatic portosystemic shunt. JOURNAL OF TRANSLATIONAL INTERNAL MEDICINE / JUL-SEP 2020 / VOL 8 |ISSUE 3 151 Benz et al.: Pulmonary complications in patients with liver cirrhosis or specific laboratory tests when chylothorax (triglyceride A continuous transcutaneous thoracic drainage is not level) or pancreatitis (amylase concentration) are considered recommended because of massive protein and electrolyte likely differential diagnoses. depletion, risk of infection, renal failure and bleeding.[33,34] Furthermore, studies show increased risk of mortality in Ultra-sonography and X-ray are valid diagnostic tools. patients who
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