Conclusions
Most internists frequently see cirrhotic patients whose general conditions have deteriorated. In this setting, infection is a common precipitating factor. Spontaneous bacterial peritonitis is common and may be fatal if not detected and managed early. The common problem of GI hemorrhage in persons with portal hypertension is frequently complicated by infection. Less common situations such as FHF or hepatic iron-overload states present special risks for infection. This increased risk of infection is due largely to reduced mononuclear phagocyte function and depressed opsonic activity of serum and ascites. Consistent with this idea, persons with chronic cholestatic liver diseases have a relative preservation of hepatocellular and phagocyte mass and have fewer infections than do those with hepatic parenchymal disease. While patients with acute hepatitis rarely have infectious complications, progression to FHF results in significant risk for serious infections. Clinicians should be aware of the infectious complications that arise in the treatment of patients with liver disease.
Similar content being viewed by others
References
Wyke RJ. Baterial infections complicating liver disease. Ballieres Clin Gastroenterol. 1989;3(1):187–210.
Wood RP, Shaw BW Jr, Starzl TE. Extrahepatic complications of liver transplantation. Semin Liver Dis. 1985;5;377–84.
MacGregor RR. Alcohol and immune defense. JAMA. 1986;256:1474–9.
Adams HG, Jordan C. Infections in the alcoholic. Med Clin North Am. 1984;68(1):179–200.
Keating JJ, O’Brien CJ, Stellon AJ, et al. Influence of aetiology, clinical and histological features on survival in chronic active hepatitis: an analysis of 204 patients. Q Med. 1987;62:59–66.
VA Cooperative Variceal Sclerotherapy Group. Prophylactic sclerotherapy for esophageal varices in men with alcoholic liver disease. N Engl J Med. 1991;324:1779–84.
Rogoff TM, Lipsky P. Role of the Kupffer cells in local and systemic immune responses. Gastroenterology. 1981;80:854–60.
Beeson PB, Brannon ES, and Warren JV. Observations on the sites of removal of bacteria from the blood in patients with bacterial endocarditis. J Exp Med. 1945;81:9–23.
Triger DR, Wright W. Hyperglobulinemia in liver disease. Lancet. 1973;1:1494–6.
Thomas HC, McSween RNM, White RG. Role of the liver in controlling the immunogenicity of commensal bacteria in the gut. Lancet. 1973;1:1288–91.
Mills LR, Scheuer PJ. Hepatic sinusoidal macrophages in alcoholic liver disease. J Pathol. 1985;147:127–32.
Lahnborg G, Friman L, Berghem L. Reticuloendothelial function in patients with alcoholic liver cirrhosis. Scand J Gastroenterol. 1981;16:481–9.
Rimola A, Soto R, Bory F, et al. Reticuloendothelial system phagocytic activity in cirrhosis and its relation to bacterial infections and prognosis. Hepatology. 1984;4(l):53–8.
Castell Do, Johnson RB. The198Au liver scan. An index of portal-systemic collateral circulation in chronic liver disease. N Engl J Med. 1966;275:188–92.
Altura BM, Hershey SG. Sequential changes in reticuloendothelial system function after acute hemorrhage. Proc Soc Exp Biol Med. 1972;139:935–9.
Wang P, Ba ZF, Burkhardt J, et al. Measurement of hepatic blood flow after severe hemorrhage: lack of restoration despite adequate resuscitation. Am J Physiol. 1992;262G:92–8.
Bleichner G, Boulanger R, Squara P, et al. Frequency of infections in cirrhotic patients presenting with acute gastrointestinal haemorrhage. Br J Surg. 1986;73(9):724–6.
Rimola A, Bory F, Teres J, et al. Oral, nonabsorbable antibiotics prevent infection in cirrhotics with gastrointestinal hemorrhage. Hepatology. 1985;5(3):463–7.
Ho H, Zuckerman MJ, Wassem C. A prospective controlled study of the risk of bacteremia in emergency sclerotherapy of esophageal varices. Gastroenterology. 1991;101:1642–8.
Naveau S, Poynard T, Abella A, et al. Prognostic value of serum fibronectin concentration in alcoholic cirrhotic patients. Hepatology. 1985;5:819–23.
Fierer J, Finley F. Deficient serum bactericidal activity againstEscherichia coli in patients with cirrhosis of the liver. J Clin Invest. 1979;63:912–21.
Altin M, Rajkovic IA, Hughes RD, et al. Neutrophil adherence in chronic liver disease and fulminant hepatic failure. Gut. 1983;24:746–50.
Campbell AC, Dronfield MW, Toghill PJ, et al. Neutrophil function in chronic liver disease. Clin Exp Immunol. 1981;45:81–9.
Rajkovic IA, Williams R. Mechanisms of abnormalities in host defenses against bacterial infection in liver disease. Clin Sci. 1985;68:247–53.
Runyon BA. Ascites, ascitic fluid infection, and hepatorenal syndrome. In: Beker S (ed). Hepatology for the Clinician: A Problem-oriented Approach. New York: Alan R. Liss, 1989;105–29.
Pinzello G, Simonetti RG, Craxi A, et al. Spontaneous bacterial peritonitis: a prospective investigation in predominantly nonalcoholic patients. Hepatology. 1983;3:545–9.
Runyon BA, McHutchison JG, Antillon MR, et al. Short-course versus long-course antibiotic treatment of spontaneous bacterial peritonitis. A randomized controlled study of 100 patients. Gastroenterology. 1991;100:1737–42.
Hoefs JC. Diagnostic paracentesis. A potent clinical tool. Gastroenterology. 1990;98:230–6.
Pare P, Talbot J, Hoefs JC. Serum-ascites albumin concentration gradient: a physiologic approach to the differential diagnosis of ascites. Gastroenterology. 1983;85:240–4.
Albillos A, Cuervas-Mons V, Millan T, et al. Ascitic fluid polymorphonuclear cell count and serum to ascites albumin gradient in the diagnosis of bacterial peritonitis. Gastroenterology 1990;98:134–40.
Runyan BA. Low-protein concentration ascitic fluid is predisposed to spontaneous bacterial peritonitis. Gastroenterology. 1986;91:1343–6.
Runyon BA, Patients with deficient ascitic fluid opsonic activity are predisposed to spontaneous bacterial peritonitis. Hepatology. 1988;8:632–5.
Wilcox CM, Dismukes WE. Spontaneous bacterial peritonitis. A review of pathogenesis, diagnosis, and treatment. Medicine. 1987:66(6)447–56.
Pelletier G, Lesur G, Ink O, et al. Asymptomatic bacterascites: is it spontaneous bacterial peritonitis? Hepatology 1991;14(1):112–5.
Bouchier IAC. Postmortem study of the frequency of gallstones in patients with cirrhosis of the liver. Gut. 1969;10:705.
Snyder N, Atterbury CE, Correia JP, et al. Increased concurrence of cirrhosis and bacterial endocarditis. Gastroenterology. 1977;73:1107–13.
Patwardhan RV, Smith OJ, Farmelant MH. Serum transaminase levels and cholescintigraphic abnormalities in acute biliary tract obstruction. Arch Intern Med. 1987;147:1249–53.
Saharia PC, Cameron JL. Clinical management of cholangitis. Surg Gynecol Obstet. 1976;142:369.
Burroughs AK, Rosenstein IJ, Epstein O, et al. Bacteriuria and primary biliary cirrhosis. Gut. 1987;25:133–7.
Davis GL, Balart LA, Schiff ER, et al. Treatment of chronic hepatitis C with recombinant interferon alfa. N Engl J Med. 1989;321:1501–6.
Perrillo RP, Schiff ER, Davis GL, et al. A randomized, controlled trial of interferon alfa-2b alone and after prednisone withdrawal for the treatment of chronic hepatitis B. N Engl J Med. 1990;323:295–301.
Czaja AJ. Diagnosis, prognosis, and treatment of classical autoimmune chronic active hepatitis. In: Krawitt EL, Wiesner RH (eds). Autoimmune Liver Disease. New York: Raven Press, 1991;143–66.
Kaplan MM, Arora S, Pincus SH. Primary sclerosing cholangitis and low-dose oral pulse methotrexate therapy. Ann Intern Med. 1987;106:231–5.
Hyams JS, Ballow M, Leichtner AM. Cyclosporine treatment of autoimmune chronic active hepatitis. Gastroenterology. 1987;93:890–3.
Hegarty JE, Nouri Aria KT, Feddleston ALW, et al. Controlled trial of a thymic hormone extract (thymostimulin) in ‘autoimmune’ chronic active hepatitis. Gut 1984;25:279–83.
Mutchnick MG, Appelman HD, Chung HT, et al. Thymosin treatment of chronic hepatitis B: a placebo-controlled pilot trial. Hepatology. 1991;14(3):409–15.
Schuman BM, Beckman JW, Tedesco FJ, et al. Complications of endoscopic injection sclerotherapy: a review. Am J Gastroenterol. 1987;82(9):823–30.
Low DE, Shoenut JP, Kennedy JR, et al. Infectious complications of endoscopic injection sclerotherapy. Arch Intern Med. 1986;146:569–71.
Runyon BA, Van Epps DE. Diuresis of cirrhotic ascites increases its opsonic activity and may help prevent spontaneous bacterial peritonitis. Hepatology. 1986;6:396–9.
Gines P, Arroyo V, Quintero E, et al. Comparison of paracentesis and diuretics in the treatment of cirrhotics with tense ascites. Gastroenterology. 1987;93:234–41.
Gines P, Arroyo V, Vargas V, et al. Paracentesis with intravenous infusion of albumin as compared with peritoneovenous shunting in cirrhosis with refractory ascites. N Engl J Med. 1991;325:829–35.
Wormser GP, Hubbard RC. Peritonitis in cirrhotic patients with LeVeen shunts. Am J Med. 1981;71:358–61.
Chapman RWG, Marborgh BA, Rhodes JM, et al. Primary sclerosing cholangitis: a review of its clinical features, cholangiography, and hepatic histology. Gut. 1980;21:870–7.
Wiesner RH, LaRusso NF. Clinicopathologic features of the syndrome of primary sclerosing cholangitis. Gastroenterology. 1980;79:200–6.
Wiesner RH, LaRusso NF, Ludwig J, et al. Comparison of the clinicopathologic features of primary sclerosing cholangitis and primary biliary cirrhosis. Gastroenterology. 1985;88:108–14.
Lindor KD, Wiesner RH, MacCarty RL, et al. Advances in primary sclerosing cholangitis. Am J Med. 1990;89:73–80.
A-Kader HH, Heubi JE, Setchell KDR, et al. The effect of ursodeoxycholic acid therapy in patients with extrahepatic biliary atresia. Gastroenterology. 1990;98:A564.
Non-transferrin-bound iron in plasma or serum from patients with idiopathic hemochromatosis. J Biol Chem. 1989;264:4417–22.
Britton RS, Ferrali M, Magiera CJ, et al. Increased prooxidant action of hepatic cytosolic low-molecular-weight iron in experimental iron overload. Hepatology. 1990;11:1038–43.
Bullen JJ, Spalding PB, Ward G, et al. Hemochromatosis, iron, and septicemia caused byVibrio vulnificans. Arch Intern Med. 1991;151:1606–9.
Cover TL, Aber RC.Yersinia enterocolitica. N Engl J Med. 1989;321:16–24.
Foberg U, Fryden A, Kihlstrom E, et al.Yersinia enterocolitica septicemia: clinical and microbiological aspects. Scand J Infect Dis. 1986;18:269–79.
Oleson, LL, Ejlertsen T, Paulsen SM, et al. Liver abscesses due toYersinia enterocolitica in patients with hemochromatosis. J Intern Med. 1989;225:351–4.
Blake PA, Merson MH, Weaver RE, et al. Disease caused by a marine vibrio. Clinical characteristics and epidemiology. N Engl J Med. 1979;300:1–5.
Hicklin H, Verghese A, Alvarez S. Dysgonic fermenter 2 septicemia. Rev Infect Dis. 1987;9(5):884–90.
Gerding DN, Khan MY, Ewing JW, et al.Pasteurella multocida peritonitis in hepatic cirrhosis with ascites. Gastroenterology. 1976;70:413–5.
Zarkin BA, Lillemoe KD, Cameron JL, et al. The triad ofStreptococcus bovis bacteremia, colonic pathology, and liver disease. Ann Surg. 1990;211(6):786–92.
Bernuau J, Rueff B, Benhamou J-P. Fulminant and subfulminant liver failure: definitions and causes. Semin Liver Dis. 1986;6:97–106.
Canalese J, Gove CD. Gimson AES, et al. Reticuloendothelial system and hepatocyte function in fulminant hepatic failure. Gut. 1982;23:265–9.
Rolando N, Harvey F, Brahm J, et al. Prospective study of bacterial infection in acute liver failure: an analysis of fifty patients. Hepatology. 1990;11:49–53
De La Mata M, Meager A, Rolando N, et al. Tumour necrosis factor production in fulminant hepatic failure: relation to aetiology and superimposed microbial infection. Clin Exp Immunol. 1990;82:479–84.
Dirix LY, Poison RJ, Richardson A, et al. Primary sepsis presenting as fulminant hepatic failure. Q J Med. 1989;73:1037–43.
Author information
Authors and Affiliations
Additional information
Received from the Department of Medicine, University of Missouri School of Medicine, Columbia, Missouri.
Rights and permissions
About this article
Cite this article
King, P.D. Infectious complications of liver disease. J Gen Intern Med 8, 327–332 (1993). https://doi.org/10.1007/BF02600149
Issue Date:
DOI: https://doi.org/10.1007/BF02600149