by Dr. Nakul Bhanuprakash KadamDr. Sourya AcharyaDr. Samarth Shukla
₹ 300
ISBN Number : 978 - 1- 73040 - 636 - 2

Dr. Nakul Bhanuprakash Kadam

Assistant Professor Department of Medicine DMIMS (DU)


Dr. Sourya Acharya

Professor Department of Medicine DMIMS (DU)


Dr. Samarth Shukla

Professor Department Of Pathology DMIMS (DU) 1


Book Overview

CIRRHOSIS Cirrhosis is defined as the histological development of regenerative nodules surrounded by fibrous bands in response to chronic liver injury that leads to portal hypertension and end stage liver disease[1]. SPONTANEOUS BACTERIAL PERITONITIS Spontaneous bacterial peritonitis (SBP) is an acute bacterial infection of ascitic fluid. Spontaneous bacterial peritonitis occurs in both children and adults and is a well–known and ominous complication in patients with cirrhosis. No race predilection is known for spontaneous bacterial peritonitis. In patients with ascites, both sexes are affected equally. Harold Conn first recognized the disorder in the 1960s. Enteric organisms have traditionally been isolated from more than 90% of infected ascites fluid in spontaneous bacterial peritonitis, suggesting that the GI tract is the source of bacterial contamination.[2] Once thought to occur only in those individuals with alcoholic cirrhosis, spontaneous bacterial peritonitis is now known to affect patients with cirrhosis from any cause. In addition, spontaneous bacterial peritonitis can occur as a complication of any disease state that produces the clinical syndrome of ascites, such as heart failure and Budd–Chiari syndrome. Children with nephrosis or systemic lupus erythematosus who have ascites have a high risk of developing spontaneous bacterial peritonitis. The preponderance of enteric organisms, in combination with the presence of endotoxin in ascitic fluid and blood, once favored the argument that spontaneous bacterial peritonitis was due to direct transmural migration of bacteria from an intestinal or hollow organ lumen, a phenomenon called bacterial translocation Predisposing factor may be the intestinal bacterial overgrowth found in people with cirrhosis, mainly attributed to delayed intestinal transit time. Intestinal bacterial overgrowth, along with impaired phagocytic function, low serum and ascites complement levels, and decreased activity of the reticuloendothelial system, contributes to an increased number of microorganisms and decreased capacity to clear them from the bloodstream, resulting in their migration into and eventual proliferationwithin ascites fluid.[3] An alternative proposed mechanism for bacterial inoculation of ascites is hematogenous transmission in combination with an impaired immune system. Nonetheless, the exact mechanism of bacterial displacement from the GI tract into ascites fluid remains controversial. Patients with cirrhosis who are in a decompensated state are at the highest risk of developing spontaneous bacterial peritonitis.[4] Low complement levels are associated with the development of spontaneous bacterial peritonitis. Patients at greatest risk for spontaneous bacterial peritonitis have decreased hepatic synthetic function with associated low total protein level or prolonged prothrombin time (PT).