Spontaneous bacterial peritonitis pathophysiology

Jump to navigation Jump to search

Peritonitis main page

Spontaneous bacterial peritonitis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Spontaneous bacterial peritonitis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History & Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Spontaneous bacterial peritonitis pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Spontaneous bacterial peritonitis pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Spontaneous bacterial peritonitis pathophysiology

CDC on Spontaneous bacterial peritonitis pathophysiology

Spontaneous bacterial peritonitis pathophysiology in the news

Blogs on Spontaneous bacterial peritonitis pathophysiology

Directions to Hospitals Treating Spontaneous bacterial peritonitis

Risk calculators and risk factors for Spontaneous bacterial peritonitis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2] Ahmed Younes M.B.B.CH [3]

Overview

Intestinal bacterial overgrowth in cirrhotic patients, defective intestinal barrier and defective host immune response are the 3 determinant factors for bacterial translocation explaining SBP.

Pathogenesis

Three factors play a role in the pathogenesis of SBP:

A. Bacterial overgrowth:

B. Increased bowel permeability:

Normally, the intestinal mucosa is impermeable to bacteria because of two lines of defense[2];the secretory component and physical component. Both are affected by the development of cirrhosis.

C. Decreased local and systemic immune responses:

Bacteria that translocate are carried through lymphatics. It can reach the ascitic fluid either through the circulation then through the liver. It can have access to the peritoneal cavity. Another way is through rupture of the lymphatic vessel carrying the contaminated lymph under pressure from portal hypertension and the increased lymph content.

References

  1. Căruntu FA, Benea L (2006). "Spontaneous bacterial peritonitis: pathogenesis, diagnosis, treatment". J Gastrointestin Liver Dis. 15 (1): 51–6. PMID 16680233.
  2. 2.0 2.1 Chang CS, Chen GH, Lien HC, Yeh HZ (1998). "Small intestine dysmotility and bacterial overgrowth in cirrhotic patients with spontaneous bacterial peritonitis". Hepatology. 28 (5): 1187–90. doi:10.1002/hep.510280504. PMID 9794900.