Peritonitis classification

Peritonitis Main Page
Patient Information
Overview
Causes
Classification Spontaneous Bacterial Peritonitis Secondary Peritonitis
Differential Diagnosis

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

Overview

Peritonitis may be classified according to the etiology into 3 subtypes: primary, secondary, and tertiary peritonitis.

Classification

Classification Based on Etiology

Peritonitis is classified based on the cause of the inflammatory process as follows:

Peritonitis

Primary peritonitis

Secondary peritonitis

Tertiary peritonitis

❑ Spontaneous peritonitis ❑ Peritonitis in patients with CAPD ❑ Tuberculous peritonitis

❑ Peritonitis without evidence for pathogens ❑ Peritonitis with fungi ❑ Peritonitis with low-grade pathogenic bacteria

Acute perforation peritonitis ❑ Gastrointestinal perforation ❑ Intestinal ischemia ❑ Pelviperitonitis and other forms

Postoperative peritonitis ❑ Anastomotic leak ❑ Accidental perforation and devascularization

Post-traumatic peritonitis ❑ After blunt abdominal trauma ❑ After penetrating abdominal trauma

Classification Based on Ascitic Fluid Analysis

Peritonitis is classified as follows based ascitic fluid analysis:

Varient of Spontaneous bacterial peritonitis (SBP)	Ascitic fluid analysis and other information
SBP culture postive	PMNs ≥250 cells/mm3 and culture positivity usually for a single organism Patients with cirrhosis and ascites in the presence or absence of symptoms and signs
Culture-negative neutrocytic ascites(CNNA) or culture-negative SBP	PMNs ≥250 cells/mm3 and culture negativity Poor culture technique and prior antibiotics or low opsonic activity in ascitic fluid. Commonly encountered phenotype and requires antibiotic therapy
Monomicrobial bacterascites	PMNs <250 cells/mm3 and culture positivity for a single organism Ascitic fluid infection which may resolve spontaneously or progress to SBP. Similar mortality to SBP and should be treated the same
Other varieties of ascitic fluid infections	Ascitic fluid analysis and other information
Polymicrobial bacterascites	PMNs <250 cells/mm3 and culture positivity (polymicrobial) Needle perforation
Secondary peritonitis	PMNs ≥250 cells/mm3 and culture positivity (polymicrobial) Intraperitoneal source of infection, e.g. diverticulitis

Classification Based on Clinical Setting

Peritonitis is classified as follows based ascitic fluid analysis:

Clinical varient of Spontaneous bacterial peritonitis	Explanation
Health care-associated SBP (HCA)	Diagnosis of peritonitis within 48 hours of hospital admission in patients with any prior health care contact in the past 90 days (e.g. recent hospitalisation, nursing home, dialysis centres and other health care setting).
Nosocomial SBP	Diagnosis of peritonitis 48 hours after the hospital admission.
Community acquired SBP (CA)	Diagnosis of peritonitis within 48 hours of hospital admission, but no history of prior health care contact in the past 90 days.
Multi-drug resistant SBP	Associate with prior history of antibiotic exposure and treat peritonitis based on culture sensitivities.
Recurrent SBP	Recurrent episodes of peritonitis increases risk of mortality compared to first episode mortality of SBP. Prophylactic antibiotics can reduce the mortality.

Classification Based on the clinical view point

Peritonitis may be classified based on the prognosis into the following types:

• Uncomplicated: In uncomplicated peritonitis, the infection only involves a single organ and no anatomical disruption is present. Usually, patients with such infections can be managed with surgical resection alone and no antimicrobial therapy besides peri-operative prophylaxis is necessary.
• Complicated:The infectious process proceeds beyond the organ that is the source of the infection, and causes either localised peritonitis, also referred to as abdominal abscess, or diffuse peritonitis, depending on the ability of the host to contain the process within a part of the abdominal cavity.They are the important cause of morbidity and more frequently associated with poor prognosis.However, an early clinical diagnosis, followed by adequate source control to stop ongoing contamination and restore anatomical structures and physiological function, as well as prompt initiation of appropriate empirical therapy, can limit the associated mortality.