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Synonyms and keywords: Acute bacterial peritonitis, acute generalized peritonitis, acute peritonitis, abscess of suppurative peritonitis, acute suppurative peritonitis, purulent peritonitis, subphrenic peritonitis, pelvic peritonitis, acute serositis, aseptic peritonitis, chronic peritonitis, continuous ambulatory peritoneal dialysis associated peritonitis, fungal peritonitis, granulomatous peritonitis, peritoneal dialysis-associated peritonitis, serositis, chemical peritonitis, neonatal peritonitis, tuberculous peritonitis, peritoneal abscess, spontaneous bacterial peritonitis, benign paroxysmal peritonitis, pyogranulomatous serositis, perforation peritonitis, CAPD peritonitis, primary peritonitis, secondary peritonitis, tertiary peritonitis.

Definition

Peritonitis is defined as inflammation of the peritoneum (a tissue that lines the inner wall of the abdominal cavity and covers most of the abdominal organs) from any cause. In contrast to peritonitis intrabdominal infection is defined as inflammation of peritoneum due to an infectious cause. The most common cause of peritonitis is perforation of a hollow viscus such as perforation of the distal esophagus (Boerhaave syndrome), of the stomach (peptic ulcer, gastric carcinoma), of the duodenum (peptic ulcer), of the remaining intestine (e.g. appendicitis, diverticulitis, Meckel's diverticulum, IBD, intestinal infarction, intestinal strangulation, colorectal carcinoma, meconium peritonitis), or of the gallbladder (cholecystitis). Other causes of infected peritonitis include spontaneous bacterial peritonitis and disruption of the peritoneum, such as in cases of trauma, surgical wounds, continuous peritoneal dialysis, and intra-peritoneal chemotherapy. Causes of non-infected peritonitis include endometriosis, blunt abdominal trauma, gastric carcinoma, peptic ulcer, pelvic trauma, and pancreatitis.

Causes

Causes of peritonitis can be divided into infected and non-infected, which are as follows:

Risk factors for Secondary peritonitis

Perforation of hollow viscus

Disruption of the peritoneum

Perforation of a hollow viscus (most common cause of peritonitis) Perforation of the distal esophagus (Boerhaave syndrome) Perforation of the stomach (peptic ulcer, Gastric carcinoma) Perforation of the duodenum (peptic ulcer) Perforations of the remaining intestine (e.g. Appendicitis, Diverticulitis, Meckel diverticulum, IBD, Intestinal infarction, Intestinal strangulation, Colorectal carcinoma, Meconium peritonitis) Perforation of the gallbladder (cholecystitis) Other possible causes for perforation Trauma Ingestion of a sharp foreign body (such as a fish bone) Perforation by an endoscope or catheter Most common organisms -mixed bacteria Gram-negative bacilli (e.g. Escherichia coli), Anaerobic bacteria (e.g. Bacteroides fragilis)

Trauma Surgical wound Peritoneal dialysis Chemotherapy Most common organisms Mixed bacteria Staphylococcus aureus Coagulase-negative staphylococci Fungi such as Candida

Causes of Non-Infected Peritonitis

Leakage of sterile body fluids into the peritoneum	Sterile abdominal surgery	Rarer non-infectious causes
Sterile body fluids such as Blood(e.g.Endometriosis, Blunt abdominal trauma), Gastric juice (e.g.Peptic ulcer, Gastric carcinoma), Bile (e.g. Liver biopsy), Urine (e.g. Pelvic trauma), Menstruum (e.g. salpingitis), Pancreatic juice (pancreatitis), These body fluids are sterile at first, they frequently become infected once they leak out of their organ, leading to infectious peritonitis within 24-48h.	Due to sterile foreign body inadvertently left in the abdomen after surgery (e.g. gauze, sponge)	Familial Mediterranean fever Porphyria Systemic lupus erythematosus

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.

Classification based on the etiological agents

• Peritonitis, caused by enteric organisms such as E.coli, Klebsiella, staphylococci, streptococci, anaerobes.
• Peritonitis, caused by bacteria residing out of GI tract such as gonococci, pneumococci.
• Aseptic peritonitis resulting from irritation of the peritoneal cavity from the extravasation of fluids such as blood, gastric juice.

Classification based on the pathological alterations in the clinical course of peritonitis

• Reactive: In the first 24 hours when there are maximal manifestations of local signs of peritonitis.
• Toxic: In 24-72 hours, when there is increased general intoxication with a gradual reduction in the local signs of peritonitis.
• Terminal: It is often the severe stage of peritonitis, usually after 72 hours characterized by irreversible intoxication in the background of a sharply expressed local manifestations of peritonitis.

Pathophysiology

Peritonitis results from contamination of normal sterile peritoneal cavity with infections or chemical irritants. Release of bile or gastric juices initially causes chemical peritonitis, infection occurs when bacteria enter and contaminate the peritoneal cavity. Bacterial peritonitis is usually caused by normal enteric flora like E.coli, Klebsiella. Inflammatory process causes shift of fluid into the peritoneal cavity(third spacing) which leads to hypovolemia, septicemia and multi-organ failure resulting in death of the patient if not adequately diagnosed and treated early.

• The main causes of peritonitis are the acute inflammation of the abdominal viscera, discontinuity and increased permeability of their walls, open and closed traumas of the abdomen with the damage of viscera followed by microbial contamination of peritoneal cavity.
• Despite the cause of peritonitis, the disease is characterized by a typical bacterial inflammation.
• Chronic peritonitis is caused mainly by extraperitoneal (lungs, lymph nodes) tuberculosis, entering the peritoneal cavity through hematogenous route.

Causes in Alphabetical Order

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Differential Diagnosis

Sign		Sypmtoms
Diabtes	Headache		Bia
HTN	EDEma	Abd pain		Koja
HLP

Differential Diagnosis

Disease	Findings

	Disease	Findings
Primary peritonitis	Spontaneous bacterial peritonitis	❑ Absence of GI perforation. ❑ More closely associated with cirrhosis and advanced liver disease. ❑ Presents with abrupt onset of fever, abdominal pain, worsening of abdominal ascites, and altered mental status. ❑ Presence of clinical and biochemical manifestations of advanced cirrhosis or nephrosis like leukocytosis,hypoalbuminemia, a prolonged prothrombin time. ❑ SAAG >1.1 g/dL, ↑s.lactic acid level, or a ↓ascitic fluid pH (< 7.31) supports the diagnosis. ❑ Gram staining reveals bacteria in only 25% of cases. ❑ Confirmed by ascitic fluid analysis which reveals WBC > 500cells/, and absolute PMN >250cells/. ❑ Culture of ascitic fluid inoculated immediately into blood culture media at the bedside usually reveals a single enteric organism, most commonly Escherichia coli, Klebsiella, or streptococci. ❑ Once diagnosed, SBP is treated with Ceftriaxone.
	Tuberculous peritonitis	❑ Seen in 0.5% of new cases of tuberculosis particularly in young women in endemic areas as a primary infection. ❑ Presents with abdominal pain, distension, fever, night sweats, weight loss, and altered bowel habits. ❑ Ascites is present in about half of cases. ❑ Abdominal mass may be felt in a third of cases. ❑ The peritoneal fluid is characterized by a protein concentration > 3 g/dL with < 1.1 g/dL SAAG and lymphocyte predominance of WBC. ❑ Definitive diagnosis in 80% of cases is by culture. ❑ Most patients presenting acutely are diagnosed only by laparotomy. ❑ Combination antituberculosis chemotherapy is preferred in chronic cases.
	CAPD peritonitis	❑ Peritonitis is one of the major complications of peritoneal dialysis & 72.6% occur within the first six months of peritoneal dialysis. ❑ Coagulase-negative staphylococci were the most common cause of peritonitis, presumably due to touch contamination or infection via the pericatheter route. ❑ Majority of cases are caused by bacteria (50% due to gram-positive organisms, 15% to gram-negative organisms). ❑ 20% were culture negative. ❑ 2% of cases are caused by fungi, mostly Candida species. ❑ Polymicrobial infection in 4%. ❑ Exit-site infection was present in 13% and a peritoneal fluid leak in 3 % and M.tuberculosis 0.1%. ❑ Treatment for peritoneal dialysis-associated peritonitis consists of antimicrobial therapy, in some cases catheter removal is also warranted. ❑ Additional therapies for relapsing or recurrent peritonitis may include fibrinolytic agents and peritoneal lavage. ❑ Most episodes of peritoneal dialysis-associated peritonitis resolves with outpatient antibiotic treatment. ❑ Initial empiric antibiotic coverage for peritoneal dialysis-associated peritonitis consists of coverage for gram-positive organisms (by vancomycin or a first-generation cephalosporin) and gram-negative organisms (by a third-generation cephalosporin or an amino glycoside). ❑ Subsequently, the regimen adjusted based on culture and sensitivity data. ❑ Cure rates are approximately 75%.
SSecondary peritonitis	Acute bacterial secondary peritonitis	❑ Occurs after perforating, penetrating, inflammatory, infectious, or ischemic injuries of the GI or GU tracts. ❑ Most often follows disruption of a hollow viscus→chemical peritonitis→bacterial peritonitis (polymicrobial, includes aerobic gram-negative {E coli, Klebsiella, Enterobacter, Proteus mirabilis} and gram-positive { Enterococcus, Streptococcus} and anaerobes {Bacteroides, clostridia}). ❑ Presents with abdominal pain, tenderness, guarding or rigidity, distention, free peritoneal air, and diminished bowel sounds—signs that reflect irritation of the parietal peritoneum resulting ileus. ❑ Systemic findings include fever, chills or rigors, tachycardia, sweating, tachypnea, restlessness, dehydration, oliguria, disorientation, and, ultimately, refractory shock. ❑ Peritoneal lavage, Laparoscopy are the treatment of choice.
	Biliary peritonitis	❑ Most often seen in cases of rupture of pathological gallbladder or bile duct or cholangitic abscess or secondary to obstruction of the biliary tract. ❑ Usually seen in alcoholic patients with ascites.
	Tertiary peritonitis	❑ Persistence or recurrence of intraabdominal infection following apparently adequate therapy of primary or secondary peritonitis. ❑ Enterococcus,Candida, Staphylococcus epidermidis, and Enterobacter are the most common organisms. ❑ Characterized by lack of response to appropriate surgical and antibiotic therapy due to disturbance in the hosts immune response. ❑ Associated with high mortality due to multi organ dysfunction. ❑ It presents in a similar way as other peritonitis but is recognized as an adverse outcome with poor prognosis.
	Familial Mediterranean fever (periodic peritonitis, familial paroxysmal polyserositis)	❑ Rare genetic condition which affects individuals of Mediterranean genetic background. ❑ Etiology is unclear. ❑ Presents with recurrent bouts of abdominal pain and tenderness along with pleuritic or joint pain. ❑ Fever and leukocytosis are common. ❑ Colchicine prevents but does not treat acute attacks.
	Granulomatous peritonitis	❑ A rare condition caused by disposable surgical fabrics or food particles from a perforated ulcer, eliciting a vigorous granulomatous (delayed hypersensitivity) response in some patients 2-6 weeks after laparotomy. ❑ Presents with abdominal pain, fever, nausea and vomiting, ileus, and systemic complaints, mild and diffuse abdominal tenderness. ❑ Diagnosed by the demonstration of diagnostic Maltese cross pattern of starch particles. ❑ Treated with corticosteroids or anti-inflammatory agents. ❑ The disease is self-liniting.
	Sclerosing encapsulating peritonitis	❑ Seen in conditions associated with long term peritoneal dialysis, shunts like VP & PV, history of abdominal surgeries, liver transplantation. ❑ Symptoms include nausea, abdominal pain, diarrhea, anorexia, bloody ascites.
	Intraperitoneal abscesses	❑ Most common etiologies include Gastrointestinal perforations, postoperative complications, and penetrating injuries. ❑ Signs and symptoms depend on the location of the abscess within the peritoneal cavity and the extent of involvement of the surrounding structures. ❑ Diagnosis is suspected in any patient with a predisposing condition. ❑ In a third of cases it occurs as a sequela of generalized peritonitis. ❑ The pathogenic organisms are similar to those for peritonitis, but anaerobic organisms occupy an important role. ❑ Diagnosed best by CT scan of the abdomen. ❑ Treatment consists of prompt and complete CT or Ultrasound guided drainage of the abscess, control of the primary cause, and adjunctive use of effective antibiotics. ❑ Open drainage is reserved for abscesses for which percutaneous drainage is inappropriate or unsuccessful. ❑ The mortality rate of serious intra-abdominal abscesses is about 30%.
	Peritoneal mesothelioma	❑ Arises from the mesothelium lining the peritoneal cavity. ❑ Its incidence is approximately 300-500 new cases being diagnosed in the United States each year. ❑ As with pleural mesothelioma, there is an association with an asbestos exposure. ❑ Most commonly affects men at the age of 50-69 years. ❑ Patients most often present with abdominal pain and later increased abdominal girth and ascites along with anorexia, weight loss and abdominal pain. ❑ CT with intravenous contrast typically demonstrates the thickening of the peritoneum. ❑ Laparoscopy with tissue biopsy or CT guided tissue biopsy with immunohistochemical staining for calretinin, cytokeratin 5/6, mesothelin, and Wilms tumor 1 antigen remain the gold standard for diagnosis. ❑ Mean time from diagnosis to death is less than 1 year without treatment. ❑ At laparotomy the goal is cytoreduction with excision. ❑ Debulking surgery and intraperitoneal chemotherapy improves survival in some cases.
	peritoneal carcinomatosis	❑ Associated with a history of ovarian or GI tract malignancy. ❑ Symptoms include ascites, abdominal pain, nausea and vomiting.

Natural history, complications and prognosis of peritonitis

The stronger predictors of poor outcome both in SBP and secondary BP patients include the concurrent development of sepsis and subsequent multiple organ failure (MOF). Sepsis may progress to conditions of varying severity. There is an increased risk of death along transition from sepsis to severe sepsis and septic shock. With insufficient treatment, sepsis may cause functional impairment of one or more organs or systems and finally lead to MOF. There is a strong correlation between mortality rate and number of failing organs. Several scoring systems have been developed to assess the clinical prognosis of patients with bacterial peritonitis. The most widely used include the APACHE-II, Mannheim Peritonitis Index (MPI), the Multiple Organ Dysfunction Score (MODS), and the Sepsis-related Organ Failure Assessment (SOFA) score. Most of the scores are based on host criteria, systemic signs of sepsis, and complications related to organ failure but these scores have limited significance in the specific, day-to-day clinical decision-making process for each individual patient.