Peritonitis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]
Synonyms and keywords:Peritoneal inflammation

Overview

Peritonitis defined as inflammation of peritoneum (serosal membrane lining the abdominal cavity and abdominal viscera) and is associated with high mortality rate secondary to bacteremia and sepsis syndrome. Most common cause of peritonitis in approximately 80% adults is perforation of the gastrointestinal or biliary tract. Other less common causes include liver cirrhosis, and peritoneal dialysis associated peritonitis. Peritonitis can also result from injury, contamination with microorganisms, chemicals or both. It may be localized or generalized, and can have an acute course in infection secondary to rupture of a hollow viscus or follows a chronic course as seen in tuberculous peritonitis. Patients present with severe abdominal pain associated with fever, chills, nausea and vomiting. Peritonitis must be differentiated from other diseases affecting the peritoneum such as peritoneal abscess, peritoneal mesothelioma and peritoneal carcinomatosis which presents with ascites and abdominal pain. Peritonitis is a emergency medical condition requiring prompt medical attention and treatment.

Causes

	Common causes	Less common causes	Comment
Spontaneous bacterial peritonitis	Aerobic gram-negative bacteria, such as Escherichia coli Gram-positive cocci, such as Streptococcus Enterococcus	Staphylococcus aureus Streptococcus salivarius Poly-microbial infection	To see a complete list of causes, click here.
Secondary peritonitis	Gram-negative bacilli (e.g. Escherichia coli), Anaerobic bacteria (e.g. Bacteroides fragilis) Enterobacter cloacae	Staphylococcus epidermidis Propionibacterium species Pseudomonas Enterococcus Candida	To see a complete list of causes, click here.

Classification

Peritonitis is classified based on the cause of the inflammatory process and the character of microbial contamination as follows:^[1]^[2]^[3]

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

Differential diagnosis

Classification of acute abdomen based on etiology		Presentation	Symptoms			Signs			Diagnosis		Comments
Classification of acute abdomen based on etiology		Presentation	Fever	Abdominal Pain	Jaundice	Guarding	Rebound Tenderness	Bowel sounds	Lab Findings	Imaging	Comments
Common causes of Peritonitis	Primary Peritonitis	Spontaneous bacterial peritonitis	+	Diffuse	–	–	–	Hypoactive	Ascitic fluid PMN>250 cells/mm³ Culture: Positive for single organism	Ultrasound for evaluation of liver cirrhosis	–
	Secondary Peritonitis	Perforated gastric and duodenal ulcer	+	Diffuse	–	+	+	N	Ascitic fluid LDH > serum LDH Glucose < 50mg/dl Total protein > 1g/dl	Air under diaphragm in upright CXR	Upper GI endoscopy for diagnosis
		Acute cholangitis	+	RUQ	+	–	–	N	Abnormal LFT	Ultrasound shows biliary dilatation	Biliary drainage (ERCP) + IV antibiotics
		Acute cholecystitis	+	RUQ	+	–	–	Hypoactive	Hyperbilirubinemia Leukocytosis	Ultrasound shows gallstone and evidence of inflammation	Murphy’s sign
		Acute pancreatitis	+	Epigastric	+/-	–	–	N	Increased amylase / lipase	Ultrasound shows evidence of inflammation	Pain radiation to back
		Acute appendicitis	+	RLQ	–	+	+	Hypoactive	Leukocytosis	Ultrasound shows evidence of inflammation	Nausea & vomiting, decreased appetite
		Acute diverticulitis	+	LLQ	+/-	+	–	Hypoactive	Leukocytosis	CT scan and ultrasound shows evidence of inflammation
		Acute salpingitis	+	LLQ/ RLQ	–	+/-	+/-	N	Leukocytosis	Pelvic ultrasound	Vaginal discharge
Hollow Viscous Obstruction		Small intestine obstruction	–	Diffuse	–	+	+/-	Hyperactive then absent	Leukocytosis	Abdominal X ray	Nausea & vomiting associated with constipation, abdominal distention
		Volvulus	–	Diffuse	–	+	–	Hypoactive	Leukocytosis	CT scan and abdominal X ray	Nausea & vomiting associated with constipation, abdominal distention
		Biliary colic	–	RUQ	+	–	–	N	Increased bilirubin and alkaline phosphatase	Ultrasound	Nausea & vomiting
		Renal colic	–	Flank pain	–	–	–	N	Hematuria	CT scan and ultrasound	Colicky abdominal pain associated with nausea & vomiting
Vascular Disorders	Ischemic causes	Mesenteric ischemia	+/-	Periumbilical	–	–	–	Hyperactive	Leukocytosis and lactic acidosis	CT scan	Nausea & vomiting, normal physical examination
	Ischemic causes	Acute ischemic colitis	+/-	Diffuse	–	+	+	Hyperactive then absent	Leukocytosis	CT scan	Nausea & vomiting
	Hemorrhagic causes	Ruptured abdominal aortic aneurysm	–	Diffuse	–	–	–	N	Normal	CT scan	Unstable hemodynamics
	Hemorrhagic causes	Intra-abdominal or retroperitoneal hemorrhage	–	Diffuse	–	–	–	N	Anemia	CT scan	History of trauma
Gynaecological Causes	Ovarian Cyst Complications	Torsion of the cyst	–	RLQ / LLQ	–	+/-	+/-	N	Increased ESR and CRP	Ultrasound	Sudden onset sever pain with nausea and vomiting
	Ovarian Cyst Complications	Cyst rupture	–	RLQ / LLQ	–	+/-	+/-	N	Increased ESR and CRP	Ultrasound	Sudden onset sever pain with nausea and vomiting
	Pregnancy	Ruptured ectopic pregnancy	–	RLQ / LLQ	–	–	–	N	Positive pregnancy test	Ultrasound	History of missed period and vaginal bleeding

**Differentiating the different causes of peritonitis**
Disease		Prominent clinical findings	Lab tests	Tratment
Primary peritonitis	Spontaneous bacterial peritonitis	Absence of GI perforation, most closely associated with cirrhosis and advanced liver disease. Presents with abrupt onset of fever, abdominal pain, distension, and rebound tenderness.	Most have clinical and biochemical manifestations of advanced cirrhosis or nephrosis like leukocytosis,hypoalbuminemia, Prolonged prothrombin time. SAAG >1.1 g/dL, increased serum lactic acid level, or a decreased ascitic fluid pH (< 7.31) supports the diagnosis. Gram staining reveals bacteria in only 25% of cases. Diagnosed by analysis of the ascitic fluid which reveals WBC > 500/ML, and PMN >250cells/ml. 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,it 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 and 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.
	Continuous Ambulatory Peritoneal Dialysis (CAPD peritonitis)	Peritonitis is one of the major complications of peritoneal dialysis & 72.6% occurred within the first six months of peritoneal dialysis. Historically, coagulase-negative staphylococci were the most common cause of peritonitis in CAPD, presumably due to touch contamination or infection via the pericatheter route. 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 resolve with outpatient antibiotic treatment.	Majority of peritonitis 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%.	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 aminoglycoside). Subsequently, the regimen should be adjusted based on culture and sensitivity data. Cure rates are approximately 75%.
Secondary 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, distension, 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.
Secondary peritonitis	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. Seen in alcoholic patients with ascites.
Tertiary peritonitis		Persistence or recurrence of intraabdominal infection following apparently adequate therapy of primary or secondary peritonitis. 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.	Enterococcus, Candida, Staphylococcus epidermidis, and Enterobacter being the most common organisms.	Characterized by lack of response to appropriate surgical and antibiotic therapy due to disturbance in the hosts immune response.
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.	The disease is self-limiting. Treated with corticosteroids or anti-inflammatory agents.
Sclerosing encapsulating peritonitis		Seen in conditions associated with long term peritoneal dialysis, shunts like VP shunts, history of abdominal surgeries, liver transplantation. Symptoms include nausea, abdominal pain, diarrhea, anorexia, bloody ascites.
Intraperitoneal abscesses		Most common etiologies being 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 responsible for peritonitis, but anaerobic organisms occupy an important role. The mortality rate of serious intra-abdominal abscesses is about 30%.	Diagnosed best by CT scan of the abdomen.	Treatment consists of prompt and complete CT or US 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.
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. Mean time from diagnosis to death is less than 1 year without treatment.	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.	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, vomiting.

**Differentiating secondary peritonitis from spontaneous bacterial peritonitis**
Characteristic	Spontaneous bacterial peritonitis	Secondary peritonitis
Presentaion	Main manifestations of peritonitis are acute abdominal pain, tenderness, and guarding, which are exacerbated by moving the peritoneum, e.g. coughing, flexing the hips, or elicitingthe Blumberg sign (a.k.a. rebound tenderness)	Similar presentation but insidious onset unlike rapid onset in SBP
Microorganism	Monomicrobial involvement is common No identifiable source of intra-abdominal infection	Polymicrobial involvement is common Identifiable source of intra-abdominal infection, with or without perforation (surgically treatable source)^[4]
Diagnostic criteria	SBP is diagnosed in the presence of:^[5] Ascitic fluid PMN count of =250/mm3 No evident intra-abdominal source of infection Positive ascitic fluid bacterial culture	Diagnosed in the presence of Positive ascitic fluid bacterial culture Ascitic fluid PMN count of =250/mm3 Evidence of a source of infection (demonstrated at surgery or autopsy], either intra-abdominal or contiguous with the peritoneal cavity
Follow-up paracentesis	Ascitic fluid usually became sterile after one dose of antibiotic	Failure of the ascitic fluid to become culture-negative despite of initial antibiotic treatment, appears to be typical of secondary peritonitis due to continuous spillage of organisms into abdominal cavity which requires surgery.^[6]^[7]

References

↑ Wittmann DH, Schein M, Condon RE (1996). “Management of secondary peritonitis”. Ann Surg. 224 (1): 10–8. PMC 1235241. PMID 8678610.
↑ Nathens AB, Rotstein OD, Marshall JC (1998) Tertiary peritonitis: clinical features of a complex nosocomial infection. World J Surg 22 (2):158-63. PMID: 9451931
↑ Mishra SP, Tiwary SK, Mishra M, Gupta SK (2014) An introduction of Tertiary Peritonitis. J Emerg Trauma Shock 7 (2):121-3. DOI:10.4103/0974-2700.130883 PMID: 24812458
↑ Runyon BA, Hoefs JC (1984). “Ascitic fluid analysis in the differentiation of spontaneous bacterial peritonitis from gastrointestinal tract perforation into ascitic fluid”. Hepatology. 4 (3): 447–50. PMID 6724512.
↑ Runyon BA, Hoefs JC (1986). “Spontaneous vs secondary bacterial peritonitis. Differentiation by response of ascitic fluid neutrophil count to antimicrobial therapy”. Arch Intern Med. 146 (8): 1563–5. PMID 3729637.
↑ Runyon BA (1986). “Bacterial peritonitis secondary to a perinephric abscess. Case report and differentiation from spontaneous bacterial peritonitis”. Am J Med. 80 (5): 997–8. PMID 3518442.
↑ Akriviadis EA, Runyon BA (1990). “Utility of an algorithm in differentiating spontaneous from secondary bacterial peritonitis”. Gastroenterology. 98 (1): 127–33. PMID 2293571.

[pmid8678610-1] Wittmann DH, Schein M, Condon RE (1996). “Management of secondary peritonitis”. Ann Surg. 224 (1): 10–8. PMC 1235241. PMID 8678610.

[pmid9451931-2] Nathens AB, Rotstein OD, Marshall JC (1998) Tertiary peritonitis: clinical features of a complex nosocomial infection. World J Surg 22 (2):158-63. PMID: 9451931

[pmid24812458-3] Mishra SP, Tiwary SK, Mishra M, Gupta SK (2014) An introduction of Tertiary Peritonitis. J Emerg Trauma Shock 7 (2):121-3. DOI:10.4103/0974-2700.130883 PMID: 24812458

[pmid6724512-4] Runyon BA, Hoefs JC (1984). “Ascitic fluid analysis in the differentiation of spontaneous bacterial peritonitis from gastrointestinal tract perforation into ascitic fluid”. Hepatology. 4 (3): 447–50. PMID 6724512.

[pmid3729637-5] Runyon BA, Hoefs JC (1986). “Spontaneous vs secondary bacterial peritonitis. Differentiation by response of ascitic fluid neutrophil count to antimicrobial therapy”. Arch Intern Med. 146 (8): 1563–5. PMID 3729637.

[pmid3518442-6] Runyon BA (1986). “Bacterial peritonitis secondary to a perinephric abscess. Case report and differentiation from spontaneous bacterial peritonitis”. Am J Med. 80 (5): 997–8. PMID 3518442.

[pmid2293571-7] Akriviadis EA, Runyon BA (1990). “Utility of an algorithm in differentiating spontaneous from secondary bacterial peritonitis”. Gastroenterology. 98 (1): 127–33. PMID 2293571.

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Peritonitis

Overview

Causes

Classification

Differential diagnosis

References

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