Peritonitis overview

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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]

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.

For more information related to Primary peritonitis click here
For more information related to Secondary peritonitis click here

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 (result of alcoholism), 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 is a emergency medical/surgical condition requiring prompt medical attention and treatment.

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.[1]

Historical Perspective

  • The first reports of SBP were seen in the German and French literatures between 1907 and 1958. Krencker 1907; Brule et al 1939; Cachin 1955; Navasa et al 1999 described that ascitic fluid infections were common in patients with liver cirrhosis. In 1963, Kerr and colleagues reported SBP as a complication in patients diagnosed with liver cirrhosis. Kerr and colleagues (1963) described 11 episodes of ascitic fluid infection in 9 cirrhotic patients. In 1964, Harold O.Conn introduced the term “spontaneous bacterial peritonitis” for the first time in English literature. [2][3][4][5]

Classification

Peritonitis is classified based on the etiology, based on the ascitic fluid analysis and based on the clinical setting in which peritonitis is present. Commonly used classification is based on the etiology and is classified into 3 subtypes: primary peritonitis, secondary peritonitis, and tertiary peritonitis.

Primary or Spontaneous Peritonitis Secondary Peritonitis Tertiary Peritonitis
  • Primary peritonitis/ spontaneous bacterial peritonitis (SBP) represents a group of diseases with different causes characterized by ascitic fluid infection of the peritoneal cavity without an evident surgically treatable intra-abdominal source of infection.
  • It is usually associated with cirrhosis and ascites in adults.[6]
  • Primary peritonitis lacks an identifiable anatomical derangement.[7]
  • Secondary peritonitis is defined as the infection of the peritoneum due to spillage of organisms into the peritoneal cavity resulting from hollow viscus perforation, anastomotic leak, ischemic necrosis, or other injuries of the gastrointestinal tract.[8]
  • Tertiary peritonitis is defined as the persistent or recurrent intra-abdominal infection that occurs in ≥48 hours following the successful and adequate surgical source control of primary or secondary peritonitis.[8][9][10]

Pathophysiology

Peritonitis results from contamination of normal sterile peritoneal cavity with infections or chemical irritants. Spillage of bile or gastric juices following a perforation of hollow viscus into the peritoneal cavity results in chemical peritonitis initially, which is followed by infection when bacteria enter and contaminate the peritoneal cavity. Bacterial peritonitis is usually caused by normal enteric flora such as 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 diagnosed early and treated adequately.

Causes

There are two forms of peritonitis: Spontaneous bacterial peritonitis (SBP) is the result of an infection of the fluid in the peritoneal cavity. Liver or kidney failure can cause this condition. Patients on peritoneal dialysis for kidney failure are also at an increased risk for SBP.Secondary peritonitis is usually due to an infection that has spread from GI tract due to perforation of the hollow viscus.The most common cause of peritonitis are 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.

Differential Diagnosis

Peritonitis has to be differentiated from other other diseases effecting the peritoneum such as peritoneal abscesses, peritoneal mesothelioma and peritoneal carcinomatosis which presents with ascites and abdominal pain.It also has to be differentiated from different forms of peritonitis like SBP, secondary peritonitis, tuberculous, CAPD peritonitis etc.Peritonitis also has to be differentiated from other causes of acute abdomen like appendicitis, diverticulitis etc.

Epidemiology and Demographics

Risk Factors

Patients with advanced liver and kidney disease are at an increased risk for SBP. Risk factors for liver disease include alcoholic cirrhosis and other diseases that lead to cirrhosis, such as viral hepatitis (Hepatitis B or C). Spontaneous peritonitis also occurs in patients who are on dialysis and chronic infections like tuberculosis.Secondary peritonitis results from rupture of a hollo viscus .

Screening

There is no routine screening for peritonitis.

Natural History, Complications and Prognosis

The prognosis depends on the cause of infection, clinical condition of the patient and the rate of progression of the disease before treatment.With timely and appropriate medical or surgical treatment for the control of local infection before it has spread systemically, patients usually do well. Without treatment, the outcome is usually poor because of entry of infection into the bloodstream causing shock and damage to other organs like kidney,liver and lung. However, in some cases, and patients with immunosuppression do poorly even with prompt and appropriate treatment.The potential complications of SBP include: progression of the liver disease leading to hepatic encephalopathy and kidney failure from hepatic-renal syndrome and sepsis.The potential complications of secondary peritonitis are progression to intra abdominal abscess, intra-peritoneal adhesions, and septic shock.

Diagnosis

History and Symptoms

The main manifestations of peritonitis are acute abdominal pain.

Physical Examination

tenderness, and guarding, which are exacerbated by moving the peritoneum, e.g. coughing, flexing the hips, or eliciting the Blumberg sign (a.k.a. rebound tenderness, meaning that pressing a hand on the abdomen elicits pain, but releasing the hand abruptly will aggravate the pain, as the peritoneum snaps back into place). Abdominal pain and tenderness: The localization of these manifestations depends on whether peritonitis is localized (e.g. appendicitis or diverticulitis before perforation), or generalized to the whole abdomen; even in the latter case, pain typically starts at the site of the causing disease. Peritonitis is an example of acute abdomen.

Laboratory Findings

A diagnosis of peritonitis is based primarily on clinical grounds, that is on the clinical manifestations described above; if they support a strong suspicion of peritonitis, no further investigation should delay surgery. Leukocytosis and acidosis may be present, but they are not specific findings.

Imaging Findings

Plain abdominal X-rays may reveal dilated, oedematous intestines, although it is mainly useful to look for pneumoperitoneum (free air in the peritoneal cavity), which may also be visible on chest X-rays. If reasonable doubt still persists, an exploratory peritoneal lavage may be performed (e.g. in cause of trauma, in order to look for white blood cells, red blood cells, or bacteria).

Other Diagnostic Studies

Treatment

Medical Therapy

Antibiotic therapy is the mainstay of treatment for spontaneous bacterial peritonitis.

Surgery

Surgery (laparotomy) is needed to perform a full exploration and lavage of the peritoneum, as well as to correct any gross anatomical damage which may have caused peritonitis.[11] The exception is spontaneous bacterial peritonitis, which does not benefit from surgery.

Prevention

Prevention of peritonitis depends on the form of peritonitis.

References

  1. Wittmann DH, Schein M, Condon RE (1996) Management of secondary peritonitis. Ann Surg 224 (1):10-8. PMID: 8678610
  2. Ribeiro TC, Chebli JM, Kondo M, Gaburri PD, Chebli LA, Feldner AC (2008). "Spontaneous bacterial peritonitis: How to deal with this life-threatening cirrhosis complication?". Ther Clin Risk Manag. 4 (5): 919–25. PMC 2621420. PMID 19209274.
  3. Garcia-Tsao, Guadalupe (2004). "Spontaneous bacterial peritonitis: a historical perspective". Journal of Hepatology. 41 (4): 522–527. doi:10.1016/j.jhep.2004.09.001. ISSN 0168-8278.
  4. CONN HO (1964). "SPONTANEOUS PERITONITIS AND BACTEREMIA IN LAENNEC'S CIRRHOSIS CAUSED BY ENTERIC ORGANISMS. A RELATIVELY COMMON BUT RARELY RECOGNIZED SYNDROME". Ann Intern Med. 60: 568–80. PMID 14138877.
  5. Crossley IR, Williams R (1985). "Spontaneous bacterial peritonitis". Gut. 26 (4): 325–31. PMC 1432517. PMID 3884467.
  6. Wiest R, Krag A, Gerbes A (2012) Spontaneous bacterial peritonitis: recent guidelines and beyond. Gut 61 (2):297-310. DOI:10.1136/gutjnl-2011-300779 PMID: 22147550
  7. 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
  8. 8.0 8.1 Calandra T, Cohen J, International Sepsis Forum Definition of Infection in the ICU Consensus Conference (2005) The international sepsis forum consensus conference on definitions of infection in the intensive care unit. Crit Care Med 33 (7):1538-48. PMID: 16003060
  9. Evans HL, Raymond DP, Pelletier SJ, Crabtree TD, Pruett TL, Sawyer RG (2001) Tertiary peritonitis (recurrent diffuse or localized disease) is not an independent predictor of mortality in surgical patients with intraabdominal infection. Surg Infect (Larchmt) 2 (4):255-63; discussion 264-5. DOI:10.1089/10962960152813296 PMID: 12593701
  10. 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
  11. "Peritonitis: Emergencies: Merck Manual Home Edition". Retrieved 2007-11-25.


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