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{{SK}} 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 [[Spontaneous bacterial peritonitis|click here]]'''''<br>
'''''For more information related to Secondary peritonitis [[Secondary peritonitis|click here]]'''''
==Overview==
==Overview==
'''Peritonitis''' is defined as [[inflammation]] of the [[peritoneum]] (the [[serous membrane]] which lines part of the [[abdomen|abdominal cavity]] and some of the [[viscera]] it contains). It may be localised or generalised, generally has an acute course, and may depend on either [[infection]] (often due to rupture of a hollow [[viscus]]) or on a non-infectious process. Peritonitis generally represents a [[surgical emergency]].
'''Peritonitis''' defined as [[inflammation]] of [[peritoneum]] ( [[serosal membrane]] lining the [[abdomen|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.<ref name="pmid8678610">Wittmann DH, Schein M, Condon RE (1996) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=8678610 Management of secondary peritonitis.] ''Ann Surg'' 224 (1):10-8. PMID: [https://pubmed.gov/8678610 8678610]</ref>


==Historical Perspective==
==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. <ref name="pmid19209274">{{cite journal| author=Ribeiro TC, Chebli JM, Kondo M, Gaburri PD, Chebli LA, Feldner AC| title=Spontaneous bacterial peritonitis: How to deal with this life-threatening cirrhosis complication? | journal=Ther Clin Risk Manag | year= 2008 | volume= 4 | issue= 5 | pages= 919-25 | pmid=19209274 | doi= | pmc=2621420 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19209274  }} </ref><ref name="Garcia-Tsao2004">{{cite journal|last1=Garcia-Tsao|first1=Guadalupe|title=Spontaneous bacterial peritonitis: a historical perspective|journal=Journal of Hepatology|volume=41|issue=4|year=2004|pages=522–527|issn=01688278|doi=10.1016/j.jhep.2004.09.001}}</ref><ref name="pmid14138877">{{cite journal| author=CONN HO| title=SPONTANEOUS PERITONITIS AND BACTEREMIA IN LAENNEC'S CIRRHOSIS CAUSED BY ENTERIC ORGANISMS. A RELATIVELY COMMON BUT RARELY RECOGNIZED SYNDROME. | journal=Ann Intern Med | year= 1964 | volume= 60 | issue=  | pages= 568-80 | pmid=14138877 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14138877  }} </ref><ref name="pmid3884467">{{cite journal| author=Crossley IR, Williams R| title=Spontaneous bacterial peritonitis. | journal=Gut | year= 1985 | volume= 26 | issue= 4 | pages= 325-31 | pmid=3884467 | doi= | pmc=1432517 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3884467  }} </ref>


==Classification==
==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.
{| class="wikitable"
|-
! style = "width: 33%;" |  '''Primary or Spontaneous Peritonitis'''
! style = "width: 34%;" |  '''Secondary Peritonitis'''
! style = "width: 33%;" |  '''Tertiary Peritonitis'''
|-
| valign = top |
* 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.<ref name="pmid22147550">Wiest R, Krag A, Gerbes A (2012) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=22147550 Spontaneous bacterial peritonitis: recent guidelines and beyond.] ''Gut'' 61 (2):297-310. [http://dx.doi.org/10.1136/gutjnl-2011-300779 DOI:10.1136/gutjnl-2011-300779] PMID: [https://pubmed.gov/22147550 22147550]</ref>
*Primary peritonitis lacks an identifiable anatomical derangement.<ref name="pmid24812458">Mishra SP, Tiwary SK, Mishra M, Gupta SK (2014) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=24812458 An introduction of Tertiary Peritonitis.] ''J Emerg Trauma Shock'' 7 (2):121-3. [http://dx.doi.org/10.4103/0974-2700.130883 DOI:10.4103/0974-2700.130883] PMID: [https://pubmed.gov/24812458 24812458]</ref>
| valign = top |
* 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.<ref name="pmid16003060">Calandra T, Cohen J, International Sepsis Forum Definition of Infection in the ICU Consensus Conference (2005) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=16003060 The international sepsis forum consensus conference on definitions of infection in the intensive care unit.] ''Crit Care Med'' 33 (7):1538-48. PMID: [https://pubmed.gov/16003060 16003060]</ref>
| valign = top |
* 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.<ref name="pmid16003060">Calandra T, Cohen J, International Sepsis Forum Definition of Infection in the ICU Consensus Conference (2005) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=16003060 The international sepsis forum consensus conference on definitions of infection in the intensive care unit.] ''Crit Care Med'' 33 (7):1538-48. PMID: [https://pubmed.gov/16003060 16003060]</ref><ref name="pmid12593701">Evans HL, Raymond DP, Pelletier SJ, Crabtree TD, Pruett TL, Sawyer RG (2001) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=12593701 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. [http://dx.doi.org/10.1089/10962960152813296 DOI:10.1089/10962960152813296] PMID: [https://pubmed.gov/12593701 12593701]</ref><ref name="pmid9451931">Nathens AB, Rotstein OD, Marshall JC (1998) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=9451931 Tertiary peritonitis: clinical features of a complex nosocomial infection.] ''World J Surg'' 22 (2):158-63. PMID: [https://pubmed.gov/9451931 9451931]</ref>
|}


==Pathophysiology==
==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.
==Pathogenesis==
===Primary peritonitis===
*The '''''route of infection''''' in primary peritonitis is usually not apparent.It is often presumed to be ''hematogenous'', ''lymphogenous'', or transmural migration through an intact gut wall from the intestinal lumen or, in women, from the vagina via the fallopian tubes. <ref name="pmid27920543">{{cite journal| author=Aguirre Valadez JM, Rivera-Espinosa L, Méndez-Guerrero O, Chávez-Pacheco JL, García Juárez I, Torre A| title=Intestinal permeability in a patient with liver cirrhosis. | journal=Ther Clin Risk Manag | year= 2016 | volume= 12 | issue=  | pages= 1729-1748 | pmid=27920543 | doi=10.2147/TCRM.S115902 | pmc=5125722 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27920543  }} </ref>.
===Postulated mechanisms===
*Bacteria have been postulated to migrate from the bowel lumen into mesenteric lymph and to enter the systemic circulation via the thoracic duct(''bacterial translocation'').
*The role of intestinal bacterial overgrowth is uncertain because different studies have provided conflicting results.  <ref name="pmid26301048">{{cite journal| author=Tsiaoussis GI, Assimakopoulos SF, Tsamandas AC, Triantos CK, Thomopoulos KC| title=Intestinal barrier dysfunction in cirrhosis: Current concepts in pathophysiology and clinical implications. | journal=World J Hepatol | year= 2015 | volume= 7 | issue= 17 | pages= 2058-68 | pmid=26301048 | doi=10.4254/wjh.v7.i17.2058 | pmc=4539399 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26301048  }} </ref> <ref name="pmid25400446">{{cite journal| author=Gómez-Hurtado I, Such J, Sanz Y, Francés R| title=Gut microbiota-related complications in cirrhosis. | journal=World J Gastroenterol | year= 2014 | volume= 20 | issue= 42 | pages= 15624-31 | pmid=25400446 | doi=10.3748/wjg.v20.i42.15624 | pmc=4229527 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25400446  }} </ref>.
*Enteric bacteria could also enter the systemic circulation from the portal vein by passage through the liver or by portosystemic shunts in patients with portal hypertension.
*The hepatic reticuloendothelial system is known to be a major site for removal of bacteria from blood. It has been postulated that organisms removed from the systemic circulation by the liver contaminate hepatic lymph and pass through the permeable lymphatic walls into the ascitic fluid.
*Results of animal studies, however, have suggested that destruction of bloodborne bacteria by the reticuloendothelial system is impaired in experimental cirrhosis and in alcoholic liver disease. Infection of ascitic fluid would be facilitated by impaired reticuloendothelial clearance of bacteria from the bloodstream, which would tend to perpetuate bacteremia and increase the opportunity to cause metastatic infection at susceptible sites, such as the ascitic collection.
*In addition, alcohol abuse and cirrhosis have been reported to be associated with impaired intracellular killing by monocytes and neutrophils and with impaired opsonization and low levels of serum complement. The decrease in phagocytic activity seen in alcoholic cirrhosis is proportional to the severity of the liver disease. Impaired local defenses in the peritoneal cavity also facilitate infection of ascites.
*Opsonic activity, as reflected by low levels of complement and immunoglobulins, is reduced in the ascitic fluid of patients with the nephrotic syndrome and cirrhosis.
*Enteric bacteria may also gain access to the peritoneal cavity by directly traversing the intact intestinal wall. In an animal model, E. coli passes from the bowel into the peritoneal cavity after the introduction of hypertonic solutions into the peritoneum. A similar mechanism may explain the enteric bacterial peritonitis that frequently complicates peritoneal dialysis.
*The infrequent occurrence of bacteremia and the multiplicity of species in peritoneal fluid when anaerobic bacteria are involved suggest that transmural migration of bacteria is the probable route of infection of ascitic fluid in most of these patients. In addition, the occurrence of polymicrobial anaerobic peritonitis in two patients after infusion of vasopressin into the superior mesenteric or gastroduodenal arteries suggested that arterial vasoconstriction decreased the intestinal mucosal barrier and permitted transmural migration of enteric organisms.
*When pneumococci are present simultaneously in vaginal secretions and peritoneal fluid in prepubertal girls, an ascending infection of genital origin is likely in these patients. The alkaline vaginal secretions of prepubertal girls may be less inhibitory to bacterial growth than the acidic secretions of postpubertal women.
*Transfallopian spread is also suggested by the development of peritonitis in women with intrauterine devices.
*In women with gonococcal or chlamydial perihepatitis (Fitz-Hugh-Curtis syndrome), the route of spread is presumably from the fallopian tubes and paracolic gutters to the subphrenic space, but it may also be hematogenous.
*Although tuberculous peritonitis may result from direct entry into the peritoneal cavity of tubercle bacilli (from the lymph nodes, intestine, or genital tract in patients with active disease of these organs), it is more likely to result from hematogenous dissemination from remote foci of tuberculosis, most commonly in the lung. Tuberculous peritonitis can become clinically evident after the initial focus has healed completely.
*Infection of ascites stimulates a dramatic increase in proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1, IL-6, interferon-γ (IFN-γ), and soluble adhesion molecules in the serum, as well as, to a much greater extent, in the peritoneal exudate. These cytokines are produced by macrophages and other host cells in response to bacteria or bacterial products, such as endotoxin. In an experimental model of peritonitis, antibodies to endotoxin, but not to TNF-α, were found to prevent death and reduce bacterial numbers in the peritoneal exudate. Another potential source is direct translocation of cytokines through the intestinal barrier. Undoubtedly, many of the systemic and abdominal manifestations of peritonitis are mediated by these molecules. Furthermore, the presence of these cytokines may lead to further reduction of effective arterial blood volume, as indicated by an increase in plasma renin activity and the development of renal insufficiency. Approximately 30% of patients with primary peritonitis develop renal insufficiency, which has been found to be the most sensitive predictor of in-hospital mortality.
 
=='''Secondary peritonitis'''==
*The virulence of the bacteria that cause peritonitis is enhanced when certain microorganisms are either combined intraperitoneally with substances such as mucus, enzymes, or hemoglobin or are combined with certain other microorganisms.  
*Chemical peritonitis can be produced by escape of bile or of gastric or pancreatic secretions into the peritoneal cavity. When ''gastric acid'' escapes into the peritoneal cavity, there is an outpouring of serum protein and electrolytes from the blood into the peritoneal cavity. The acidity is neutralized quickly by these buffers and by diffusion of hydrogen ions into the body fluids. Widespread necrosis may result from enzymatic digestion after intraperitoneal spillage of potent pancreatic enzymes. Escape of ''bile'' into the peritoneal cavity is generally considered to be a grave, often fatal situation. *The severity of peritonitis after escape of these intestinal secretions results in subsequent bacterial peritonitis. *Bacteria may enter the peritoneal cavity with contaminated intestinal secretions through perforations in the gastrointestinal wall or by migration through the wall of the intact gastrointestinal tract in response to irritation of the serosal surface by bile and possibly other intestinal tract secretions.
*Establishment of an anaerobic infection requires a favorable environment. These requirements are usually met by tissue devitalized as a consequence of ischemia, trauma, or neoplastic growth. When proper conditions are obtained, anaerobic organisms can achieve doubling rates equivalent to rates seen with aerobic enteric bacilli. In vivo, the rapidly expanding bacterial and inflammatory cell mass, frequently accompanied by gas production, can interrupt the blood supply to the immediately surrounding tissue and cause further tissue necrosis.
*Gram-negative anaerobic cocci and bacilli (including B. fragilis) possess endotoxins, although with much weaker biologic activity in comparison with endotoxins extracted from their aerobic counterparts. In addition, anaerobes may be resistant to host defenses.


==Causes==
==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]], [[abdominal trauma|blunt abdominal trauma]], [[gastric carcinoma]], [[peptic ulcer]], [[pelvic trauma]], and [[pancreatitis]].


==Causes (Microbiology)==
==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.
==Differentiating Peritonitis from Other Diseases==


==Epidemiology and Demographics==
==Epidemiology and Demographics==


==Risk Factors==
==Risk Factors==
Patients with liver disease are at increased risk. 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]] for [[kidney failure]].
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==
==Screening==
There is no routine screening for peritonitis.


==Natural History, Complications and Prognosis==
==Natural History, Complications and Prognosis==
===Natural History===
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.
 
===Complications===
 
===Prognosis===
With treatment, patients usually do well. Without treatment, the outcome is usually poor. However, in some cases, patients do poorly even with prompt and appropriate treatment.


==Diagnosis==
==Diagnosis==
===Diagnostic Criteria===
===History and Symptoms===
===History and Symptoms===
The main manifestations of peritonitis are acute abdominal [[abdominal pain|pain]], [[abdominal tenderness|tenderness]], and [[abdominal guarding|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).
The main manifestations of peritonitis are acute [[abdominal pain|abdominal pain.]]
 
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]].


===Physical Examination===
===Physical Examination===
[[abdominal tenderness|tenderness]], and [[abdominal guarding|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===
===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. 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 [[physical trauma|trauma]], in order to look for [[white blood cells]], [[red blood cells]], or [[bacteria]]).
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===
===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 [[physical trauma|trauma]], in order to look for [[white blood cells]], [[red blood cells]], or [[bacteria]]).


===Other Diagnostic Studies===
===Other Diagnostic Studies===
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==Treatment==
==Treatment==
===Medical Therapy===
===Medical Therapy===
Antibiotic therapy is the mainstay of treatment for spontaneous bacterial peritonitis.


===Surgery===
===Surgery===
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===Prevention===
===Prevention===
Prevention of peritonitis depends on the form of peritonitis.


==References==
==References==
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[[Category:Surgery]]
[[Category:Surgery]]
[[Category:Emergency medicine]]
[[Category:Emergency medicine]]
[[Category:Infectious disease]]
 


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Latest revision as of 18:41, 18 September 2017

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

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  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.
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  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
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