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This is a term used for a condition in which inflammation occurs in the peritoneum itself rather than as a result of pathology arising in another organ. Bacterial infection arising from intraperitoneal dialysis is a typical example. Spontaneous bacterial peritonitis (SBP) is a specific condition which occurs in patients with ascites secondary to chronic liver disease; it is seen mainly in hospitalised patients and is rare in asymptomatic outpatients.
This occurs when a pathological process adjacent to the peritoneum causes inflammation. Perforation of a viscus is a typical example.
This term is used when the inflammation is in a limited area, such as adjacent to an inflamed appendix or diverticulum prior to rupture.
As one might suspect, this term is used when the inflammation is widespread - eg, after the rupture of a viscus.
This is a term used for any intra-abdominal infection and encompasses both localised and generalised peritonitis.
These are localised collections of infected fluid and can be simple or complex (multiloculated). The most common areas are subhepatic, pelvic and paracolic gutters but abscesses can also develop in the lesser sac, perisplenic area and between small loops of bowel and their omentum.
Histopathology of peritonitis
The pathological process underpinning peritonitis involves the omentum (the 'abdominal policeman') which attempts to confine the area by wrapping around the infection. Adjacent bowel and fibrinous adhesions are also involved. It is thought that chemical mechanisms such as the release of cytokines and antimicrobial peptides also contribute to the process. If this process fails, generalised life-threatening peritonitis occurs.
The cause of intra-abdominal sepsis and abscesses is wide. Examples include:
- Upper gastrointestinal tract (oesophagus, stomach and duodenum) - malignancy, trauma, peptic ulcer perforation, iatrogenic (eg, endoscopy).
- Lower gastrointestinal tract (colon, caecum, rectum and anus) - ischaemic bowel, diverticulitis, hernia, obstruction, inflammatory bowel disease, appendicitis, trauma.
- Liver/biliary tract/pancreas/spleen/kidneys - cholecystitis. malignancy, pancreatitis, endocarditis.
- Genitourinary tract - pelvic inflammatory disease, malignancy.
The incidence depends on the cause. In a hospital setting the prevalence of SBP is around 10%.Three studies of patients with perforated appendicitis found an incidence of postoperative abscess formation of 20%. Another study of patients undergoing appendectomy found an incidence of localised and generalised peritonitis of 26.4% and 14.0% respectively.
The symptoms are highly variable and depend on the location of the abscess. Symptoms may include fever, pain anywhere in the abdomen, diarrhoea or ileus. A subphrenic abscess can cause chest pain and also shoulder pain. Psoas muscle abscesses may lead to flank pain which radiates to the groin.
The principal feature is abdominal pain. Depending on the site of the infection and the underlying pathology, it may be insidious, dull and poorly localised from the outset, becoming gradually worse and more localised as the infection spreads. More generalised pain may develop if the condition is not contained. In some cases (eg, gastric perforation) acute generalised pain is present from the onset. Anorexia, nausea and vomiting may also be present.
The temperature chart is typically described as 'swinging' or 'spikey' (swinging pyrexia). There may be a palpable abdominal inflammatory mass or a hot tender mass on rectal examination (typical after appendectomy). In the early stages, the clinical picture may be one of an ill patient with few physical signs, especially if the abscess is deep-seated.
The patient usually appears unwell and distressed. A high fever is present in the initial stages but in severe peritonitis there may be hypothermia. Tachycardia is usually present. The classic abdominal signs are tenderness on palpation, guarding and rebound tenderness. The tenderness will be maximal over the area of pathology. Severely ill patients will have rigidity and may lie with their knees flexed to minimise movement of the abdominal wall. They may be hypotensive due to dehydration and show signs of septic shock. Bowel sounds may be absent. Rectal examination may increase the abdominal pain (typically to the right if the appendix is involved and anteriorly if there is pelvic inflammation).
These will depend on the suspected pathology but the following are likely to be contributory in most cases.
- FBC - there is usually a leukocytosis.
- U&Es and creatinine - dehydration may be present.
- LFTs, amylase and lipase - particularly if pancreatitis is suspected.
- Blood cultures - aerobic and anaerobic to exclude blood sepsis.
- Peritoneal fluid - for culture and amylase level.
- Urinalysis - to exclude renal tract pathology.
- Imaging - this may include abdominal X-ray, upright CXR, ultrasound, CT scanning, MRI and contrast studies.
Antibiotics are usually required parenterally. Treatment should be based on the results of blood or abscess culture material. Both aerobic and anaerobic organisms need to be dealt with, so a combination of two agents or a broad-spectrum antibiotic is required.
'To drain or not to drain' is a question which has been raging in the literature for many years, The question has to a large extent been answered with the advent of percutaneous drainage under CT or ultrasound guidance. This is relatively low-risk and effective in the majority of patients. Failure is usually due to other complicating factors, such as immune deficiency (the abscess is often tubercular) or multilocular abscesses.
SBP will initially require a third-generation cefalosporin, with further therapy guided by microbiological culture results. In secondary peritonitis, systemic antibiotic therapy is also used but patients may also need organ support. Best results are achieved when antibiotics are started early. All patients are likely to require supportive therapy with intravenous fluids.
An attempt to identify the cause of the infection should be made prior to surgery if possible. In the early stages it may be possible to adopt a 'wait and see' approach (particularly if pancreatitis is suspected); otherwise, the options are localised percutaneous drainage of abscesses, open surgery or laparoscopy. The choice will depend on the likely pathology and the clinical state of the patient. Emergency exploratory surgery will be required if the patient is rapidly deteriorating, even if the underlying cause cannot be found. Open surgery is also indicated if there is significant intestinal distension or extensive oedema of the abdominal wall, or organ oedema. In such circumstances, primary fascial closure under tension may be difficult and is associated with multiple organ failure, necrotising abdominal wall infection and increased mortality. An initial operation may be required for drainage and to remove necrotic tissue. Further operations may then follow to remove the abscess completely.
Pancreatitis-associated peritonitis often needs intensive medical treatment for 12-24 hours before any surgical procedures are contemplated. Surgical debridement and repeated exploration are preferred and a percutaneous approach should be avoided unless defined collections of fluid around the pancreas require drainage in stable patients.
The prognosis has improved considerably with the advent of drainage under CT scanning. Deaths are generally due to the underlying disease process or unsuspected foci of infection. Risk factors for adverse clinical outcomes include older age and need for multiple surgical procedures.
The main prognostic factor in SBP in cirrhotic patients is renal dysfunction. One study reported that the mortality rate among patients with renal dysfunction was 67%, compared with only 11% of patients who maintained normal renal function.
Various scoring systems have been used to predict the prognosis of peritonitis, most of which rely on systemic signs of the patient and the degree, if any, of organ failure. One of the most commonly used is the Acute Physiology and Chronic Health Evaluation II (APACHE II) scoring system.
One study found that the prognosis in secondary peritonitis was more related to the organisms present in peritoneal fluid than to the cause of the peritonitis. Thus, whereas there was no difference in the incidence of shock and outcome between patients with postoperative peritonitis and those with community-acquired peritonitis, enterococci and yeast in the peritoneal fluid were associated with worse outcome. Biliary origin of peritonitis was an independent risk factor for mortality.
Further reading and references
; Prevalence and risk factors for unsuspected spontaneous ascitic fluid infection in cirrhotics undergoing therapeutic paracentesis in an outpatient clinic. Indian J Gastroenterol. 2011 Sep30(5):221-4. Epub 2011 Sep 29.
; The anti-inflammatory and antibacterial basis of human omental defense: selective expression of cytokines and antimicrobial peptides. PLoS One. 20116(5):e20446. Epub 2011 May 24.
; EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis. J Hepatol. 2010 Sep53(3):397-417. doi: 10.1016/j.jhep.2010.05.004. Epub 2010 Jun 1.
; A clinicopathological review of 324 appendices removed for acute appendicitis in Durban, South Africa: a retrospective analysis. Ann R Coll Surg Engl. 2009 Nov91(8):688-92.
; Current concepts in the management of tuberculosis. Mayo Clin Proc. 2011 Apr86(4):348-61.
; Renal dysfunction is the most important independent predictor of mortality in cirrhotic patients with spontaneous bacterial peritonitis. Clin Gastroenterol Hepatol. 2011 Mar9(3):260-5. Epub 2010 Dec 8.
; APACHE II scoring system is superior in the prediction of the outcome in critically ill patients with perforative peritonitis. Med Arh. 201165(2):82-5.
; Factors associated with septic shock and mortality in generalized peritonitis: comparison between community-acquired and postoperative peritonitis. Crit Care. 200913(3):R99. Epub 2009 Jun 24.
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