Intra-abdominal Sepsis and AbscessesIntroductionTerminologyPrimary peritonitis: this is a term used for a condition in which inflammation occurs in the peritoneum itselfrather than as a result of pathology arising in another organ. Bacterial infection arising from intraperitoneal dialysisis a typical example. Spontaneous bacterial peritonitis (SBP) is a specific condition which occurs in patients withascites secondary to chronic liver disease; it is seen mainly in hospitalised patients and is rare in asymptomaticoutpatients. [1]

Secondary peritonitis: this occurs when a pathological process adjacent to the peritoneum causesinflammation. Perforation of a viscus is a typical example.

Localised peritonitis: this term is used when the inflammation is in a limited area, such as adjacent to aninflamed appendix or diverticulum prior to rupture.

Generalised peritonitis: as one might suspect, this term is used when the inflammation is widespread, eg afterthe rupture of a viscus.

Intra-abdominal sepsis: this is a term is used for any intra-abdominal infection and encompasses both localisedand generalised peritonitis.

Abscesses: [2] these are localised collections of infected fluid. Approximately 50% of patients have simpleabscesses, with the remainder having complex multiloculated abscesses, which are divided by fibrous tissueand organisation of infected material. The most common areas are subhepatic, pelvic and paracolic gutters butabscesses can also develop in the lesser sac, perisplenic area and between small loops of bowel and theiromentum.

Histopathology of peritonitisThe pathological process underpinning peritonitis involves the omentum (the 'abdominal policeman') whichattempts to confine the area by wrapping around the infection. Adjacent bowel and fibrinous adhesions are alsoinvolved. It is thought that chemical mechanisms such as the release of cytokines and antimicrobial peptides alsocontribute to the process. If this process fails, generalised life-threatening peritonitis occurs. [3]

Causes

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Causes of Intra-abdominal Sepsis and Abscesses[2]

Source Causes

Oesophagus Boerhaave's syndrome (spontaneous rupture of oesophagus - usually after forcedemesis.Malignancy.Trauma (mostly penetrating).Iatrogenic (usually endoscopy).

Stomach Peptic ulcer perforation.Malignancy (eg adenocarcinoma, lymphoma, gastrointestinal stromal tumour).Trauma (mostly penetrating).Iatrogenic (usually endoscopy).

Duodenum Peptic ulcer perforation.Trauma (blunt and penetrating).Iatrogenic (usually endoscopy).

Biliary tract Cholecystitis.Stone perforation from gallbladder (ie gallstone ileus) or common duct.Malignancy.Choledochal cyst (rare).Trauma (mostly penetrating).Iatrogenic (usually endoscopy).

Pancreas Pancreatitis (eg alcohol, drugs, gallstones).Trauma (blunt and penetrating).Iatrogenic (usually endoscopy).

Small bowel Ischaemic bowel.Incarcerated hernia (internal and external).Closed loop obstruction.Crohn's disease.Malignancy (rare).Meckel's diverticulumTrauma (mostly penetrating)

Large bowel and appendix Ischaemic bowel.Diverticulitis.Malignancy.Ulcerative colitis and Crohn's disease.Appendicitis.Colonic volvulus.Trauma (mostly penetrating).Iatrogenic (usually mechanical or thermal damage, or dehiscence of an anastamosis).

Uterus, salpinx, andovaries

Pelvic inflammatory disease (eg salpingo-oophoritis, tubo-ovarian abscess, ovariancyst).Malignancy (rare).Trauma (uncommon).

EpidemiologyThe incidence depends on the cause. 10-30% of patients with cirrhosis develop spontaneous bacterial peritonitis(SBP). [4] Three studies of patients with perforated appendicitis found an incidence of postoperative abscessformation of 20%. Another study of patients undergoing appendectomy found an incidence of localised andgeneralised peritonitis of 26.4% and 14.0% respectively. [5]

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PresentationSymptomsAbscess - the symptoms are highly variable but may include fever, pain anywhere in the abdomen, diarrhoea orileus. A subphrenic abscess can cause pulmonary symptoms and a pelvic abscess can cause urinarysymptoms. [2]

Peritonitis - the principle feature is abdominal pain. Depending on the site of the infection and the underlyingpathology it may be insidious, dull and poorly localised from the outset, getting gradually worse and morelocalised as the infection spreads. More generalised pain may develop if the condition is not contained. In somecases (eg gastric perforation) acute generalised pain is present from the onset. Anorexia, nausea and vomitingmay precede the pain, particularly if a degree of obstruction is present. [4]

SignsAbscess- the temperature chart is typically described as 'swinging' or 'spikey' (swinging pyrexia). There may bepalpable abdominal inflammatory mass or hot tender mass on rectal examination (typical after appendectomy). Inthe early stages, the clinical picture may be one of an ill patient with few physical signs. There may be little or noabdominal tenderness, particularly if the abscess is deep-seated. [2]

Peritonitis - the patient usually appears unwell and distressed. A high fever is present in the initial stages but insevere peritonitis there may be hypothermia. Tachycardia is usually present. The classic abdominal signs aretenderness on palpation, guarding and rebound tenderness. The tenderness will be maximal over the area ofpathology. Severely ill patients will have rigidity and may lie with their knees flexed to minimise movement of theabdominal wall. They may be hypotensive due to dehydration and show signs of septic shock. Bowel soundsmay be absent. Rectal examination may increase the abdominal pain (typically to the right if the appendix isinvolved and anteriorly if there is pelvic inflammation). [4]

Investigations [2]

These will depend on the suspected pathology but the following are likely to be contributory in most cases.

FBC - there is usually a leukocytosis.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 straight abdominal X-ray, upright CXR, ultrasound, CT scanning, MRI andcontrast studies.

Management [2] [4]

AbscessDrugs - antibiotics are usually required parenterally. Treatment should be based on the results of blood orabscess culture material. Both aerobic and anaerobic organisms need to be dealt with, so a combination of twoagents or a broad spectrum antibiotic (eg ciprofloxacin plus metronidazole) is required.

Surgery - 'To drain or not to drain' is a question which has been raging in the literature for many years, Thequestion has to a large extent been answered with the advent of percutaneous drainage under CT or ultrasoundguidance. This is relatively low-risk and effective in the majority of patients. Failure is usually due to othercomplicating factors, such as immune deficiency (the abscess is often tubercular) or multilocularabscesses. [6] [7]

Peritonitis

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Drugs - spontaneous bacterial peritonitis (SBP) will initially require a third-generation cefalosporin, with furthertherapy guided by microbiological culture results. In secondary peritonitis, the patient is likely to require medicaltreatment to stabilise renal, haemodynamic and pulmonary function, nutritional and metabolic support andsystemic antibiotic therapy. Best results are achieved when antibiotics are started early, before culture results arereceived, with a second- or third-generation cefalosporin (eg cefotaxime) or a quinolone (eg ciprofloxacin) with orwithout metronidazole.

Surgery - an attempt to identify the cause of the infection should be made prior to surgery if possible. In the earlystages it may be possible to adopt a 'wait and see' approach (particularly if pancreatitis is suspected); otherwisethe options are localised percutaneous drainage of abscesses, open surgery or laparoscopy. The choice willdepend on the likely pathology and the clinical state of the patient. Emergency exploratory surgery will be requiredif the patient is rapidly deteriorating, even if the underlying cause cannot be found. Open surgery is also indicatedif there is significant intestinal distension or extensive oedema of the abdominal wall, or organ oedema. In suchcircumstances, primary fascial closure under tension may be difficult and is associated with multiple organfailure, necrotising abdominal wall infection and increased mortality. An initial operation may be required fordrainage and to remove necrotic tissue. A second operation may be required to deal with the underlying pathologyand provide further clearance of infection. Studies suggest that further surgery after this point is less beneficial. [4]

Pancreatitis-associated peritonitis often needs intensive medical treatment for 12-24 hours before any surgicalprocedures are contemplated. Surgical debridement and repeated exploration are preferred and a percutaneousapproach should be avoided unless defined collections of fluid around the pancreas require drainage in stablepatients.

PrognosisAbscess [2]

The prognosis has improved considerably with the advent of drainage under CT scanning. Deaths are generallydue to the underlying disease process or unsuspected foci of infection. Risk factors for adverse clinicaloutcomes include age over 50 and multiple surgical procedures.

PeritonitisThe main prognostic factor in spontaneous bacterial peritonitis (SBP) in cirrhotic patients is renal dysfunction.One study reported that the mortality rate among patients with renal dysfunction was 67%, compared with only11% of patients who maintained normal renal function. [8]

Various scoring systems have been used to predict the prognosis of peritonitis, most of which rely on systemicsigns of the patient and the degree, if any, of organ failure. One of the most commonly used is the AcutePhysiology and Chronic Health Evaluation II (APACHE II) scoring system. [9]

One study found that the prognosis in secondary peritonitis was more related to the organisms present inperitoneal fluid than in the cause of the peritonitis. Thus, whereas there was no difference in incidence of shockand outcome between patients with postoperative and those with community-acquired peritonitis, enterococciand yeast in the peritoneal fluid were associated with worse outcome. Biliary origin of peritonitis was anindependent risk factor for mortality. [10]

Further reading & references1. Mohan P, Venkataraman J; Prevalence and risk factors for unsuspected spontaneous ascitic fluid infection Indian J

Gastroenterol. 2011 Sep;30(5):221-4. Epub 2011 Sep 29.2. Saber AA et al , Abdominal Abscess, Medscape, May 20093. Chandra A, Srivastava RK, Kashyap MP, et al; The anti-inflammatory and antibacterial basis of human omental defense:

selective PLoS One. 2011;6(5):e20446. Epub 2011 May 24.4. Peralta R et al, Surgical Approach to Peritonitis and Abdominal Sepsis, Medscape, Mar 20115. Chamisa I; A clinicopathological review of 324 appendices removed for acute appendicitis in Ann R Coll Surg Engl. 2009

Nov;91(8):688-92.6. Slater B, Acute Abdomen and HIV/AIDS, Mount Sinai School of Medicine, 20037. Sia IG, Wieland ML; Current concepts in the management of tuberculosis. Mayo Clin Proc. 2011 Apr;86(4):348-61.8. Tandon P, Garcia-Tsao G; Renal dysfunction is the most important independent predictor of mortality in Clin Gastroenterol

Hepatol. 2011 Mar;9(3):260-5. Epub 2010 Dec 8.9. Delibegovic S, Markovic D, Hodzic S; APACHE II scoring system is superior in the prediction of the outcome in Med Arh.

2011;65(2):82-5.

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10. Riche FC, Dray X, Laisne MJ, et al; Factors associated with septic shock and mortality in generalized peritonitis: Crit Care.2009;13(3):R99. Epub 2009 Jun 24.

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Original Author:Dr Huw Thomas

Current Version:Dr Laurence Knott

Peer Reviewer:Prof Cathy Jackson

Last Checked:19/01/2012

Document ID:4138 (v22)

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