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Intra-abdominal Sepsis and Abscesses

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Sepsis

Intra-abdominal sepsis is a term generally used for any intra-abdominal infection. It thus encompasses both localised and generalised peritonitis. Spontaneous bacterial peritonitis (SBP) is a common cause of primary peritonitis and occurs in patients with ascites secondary to chronic liver disease.1 The commonest cause of secondary peritonitis is perforation of a visceral organ.

The pathological process involves the omentum (the 'abdominal policeman') which attempts to confine the area by wrapping around the infection.2 Adjacent bowel and fibrinous adhesions are also involved. If this process fails, generalised life-threatening peritonitis occurs.1

Abscess

Abscesses are localised collections of infected fluid. Approximately 50% of patients have simple abscesses, whist the remainder have complex multi-loculated abscess which are divided by fibrous tissue and organisation of infected material. The commonest areas are subhepatic, pelvic and paracolic gutters but abscesses can also develop in the lesser sac, parasplenic and between small loops of bowel and their omentum.3

Causes3

Causes of Intra-abdominal Sepsis and Abscesses3

Source

Causes

Oesophagus
  • Boerhaave's syndrome (spontaneous rupture of oesophagus - usually after forced emesis
  • Malignancy
  • Trauma (mostly penetrating)
  • Iatrogenic (usually endoscopy)
Stomach
  • Peptic ulcer perforation
  • Malignancy (e.g. adenocarcinoma, lymphoma, gastrointestinal stromal tumor)
  • Trauma (mostly penetrating)
  • Iatrogenic (usually endoscopy)
Duodenum
  • Peptic ulcer perforation
  • Trauma (blunt and penetrating)
  • Iatrogenic (usually endoscopy)
Biliary tract
  • Cholecystitis
  • Stone perforation from gallbladder (i.e. gallstone ileus) or common duct
  • Malignancy
  • Choledochal cyst (rare)
  • Trauma (mostly penetrating)
  • Iatrogenic (usually endoscopy)
Pancreas
  • Pancreatitis (e.g. 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 diverticulum
  • Trauma (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, and ovaries

Epidemiology

The incidence depends on the cause. 10-30% of patients with cirrhosis develop SBP.3 One large study of patients admitted with acute appendicitis found abscess formation in 7% and peritonitis in a further 18%.4

Presentation

Symptoms

Abscess - the symptoms are highly variable but may include fever, pain anywhere in the abdomen, diarrhoea or ileus. A subphrenic abscess can cause pulmonary symptoms and a pelvic abscess can cause urinary symptoms.5

Peritonitis - the principle 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, getting gradually worse and more localised as the infection spreads. More generalised pain may develop if the condition is not contained. In some cases (e.g. gastric perforation) acute generalised pain is present from the onset. Anorexia, nausea and vomiting may precede the pain, particularly if a degree of obstruction is present.3

Signs

Abscess- the temperature chart is typically described as 'swinging' or 'spikey' (swinging pyrexia). There may be palpable abdominal inflammatory mass or 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. There may be little or no abdominal tenderness, particularly if the abscess is deep-seated.5

Peritonitis - 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).3

Investigations

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

  • Full blood count - there is usually a leucocytosis.
  • Liver function tests, 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 chest X-ray, ultrasound, CT scanning, MRI and contrast studies.
Management

Abscess

Drugs - 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 (e.g. 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, 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.6,7

Peritonitis

Drugs - SBP will initially require a third generation cefalosporin, with further therapy guided by microbiological culture results. In secondary peritonitis, the patient is likely to require medical treatment to stabilise renal, haemodynamic and pulmonary function, nutritional and metabolic support and systemic antibiotic therapy. Best results are achieved when antibiotics are started early, before culture results are received, with a second or third generation cefalosporin (e.g. cefotaxime) or a quinolone (e.g. ciprofloxacin) with or without metronidazole.

Surgery - 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. An initial operation may be required for drainage and to remove necrotic tissue. A second operation may be required to deal with the underlying pathology and provide further clearance of infection. Studies suggest that further surgery after this point is less beneficial. 3

Prognosis

Abscess5

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 age over 50 and multiple surgical procedures.

Peritonitis

The mortality rate of SPB is 30-50% and prognosis is worse in older age groups.8

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 commonest used is the APACHE II system.9 In one study of patients with generalised peritonitis, 38% died. Patients were divided into causative groups :

  • Appendicitis and perforated duodenal ulcer
  • Intraperitoneal origin other than appendix or duodenum
  • Post-operative peritonitis

Mortalities were 10%, 50% and 60%, respectively.10


Document references
  1. Natarajan SK, Mukhopadhya A, Ramachandran A, et al; Spontaneous bacterial peritonitis results in oxidative and nitrosative stress in ascitic fluid. J Gastroenterol Hepatol. 2007 Feb;22(2):177-81. [abstract]
  2. Platell C, Cooper D, Papadimitriou JM, et al; The omentum. World J Gastroenterol. 2000 Apr;6(2):169-176.
  3. Peralta R, Genuit T; Peritonitis and Abdominal Sepsis eMedicine.com 2006
  4. Kaminski A, Liu IL, Applebaum H, et al; Routine interval appendectomy is not justified after initial nonoperative treatment of acute appendicitis. Arch Surg. 2005 Sep;140(9):897-901. [abstract]
  5. Saber A, LaRaja A; Abdominal Abscess eMedicine.com updated 2007.
  6. Wilson SE, Robinson G, Williams RA, et al; Acquired immune deficiency syndrome (AIDS). Indications for abdominal surgery, pathology, and outcome. Ann Surg. 1989 Oct;210(4):428-33; discussion 433-4. [abstract]
  7. Malangoni MA, Shumate CR, Thomas HA, et al; Factors influencing the treatment of intra-abdominal abscesses. Am J Surg. 1990 Jan;159(1):167-71. [abstract]
  8. Thuluvath PJ, Morss S, Thompson R; Spontaneous bacterial peritonitis--in-hospital mortality, predictors of survival, and health care costs from 1988 to 1998. Am J Gastroenterol. 2001 Apr;96(4):1232-6. [abstract]
  9. Bohnen JM, Mustard RA, Oxholm SE, et al; APACHE II score and abdominal sepsis. A prospective study. Arch Surg. 1988 Feb;123(2):225-9. [abstract]
  10. Bohnen J, Boulanger M, Meakins JL, et al; Prognosis in generalized peritonitis. Relation to cause and risk factors. Arch Surg. 1983 Mar;118(3):285-90. [abstract]
Acknowledgements EMIS is grateful to Dr Laurence Knott for writing this article and to Dr Huw Thomas for earlier versions. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2009.
Document ID: 4138
Document Version: 21
Document Reference: bgp234
Last Updated: 1 Apr 2009
Planned Review: 1 Apr 2011

The authors and editors of this article are employed to create accurate and up to date content reflecting reliable research evidence, guidance and best clinical practice. They are free from any commercial conflicts of interest. Find out more about updating.

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