M62 Coloproctology Course

Rick Nelson from Chicago was the keynote speaker, lecturing on the evidence for fissure-in-ano. Other topics included T4 rectal cancer, volvulus and immunonutrition.

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Paul Finan, Leeds General Infrimary

Powerpoint File

Introduction

Peritonitis, from whatever cause, is one of the major issues facing the general surgeon. It can present in a variety ways, from the localised contained peritonitis of an acutely inflamed appendix or gall bladder to the fulminant picture seen with systemic sepsis, and its associated multi organ dysfunction, secondary to faecal peritonitis.

 

Although the clinical spectrum may vary, the principles of management remain the same. These include control of the ongoing septic process, liberal use of CT imaging to diagnose and, on many occasions, treat the septic foci, appropriate surgery and prompt introduction of full supportive measures including appropriate antibiotic therapy, and damage limitation with early recognition of the need for further supportive measures.


Classification

Peritonitis can be classified as primary, secondary or tertiary. Exposure to primary peritonitis is limited. Although acute abdominal pain may be a presenting feature in such cases and therefore present to the general surgeon, it is usually associated with a single organism and can often be treated conservatively. Perhaps the most common presenting cases are those associated with CAPD. Tertiary peritonitis is very often seen within the context of the terminally ill on the ICU. Organisms seen in such cases are often atypical e.g. fungi, and represent the inability of the host to mount an immunological response as part of their severe illness. Secondary peritonitis, which can be localised or generalised, is invariably due to a surgical problem and is the subject of the remainder of this talk. The origin may be primary intra-abdominal pathology e.g. acute cholecystitis, appendicitis or diverticulitis or secondary to a complication of a previous surgical procedure. It can be subdivided into localised or diffuse depending on whether the infective process remains contained within, or adjacent to, the inflamed organ or has spread throughout the abdominal cavity.


Recognition


Although the classical features of peritonitis may be present, one needs to be aware of atypical features. The common symptoms, signs and abnormal investigations may be absent or moderated particularly at the extremes of age. Similarly, as the systemic effects of peritonitis are a balance between the infectivity of the infective organism(s) and the host response, then other factors e.g. steroid usage, may mask the characteristic features of this condition. It is also well recognised that cardiac arrythmias in the post-operative period may be the first manifestation of intra-abdominal problems.

Whilst accepting that clinical examination remains important, the diagnosis is often made with the assistance of radiological investigations. Whilst simple plain radiography may give the diagnosis, increasingly CT scanning is the radiological modality of choice. It has applications in the initial assessment of the patient with suspected peritonitis but has its major role in the post-operative period. The value of CT over ultrasound has been repeatedly confirmed. CT scanning can also contribute to the management of the condition as will be mentioned later.


Management

The principles of management are two-fold, control of the infective process, source control, and damage limitation. The control of the infective process may be to remove the source e.g. appendicectomy or cholecytectomy. Such problems, whilst serious,

seldom lead to the demise of the patient. Infection from the intestinal tract in the post-operative patient however may go unrecognised and the subsequent peritonitis may lead to the full blown systemic inflammatory response syndrome, SIRS. Whilst necessitating the full support of the ICU, failure to correct or limit the infective source will lead to deterioration. The development of scoring systems which take account of the systemic signs of sepsis, whilst not determining treatment, allow for comparisons of treatment to be made.

The more distal the problem within the GI tract the more serious the peritonitis. Although the stomach and proximal duodenum are, to all extents and purposes, sterile, the bacterial count can rise in cases of obstruction or cancer. Peritonitis arising from the colon and rectum invariably leads to infections with pathogenic coliforms and species of bacteroides.

Following initial, and prompt resuscitation, a laparotomy becomes the most important treatment modality. Localised peritonitis e.g. a post-operative abscess, may not only be diagnosed but treated by CT drainage. This can be successful in selected cases but will be of little value if the underlying infective process is on-going e.g. an anastamotic leak or necrotising pancreatitis. The decisions taken at the initial laparotomy are probably the most important. Simple suturing of perforated ulcers is clearly appropriate, but attempts at repair of leaking anastamoses with further suturing is often futile and exteriorisation of the two ends may be the wise decision.

Removal of particulate matter is important but attempts at doing the same to the fibrinous covering of the bowel is probably of little importance and may damage the already friable intestine. Lavage of the peritoneal cavity is much loved by the surgeon but has not been shown to be of value in the controlled trial setting. It does however allow thorough cleansing of the peritoneal cavity. Certainly continued lavage in the post-operative period seems of little value.

The formation of a laparostomy i.e. not closing the abdominal wound has become popular in some cases of peritonitis. There are several indications for this procedure. Concern as to the success of source control and a decision at the time of initial surgery to return the patient to theatre 24 hours later would be one such indication. A further reason would be the onset of the intra-abdominal compartment syndrome and a judicious laparostomy may be of considerable value. Such a procedure may be reversed after a few days if all seems well and a secondary suture of the abdomen performed. Alternatively, the abdomen can be left open and the abdominal contents covered with an absorbable mesh. This procedure, whilst being necessary in particularly complicated cases of peritonitis, will almost invariably lead to an incisional hernia. Suction wound dressing systems have gained in popularity but our experience, and that of others, is that such systems may lead to intestinal fistulation.

Antibiotic therapy is clearly of importance, although the duration of treatment is often extended unnecessarily. Studies have shown that the peritoneal cavity can become almost sterile after a few days. Further treatment with antibiotics should be reserved for those patients showing signs of the systemic infection, or a failure to control the infection within the peritoneal cavity. A recent meta-analysis of antibiotic regimens has failed to show an advantage of one particular regimen over another, but current practice would include a broad spectrum cephalosporin and metronidazole.


Conclusion

Peritonitis carries a high mortality. Early recognition, prompt resuscitation, liberal use of CT imaging, correct decisions at the time of surgery with attention to source control and damage limitation, and a multi-disciplinary approach, offer the best chance of a successful outcome

 

References

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Emmanuel K. Current and future concepts of abdominal sepsis. World J. Surg. 2005; 29: 3-9

Deans KJ. et al. Novel therapies for sepsis: a review. J. Trauma 2005; 58: 867-874

Lamme B et al. Meta-analysis of relaparotomy for secondary peritonitis. Br. J. Surg. 2002; 89: 1516-1524

vanSonnnenberg E et al. Percutaneous abscess drainage: update. World J. Surg. 2001; 25: 362-372

Stafford et al. Surgical infections in the critically ill. Curr Opin Crit Care 2002; 8: 449-452

Mulier et al Factors affecting mortality in generalised postoperative peritonitis: multivariate analysis in 96 patients. World J. Surg. 2003; 27: 379-384

Solomkin et al. Guidelines for the selection of anti-infective agents for complicated intra-abdominal infections. Clin Infect Dis. 2003; 37: 997-1005

Jimenez MF et al. Source control in the management of sepsis. Intensive Care Med. 2001; 27: S49-S62

Hotchkiss RS et al Medical progress: the pathophsiology and treatment of sepsis. N Engl J Med. 2003; 348: 138-150

Cinat ME et al Determinants for successful percutaneous image-guided drainage of intra-abdominal abscess. Arch Surg. 2002; 137: 845-849

Betsch et al. CT-guided percutaneous drainage of intra-abdominal abscesses: APACHE III score stratification of 1-year results. Eur Radiol. 2002; 12: 2883-2889

Genuit T et al Peritonitis and abdominal sepsis. E-medicine at www.e- medicine.com/med/topic2737.htm

Woltmann A. et al. Molecular mechanisms of sepsis. Langenbeck’s Arch Surg. 1998; 383: 2-10

Van Nieuwenhoven et al. Clinical relevance of sepsis scores. Langenbeck’s Arch Surg. 1998; 383: 11-14

Wittmann et al. Scope and limitations of antimicrobial therapy of sepsis in surgery. Langenbeck’s Arch Surg. 1998; 383: 15-25

Neugebauer et al. Thirty years of anti-mediator treatment in sepsis and septic shock – what have we learned? Langenbeck’s Arch Surg. 1998; 383: 26-34

Berger et al. Management of abdominal sepsis. Langenbeck’s Arch Surg. 1998; 383: 35-43

Schoenberg et al. Outcome of patients with sepsis and septic shock after ICU treatment. Langenbeck’s Arch Surg. 1998; 383: 44-48

Wong et al. Antibiotic regimens for secondary peritonitis of gastrointestinal origin in adults. Cochrane database Syst Rev. 2005; Apr 18; (2): CD004539

To register fill in the registration form and send it off complete with a cheque to pay for your course.

Course Fee: £240

Mr J Hartley
Consultant Surgeon
Academic Surgical Unit
Castle Hill Hospital
Cottingham
East Yorkshire
HU16 5JQ

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