Faecal Peritonitis

John Hartley

Powerpoint File

Introduction

For the purposes of this paper the term faecal peritonitis refers to the clinical sequela of free faecal contamination of the peritoneal cavity. Faecal peritonitis is most commonly seen as the most dramatic manifestation of perforated sigmoid diverticular disease. Other common causes of faecal peritonitis include stercoral perforation, pressure necrosis of the caecum due to progressive distal colonic obstruction in the presence of a competent ileocaecal valve, or anastomotic failure after colorectal resection. Perforation of toxic megaocolon should be rare given appropriate multidisciplinary management of acute colitis, whilst perforation of the caecum in pseudoobstruction should also be uncommon.

Pathophysiology

The clinical picture resulting from free faecal contamination differs from purulent peritonitis (resulting perhaps from perforated appendicitis or rupture of a pericolic abscess in diverticulitis), in the severity of the systemic inflammatory response. Free colonic perforation releases large numbers of gram negative (usually pathogenic coliforms) and anaerobic bacteria (typically bacteroides species) into the peritoneal cavity. The degree of bacterial infection correlates with the magnitude of release of endotoxin, TNF alpha, interleukins 1 and 6 and other pro-inflammatory cytokines. Release of such cytokines within the peritoneal cavity leads to rapid progression of the sytemic inflammatory response syndrome (SIRS).

Recognition

Early recogntion is vital to the successful management of faecal peritonitis. If faecal contamination and secondary bacterial infection go unchecked then progression through the SIRS picture to septic shock and multiple organ failure (MOF) can be extremely rapid. This is particularly the case in the group of elderly patients with co-morbidity from which the majority of cases of colonic preforation are drawn. Physical findings consistent with widespread peritonitis are usually obvious, although it must be remembered that these may be less apparent at the extremes of age and in the presence of other factors which affect the host reponse such as steroid usage and other forms of immunosuppression. In addition the postoperative abdomen may be difficult to interpret. The systemic features which are required for the definition of SIRS are listed below:

SIRS if 2 or more of the following are present:

Temp. >38c. or <36c.
Heart rate >90BPM
Resp rate > 20BPM, or PaCO2 <4.3 Kpa (32mmHg)
WBC’s >12 or <4 (or >10% immature forms)
Management

The successful management of faecal peritonitis relies upon rapid resuscitation of the patient in order to allow removal of the source of contamination. Thereafter supportive therapy is required until such time as the patient recovers from the physiological insult, or it becomes apparent that death through MOF is inevitable. Volume rescuscitation should commence immediately and be guided by response in central venous and mean arterial pressure as well as urine output. Broad spectrum antibiotics should be commenced and targeted at gram negative organisms and anaerobes. A recent Cochrane review has shown no convincing evidence in favour of one particular regimen over another, and in practice a 2nd or 3rd generation cephalosporin in combination with metronidazole would be the norm. Appropriate inotropes will be required if volume resuscitation is unable to achieve a satisfactory mean arterial pressure.
Within an HDU setting (or even in the anaesthetic recovery area) it should be possible to optimise patients in the above fashion in a relatively short period of time. After 4 to 6 hrs of the above treatment (and usually considerably less) the patient will be in as optimal a state as it is possible to render them without attention to the source of sepsis – in other words laparotomy. Faecal peritonitis thus represents a true surgical emergency and laparotomy should not be delayed beyond this point. At the same time careful consideration should be given as to whether a laparotomy is appropriate in a patient who shows little or no response to vigorous resuscitation as outlined above. These decisions require senior input.

Surgery

The initial intervention at an appropriately timed laparotomy is crucial to successful outcome. Such patients will usually tolerate anaesthesia poorly, and the surgeon will usually only get a single opportunity upon which success or failure depends. Re-laparotomy in this situation because of a failure to control sepsis at initial procedure is usually associated with a poor outcome. Removal of the source of sepsis is the goal, and this should be undertaken by the most simple and expeditious means possible. Excision or exteriorisation of the perforation is required and primary anastomosis unwise. Thus for diverticular or stercoral perforations a Hartmann’s resection is usually appropriate. A burst caecum secondary to left sided obstruction will require a more extensive procedure, usually involving subtotal colectomy and end ileostomy. Similarly a leaking anastomosis should be exteriorised. In all but the most difficult circumstances management should be as above. However, peritoneal lavage with drainage and proximal faecal diversion is on occasion all that can be achieved in cases of established peritonitis in a particularly hostile abdomen, or in a patient so unstable that there is time for nothing else.

There is debate regarding the use of primary anastomosis rather than Hartmann’s procedure in perforated diverticular disease. Support for this approach comes from non-randomised studies in small numbers of patients in whom the degree of peritonitis is often unclear, or where patients with faecal peritonitis were excluded. Whilst primary anastomosis may be used in carefully selected patients with purulent peritonitis it is difficult to recommend this practice in patients with faecal peritonitis.

Following source control generous peritoneal lavage with warmed saline is commonly undertaken, along with removal of obvious faecal and particulate matter, although none of this has been shown to be of value in the setting of a controlled trial. Extensive removal of adherent fibrin and pyogenic membrane from peritoneal and serosal surfaces is not required and may be lead to enteric injury. Addition of antibiotics to the lavage solution confers no additional benefit.

There is a current vogue for managing critically ill patients with an open abdomen in order to avoid some of the hazards of the abdominal compartment syndrome (ACS). At present it is difficult to give evidence based guidelines on this issue. However, a reasonable approach is to adopt an expectant approach to ACS; thus where abdominal closure is technically possible then to do so and to deal with elements of ACS if an when they arise. On occasion concerns over control of sepsis or ongoing intestinal ischaemia may mandate a planned second look in which case some form of temporary closure can be undertaken or a laparostomy dressing applied.

Aftercare

Patients who are to survive emergency surgery for faecal peritonitis will frequently require a protracted period of ICU care, often with prolonged respiratory cardiovascular and or renal support, with the obvious requirement for multidisciplinary involvement. Mortality rates in the region of 30 to 80% can be anticipated depending upon such factors as age, co-morbidity, response to resuscitation, and degree of peritoneal soiling. Scoring systems for prediction of outcome are widely available, and may aid decision making. When there are signs of ongoing sepsis or failure to progress, the abdomen is often deemed to be the likely source. CT scanning and percutaneous drainage will often be useful in dealing with residual collections. However, the limitations of CT in the early postoperative period should be remembered. The use of planned re-laparotomy for severe sepsis rather than “laparotomy on demand” is controversial and such evidence as exists is in support of the latter approach. The decision to re-open such a patient for failure to progress in the absence of some objective radiological or clinical evidence of a remediable problem within the abdomen should be taken very carefully.

Conclusions

The successful management of faecal peritonitis relies upon early diagnosis and rapid optimisation of the patient so as to allow laparotomy and control of the source of sepsis. High morbidity and mortality can be anticipated despite best practice.

References
Schein M. Surgical management of intra-abdominal infection: is there any evidence? Langenbeck’s Arch Surg 2002; 387: 1-7
Wittmann D et al. Management of secondary peritonitis. Ann. Surg 1996; 224: 10-18
Lamme B et al. Meta-analysis of relaparotomy for secondary peritonitis. Br. J. Surg. 2002; 89: 1516-1524
Mulier et al Factors affecting mortality in generalised postoperative peritonitis: multivariate analysis in 96 patients. World J. Surg. 2003; 27: 379-384
Hotchkiss RS et al Medical progress: the pathophsiology and treatment of sepsis. N Engl J Med. 2003; 348: 138-150
Wong et al. Antibiotic regimens for secondary peritonitis of gastrointestinal origin in adults. Cochrane database Syst Rev. 2005; Apr 18; (2): CD004539
Krukowski ZH, Matheson NA. Emergency surgery for diverticular disease complicated by generalized and faecal peritonitis: a review. Br J Surg 1984; 12:921-7.
Hau T, Ohmann C, et al. Peritonitis study group of the Surgical Infection Society of Europe. Planned relaparotomy vs relaparotomy on demand in the treatment of intr-abdominal infections. Arch Surg 1995; 130:1193-1197
Nathens AB, Rotstein OD. Therapeutic options in peritonitis. Surg Clin North Am 1994; 74:677-692
Anderson ID, Fearon KC, Grant IS. Laparotomy for abdominal sepsis in the critically ill. Br J Surg 1996; 83: 535-539
Constantinides VA, Heriot A, Remzi F Et al. Operative strategies for diverticular peritonitis: a decision analysis between primary resection and anastomosis versus Hartmann’s procedures. Ann Surg 2007; 245:94-103.
Surgue M, Buist D et al. Prospective study of intra-abdominal hypertension and renal function after laparotomy. Br J Surg 1995; 82:235-238