Peritonitis – the Eastern experience

Perforations of peptic ulcers form the major group among the gastroduodenal perforations [Table 2]. These perforations are usually encountered along the first part of the duodenum anteriorly and in the pylorus of the stomach. The advances in the medical treatment of the peptic ulcer disease have led to a dramatic decrease in the number of elective surgeries performed. However, the number of patients undergoing surgical intervention for complications such as perforation remains relatively unchanged or has increased [21, 22]. Such patients present with the classical signs and symptoms of peritonitis, and need early surgery for a favourable outcome. Although the surgical options are many – from simple closure to definitive acid reducing procedures – it has been our experience that simple closure of the perforation using a pedicled omental patch gives good results, even in large perforations upto 3 cms diameter [23]. This should therefore, be the preferred surgical method of closure, as it is easy to perform, is technically straightforward, and gives comparable results to that of definitive surgery [23, 24]. The mortality rate of these perforations varies from 4 – 11% [17‐19, 23, 25], and is higher in the elderly, those with concomitant disease, preoperative shock, larger size of the perforation, delay in presentation and delay in operation [17‐19]. Perforation of ulcers at other sites within the stomach and gastric cancers has been uncommonly reported, and emergency gastrectomy is the treatment of choice [26, 27].

The next common types of perforations encountered are those arising in the small intestine [Table 3]. These usually arise on a background of enteric fever, when the ulcerated peyer's patches in the terminal ileum perforate to give frank peritonitis. These typhoid ileal perforations have a high mortality rate, upto 60% [28‐32]. Aggressive resuscitation, antibiotics and early surgery has reduced the mortality rate and complications in this subset of small bowel perforations to less than 10% [28]. Although early surgery is associated with a better outcome, there is, however, no uniformity of opinion about the operative procedure to be performed in these perforations, and various procedures have been described such as simple closure, wedge excision or segmental resection and anastomosis, ileostomy, and even, side to side ileo-transverse anastomosis after primary repair of the perforation [28‐33]. However, it is our experience and teaching, that these patients have bowel oedema that precludes any suturing, and therefore, exteriorization of the perforation as a 'loop' ileostomy is the safest and fastest procedure to be done. Closure of this loop ileostomy is performed electively after 6 to 8 weeks, and is safe. A primary anastomosis (simple closure) is to be considered only when the patient presents early and the bowel is healthy.

A 'non specific' etiology is attributed to small bowel perforations when the perforation cannot be classified on the basis of clinical symptoms, gross examination, serology, culture and histopathological examination into any disease state such as enteric fever, tuberculosis or malignancy [20, 34, 35]. These ulcers are usually single and commonly involve terminal ileum [34]. It has been proposed that submucus vascular embolism [36], chronic ischemia due to atheromatous vascular disease or arteritis [37], or drugs such as enteric coated potassium tablets [38] are responsible for them.

These 'non specific' ileal perforations are closely followed by small bowel perforations occurring in intestinal tuberculosis. Most of these (50 – 80 %) occur in the ileum, usually proximal to strictures of the bowel [39]. Free tubercular perforations are rare [40]. The mortality rate reported in these tubercular perforations is very high, upto 70 % [41]. The diagnosis of perforated tubercular enteritis is usually not one that is made pre-operatively, because of the non-specific signs and symptoms and absence of radiological evidence of tuberculosis in the chest. Even in the presence of tubercular lesions in the chest skiagram, the diagnosis is not entertained or established until the histology and culture of the biopsied tissue turns out to be positive [42]. The recommended treatment after source control is multidrug anti tubercular therapy [43].

In contrast to these common causes of small bowel perforation in the developing countries, small bowel perforations are rare in the oriental countries [14, 20]. Apart from enteric fever and 'non specific' ulcers [20, 44], the other reported causes of such perforations from these countries include Crohn's disease, Behcet's disease, radiation enteritis, adhesions, ischemic enteritis, SLE and very rarely, intestinal tuberculosis [20, 45‐47]. Free perforations are a rare complication of Crohn's disease, and their incidence is reportedly highest from Japan, where it ranges from approximately 3% to 10%. These perforations are usually solitary, and occur mainly in the ileum. However, they can be multiple, and can occur at any site in the small or large bowel [45]. Similarly the incidence of Behcet's disease is much higher in Japan, and perforation of the intestinal ulcers can occur in upto 56% of cases. These are usually multiple and occur commonly in the terminal ileum and caecum, and need removal of a long segment of the ileum to prevent post-operative recurrence [46].

Gastroduodenal and small bowel perforations form the majority of cases encountered. Few series have shown higher or equal incidence of appendicular perforations [7, 21]. However, this high incidence of appendicular perforations probably reflects the younger age of patients in the reported series where appendicitis and consequently the complications are known to be much higher [7]. Colorectal perforations are uncommon, and apart from occasional case reports, we could come across only a single series from Japan that dealt with non appendicular colorectal perforations [48]. Perforations secondary to colonic neoplasms account for the majority of such cases. The perforation may occur at the site of the malignancy or proximally, as a 'blow out' of the proximal large bowel due to obstruction from the lesion. The incidence of such perforations is low, but carries a high mortality of about 17% [48, 49].

The other causes that have been reported are perforation of colonic diverticula, inflammatory conditions of the colon, volvulus, mesenteric ischemia, trauma, iatrogenic complications, idiopathic and stercoral perforations [48, 50]. In the Asian communities diverticular disease is more common in a younger age group, and the right colon is more commonly involved. One-third of these patients present with perforation of the large bowel and fecal peritonitis that requires surgical intervention [51, 52]. Amoebic colitis is another condition that is common in the tropical countries, with an incidence of perforation around 2 %, but with a high mortality rate (up to 50%) regardless of the treatment [53].

Rare sites of perforation leading to secondary peritonitis that have also been reported in the literature arise from the biliary tree, uterus, splenic and liver abscesses. Of these, ruptured amoebic liver abscesses are frequently encountered in tropical countries. These are seen in 3–7% of cases of intestinal amoebiasis, and upto 22% can rupture to give peritonitis, which carries a high mortality [54]. The management is by laparotomy and drainage or non-operatively, by means of metronidazole and/or radiologically guided drainage [54, 55]. Rupture of pyogenic liver abscess is rarer by comparison [56].

The bacterial analysis of the peritoneal fluid encountered showed E. coli to be dominant pathogen isolated, ranging from 25–71% [3, 6, 7, 10, 57, 58]. This was followed by Bacteroides fragilis, [57, 58] Klebsiella sp., and Pseudomonas sp [6, 7], in the few series that dealt with this aspect of peritonitis. A sterile culture was encountered in 8–59.1% [3, 6, 10, 58]. Depending on the site of the perforation gram positive cocci are predominantly isolated in gastroduodenal perforations; Pseudomonas sp. in small bowel perforations; and E.coli in appendicular and colonic perforations [12]. However, a higher incidence of fungal isolates has also been reported after gastroduodenal perforations [59].