Treatment
Following intravenous fluid resuscitation and antibiotic therapy to cover gut flora, laparotomy
to lavage the abdominal cavity and either place a protecting stoma or an end colostomy is
generally indicated for the more severe anastomotic leak. In less severe cases, where rectal
contrast is seen to be contained by CT imaging, further surgery is not always necessary. In
either event, any abscess formed must be drained, preferably percutaneously with CT
guidance when possible (26).
Perforated Gastroduodenal Ulcer
Although markedly decreased in incidence by improved critical care management, gastro-
duodenal ulceration leading to perforation and peritonitis may complicate the course of ICU stays.
Risk Factors
Perforated ulcer represents yet another potential source of abdominal infection in the postop-
erative patient. Nonsurgical patients in the ICU are also predisposed to the development of ulcers.
Curling’s ulcers, or stress ulcers, affect in particular burn patients with septic complications;
Cushing’s ulcers develop in patients with central nervous system pathology involving midbrain
damage, such as occurs after head trauma. In addition, many patients will be treated with
nonsteroidal anti-inflammatory drugs and exogenous steroids during their ICU stay, which may
contribute to mucosal barrier breakdown and delay recognition of ensuing infection. Risk factors
predicting ulcer perforation include smoking, exposure to nonsteroidal anti-inflammatory drugs,
cocaine abuse, andHelicobacter pyloriinfection (27,28). Effective, as they are, acid-suppressing
drugs do not eliminate the risk entirely (29), and thus the possibility of ulcer perforation should
be considered as an explanation of intra-abdominal infection in the ICU patient.
Presentation and Diagnosis
Perforation most typically presents as an acute abdomen with sudden onset of pain,
occasionally accompanied by nausea and vomiting, diffuse abdominal tenderness, rigidity of
the abdominal wall, and ileus. As with other illnesses, perforation in the ICU patient may
manifest in less obvious ways. Plain abdominal and upright chest films exhibiting signs of free
air may detect 85% of free perforations (30) and is often the radiologic modality of first choice.
CT scan, although frequently rendered unnecessary in the face of a positive plain film, may
nevertheless disclose a remaining few diagnoses: Chen et al. found pneumoperitoneum on CT
to be 100% sensitive (31). Moreover, other signs such as fluid collections and soft tissue
inflammation also demonstrated by CT may be of further help.
Treatment
Although there has been debate in recent years with regard to a 12-hour period of observation
and supportive treatment before proceeding to surgical intervention for perforation, the poor
prognosis associated with delay in definitive treatment and the relatively straightforward
surgical procedure has persuaded many surgeons against this approach (28). Currently, direct
suture repair, often with omental patch reinforcement, is the usual treatment of choice.
Subsequent eradication ofH. pylori—for example, using ampicillin, metronidazole, and a
proton pump inhibitor, otherwise known as “triple therapy”—has been shown to decrease the
recurrence of ulcers at one year from 38% to 5% (27).
Spontaneous Bacterial Peritonitis
Spontaneous bacterial peritonitis (SBP) is a bacterial infection of intraperitoneal ascitic fluid
and resulting peritoneal inflammation that occurs in the absence of other inciting factors, e.g., a
perforated viscus. With a 10% to 30% incidence of SBP among random hospital admissions of
cirrhotic patients with ascites, and a mortality of 20% to 40% equivalent to that of an
esophageal variceal bleed, SBP is a formidable threat to the cirrhotic ICU patient (32,33).
Risk Factors and Pathogenesis
SBP occurs when enteric bacteria, most commonly E. coli, Klebsiella pneumoniae,and
pneumococcus, translocate across the gut mucosa to mesenteric lymph nodes. From there,
Intra-abdominal Surgical Infections and Their Mimics in Critical Care 265