body temperature is slightly up, and the WBC count is 17,000 this morning.” You know exactly what will happen next. Or at least you fear you know what will happen next: fascial dehiscence, due to a missed intestinal injury that you caused while dissecting those severe adhesions. What else it could be? Multiple stulas, but why?

* Several patients used as examples have been

created for illustrations, and some are real.

anatomy (of the stula), timing of surgery, and surgical strategy) in 135 patients treated for ECFs

While the reported mortality rate resulting from treating ECFs has dropped from 44% in 1960 [5] to around less than 10% presently [6], patients with ECFs still present the most difcult and complex challenge to any patient and a gen­eral surgeon. Despite the developments in surgi­cal techniques, wound care, nutritional support, and overall intensive and surgical care, patients with high-output stulas (>500ml/d) are still at risk of severe malnutrition, bloodstream catheter­related sepsis, intra-abdominal sepsis, and death [2, 7]. Dealing with ECF or entero-atmospheric stula (EAF) is considerably complex and will test the skills of even the most experienced sur­geon [8].

The diagnosis, that is the early identication of the stulas, needs to be established in a timely fashion and without much delay, while the pre­sentation depends on the clinical situation [9]. The cause of postoperative wound infections and abdominal dehiscence is not straightforward, and one has to fear intra-abdominal catastrophe before “blaming” technical reasons for suture failure of the closure. The rst cause of abdomi­nal wound dehiscence, with or without stula after the creation of a single or multiple anasto­moses, with or without lysis of adhesions, should be sought in some other sort of abdominal catas­trophe, such as severe infection (abscess), due to missed injury or anastomotic leak.

Over the years, the senior author (RL) has observed an interesting phenomenon in surgeons’ behavior. As surgeons, we not only behave differ­ently in novel situations, but we also vary our behavior in the same scenarios with different patients. The best examples are among acute care surgeons or trauma surgeons. When a trauma patient is not doing well postoperatively, we, the trauma surgeons, immediately think that we have missed an injury or there is something new hap­pening and take the patient back to the operating room for an “eye-scan” exploration. And we do that exact thing, most of the time. Yet, when we perform an elective surgery, or even emergency general surgery, such as the patient with elective colostomy take-down described later on in this chapter, and they develop a severe complication like a wound infection, even with questionable fascial integrity, we hesitate and use any possible imaging technique to avoid returning to the oper­ating room, often causing signicant delays in dealing with the problem at hand. I cannot entirely explain such a change in a surgeon’s behavior. Perhaps it is an ego thing.

The patient from our example was barely started on a clear liquid diet by day 5. On the 6th postoperative day, he was not feeling well, and now you receive the call on day 7. At this point, the patient has developed complications, and this process of starvation will be prolonged ever fur­ther. One has to remember that we should initiate and maintain nutritional therapy enterally or par­enterally throughout the hospitalization. However, in a very busy practice, it is easily forgotten that a patient who underwent a major surgical operation needs aggressive nutritional support.

ever, collecting all the uids from patients with large open abdominal wall defects (which the senior author (RL) has termed “a stula city”) (Fig. 11.1) may prove extremely difcult. Controlling sepsis, providing adequate wound care and tissue coverage (native or biologic) of the abdominal wall, and maintaining nutritional sup­port will result in patient improvement. They may of course eventually develop a major hernia that also needs to be xed at a later time. One major aspect of this surgical decision- making process is

gical treatment of a stula include high output and the presence of multiple stulas [1]. To rees­tablish intestinal continuity, the bowel segment giving rise to the stula is resected, and some have recommended long intestinal tube stenting of the entire small bowel afterward [11]. The sur­gery for ECFs should be timed after sepsis has been addressed and nutritional status improved, but there are cases when neither intra-abdominal infections nor malnutrition will not resolve until you resolve the source of the problem. In order to protect the surrounding skin from the caustic effects of intestinal contents, the output of the s­tula needs to be controlled [12]. Patients who develop a stula at the anastomosis (Fig.11.2a,b) or elsewhere, following dense adhesions release, in the perioperative phase, should be operated on at once. That segment of the intestines should be resected completely and never close with just one or two stitches. For patients with an abdominal wound that cannot immediately be closed and are at high risk for complications, a vacuum-assisted

It was a colostomy take-down that ended up with major complications, despite all prepara­tions. Moreover, one does not think of NSTI of this magnitude, when taking down colostomy as the rst complication.

abdomen rst, discussed later in this chapter. Necrotizing soft tissue infections (NSTIs) are rapidly progressing conditions with high mortal­ity and include fasciitis, gas gangrene, Fournier gangrene, or anaerobic myositis, but postopera­tive NSTIs, while rare, have high mortality if not addressed immediately and without delay [13] and require multidisciplinary approach, includ­ing intensive care unit (ICU) [14]. Patients with NSTI classically present with fever, signs of sys­temic toxicity, and severe pain that is dispropor­tionate to the clinical ndings [14–16]. Common risk factors include diabetes mellitus, obesity, peripheral vascular disease, chronic renal failure, intravenous drug use (particularly black tar her­oin), alcoholism, immunosuppression, and old age (>50 years) [15–17]. While the overall patho­physiology is common among all necrotizing infections, the rate at which clinical symptoms develop are dependent upon the particular patho­gen [15].

The US Food and Drug Administration (FDA) excludes necrotizing soft tissue infections from therapeutic trials, and therefore current recom­mendations have been inferred from complicated skin and soft tissue infections (cSSTIs) [18]. Complicated SSTIs are generally classied by either their anatomical site, microbial etiology, or severity, with complicated cases being those requiring surgery [14]. The management applied to NSTI includes a combination of aggressive surgical debridement and antibiotic management [14, 19, 20]. However, prompt recognition of NSTIs is essential, and delay in treatment is asso­ciated with increased mortality, particularly if surgery is delayed [13, 16]. Antibiotic therapy should initially be broad, as the necrotizing infection may be the result of multiple organ­isms, and targeted at the most likely pathogen but then quickly adjusted after culture and sensitivity laboratory results become available [20, 21].

cant difference in the mortality between the groups based on the timing of surgical interven­tion (17.5% in late vs. 7.5% in early intervention group), this did not reach statistical signicance.

one must keep in mind that the source control of the infection is the number one priority in the management of any critically ill patients. These patients should be treated with the same urgency as a gunshot wound or any other major insult to the body.

0.008) in comparison to the early group (< 6 h). With every 1 h delay in time to surgery, there is a