Definition and Etiology

Abdominal abscesses are well-defined collections of infected purulent material that are walled off from the rest of the peritoneal cavity by inflammatory adhesions, loops of intestine and their mesentery, the greater omentum, or other abdominal viscera. Abscesses may occur in the peritoneal cavity, either within or outside of abdominal viscera (extravisceral), as well as in the retroperitoneum.¹ Most relevant to the surgeon are extravisceral abscesses that usually arise in 1 of 2 situations: (1) after resolution of diffuse peritonitis in which a loculated area of infection persists and evolves into an abscess and (2) after perforation of a viscus or an anastomotic breakdown that is successfully walled off by peritoneal defense mechanisms. More than 80% of intra-abdominal abscesses occur in the postoperative period, the majority of which occur after pancreaticobiliary or colorectal surgery and are usually related to anastomotic dehiscence.^2,3

Occasionally, postsurgical abscesses result from infection of an intraperitoneal hematoma that develops following surgery. Less frequently, intra-abdominal abscesses are unassociated with previous surgery and are usually attributable to spontaneous inflammatory processes associated with a small, localized perforation, such as in appendicitis, diverticulitis, and Crohn disease.^3,4 Visceral abscesses are most commonly caused by hematogenous or lymphatic spread of bacteria to the organ. Retroperitoneal abscesses may be caused by several mechanisms, including perforation of the gastrointestinal (GI) tract into the retroperitoneum and also hematogenous or lymphatic spread of bacteria to the retroperitoneal space, where seeding of uninfected collections such as peripancreatic necrosis or hematomas may occur.

Pathophysiology of Abscess Formation

After bacterial contamination of the peritoneal cavity, a complex series of events is initiated that, under ideal circumstances, effects complete eradication of invading bacteria. The 3 major defense mechanisms in the peritoneal cavity are (1) mechanical clearance of bacteria via the diaphragmatic lymphatics, (2) phagocytosis and destruction of suspended or adherent bacteria by phagocytic cells, and (3) sequestration and walling off of bacteria coupled with delayed clearance by phagocytic cells.⁵ The first 2 mechanisms act rapidly, usually within hours. Egress of bacteria from the peritoneal cavity via the lymphatics is responsible for the early septic response due to bacteremia and initiation of the innate immune response to infection.

The initial peritoneal response to bacterial contamination is characterized by hyperemia, exudation of protein-rich fluid into the peritoneal cavity, and a marked influx of phagocytic cells. Resident peritoneal macrophages predominate early in the infection, but the rapid influx of neutrophils after a 2- to 4-hour delay makes them the predominant phagocytic cell in the peritoneal cavity for the first 48 to 72 hours.⁶ The combination of resident peritoneal cells plus the migration of these cells into the peritoneum serves to propagate the initiation of the innate immune response, including the elaboration of inflammatory cytokines and the procoagulant response. In humans with severe intra-abdominal infection, peritoneal levels of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1, and IL-6 are higher than levels measured simultaneously in plasma.^7,8 Haecker and colleagues reported that TNF-α and IL-10 levels are increased and reach 100- to 1000-fold in the plasma following appendiceal perforation. In adult patients, a correlation between the magnitude of the cytokine response and outcome in infected patients has been demonstrated in several clinical studies.⁹ Higher levels of circulating TNF-α and IL-6 have been recorded in patients who later die with intra-abdominal infection.⁷ Interestingly, elevated peritoneal levels persist even after systemic inflammatory response has abated. This suggests that during resolving peritonitis, there is compartmentalization of the response with local cytokine elaboration, thereby promoting local resolution of infection.

Other cell types are likely important in the initiation of the local peritoneal response. Peritoneal mast cells and mesothelial lining cells have also been shown to be potent producers of a range of cytokines and procoagulants. Fibrin deposition appears to play an important role in this compartmentalization of infection, not only by incorporating large numbers of bacteria within its interstices¹⁰ but also by causing loops of intestine to adhere to each other and the omentum, thereby creating a physical barrier against dissemination. Fibrin deposition is initiated after the exudation of protein-rich fluid containing fibrinogen into the peritoneal cavity. The conversion of fibrinogen to fibrin is promoted by the elaboration of tissue factor by both mesothelial cells and stimulated peritoneal macrophages.¹¹ In addition, generation of other inflammatory mediator molecules and components of the complement cascade (eg, C3a and C5a) further promotes the development of local inflammation. The net effect of these responses is the localization of the bacterial infection in the peritoneal cavity, wherein ultimate resolution can occur. However, a number of local factors thwart complete resolution and presumably establish the local environment for persistent infection and hence abscess formation. These include regional fibrin deposition that impedes phagocytic cell migration, factors that inhibit phagocytic cell function such as hemoglobin, particulate stool, low pH, and hypoxia.

On the microbial side, polymicrobial flora of these infections as well as the near ubiquitous presence of Bacteroides fragilis and its unique capsular polysaccharide have been implicated in persistence of infection and abscess formation. Considered together, while the process of abscess formation represents a successful outcome of the peritoneal response to bacterial contamination of the peritoneal cavity, one is left with a residual infection that carries with it morbidity and potential mortality and must be actively managed.

Clinical Presentation and Diagnosis

CLINICAL PRESENTATION

Diagnosis of an intra-abdominal abscess is based on clinical suspicion complemented by radiologic confirmation of the presence of the abscess. High spiking fevers, chills, tachycardia, tachypnea, and leukocytosis, associated with localized abdominal pain, anorexia, and delay in return of bowel function in the postoperative patient, are the classic signs and symptoms associated with the presence of an intra-abdominal abscess. The presence of a well-localized tender mass on clinical examination is consistent with the presence of an abscess. However, there may be considerable variability in the clinical appearance of the patient with this infection, ranging from a relatively mild picture where the patient appears generally well but is “slow to recover” from his or her surgical procedure to those who manifest evidence of profound systemic inflammation. There may be no mass palpable on clinical examination. A number of factors may contribute to this variability, including patient factors such as age, immunocompetence, and concurrent use of antimicrobials, as well as abscess factors such location and size of the abscess and how well walled off the abscess is. For example, subphrenic abscesses can present with vague upper quadrant abdominal pain, referred shoulder pain, and occasionally hiccoughs but with no localized abdominal tenderness or palpable mass. By contrast, paracolic abscesses present with localized tenderness and may manifest as a palpable mass on abdominal examination. Pelvic abscesses may also cause local irritation of the urinary bladder, causing frequency, or of the rectum, resulting in diarrhea and tenesmus. Retroperitoneal collections, particularly psoas abscesses, can manifest as leg and back pain with muscular spasm and flexion deformity of the hip. In reality, with the ready availability of computed tomography (CT) scanning in most institutions, almost any deviation from the normal recovery trajectory in the postoperative period will prompt a CT scan and possible early detection of the abscess.

DIAGNOSTIC TESTS

Imaging provides the definitive evidence of the presence of an intra-abdominal abscess. Abdominal plain films can be helpful in identifying air-fluid levels in the upright or decubitus positions, extraluminal gas, or a soft tissue mass displacing the bowel. In the postoperative patient, however, extraluminal gas may be present for up to 7 days. Overall, plain radiography may suggest the presence of an abscess, but other imaging modalities have essentially replaced plain films in the evaluation of intra-abdominal abscesses.

CT scanning has emerged as the radiologic investigation of choice in the diagnosis of intra-abdominal abscess.¹² With its ready availability, it has essentially supplanted abdominal ultrasound (US) as the main diagnostic tool in this setting, mainly because of its accuracy, but also because its functionality is not impaired in the setting of ileus, wound dressings, stomas, and the open abdomen. The accuracy of the scan is improved if contrast is used. Intravenous contrast increases the accuracy of defining the presence of an abscess, while GI tract contrast helps to distinguish fluid-filled bowel loops from an abscess and, in addition, may detect the presence of an anastomotic leak. In a retrospective study that compared US and CT in diagnosing intra-abdominal abscesses, the sensitivity of US in 123 patients was 82% compared to 97% in 74 patients by CT, and the overall accuracy of US was found to be 90% versus 96% for CT.¹³

Criteria for identification of an abscess by CT have been well described and include identification of an area of low CT attenuation in an extraluminal location or within the parenchyma of solid abdominal organs. The density of abscesses usually falls between that of water and solid tissue.¹⁴ Other radiologic signs of an abscess are mass effect that replaces or displaces normal anatomic structures, a lucent center that is not enhanced after the intravenous administration of a contrast medium, enhancing rim around the lucent center after IV contrast administration, and gas in the fluid collection (Fig. 16-1).

One of the major advantages of CT over US is the ability to detect abscesses in the retroperitoneum and pancreatic area. There are also some disadvantages to CT scanning. In the absence of contrast rim enhancement, gas, or visible septations, CT cannot distinguish between sterile and infected fluid collections. Occasionally, there may be a solid-appearing collection that is really an abscess with a high leukocyte and protein content. Septations and other signs of loculated abscesses can often be better visualized with US than CT. Finally, CT scanning is sometimes unable to differentiate between subphrenic and pulmonic fluid, a relatively common situation in abdominal surgery.¹⁵ In these limited circumstances, US may be considered as a complement to CT imaging.

Other modalities include magnetic resonance imaging (MRI). While MRI can sometimes better delineate the extent of an abscess, particularly in relation to adjacent soft tissue structures such as muscles and major blood vessels, it does not clearly have advantages over CT scanning and its practicality may be limited in the sick surgical patient.¹⁶ One area where US and MRI may be relevant is in the investigation of the pregnant patient with abdominal pain.¹⁷ US is particularly useful when appendicitis/appendiceal abscess is suspected, and MRI may be useful when localization is less clear. The roles of radiolabelled compounds in the diagnosis of abdominal abscesses are limited at present.¹⁸

Management

The basic principles underlying the successful treatment of intra-abdominal abscesses are three fold:

1. 
   

   Adequate resuscitation and support

   
   
2. 
   

   Antimicrobial therapy

   
   
3. 
   

   Source control/abscess drainage

RESUSCITATION AND SUPPORT

In keeping with the variable presentation of patients with intra-abdominal abscesses, the initial approach to resuscitation and support will vary considerably. Attention to the ABCs (airway, breathing, circulation) while individualizing the intervention for each patient according to his or her deviation from normal physiology is appropriate. Particularly in the postsurgical patient, nutritional support should be considered.

When feasible, oral nutrition should be given in preference to total parenteral nutrition. Some patients are able to ingest food and/or supplements by mouth, while others might require an enteral feeding tube, due to anorexia, precluding adequate ingestion of nutrients. Systematic review of the literature suggests that infectious complications and cost are reduced in critically ill patients receiving enteral nutrition compared to parenteral nutrition.¹⁹ One can presumably extrapolate to patients with intra-abdominal infection. When abscess formation occurs due to an anastomotic leak, there is a sense that this might preclude use of enteral nutrition. This concern is likely unfounded, unless there is profound ileus associated with the infection.

ANTIMICROBIAL THERAPY

Considerations regarding antimicrobial use are based on the microbial flora recovered from the infections. Over the past decade, there has been increasing appreciation that there is an evolution of the flora with increasing severity of abdominal infection.²⁰ For example, Table 16-1 shows the bacteriology of peritonitis in patients with community-acquired peritonitis and those with postoperative peritonitis.

The major pathogens in community-acquired intra-abdominal infections are coliforms (especially Escherichia coli) and anaerobes (especially B fragilis). As illustrated, while both are polymicrobial, postoperative peritonitis has a higher incidence of more resistant microbes. Aside from patients with postoperative peritonitis, other factors predict this shift in microbiology, including advanced age, severe physiologic derangement, immunosuppression, previous use of antibiotics, and residence in a health care institution in hospitals and nursing homes.

Guidelines have been developed by the Surgical Infection Society and the Infectious Diseases Society of America regarding the use of antimicrobial therapy in intra-abdominal infection.²¹ These authors have risk-stratified patients into 3 categories and provided recommendations for empiric antimicrobial regimens according to category. The 3 categories are (1) community-acquired infections of mild to moderate severity; (2) high-risk or severe community-acquired infections; and (3) health care–associated infections. Factors that dictate conversion from mild-to-moderate severity to high severity include severe physiologic derangement (eg, high Acute Physiology and Chronic Health Evaluation II [APACHE II] score), advanced age, or immunocompromised state. Our institution follows the best practice in general surgery guidelines of the University of Toronto–affiliated hospitals (Table 16-2). Even though these guidelines are readily applicable to decision making regarding patients coming to the hospital with abscesses, they are not to be considered a meta-analysis subjected to formal peer review process. It is noteworthy that while Enterococcus is frequently recovered in isolates in these infections, the evidence demonstrates no additional benefit to treating this microbe as part of empiric therapy.

When possible, switchover to oral agents is appropriate. Traditionally, the duration of antibiotics was based on resolution of the clinical signs and symptoms of infection, a period that usually ranged from 4 to 7 days. Should there be no resolution by this time, reevaluation of the patient for the presence of persistent infection in the abdomen and elsewhere is appropriate. A clinical trial randomly assigned 518 patients with complicated intra-abdominal infections to receive antibiotics until 2 days after the resolution of fever, leukocytosis, and ileus with a maximum of 10 days, or to receive a fixed course of antibiotics of 4 ± 1 calendar days. Patients in both groups underwent adequate source control. The results of that study showed similar outcomes after fixed-duration antibiotics (approximately 4 days) compared to a longer course of antibiotics until the resolution of physiologic abnormalities (approximately 8 days).²² This study successfully challenged the paradigm that discontinuation be based on clinical signs of infection and suggests that a shorter fixed duration of treatment may be acceptable therapy.

Patients who present in the postsurgical period fall into the category of patients with health care–associated infection. In these patients, empiric therapy should include agents with expanded spectra against gram-negative aerobic and facultative bacilli, including meropenem, imipenem-cilastatin, doripenem, piperacillin-tazobactam, or ceftazidime or cefepime in combination with metronidazole. Table 16-3 shows the considerations regarding selection depending on local institutional microbial isolates. Empiric anti-enterococcal treatment should be given. Treatment of Candida with fluconazole when recovered from cultures and treatment of methicillin-resistant Staphylococcus aureus with vancomycin should be followed if the patient is colonized with the microbe.

SOURCE CONTROL

Source control is a term used to include all physical measures taken to control a focus of infection. Here we focus our discussion to abscess drainage, but adequate source control may also include debridement of necrotic tissue, surgical repair, resection, and/or exteriorization of the anatomic defect causing peritoneal contamination.²³

Over the past 2 decades, percutaneous drainage of abscesses has become an established technique and a safe alternative to surgery. This evolution of care has not been based on a series of strong randomized trials showing equivalence or superiority of this approach. Rather, observational studies from a number of centers have shown it to be a safe effective alternative to surgical intervention, with equivalent success rates, comparable mortality (10%-20%) and morbidity (~25%).^24-26 Combined with other advantages of percutaneous approaches including avoidance of general anesthesia, lower costs, and the potential for fewer complications, it has now become the default approach to abscess management. Prerequisites for catheter drainage include an anatomically safe route to the abscess, a well-defined unilocular abscess cavity, concurring surgical and radiologic evaluation, and surgical backup for technical failure. Multiple abscesses, abscesses with enteric connections as seen with enterocutaneous fistulas, and the need to traverse solid viscera are not contraindications. Indeed, as the technique has evolved over several decades, the barriers to accessing unusually positioned collections have disappeared with the use of unconventional routes (transgluteal, transvaginal, transrectal) and the advent of new technologies including endoscopic US.^27,28 Even the presence of septations and loculations has not precluded at least an attempt to use percutaneous drainage.²⁹

Percutaneous drainage can be performed with US or CT guidance. CT provides for more precise identification of organs and bowel loops and is more accurate for planning of drainage route.¹⁵ Once the abscess is identified, initial diagnostic aspiration should be sent for Gram stain and microbiological culture. The catheter used for drainage should be as small as possible for safety, yet large enough so that the tubing does not become obstructed. Most commonly used catheters range in size from 8 to 12 F. With appropriate catheter placement, the abscess cavity typically decompresses and collapses. Irrigation of the catheter should be done once daily to ensure tube patency. As catheter drainage decreases, repeat CT scanning can be performed to evaluate for residual contents. If drainage increases over time or continues at a steady rate, the development of an enteric fistula must be suspected. This may not have been unexpected when the catheter was initially placed near a perianastomotic abscess or an abscess adjacent to some underlying pathologic process. Potential complications of catheter placement include bacteremia, sepsis, vascular injury, enteric puncture, cutaneous fistula, and transpleural catheter placement.

Catheters should be maintained on closed drainage systems. There does not appear to be benefit to the use of suction or irrigation of these catheters, although flushing once per day with saline ensures patency. Patients should respond with defervesce of symptoms within 48 hours of catheter insertion. If they do so, a repeat CT scan is done at approximately 5 to 7 days to ensure shrinkage of the abscess. Criteria for removal of the drain include (1) clinical resolution of septic parameters, including patient well-being, normal temperature, and leukocyte count; (2) minimal drainage from the catheter; and (3) CT evidence of the resolution of the absence.

As noted previously, studies comparing outcomes of surgical and percutaneous drainage of intra-abdominal abscesses demonstrate comparable efficacy. In one study, patients were matched for age, abscess location, and etiology, and had similar APACHE II scores. There were no differences between percutaneous and surgical drainage in patient morbidity, mortality, or duration of hospital stay.²⁵ Furthermore, initial percutaneous drainage of abscesses in the context of diverticular disease allowed for subsequent definitive operative resection and primary anastomosis in 1 rather than 2 operations. Another group retrospectively examined postoperative intra-abdominal abscesses after laparotomy. This study similarly demonstrated that use of either form of drainage resulted in similar cure rates for postoperative intra-abdominal abscesses.²⁶

With clear demonstration of its efficacy when compared to surgical drainage, percutaneous drainage should be considered the preferred approach in source control of abscesses. Table 16-4 shows outcome of percutaneous drainage according to underlying pathologic processes. In general, one should predict a successful outcome in patients with a single, well-defined abscess with no enteric communication. The presence of enteric communication per se does not reduce the likelihood of success as it is defined by the resolution of the infection. In a postoperative abscess, following drainage of the infection, the underlying anastomotic defect will usually close. In other settings, there may be a requirement for subsequent surgery to manage the underlying disease process such as diverticular disease or Crohn disease. For example, in one study, approximately 75% of patients with large peridiverticular abscesses were drained percutaneously and then they underwent a single-stage sigmoid colectomy.²⁹ Other circumstances such as fungal abscesses, infected hematomas, peripancreatic necrosis, or necrotic-infected tumor have a lower success rate for percutaneous drainage and early consideration for surgical intervention.³⁰ CT features such as the presence of a “rind,” a sharp exterior margin, air-fluid levels, and septations do not predict outcome and therefore should not be determinants as to whether or not initial percutaneous drainage should be used.³¹ Finally, one should use clinical judgment as to the need for percutaneous drainage for small abscesses (<5-cm diameter) such as those that might occur with acute diverticulitis, Crohn disease, and interloop collections. These may respond well to antibiotics alone, and the use of percutaneous drainage may be meddlesome and potentially morbid.³²

There are circumstances where percutaneous drainage should be considered contraindicated. Most important among these is the circumstance where peritoneal infection is not localized, such as in the early postsurgical period where an anastomotic leak leads to diffuse peritonitis. Abdominal CT scans performed in this scenario may demonstrate 1 or more discrete fluid collections. When there is diffuse peritoneal irritation on clinical examination, fluid collections distant from the anastomosis, or the presence of massive intraperitoneal air, surgical intervention is clearly indicated. Attempts to manage such situations with percutaneous interventions invariably lead to delayed definitive surgical management and adverse outcome.

SURGICAL DRAINAGE

As stated previously, percutaneous drainage is the procedure of choice for the majority of intra-abdominal abscesses, with the caveats being those indicated. Specifically, when the infection is diffuse rather than localized, surgical intervention is clearly indicated. Second, when the content of the abscess is too thick for percutaneous drainage, an initial percutaneous attempt may be reasonable, but conversion to surgery early in the course is reasonable. Finally, when access is impossible, surgery is indicated. This last circumstance is increasingly rare.

The transperitoneal approach allows for examination of the entire abdominal cavity and allows for the drainage of multiple abscesses. Subphrenic abscesses and right subhepatic abscesses may also be approached by lateral abdominal incisions. Once abscess cavities are identified, they are entered and drained quickly to minimize spillage and contamination of the rest of the peritoneal cavity. The abscess cavity should then be widely opened. Specimens should be sent for Gram stain and culture. Copious warm irrigation must be used at the end of the operation to properly cleanse the abdominal cavity. Closed-suction drains should be placed in dependent positions to reduce the risk of reaccumulation. In extremely contaminated cases, the incision may be left open and packed to prevent wound infection.

Definition and Etiology

A fistula is defined as an abnormal communication between 2 epithelial surfaces. Enteric fistulas may arise in a number of settings: (1) diseased bowel extending to surrounding epithelialized structures; (2) extraintestinal disease eroding into otherwise normal bowel; (3) surgical trauma to normal bowel including inadvertent or missed enterotomies; or (4) anastomotic disruption following surgery for a variety of conditions. The first 2 generally occur spontaneously, while the latter 2 occur following surgical procedures. For the surgeon, the latter 2 are generally more problematic, in part because they are iatrogenic complications of surgery, but also because their early management often requires treatment of the critically ill patient with sepsis.

While this chapter overviews general considerations regarding the pathophysiology and management of enteric fistulas, it focuses on postsurgical enteric fistulas, particularly fistulas to the skin, that is, enterocutaneous fistulas. In this particular patient population, the mortality rate remains high, between 3 and 22% in series dating back 6 decades, largely due to the frequent complications of sepsis and malnutrition (Table 16-5). Successful outcome requires a multidisciplinary team of health care workers, including surgeons, infectious disease specialists, intensivists, radiologists, nurses, enterostomal therapists, and nutrition specialists. Management of these patients must also take into account the psychosocial and emotional needs of the patient and his or her family through a prolonged and often complex treatment course.

One of the challenges in attempting to discern optimal management of these patients relates to the quality of the medical literature. Most reports are retrospective reviews of large case series emanating from referral institutions. Notwithstanding this shortcoming, these series provide general approaches to therapy, which help to guide treatment.

Classification

Fistulas involving the alimentary tract have traditionally been classified in 3 distinct ways: by the etiology responsible for their formation, that is, spontaneous versus postoperative; by the anatomy of the structures involved; and finally, by the amount and composition of drainage from the fistula. Such distinctions may provide important prognostic information about the physiologic impact of fistulas and the likelihood that they will close without surgical intervention.

SPONTANEOUS VERSUS POSTOPERATIVE

Enterocutaneous fistulas may be classified as either spontaneous or postoperative. Approximately three-quarters of fistulas occur in the postoperative setting, most commonly subsequent to procedures performed for malignancy, inflammatory bowel disease (IBD), or adhesive bowel obstruction.³³ These fistulas become evident to the surgeon in a number of different ways: (1) They may occur in the early postoperative period as a septic complication of surgery, sometimes with catastrophic physiologic deterioration. This is usually a result of uncontrolled diffuse intra-abdominal infection caused by anastomotic leakage, breakdown of enterotomy closure, or a missed enterotomy. (2) They may occur in a more delayed manner, following treatment of a postsurgical infection with percutaneous drainage of a deep abscess or opening of a superficial wound infection that may reveal an underlying connection to the GI tract as a cause. (3) They may occur very late after the surgery due to unanticipated injury to the GI tract. The development of a wound infection following use of mesh for hernia repair would fall into this category either through erosion of mesh into bowel or due to iatrogenic injury to the bowel as one attempts to debride infected mesh.

Overly aggressive management of an open abdominal wound can also lead to intestinal injury and fistula formation, underscoring the importance of early definitive closure of the abdominal wall, preferably within the first 8 days from the original laparotomy.³⁴ Fistulas have been reported to occur in up to 25% of patients during treatment with an open abdomen for abdominal sepsis.³⁵ Two easily avoidable causes of fistulas in open abdomens managed with vacuum-assisted closure devices are feeding tubes inserted through the bowel wall during surgery and manipulation of anastomoses during VAC dressing changes.

The remaining 25% of fistulas occur spontaneously, that is, without an antecedent surgical intervention. These fistulas often develop in the setting of cancer or inflammatory conditions. Fistulas occurring in the setting of malignancy or irradiation are unlikely to close without operative intervention. Inflammatory conditions such as IBD, diverticular disease, perforated ulcer disease, or ischemic bowel can result in fistula development.³⁶ Of these, fistulas in patients with IBD are most common; these fistulas may close following a prolonged period of parenteral nutrition, only to reopen when enteral nutrition resumes.³⁷

ANATOMIC CLASSIFICATION

Fistulas may communicate with the skin (external fistulas: enterocutaneous or colocutaneous fistulas) or other intra-abdominal or intrathoracic organs (internal fistulas). Internal fistulas that bypass only short segments of bowel may not be symptomatic; however, internal fistulas of bowel that bypass significant length of bowel or that communicate with either the bladder or vagina typically cause symptoms and become clinically evident. Fistulas that occur in the absence of overlying soft tissue cover, known as enteroatmospheric fistulas, are among the most challenging types of fistulas. Identification of the anatomic site of origin of external fistulas may provide further information on the etiology and management of the fistula.

Oral, Pharyngeal, and Esophageal Fistulas

Radical resections and reconstructions for head and neck malignancy may be complicated by postoperative fistulas in 5% to 25% of cases.³⁸ Alcohol and tobacco use, poor nutrition, and preoperative chemoradiation all contribute to poor wound healing and increase the risk of fistula formation. Failure of closure of the pharyngeal defect at the base of the tongue most commonly leads to fistula formation, and free microvascular flaps are the preferred method for closure. Brown and colleagues reported a significantly decreased postoperative fistula rate in patients who underwent free flap closure versus those with pedicled pectoralis flap closure, 4.5 versus 21%, respectively.³⁹

Most esophagocutaneous fistulas result from breakdown of the cervical anastomosis either following resection of esophageal malignancy or following esophageal trauma. Less common causes of oropharyngeocutaneous or esophagocutaneous fistula include tuberculosis, laryngeal or thoracic surgery, trauma, congenital neck cysts, anterior cervical spine fusion, and foreign body perforations.^40-42

Gastric Fistulas

The most commonly reported procedure associated with gastrocutaneous fistula formation is the removal of a gastrostomy feeding tube, particularly in children. The duration of gastrostomy tube placement appears to be related to the likelihood of development of a fistula after tube removal, with nearly 90% of children developing a fistula when the tube had been in situ for more than 9 months.⁴³ The rate of gastrocutaneous fistula following operations for nonmalignant processes such as ulcer disease, reflux disease, and obesity is between 0.5% and 3.9%.⁴⁴ The recent rapid increase in the number of bariatric surgical procedures was anticipated to lead to an increase in the incidence of gastrocutaneous fistula following surgery for benign disease, as the rate of anastomotic leakage after gastric bypass surgery is 2% to 5%. One study has reported that approximately 10% of patients with staple line leaks go on to form chronic fistulas, making the overall rate less than 0.5%.⁴⁵ Fistula formation following resection for gastric cancer remains a dreaded complication with significant mortality rates. Spontaneous gastrocutaneous fistulas are uncommon but can result from inflammation, ischemia, cancer, and radiation.

Duodenal Fistulas

The majority of duodenocutaneous fistulas develop after distal or total gastric resections or surgery involving the duodenum or pancreas. Inadvertent injury to or intentional excision of a portion of the duodenum during surgery of the colon, aorta, kidney, or biliary tract may also result in fistula formation. Spontaneous cases resulting from trauma, malignancy, Crohn disease, and ulcer disease account for the remaining duodenal fistulas.^46,47 Prognostically, duodenal fistulas segregate into 2 groups: lateral duodenal fistulas and duodenal stump fistulas. Some authors have reported a decreased spontaneous closure rate with lateral duodenal fistulas when compared to that with duodenal stump fistulas.^33,48

Small Bowel Fistulas.

Fistulas arising in the small bowel account for the majority of GI-cutaneous fistulas, the majority of which (70%-90%) occur in the postoperative period.^37,49,50 Postoperative small bowel fistulas result from either disruption of anastomoses (either small bowel anastomoses or small bowel to colon anastomoses) or inadvertent and unrecognized injury to the bowel during dissection or closure of the abdomen. Operations for cancer, IBD, and adhesiolysis for bowel obstruction are the most common procedures antecedent to small bowel fistula formation. As noted previously, spontaneous small bowel fistulas arise from IBD, cancer, peptic ulcer disease, or pancreatitis.

Crohn disease is the most common cause of spontaneous small bowel fistula. The transmural inflammation underlying Crohn disease may lead to adhesion of the small bowel to the abdominal wall or other abdominal structures. Microperforation may then cause abscess formation and erosion into adjacent structures or the skin. Approximately half of Crohn fistulas are internal and half are external.^51-53 Crohn fistulas typically follow 1 of 2 courses. The first type represents fistulas that present in the early postoperative period following resection of a segment of diseased bowel. These fistulas arise in otherwise healthy bowel and follow a course similar to non-Crohn fistulas with a significant likelihood of spontaneous closure. The other group of Crohn fistulas arises in diseased bowel and has a low rate of spontaneous closure.

Appendiceal Fistulas

Fistulas of appendiceal origin may result from drainage of an appendiceal abscess or after appendectomy in a patient either without or with Crohn disease.^54,55 In the latter case, the fistula often originates from the terminal ileum, not the cecum. The inflamed ileum adheres to the abdominal wall closure and subsequently results in fistula formation.

Colonic Fistulas

While spontaneous fistulas of the colon may result from inflammatory conditions such as diverticulitis, appendicitis, and IBD, or from advanced malignancy, the majority of colocutaneous fistulas are postsurgical, usually secondary to anastomotic breakdown following colonic resection for 1 of these conditions. Preoperative radiation therapy reduces the risk of local recurrence and death from advanced rectal cancer and is an accepted practice.⁵⁶ However, radiation therapy contributes to both spontaneous and postoperative colocutaneous fistulas. Russell and Welch reported a 31% incidence of breakdown of primary anastomoses performed in irradiated tissues with resulting sepsis or fistula formation.⁵⁷

Enteroatmospheric Fistulas

Enteroatmospheric fistulas tend to occur within the first week of the open abdomen. The incidence of these fistulas depends on the baseline abdominal problem. In trauma patients managed with open abdomen, the incidence of enteroatmospheric fistulas varies between 2% and 25%. The incidence increases to more than 25% in open abdomens for intra-abdominal sepsis, and up to 50% in the setting of infected pancreatic necrosis.