Crohn disease is a chronic inflammatory disease that commonly affects the small bowel, colon, rectum, and anus, but it can also involve the stomach, esophagus, and mouth. CD is a panintestinal condition which may affect any area from the mouth to the anus. The most commonly affected location is the terminal ileum and one-fifth of all patients have more than one intestinal segment affected simultaneously.
The United States, Canada, and Europe have the highest incidence of CD. The current estimated incidence of CD in the United States is approximately four new cases per year for every 100,000 persons, while the prevalence is much higher, between 80 and 150 cases per 100,000.
It is much less common in Asia, South America, and Japan, while accurate data regarding its incidence in Africa are lacking. The peak age for contracting CD is between 15 and 25 years. Familial clusters of disease are not uncommon, with a six- to tenfold increase in the risk of CD in first-degree relatives of those affected by CD or its sister ailment, ulcerative colitis. Although familial aggregations are common, the distribution within families does not indicate a pattern of simple Mendelian inheritance.
The etiology of CD is not known. CD is an altered immune response that results in inflammation and destruction of intestinal tissues. If this altered immune response is the result of a primary dysfunction in the gut-related immune system or whether an unknown pathological trigger induces an otherwise normal immune system to overreact is still unclear. CD may occur in individuals with a genetic predisposition, while environmental triggers may start the pathological sequence that ultimately manifests as CD.
To date, even though an increase in intestinal permeability in both CD patients and their symptom-free first-degree relatives has been demonstrated no specific primary defect in the systemic or mucosal immune system has been identified. This may lead to an altered mucosal barrier function with abnormal interactions between the multitude of antigenic substrates normally found in the gut lumen and the immunocompetent tissue of the submucosa.
Concerning genetic predisposition, the CARD15/NOD2 gene has been linked to susceptibility to CD. CARD15 is a gene product related to innate immunity and it is preferentially expressed to Paneth cells of the ileum. Nevertheless, the known mutations of CARD15 are neither necessary nor sufficient to contract the disease. Hence, it appears that the genetic relationship of CARD15/NOD2 to CD is complex and still poorly understood.
The hypothesis that infectious agents may play a role, either directly as a primary cause of CD, or indirectly as a trigger to stimulate a defective immune system, has always found strength in the identification of noncaseating granulomas as the characteristic histopathologic lesion found in Crohn specimens, and in the isolation of Mycobacterium paratuberculosis from resected CD specimens. Nevertheless, even sensitive preliminary chain reaction studies have been unable to provide definitive evidence for the presence of Mycobacterium paratuberculosis-specific DNA in CD-affected segments of the bowel. Other infectious agents, including measles virus, non-pylori Helicobacter species, Pseudomonas, and Listeria monocytogenes have been studied, but none of them has been consistently associated with CD.
Although diet modification can ameliorate the symptoms of CD, no dietary factor has been identified as a cause of CD. Smoking, however, has been associated with the development of CD. In addition, smoking is known to exacerbate existing CD and can accelerate the recurrence of disease after resection.
Histopathologic examination of CD typically demonstrates transmural inflammation characterized by multiple lymphoid aggregates in a thickened and edematous submucosa that can be found within the muscularis propria. Another typical microscopic feature of CD is the noncaseating granuloma. However, it is demonstrated in only 50% of resected specimens and is rarely detected on endoscopic biopsies. Additionally, the presence of granulomas does not correlate with disease activity.
Small mucosal ulcerations, called aphthous ulcers, are the earliest gross manifestations of CD. They appear as red spots or focal mucosal depressions, typically directly over submucosal lymphoid aggregates. As the inflammation progresses, the aphthous ulcers enlarge and become stellate. They then coalesce to form longitudinal mucosal ulcerations always along the mesenteric aspect of the bowel lumen. Further progression leads to a serpiginous network of linear ulcerations that surround islands of edematous mucosa producing the classic “cobblestone” appearance. Mucosal ulcerations may penetrate through the submucosa to form intramural channels that can bore deeply into the bowel wall and create sinuses, abscesses, or fistulas.
The inflammation of CD also involves the mesentery and regional lymph nodes such that the mesentery may become massively thickened. With early acute intestinal inflammation, the bowel wall is hyperemic and boggy. As the inflammation becomes chronic, fibrotic scarring develops and the bowel wall becomes thickened and leathery in texture.
The clinical presentation and symptoms of CD depend on the involved segment, the pattern and the severity of disease, and the associated complications. The onset of CD is often insidious and many patients will experience some symptoms for months or even years before the diagnosis is made. The most common complaints are intermittent abdominal pain, bloating, diarrhea, nausea, vomiting, weight loss, and fever. Abdominal pain occurs in 90% of cases: when related to partial obstruction it is mostly postprandial and crampy in nature, while when it is from septic complications it is typically steady and associated with fever. Weight loss is usually related to food avoidance, but in severe cases weight loss may be the result of malabsorption. Symptoms can also be related to complications including abdominal mass, pneumaturia, perianal pain and swelling, or skin rash. Rarely some patients can experience a more sudden onset of pain in the right-lower quadrant, mimicking an acute appendicitis.
In patients suspected of having CD, a complete physical exam should include a thorough abdominal evaluation. In cases of ileal CD, tenderness is typically present in the right-lower quadrant and occasionally a palpable mass is present. The oral cavity should be examined for aphthous ulcers, while the presence of fistulas, abscesses, or enlarged skin tags should be assessed in the perianal area. A digital rectal examination should assess for the presence of anal strictures, fissures, and rectal mucosal ulcerations. The skin in the extremities should be examined for the presence of erythema nodosum and pyoderma gangrenosum.
Even though CD can be categorized into three general manifestations, such as stricturing, perforating, and inflammatory disease, these three classes do not represent truly distinct forms of the disease. It is typical that the same patient can present with more than one pattern even in the same segment of bowel. Nevertheless, one pattern tends to be predominant in most cases, determining the clinical presentation and affecting the therapeutic options.
Fibrotic scar tissue is the result of chronic inflammation of CD, and it constricts the intestinal lumen with cicatricial strictures often referred to as “fibrostenotic lesions.” Patients with a stricturing pattern of disease generally develop partial or complete intestinal obstruction, and hence their symptoms are primarily obstructive in nature. Being the result of scar tissue, these strictures are not reversible with medical therapy and surgical intervention is often required.
Perforating CD is characterized by the development of sinus tracts, fistulae, and abscesses. The sinus tracts penetrate through the muscularis propria and give rise to abscesses or to fistulas if they penetrate into surrounding structures. Inflammatory response around the advancing sinus tract typically results in adhesion to surrounding structures, therefore, free perforation with spillage of intestinal contents into the abdominal cavity is uncommon. Typically, perforating disease is accompanied by a degree of stricture formation, but the fistula or abscess generated by the perforating component of the disease dominates the clinical picture.
The inflammatory pattern of CD is characterized by mucosal ulceration and bowel wall thickening. The edema that results from inflammation can lead to an adynamic segment of intestine and luminal narrowing. This pattern often gives rise to obstructive symptoms. Of the three patterns of disease, the inflammatory pattern is much more likely to respond to medical therapy.
Other common symptoms and findings include anorexia and weight loss. Patients may develop a palpable mass, usually located in the right-lower quadrant, related to an abscess or phlegmon in perforating disease or a thickened loop of intestine in obstructive disease. Evidence of fistulization to the skin, urinary bladder, or vagina may also be elicited with an accurate history and physical exam.
There is no specific laboratory test that is diagnostic for CD. The diagnosis is made by a thorough history and physical examination along with intestinal radiography and endoscopy. Advanced imaging studies such as CT scan or magnetic resonance imaging (MRI) can assess or detect some of the complications and manifestations of CD, but they are generally not useful in making the initial diagnosis of CD.
Small bowel follow-through or enteroclysis are the best means for assessing the small bowel for CD. The radiographic abnormalities are often distinctive. Mucosal granulations with ulceration and nodularity can be identified in the early stages of the disease. Thickening of the mucosal folds and edema of the bowel wall can be demonstrated as the disease progresses. With more advanced disease, cobblestoning becomes radiographically apparent. Small bowel contrast studies can also provide information regarding enlargement of the mesentery, as well as formation of an inflammatory mass or abscess demonstrated by a general mass effect separating and displacing contrast-filled loops of small intestine. Even though small bowel contrast studies can demonstrate some of the complications of CD, including high-grade strictures and fistulas, they may not identify all such lesions, including ileosigmoid and ileovesical fistulas. Additionally, small bowel studies may not demonstrate all the areas of disease with significant strictures. Small bowel radiographs can also help in assessing the extent of the disease by identifying the location and length of involved and uninvolved small bowel, and by recognizing whether the disease is continuous or discontinuous with skip lesions separated by areas of normal intestine. Experienced radiologists can also assess areas of luminal narrowing and determine if they are the result of acute inflammatory swelling or are the result of fibrostenotic scar tissue. Such a distinction provides valuable information regarding the value of medical therapy versus early surgical intervention, as inflammatory stenoses are likely to respond to medical therapy while fibrotic strictures are best treated with surgery.
Computed tomography findings of uncomplicated CD are nonspecific and routine CT is not necessary for the diagnosis of CD. CT, however, is very useful in identifying the complications associated with CD—thickened and dilated intestinal loops, inflammatory masses, abscesses, and hydronephrosis resulting from retroperitoneal fibrosis and ureteral narrowing (Figure 29–4). CT is also the most sensitive indicator of an enterovesical fistula as suggested by the presence of air within the urinary bladder. More recently cross-sectional imaging techniques have assumed an increasing role in the imaging of patients with CD. Computed tomography enterography (CTE) has been shown to have a higher sensitivity than barium small-bowel follow through. Based on these findings, CTE is often used combined with ileocolonoscopy as a first-line test for the diagnosis and staging of CD. CTE has several potential advantages over barium studies in the identification of fistulizing disease. CTE does not suffer from superimposition of bowel loops, and it displays the mesentery, retroperitoneum, and abdominal wall musculature, typically involved by fistulas. CTE can also readily identify sinus tracts and abscesses. However, recent concerns about radiation-induced cancer arising from medically related CT in young CD patients have encouraged the use of magnetic resonance enterography (MRE). MRE has the same advantages of CTE but does not require ionizing radiation.
CT scan showing a markedly thickened loop of distal ileum (arrow) causing obstruction of the more proximal small bowel in regional enteritis.
While upper endoscopy is useful in the diagnosis of mucosal lesions of the esophagus, stomach, and duodenum a colonoscopy often allows the evaluation of the terminal ileum.
Capsule endoscopy can detect subtle mucosal lesions that may not be apparent on small bowel x-rays. The value of capsule endoscopy in the diagnosis of CD has been recently evaluated: the rate of abnormalities detected on capsule endoscopy is higher than that of CTE only for the subgroup of patients with known CD. The need for a preliminary small bowel contrast study to detect asymptomatic partial small-bowel obstruction before the capsule endoscopy and the lack of a clear advantage over other imaging studies, limits the utility of capsule endoscopy as a first-line test in CD, and perhaps reserve this study for those cases in which there is a substantial diagnostic uncertainty.
The differential diagnosis includes irritable bowel syndrome, acute appendicitis, intestinal ischemia, pelvic inflammatory disease, endometriosis, and gynecological malignancies. Other disorders are radiation enteritis, Yersinia infections, intestinal injury from nonsteroidal anti-inflammatory agents, intestinal tuberculosis, and small bowel tumors.
When malignancy is suspected, resection should be undertaken to make the diagnosis certain. The exclusion of intestinal tuberculosis can be difficult, as the inflammation and strictures of the terminal ileum can occur very similarly to CD. A previous exposure to tuberculosis should be evaluated and purified protein derivative skin test should be performed, along with chest radiography. Even when the diagnosis of CD is certain, patients who coincidentally are found to also have latent tuberculosis should be treated in accordance with the American Thoracic Society guidelines prior to the initiation of immunosuppressive therapy for management of CD.
Intestinal injury from nonsteroidal anti-inflammatory drugs (NSAIDs) can result in focal enteritis with ulcerations and strictures. These manifestations can be very difficult to distinguish from CD of the small bowel, and often require resection or biopsy to confirm the diagnosis.
Long-lasting symptomatic relief while avoiding excessive morbidity is the goal of medical treatment of CD. Even though CD cannot be cured by medical treatment long periods of disease control can be obtained avoiding a surgical intervention. Medical treatment for each individual is based on the course of the disease, the clinical presentation and associated complications.
Corticosteroids are the most effective agents for controlling acute exacerbations of CD, but their use is limited due to the risk of serious side effects, including diabetes, osteoporosis, cataracts, osteonecrosis, myopathy, psychosis, opportunistic infections, and adrenal suppression, that are related to both the dose and the duration of steroid therapy. The majority of patients with active small bowel CD will experience clinical remission with a short course of oral prednisone given in a dose between 0.25 and 0.5 mg/kg/d. For patients unable to take oral medications, methylprednisolone can be administered in the adult at doses of 40-60 mg given as a daily infusion.
The aminosalicylates include sulfasalazine and 5-aminosalicylic acid (5-ASA) derivatives. They inhibit leukotriene production by inhibiting 5-lipooxygenase activity and the production of inter-leukin-1 and tumor necrosis factor (TNF). Aminosalicylates are effective in the treatment of mild to moderate CD. 5-ASA given in a controlled-release preparation is also effective as maintenance therapy to prevent recurrence after a flare of disease has been effectively managed either medically or surgically.
Aminosalicylates come in a variety of preparations, each designed to deliver the drug in a topical fashion to the affected bowel segments. For instance, Asacol is 5-aminosalicylic acid contained within a pH-dependent resin that releases the drug in the terminal ileum and colon where the pH is greater than 7.0. Pentasa is 5-aminosalicylic acid contained within ethylcellulose-coated microgranules that slowly releases the active compound throughout the entire small bowel and colon. Azathioprine and 6-mercaptopurine (6-MP) are immunosuppressive agents that inhibit cytotoxic T-cell and natural killer cell function. These agents are effective in treating mild to moderate CD. Azathioprine given at 2.0-2.5 mg/kg/d or 6-MP in doses of 1.0-1.5 mg/kg/d will result in a 50%-60% response rate in patients with active CD. Both 6-MP and azathioprine are also effective in maintaining remission following surgery or successful medical management.
Infliximab is a chimeric mouse-human monoclonal antibody to TNF that is a proinflammatory cytokine that may be important in the pathophysiology of CD. Infliximab binds to both free and membrane-bound TNF, and prevents TNF from binding to its cell surface receptors. Clinical trials have demonstrated an 80% response rate with a single dose of infliximab. It is important to note that the doses and dosing intervals of infliximab must be individualized, but a typical regimen would include 5 mg/kg of infliximab given IV at weeks 0, 2, and 6, with a dose of 5 mg/kg every 8 weeks thereafter. Because Infliximab is a potent immunosuppressive agent concerns have been raised about the risk for poor wound healing and postoperative septic complications. Nevertheless, current available data on the perioperative risks associated with infliximab does not seem to support this hypothesis.
Other agents that are used with varying success in the treatment of CD include methotrexate, metronidazole, cyclosporine, tacrolimus, and thalidomide.
Similarly to medical treatment, the goal of surgical treatment of CD is to provide long-lasting symptomatic relief while avoiding excessive morbidity. Like medical treatment, surgery should be considered palliative. Therefore, treatment of complications and palliation of symptoms while avoiding excessive resection of small bowel should be the main aims of surgical treatment.
To avoid excessive loss of small bowel, nonresectional techniques such as strictureplasty may be required. In addition, optimal surgical therapy should be the resection of the only areas of severe and symptomatic CD, leaving behind segments of small bowel affected by mild but asymptomatic CD based on the high risks of recurrence and repeated operations.
C. Indications for Surgery
1. Failure of medical treatment
The failure to respond to medical treatment, the inability to tolerate effective therapy are the most common indications for surgical treatment of CD, as the occurrence of complications related to the medical treatment or the progression of disease while on maximal medical treatment. Some patients may respond to the initial medical therapy only to rapidly relapse with tapering of the medical treatment. For example, some patients respond well to steroid therapy, but become steroid-dependent as tapering of the steroid dose results in recurrent symptoms. Due to the severe complications that are virtually inevitable with prolonged steroid treatment, surgery is warranted if the patient cannot be weaned from systemic steroids within 3-6 months.
2. Intestinal obstruction
Partial or complete intestinal obstruction is a common indication for operation. The clinical presentation of chronic partial SBO is much more typical than complete obstruction, and postprandial cramps, abdominal distension, borborygmi, and weight loss are common symptoms. To avoid them, many patients restrict the diet to soft foods or even liquids. In case of partial obstruction primarily due to acute inflammation and bowel wall thickening, initial medical therapy is warranted. If, however, the obstructive symptoms are secondary to high-grade fibrostenotic lesions, surgery is indicated because medical treatment will not reverse these lesions.
When complete intestinal obstruction occurs, initial conservative treatment consists of nasogastric decompression and intravenous hydration along with administration of intravenous steroids. This treatment leads to decompression of acutely distended and edematous bowel, and in most cases, to resolution of the complete obstruction. However, even patients with complete resolution of the acute obstruction after the initial conservative treatment are at high risk for recurrent episodes of obstruction and are best managed with elective surgery once adequate decompression and resuscitation is achieved. If the obstruction fails to respond to appropriate conservative treatment, then surgery is required. In these situations, a high index of suspicion for small bowel cancer as the cause of the obstruction is mandatory, as obstructions from cancers do not respond to bowel decompression and steroid treatment.
Intestinal fistulas occur in one-third of CD patients. However, the presence of an intestinal fistula is not in and of itself an indication for surgery. In general, it is the primary indication for surgery if the fistula is in connection with the genitourinary tract, or if their drainage causes personal embarrassment and discomfort (enterocutaneous and enterovaginal fistulas), or if a bypass causing intestinal malabsorption is created.
Fistulas can be classified according to anatomic site, characteristics of the tract (simple vs. complex), and volume of output (high vs. low). A low volume output is less than 200 mL/24 h, while a high volume output is more than 500 mL/24 h.
Ileosigmoid fistula is a common complication of perforating CD of the terminal ileum. Typically, the inflamed terminal ileum adheres to the sigmoid colon that is otherwise healthy. Most ileosigmoid fistulas are small and asymptomatic. These ileosigmoid fistulas do not in and of themselves require operative management. On the other hand, large ileosigmoid fistulas can result in bypass of the intestinal contents from the terminal ileum to the distal colon and thus give rise to debilitating diarrhea. Such symptomatic fistulas should be managed surgically, as they often fail to respond to medical therapy.
More than half of the ileosigmoid fistulas from CD are recognized intraoperatively. Ileosigmoid fistulas can be managed by simple division of the fistulous adhesion and resection of the ileal disease. The defect in the sigmoid colon is then debrided and simple closure is undertaken. In about 25% of cases, resection of the sigmoid colon is needed, particularly when primary closure of the fistula is at risk for poor healing. This is the case when either the sigmoid is also involved in CD, when the fistulous opening is particularly large, or when there is extensive fibrosis extending along the sigmoid colon. Also, fistulous tracts that enter the sigmoid colon in proximity to the mesentery can be difficult to close and often require resection and primary anastomosis.
Ileovesical fistulae occur in approximately 5% of CD patients. Although hematuria and fecaluria are virtually diagnostic of ileovesical fistula, these symptoms are absent in almost 30% of cases. Air within the bladder, as noted on CT scan, is often the best indirect evidence for the presence of an enterovesical fistula, while small bowel x-rays, cystogram, and cystoscopy often do not detect the fistula. An ileovesical fistula is an indicator of complex fistulizing disease, as most ileovesical fistulas occur along with other enteric fistulae.
The necessity for surgery for ileovesical fistula is controversial. While it is not mandatory to operate on all cases of enterovesical fistulas, surgery is warranted to avoid deterioration of renal function with recurrent infections or if symptoms persist in spite of appropriate medical therapy.
Surgical treatment of ileovesical fistulae requires resection of the ileal disease with closure of the bladder defect. Most ileovesical fistulas involve the dome of the bladder, and thus debridement and primary closure can be accomplished without risk of injury to the trigone. Decompression of the bladder with an indwelling Foley catheter should be continued postoperatively until the bladder is confidently healed without leaks. A cystogram taken postoperatively is useful to confirm the seal of the bladder repair, before removing the Foley catheter.
6. Enterovaginal and enterocutaneous fistulas
These are rare fistulas caused by perforating small bowel disease draining through the vaginal stump in a female who has previously undergone a hysterectomy or through the abdominal wall, usually at the site of a previous scar. These fistulas often require surgical intervention because they cause physical discomfort and personal embarrassment. Surgical treatment requires resection of the small bowel disease. The vaginal cuff does not need to be closed; the chronic infection along the abdominal wall fistulous tract requires debridement and wide drainage to allow healing by secondary intention.
Intra-abdominal CD abscesses tend to have an indolent course with modest fever, abdominal pain, and leukocytosis. In up to 30% of cases preoperative clinical signs of localized infection are absent and the abscesses are discovered only at the time of operation. When an abscess is suspected or an abdominal mass is palpated, a CT scan should be obtained, as 50% of tender intra-abdominal masses will harbor an abscess collection within. The CT scan can detect most chronic abscesses and can also delineate the size and location of the abscess as well as the relationship of the abscess to critical structures such as the ureters, duodenum, and the inferior vena cava.
In the majority of cases, abscesses are very small collections contained within the area of diseased small bowel and its mesentery. In the case of small intraloop or intramesenteric abscesses, resection of the involved bowel segment and its mesentery often extirpates the abscess such that drains are not necessary and primary anastomosis can be performed without risk.
Large abscesses are best managed with CT-guided percutaneous drainage. However, abscess drained percutaneously is very likely to recur or result in an enterocutaneous fistula, and surgical resection is often advised even after successful drainage. Such a fistula may spontaneously close or it may persist and the intestine may continue to be a source of sepsis. With successful drainage of the abscess, the sepsis often clears well enough that it can be tempting to try to manage the disease without subsequent surgery. In the absence of symptoms, initial non-operative management after successful percutaneous drainage can be undertaken in carefully selected patients. If drainage through the fistula continues, surgical resection of the affected segment of intestine becomes necessary.
Free perforation is a rare complication of CD occurring in less than 1% of patients because the chronic progressive inflammation of CD usually leads to adhesions with adjacent structures, and it is an obvious indication for urgent operation with resection of the diseased segment and exteriorization of the proximal bowel as an end ileostomy. The diagnosis of free perforation is made by detecting a sudden change in the patient’s symptoms along with the development of the physical findings of peritonitis or the identification of free intraperitoneal air as demonstrated on plain x-rays or CT scan. The use of immunosuppressants and glucocorticosteroids can blunt many of the physical findings of acute perforation; therefore the index of suspicion for perforation must be higher in immunocompromised patients.
Creation of a primary anastomosis even with a proximal protecting loop ileostomy carries a high risk of anastomotic breakdown and should be avoided. Primary closure of the perforation should never be attempted, as sutures will not be able to approximate the edges of the perforated, edematous, and diseased bowel in a satisfactory and tension-free way and the presence of a distal intestinal stenosis or partial obstruction will cause an increase in the intraluminal pressure at the level of the local repair with subsequent dehiscence.
Hemorrhage is an uncommon complication from small bowel CD. Angiography in the presence of brisk bleeding leads to localization of the site of bleeding. Bleeding from small bowel tends to be indolent with episodic or chronic bleeding requiring intermittent transfusions, but rarely requires emergent surgery. However, because the risk of recurrent bleeding is high, elective resection of the areas of CD is recommended. Finally, risk for bleeding from peptic ulcer disease is increased in patients, particularly in those receiving corticosteroids.
10. Cancer or suspicion of cancer
The presence of CD increases the risk of adenocarcinoma of the small bowel. The diagnosis of adenocarcinoma of the small bowel is difficult because symptoms and radiographic findings can be similar to those of the underlying CD. Male patients, patients with long-standing disease and patients with defunctionalized segments of bowel appear to be at increased risk for small bowel adenocarcinoma. For this reason, bypass surgery should be avoided for CD of the small intestine and defunctionalized rectal stumps should either be restored to their function or excised.
Adenocarcinoma of the small intestine should be suspected in any patient with long-standing disease whose symptoms of obstruction progress after a lengthy quiescent period.
Growth retardation occurs in a quarter of children affected by CD. Although steroid treatment may delay growth in children, the major cause of growth retardation in CD patients is due to the malnutrition associated with active intestinal disease.
Intestinal resection with anastomosis is the most common surgical procedure performed for the treatment of small bowel CD. In most cases of CD only limited resections are required with no risk for short bowel syndrome. Only grossly apparent disease should be resected, as wider resections do not improve the surgical outcomes. Grossly normal resection margins with microscopic evidence for CD activity are not associated with early recurrence or other complications. Therefore, intraoperative frozen section of the resection margins is not necessary.
The extent of mesenteric dissection does not affect the long-term results. Division of the thickened mesentery of small bowel CD can be the most challenging aspect of the procedure, as identification and dissection of individual mesenteric vessels is often not feasible. A common technique consists of the application of overlapping clamps on either side of the intended line of transection. The mesentery is then divided between the clamps and the tissue contained within the clamps is suture ligated. In severe cases, a vascular clamp may be used at the root of the small bowel mesentery to obtain proximal control: mattress sutures may then be need to be applied to the cut edge of the mesentery to control bleeding. Even when tissue welding devices such as the LigaSure device are used, mattress sutures in the mesentery are commonly needed for complete hemostasis.
There is no consensus regarding the optimal technique for intestinal anastomosis in CD. Recurrent CD after resection of terminal ileum is most likely to occur at the ileocolonic anastomosis or at the pre-anastomotic ileum. It has been proposed that large caliber anastomoses require a longer period to stricture down to a critical diameter that becomes symptomatic. The argument is made that a longer side-to-side anastomosis may be beneficial over an end-to-end or end-to-side anastomosis. To date, however, clinical data do not indicate a benefit for one particular intestinal configuration over another. Intestinal anastomosis for CD cases can be fashioned with a stapling device or may be hand sutured. Under selective conditions, small bowel anastomotic dehiscence rates is under 1%. In the presence of sepsis, severe scarring, malnutrition, or recent treatment with methotrexate or infliximab, it may be wise to protect the anastomosis with a proximal loop stoma or to forego the anastomosis altogether and bring out an end stoma at the point of resection.
Initially conceived to bypass an area of stricture or obstruction, the use of bypass procedures was eventually extended to CD complicated by septic complications. Increased experience with bypass procedures revealed that patients with persistent disease are at higher risk of persistent sepsis, and eventually neoplastic transformation. Therefore, bypass procedures were supplanted by limited intestinal resection as the main surgical option in the late 1960s in all intestinal districts except the duodenum, where a simple side-to-side retrocolic gastrojejunostomy adequately relieves the obstructive symptoms. With increased experience in the performance of strictureplasty, duodenal disease is nowadays more and more commonly handled with strictureplasties.
Strictureplasties are best performed when resection would otherwise result in loss of a long segment of bowel with an increased risk for short bowel syndrome, including cases of stricturing disease involving long segments of bowel and patients with multiple prior resections. They are also indicated as a simpler alternative to resection in case of short recurrent disease at a previous ileocolic or enteroenteric anastomosis.
There is increased evidence that the acuity of the disease decreases at the site of the strictureplasty and the disease becomes quiescent, maybe in correlation with a simultaneous restoration of absorptive function.
The most commonly performed strictureplasty is the Heinecke–Mikulicz strictureplasty, that is appropriate for short segment strictures of 2-5 cm in length. A longitudinal incision is made along the antimesenteric border of the stricture extending for 1-2 cm into the normal elastic bowel on either side of the stricture. Once the enterotomy is made, the area of the stricture should be closely examined to rule out a malignancy. The longitudinal enterotomy of the Heinecke-Mikulicz strictureplasty is then closed in a transverse fashion with either single- or double-layered sutures.
The Finney strictureplasty can be used for strictures up to 15 cm in length. The strictured segment is folded onto itself in a U-shape, and a row of seromuscular sutures is placed between the two arms of the U. A longitudinal U-shaped enterotomy is then made paralleling the row of sutures. The mucosal surface is examined and biopsies are taken as necessary. In essence, the Finney is a short side-to-side functional anastomosis. A very long Finney strictureplasty may result in a functional bypass with a large lateral diverticulum that, in theory, could be at risk for bacterial overgrowth and the blind loop syndrome. However, this theoretical concern has not been observed in clinical practice.
Repeated Heinecke–Mikulicz or Finney strictureplasties to manage multiple strictures should be separated from each other by at least 5 cm, in order to avoid excessive tension on each suture line.
Patients with long segment stricturing disease and multiple strictures grouped close together are best managed with a side-to-side isoperistaltic strictureplasty, also called Michelassi strictureplasty. The segment of stricturing disease is divided at its midpoint. The proximal and distal ends are then drawn onto each other in a side-to-side fashion. Division of some of the mesenteric vascular arcades facilitates the positioning of the two limbs over each other. The proximal and distal loops are then sutured together with a layer of interrupted seromuscular sutures. A longitudinal enterotomy is then made along both of the loops. The intestinal ends are spatulated to provide a smoothly tailored fit to the ultimate closure of the strictureplasty. The outer suture line is reinforced with an interior row of either interrupted or running full-thickness sutures. This inner suture line is continued anteriorly. The anterior closure is then reinforced with an outer layer of interrupted seromuscular sutures to complete the strictureplasty. In appropriately selected patients, perioperative morbidity from strictureplasty appears to be similar to that of resection and primary anastomosis. Specifically, intestinal suture line dehiscence appears to be uncommon with any of the described strictureplasty techniques. The most common postoperative complication directly related to strictureplasty is hemorrhage from the strictureplasty site, in up to 9% of cases. Usually, the gastrointestinal hemorrhage following strictureplasty is minor and can be managed conservatively with transfusions alone. Rarely, a reoperation to control hemorrhage after strictureplasty is necessary. It is by now also well established that strictureplasty techniques provide excellent long-term symptomatic relief which is comparable to resections with anastomosis.
Most CD patients are well suited for laparoscopy. They are usually young, otherwise healthy, and interested in undergoing an operation that involves minimal scarring, since they are facing the risk of multiple major abdominal operations in their lifetime.
The indications for laparoscopic surgery for CD should not differ from conventional open surgery as described before. Contraindications to a laparoscopic approach include patients who are critically ill and unable to tolerate the pneumoperitoneum due to hypotension or hypercarbia, patients with extensive intra-abdominal sepsis (abscess, free perforation, or complex fistula), and difficulty in identifying the anatomy (previous surgery, obesity, or adhesions). The same variety of surgical procedures described earlier can be performed laparoscopically.