Inflammatory Diseases of the Intestines
Sean P. Whelan
Vaishali D. Schuchert
Brian S. Zuckerbraun
Inflammatory Diseases of the Stomach and Small Intestine
I. Gastroduodenal Perforation
Perforation of the stomach or duodenum can be secondary to trauma, neoplasm, foreign body ingestion, or iatrogenic perforation from diagnostic or therapeutic procedures. The most common cause of gastroduodenal perforation is ulcer disease, with an incidence between 2% and 10% in patients with ulcers. For more details regarding peptic ulcer disease refer to Chapter 51. In this section we will focus on other common causes of perforation including marginal ulcer and iatrogenic perforation.
Marginal ulcer
A perforated marginal (perianastomotic) ulcer occurs in a patient who has surgically altered anatomy by previous gastrojejunostomy or other gastric anastomosis. With increasing numbers of patients undergoing bariatric surgery, understanding short- and long-term complications is key. Elective surgery is occasionally performed for intractable ulcers (not responding to maximal medical therapy after 3 months.) Emergency surgery may be necessary in the case of perforated marginal ulcers.
Incidence
The reported incidence of marginal ulcer after Roux-en-Y gastric bypass (RYGB) varies from 1% to 16%, with a median time of presentation 18 months after RYGB. Gastric partition without transection (commonly performed in open gastric bypass) has a higher incidence of marginal ulcer than with transection of the stomach.
Pathophysiology
Smoking, excessive alcohol intake, NSAID, and steroid use increase risk for the development of marginal ulcers. Ulceration is most commonly on the jejunal side of the anastomosis, suggesting acid exposure from the stomach as a causative factor. Neither prophylactic acid suppression nor vagotomy reduces the rate of marginal ulcers after RYGB.
Management
Goals of an emergency operation for perforated marginal ulcer are the same as in any upper gastrointestinal perforation: Close the defect, ensure adequate drainage, and manage sepsis. Alternate enteral access for postoperative nutritional support may be required, generally jejunostomy.
A large ulcer or abscess may require resection. Anastomosis in the face of frank purulence or shock should be deferred until the patient has recovered. Laparoscopic repair of perforated marginal ulcer is an option in stable patients without abscess.
Iatrogenic perforation
With more liberal use of esophagoduodenoscopy for diagnostic and therapeutic purposes, iatrogenic injury is an increasingly common cause of gastroduodenal perforation. Endoscopic retrograde cholangiopancreatography (ERCP) carries a risk of perforation between 0.5% and 2%. Perforation is described rarely following placement of inferior vena cava filters or biliary stents.
Management
Microperforation secondary to a wire or sphincterotomy during ERCP often may be managed non-operatively. If needed, the standard therapy for free
duodenal wall rupture has traditionally been surgical repair. Advances in endoscopic techniques now allow possible closure of a duodenal perforation endoscopically if recognized immediately and the defect is small.
Intravenous antibiotics and close observation are mandatory.
If surgical repair of an iatrogenic gastric or duodenal perforation is indicated (size, ongoing leak), the patient’s hemodynamic status guides surgical management. Repair of the defect, peritoneal lavage, and placement of drains can be done by laparoscopy or laparotomy.
The patient with peritonitis and in shock should be managed with laparotomy with antifungal therapy added to broad antibiotic therapy.
A repaired gastric defect may not require extraluminal drains, but a duodenal perforation should be drained widely after repair.
Proximal decompression in either case is achieved adequately with a well-positioned nasogastric tube on sump suction.
We do not recommend lateral duodenostomy, but favor placement of closed suction drains in Morison’s pouch to provide egress for potential duodenal leak in the form of a controlled fistula.
Create surgical enteral access for postoperative nutritional support.
II. Crohn’s disease of the small bowel
Introduction. Crohn’s disease is the most common primary surgical disease of the small intestine. It is an inflammatory process which can affect any portion of the alimentary tract from mouth to anus, but most commonly affects the terminal ileum. Up to 55% of patients with Crohn’s disease have ileocolic disease, 30% have isolated small bowel disease, and 15% to 30% have disease involving only the colon or anorectum.
Pathophysiology
Unlike ulcerative colitis, Crohn’s disease is transmural and often discontinuous. Grossly, the affected bowel is characterized by creeping fat and a thickened bowel wall and mesentery. Cobblestoning of the mucosa is characteristic but is not pathognomonic of Crohn’s disease.
Crohn’s disease is associated with a greater degree of extraintestinal manifestations as compared to ulcerative colitis, with up to 25% of patients having at least one extra-intestinal manifestation of disease (Table 52-1).
Etiology/risk factors
The incidence of Crohn’s disease is highest in North America and Northern Europe. Males and females appear to be affected equally.
Peak incidence is in the third decade of life with a smaller peak in the sixth decade of life.
Management
No cure is known for Crohn’s disease; the goals of treatment are amelioration of symptoms and improvement in quality of life. Fifty percent to 70% of patients with Crohn’s disease will require an operation at some point, but surgery is reserved for refractory cases or in those with complications.
Initiate prophylaxis for all hospitalized patients against venous embolism since inflammatory bowel disease (IBD) is a risk factor for development of deep venous thrombosis.
Clinical patterns of Crohn’s disease are stricturing, perforating, and inflammatory. Fibrosis and stenosis of discontinuous segments of bowel are the hallmark of the stricturing pattern. Repeated episodes eventually lead to strictures that no longer respond to medical therapy and ultimately require surgery. Abscess and fistulae characterize the perforating pattern. The inflammatory pattern tends to produce a more diffuse distribution, generally treated medically.
Extraintestinal Manifestations of Crohn’s Disease (from Schuchert et al.)
Eyes
Uveitis
Iritis
Episcleritis
Conjunctivitis
Skin
Erythema nodosum
Erythema multiforme
Pyoderma gangrenosum
Blood
Deep venous thrombosis/pulmonary embolism
Hemolytic anemia
Thrombocytosis
Liver and pancreas
Sclerosing cholangitis
Triaditis
Pancreatitis
Joints and bones
Ankylosing spondylitis
Arthritis
Spondyloarthropathy
Osteoporosis
Clubbing
Kidney
Nephrotic syndrome
Amyloidosis
Nervous system
Seizure
Stroke
Myopathy
Peripheral neuropathy
Headache
Treatment of inflammatory Crohn’s disease
First line therapy for mild symptoms is 5-ASA (Pentasa, Asacol).
For a severe acute episode, or “Crohn’s flare,” corticosteroids are the usual treatment to induce remission.
Budesonide is often used to induce remission because of less systemic absorption and more tolerable side effects compared to prednisone.
Antibiotics, typically metronidazole, may be used as adjunctive therapy.
Infliximab, a monoclonal antibody against TNF-alpha, is used for the treatment of severe active Crohn’s disease resistant to conventional therapy. Infliximab is effective as an induction agent, up to 70% patients responding within 1 to 2 weeks from a single infusion.
Following successful induction therapy, the goal of treatment becomes maintenance of remission. Steroids are ineffective as maintenance therapy. The two most common agents used for maintenance of remission are azathioprine and 6-mercaptopurine. Patients must be monitored closely for complications which include bone marrow suppression, hepatotoxicity, and pancreatitis.
Treatment of perforating Crohn’s disease
The primary goal of treatment for abscess or fistula is control of sepsis. Image-guided drainage of an abdominal abscess with parenteral antibiotics is the mainstay of therapy.
Nutritional and metabolic support are essential.
The three most important types of fistulae are enterocutaneous, enteroenteral, and enterovesical.
Enterocutaneous fistulae (ECF) occur in 4% of patients with Crohn’s disease. Medical management should be initiated with antibiotics, nutritional support, and infliximab, the latter associated with greater than 60% response rate for closure.
Enteroenteral fistulae in themselves do not mandate operation. Surgery is indicated if the fistulae are associated with an acute inflammatory exacerbation refractory to medical management, abdominal mass, hemorrhage, or uncorrectable malnutrition.
Enterovesical fistula is characterized by chronic or recurrent urinary tract infection (88%), pneumaturia (88%), fecaluria (38%), and hematuria (63%). Do operative repair of enterovesical fistulae to prevent injury to the kidneys from recurrent urinary tract infections.
Diagnostic imaging
Radiographs with oral contrast and small bowel follow-through help determine length of bowel and location of disease, identify fistulae, and evaluate strictures.
CT identifies masses, fluid collections, and bowel wall thickening.
Colonoscopy may help establish the presence and extent of disease.
Preoperative workup
Assess and optimize the nutritional status prior to surgery.
A bowel prep should be performed if possible.
Consult with the stoma care nursing team for preoperative counseling and marking potential stoma sites is helpful.
Seek any history of recent corticosteroid use to determine whether perioperative steroid replacement or stress dosing is needed. Perioperative corticosteroid use increases postoperative complications, so a rapid taper postoperatively should be a goal when possible.
Other immunosuppressive medications may be safely discontinued preoperatively.
Operative indications
Surgical therapy of Crohn’s disease is aimed at treatment of complications, relief of symptoms, and optimization of quality of life. Urgent operation may be necessary for free perforation (rare), acute hemorrhage, or uncontrolled sepsis from abscesses not amenable to percutaneous drainage.
Less urgent operation is indicated for enterovesical fistula or acute Crohn’s flare, obstruction, or fistula refractory to medical management.
Operative approach
Whether elective or emergent, open or laparoscopic, certain basic principles apply to the surgical management of Crohn’s disease.
Resect only the segment causing complications and only to grossly (not microscopically) negative margins; minimize length of resected intestine.
Stricturoplasty is a good option when dealing with obstruction.
Consider bypass a last resort because of the risk of bleeding, perforation, and future malignancy in the bypassed portion, although it may be the only viable option with duodenal disease.
In high-risk patients (high-dose steroids, profound malnutrition) endostomy or protective loop ileostomy for a distal anastomosis is advisable.
Perform an appendectomy when safe to avoid future diagnostic dilemma (base of the appendix and adjacent cecum should be free of active Crohn’s disease).
In the patient with peritoneal contamination or shock, primary anastomosis is associated with a high leak rate; here, a damage control approach is prudent. This includes resection of bowel to grossly negative margins, peritoneal lavage, and planned re-operation 24 to 48 hours later.
Stricturoplasty may be more appropriate than resection in the patient with concern for short gut. A Heineke–Mikulicz-type stricturoplasty is typically used for strictures less than 10 to 12 cm in length. For longer strictures, up to 25 cm in length, a Finney-type stricturoplasty is preferred.
Selected patients are candidates for laparoscopic surgery for Crohn’s disease. Length of stay, morbidity, and overall cost in the first 3 postoperative months are lower in patients undergoing a minimally invasive surgical approach.
Diagnosis
Most patients presenting with severe colitis from IBD already have that underlying diagnosis. In those who do not, it is important to consider alternative diagnoses such as infectious or ischemic colitis. In patients with a
diagnosis of IBD, consider cytomegalovirus (CMV) or Clostridium difficile infection.
Plain films of the abdomen can evaluate for perforation, disease, extent, or toxic megacolon; CT is more accurate for these findings.
Colonoscopy assesses the severity and the extent of mucosal inflammation and ulceration. Biopsy and inspection may help diagnose ischemic colitis, Crohn’s colitis, CMV infection, C. difficile, or other infectious colitides.
Management
Medical management parallels that noted in small bowel IBD (see earlier).
Operative indications
Failure of medical therapy, clinical deterioration, perforation, or toxic megacolon requires operative intervention.
Patients will generally undergo a subtotal abdominal colectomy, end-ileostomy, and creation of a Hartmann’s pouch. Total proctocolectomy is usually avoided in the acute setting if a restorative procedure is possible in the future.
Early consultation with a stoma therapist will help guide management and enhance patient understanding.
III. Enterocutaneous Fistula
General. The management of (ECF is challenging. Fistulae are often complicated by sepsis, fluid and electrolyte abnormalities, malnutrition, and complex wound management issues; mortality ranges from 10% to 20%. ECF develop as a result of technical factors from a previous operation, factors related to healing and tissue integrity inherent to the patient, and factors related to specific disease processes.
Pathophysiology
The majority of ECF occur as a complication of an abdominal operation, often from anastomotic leak, unrecognized enterotomy, incorporation of bowel in the fascial closure, or ischemia. Risk factors include emergency abdominal procedures, contaminated operations, severe malnutrition, steroid use, radiation, or chemotherapy. Serum albumin levels less than 3.0 g/dL is a risk factor for the development of ECF.
Clinical manifestation
ECF classically presents as a wound infection following abdominal surgery. Wound drainage with the appearance and odor of enteric contents is diagnostic. Evaluate the underlying fascial integrity since ongoing leakage of enteric contents may lead to fascial dehiscence and evisceration. Conversely, ECF is in the differential diagnosis of a patient presenting with fascial dehiscence or evisceration.
In general, the more proximal the fistula, the more pronounced the electrolyte abnormalities, fluid losses, and malnutrition. Distal fistulae may essentially function as an ileostomy or colostomy without fluid, electrolyte, or nutritional abnormalities.
Diagnostic imaging
Upper GI contrast study or CT with oral contrast may demonstrate an ECF along with possible obstruction, abscess, potential foreign body, or loss of domain (large ventral defect). A chronic fistula tract can be injected with oral contrast to locate the site of communication with the intestinal tract (fistulogram).
Management
The primary goal of treatment of an ECF is source control and control of sepsis. Uncontrolled sepsis is the major cause of mortality in patients with ECF. Correction of fluid and electrolyte imbalances, nutritional support, and skin care are essential adjuncts.Related posts:
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