Inflammatory Bowel Disease (IBD)

The two most common types of inflammatory bowel disease are Crohn's disease and ulcerative colitis.

Ulcerative colitis (UC) and Crohn's disease (CD) are known as inflammatory bowel diseases (IBD).

The precise cause of IBD remains unknown. These diseases are believed to be caused by a combination of genetic and non-genetic, or environmental factors (for example, infections) that interact with the body's immune (defense) system. When the intestinal immune system does not function properly, many white blood cells accumulate in the inner lining (mucosa) of the gut. The white cells then release chemicals that lead to tissue injury (inflammation). This inflammation of the mucosa can cause diarrhea, which is the most common symptom of ulcerative colitis and Crohn's disease, with or without intestinal complications.

Small intestinal bacterial overgrowth (SIBO) can occur as a complication of Crohn's disease but not of ulcerative colitis since the small intestine is not involved in ulcerative colitis. SIBO can result when a partially obstructing small bowel stricture is present or when the natural barrier between the large and small intestines (ileocecal valve) has been surgically removed in Crohn's disease. Normally, the small bowel contains only a few bacteria, while the colon has a tremendous number of resident bacteria. If a stricture is present or the ileocecal valve has been removed, bacteria from the colon gain access to the small bowel and multiply there. With SIBO, the bacteria in the small bowel begin to break down (digest) food higher up than normal in the GI tract. This digestion produces gas and other products that cause abdominal pain, bloating, and diarrhea. In addition, the bacteria chemically alter the bile salts in the intestine. This alteration impairs the ability of the bile salts to transport fat. The resulting malabsorption of fat is another cause of diarrhea in Crohn's disease. (As previously mentioned, inflammation of the intestinal lining is the most common cause of diarrhea in patients with IBD.)

SIBO diagnosis

SIBO can be diagnosed with a hydrogen breath test (HBT). In this test, the patient swallows a specified amount of glucose or another sugar called lactulose. If bacteria have reproduced in the small bowel, the glucose or lactulose is metabolized by these bacteria, which causes the release of hydrogen in the breath. The amount of hydrogen in the breath is measured at specific time intervals after the ingestion of the sugar. In a patient with SIBO, the hydrogen is eliminated into the breath sooner than the hydrogen that is produced by the normal bacteria in the colon. Accordingly, the detection of large amounts of hydrogen at an early interval in the testing indicates the possibility of SIBO. Another test, which may be more specific, uses a sugar called xylose. In this test, the swallowed xylose is tagged with a very small amount of radioactive carbon 14 (C14). The C14 is measured in the breath and interpreted by applying the same principles as used for hydrogen in the HBT.

SIBO treatment

The best treatment for bacterial overgrowth is antibiotics for approximately 10 days using, for example, neomycin, metronidazole, or ciprofloxacin. After this treatment, the breath test may be repeated to confirm that the bacterial overgrowth has been eliminated. SIBO may recur, however, if the stricture itself is not treated, or if the bacterial overgrowth is due to the surgical removal of the ileocecalvalve.

Fissures are tears in the lining of the anus. They may be superficial or deep. Fissures are especially common in Crohn's disease. They differ from fistulas in that fissures are confined to the anus and do not connect to other parts of the bowel, other internal organs, or the skin. Still, fissures can cause mild to severe rectal pain and bleeding, especially with bowel movements.

The most common treatment for anal fissures is periodic sitz baths or topical creams that relax the muscle (sphincter) around the anus. Injections of tiny amounts of botulinum toxin into the muscles around the anus have been reported to help relax the sphincter, thereby allowing the fissures to heal. The benefit of this type of therapy, however, is still controversial.

Sometimes, surgery is needed to relieve the persistent pain or bleeding of an anal fissure. For example, the surgeon may cut out (excise) the fissure. Alternatively, the muscle around the anus can be cut (sphincterotomy) to relax the sphincter so that the fissure can heal. However, as is the case with any surgery in patients with Crohn's disease, post-operative intestinal complications can occur frequently.

Intestinal fistulas are tubular connections between the bowel and other organs or the skin. Fistulas form when inflammation extends through all of the layers of the bowel and then proceeds to tunnel through the layers of other tissues. Accordingly, fistulas are much more common in Crohn's disease than in ulcerative colitis. (In the latter, as you recall, the inflammation is confined to the inner lining of the large intestine.)

Fistulas often are multiple. They may connect the bowel to other loops of the bowel (enteroenteric fistulas), to the abdominal wall (enterocutaneous), to the skin around the anus (perianal), and to other internal locations such as the urinary bladder (enterovesical), vagina (enterovaginal), muscles, and scrotum.

In Crohn's disease patients, fistulas may form in conjunction with intestinal strictures. One reason for this association is that both fistulas and strictures can begin with inflammation of the entire thickness of the bowel wall (transmural inflammation). Subsequent scarring (fibrosis) causes strictures while continuing inflammation and tissue destruction lead to fistulas. A stricture can also help create a fistula. As already mentioned, perforation of the intestine can occur above an obstructing stricture. The perforation can create a tract outside of the bowel wall. A fistula then may develop in this tract.

The risk of developing colon cancer is 20 times higher for patients with IBD than it is for the general population. The association with colon cancer is more clearly established in ulcerative colitis than in Crohn's disease. The increased risk most likely also exists, however, for patients with Crohn's disease that affects the colon. In ulcerative colitis, the risk of acquiring colon cancer increases according to how much of the colon is involved and the duration of colitis.

Thus, after about 8 to 10 years of ulcerative colitis, especially if the entire colon is involved, the risk of developing colon cancer substantially increases. Other risk factors for colon cancer in IBD patients include a liver disease called primary sclerosing cholangitis (PSC), a family history of colon cancer, and a history of liver transplantation. Additional possible risk factors include the use of concurrent immunosuppressive medications and a deficiency of the vitamin, folic acid.

When the inflammation in the inner lining of the intestine becomes severe, it can break through the inner lining to form ulcers.

The ulcers associated with ulcerative colitis are located in the colon, whereas ulcers in Crohn's disease may be found anywhere in the gut from the mouth (aphthous ulcers) to the anus. When examined, ulcerative colitis ulcers are typically shallow and more numerous, while Crohn's disease ulcers are usually deeper and with more distinct borders.

The symptoms caused by intestinal ulcers are predominantly abdominal pain, cramps, and bleeding. Sometimes, however, ulcers may be present in IBD but are not associated with any symptoms (asymptomatic).

In Crohn's disease, the inflammation and accompanying ulcers occur most commonly in the ileum, jejunum, and colon, but can occasionally occur in the duodenum. Note, however, that these ulcers are entirely different from the far more common acid-related peptic ulcers in the duodenum.

In patients with Crohn's disease, there is an increased risk of developing lymphoma or adenocarcinoma of the small intestine. Since the small intestine is not involved in ulcerative colitis, there is no increased risk of this cancer in ulcerative colitis patients. Even though there is a higher risk of these cancers in Crohn's disease, the percentage of patients contracting them is very small. Still, certain conditions predispose Crohn's disease patients to even higher cancer risk. These conditions include bypassed segments of the bowel and chronic fissures, fistulas, or strictures.

Even so, routine monitoring for small bowel cancer in Crohn's disease patients by X-ray or enteroscopy is not currently recommended because these diagnostic procedures are difficult, time-consuming, and not very effective for this purpose. If however, after many years of Crohn's disease, the disease suddenly changes its course or becomes difficult to treat, the possibility of small bowel cancer should be investigated.

Bleeding from the intestinal tract, or gastrointestinal (GI) bleeding, may complicate the course of both ulcerative colitis and Crohn's disease. GI bleeding is often referred to as rectal bleeding when the blood comes out of the rectum, usually with the stools. If the source of bleeding is in the colon, the blood is usually red. The longer the blood remains in the intestine, however, the darker it becomes. Thus, rectal bleeding originating from higher up in the intestinal tract is usually black, except for very rapid bleeding, which can still be red.

Patients with ulcerative colitis usually experience some degree of chronic rectal bleeding, which can be continuous or intermittent. The bleeding may be mild, as when it is limited to occasional drops on the toilet paper or streaks of blood around the stools. At times, however, the bleeding may be more severe or acute, with the passage of greater amounts of blood or large blood clots. The more severe rectal bleeding is most likely due to more severe inflammation and extensive ulceration of the colon.

In Crohn's disease, mild or severe intestinal inflammation also may occur, but the ulcers and bleeding are less frequent than in ulcerative colitis. Because of the deep nature of ulcers in Crohn's disease, however, the GI bleeding tends to be acute (sudden and brief) and sporadic. Furthermore, in Crohn's disease, the site of bleeding can be anywhere in the GI tract, including the colon.

When inflammation is present for a long time (chronic), it sometimes can cause scarring (fibrosis). Scar tissue is typically not as flexible as healthy tissue. Therefore, when fibrosis occurs in the intestines, the scarring may narrow the width of the passageway (lumen) of the involved segments of the bowel. These constricted areas are called strictures. The strictures may be mild or severe, depending on how much they block the contents of the bowel from passing through the narrowed area.

Crohn's disease is characterized by inflammation that tends to involve the deeper layers of the intestines. Strictures, therefore, are more commonly found in Crohn's disease than in ulcerative colitis. Additionally, strictures in Crohn's disease may be found anywhere in the gut. Remember that the intestinal inflammation in ulcerative colitis is confined to the inner lining (mucosa) of the colon. Accordingly, in chronic ulcerative colitis, benign (not malignant) strictures of the colon occur only rarely. A narrowed segment of the colon in ulcerative colitis may well be caused by colon cancer rather than by a benign (non-cancerous), chronic inflammatory stricture.

Toxic megacolon is a widened (dilated) segment of the colon in a patient with severe inflammation of the colon (colitis). The megacolon develops when the lining of the colon is so inflamed that the colon loses its ability to contract properly. When this happens, the propelling (peristaltic) contractions are unable to move the intestinal gas along through the colon. The colon, therefore, accumulates excessive amounts of gas. The gas then increases the pressure on the bowel wall, which causes the colon to dilate.

How colon cancer develops in IBD patients is thought to be different from how it develops in other people. In individuals without IBD, usually a benign (not malignant) polyp initially forms in the colon. Then, depending on the type of polyp and the genetic makeup of the patient, the polyp may eventually become cancerous. In IBD, the constant process of inflammatory injury and repair of the lining of the colon (colonic mucosa) is believed to make the individual more susceptible to cancer. The idea is that the mucosal cells are dividing so rapidly that they are liable to make mistakes in their DNA (mutations). These mutated cells can then become pre-cancerous (dysplastic) cells, which later can turn into cancer.

Additionally, pre-cancerous cells in IBD develop in ways other than in a polyp. Pre-cancerous cells can develop in tissue that appears completely normal or exhibits only mild irregularities. For this reason, colon cancer may not be discovered in IBD patients until the cancer has progressed to a later stage. In later stages, cancer can invade tissues beyond the colon or spread (metastasize) to other parts of the body.

Individuals may not know that they have an intestinal stricture. The stricture may not cause symptoms if it is not causing a significant blockage (obstruction) of the bowel. If a stricture is narrow enough to hinder the smooth passage of the bowel contents, however, it may cause abdominal pain, cramps, and bloating (distention). If the stricture causes even more complete obstruction of the bowel, patients may experience more severe pain, nausea, vomiting, and an inability to pass stools.

An intestinal obstruction that is caused by a stricture can also lead to perforation of the bowel. The bowel must increase the strength of its contractions to push the intestinal contents through a narrowing in the bowel. The contracting segment of the intestine above the stricture, therefore, may experience increased pressure. This pressure sometimes weakens the bowel wall in that area, thereby causing the intestines to become abnormally wide (dilated). If the pressure becomes too high, the bowel wall may then rupture (perforate). This perforation can result in a severe infection of the abdominal cavity (peritonitis), abscesses (collections of infection and pus), and fistulas (tubular passageways originating from the bowel wall and connecting to other organs or the skin). Strictures of the small bowel also can lead to bacterial overgrowth, which is yet another intestinal complication of IBD.

Some fistulas, especially those that connect adjacent loops of the bowel, may not cause significant symptoms. Other fistulas, however, can cause significant abdominal pain and external drainage, or create a bypass of a large segment of the intestine. Such a bypass can occur when a fistula connects one part of the bowel to another part that is further down the intestinal tract. The fistula thereby creates a new route for the intestinal contents. This new route bypasses the segment of the intestine between the fistula's upper and lower connections to the intestine.

Sometimes, fistulas can open and close sporadically and unevenly. Thus, for example, the outside of a fistula might heal before the inside of the fistula. Should this occur, the bowel contents can accumulate in the fistulous tract and result in a pocket of infection and pus (abscess). An abscess may be quite painful and can be dangerous, especially if the infection spreads to the bloodstream.

Malabsorption means abnormal intestinal absorption. Crohn's disease usually affects the small intestine, which is the part of the gut that absorbs most nutrients. Remember that Crohn's disease involves the small bowel and/or the colon, while ulcerative colitis involves only the colon. Crohn's disease of the upper part (duodenum) and middle part (jejunum) of the small intestine may interfere with the absorption of proteins, sugars, iron, vitamins, and fats. This widespread malabsorption in Crohn's disease, which does not occur in ulcerative colitis, may lead to weight loss and malnutrition.

In addition, some unabsorbed nutrients can cause the small or large intestine to secrete increased amounts of liquid, which worsens diarrhea in Crohn's disease. (As previously mentioned, diarrhea is the most common symptom in patients with IBD, with or without intestinal complications.) The lower end (ileum) of the small intestine is the part of the bowel most commonly involved in Crohn's disease. In ulcerative colitis, however, the function of the ileum is normal. When the ileum is involved in patients with Crohn's disease (or surgically removed), a decreased absorption of vitamin B12 may occur. If a deficiency of B12 develops, a particular type of anemia called pernicious anemia can result.

The ileum is also the major area for intestinal absorption of bile acids. The bile acids are compounds that are secreted in the bile by the liver into the duodenum. The major function of bile acids is to help transport and absorb fats, mostly in the jejunum. Bile acids that are not absorbed by diseased or removed ileum pass into the colon. The bile acids then induce the colon to secrete liquid, which aggravates diarrhea. If the bile acids are not sufficiently absorbed in the colon and consequently become deficient, fat malabsorption and more diarrhea can result.

Extensive Crohn's disease, usually involving the surgical removal of several intestinal segments over the years, can lead to a debilitating condition known as short bowel syndrome. In this condition, the patients have many of the intestinal complications of Crohn's disease, including severe malabsorption. They can also suffer from the previously mentioned complications not directly affecting the intestinal tract (extraintestinal). Additionally, these patients frequently have certain other extraintestinal complications, such as osteoporosis (thin or porous bones), osteomalacia (soft bones), gallstones, and kidney stones.

Patients with toxic megacolon usually are very ill, with abdominal pain, bloating (distention), and fever. The dilated colon can allow bacteria to leak through the bowel wall into the bloodstream (septicemia). With continuing dilation, the inflamed colonic wall becomes at high risk for bursting (perforating) and causing inflammation of the abdominal cavity (peritonitis). Both septicemia and peritonitis are serious infections, which, in some cases, can even lead to death.

Toxic megacolon typically occurs when inflammation of the colon is severe. This complication, however, does not occur exclusively in patients with ulcerative colitis or Crohn's disease. Thus, toxic megacolon can develop in other types of colitis, such as amebiasis or bacillary dysentery (shigella). Narcotics, codeine, or anti-diarrheal medications such as diphenoxylate (Lomotil) or loperamide (Imodium) can decrease the contractions of the colon and allow excessive gas to accumulate. These medications, therefore, predispose to the development of toxic megacolon and should be avoided during severe episodes (flares) of colitis.

Intestinal ulcers can be diagnosed by directly viewing the lining of the intestines. Various procedures, utilizing viewing instruments called endoscopes, are available. Endoscopes are flexible, thin, tubular instruments that are inserted into the gastrointestinal (GI) tract through either the mouth or rectum, depending on the procedure. Which procedure is done depends on the part of the GI tract that is being examined. Endoscopy can be done for either the upper or lower GI tracts. The endoscope is inserted through the mouth for upper endoscopy or through the rectum for lower endoscopy. The colon is examined either by sigmoidoscopy (using sigmoidoscopes) for the lower (sigmoid) part of the colon or by colonoscopy (using a colonoscope) for the entire colon.

The upper GI tract is examined by a procedure called esophago-gastro-duodenoscopy (EGD). An upper GI endoscope is used for this procedure. EGD is useful in detecting Crohn's disease ulcers in the esophagus, stomach, and duodenum.

Crohn's disease ulcers in the small intestine may be seen by a procedure called enteroscopy, in which a special endoscope (called an endoscope) is used. But enteroscopy needs special equipment and is not widely available. Ulcers in the small intestine, however, are more often diagnosed with an X-ray study called a "small bowel follow-through" (SBFT). In this test, the patient swallows a few cups of barium, which coats the lining of the small intestine. On the X-ray, the barium may show the presence of ulcers. However, SBFT may not be accurate, and may not detect small ulcers in the small bowel. In patients suspected of having small bowel Crohn's disease ulcers and yet have normal SBFT studies, CT (computerized tomography) of the small bowel and capsule enteroscopy may be helpful in diagnosis.

Capsule enteroscopy is a procedure where a patient swallows a small camera the size of a pill. The camera located inside the pill takes multiple images of the inside of the small bowel and transmits these images wirelessly onto a recorder worn around the patient's waist. The recorded images are later reviewed by a doctor. Both CT of the small bowel and capsule enteroscopy in some studies are more accurate than the traditional SBFT in diagnosing Crohn's disease of the small bowel.

Intestinal bleeding in IBD is usually diagnosed by EGD for the upper GI tract or colonoscopy for the lower GI tract. These methods allow for direct visualization of the bleeding site, which can be particularly helpful. Additionally, special instruments can be used through upper GI endoscopes or colonoscopes, which may effectively treat the bleeding lesions and stop ongoing blood loss.

Sometimes, if the bleeding is severe and the bleeding site is suspected to be in the small intestine, other tests may be needed.

• One of these tests is a special X-ray study called an angiogram, which uses a dye to visualize the intestinal blood vessels that may be bleeding.
• Another test is a nuclear medicine study called a tagged red blood cell scan, which tracks the red blood cells from the bloodstream to the gut.

Each of these tests can help identify the site of bleeding. Pinpointing the bleeding site becomes additionally important if surgery is ultimately needed.

Intestinal strictures of the small intestine may be diagnosed with a small bowel follow-through (SBFT) X-ray. For this study, the patient swallows barium, which outlines the inner lining of the small intestine. Thus, the X-ray can show the width of the passageway, or lumen, of the intestine. Upper GI endoscopy (EGD) and enteroscopy are also used for locating strictures in the small intestine. For suspected strictures in the colon, barium can be inserted into the colon (barium enema), followed by an X-ray to locate the strictures. Colonoscopy is another diagnostic option.

Fistulas sometimes are difficult to detect. Although the outside opening of a fistula may be simple to see, the inside opening that is connected to the bowel may not be easy to locate. The reason for this difficulty is that fistulas from the bowel can have long, winding tunnels that finally lead to the skin or an internal organ. Endoscopy might detect the internal opening of a fistula, but it can easily be missed. Sometimes, a small bowel barium X-ray will locate a fistula. Often, however, an exam under general anesthesia may be required to fully examine areas that have fistulas, especially around the anus and vagina.

No medications as yet have been shown to specifically stop acute GI bleeding in IBD. Nevertheless, the initial approach to IBD-associated GI bleeding is the aggressive medical treatment of the underlying inflammation and ulceration. Chronic bleeding might respond to medications if the inflammation resolves and the ulcers heal. If the medications or endoscopic treatments do not stop acute or severe chronic bleeding, however, surgical removal (resection) of the bleeding area of the gut may be necessary.

The treatment of ulcers in IBD is aimed at decreasing the underlying inflammation with various medications, which include:

• mesalamine (Asacol, Pentasa, or Rowasa)
• Corticosteroids
• Antibiotics
• Immunosuppressive medications such as 6-MP (6-mercaptopurine, Purinethol) or azathioprine (Imuran)

In some cases, ulcers can be very resistant to these treatments and the use of stronger drugs may be required. These drugs include an immunosuppressive medication, cyclosporine (Neoral or Sandimmune), or the newer infliximab (Remicade), which is an antibody to one of the body's inflammation-inducing chemicals called tumor necrosis factor (TNFa). Adalimumab (Humira) and certolizumab (Cimzia) are also in the same class of drugs as infliximab. Occasionally, therapy with medications fails to heal IBD ulcers, and surgical treatment is needed.

Intestinal strictures may be composed of a combination of scar tissue (fibrosis) and tissue that is inflamed and, therefore, swollen. A logical and sometimes effective treatment for these strictures, therefore, is medication to decrease inflammation. Some medications for IBD, such as infliximab, however, may make some strictures worse. The reason is that these medications may promote the formation of scar tissue during the healing process. If the stricture is predominantly scar tissue and is only causing a mild narrowing, symptoms may be controlled simply by changes in the diet. For example, the patient should avoid high-fiber foods, such as raw carrots, celery, beans, seeds, nuts, fiber, bran, and dried fruit.

If the stricture is more severe and can be reached and examined with an endoscope, it may be treated by stretching (dilation) during the endoscopy. In this procedure, special instruments are used through the endoscope to stretch open the stricture, usually with a balloon that is passed through an endoscope. Once the balloon traverses the stricture, it is inflated and the force of the balloon dilates the stricture to a bigger size, thus opening the lumen to make it wider. If that doesn't work, some patients will require surgery. Typically, this procedure does not produce long-lasting results.

Surgery sometimes is needed to treat intestinal strictures. The operation may involve cutting out (resecting) the entire narrowed segment of the bowel, especially if it is a long stricture. More recently, a more limited operation, called stricturoplasty, has been devised. In this procedure, the surgeon simply cuts open the strictured segment lengthwise and then sews the tissue closed crosswise to enlarge the width of the bowel's passageway (lumen). After surgery in Crohn's disease patients, medication still should be taken to prevent inflammation from recurring, especially at the site of the stricture. The reason for this recommendation is that after abdominal operations, recurrent intestinal inflammation is a common problem in Crohn's disease. Furthermore, the risk of post-operative intestinal fistulas and abscesses is increased in Crohn's disease patients. Therefore, necessary and only abdominal surgery should be done in patients with Crohn's disease.

Intestinal fistulas that do not cause symptoms often do not require treatment. Fistulas that cause significant symptoms, however, usually require treatment, although they are frequently difficult to heal.

Fistulas located around the anus (perianal) sometimes can be improved by treatment with antibiotics, metronidazole (Flagyl), or ciprofloxacin (Cipro). In response to the antibiotics, some of these fistulas even close completely. Also, treatment with the immunosuppressive medications, azathioprine or 6MP, improves fistulas located around the anus (perianal) in almost two-thirds of patients, including complete healing in one-third. More recently, the new drug infliximab (Remicade), which is an antibody to one of the body's inflammation-inducing chemicals, has been shown to produce very similar results. Remember, however, that infliximab might worsen strictures, which, as mentioned, can sometimes be associated with fistulas.

When medications for the treatment of fistulas are discontinued, they usually re-open within 6 months to a year. Steroids do not heal fistulas and should not be used for this purpose. Other medications that suppress the immune system, such as cyclosporine or tacrolimus (FK506 or Prograf), are currently being studied for the treatment of fistulas. Sometimes, resting the bowel by feeding the patient solely with total parenteral (intravenous) nutrition (TPN), and thus nothing by mouth, is required to treat fistulas. Even if these fistulas heal in response to the TPN, they commonly recur when eating is resumed.

Fistulas sometimes require surgery. For example, when fistulas around the anus become very severe, they can interfere with the patient's ability to control bowel movements (continence). In this situation, the surgeon might make an opening (ostomy) to the skin from the bowel above the fistulas. The intestinal contents are thereby diverted away from the fistulas. Occasionally, when necessary, intestinal fistulas are surgically removed, usually along with the involved segment of the bowel. Fistulas from the intestine to the bladder or vagina are frequently very difficult to close with medical treatment alone and often require surgery.

Not all polyps that are found in IBD patients are pre-cancerous or cancerous. Some polyps form as a result of the inflammatory and healing processes. These polyps are called inflammatory polyps or pseudopolyps, and they do not turn into cancer. The only way to make sure that polyps do not have pre-cancerous or cancerous cells, however, is to remove (biopsy) and examine them under the microscope.

The treatment of malabsorption in patients with IBD includes medications to treat the underlying intestinal inflammation. Decreasing the inflammation can improve the intestinal absorption of the nutrients that were malabsorbed. The malabsorption or deficiency of B12 may need to be treated by administering the vitamin in the vein or into the muscle. Diarrhea that is induced by bile acid can be treated with cholestyramine, a compound that works by binding the bile acids.

Supplemental calories and nutrients may be administered as special liquid diets. These so-called elemental diets are composed of proteins, carbohydrates, vitamins, and fats that are broken down into smaller particles that are easier for the intestine to absorb. Unfortunately, however, these diets often do not smell or taste very good. Nevertheless, they can be administered through a small tube inserted through the nose (enteral feeding). For patients who are unable to tolerate any food or liquid by mouth or by enteral feeding, nutrition may need to be given solely through the veins (total parenteral nutrition). Finally, a small bowel transplant can now be done for patients with severe Crohn's disease or otherwise unmanageable short bowel syndrome.

The intestinal complications of IBD occur when the intestinal inflammation is severe, extends beyond the inner lining (mucosa) of the intestines, is widespread, and/or is of long duration (chronic). For example, severe mucosal inflammation can cause ulcers, bleeding, and toxic megacolon (a condition in which the colon widens or dilates and loses its ability to properly contract).

Inflammation that extends beyond the inner lining and through the intestinal wall is responsible for strictures (scarring that causes narrowing of the intestinal wall) and fistulas (tubular passageways originating from the bowel wall and connecting to other organs or the skin). Strictures, in turn, can lead to bacterial overgrowth of the small intestine (SIBO). If the inflammation of the small bowel is widespread, malabsorption of nutrients can be a complication. Chronic inflammation can also be associated with colon cancer.

The majority of IBD patients experience periods during which their disease intensifies (flares) or subsides (remission). Although most patients require medication for IBD, they can live normal, productive lives. Some patients, but certainly not all, will develop intestinal complications of IBD. When these complications occur, they should be recognized and usually treated. Some patients with IBD develop complications outside of the intestine (extraintestinal), such as certain kinds of arthritis, skin rashes, eye problems, and liver disease. These extraintestinal complications are discussed in other articles on IBD.

This review will describe the various types of intestinal complications that are associated with IBD, and will also summarize methods for their diagnosis and treatment. Please note that the terms bowel, intestine, and gut are used synonymously. The small bowel, or intestines, includes from top to bottom, the duodenum, jejunum, and ileum. The large bowel is also called the colon.

Some intestinal complications of IBD occur in both ulcerative colitis and Crohn's disease. For example, ulceration of the inflamed inner intestinal lining (mucosa), which causes abdominal pain and intestinal bleeding, may complicate both diseases.

Since both diseases involve the colon, complications that are associated with the colon, such as toxic megacolon and colon cancer, occur in both diseases. Additionally, there are no intestinal complications that occur only in ulcerative colitis and not in Crohn's disease. On the other hand, certain intestinal complications of IBD occur predominantly in Crohn's disease (for example, fistulas) or exclusively in Crohn's disease and not in ulcerative colitis (for example, malabsorption and SIBO).

The differences in intestinal complications between ulcerative colitis and Crohn's disease depend on the characteristically dissimilar behaviors of the inflammation associated with these diseases. In Crohn's disease, the inflammation usually extends from the inner lining (mucosa) through the entire thickness of the bowel wall. This spreading inflammatory process may thereby lead to fistulas, abscesses, or strictures of the bowel. By contrast, the inflammation in ulcerative colitis is limited to the inner lining of the colon. The development of these particular complications is, therefore, much less common in ulcerative colitis. Also, Crohn's disease can affect any area of the GI tract from the mouth to the anus, whereas ulcerative colitis is limited to the colon. Therefore, complications involving the small intestine, such as malabsorption and SIBO, as previously noted, occur only in Crohn's disease and not in ulcerative colitis.

As already mentioned, patients with IBD, especially ulcerative colitis, have an increased risk of developing colon cancer. Performing a colectomy (removal of the colon)before cancer develops in these patients is a sure way to prevent colon cancer. The concept is to remove the pre-cancerous cells (dysplasia)in the colon before they can turn into cancer.

Accordingly, inspection for dysplasia and cancer by yearly colonoscopies with multiple colonic biopsies is recommended for patients with ulcerative colitis. The monitoring is suggested to begin after the patient has had ulcerative colitis for 8-10 years. Many physicians recommend a similar monitoring program for Crohn's disease patients who have inflammation of the colon (colitis), even though the association with colon cancer is less well-established in Crohn's disease. Remember that ulcerative colitis involves only the colon, whereas Crohn's disease, which involves the small bowel, colon, or both, often does not affect the colon.

A colonoscopy is the best method for monitoring colon cancer. An otherwise negative colonoscopy in ulcerative colitis, however, does not guarantee that the colon is free of cancer or pre-cancerous cells. The reason for this is that the multiple biopsies that are done during the colonoscopy still make up only a tiny percentage of the entire lining of the colon. However, if pre-cancerous cells are found on a microscopic examination of the biopsies, a colectomy (surgical removal of the colon) may be recommended to prevent cancer from developing. One caution here is that the diagnosis of dysplasia should be made only in the absence of concurrent, active, inflammation of the colon. This is because inflammation sometimes can mimic the microscopic appearance of dysplasia.