Causes and Symptoms The colon is the section of the lower bowel, or intestines, extending from the ileocecal valve to the rectum. It is wider in diameter than the small bowel, although shorter in length at about one meter. From behind the pelvis, the colon rises along the right side of the body (ascending colon), turns left to cross the upper abdominal cavity (transverse colon), and then turns down along the left side of the body (descending colon) until it joins the sigmoid (S-shaped) colon. The sigmoid colon empties into the rectum, a pouch that stores the waste products of digestion that are excreted through the anus. The colon absorbs most of the fluid passed to it from the small bowel, so that wastes solidify; meanwhile, bacteria in the colon break down undigested proteins and carbohydrates, creating hydrogen, carbon dioxide, and methane gases in the process.
A key structure in colonic activity is its mucosa. This thin sheet of cells lining the bowel wall permits passage of fluids and certain nutrients into the bloodstream but resists bacteria and toxins (poisonous chemical compounds). When the mucosa is torn or worn away, bacteria and toxins enter, infecting the bowel wall. The body responds to infection by rushing fluids and powerful chemicals to the endangered area to confine and kill the infecting agents. In the process, the tissues of the bowel wall swell with the fluids; this is known as "inflammation." The medical suffix denoting this response is -itis; when it occurs in the colon, physicians call it "colitis."
A variety of agents can cause colitis, which is divided into two major types depending on the duration of the disease: acute colitis and chronic ulcerative colitis. Acute colitis is a relatively brief, single episode of inflammation. It is often caused by bacteria or parasites. For example, Giardia lamblia, a bacterium in many American streams, is a common infectious agent in colitis, and the amoebas in polluted water supplies are responsible for the type of colitis known as "amebic dysentery." Some medicines, however, especially antibiotics, can also induce colitis. Acute colitis either disappears on its own or can be cured with drugs. Untreated, however, it may be fatal.
Chronic ulcerative colitis and
Crohn’s disease constitute a category of serious afflictions called inflammatory bowel disease (IBD), whose primary physical effects include swelling of the bowel lining, ulcers, and bloody diarrhea. Although some medical researchers think that these afflictions may be two aspects of the same disease, ulcerative colitis affects only the colon, whereas Crohn’s disease can involve the small bowel as well as the colon. Moreover, colitis chiefly involves the colonic mucosa, but Crohn’s disease delves into the full thickness of the bowel wall.
Chronic ulcerative colitis is a permanent disease that manifests itself either in recurring bouts of inflammation or in continuous inflammation that cannot be cleared up with drugs. It is commonly called "ulcerative colitis" because ulcers, open sores in the mucosa, spread throughout the colon and rectum, where the disease usually starts. Researchers have not yet discovered the causes of chronic ulcerative colitis although there are many theories, of which three are prominent. The first is bacterial or viral infection, and many agents have been proposed as the culprit. Because such a multitude of organisms commonly reside in or pass through the colon, researchers have enormous difficulty separating out a specific kind in order to show that it is always present during colitis attacks. Second is autoimmune reaction. Research in other diseases has shown that sometimes the body’s police system, enforced by white blood cells, mistakes native, healthy tissue for a foreign agent and attacks that tissue in an attempt to destroy it. Yet no testing in chronic ulcerative colitis has yet proven the theory. Third is a combination of foreign infection and autoimmune response; it is as if the immune system overreacts to an infectious agent and continues its attack even after the agent has been neutralized. Many researchers have suspected that the disease is inherited, because certain families have higher rates of the disease than others. This genetic theory is not universally accepted, however, because it is just as likely that family members share infection rather than having passed on a genetic predisposition for the disease. Other theories propose food allergies as the cause; even toothpaste has been considered.
Regardless of the cause, there is no doubt that colitis is a painful, disabling, bewildering disease. When the bowel inflames, the tissues heat up and fever results. Cramps are common, and sufferers feel an urgent, frequently uncontrollable urge to defecate. When they reach the toilet (if they do so in time), they have soft, loose stool or diarrhea, which can seem to explode from the anus. They may have as many as ten to twenty bowel movements a day. Because ulcers often erode blood vessels, blood can appear in the stool, as well as mucus and pus from the bowel wall. Severe weight loss, anemia, lack of energy, dehydration, and anorexia often develop as the colitis persists. The symptoms may clear up on their own only to recur months or years later; attacks may come with increasing frequency thereafter. The first attack, if it worsens rapidly, is fatal in about 5 to 10 percent of patients, although the death rate can rise to 25 percent among first-time sufferers who are more than sixty years old.
Complications from colitis can be life threatening. These include perforation of the bowel wall, strictures, hemorrhaging, and toxic megacolon (hyperinflation of the colon, an emergency medical condition). If left untreated or if unresponsive to treatment, ulcerative colitis can led to bone loss or arthritis, rashes, inflammation of the eye, liver disease, or painful kidney stones. Furthermore, studies show that patients who have had ulcerative colitis for more than ten years have about a 20 percent chance of developing cancer in the colon or rectum.
Because colitis is a relapsing, embarrassing disease, patients often suffer psychological turmoil. In Colitis (1992), Michael P. Kelly reports the results of his study of forty-five British colitis patients. According to Kelly, they typically denied that early symptoms were the signs of serious illness, passing them off as the result of overeating or influenza. The denial continued until the continual, desperate urge to defecate made them despair of controlling their bowels without help. Often, they suffered embarrassment because they had to flee family gatherings or work in order to find a toilet or because they passed stool inadvertently in public. Many feared being beyond easy access to a toilet, shunned public places, and felt humiliated. Only then did some visit a physician, and even after chronic ulcerative colitis was diagnosed, a portion hoped they could still cope on their own. When they could not, they grew depressed, insomniac, angry at their fate, or antisocial. Even with treatment, the strain of enduring the disease can be debilitating.
Treatment and Therapy Fortunately, medical science has several well-tested methods of controlling or curing colitis. In the case of acute colitis, patients usually resume normal bowel functions on their own and emerge as healthy as they were before the onset of symptoms. For chronic ulcerative colitis patients, however, the body is rarely the same again, and they must adjust to the effects of medication, surgery, or both—an adjustment that some authors claim is essentially a redefinition of the self.
After interviewing a patient and assessing the reported symptoms, the physician suspecting colitis orders a stool sample to check for blood, bacteria, parasites, and pus. If any of these are present, the physician directly examines the rectum and colon by inserting a fiber-optic endoscope into the rectum and up the colon. Early in the disease, the mucosa looks granular with scattered hemorrhages and tiny bleeding points. As the disease progresses, the mucosa turns spongy and has many ulcers that ooze blood and pus. An x-ray often helps determine the extent of inflammation, and tissue samples taken by endoscopic biopsy can establish if it is ulcerative colitis or infection, and not Crohn’s disease, that is present.
There is no easy treatment for chronic ulcerative colitis. Dietary restrictions—especially the elimination of fibrous foods such as raw fruits and vegetables, of milk products, or of certain seasonings—may reduce the irritation to the inflamed colon, and symptoms then may improve if the disease is mild. Antidiarrheal drugs can firm the stool and reduce the patient’s urgency to defecate, although such drugs must be used very cautiously to avoid dangerous dilation of the bowels.
Such nonspecific measures are seldom more than delaying tactics, and drugs are needed to counteract the colon’s inflammation. The most common types are aminosalicylates, corticosteroids, oral immunosuppressants, and intravenous infliximab, an antitumor necrosis factor agent. Among the first class, sulfasalazine is a sulfa drug developed in the 1940s. It is an anti-inflammatory agent that is most effective in mild to moderate ulcerative colitis and helps prevent recurrence of inflammation. Aminosalicylates may be administered as pills, suppositories, or enemas. Corticosteroids behave like the hormones produced by the adrenal gland that suppress inflammation. Administered orally, intravenously, or rectally, these drugs work well in relieving the symptoms of moderate to moderately severe attacks. Immunosuppressants and infliximab may be prescribed for severe, unresponsive cases of ulcerative colitis. All of these types of drugs have serious side effects, so physicians must carefully tailor dosages for each patient and check repeatedly for reactions. In some patients, sulfasalazine induces nausea, vomiting, joint pain, headaches, rashes, dizziness, and hepatitis (liver inflammation). The effects of corticosteroids include sleeplessness, mood swings, acne, high blood pressure, diabetes, cataracts, thinning of the bones (especially the spine), and fluid retention and swelling of the face, hands, abdomen, and ankles. Women may grow facial hair, and adolescents may have delayed sexual maturation. In most cases, the side effects clear up when patients stop taking the drugs. Immunosuppressants and infliximab can lead to toxicity.
With medication, people who suffer mild or moderate chronic ulcerative colitis can control it for years, often for the rest of their lives. Severe colitis requires surgery, and sometimes patients with milder forms choose to have surgery rather than live with the disease’s unpredictable recurrence or the ever-present side effects of drugs. In any case, surgery is the one known cure for chronic ulcerative colitis, although fewer than one-third of patients undergo surgical procedures. Several types of these surgeries have high success rates.
Because ulcerative colitis eventually spreads throughout the colon, complete removal of the large bowel and rectum is the surest way to eliminate the disease. This “total proctocolectomy” takes place in three steps. The surgeon first cuts through the wall of the abdomen, the incision extending from the mid-transverse colon to the rectum, and removes the colon. Next, the end of the ileum is pulled through a hole in the abdomen to form a stoma (a procedure called an ileostomy). Finally, the rectum is removed and the anus sutured shut. Thereafter the patient defecates through the stoma. Either of two arrangements prevents stool from simply spilling out unchecked. Most patients affix plastic bags around their stomas into which stool flows without their control; when full, the bag is either emptied and reattached or thrown away and replaced. To avoid external bags, some patients prefer a “continent ileostomy,” so called because it allows them to control defecation. The surgeon constructs a pouch
out of a portion of the ileum and attaches it right behind the stoma, a procedure called a "Kock pouch" after its inventor, Nils Kock of Sweden. When this pouch is full, the patient empties it with a catheter inserted through the stoma. Some patients can choose to have an ileoanal anastomosis. In this procedure, the surgeon forms the end of the ileum into a pouch, which is attached to the anus and collects wastes in place of the rectum. The patient continues to defecate through the anus rather than through a stoma.
None of these surgical procedures is free of problems, and all require extensive recovery in the hospital and rehabilitation. Moreover, both infections and mechanical failures can occur. If healthy portions of the colon are left intact, they often flare with colitis later, and more operations become necessary. Patients with stomas are vulnerable to bacterial inflammation of the small intestine, resulting in diarrhea, vomiting, and dehydration. Stomas and pouches sometimes leak or close up, and even after successful operations patients lose some capacity to absorb zinc, bile salts, and vitamin B12, although food supplements can make up for these deficiencies.
Any major surgery is an emotional trial. One that leaves a basic function of the body permanently altered, as with proctocolectomy or ileostomy, is difficult to accept afterward, even when the surgery was an emergency measure to save the patient’s life. Patients must live with a bag of stool on their abdomen or a pouch that they must empty with a plastic straw—bags and pouches that sometimes leak stool or gas and that, even when functioning smoothly, are not pleasant to handle. They must pay close attention to body functions that they rarely had to think about before the ulcerative colitis began. The changes can severely depress patients, who then may need psychiatric help and antidepressant drugs to recover their spirits. Patients with anastomoses, who continue to defecate through their anus, also find their bowel functions changed, although not so severely. For example, it takes many months before normal stool forms, and diarrhea plagues these patients.
After their operations, patients have access to considerable help in addition to physicians and surgeons. Special nurses train patients to care for their stomas, check regularly for infection or malfunction, and generally ease them into their new lives. Formal support groups and informal networks are common and provide the afflicted with information and reassurance.
Perspective and Prospects Acute forms of colitis, especially amebic dysentery, have long been recognized as among the endemic diseases of polluted water, and until the development of antibiotics, they regularly killed significant portions of local populations, especially the young and elderly. Chronic ulcerative colitis was first described in 1859, but no effective treatment for it existed until the 1940s. At that time, Nana Svartz of Sweden noticed that when rheumatoid arthritis patients were given sulfasalazine, the bowel condition of those who had colitis improved as well. J. Arnold Bargen, an American physician, confirmed Svartz’s observation in a formal clinical trial, and sulfasalazine soon was mass-produced for distribution in the United States and later throughout the world. Since the 1940s, medications and surgical techniques for ulcerative colitis have proliferated, although none restores a patient’s original state of health.
Because the agents causing ulcerative colitis are unknown, the historical and geographical origin of the disease likewise cannot be determined. Nevertheless, three somewhat odd social facets of the disease are recognized.
Evidence suggests that ulcerative colitis is a disease of urban industrial society. Along with Crohn’s disease, colitis appears to be entrenched in Scandinavia, the United States, Western Europe, Israel, and England. It rarely occurs in rural Africa, Asia, or South America, despite the poor nutrition and sanitation in some of these areas. Yet the disease does not appear to vary solely by racial type or nationality, although Jewish people tend to fall ill with it more often than any other group. For example, African Americans, whether from families long-established in the United States or recently immigrated, show an incidence of colitis as high as residents of European descent.
Furthermore, ulcerative colitis strikes the young. It most often begins between the ages of fifteen and thirty; men and women are equally likely to come down with it. This fact, taken with the high rate of inflammatory bowel disease (IBD) sufferers who have family members also with the disease (20 to 25 percent), has led some researchers to believe that a genetic factor creates a susceptibility for IBD.
Finally, IBD patients bear some social stigma or at least believe they do. Ulcerative colitis involves bowel incontinence and often ends with surgical replacement of the anus with a stoma; in such cases, bowel movements can dominate a patient’s life and become obvious to family members, coworkers, and even strangers. Because the subject of stool is taboo to many and the odor offends most people, patients can feel severe embarrassment and come to see themselves as pariahs. Even though the causes of ulcerative colitis remain obscure and the treatment is often distressing, modern medicine saves people who otherwise would die.
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