Perspective

Irritable bowel syndrome (IBS) is a chronic non–life-threatening disorder characterized by abdominal pain and alteration in bowel habits. IBS is an extremely common disorder; estimates put the prevalence in the North American population at 10 to 15%, with women affected twice as often as men.1,2 Although only one third of patients who have the clinical syndrome ever seek medical attention, IBS accounts for more than 10% of all visits to primary care physicians and more than 25% of all visits to gastroenterologists. IBS is said to contribute more impairment to quality of life than either diabetes or renal failure.

No specific physical or laboratory abnormalities defining IBS have been identified. IBS is a functional somatic syndrome that is diagnosed by clinical criteria in the absence of “alarm” symptoms and findings that suggest other, more urgent diagnoses. Diagnosing IBS is problematic in the emergency department (ED), and typically patients are discharged with a diagnosis of “abdominal pain of unclear cause” or the equivalent. Patients with known IBS who are experiencing acute symptoms may also pose a diagnostic challenge. Symptoms of IBS overlap with those of other conditions, including some that are life-threatening, which must be excluded before hospital discharge.

Principles of Disease

Although the cause of IBS is unknown, it is associated with several pathophysiologic findings suggesting that it is a disorder of altered gut motility, gut sensation, and perception of intestinal activity. IBS was originally thought to be primarily a psychiatric disorder because there are no visible anatomic abnormalities and because stress is an exacerbating factor. Physiologic testing has since shown that patients with IBS have disturbances in the rhythmic pattern of electrical activity in the intestine and in how the intestine responds to stimulation. Patients with IBS seem to be more attuned to activity in the abdomen as well, sensing different phases of intestinal motor activity and intestinal content movement to a greater extent than people without IBS.

Psychiatric conditions often coexist with IBS, ranging from generalized anxiety disorder to major depression. IBS has been associated with fibromyalgia, chronic fatigue syndrome, and chronic pelvic pain.² An association with previous sexual abuse also has been reported. In women, symptoms often are related to the menstrual cycle, suggesting a hormonal influence. A familial predisposition for the symptoms of IBS has been described, suggesting a genetic component. Bacterial overgrowth and infection have also been associated with IBS.²

Clinical Features

The diagnosis of IBS is defined by clinical criteria in a patient whose symptoms have no other organic explanation. Several sets of clinical criteria have been published, one set of which is the Rome III criteria (Box 95-1). Patients with IBS experience symptoms intermittently, with the typical patient averaging symptoms on 1 of every 3 days. Complaints include abdominal pain, bloating, and constipation or diarrhea. Pain typically is relieved with defecation; pain that persists suggests another diagnosis. A mucoid discharge from the rectum often accompanies diarrhea. Upper gastrointestinal symptoms such as nausea and dyspepsia can also occur. Patients may come to the ED with an exacerbation of their previous symptoms or with a new abdominal complaint and often report that they are undergoing a period of stress. Physical examination may reveal either mild focal abdominal tenderness that can vary in location, or diffuse tenderness. IBS is subdivided into three categories: constipation-predominant (IBS-C), diarrhea-predominant (IBS-D), and mixed pattern (IBS-M).²

Pain that is progressive or is associated with anorexia or significant abdominal tenderness suggests an alternate diagnosis. Signs and symptoms that point away from the diagnosis of IBS (alarm symptoms) include onset of symptoms after age 50, unintentional weight loss, anorexia, bloody stools, nocturnal diarrhea, or a family history of significant colon disease.² In the absence of symptoms suggesting another diagnosis, the clinical criteria have a specificity ranging from 87 to 100%, although sensitivity may be only 60%. In patients determined to have IBS through correct use of the clinical criteria, follow-up evaluation over many years rarely leads to a change in the diagnosis.²

A final diagnosis of IBS usually is made in the primary care setting and not in the ED. Studies that are sometimes performed in the evaluation for IBS may include a complete blood count, thyroid studies, stool examination for ova and parasites, evaluation for lactose intolerance, and possibly lower gastrointestinal endoscopy, although current approaches try to limit testing in cases in which the clinical picture is clearly IBS.³ The ED evaluation seeks to exclude other, more urgent causes for the patient’s symptoms. In this setting, testing for pancreatitis, hepatitis, biliary colic, or urologic disorders, including urolithiasis, may be appropriate as indicated by the pattern of the presenting complaints.

Diagnostic Strategies

No specific testing should be done in the ED on individuals who fit the pattern of IBS. In the primary care setting patients may benefit from lactose intolerance or celiac disease testing. Other tests, including colonoscopy, are not found to be helpful.

Differential Considerations

The differential diagnosis of symptomatic IBS depends on the predominant symptoms and includes a host of disorders (Box 95-2). Patients may report pain, constipation, or diarrhea or any combination of the three.

Management

Not all patients with IBS require treatment. It is recommended that therapy be initiated only if symptoms diminish the quality of life.¹ Because no curative therapy is available, treatment is directed toward the relief of symptoms. Diet, behavioral, and pharmacologic therapies all are used in IBS. Specific therapy will be determined by the type of IBS: IBS-C, IBS-D, or IBS-M. Dietary suggestions include a low-fat diet, reduced nondigestible sugars, and avoidance of gas-forming foods, although none of these has any proven benefit. Fiber supplementation may aid IBS-C.

Medications with antispasmodic activity, such as anticholinergics and calcium channel blockers, are used for abdominal cramping, and peripherally acting narcotics, such as loperamide, are used to reduce diarrhea. Osmotic laxatives such as lactulose sometimes are helpful in constipation. Tricyclic antidepressants have been effective in certain classes of patients with IBS. Serotonin receptor antagonists, serotonin receptor agonists, chloride channel activators, and prokinetic agents also are used (Box 95-3), but the serotonin receptor drugs have significant side effects, including adverse cardiovascular events and ischemic colitis, and thus are reserved for patients with severe symptoms unresponsive to other agents. Nonsteroidal anti-inflammatory drugs (NSAIDs) may worsen symptoms.³

Behavioral therapy may benefit patients who are unresponsive to medication, but high-quality evidence of its effectiveness is lacking. A role for nontraditional therapies such as arrowroot, artichoke leaf, and some Chinese traditional herbal medicines is supported by limited scientific evidence.

Disposition

IBS is not a life-threatening disease and can be managed on an outpatient basis as long as other disorders have been excluded. The search for optimal therapy usually involves empirical trials until the correct fit is found. This process is best accomplished through a well-established primary care relationship. The disorder is chronic, but with appropriate therapy, many patients experience significant improvement in their quality of life.

Perspective

Diverticular disease is an affliction of middle age that seems to be a direct consequence of the diet of modern Western civilization. Diverticular disease was virtually unknown in the Western world before the 20th century and is still rare in other cultures. In 1925 only 9% of people older than 50 years of age in the United States had diverticula; by 1968 the percentage had increased to 30%.⁴ Today it is estimated that 5 to 10% of people older than 45 years and 80% of people older than 85 years have diverticula. Diverticula are less common in people younger than age 40, representing only approximately 2 to 5% of all patients with the disease. The proliferation of this disease was coincident with the invention and widespread use of the flour rolling mill, which removes the fiber-containing outer part of the wheat kernel. This coincidence has prompted the labeling of diverticulosis as a “modern deficiency disease,” which is supported by the fact that adding fiber back into the diet seems to be protective against the development of diverticulosis.⁴ In rural Africa and Asia, where the diet is high in fiber, diverticular disease is virtually unknown. Over the last decade the incidence of diverticulitis has increased in the United States, especially in people aged 18 to 44.⁵

Diverticulosis denotes the presence of diverticula in the colon. Most patients with this condition are asymptomatic. Diverticulitis denotes inflammation of diverticular tissue, which is usually painful. It is estimated that 10 to 25% of patients with diverticulosis will develop diverticulitis.⁵ Complicated diverticulitis is defined by the presence of more extensive disease, including abscess formation, peritonitis, intestinal obstruction, or fistula formation.

Principles of Disease

The wall of the colon is penetrated at regular intervals by blood vessels, collectively known as the vasa recta, that supply the internal intestinal layers. The site of vessel penetration is apparently the weakest part of the colon wall because it is at these sites that diverticula form. Although the exact pathogenic mechanism is unknown, the current theory is that diverticula form in response to increased intracolonic pressures generated when the colon is processing smaller, non–fiber-containing stools. Patients with diverticular disease exhibit normal resting colonic pressure but higher peak pressure than those without diverticular disease⁵; higher peak pressures lead to a herniation of colonic mucosa through the intestinal wall at the vasa recta, creating small, saclike appendages. These appendages (diverticula) typically measure 5 to 10 mm in diameter but on rare occasions can grow into huge sacs measuring many centimeters across (giant colonic diverticula). Diverticula are generally asymptomatic; symptoms are believed to develop when diverticula become obstructed, presumably with inspissated stool. When obstruction occurs, inflammation sets in and microperforations of the sac develop, resulting in inflammation of pericolonic structures and abdominal pain.

In the Western world, most diverticular disease occurs in the left colon, usually the sigmoid. This is not the case in Japan, where right-sided diverticular disease is more common. Japanese-Hawaiians consuming a low-fiber Western diet have a significantly increased incidence of diverticular disease, but it remains in the right colon.⁴ This finding suggests that although diet plays a significant role in the formation of diverticula, the location of diverticula is genetically determined.

A spectrum of disease is observed in relation to diverticular inflammation. In uncomplicated diverticulitis, only the pericolonic fat is inflamed. With time, a phlegmon, abscess, or gross perforation may develop. Any extension of disease beyond the pericolonic fat is considered to represent complicated diverticulitis. The involved colonic segment may fistulize to any adjacent organ, most commonly the bladder. Adjacent bowel may become obstructed by mass effect from an abscess or may incur an inflammatory ileus. Recurrent episodes of diverticulitis can lead to strictures in the colon with subsequent colonic obstruction.

Diverticula can also bleed, presumably from erosion into the mucosal wall by dried stool trapped in the diverticular sac. Severe hemorrhage occurs in 3 to 5% of all patients with diverticulosis and accounts for approximately 40% of all instances of lower gastrointestinal hemorrhage.⁴ Bleeding notably occurs in the absence of inflammation and typically is painless. NSAID use is associated with this complication.

Clinical Features

Diagnostic Strategies

Differential Considerations

In a patient with more serious disease, making the correct diagnosis usually poses no great dilemma because more extensive laboratory testing and diagnostic imaging typically have been performed. In a patient with milder disease, in whom a tentative diagnosis of diverticulitis may be based on clinical grounds alone, the differential diagnosis presents more of a challenge. An important consideration is whether or not the patient has colonic carcinoma; however, it usually is safe to wait until after the acute episode has resolved to investigate this possibility. Additional diagnoses to consider include colitis (either inflammatory or ischemic); ureteral stones; inguinal hernia; and pelvic pathology, including ectopic pregnancy or pelvic inflammatory disease, and ovarian pathology with or without ovarian torsion. Appendicitis should be suspected when symptoms are predominantly right sided. Diffuse abdominal pain should prompt an evaluation for other life-threatening problems, including leaking abdominal aortic aneurysm, peritonitis, hemoperitoneum from ectopic pregnancy, and bowel obstruction.

Management

Definitive Management

It is not known whether medical or dietary treatment is of benefit in diverticulitis. The only proven way to eradicate diverticula is to remove the affected segment of colon surgically. Most patients who recover from their first attack of diverticulitis are likely to remain asymptomatic for many years. With subsequent attacks, the likelihood of recurrence increases. Elective resection of diverticula generally is reserved for patients who have had more than one attack of diverticulitis. According to some experts, younger patients (i.e., younger than 40 years) should undergo elective resection after their first bout of diverticulitis because of concerns about a higher risk for a second attack, but this recommendation is controversial, with recent evidence suggesting that outcomes are better without surgery.⁶ Most resections can be done laparoscopically with a single-stage procedure (no colostomy). Estimates on recurrence of diverticular disease after resection vary, ranging from 3 to 27%.^7,14

Disposition

Perspective

Large bowel obstruction (LBO) is much less common than small bowel obstruction, but LBO is a more ominous condition because it is frequently associated with malignant disease. One half of all operative cases involving LBO in the United States are the result of colorectal cancer, and up to 20% of patients with colon cancer will develop acute obstruction.¹⁵ Adhesions, a common cause of small bowel obstruction, cause only a small number of LBOs. Other causes of LBO include volvulus, diverticular disease, fecal impaction, strictures (often related to inflammatory bowel disease [IBD] or chronic colon ischemia), adhesions, hernia, and pseudo-obstruction. Most causes are managed surgically, but pseudo-obstruction responds well to medical management alone.

Principles of Disease

When mechanical obstruction is secondary to an obstructing lesion, either inside the bowel (carcinoma) or outside the bowel (diverticular abscess, volvulus), the bowel becomes increasingly dilated with air and fluid that cannot be passed distally. As the distention increases, the intraluminal pressure increases. When intraluminal pressure approaches systolic blood pressure, blood flow to the bowel wall is compromised and edema sets in, with subsequent transudation of fluid into the lumen. Transudation along with decreased resorption of intraluminal fluid leads to dehydration. Eventually, as arterial flow to the bowel wall is compromised, ischemia and gangrene develop. Translocation of bacteria from compromised bowel can lead to sepsis. Perforation of the bowel wall follows if the process is not interrupted.

Pseudo-obstruction, also called Ogilvie‘s syndrome, occurs through a completely different mechanism. Pseudo-obstruction is defined as LBO in which no obstructing lesion can be identified. This condition usually is found in patients with significant acute comorbid conditions.¹⁶ Patients typically have a history of significant spine or retroperitoneal trauma, severe electrolyte disturbances, or narcotic exposure. Although the exact mechanism is unknown, it is believed to involve malfunction of autonomic control of the bowel. Normal balance between parasympathetic and sympathetic input is disrupted, resulting in changes in motility that lead to obstruction. The pathophysiologic changes observed with pseudo-obstruction are the same as those described for mechanical obstruction.

Clinical Features