Inflammatory Bowel Disease (IBD)
An elaborate article by William A Rowe, MD
Breakthroughs in the management of IBD
Last Updated: June 9, 2004
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Synonyms and related keywords: IBD, Crohn disease, Crohn's disease,
terminal ileitis, granulomatous enteritis, ulcerative colitis, gastrointestinal
tract disease, GI tract disease, gastrointestinal disease, GI disease,
Clostridium difficile, C difficile, irritable bowel syndrome, IBS, pyoderma
gangrenosum, bloody diarrhea, inflamed colon, colonoscopy, proctocolectomy,
continent ileostomy, Koch pouch, colonic disease, ileoanal anastomosis,
segmental colon resection.
Author: William A Rowe, MD, Consulting Staff, Gastroenterology
William A Rowe, MD, is a member of the following medical societies: American
Gastroenterological Association, and American Society for Gastrointestinal
Editor(s): Rajeev Vasudeva, MD, FACG, Director, Clinical Professor,
Department of Internal Medicine, Division of Digestive Diseases and Nutrition,
University of South Carolina School of Medicine; Francisco Talavera, PharmD,
PhD, Senior Pharmacy Editor, eMedicine; Oscar S Brann, MD, Associate Clinical
Professor, UCSD School of Medicine; Program Director of Gastroenterology
Fellowship, Department of Internal Medicine, Naval Medical Center San
Diego; Alex J Mechaber, MD, FACP, Director of Clinical Skills Program,
Assistant Professor, Department of Internal Medicine, Division of General
Internal Medicine, University of Miami School of Medicine; and Julian
Katz, MD, Professor, Department of Internal Medicine, Division of Gastroenterology,
MCP Hahnemann University.
Inflammatory bowel disease (IBD) is an idiopathic disease, probably
involving an immune reaction of the body to its own intestinal tract.
The 2 major types of IBD are ulcerative colitis and Crohn disease. As
the name suggests, ulcerative colitis is limited to the colon; Crohn disease
can involve any segment of the gastrointestinal tract from the mouth to
Although ulcerative colitis and Crohn disease have significant differences,
many (but not all) of the treatments available for one are also effective
for the other. Likewise, both diseases share many extraintestinal manifestations,
although some of these tend to occur more commonly with one disease or
Both ulcerative colitis and Crohn disease usually have waxing and waning
intensity and severity. When the patient is actively symptomatic, indicating
significant inflammation, the disease is considered to be in an active
stage; the patient is having a flare of the IBD.
When the degree of inflammation is less (or absent) and the patient is
usually asymptomatic, then the patient's disease is considered to be in
remission. In most cases, symptoms do correspond well with the degree
of inflammation present for either disease, although this is not universally
true. In some patients, objective evidence for disease activity should
be sought before administering medications with significant adverse effects.
The pathophysiology of IBD is under active investigation. The common
end pathway is inflammation of the mucosal lining of the intestinal tract,
causing ulceration, edema, bleeding, and fluid and electrolyte loss.
Persons with IBD have a genetic predisposition (or perhaps susceptibility)
for the disease. The triggering event for the activation of the immune
response has yet to be identified. Possible factors related to this event
include a pathogenic organism (as yet unidentified), an immune response
to an intraluminal antigen (eg, protein from cow milk), or an autoimmune
process whereby an appropriate immune response to an intraluminal antigen
and an inappropriate response to a similar antigen is present on intestinal
A great deal of research has been performed to discover potential genes
linked to IBD. One of the early linkages discovered was on chromosome
16 (IBD1 gene), which led to the identification of the NOD2 gene (now
called CARD15) as the first gene clearly associated with IBD (as a susceptibility
gene for Crohn disease). Studies have also provided strong support for
IBD susceptibility genes on chromosomes 5 (5q31) and 6 (6p21 and 19p).
NOD2/CARD15 is a polymorphic gene involved in the innate immune system.
The gene has more than 60 variations. Three of these variations play a
role in 27% of patients with Crohn disease, primarily in patients with
ileal disease. One important point to note with all of these potential
genes is that they appear to be permissive (ie, allow IBD to occur) but
not causative (ie, just because the gene is present does not necessarily
mean the disease will develop).
None of these mechanisms has been implicated as the primary cause, but
they are postulated as potential causes. The lymphocyte population in
persons with IBD is polyclonal, making the search for a single precipitating
cause difficult. In any case, activation of the immune system leads to
inflammation of the intestinal tract, both acute (neutrophilic) and chronic
Many of the mucosal changes seen in persons with IBD are nonspecific
in nature; they are seen in any organ system in which active inflammation
is occurring. Many inflammatory mediators have been identified; antibodies
against these mediators or methods to block the production or receptors
for these mediators hold great promise for potential therapy for IBD.
In the US: Approximately 1 million people in the United States have ulcerative
colitis or Crohn disease. Before 1960, the incidence of ulcerative colitis
was several times higher than that of Crohn disease. The latest data suggest
that the current incidence of Crohn disease is approaching that of ulcerative
colitis, although this change may reflect improved recognition and diagnosis
of Crohn disease.
In the United States, the rates of IBD among persons of European descent
have been measured in Olmstead County, Minn. In this population, the incidence
of ulcerative colitis is 7.3 cases per 100,000 people per year and the
prevalence is 116 cases per 100,000 people; the incidence of Crohn disease
is 5.8 cases per 100,000 people per year and the prevalence is 133 cases
per 100,000 people.
The prevalence of IBD among Americans of African descent is estimated
to be the same as the prevalence among Americans of European descent.
The prevalence is lower among Americans of Asian and Hispanic descent.
Internationally: The incidence of IBD is assumed to be highest
in developed countries and lowest in the developing regions of the world.
A recent study in Italy showed the incidences of ulcerative colitis and
Crohn disease to be similar to those found in the United States. Persons
living in colder climates have a greater rate of IBD than persons living
in warmer climates. Persons living in urban areas have a greater rate
of IBD than persons living in rural areas.
Multiple studies have been conducted from regions throughout the world
on mortality in patients with IBD. The mortality from ulcerative colitis
has decreased over the past 40-50 years.
One study suggested decreased mortality for ulcerative colitis (standardized
mortality ratio of 0.6 in Florence, Italy), but the vast majority of studies
indicate a small but significant increase in mortality associated with
IBD. The standardized mortality ratio for IBD generally ranges from approximately
1.4 times the general population (Sweden) to 5 times the general population
(Spain). In general, the 95% confidence intervals suggest that the increase
in relative risk is real. Ulcerative colitis and Crohn disease have approximately
equal mortality rates.
The most frequent cause of death in persons with IBD is the primary disease,
followed by malignancy and thromboembolic disease.
A generally accepted postulation is that the risk of colorectal cancer
is not significantly higher in persons with ulcerative colitis compared
with the general population until several years after diagnosis. Beyond
8-10 years after diagnosis, the risk of colorectal cancer increases by
0.5-1.0% per year. Recent data suggest that surveillance colonoscopies
with random biopsies reduce mortality from colorectal cancer in patients
with ulcerative colitis, primarily by allowing the detection of carcinoma
at an earlier Duke stage. Recent data suggest that persons with Crohn
colitis involving the entire colon have a risk of developing malignancy
equal to that of persons with ulcerative colitis; however, the risk for
most patients with Crohn disease is much smaller (albeit poorly quantified).
Race: The incidence of IBD has been reported to be highest in
Jewish populations, followed by nonJewish white populations. However,
more recent data suggest that incidences in non-Jewish, black, and Hispanic
populations are increasing. The American Jewish population has one of
the highest prevalences of IBD, 4-5 times that of the general population.
Sex: The male-to-female ratio is approximately equal for both
ulcerative colitis and Crohn disease.
Age: Ulcerative colitis and Crohn disease are diagnosed most commonly
in young adults (ie, late adolescence to the third decade of life). The
age distribution of newly diagnosed IBD cases is bell-shaped; the peak
incidence occurs in people in the early part of their second decade of
life, with the vast majority of new diagnoses made in people aged 15-40
years. However, children younger than 5 years and elderly persons are
occasionally diagnosed. Of patients with IBD, 10% are younger than 18
History: The manifestations of IBD generally depend on the area
of the intestinal tract involved. Patients with ulcerative colitis or
Crohn colitis frequently have bloody diarrhea, occasionally with tenesmus.
Patients with Crohn disease involving the small intestine frequently have
abdominal pain and diarrhea, and occasionally they have symptoms of intestinal
obstruction. A variety of intestinal and extraintestinal manifestations
of IBD also may be observed in conjunction with either ulcerative colitis
or Crohn disease.
The most typical manifestation of ulcerative colitis is bloody diarrhea.
Pain is uncommon but may occur.
Patients are commonly fatigued, which is often related to the inflammation
and anemia that accompany disease activity.
The most typical manifestations of Crohn disease are abdominal pain and
diarrhea. Not uncommonly, patients have been diagnosed with irritable
bowel syndrome before being diagnosed with IBD.
Pain is particularly common, especially when some degree of obstruction
is present. The pain may be almost anywhere within the abdominal cavity,
although the classic location is the lower abdomen or right lower quadrant
Patients are commonly fatigued, which is often related to the pain, inflammation,
and anemia that accompany disease activity.
Strictures and obstructions are not uncommon in persons with Crohn disease
(see Image 2 and Image 4). These strictures are often inflamed and frequently
resolve with medical treatment. Fixed (scarred or cicatrix) strictures
may require endoscopic or surgical intervention to relieve obstructions.
However, in persons with ulcerative colitis, colonic strictures are of
significant concern and should be presumed to be malignant unless proven
otherwise (usually by resection).
Fistulae and perianal disease are not uncommon in persons with Crohn
disease and may be refractory to vigorous medical treatment, including
antibiotic therapy (see Image 3). Surgical intervention is often required
for fistulae and perianal disease treatment, but both are associated with
a high risk of recurrence.
Toxic megacolon is a life-threatening complication of ulcerative colitis
and requires urgent surgical intervention.
Infectious colitis is in the differential diagnosis of ulcerative colitis
and must be excluded before the diagnosis of ulcerative colitis can be
made. However, in patients with well-established ulcerative colitis, superimposed
infection can occur. Infection with Clostridium difficile is by far most
common. Stools of patients hospitalized for a flare of ulcerative colitis
should be tested for C difficile toxin. Treatment of C difficile (if present)
infection generally helps put the flare into remission.
Malignancy is the most dreaded long-term intestinal complication of ulcerative
colitis. The risk of colon cancer for persons with ulcerative colitis
begins to rise significantly above that of the general population approximately
8-10 years after diagnosis. For cancer prevention, surveillance colonoscopy
every 2 years after 8 years of disease is recommended, more frequently
if areas of pathologic concern are evident. The risk of cancer in persons
with Crohn disease may equal to that of persons with ulcerative colitis
if the entire colon is involved, and screening may be beneficial for patients
with pancolitis Crohn disease. The risk of small intestine malignancy
is increased in persons with Crohn disease, but the malignancy is as likely
to arise in a previously normal area as in an inflamed area. No screening
protocol has ever been demonstrated to be effective for small bowel Crohn
Presenting signs of ulcerative colitis include diarrhea with occult or
frank blood loss (see Image 1). Weight loss and anemia are also common.
Persons with ulcerative colitis typically do not develop fistulae or perianal
disease, although they may have perianal abscesses.
Diagnosis can be made endoscopically or radiologically, with contrast
radiographs typically showing loss of the normal mucosal pattern and,
with more advanced disease, loss of colonic haustrae.
Sigmoidoscopy or colonoscopy reveals that the rectum is almost always
involved. The disease can be limited to the rectum (proctitis); to the
rectum, sigmoid, and descending colon (left-sided colitis); or to the
entire colon (pancolitis). Ulcerative colitis does not involve any other
segment of the gastrointestinal tract. Colectomy is curative.
Presenting signs of Crohn disease include occult blood loss and low-grade
fever; weight loss and anemia are common. Growth retardation is seen in
children and may be the only presenting sign in young patients. Fistulae
and perianal disease are not uncommon.
Diagnosis can be made endoscopically or radiologically, with contrast
radiographs typically showing a cobblestone pattern to the mucosa and
areas of normal mucosa alternating with areas of inflamed mucosa (skip
Sigmoidoscopy or colonoscopy reveals that the rectum is frequently spared
and right colonic predominance is common. Occasionally, gastric or duodenal
Crohn disease manifests as seemingly refractory ulcer disease.
Many complications associated with IBD can occur with either ulcerative
colitis or Crohn disease. In addition, many of the medications used to
treat IBD may cause significant adverse systemic effects.
In addition to medication-induced arthropathies, the arthritides associated
with the IBD are of 2 varieties, axial (or central) arthritis and peripheral
The axial arthritis associated with IBD consists of ankylosing spondylitis
and sacroiliitis. Axial arthritis occurs in approximately 5% of patients
with IBD (often Crohn disease) and typically is independent of disease
activity. Axial arthritis is often associated with HLA-B27.
The peripheral arthritides vary with the activity of the underlying IBD.
Peripheral arthritis occurs in approximately 10% of patients with IBD;
it is a nondestructive arthritis, and patients have seronegative findings
for rheumatoid factor. The peripheral arthritis typically is asymmetric,
and it can be monoarticular or may involve different joints on different
sides of the body. The classic peripheral arthritis affects large weight-bearing
joints, although any joint may be involved.
Diseases of the eye associated with ulcerative colitis are episcleritis
and iritis (uveitis). Treatment of these complications often requires
high-dose systemic steroids or infliximab, and either condition can cause
significant vision loss if left untreated.
The major skin diseases associated with IBD are erythema nodosum and
Erythema nodosum is a painful, tender, raised, purplish lesion
on the anterior surface of the tibia. Erythema nodosum tends to correlate
well with the activity of the underlying bowel disease; with bowel disease
treatment, the erythema nodosum usually dissipates.
Pyoderma gangrenosum, on the other hand, typically is not associated
with disease activity (see Images 6-7). This skin lesion starts as an
inflamed patch of skin ranging from one to several centimeters in diameter
that progresses until it ulcerates. Upon ulceration, the lesion may persist
for many months before healing. Treatments that have been tried that may
have some efficacy include dapsone, metronidazole (MetroGel), cyclosporine,
and infliximab. Surgical removal of the diseased bowel (eg, colectomy)
does not ameliorate pyoderma gangrenosum.
Infectious skin lesions related to immune suppression may also be seen
(eg, herpetic lesions)
The urinary complications of IBD are more common in persons with Crohn
disease. Calcium oxalate stones are the most common type of renal calculi
associated with Crohn disease; treatment is to increase hydration and
to use oral calcium citrate supplements, which bind the oxalate within
the intestinal tract and prevent its excretion in the urinary tract. Because
of its proximity to the ureters, inflammation of the small bowel may involve
the ureters, causing obstruction and hydronephrosis. Fistulae occasionally
occur between the bowel and bladder or ureters.
Sclerosing cholangitis is most commonly associated with ulcerative colitis.
Sclerosing cholangitis is a disease of the biliary tree. Although sclerosing
cholangitis typically manifests as fatigue and, perhaps, jaundice, it
is far more commonly sought when abnormal LFT results in a cholestatic
pattern are found in a patient with ulcerative colitis.
Although ursodeoxycholic acid may help improve serum LFT results, this
has not been translated into improved survival. If sclerosing cholangitis
is diagnosed in the absence of a known history of ulcerative colitis,
colonoscopy is indicated.
Ulcerative colitis may be expected to be clinically evident within 2
years of diagnosis of sclerosing cholangitis if the colitis is present
and has not been diagnosed first. Sclerosing cholangitis may be indolent
for many years but may progress to cirrhosis, for which hepatic transplantation
may be necessary. The most dreaded complication of sclerosing cholangitis
is the development of cholangiocarcinoma.
Gallstones are common in persons with Crohn disease, but these persons
are usually asymptomatic; occasionally, cholecystectomy is necessary.
The anemia associated with IBD may be of 2 types, (1) iron deficiency
anemia secondary to chronic blood loss and (2) anemia of chronic disease.
Because iron is absorbed in the duodenum, patients with Crohn disease
involving the proximal small intestine may have difficulty absorbing oral
iron; occasionally, parenteral iron replacement is necessary. IBD is a
recognized cause of anemia of chronic disease.
A hypercoagulable state is associated with IBD. It is estimated to occur
in as many as one third of patients with IBD, but it may go unrecognized
until a thrombotic event occurs. Strokes, retinal thrombi, and pulmonary
emboli are not uncommon in patients with IBD.
Causes: The causes of IBD are currently unknown. Also see Pathophysiology.
Genetics: IBD clearly has a familial tendency. A parent with IBD
has approximately a 4% chance of having a child develop IBD. Of patients
with IBD, 10-25% are estimated to have a first-degree relative with the
disease. Monozygous twin studies show a high concordance for Crohn disease
but less so for ulcerative colitis.
Animal models: Several animal models are used to study IBD. A
local irritant (eg, acetic acid, trinitrobenzene sulfonic acid) can be
inserted via an enema into the colon of rats or rabbits to induce a chemical
colitis. An interleukin-10 knockout mouse has been genetically engineered
to have some characteristics similar to those of a human with IBD.
The cotton-top marmoset, a South American primate, develops a colitis
very similar to ulcerative colitis when the animal is subjected to stress.
C1 Esterase Deficiency
Chronic Pelvic Pain
Clostridium Difficile Colitis
Collagenous and Lymphocytic Colitis
Intestinal Motility Disorders
Intestinal Radiation Injury
Irritable Bowel Syndrome
Other Problems to be Considered:
Laboratory studies are of value in assisting with the management of IBD
but are of minimal help in establishing the diagnosis. Laboratory values
may be used as surrogate markers for inflammation and nutritional status
and to look for deficiencies of necessary vitamins and minerals. Serologic
studies have been proposed to help diagnose IBD and to differentiate Crohn
disease from ulcerative colitis.
Stool studies: Perform a stool culture (and C difficile toxin
assay) on patients before making a definitive diagnosis of idiopathic
IBD. Any patient hospitalized with a flare of colitis should, at a minimum,
have a C difficile toxin assay performed because, commonly, pseudomembranous
colitis is superimposed on ulcerative colitis.
Complete blood cell count: The components of the CBC count can
be useful indicators of disease activity and iron or vitamin deficiency.
An elevated WBC count is common in patients with active inflammatory disease
and does not necessarily indicate infection. Anemia is common and may
be either an anemia of chronic disease (usually normal mean corpuscular
volume [MCV]) or an iron deficiency anemia (MCV is often low). Generally,
the platelet count is normal, or, it may be mildly to moderately elevated
if active inflammation is occurring, particularly if gastrointestinal
blood loss occurs. Note that the MCV can be elevated in patients taking
azathioprine (Imuran) or 6-mercaptopurine (6-MP).
Erythrocyte sedimentation rate: The erythrocyte sedimentation
rate (ESR) is used as a surrogate marker for inflammation; an elevation
above normal generally indicates the presence of an inflammatory response.
For most, but not all, patients, the ESR can be used to help determine
whether active IBD is present. Persons with cicatrix strictures are not
expected to have an elevated ESR.
Nutritional markers: Blood tests can also be used to help determine
nutritional status. The most commonly used marker is serum albumin; prealbumin
and transferrin can also be used, although the latter is an acute phase
reactant and can be falsely elevated in persons with active IBD. Hypoalbuminemia
may reflect malnutrition; it can also develop because of the protein-losing
enteropathy that can occur with active IBD.
Serum vitamin B-12: Vitamin B-12 deficiency can occur in patients
with Crohn disease who have significant terminal ileum disease or in patients
who have had terminal ileum resection. The standard replacement dose of
vitamin B-12 is 1000 mcg subcutaneously every month.
Serum iron studies: Because active IBD is a source for gastrointestinal
blood loss, iron deficiency is common. A microcytic hypochromic anemia
suggests iron deficiency; if confirmed with serum iron/total iron-binding
capacity, iron can be replaced either enterally or parenterally. For parenteral
replacement, intravenous iron dextran can be used and is dosed based on
the table in the package insert, with a maximum of 30 mL (1500 mg) at
Red blood cell folate: While folate deficiency is not common in
persons with IBD, several concerns have been raised regarding this vitamin.
Sulfasalazine (Azulfidine) is a folate reductase inhibitor and may inhibit
normal uptake. Although some practitioners administer folate supplements
in patients taking sulfasalazine, few data demonstrate that this is universally
necessary. Folate supplements are indicated in all women who are pregnant
to help prevent neural tube defects; this is particularly true for patients
with IBD, and supplementation with 2 or more mg/d (rather than the usual
1 mg/d) should be considered.
Abdominal flat plate: For the patient with IBD, kidneys, ureter,
bladder radiography can provide a great deal of information. Evidence
of obstruction can be seen. Evidence of inflammatory disease, especially
involving the colon, can often be discerned, perforation can be detected,
and toxic megacolon can be diagnosed. More subtle findings can include
indications of osteopenia and nephrolithiasis.
Barium enema: This was one of the first studies that allowed characterization
of the typical findings associated with IBD. Normal barium enema findings
virtually exclude active ulcerative colitis, whereas abnormal findings
can be diagnostic. Several terms have been used to describe abnormalities
found after barium studies of the colon. These include (1) a stove-pipe
appearance, which suggests chronic colitis that has resulted in a loss
of colonic haustrae; (2) rectal sparing, which suggests Crohn
colitis in the presence of inflammatory changes in other portions of the
colon; (3) thumbprinting, which indicates mucosal inflammation
(which can also be seen frequently on the abdominal flat plate); and (4)
skip lesions, which suggests areas of inflammation alternating
with normal-appearing areas, again suggesting Crohn colitis. Barium can
be refluxed into the terminal ileum in many cases, which can assist in
the diagnosis of Crohn disease.
Small bowel series/small bowel follow-through: The small bowel
series, with or without an upper gastrointestinal tract series, provides
invaluable information about Crohn disease. This study can reveal if inflammation
is present, can assist in the assessment of stricture length and severity,
and can help decide the most appropriate surgical approach. Fistulae are
often demonstrated on films from a small bowel series, even if they are
not suggested based on the clinical evaluation. The small bowel series
is usually sufficient for the evaluation of small intestine Crohn disease;
rarely, it affords an inadequate view of the terminal ileum and enteroclysis
must be performed. Although radiologists may remark on abnormalities suggested
in the cecum or ascending colon when the barium from a small bowel series
enters the colon, independent confirmation must be sought because the
presence of stool and dilution of the barium make proper interpretation
of colon findings difficult.
Small bowel enteroclysis: The enteroclysis differs from a small
bowel series in that a nasoenteric or oroenteric tube is placed and contrast
is instilled directly into the small intestine. This is usually performed
when fine detail of the intestinal mucosa is required or the distal small
intestine is not adequately seen on the small bowel series because the
contrast is diluted as it passes through the (usually dilated) small bowel.
Computed tomography scan of the abdomen and pelvis: CT scanning
of the abdomen and pelvis has limited use in the diagnosis of IBD, but
findings may be very suggestive of IBD. Wall thickening on CT scans is
nonspecific and may occur from smooth muscle contraction alone, especially
in the absence of other extraintestinal inflammatory changes; however,
the presence of inflammatory changes significantly increases the predictive
value of the CT scan. CT scanning is the ideal study to determine if the
patient has abscesses, and it can be used to guide percutaneous drainage
of these abscesses. Fistulae also may be detected on CT scans.
Fistulogram: Contrast can also be inserted directly into an enterocutaneous
fistula in order to help determine the course of the fistula in anticipation
of surgical correction and to assist in guiding the surgical approach.
This is one of the most valuable tools available to the physician for
the diagnosis and treatment of IBD, although its limitations must be recognized.
Foremost, not all mucosal inflammation is idiopathic IBD. Infectious causes
of inflammation must always be considered, as should diverticulitis and
ischemia (which are far more common as new diagnoses in an elderly population
than IBD, despite the similar colonoscopic and histologic appearance).
When used appropriately, colonoscopy can help determine the extent and
severity of colitis, assist in guiding treatment, and provide tissue to
assist in the diagnosis. In skilled hands, the colonoscope can frequently
reach the terminal ileum and permit assessment of inflammation to assist
in the diagnosis or exclusion of Crohn disease. Inflammation may occasionally
occur in the terminal ileum in patients with ulcerative colitis; this
is referred to as a backwash ileitis and is mild, nonulcerating, and may
occur when a widely patent ileocecal valve is present.
Be cautious with colonoscopic intervention in patients with IBD. The
usual risks of colonoscopy apply (eg, reaction to medication, bleeding,
perforation); the risk of bleeding is increased in the presence of inflammation,
and even mucosal biopsies may require cautery to limit bleeding. The risk
of perforation is also increased, particularly in patients taking high
doses of steroids long-term. Also, weigh the risks and benefits of continuing
colonic intubation in a patient with IBD who has significant inflammation.
Colonoscopy can also be used for therapeutic intervention in patients
with IBD. The most common therapeutic use is stricture dilation in persons
with Crohn disease; colonic, anastomotic, and even small bowel strictures
can often be dilated using pneumatic through-the-scope dilators. Intralesional
injection of steroids (eg, triamcinolone at 5 mg in 4 quadrants) may help
prevent reformation of the stricture, although this has yet to be demonstrated
in controlled trials.
This study is useful for a preliminary diagnosis in patients with chronic
diarrhea or rectal bleeding; however, because of the limited length of
the scope (60 cm), it can only help diagnose distal ulcerative colitis
or proctitis, but not pancolitis. Rarely, Crohn colitis can be diagnosed
based on flexible sigmoidoscopy findings; use caution interpreting sigmoid
inflammation, particularly in older patients, because Crohn colitis may
be confused with diverticulitis or ischemia.
Esophagogastroduodenoscopy is used for the evaluation of upper gastrointestinal
tract symptoms, particularly in patients with Crohn disease. Aphthous
ulceration occurs in the stomach and duodenum in 5-10% of patients with
Crohn disease. The diagnosis of Crohn disease is occasionally made after
gastric or duodenal ulcers fail to heal with acid suppression alone.
Small bowel enteroscopy:
This is of limited use in patients with Crohn disease and is of almost
no value in those with ulcerative colitis. Although ulcerations and strictures
in the upper half of the jejunum can be demonstrated with enteroscopy,
the same information (and often more information) can be demonstrated
on the small bowel follow-through x-ray film.
In ulcerative colitis, the inflammation is limited to the mucosa. Inflammation
almost always involves the rectum and is contiguous, virtually regardless
of the extent of the colon involved. The exception to this rule is that
the initial inflammation may appear patchy during colonoscopy performed
very early in the ulcerative colitis process, although biopsy specimens
of intervening normal-appearing mucosa often do reveal inflammation. The
intestinal inflammation of ulcerative colitis only involves the colon;
the remainder of the gastrointestinal tract is not inflamed. Biopsy specimens
demonstrate neutrophilic infiltrate along with crypt abscesses and crypt
distortion. Granulomas do not occur in ulcerative colitis.
The entire intestinal wall is involved with inflammation in Crohn disease,
not just the mucosa, as in ulcerative colitis. Biopsy specimens frequently
demonstrate granulomas (approximately 50% of the time). The presence of
granulomas is often helpful for making the diagnosis but is not necessary.
Because biopsy specimens obtained at colonoscopy are generally superficial
mucosal tissue samples, the pathologist often has difficulty making a
definitive diagnosis of ulcerative colitis or Crohn disease based on histologic
findings alone. However, other causes of inflammation may be suggested
based on pathology findings (eg, infectious colitis).
The care of a patient with IBD can be either medical or surgical in nature.
The medical approach for patients with IBD is symptomatic (flaring) care
and generally follows a step-wise approach to medication therapy, with
progression of the medical regimen until a response is achieved. Whether
patients whose disease is in remission benefit from continuing to take
aminosalicylate is controversial. In persons with Crohn disease, earlier
data suggested that postoperative recurrences are decreased in frequency
and severity, although later data suggest that this preventive effect
may not apply to flares of this IBD.
The first step in medication therapy is usually aminosalicylates;
no advantage has been demonstrated for any particular agent for either
ulcerative colitis or Crohn disease. For Crohn disease, metronidazole
or ciprofloxacin is occasionally used, particularly for perianal disease
or an inflammatory mass.
If the IBD fails to respond to aminosalicylates, the second step is
corticosteroids. Corticosteroids tend to provide rapid relief of symptoms
and a significant decrease in inflammation, but they are limited by their
adverse effects, particularly for prolonged use.
The consensus regarding treatment with corticosteroids is that they should
be tapered as rapidly as possible. Corticosteroids do not have a role
in maintaining remission.
If patients have difficulty reducing the dose of corticosteroids, have
IBD that is refractory to corticosteroid therapy, or have frequent flares
that require corticosteroid therapy, the third step for medication
is one of the immunomodulatory agents, either 6-MP or azathioprine.
These agents are not used for acute flares because the time from the
initiation of treatment to the onset of significant action may be as long
as 2-3 months. Response to these agents may be dose dependent; monitoring
of blood counts is required to protect the patient from the hematological
toxicity associated with these agents. Some authors suggest earlier use
of these agents.
An alternative third step is available for persons with Crohn
disease. This alternative is infliximab, a monoclonal antibody against
tumor necrosis factor (TNF)alpha. Administer this agent by intravenous
infusion. It may occasionally be given as a single dose or, more commonly,
3 doses (for fistulizing Crohn disease) followed by a maintenance regimen.
Administering the drug every 8 weeks has been demonstrated to be effective
for maintaining remission. The practitioner is advised to have the patient
seek insurance approval for the administration of this medication because
it is extremely expensive (typically, several thousand dollars per dose).
As of this writing, the medications approved by the US Food and Drug Administration
for the treatment of Crohn disease are prednisone, budesonide, and infliximab.
The final step for the treatment of IBD involves agents that have
less well-demonstrated levels of efficacy but have been shown to be useful
in some subsets of patients. For Crohn disease, methotrexate at 12.5-25
mg/wk may fall into this category. For ulcerative colitis, cyclosporine
A (usually started intravenously for overwhelming disease) and nicotine
patches fall into this category. Finally, a number of clinical trials
of biological agents and diets are being conducted and may demonstrate
efficacy in persons with IBD.
The approach to surgical treatment of IBD varies depending on the disease.
Importantly, ulcerative colitis is a surgically curable disease because
the disease is limited to the colon.
However, Crohn disease can involve any segment of the gastrointestinal
tract from the mouth to the anus; thus, surgical resection is not curative.
On the contrary, excessive surgical intervention can leave the patient
with a crippling short bowel syndrome.
Situations arise in Crohn disease in which surgical intervention without
resection can be used to defunctionalize the colon in order to possibly
allow healing of distal disease.
Surgery for ulcerative colitis
Surgical intervention for ulcerative colitis is curative for colonic
disease and potential colonic malignancy. The indications for colectomy
are (1) inflammation that is difficult to control, (2) early changes found
during surveillance (high-grade dysplasia, low-grade dysplasia in some
instances), (3) strictures; (4) significant adverse medication effects,
and/or (5) an unacceptable quality of life referable to the ulcerative
The surgical options for ulcerative colitis vary. While segmental resection
is rarely performed, total proctocolectomy is common. Total proctocolectomy
with ileostomy creation is the simplest procedure with the lowest overall
complication rate. A variation on this is the continent ileostomy or Koch
pouch. This procedure creates an ileal reservoir that can be emptied with
catheterization several times per day. However, incontinence from the
pouch may necessitate use of an ileostomy bag. A colectomy may be performed,
leaving a few centimeters of rectum intact; this ensures anal continence,
but continued malignancy surveillance is needed for any colonic mucosa
that remains and the remaining diseased rectal mucosa can continue to
be problematic from a symptomatic standpoint.
The most technically demanding option is ileoanal anastomosis. In this
multistage procedure, a diverting ileostomy is performed and an ileal
pouch is created and anastomosed directly to the anus, with complete removal
of the rectal mucosa. After the ileoanal anastomosis is healed, the ileostomy
is taken down and flow through the anus is reestablished. The major complications
of this procedure are anal incontinence and impotence. Pouchitis occasionally
is a problem. If the diagnosis is incorrect and this procedure is performed
on a patient with colonic Crohn disease, the likelihood of disease recurrence
at the ileoanal anastomosis is high, which requires takedown, ileostomy
creation, and loss of additional small bowel. When performed by a surgeon
skilled in this technique, it offers an excellent option for younger patients
with ulcerative colitis and concerns about body image.
Surgery for Crohn disease
The most straightforward surgery for Crohn disease is the segmental resection,
in which a segment of intestine with active Crohn disease or a stricture
is resected and the remaining bowel is reanastomosed. This surgery requires
margins of resection; in general, as little bowel as possible is resected
because the risk of disease recurrence is significant.
In patients with a very short cicatrix (scar tissue) stricture, a bowel-sparing
stricturoplasty can be performed. In this procedure, a longitudinal incision
is made across the stricture and then the incision is repaired with a
vertical suture. All mucosa is spared, and the obstruction is relieved.
As many as 6-8 stricturoplasties can be performed in a single operative
session. Stricturoplasty is associated with a 6-8% septic complication
rate (2-3% of patients require reoperation); this can generally be prevented
with optimal preoperative management to control the inflammatory component
of the stricture before surgical intervention.
Ileorectal or ileocolonic anastomosis is an option available to some
patients who have distal ileal or proximal colonic disease. This is a
variation on the simple segmental resection.
In patients with severe perianal fistulae, a diverting ileostomy or colostomy
is a surgical option. In this procedure, the distal colon is defunctionalized
and a temporary ileostomy or colostomy is created. The defunctionalized
rectum is allowed to heal, and the ileostomy or colostomy is then taken
down 6 months or a year later. Many patients who pursue this option choose
to forego reanastomosis after experiencing a stoma and a consequent improvement
in quality of life. Approximately 50% of patients who have the reanastomosis
performed have recurrences of perianal disease.
In addition to possible studies performed by an endoscopist or radiologist,
patients with IBD who are admitted to a medical service facility typically
require consultation with a surgeon.
Colorectal surgeon (where available) or general surgeon: Early
consultation with a surgeon is particularly useful in patients with stricturing
or fistulizing disease and in patients with ulcerative colitis who experience
frequent flares, have significant adverse effects from medications, or
have an unacceptable quality of life.
Radiologist: An interventional radiologist may be consulted when
percutaneous drainage of an abscess is desired.
Diet: No known dietary substances cause activation of IBD. Diet
may influence intestinal inflammation in persons with Crohn disease, but
it does not play a role in influencing inflammation in those with ulcerative
Lactose intolerance is common in persons with Crohn disease or
ulcerative colitis and some patients with other types of IBD.
Diet has been well demonstrated to have little or no influence on inflammatory
activity in persons with ulcerative colitis. However, diet may influence
symptoms. For this reason, patients are often advised to make a variety
of diet modifications, especially the adaptation of a low-residue diet.
Evidence does not support a low-residue diet as beneficial in the treatment
of ulcerative colitis, although it might decrease the frequency of bowel
Unlike in persons with ulcerative colitis, diet can influence inflammatory
activity in persons with Crohn disease. Nothing by mouth (status NPO)
can hasten the reduction of inflammation, as might the use of a liquid
or predigested formula for enteral feeding.
Although a meta-analysis in 1993 demonstrated that steroids were superior
to liquid diet alone for Crohn disease, a liquid diet seemed superior
to a regular diet for reducing inflammation. The problem with using enteral
liquid diets, especially the predigested formulations, is that palatability
limits the intake of adequate energy (calories) to meet patient requirements.
Parenteral alimentation may be needed.
Activity: Generally, patients do not need to limit activity when
IBD is quiescent. Even during flares of disease activity, activity is
limited only by the extent of fatigue and the abdominal pain or diarrhea
the patient is experiencing.
Abdominal pain may limit the ability of the patient to work productively
during flares of disease. When abdominal pain persists beyond medical
therapyinduced resolution of the active inflammation, other causes
of pain must be considered, including nephrolithiasis, abscess, stricture,
irritable bowel syndrome, and psychiatric disease.
In most instances, diarrhea limits activity primarily because of the
lack of immediate access to toilet facilities in many locations and/or
occupations. This can often be resolved with employers. Occasionally,
dehydration may be an issue, requiring intravenous hydration or the use
of oral rehydration solutions.
While several drugs have been used successfully for the treatment of
IBD for many years, medical treatment has advanced rapidly. The medications
used are broken down into several classes based on the chemical similarities
of the individual agents and similarities in the mechanisms of action.
A step-wise approach may be taken. With this approach, the most benign
(or temporary) drugs are used first. As they fail to provide relief, drugs
from a higher step are used.
The aminosalicylates and symptomatic agents are step I drugs under this
scheme; the antibiotics are a step IA, given the limited situations in
which they are used. The corticosteroids constitute the step II drugs
to be used if the step I drugs fail to adequately control the IBD. The
immune-modifying agents are step III drugs and are used if corticosteroids
fail or are required for prolonged periods. Infliximab is also a step
III drug and is used in limited situations in patients with Crohn disease.
The experimental agents are step IV drugs and are used only after the
previous steps fail and, then, are administered only by physicians familiar
with their use.
Note that drugs from all steps may be used additively; in general, the
goal is to wean the patient off steroids as soon as possible to prevent
long-term adverse effects from these agents. Opinions differ regarding
the use of certain agents in this step-wise approach.
Step I (aminosalicylates)
The 5 oral aminosalicylate preparations available for use in the United
States are sulfasalazine (Azulfidine), mesalamine (Asacol, Pentasa), balsalazide
(Colazal), and olsalazine (Dipentum). Enema and suppository formulations
are also available. All of these are derivatives of 5-aminosalicylic acid
(5-ASA); the major differences are in the mechanism of delivery. Some
of these also have unique adverse effects that other agents of this class
lack. All of the aminosalicylates are useful for treating flares of IBD
and for maintaining remission. None of the aminosalicylates has been proven
to have greater efficacy for the treatment of ulcerative colitis or Crohn
disease over any of the others. All of them are clearly more effective
in persons with ulcerative colitis than in persons with Crohn disease;
in persons with Crohn disease, the primarily utility is for colonic disease.
Step IA (antibiotics)
The antibiotics metronidazole and ciprofloxacin are the most commonly
used antibiotics in persons with IBD. Antibiotics are used only sparingly
in persons with ulcerative colitis because ulcerative colitis increases
the risk of developing antibiotic-associated pseudomembranous colitis.
When used in persons with ulcerative colitis, antibiotics are most commonly
administered in the perioperative setting. However, in persons with Crohn
disease, antibiotics are used for a variety of indications, most commonly
for perianal disease. They are also used for fistulae and inflammatory
masses in the abdomen, and they may have some efficacy in treating ileitis.
The antibiotics have potential adverse effects, including nausea, anorexia,
diarrhea, and monilial (candidal) infections; peripheral neuropathy can
be observed in association with metronidazole use and, when present, requires
discontinuation of therapy with that drug.
Step II (corticosteroids)
Corticosteroids are rapid-acting anti-inflammatory agents used in the
treatment of IBD. Indications are for acute flares of disease only; corticosteroids
have no role in the maintenance of remission. Corticosteroids may be administered
by a variety of routes depending on the location and severity of disease;
they may be administered intravenously (ie, methylprednisolone, hydrocortisone),
orally (ie, prednisone, prednisolone, budesonide, dexamethasone), or topically
(ie, enema, suppository, or foam preparations).
Intravenous corticosteroids are often used for patients who are severely
ill and hospitalized; few data have been published on the optimum dosage
of intravenous (or oral form) corticosteroids. The generally used upper
ends of dosing are methylprednisolone at 40 mg intravenously every 6 hours
or hydrocortisone at 100 mg intravenously every 8 hours. Some situations
mandate a higher initial intravenous dose, but many practitioners start
hospitalized patients at lower intravenous doses.
In general, once a clinical response is observed (typically within a
1-2 d, occasionally longer), the dose of the intravenous corticosteroid
can be tapered. Before hospital discharge, conversion to an oral corticosteroid
is made; further dosage tapering can be accomplished in an outpatient
setting. When oral corticosteroids are used, dosing is highly variable
and few data have been published to guide optimal dosing. The most common
range for moderate flares of IBD is prednisone at 10-40 mg/d; for more
severe flares, the higher end of the range is used (occasionally even
higher doses are used). Again, once a clinical response is seen, the dose
is tapered. Most patients who use oral corticosteroids can only occasionally
tolerate a relatively rapid taper after a response is achieved; occasionally,
a very prolonged steroid taper is necessary to prevent relapse. When the
latter situation occurs, consider the use of alternative drugs (immune
modifiers or anti-TNF therapy).
Topical corticosteroids are used in persons with distal colonic disease
in a manner similar to topical mesalamine; the major difference is that
even though topical mesalamine may be used to help maintain remission,
topical corticosteroids are used for active disease and have only a small
role in the maintenance of remission. The potential complications of corticosteroid
use are multiple and include fluid and electrolyte abnormalities, osteoporosis,
aseptic necrosis, peptic ulcers, cataracts, neurologic and endocrine dysfunctions,
infectious complications, and occasional psychiatric disorders (including
psychosis). Patients who are taking corticosteroids, especially for longer
than a few weeks, must be warned about the associated complications; this
discussion should be documented in the medical record. Some recent data
assert that some agents used for osteoporosis prevention and treatment
(eg, the bisphosphonates) are useful for preventing the bone loss associated
with corticosteroid use.
Step III (immune modifiers)
The immune modifiers 6-MP and azathioprine are used in patients with
IBD in whom remission is difficult to maintain with the aminosalicylates
alone. Immune modifiers work by causing a reduction in the lymphocyte
count, and because of that mechanism of action, their onset of action
is relatively slow (typically 2-3 mo). They are used most commonly for
their steroid-sparing action in persons with refractory disease; they
are also used as primary treatment for fistulae and the maintenance of
remission in patients intolerant of aminosalicylates. Use of these agents
mandates monitoring of blood parameters; they can cause significant neutropenia
or pancytopenia that would warrant a dose reduction or discontinuation.
Routine CBC counts with differentials and platelet counts are checked
monthly, and LFTs can be performed intermittently. After a year of stable
dosing with no difficulties with blood counts (except the expected lymphopenia),
the intervals between blood count monitoring can be increased.
The cytopenic effect is typically dose dependent, although some patients
are more sensitive than others. Typical dosing of the immune modifiers
(either 6-MP or azathioprine) is 1-2 mg/kg/d. If needed, the dose can
be increased to the point when cytopenia occurs; obviously, at higher
doses, closer monitoring is warranted. Blood tests are available to measure
metabolite levels, but the results have not been shown in independent
studies to have any correlation with clinical efficacy. These blood tests
for monitoring toxicity offer little advantage (but much greater expense)
over monitoring CBC counts and LFT results.
Other adverse effects of the immune modifiers include fever, rash, infectious
complications, hepatitis, pancreatitis, and bone marrow depression. The
most common reason for discontinuing the immune modifiers within the first
few weeks is the development of abdominal pain; occasionally, a biochemically
demonstrable pancreatitis occurs.
Concerns have been raised about the development of malignancy in patients
taking azathioprine and 6-MP. Because the population that requires these
medications is already at higher risk for the development of malignancy,
the author believes that the available data on the use of azathioprine
or 6-MP are insufficient and do not demonstrate a significant increase
in the risk of malignancy.
An additional step III agent works by a different mechanism. Infliximab
(Remicade) is an antiTNF-alpha monoclonal antibody administered
by infusion for the treatment of Crohn disease. Data supporting its use
in persons with ulcerative colitis are not as convincing as the data for
using it in persons with Crohn disease. Infliximab is administered as
a single infusion of 5 mg/kg for the treatment of moderate-to-severe Crohn
disease. For this indication, the response rate is 80% and the induction
of remission rate is 50% after a single dose; with multiple dosing, higher
rates of remission are attained.
Infliximab is also indicated for the treatment of fistulizing Crohn disease;
for this indication, it is administered as 3 separate infusions of 5 mg/kg
at weeks 0, 2, and 6, often followed by doses every 8 weeks. The fistula
responds (closes) in 68% of patients treated with infliximab, although
12% develop an abscess. The duration of response is variable, lasting
weeks to months; the duration of response can be increased with the concomitant
use of immune modifiers. The response can be maintained by continuing
regular dosing (ie, every 8 wk) after the induction dose. The response
rate in persons with ulcerative colitis is not as good as in those with
Crohn disease; from multiple small studies, the response rate in persons
with ulcerative colitis is approximately 50%.
The adverse effects of infliximab commonly include hypersensitivity and
flulike symptoms; the latter can often be avoided by pretreatment with
acetaminophen and diphenhydramine. Rare reports of lupuslike reactions
and lymphoproliferative malignancies have been reported, although whether
these are related to the drug remains uncertain.
Step IV (experimental treatments)
Generally, use these agents as part of an experimental protocol or in
a setting in which the toxicities of the agents can be rapidly recognized
and managed. Examples of some agents are provided, but a review of the
literature is warranted before using them. In most cases, some subsets
of patients respond; in general, large placebo-controlled trials have
not yet established efficacy for these agents for the treatment of IBD.
Various experimental agents tend to be more disease-specific, ie, an
agent works for Crohn disease but not ulcerative colitis, or vice versa.
Experimental agents used in persons with Crohn disease include methotrexate
(12.5-25 mg/wk orally or intramuscularly), thalidomide (50-300 mg/d orally),
and interleukin 11 (1 mg/wk subcutaneously). Experimental agents used
in persons with ulcerative colitis include cyclosporine A at a dose of
2-4 mg/kg/d intravenously (measure level; convert to oral dosing at 2-3
times the intravenous dose), nicotine patch (14-21 mg/d via topical patch),
butyrate enema (100 mL per rectum twice daily), and heparin (10,000 U
subcutaneously twice daily). Multiple contraindications, interactions,
and precautions are associated with these drugs.
Because patients report symptoms (eg, diarrhea, spasm/pain, epigastric
discomfort) and not inflammation per se, symptomatic relief is appropriate
when indicated. This includes therapy with antidiarrheal agents, bile
acidbinding agents, antispasmodics, and acid suppressants, as needed.
These medications are not without complications, and caution is necessary.
Further Inpatient Care:
Day of admission
Admit the patient to the hospital if surgical intervention is anticipated
or if he or she does not respond to outpatient treatment, is dehydrated,
or has uncontrolled pain or diarrhea.
Start intravenous hydration. If indicated, obtain an abdominal flat plate
image to exclude obstruction or megacolon. If the patient is nauseated
or vomiting or has evidence of obstruction or megacolon, nasogastric intubation
is indicated. Consider consultation with a surgeon.
If the patient has colitis, send a stool sample for C difficile toxin
titer testing; also send one for routine culture and sensitivity testing
if the patient has a new diagnosis of IBD. Laboratory studies to be considered
include CBC count with differential, albumin level, ESR, glucose value,
calcium level, magnesium level, phosphate value, electrolyte status, BUN/creatinine
values, and a pregnancy test in females of childbearing age.
Initiate treatment with an oral aminosalicylate, intravenous corticosteroids,
and metronidazole or ciprofloxacin (if antibiotics are indicated). Electrolyte
correction and, potentially, transfusion, can be performed if indicated
based on laboratory findings.
Keep patients NPO, except for medications (Crohn disease only); patients
with ulcerative colitis may maintain a regular diet unless megacolon is
present or surgery is being contemplated. Consider additional consultations
with a registered dietitian and a stoma nurse if indicated. Consider line
placement of central venous access.
Hospital day 1
If the abdominal flat plate findings were not diagnostic or if diagnostic
concerns remain, order a barium study (small bowel series or barium enema).
Although a colonoscopic evaluation also may be contemplated, consider
the increased risk of perforation in persons with acute colitis.
Assess and correct the posthydration CBC count and electrolyte values,
as indicated. Depending on the response to the initial interventions,
advancement of the diet may be considered.
Hospital days 2 and 3
By the second hospital day, most patients should be showing clear evidence
of clinical improvement. Assess the electrolyte status if intravenous
fluids are still being administered. Consider advancement of the diet.
The corticosteroid dose can be tapered. If the patient is not improving,
consider other treatment options; these may include hyperalimentation,
other medical therapies, surgical intervention, or transfer to a tertiary
care facility. Consider skipping to interventions typically enacted on
day 3 or 4 (or discharge).
Hospital day 3 is similar to day 2. The corticosteroid dose can be reduced,
and a switch to oral forms of all medications can be contemplated. If
home treatments are needed (eg, home hyperalimentation), initiate arrangements
for these. The diet can be advanced as tolerated. Consider skipping to
day 4 or 5 interventions.
Hospital day 4
Continue to advance the diet, as tolerated. Continue the switch to oral
medications. Many patients with a flare of Crohn disease or ulcerative
colitis may be discharged by this time (occasionally even sooner); some
may require another day of intravenous therapy.
If no progress has been made in the patient's condition since admission,
additional treatments are necessary, including surgery or more aggressive
medical treatments. Again, consider transfer to a tertiary care facility.
If the patient has been unable to tolerate an oral diet, initiate hyperalimentation
and/or reconsider surgical intervention.
Day of discharge/hospital day 5
Most patients should be able to be discharged on or before the fifth
hospital day. A regular diet should be tolerated, with some restrictions
if strictures are present. An ESR may be obtained to assist in future
disease assessment but is unlikely to alter current management.
Discharge the patient on oral medications, with appropriate follow-up
as an outpatient, typically within a few weeks.
Further Outpatient Care:
Outpatient medical care follows the approach outlined earlier in the
article (see Medical Care) using the medications described (see Medication).
Most outpatients' disease is in remission and requires little or no medication
other than aminosalicylates (perhaps). Flares of IBD can generally be
managed in an outpatient setting, primarily by stepping up the medication
as described in the step-wise approach (see Medication).
The biggest concern for outpatients is the duration and dosing of oral
corticosteroids. This author uses a dose that is adequate to suppress
inflammation (and thus symptoms), typically in the range of 20-40 mg of
prednisone per day. Once symptoms are controlled, a rapid taper of the
steroid follows. Patients in whom flares are frequent (>1-2 times/y),
in whom the duration of steroid use is long (more than a few weeks each
year), in whom reduction of the steroid dose causes recurrence of symptoms,
or in whom steroids do not appear to be working are candidates for more
intensive therapy. This higher step would include immune-modifying agents,
infliximab, or experimental agents.
One health maintenance issue of particular importance to patients with
IBD is a reduction in bone density, either from decreased calcium absorption
(because of the underlying disease process) or because of corticosteroid
use. Crippling osteoporosis can be a very serious complication for patients
with IBD. The threshold for obtaining bone density studies should be low,
and treatment (with bisphosphonates and calcium supplements) can be initiated
in patients with significantly low bone density.
In/Out Patient Meds:
If a step-wise approach is observed, the least amount of medication that
is effective can be used (see Medication). Despite the widespread availability
of home infusion, intravenous corticosteroids are still used only in hospital
settings because of potential problems and the dosing schedule.
Home infusion of intravenous hyperalimentation is increasingly available
for rare patients with Crohn disease in whom prolonged bowel rest is necessary.
The short bowel may require prolonged hyperalimentation. Home intravenous
antibiotics can also be arranged in this setting, if necessary.
The decision to transfer care of a patient (inpatient or outpatient)
depends on the expertise and comfort level of the treating physician.
Outpatient requests for a tertiary opinion should occur when patients
have disease that is difficult to control with aminosalicylates and occasional
brief courses of corticosteroids.
Relatively infrequent use and the monitoring necessary for azathioprine,
6-MP, and infliximab prompt some physicians to choose to refer patients
to tertiary care centers when the need for these agents becomes apparent;
others are comfortable handling these agents themselves.
For patients with refractory disease or those in whom corticosteroids
cannot be weaned, referral for a second opinion generally is wise. Transfer
inpatients for a tertiary opinion if the patient is not responding to
intravenous steroids within a few days of admission; alternatively, strongly
consider surgical intervention.
No known dietary or lifestyle changes prevent IBD.
Dietary manipulation may help symptoms in persons with ulcerative colitis,
and it actually may help reduce inflammation in persons with Crohn disease
(see Diet). However, no evidence indicates that consuming or avoiding
any particular food item causes or avoids flares of IBD.
Smoking cessation is the only lifestyle change that may benefit patients
with Crohn disease. Smoking has been linked to increases in the number
and severity of flares of Crohn disease. Smoking cessation is occasionally
sufficient to achieve remission in a patient with refractory Crohn disease.
See the subtopics in Clinical for the various complications that occur
Prognosis is discussed in Mortality/Morbidity. The typical course of
IBD (for the vast majority of patients) includes periods of remission
interspersed with occasional flares.
The average patient with ulcerative colitis has a 50% probability of
having another flare during the next 2 years. However, the range of experiences
is very broad; some patients may only have one flare over 25 years (as
many as 10%), and others may have almost constant flares (much less common).
Patients with ulcerative colitis limited to the rectum and sigmoid at
the time of diagnosis have a greater than 50% chance of progressing to
more extensive disease and a 12% rate of colectomy over 25 years. More
than 70% of patients presenting with proctitis alone continue to have
disease limited to the rectum over 20 years. Most who develop more extensive
disease do so within 5 years of diagnosis. Of patients with ulcerative
colitis involving the entire colon, 60% eventually require colectomy,
whereas very few of those with proctitis require colectomy. Of interest,
most surgical interventions are required in the first year of disease;
the annual colectomy rate after the first year is 1% for all patients.
Surgical resection for ulcerative colitis is considered curative for that
disease, although postoperative pouchitis may occur in some patients.
Of note, pouchitis is far more common in patients who have had a colectomy
for ulcerative colitis than in those who have had a colectomy for other
reasons (eg, familial adenomatous polyposis).
The clinical course of Crohn disease is much more variable than that
of ulcerative colitis. The clinical activity of Crohn disease is independent
of the anatomic location and extent of disease. A patient in remission
has a 42% likelihood of being free of relapse for 2 years and only a 12%
likelihood of being free of relapse for 10 years. Over a 4-year period,
approximately one quarter of patients remain in remission, one quarter
have frequent flares, and one half have a course that fluctuates between
periods of flares and remissions.
Surgery for Crohn disease is generally performed for complications (eg,
stricture, stenosis, obstruction, fistula, bleeding) rather than for the
inflammatory disease itself. After operation, the frequency of recurrence
of Crohn disease is high, generally in a pattern mimicking the original
disease pattern, often on one or both sides of the surgical anastomosis.
Approximately one third of patients with Crohn disease who require surgery
require surgery again within 5 years, and two thirds require surgery again
within 15 years. Endoscopic evidence of recurrent inflammation is present
in 93% of patients 1 year after surgery for Crohn disease. Surgery is
an important treatment option for Crohn disease, but patients should be
aware that it is not curative and that disease recurrence after surgery
is the rule.
Patients with IBD benefit tremendously from education about their disease.
As a chronic, often life-long disease that is frequently diagnosed in
young adulthood, increasing patient knowledge improves medical compliance
and assists in the management of symptoms.
The Crohn's & Colitis Foundation of America (available at: www.ccfa.org)
is the most prominent organization in the United States that can directly
provide educational materials for patients. This organization also supplies
physicians with educational brochures at no cost upon request.
For excellent patient education resources, visit eMedicine's Crohn Disease
Center and Esophagus, Stomach, and Intestine Center. Also, see eMedicine's
patient education articles, Inflammatory Bowel Disease, Crohn Disease,
Crohn Disease FAQs, and Irritable Bowel Syndrome.
Physicians may be at risk in certain areas of the treatment of patients
with IBD. In general, these may be easily avoided by documenting appropriate
education of the patient in the patient's medical record.
Patients with IBD are more prone to the development of malignancy. Persons
with Crohn disease have a higher rate of small bowel malignancy. Because
no effective screening protocol is available, this should not be an issue.
Patients with pancolitis, particularly ulcerative colitis, are at a higher
risk of developing colonic malignancy after 8-10 years of disease. The
current standard of practice is to screen these patients with colonoscopy
at 1- to 2-year intervals once they have had the disease for that duration.
If a patient refuses appropriate screening, document it in the medical
Use of corticosteroids may lead to debilitating illness, particularly
after long-term use. Warn patients who refuse to try more aggressive therapies
and insist on continuing to take corticosteroids of the potential for
long-term harm with these drugs, and take care to document these warnings
and the alternatives offered in the medical record. Recommend to any patient
who requires more than the rare short course of steroids that a yearly
ophthalmologic examination is warranted because of the risk of cataract
Patients with IBD who are undergoing endoscopic procedures have higher
complication rates than the general population; the informed consent obtained
for endoscopic procedures should always mention bleeding and perforation
as potential complications.
The single factor cited in most lawsuits involving endoscopy is failure
to obtain adequate informed consent; missed malignancy and perforation
Ulcerative colitis is a surgically curable disease. Keep this in mind
in patients who are having significant difficulty with their disease or
are having significant adverse effects from medications (particularly
those related to long-term steroid use). This author makes certain to
mention this (and document it) when first meeting any patient with ulcerative
If a decision is made to use or to continue immunosuppressant agents
(ie, azathioprine, 6-MP) in a pregnant patient with IBD, the physician
should be aware of the latest literature and should document the discussion
of such with the patient, particularly given that these agents are still
rated pregnancy class D by the Food and Drug Administration.
Because patients with IBD are often diagnosed in the peak of childbearing
years, issues related to fertility, pregnancy, and childbearing are always
a concern with the disease and its treatment.
In women, fertility is normal or only minimally impaired. Women considering
pregnancy should not take immune modifiers (ie, 6-MP, azathioprine). Although
some case reports and small series show no adverse outcomes of pregnancies
in patients with IBD who are taking immune modifiers, birth defects are
also reported. If a patient is taking an immune modifier and becomes pregnant,
stopping the immune modifier and using steroids, as needed, is advisable
in most instances. Vigilance for birth defects is appropriate.
For men with IBD, the major concern is the medications needed for treatment.
Sulfasalazine can decrease sperm counts and sperm motility, causing a
functional azoospermia; the other aminosalicylates do not seem to have
this effect. The sperm effects are reversible by discontinuing the sulfasalazine.
No firm evidence indicates that the use of immune modifiers in the father
leads to more birth defects, although this has been suggested.
Most infants are born healthy. The prevalence of prematurity, stillbirth,
and birth defects is similar to that of the general population. The prevalence
of spontaneous abortion is slightly higher in patients with IBD (12.2%
vs 9.9% in the general population). Prior proctocolectomy or ileostomy
is not an impediment to successful pregnancy.
In general, the aminosalicylates, including sulfasalazine, are safe during
pregnancy. Folate supplements should be taken. Corticosteroids are also
safe, but if high doses are needed near the end of the pregnancy, monitor
the infant for signs of adrenal suppression. Current literature suggests
that continuation of immune modifiers (ie, azathioprine, 6-MP) may be
safe in pregnancy. Metronidazole (Flagyl) and ciprofloxacin (Cipro) are
safe in pregnancy. The topical agents are generally safe in pregnancy.
Mothers who require medication to control of their IBD should strongly
consider bottle feeding their infants. Sulfasalazine metabolites can be
detected in breast milk; exercise caution. Low concentrations of mesalamine
and higher concentrations of its metabolites can be detected in breast
milk. The significance of this is unknown. Corticosteroids can also be
detected in breast milk. Immune modifiers are excreted in breast milk;
either the immune modifier should be discontinued or the infant should
be bottle fed. Metronidazole (Flagyl) and ciprofloxacin (Cipro) are excreted
in breast milk; discontinue nursing or discontinue the drugs.
Although small amounts of the topical agents are absorbed, and thus may
be excreted in breast milk, the concentrations are much lower than with
the oral forms of the same medications. These medications are probably
reasonably safe in breastfeeding.
Medications, safety in pregnancy
All of the aminosalicylates and the corticosteroids appear to be safe
in women in all phases of fertility, pregnancy, and lactation. Men should
avoid sulfasalazine (Azulfidine) during periods when they and their mates
are attempting to become pregnant.
The antibiotics (ie, metronidazole, ciprofloxacin) should generally be
avoided during lactation; they are probably safe for fertility and during
The immune-modifying agents (ie, 6-MP, azathioprine) should be considered
only on a case-by-case basis.
Aspirin and nonsteroidal anti-inflammatory agents in IBD
Currently, substantial controversy has been raised in the medical/IBD
community regarding the effects of aspirin or nonsteroidal anti-inflammatory
drugs (NSAIDs) on IBD. Published data and recommendations indicate that
aspirin and NSAIDs cause a number of flares of IBD and, thus, should be
avoided in all patients with IBD. On the other hand, studies also indicate
that only a very minor link exists between the use of aspirin or NSAIDs
and flares of IBD.
This author's practice is to administer aspirin or NSAIDs judiciously
when indicated (eg, with arthritis and/or arthralgias associated with
IBD), with the caveat that the patient is warned of the possibility that
the medication may cause a flare of the IBD. If, shortly after starting
the NSAID, a flare occurs, then the NSAID should be discontinued. If the
patient's disease remains in remission, the patient can be maintained
on the NSAID as necessary.
INFLAMMATORY BOWEL DISEASE
BREAKTHROUGHS IN THE MANAGEMENT
OF INFLAMMATORY BOWEL DISEASE
N H Banka
Consultant Gastroenterologist and Hepatologist, Bombay Hospital and Medical
Research Centre, Formerly, Consultant gastroenterologist at Sir JJ Group
of hospitals and Grant Medical College, Sir Hurkisondas Hospital and Nanavati
Breakthroughs in newly developed agents have included not only new compounds
and modes of delivery, but also entirely novel therapeutic modalities.
Biologic therapies have begun to assume prominent role. Clinical observations,
pilot studies and extrapolation of results from other Immuno-inflammatory
diseases (Rheumatoid arthritis), provide important insights into mechanism
of risk benefit, action and sample size estimates for the design and implementation
of controlled trials. This is true for inflammatory bowel disease (IBD)
where a constant flow of breakthroughs are reaching the professional and
layman journals. However, even with the advent of regulatory approval
of new treatments, such as Infliximab, the evidence base may be insufficient
to predict the eventual optimisation of treatment strategies until years
after the agents availability in the market.
The only "new" aminosalicylate is Balsalazide, which is a pro-drug. In
recent trials this molecule has comparable efficacy and safety to mesalamine
in the induction and maintenance of remission for ulcerative colitis.
Budesonide is marketed in different countries for the treatment of IBD.
Potential therapeutic advantage over systemic steroids include a) an increased
binding potency for the glucocoticoid receptor and b) increased "first-pass"
hepatic metabolism. This drug can also be used to reach specific sites
in the form of targeted delivery. The therapeutic efficacy has been similar
to other steroids without inhibition of the hypothalamus-pituitary-adrenal
Budesonide enemas are not as efficacious as topical mesalamine.
Niether azathioprine nor mercaptopurine is considered a new therapy for
IBD. Important and practical aspects of their usage remains to be defined
in ulcerative colitis (UC) and Crohn's disease (CD). It could prove to
be efficacious drug with initial steroid therapy and concurrent treatment
A recent, small trial has suggested that intravenous cyclosporin without
steroids may be efficacious for acute UC. Long term immunomodulation is
beneficial after acute cyclosporin therapy with azathioprine. Other oral
agents such as tacrolimus also have been evaluated in preliminary trials
of UC and CD but controlled data is lacking.
Mycophenolate has also been studied but requires additional studies of
safety and efficacy before it can be considered a standard approach.
The introduction of infliximab into the US marketplace has been the first
real advance for the treatment of IBD since the general acceptance of
immunomodulation. Three controlled trials have set the expectations for
these new therapies andpredict the eventual utility of infliximab. There
was excellent efficacy for refractory disease but a gradual decline in
efficacy over the ensuing 12 month period, particularly in patients who
did not receive re-treatment. Similar results were obtained in fistulising
Tight on the heals of infliximab are other anti-TNF strategies as an
humanised version of a monoclonal anti-TNF (CDP571) and the potential
use of eternacept, humanised soluble receptors for TNF. Most recently,
thalidomide has also been explored in early trials for CD with optimistic
reports of efficacy.
Molecular engineered formulations of human recombinant interleukin-10
and interleukin-11 have entered clinical trials in IBD as have anti-sense
compounds targeting inhibition of adhesion molecules (ICAM-1). It is anticipated
that monoclonal antibody and anti-sense technologies will continue to
assess specific mediators such as NF kappa, gamma-interferon and interleukin-12.
Evolving methods of influencing cytokine production and regulation, including
the use of viral vectors are presently on the horizon.
The protective role of cigarette smoking against the development of UC
has led to trials utilising nicotine as adjunctive therapy. A series of
trials using nicotine patches has supported a role for nicotine therapy
in the symptomatic management of UC. At present nicotine should not be
used as a proven therapy for UC but may be considered in the patients
whose UC aggravated after smoking cessation.
Short Chain Fatty Acids
Short chain fatty acids enhance the colonocyte-nutrient oxidation, thus
improving the ongoing colonocyte dysfunction. It has been used as mixed
SCFD or butyrate as enematas in distal UC. While in most studies there
was a positive benefit, the overall response rate is not substantially
different from placebo. At the present time this mode of therapy cannot
be advocated for the routine management of UC.
Fish Oil, Omega-3 fatty Acids and Leukotriene Inhibitors
Trials involving omega-3 fatty acids were performed in the early and
mid-1990s for refractory UC or as maintenance therapy. In these trials
the clinical benefit was modest, at best, and these therapies have not
been accepted within the current practice guidelines for UC. The development
of an enteric coated fish oil preparation, recently effective in a Crohn's
disease maintenance trial, may eventually offer an alternative therapeutic
option in IBD.
The potential role of inhibition of 5-lipoxygenase and leukotriene B4
led to development of specific 5-lipoxygenase inhibitors. However, in
contrast to asthma, specific inhibition of a distal mediator of inflammation
has failed to provide adequate therapy for either active UC or prevention
Observations regarding a "paradoxical" improvement in colitis with heparin
therapy and improvement in extraintestinal manifestations of IBD have
led to the possibility that heparin may have a therapeutic role in IBD.
While heparin does appear to be safe in the setting of UC it remains to
be determined where heparin therapy will fall in the armamentarium for
IBD and whether the new developments in low molecular weight heparin will
provide similar therapeutic potential.
An intriguing area of therapy has been the potential for probiotic therapy
for IBD. Recent european trials have begun to suggest efficacy for probiotic
therapy for UC and CD. We anxiouslyawait further evidence for this expanding
Challenges in the field of IBD is not only identifying the novel agents,
but also defining the end points and identifying the efficacy at the biologic
level. Clinicians are only just beginning to recognize subclinical markers
of response. Looking back at successes and failures in newer breakthroughs
to treating IBD, it may be tempting, although extremely difficult to draw
conclusions about pathogenesis. Even with a therapy as specific as anti-TNF
antibody, it is not clear if the benefit is simple binding and clearing
or deletion of the activated macrophage. Thus, when a therapy proves effective,
do clinicians truly know how it works? In this context it is the write
time to remember Sir William Osler's saying -"I always use the newest
medicine first, Before its effectiveness wears off".
Inflammatory Bowel Disease
What Causes IBD?
How Do I Know if I Have Ulcerative Colitis?
Does Ulcerative Colitis Increase the Risk of Colon Cancer?
How Do I Know if I Have Crohns Disease?
What are the Complications Associated with Crohn s
What is the Treatment for IBD?
Should I Modify or Change My Diet?
How Do I Cope with IBD?
When is Surgery Needed?
Digestion of food begins in the mouth and moves through the esophagus,
stomach, and the small and large intestine. In the mouth, stomach, and
the small intestine, food is mixed with digestive juices. The digestive
juices break the food down into smaller chemical pieces or nutrients.
These nutrients move along the small intestine, which is made up of three
parts: the duodenum, jejunum, and ileum. The nutrients are absorbed into
the bloodstream through the small intestine and carried to all parts of
the body. Nutrients are needed for the body to grow and remain healthy.
The water and solid waste that remain after the nutrients are absorbed
move into the large intestine. Most of the remaining water is absorbed
into the bloodstream from the colon. The solid waste is passed out of
the body as a bowel movement (BM) through the anus.
Inflammatory Bowel Disease (IBD) is a term that refers to both ulcerative
colitis and Crohns disease. Ulcerative colitis causes inflammation
of the lining of the large intestine. Crohns disease causes inflammation
of the lining and wall of the large and/or small intestine. When inflamed,
the lining of the intestinal wall is red and swollen, becomes ulcerated,
What Causes IBD?
The cause(s) of IBD are not known, but there are several theories. One
theory is based on genetics indicating that IBD does run in families.
About 15 percent to 30 percent of patients with IBD have a relative with
the disease. There is research going on to find out if a specific gene
or a group of genes makes a person more susceptible to getting the disease.
Many changes in the bodys immune system (bodys natural defense
system against disease) have been discovered in patients with IBD. What
is still unknown is what causes those changes to happen. There is a large
amount of research being done in this area.
There is little evidence that stress causes IBD. As with other illnesses,
stress may aggravate symptoms and require a treatment program.
IBD occurs most frequently in people in their late teens and twenties.
There have been cases in children as young as two years old and in older
adults in their seventies and eighties. Men and women have an equal chance
of getting the disease.
Most often ulcerative colitis occurs in young people 15 to 40 years of
age. Ulcerative colitis occurs only in the inner lining of the colon (large
intestine) or rectum. When it is located only in the rectum, it is called
proctitis. Inflammation of the rectum and colon keeps water from being
absorbed into the bloodstream and results in diarrhea.
Symptoms of Ulcerative Colitis
The most common symptoms of ulcerative colitis are diarrhea, abdominal
cramps, and rectal bleeding. Some people may be very tired and have weight
loss, loss of appetite, abdominal pain, and loss of body fluids and nutrients.
Bleeding may be serious, leading to anemia (low red blood cell count).
Joint pain, redness and swelling of the eyes, and liver problems can also
occur. No one knows for sure why problems outside the colon are linked
with colitis. These problems may improve when the colitis is managed.
Ulcerative colitis is an illness that has periods of remission (time
when you feel well) and relapse (time when you feel ill). Half of the
people who have ulcerative colitis have only mild symptoms. Others have
frequent fever, bloody diarrhea, nausea, and severe abdominal cramps.
Some people with severe symptoms of ulcerative colitis must go to the
hospital to correct malnutrition and stop diarrhea and loss of blood.
In the hospital, a patient may need a treatment program including a special
diet and feeding through a vein. Sometimes surgery is needed.
How Do I Know if I Have Ulcerative Colitis?
To find out if you have ulcerative colitis, your doctor must take your
medical history and perform a physical examination. The exam may include
blood tests and samples of a bowel movement. Other tests include:
Flexible Sigmoidoscopy or Colonoscopy - A small flexible tube
inserted by your doctor into the anus. The flexible tube is slowly passed
into the lower third of the colon in flexible sigmoidoscopy and through
the entire colon in a colonoscopy, allowing your doctor to see the lining
of the colon. If necessary, the doctor can take a tissue sample called
a biopsy to make a diagnosis of your condition.
Barium Enema---This is an X-ray of the colon. A white substance
called barium is put into the colon by an enema. This test may allow your
doctor to see areas of the colon that are abnormal.
Does Ulcerative Colitis Increase the Risk of Colon Cancer?
Risk of colon cancer is higher in ulcerative colitis patients with involvement
of the entire colon and in patients who have had the diagnosis for eight
to ten years. Patients with a diagnosis of left-sided ulcerative colitis
for 15-20 years also fall into a higher risk group for developing cancer.
Individuals in these groups should consult their doctor and plan for periodic
colonoscopy with biopsy.
Crohns is a chronic disease that has periods of remission (time
when person feels well) and relapse (when a person feels ill).
Crohns disease is an inflammation and ulceration process that occurs
in the deep layers of the intestinal wall. The most common areas affected
are the lower part of the small intestine, called the ileum, and the first
part of the colon. This type of Crohns disease is called ileocolitis.
Crohns disease can infrequently affect any part of the upper gastrointestinal
tract. Aphthous ulcers, which are similar to cold sores, are common. Ulcers
can also occur in the esophagus, stomach, and upper small intestine (duodenum).
It is difficult to tell these ulcers from peptic ulcers except by biopsy
Symptoms of Crohns Disease
The most common symptoms of Crohns disease are pain in the abdomen,
often in the lower right side, diarrhea, and weight loss. There may also
be rectal bleeding and fever. Chronic bleeding may lead to a low red blood
cell count called anemia. Children who develop Crohns disease may
have delayed development and stunted growth.
How Do I Know if I Have Crohns Disease?
To find out if you have Crohns disease, your doctor must take your
medical history and do a physical exam. The exam may include blood tests
and samples of a bowel movement. Other tests are the same as described
in the section on Ulcerative Colitis; a barium enema and a colonoscopy
examination. In addition, a small bowel X-ray may be required.
What are the Complications Associated with Crohns
The most common complication of Crohns disease is blockage of
the intestine. Blockage or stricture occurs when the disease thickens
the bowel wall with swelling and scar tissue. The intestine passage becomes
smaller and smaller, until it is completely closed.
Fistulas are a common complication of this disease. Fistulas occur
when ulcers in the intestine break through the intestine wall making tunnels
into surrounding tissues of the bladder, vagina, or into the skin. Fistulas
occur frequently around the anus and rectum.
These fistulas can become infected and may result in abscess formation.
Treatment programs are used to manage infected fistulas, but often surgery
What is the Treatment for IBD?
Your doctor will discuss with you a treatment plan that may include any
of the following:
There are many different types of treatment plans that your doctor can
prescribe to control the symptoms of IBD, and each of these has specific
actions and side effects. Be sure to follow all of your doctors
directions. Never stop your treatment plan until you have completed it
or your doctor instructs you to stop.
Should I Modify or Change My Diet?
What you eat does not cause IBD, but can cause symptoms when the disease
The goal of nutritional management for people with IBD is to modify the
diet to decrease gastrointestinal (GI) symptoms while maintaining adequate
nutrient intake. Your doctor may do a nutritional assessment to determine
if you are taking in enough calories, vitamins, and minerals. When nutritional
needs are not being met, your doctor may suggest a liquid supplement.
How Do I Cope with IBD?
Although IBD is a chronic disease that has periods of remission and relapse,
most people have a normal life span and a good quality of life.
For those who have chronic and continuing symptoms, the following apply:
Know your body and how IBD affects you
Learn to care for yourself, have control over those things you can control
Develop a support system that works for you: family, friends, and support
Be sure to follow instructions from your medical team
When is Surgery Needed?
Most people who have IBD respond to their treatment program, including
medications and nutritional planning. Many patients have mild episodes
of illness after long periods of feeling well. Your doctor will consider
surgery usually when certain conditions are present. Surgery may be needed
if there is:
A large amount of bleeding
Long-lasting and serious illness
Ulceration that makes a hole in the intestinal wall
Medical treatment plan is not controlling the disease
There are several surgical choices. Each has advantages and disadvantages.
The surgeon and patient must decide on the best option.
Staying informed is an important aspect of dealing with IBD.
Absorption - the process of nutrients passing from the intestine into
the blood stream.
Anemia - a condition in which the blood does not have enough red blood
Anus - opening at the end of the rectum that allows solid waste to be
Aphthous Ulcers - a sore on the mouth that is associated with CrohnÕs
Chronic Disease - illness that occurs at frequent intervals over a long
period of time.
Colon - the large intestine.
Chrohns Disease - an inflammatory and ulcerative process that occurs
in the deep layers of the small and sometimes large intestine.
Digestion - the process of breaking down food into its simplest chemical
compounds so that it can be absorbed.
Duodenum - the first portion of the small intestine. Connects the stomach
to the small intestine.
Fistulas - an abnormal passage leading from the colon to other organs
in the lower abdominal cavity.
Ileocolitis - a common form of Crohns disease that affects the
lower portion of the small intestine and the first portion of the colon
called the ileum.
Ileum - the last portion of the small intestine that connects to the
Immune System - the bodys natural defense system that fights against
Inflammation - a response to tissue injury that causes redness, swelling,
Jejunum - the middle portion of the small intestine.
Large Intestine - also known as the colon. Primary function is to absorb
water and get rid of solid waste.
Malnutrition - condition that occurs when the body does not have enough
calories, vitamins, and minerals to maintain growth and health.
Proctitis - inflammation of the rectum.
Rectum - lowest portion of the colon.
Small Intestine - Connects to the stomach and large intestine. Absorbs
Stricture - closure or obstruction of the intestine.
Brandt LJ, Steiner-Grossman P, eds. Treating IBD: A Patients Guide
to the Medical and Surgical Management of Inflammatory Bowel Disease.
New York: Raven Press, 1989
Steiner-Grossman P, Banks PA, Present DH, eds. The New People Not Patients:
A Source Book for Living with IBD. Dubuque, Iowa: Kendall/Hunt Publishing
Crohns and Colitis Foundation of America>
(CCFA). 386 Park Ave., South, New York, NY, 10016-8804. (212) 685-3440,
or (800) 932-2423.