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Acknowledgement
This chapter in the sixth edition was written by Mark Thompson-Fawcett and we are grateful to him for those parts of the chapter, which we have kept in this edition.
Introduction
Crohn’s disease is a chronic, relapsing illness of unknown cause with a transmural inflammatory process that can affect the gastrointestinal tract anywhere from mouth to anus, and which may be associated with extra-intestinal manifestations. The most frequent disease distributions include ileal, ileocolic and colonic. Perianal disease often co-exists. Classically, there are discontinuous segments of disease (‘skip lesions’) with areas of normal mucosa intervening. Inflammation may cause ulceration, fissures, fistulas and fibrosis with stricturing. Histology reveals a chronic inflammatory infiltrate that is typically patchy and transmural and may reveal classic granulomas with giant cell formation. Clinically, a characteristic triad of symptoms may be seen: abdominal pain, diarrhoea and weight loss. Complications include intestinal obstruction caused by stricturing disease or intestinal fistulas. A combination of clinical, macroscopic, radiological and pathological features is required to make the diagnosis. Remission of varying duration is interspersed with acute episodes or ‘flares’.
Epidemiology
Peak age of onset is 20–30 years, with a second peak at age 50–60 years. Sex distribution is equal. The incidence has increased gradually in most regions around the world, with a higher prevalence in developed countries, particularly in urban areas. The prevalence is highest in Europe and Northern America (around 200–300 per 100 000). It is notable that areas with a low incidence and prevalence have shown a steady increase in rates in parallel with their economic development. This is particularly the case in Asia where increases in incidence have been associated with rapid urbanisation suggesting that environmental factors may have a role. From genetic studies, there are some risk loci that are specific to ethnicity, but many are shared.
Aetiology
The aetiology involves interplay between environmental factors and genetic susceptibility, along with changes in the intestinal microflora.
Environmental factors
Smoking is the most studied environmental factor, doubling the relative risk of Crohn’s. Antibiotic exposure in childhood may also increase risk. Other medications potentially increasing risk include oral contraception and non-steroidal anti-inflammatory drugs. Dietary factors including reduced fibre and increased saturated fat, and micronutrients such as Vitamin D, zinc and iron may be associated with a small increase in risk, but whether any of these factors are causal or simply associated is not clear.
Genes
There is a genetic predisposition to Crohn’s disease. About 12% of patients with Crohn’s will have a family history. Ashkenazi Jews have a three- to fourfold greater risk of disease than non-Jewish populations and those of Asian and African-American descent have the lowest risk of developing the disease. Relatives of patients with Crohn’s disease also have an increased risk of developing ulcerative colitis. Crohn’s disease and ulcerative colitis are polygenic disorders with some shared susceptibility genes.
Linkage studies have identified gene associations including NOD2 mutations, HLA , MUC2 and JAK2 . All play a role in bacterial handling in the gut, a key factor for disease. However, only a small proportion of disease hereditability is explained by genetic variation and genetics alone has so far failed to explain disease variance and phenotypes, highlighting the potential importance of epigenetic and environmental factors in disease susceptibility and course.
The microbiome
Microbiome imbalance or maladaptation (dysbiosis) has been demonstrated in Crohn’s patients at the time of diagnosis. This dysbiosis provides a compelling theoretical pathogenic pathway to development of disease. For instance, approximately one third of patients have an increased abundance of mucosa associated adherent-invasive Escherichia coli , which can cross the mucosal barrier, adhere to and invade intestinal epithelial cells and survive and replicate within macrophages provoking release of tumour necrosis factor (TNF)-α. Despite significant research in this area, manipulation of the microbiome has so far mainly failed to significantly impact on treatment.
Pathogenesis
Normally, the gut exists in a state of tolerance to the stream of microbial, dietary and other antigens in contact with the mucosa, but this tolerance and the ability to suppress an immune-mediated inflammatory response is lost. Defects in immunoregulation are coupled with an increased mucosal permeability because of leaky paracellular pathways.
Defects in immunoregulation may include disturbed innate immune mechanisms at the epithelial barrier, problems with antigen recognition and processing by dendritic cells, and effects of psychosocial stress via a neuroimmunological interaction. In Crohn’s disease, the cell-mediated response is predominant, with excessive activation of effector T cells that predominate over the regulatory T cells that turn off the process. Pro-inflammatory cytokines released by effector T cells stimulate macrophages to release TNF-α, interleukin (IL)-1 and IL-6. In addition, abnormal dendritic cell function may further drive the inflammatory response. Leucocytes then enter from the local circulation releasing further chemokines, amplifying the inflammatory process. The result is a local and systemic response, including fever, an acute-phase response, hypoalbuminaemia, weight loss, increased mucosal epithelial permeability, endothelial damage and increased collagen synthesis. Because of immune dysregulation, the inflammatory response in the intestinal mucosa proceeds unchecked, producing a chronic inflammatory state.
Pathology
The macroscopic appearance and distribution are important in differentiating Crohn’s disease from other forms of inflammatory bowel disease (IBD), particularly ulcerative colitis. Frequencies of regions involved are:
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small bowel alone, 30% colon alone, 25–35%;
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small bowel and colon, 30–50% (usually ileocolic);
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perianal lesions, over 50%;
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stomach and duodenum, 5% (minor subclinical mucosal abnormalities in 50%).
Skip lesions strongly suggest Crohn’s disease, although occasionally, a periappendiceal or caecal patch of overt colitis may be observed with distal ulcerative colitis.
The combination of disease behaviour (stricturing, penetrating), distribution and perianal disease is captured in the Montreal classification ( Table 11.1 ).
Table 11.1
Phenotyping Crohn’s disease: Montreal classification for Crohn’s disease
Age at diagnosis: <17 years (A1); between 17 and 40 years (A2); or ≥40 years (A3 Location of disease:
Behaviour:
|
Perianal disease [p] is added if present.
The classification was modified to the Paris classification to include growth failure in a paediatric population.
Macroscopic appearance
The unmistakable appearance of Crohn’s disease is of a stiff, thick-walled segment of bowel with fat wrapping and serosal ‘corkscrew’ vessels. There is creeping extension of mesenteric fat around the serosal surface of the bowel wall towards the anti-mesenteric border. This is part of the connective tissue change that affects all layers of the bowel wall. As inflammation is full thickness, there can be fibrinous exudate and adhesions on the serosal surface. Narrow linear ulcers with intervening islands of oedematous mucosa give the mucosal surface its classic cobblestone appearance. Ulceration is discrete, and serpiginous linear ulcers usually run along the mesenteric aspect of the lumen. Deep fissuring from linear ulceration may lead to formation of fistulas through the bowel wall. Closer inspection may reveal multiple aphthous ulcers that usually develop on the surface of submucosal lymphoid nodules. Aphthous ulcers are the earliest macroscopic lesions in Crohn’s disease and are seen before the classic appearances of more established disease. Inflammatory polyps are often found in the involved colon but are unusual in the small bowel. Enlarged lymph nodes may be present in the resected mesentery but are not caseated or matted together. Strictures can vary in length and may be stiff, like a hosepipe, with turgid oedema, or tight fibrotic strictures from burnt-out inflammation. The narrowing of the lumen may be sufficient to produce obstruction and proximal dilatation, and there may be multiple dilated segments between multiple tight strictures. Fistulas, sinuses and abscesses are often present in the ileocaecal region but may arise from any segment of active disease and can communicate with other loops of bowel, stomach, bladder, vagina, skin or intra-abdominal abscess cavities.
Microscopy
The main questions asked by the histopathologist when assessing an initial biopsy for IBD are;
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Is the mucosa inflamed?
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If the mucosa is inflamed: is it IBD or not?
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If it is IBD: is it ulcerative colitis, Crohn’s disease, or IBD unclassified?
Inflammation involves the full thickness of the bowel wall. Early mucosal changes show neutrophils infiltrating the base of crypts, causing injury and focal crypt abscesses. The formation of mucosal lymphoid aggregates followed by overlying ulceration produces aphthous ulcers. Lymphoid follicles may be seen in the base of the mucosa in severe ulcerative colitis, but they are a prominent feature of Crohn’s disease, where they are transmural, leading to the formation of a Crohn’s ‘rosary’ on the serosal surface.
In Crohn’s disease, there is relative preservation of goblet cell mucin, whereas mucin depletion is a feature of ulcerative colitis (with the exception of fulminant ulcerative colitis, where there may be surprisingly little mucin depletion).
As the disease progresses, connective tissue changes occur in all layers of the bowel wall giving the stiff, thick-walled, macroscopic appearance. There is submucosal fibrosis and muscularisation. The muscularis mucosa and muscularis propria are thickened from increased amounts of connective tissue. Typically, the chronic inflammatory infiltrate and the architectural changes in the mucosa are patchy.
The following three features are diagnostic hallmarks of Crohn’s disease:
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deep non-caseating granulomas are present in 60–70% of patients and are commonly located in the bowel wall but also the mesentery, regional lymph nodes, peritoneum, liver or contiguously involved tissue;
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intra-lymphatic granulomas;
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granulomatous vasculitis.
Differentiating Crohn’s colitis from ulcerative colitis
Differentiation is important for planning medical and surgical treatment. Consideration of the clinical picture, radiological and endoscopic features and histological findings is essential – with the cumulative evidence informing the diagnosis.
It may be difficult even for an experienced gastrointestinal pathologist to distinguish between Crohn’s colitis and ulcerative colitis on histology. No individual histological feature is diagnostic of IBD or a type of IBD but features may be more frequent in one IBD type compared to another. Considerable inter-observer variation is reported. Where the distinction between ulcerative colitis and Crohn’s cannot be made, the term IBD-unclassified is used. During the course of the disease, behaviour may change, resulting in a change of diagnosis.
The following histological features favour a diagnosis of Crohn’s disease over ulcerative colitis:
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Granuloma (non-cryptolytic)
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Focal or patchy lamina propria chronic inflammation (rather than continuous/diffuse)
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Focal or segmental crypt distortion (rather than continuous/diffuse)
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Ileal involvement.
Rectal sparing may be seen in ulcerative colitis, especially if topical (local) treatment has been used. Treated ulcerative colitis may also demonstrate the patchy changes listed earlier. Perianal disease is very suggestive of Crohn’s, although patients with ulcerative colitis can develop cryptoglandular fistulas and abscesses. Established diversion proctitis or pouchitis may also mimic Crohn’s disease.
Clinical
Clinical features include a typical triad of diarrhoea (70–90%), abdominal pain (45–65%) and weight loss. Perianal disease is an important and debilitating manifestation (30%).
The Crohn’s disease phenotype for an individual is described using the Montreal classification – see Table 11.1 .
Systemic symptoms
Weight loss is reported by 65–75% of patients. This is the result of active inflammation, anorexia, food fear and, less often, malabsorption. The latter may be caused by extensive inflammatory disease but also from bacterial overgrowth as a result of coloenteric fistulas, blind loops or stasis from chronic obstruction. With an aggressive approach to assessment and treatment, these should occur infrequently. If there is extensive small-bowel disease, there may be poor absorption of fat-soluble vitamins leading to symptoms and signs of osteomalacia (vitamin D) or a bleeding tendency (vitamin K). These are all rare. Other deficiencies are also uncommon and usually result from inadequate intake rather than increased losses. They may include deficiencies of magnesium, zinc, ascorbic acid and the B vitamins. Anaemia, however, is common and results from iron deficiency because of impaired iron utilisation or intestinal blood loss and, less commonly, from vitamin B 12 or folate deficiency. Any fever, particularly if high and spiking, or associated with rigors, should prompt careful consideration of suppurative intra-abdominal complication being present.
Gastrointestinal symptoms
Clinical presentation varies depending on the site of disease. Initial presentation as an emergency is uncommon, but ileal disease can mimic acute appendicitis and colonic disease may present as a fulminating colitis.
Abdominal pain occurs because of inflammatory disease, obstructing or sub-acutely obstructing lesions. Terminal ileal disease is the most common site for obstructive lesions.
Diarrhoea results most frequently from mucosal inflammation but can also be caused by bile salt malabsorption from terminal ileal disease or resection, fistulation between loops of bowel, short bowel from previous resections or bacterial overgrowth from obstructed segments. Bile salts and vitamin B12 are absorbed from the terminal ileum. Resection of the terminal ileum – or sometimes severe disease at that site – can cause malabsorption of these. Bile salt malabsorption disrupts their enterohepatic circulation and results in a cathartic effect as the bile salts reach the colon causing diarrhoea. This is treated by bile-salt chelating agents such as cholestyramine or colesevelam. B12 replacement injections are usually advised after terminal ileal resection.
Distal colitis and proctitis, and decreased rectal compliance, produce tenesmus and frequent bowel motions. Rectal bleeding may occur in 50% of patients with colonic involvement.
Symptoms can also be those of complications – described in the Montreal classification: stricturing or perforating disease (leading to local abscess formation, internal fistula and fistulae to the skin) ( Fig. 11.1 ).
Perianal disease
Perianal disease varies from an asymptomatic fissure or inflamed skin tags, individual fistulas to severe disease with erythema, large fleshy skin tags, deep chronic fissures with bridges of skin and multiple fistulas creating the so-called ‘watering-can perineum’. Fibrosis from chronic inflammation may produce a woody, stiff anal canal or anal/rectal stenosis. The impact of perianal disease is underestimated by clinicians and may be underreported by patients. It can present before intestinal disease is apparent.
Perianal abscesses will present with local pain and swelling – with a discharge if this spontaneously leaks, particularly if there is associated fistulating disease. Perianal fistula can be complex and asymmetrically distributed when compared to idiopathic fistulas. Fistulating disease may cause local discomfort and discharge, which can by mucopurulent, bloody or faeculent. Significant perianal pain suggests undrained sepsis. Fistulas extending to the bladder can produce pneumaturia and recurrent urinary tract infection while those extending to the vagina may cause flatus or faeces vaginally. Fissures may be painful but can be large, indolent and painless.
Gastrointestinal complications
Stricturing disease
Chronic fibrosis results in stricturing disease – causing luminal narrowing and clinical features of obstruction. Acute inflammatory change can also contribute to the narrowing. Patients can present with complete obstruction or with milder and self-limiting episodes of sub-acute obstruction. These usually occur in patients known to have Crohn’s but rarely can be the initial presenting feature. Differential diagnosis includes adhesions from previous surgery as well as other causes of obstruction, including strictures due to non-steroidal anti-inflammatory drugs.
Perforating disease
Transmural inflammation can result in perforation with local abscess formation. Fistulation to a range of other adjacent structures may occur, for example to:
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other loops of adjacent small or large bowel: (enteroenteric, enterocolic fistulas) presenting with diarrhoea relating to reduced transit time and bacterial overgrowth
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bladder (enterovesical or colovesical) – presenting with recurrent urine infection or sterile pyuria
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skin (enterocutaneous)
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vagina (entero-, colo- or rectovaginal fistulas) – presenting with passing gas or faeces per vaginam.
Free perforation with generalised peritonitis can occur but is rare.
Colon cancer
In Crohn’s colitis, there is an increased risk of colorectal cancer similar to ulcerative colitis, with similar risk factors: duration of disease and extensive disease. Field change in the colonic mucosa with areas of dysplasia is observed, as in ulcerative colitis. Compared to the general population, the relative risk of adenocarcinoma of the colon complicating Crohn’s colitis is 1.4 to 1.9 and the relative risk of small-bowel carcinoma, 21 to 27. Surveillance colonoscopy should be offered, and this is probably best done with dye spray and targeted biopsies. Particular care is needed in the presence of colonic strictures, which should always be regarded as malignant until proven otherwise; this may entail a resection to make the diagnosis.
Haemorrhage
Massive bleeding occurs in 1–2%.
Extra-intestinal manifestations
These are outlined in Box 11.1 and are more common in association with Crohn’s colitis than isolated small-bowel disease. Manifestations are similar to those that occur in ulcerative colitis, and may precede, be independent of or accompany active IBD, and can cause significant morbidity. They may be experienced by up to 50% of patients and are life-long in 25–30%.
Box 11.1
Extra-intestinal manifestations of Crohn’s disease
Related to disease activity
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Aphthous ulceration (10%)
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Erythema nodosum (5–10%)
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Pyoderma gangrenosum (0.5%)
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Acute arthropathy (6–12%)
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Eye complications (conjunctivitis, etc.) (3–10%)
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Amyloidosis (1%)
Unrelated to disease activity
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Sacroiliitis (often minimal symptoms) (10–15%)
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Ankylosing spondylitis (1–2%)
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Arthritis
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Primary sclerosing cholangitis (rare)
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Chronic active hepatitis (2–3%)
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Cirrhosis (2–3%)
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Gallstones (15–30%)
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Renal calculi (5–10%)
Steatorrhoea may promote increased absorption of oxalate and increase the incidence of oxalate renal stones – though this is usually only after extensive small-bowel resection.
Primary sclerosing cholangitis may be associated with colonic disease. Patients may develop a fatty liver as a result of malnutrition or from receiving total parenteral nutrition. Mild abnormalities of liver function are common with active disease, and do not necessarily indicate significant liver disease.
Thromboembolic complications are an important association of IBD and an important source of morbidity. These are predominantly venous but can be arterial. They can be associated with active disease but there is an increased risk even without active disease. Common sites are the lower extremities and pelvic veins, and pulmonary emboli but cerebrovascular accidents have also been reported.
The increased risk of thromboembolic complications is clinically important, particularly for any hospital admission or after surgery, where extended prophylaxis should be standard. ,
Skin manifestations include erythema nodosum and pyoderma gangrenosum. Appearances are usually typical, but sometimes skin biopsy is needed to confirm the diagnosis. Metastatic Crohn’s disease is an unusual complication in which nodular ulcerating skin lesions occur at distant sites including the vulva, sub-mammary areas and extremities, and sometimes peristomal. Biopsies show non-caseating granulomas. Clubbing is seen in some cases of extensive small-bowel disease.
Amyloidosis is reported in 25% of patients with Crohn’s disease at post-mortem but only 1% have clinical manifestations. It can occur in the bowel or within other organs, including the liver, spleen and kidneys. If renal function is affected, resection of the diseased bowel may result in regression of amyloid and improvement of renal function.
Physical signs
Patients may appear well and have a normal physical examination. With more severe disease there may be evidence of weight loss, anaemia, iron deficiency, clubbing, cachexia, proximal myopathy, easy bruising, elevated temperature, tachycardia and peripheral oedema. Signs of extra-intestinal manifestations may be present.
Abdominal examination can be normal but tenderness in the right iliac fossa is common. An abdominal mass may be palpable because of thickened loops of matted bowel or if an abscess is present. A psoas abscess may cause fixed hip flexion (or pain on stepping down). Occasionally, there is general peritonitis. Enterocutaneous fistulas may be evident and may present through a scar.
Paediatric age group
In children and adolescents, the gastrointestinal manifestations are similar but extra-intestinal and systemic manifestations become more important. About 15% have arthralgia and arthritis that often precedes bowel symptoms by months or years. Diagnosis may be delayed by a non-specific presentation with systemic symptoms of weight loss, growth failure, unexplained anaemia and fever. If active disease is dealt with promptly by medical or surgical treatment and adequate nutrition is maintained, retardation of growth and sexual development can usually be reversed.
Pregnancy
The disease frequently affects young adults and therefore may require management during or before pregnancy. Reduced fertility may have a number of contributing factors including reduced libido, dyspareunia and psychological morbidity. The risk of adverse outcomes in pregnancy is related to disease activity. In the absence of active disease, the outcome of pregnancy is the same as that of matched controls. With active disease at conception, there is an increase in spontaneous abortions and premature delivery, and a greater than 50% chance of relapsing disease during pregnancy. The risk of relapse is only 20–25% if disease is inactive at conception. It is therefore advisable to avoid conception during an acute flare-up. Pregnancy does not affect the long-term course of the disease.
Drug treatment during pregnancy should be discussed –taking into consideration the importance of ensuring optimum disease control. Steroids can be used if necessary. Thiopurines are normally continued during pregnancy as withdrawal may be associated with an increased risk of flare. Biological agents can be continued throughout pregnancy, but the risks and benefits need to be discussed. Withdrawal may carry a risk of poor disease control and therefore adverse pregnancy outcomes. They cross the placenta to the foetus in the third trimester, which therefore carries a risk of immunosuppression in the neonate. Live vaccines must be avoided. Detectable levels of biological drugs may still occur at 9 months. For those with inactive disease who wish to discontinue treatment, it may be reasonable to stop at the start of the third trimester. The use of methotrexate is contraindicated.
Investigations
Laboratory
Common laboratory findings include raised acute phase proteins (especially C-reactive protein [CRP]) a raised platelet count and anaemia. Mild episodic elevations of liver function tests are common but persistent abnormalities require further investigation. A neutrophil leucocytosis may indicate infection. CRP is used to monitor disease activity but does not necessarily correlate with endoscopic activity and in some patients with active disease is found to be normal. Erythrocyte sedimentation rate is useful in Crohn’s colitis but less so in small-bowel disease.
Serum albumin is often low in active disease because of downregulation of albumin synthesis by cytokines (IL-1, IL-6, TNF).
Anti-microbial antibodies particularly anti- Saccharomyces cervisiae antibodies (ASCAs) may be raised and if high titres, may suggest a more aggressive phenotype. However, the sensitivity and specificity of such markers are too low for diagnostic purposes.
Stool biomarkers including faecal calprotectin are surrogate markers for intestinal inflammation and are being increasingly used as screening tests to differentiate inflammatory bowel syndrome (IBS) from IBD in primary care, monitoring disease activity and response to treatment and predicting post-operative relapse.
Magnesium, zinc and selenium levels may be low.
Endoscopy
Ileocolonoscopy is the first-line investigation for suspected Crohn’s disease, particularly as it allows biopsies to support diagnosis. It provides a macroscopic view that can be recorded, enables assessment and biopsy of strictures, and can clarify the situation where significant symptoms are not backed up by clinical evidence of disease. Intubation of the ileocaecal valve allows examination and biopsy of the terminal ileum. It may not always be possible and in about 20% of cases there is isolated proximal small-bowel disease beyond the reach of the colonoscope. Endoscopic appearances are typically discontinuous and include small (<5 mm) aphthous ulcers, larger ulcers, which may be deep and linear fissuring ulcers, which may give a cobblestone appearance. Erythema and loss of vascular pattern may also occur as in ulcerative colitis but differs in usually being discontinuous.
Use of endoscopic scoring systems is essential in randomised clinical trials but could be used in clinical practice to support more consistent reporting. The simplified endoscopic score for Crohn’s disease (SES-CD) evaluates ulceration, extent of inflammation and stenosis in five colonic segments. The Rutgeerts score evaluates the extent of ulceration in the neoterminal ileum has proved useful in practice as more severe ulceration predicts clinical recurrence.
Multiple biopsies should be taken even if the mucosa appears normal, as granulomas may be present that can confirm the diagnosis. There is not usually a role for routine follow-up endoscopy (except after surgery) and endoscopic findings correlate poorly with clinical remission. There is a cancer risk in long-standing Crohn’s colitis and the same colonoscopic surveillance as for extensive ulcerative colitis is required.
Endoscopy of the upper gastrointestinal tract is indicated only if symptoms suggest upper gastrointestinal involvement from symptoms or imaging. Findings may include rugal hypertrophy, deep longitudinal ulcers and a cobblestone mucosa. Biopsies should be taken but granulomas are often absent.
Small-bowel endoscopy is now possible through video capsule endoscopy or double-balloon assisted enteroscopy. The latter can be undertaken per anum or per orally. It is more invasive and uncomfortable requiring deep sedation or general anaesthetic and with risks that include perforation and pancreatitis but does allow tissue biopsy. Capsule endoscopy is sensitive but does not allow biopsy. Capsule retention may occur if the procedure is undertaken in the presence of a stricture – which may then need surgical retrieval. If there is any significant concern that this may happen, a dummy dissolvable capsule should be used first, to assess luminal patency.
Radiology
Radiological imaging allows non-invasive assessment of:
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disease activity
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site of disease
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extent of disease
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complications.
Luminal barium fluoroscopic imaging was traditionally the mainstay of radiological investigation but has largely been replaced by cross-sectional imaging (magnetic resonance enterography [MRE] and computerised tomography [CT]). These techniques provide additional transmural information about inflammation or fibrosis and about extra-mural complications. Choice of modality depends on the clinical question, the clinical setting, local expertise and radiation exposure.
Magnetic resonance
MRE is more frequently chosen in the elective, outpatient setting. It is free of ionising radiation and not limited by poor renal function. It helps define whether changes are acute inflammatory or chronic fibrotic. It also identifies extra-luminal complications. Strictures can be identified ( Fig. 11.2 ) aided by dynamic imaging to differentiate fixed narrowing from contractions. Abdominal abscesses can also be identified.
MR imaging (MRI) is also the investigation of choice for complicated perianal sepsis.
Computerised tomography scanning
CT scanning is often undertaken in the emergency setting. It is frequently used to investigate acute abdominal pain when the diagnosis of Crohn’s is suggested by thickened small-bowel loops, especially in the terminal ileum ( Fig. 11.3 ). CT will also demonstrate intra-abdominal abscesses and dilatation in those presenting with obstructive features. Cumulative radiation exposure is an important consideration for people with Crohn’s disease who need repeated imaging over many years. If CT enterography is used, a low-dose protocol should be considered.
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