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Crohn’s disease

Crohn’s disease is a chronic inflammatory disease that mainly affects 
the gastrointestinal tract. It is characterized by transmural inflammation
 ( extending through all layers ) , deep ulceration and fissuring of the mucosa 
and the presence of granulomas .

It may involve any or all parts of the entire GI tract from mouth to 
peri-anal area ( although seen usually in terminal ileum and perianal locations ) interspersed with areas of relatively normal tissue

Rising incidence and prevalence globally Currently no cure for IBD Affects about 1 in 300 people in the Western World At-least 115,000 people in UK with Crohn’s disease ( NICE 2012 ) Can occur at any age but most commonly presents in adolescence and early adulthood 20-30 % cases present in people < 20 yrs Median age of diagnosis is 30 yrs Occurs with equal rate in men and women Rising incidence and prevalence globally A Lancet report mentions that the prevalence of IBD has increased substantially in many regions from 1990-2017 ( Jairath et al 2017 ) CD is more common in the industrialized world ( N America and Western Europe ) At-least 115,000 people in UK with Crohn’s disease ( NICE 2012 ) About 70,000 cases / year – of IBD are diagnosed in the US and it is estimated that about 1.3 % the US population has IBD Median age of diagnosis is 30 yrs- has two peaks the 1st is between age of 20-30 followed by a smaller peak around 50 years Occurs with equal rate in men and women

Thought to be an immune mediated condition caused by environmental triggering 
events in genetically susceptible people. Chronic inflammation from T-cell activation
 leading to tissue injury is implicated in the pathogenesis Aetiology remains unclear and is widely debated. Possible factors include

risk factors-White ancestry Family history Smoking Infectious gastroenteritis Appendectomy Drugs eg COCP , NSAIDs Not breastfed alteration in gut microbiome or disruption in intestinal mucosa cigarette smoking- smokers have 2 fold increased risk ( confers a protective role for UC ) Vitamin D deficiency Antibiotics and NSAIDs increases risk Use of hormonal preparations- both OCP and HRT Enteric infections for e.g Clostridium difficile , Salmonella and Campylobacter Pre-illness stress , depression or anxiety Diet association not clear but possible association with intake of fiber , fruits and vegetable

When to suspect- Most patients diagnosed in their teens and twenties Consider if
○ unexplained wt loss
○ anaemia
○ family h/o IBD
○ extra-intestinal manifestations

Atleast 50 % patients experience atleast one EIM before diagnosis
 In children –> diarrhoea may not be present in up to 44 % of children with IBD
○ delayed growth and development
 Faecal calprotectin can help differentiate between IBD and irritable bowel syndrome

Presentation- Symptoms can be heterogeneous 

○ diarrhoea ( including nocturnal diarrhoea ) of more than 6 weeks. Caused by
- bacterial overgrowth in obstructed areas
- fistulization
- bile acid malabsorption
- intestinal inflammation with ↓↓ water absorption and ↑↑ secretion of electrolytes Systemic symptoms like malaise , anorexia or fever are common Bowel obstruction due to
acute inflammatory oedema and spasm of the bowel or chronic scarring and stricture Acute terminal ileal CD may be mistaken for acute appendicitis
○ pain often in RLQ ( most common site terminal ileum → ileocolitis ) Abdominal pain and weight loss are seen in about 70 % and 60 % Blood and / or mucus in stool Oral lesions ( apthous ulcers ) Weight loss , faltering growth or delayed puberty in children
 Patients may present with extraintestinal manifestations of CD before intestinal presentations become prominent
 Malabsorption and steatorrhoea

Symptoms can be heterogeneous – based on disease phenotype and location Presenting symptoms may include
○ persistent diarrhoea ( can include mucus and blood )
○ abdominal pain ( rt lower quadrant )
pain is typically crampy or colicky in nature ( as with most forms of bowel inflammation )
○ flatulence / bloating / vomiting
○ loss of appetite , weight loss and fever Chronic diarrhoea is the most common presenting symptom Presentation may also be with
○ bowel obstruction ( stricturing disease )
○ acute peritonitis
○ fistula or abscess- important to ask about genitourinary symptoms as fistula formation can lead to blood or faecal matter in the urine as well as urinary tract infections Extra intestinal manifestations- about a 3rd of patients and may include
○ peripheral arthritis
○ aphthous stomatitis
○ uveitis
○ erythema nodosum and pyoderma gangrenosum
○ ankylosing spondylitis

FBC – look for anaemia , raised platelet count , leukocytosis Inflammatory markers – CRP and ESR Urea and Electrolytes LFTs including albumin Iron studies -Ferritin , serum iron , TIBG Serum Vit B12 , Folate and Vitamin D Magnesium , Phosphate Coeliac screen Stool microscopy and culture including C Diff and
Y enterocolitica Faecal calprotectin Plain abdominal radiograph – still essential if intestinal obstruction suspected
as in UC it helps to estimate the extent & severity of Crohn’s colitis
 
 CT , MRI , US , Barium contrast studies Endoscopic visualization and biopsy Colonoscopy , ileocolonoscopy Small bowel enteroscopy Interventional radiology

Ulcerative colitis Infective colitis Pseudomembranous colitis Macroscopic colitis Intestinal ischaemia Acute appendicitis Diverticulitis Coeliac disease Irritable bowel syndrome Anal fissure Malignancy eg
colorectal cancer
small bowel cancer
lymphoma Endometriosis Laxative abuse

Complications- Psychological Abscesses Intestinal strictures Fistulas Anaemia Malnutrition Colorectal and small bowel cancer

5-Aminosalicylic acid derivative agents Corticosteroids Immunosuppressive agents Monoclonal antibodies Antibiotics Antidiarrhoeal agents Bile acid sequestrants Anticholinergic agents

Check BP , respiratory rate and heart rate , temp R/O any enterocutaneous fistula Examine the abdomen
○ auscultate the abdomen
○ percussion
○ palpation for focal tenderness Rectal examination Extra-intestinal manifestations

The aim of examination would be to

○ identify any complications
○ r/o common differentials particularly appendicitis
○ r/o a presentation which needs immediate medical / surgical attention

 

Acute Appendicitis Ulcerative colitis Infective colitis Pseudomembranous colitis Macroscopic colitis Intestinal ischaemia Diverticulitis Coeliac disease Irritable bowel syndrome Anal fissure Bechet disease Malignancy eg
colorectal cancer
small bowel cancer
lymphoma Endometriosis Laxative abuse

 

Reduced QoL Psychological Abscesses Intestinal strictures Intestinal obstruction Fistulas Anaemia Malnutrition Colorectal and small bowel cancer- patients are at increased risk and need ongoing surveillance

Diagnosis is clinical Diagnosis is established by
○ history
○ endoscopy / capsule endoscopy
○ histopathology
○ appropriate radiology like computed tomography enterography and magnetic resonance enterography Various factors can make the process of diagnosing CD difficult as
○ presenting symptoms can be insidious & non-specific
○ disease is often present for months or even years before the symptoms manifest

Mild disease –This is generally treated using oral mesalazine , immunomodulators as thiopurines
 ( mercaptopurines , azathioprine , methotrexate and steroids )

Moderate to severe disease –Treatment options here include using a combination of immunomodulators and biologics as infliximab , adalimumab , golimumab , vedolizumab or biologics alone

 

Treatment of CD is complex and evolving Aim of medical therapy is to maintain remission without the need for surgery Tools to deliver appropriate evidence based care for primary care clinicians are lacking although it is thought that a large proportion of people with IBD are managed in primary care Aim of management is to achieve sustained disease remission with the least toxic therapy to avoid complications Mesalazine appears little better than placebo for mild to moderate CD- works possibly by anti-inflammatory action Sulfasalazine is a mesalazine derivative which is used to induce remission in active disease , particularly in those with colonic vinvolvement Corticosteroids can induce remission but do not prevent relapse Immunomodulators help to maintain remission and are increasingly considered sooner rather than later In CD cytokine tumour necrosis factor ( TNF alpha ) mediates inflammation and the therapeutic antibodies infliximab and adalimumab block its action Surgery is used for treatment of complications as bowel obstruction , abscess , fistulas or bowel perforation Surgery is not curative. Relapse following surgery is common but most patients ( 70 to 80 % ) with CD will require surgical intervention during their lifetime. Patients still need therapy even after surgery for disease recurrence NSAIDs may exacerbate disease ( avoid ) Mild diarrhoea can be managed with anti-diarrheals

 

Prognosis can be influenced by factors which indicate aggressive disease activity 
 Early age of onset ( < 30 yrs ) Extensive anatomical involvement Perianal disease deep ulcers prior surgery stricturing and or penetrating disease

References

  1. BMJ Best Practice Crohn’s disease
  2. NICE guideline Crohns disease October 2012
  3. CKS NHS Crohn’s disease in September 2017
  4. The second European evidence-based consensus on the diagnosis and management of Crohn’s disease: Definition and diagnosis European Crohn’s and Colitis Organisation September 2012
  5. Clinical Evidence Handbook Crohn Disease
  6. AAFP org Management of Crohn’s Disease in Adults Practice Guidelines The American Journal of Gastroenterology Vol 96 , No 3 , 2001
  7. Crohn’s Disease Medscape Leyla J Ghazi , MD et al Jan 2017
  8. American Gastroenterological Association Institute Technical Review on the Management of Crohn’s Disease After Surgical Resection Gastroenterology 2017 ;152:277-295
  9. Point-of-care and home faecal calprotectin tests for monitoring treatment response in inflammatory bowel disease NICE December 2017
  10. Clinical Review Management of Crohn’s Disease BMJ 1999 ; 319 : 1480
  11. NICE Pathways Crohn’s Disease
  12. Ha, Francis, and Hanan Khalil. “Crohn’s disease: a clinical update.” Therapeutic advances in gastroenterology vol. 8,6 (2015): 352-9. doi:10.1177/1756283X15592585 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4622286/
  13. Genetics Home Reference Crohn disease https://ghr.nlm.nih.gov/condition/crohn-disease#diagnosis
  14. Liu, Jimmy Z, and Carl A Anderson. “Genetic studies of Crohn’s disease: past, present and future.” Best practice & research. Clinical gastroenterology vol. 28,3 (2014): 373-86. doi:10.1016/j.bpg.2014.04.009
  15. Ranasinghe IR, Hsu R. Crohn Disease. [Updated 2019 Dec 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK436021/
  16. Cummings, J R Fraser et al. “Medical management of Crohn’s disease.” BMJ (Clinical research ed.) vol. 336,7652 (2008): 1062-6. doi:10.1136/bmj.39547.603218.AE https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2376027/
  17. Bennett, Alice L et al. “Tools for primary care management of inflammatory bowel disease: do they exist?.” World journal of gastroenterology vol. 21,15 (2015): 4457-65. doi:10.3748/wjg.v21.i15.4457
  18. Mazal, Jonathan. (2014). Crohn disease: Pathophysiology, diagnosis, and treatment. Radiologic technology. 85. 297-316.
  19. Feuerstein JD, Cheifetz AS. Crohn Disease: Epidemiology, Diagnosis, and Management. Mayo Clin Proc. 2017;92(7):1088‐1103. doi:10.1016/j.mayocp.2017.04.010
  20. Environmental Risk Factors for Inflammatory Bowel Disease Ashwin N. Ananthakrishnan, MD, MPHGastroenterology & Hepatology June 2013, Volume 9, Issue 6

     

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