Crohn’s Disease is a chronic inflammatory disease of unknown etiology. It affects the wall of the gastrointestinal tract. The single strongest risk factor for its development is a family history of the disease. The underlying cause could be an autoimmune reaction.
The disease is often insidious, slowly progressing with a protracted course, commonly affecting young adults in the second or third decade of life. Intermittent lower abdominal colic, diarrhea and weight loss are the presenting symptoms. Anal fissures are also commonly seen. Many cases of fistulas are also reported.
Crohn’s Disease is categorized into two major types:
- Inflammatory bowel disease
- Ulcerative colitis
Crohn’s Disease can affect any part of the gastrointestinal tract from the mouth to the anus. It also affects the skin, joints, eyes, liver, kidneys and pancreas. Some 30-40% of patients suffering from Crohn’s Disease have small intestinal affections. 15-25% of patients have large intestine affections. In 75% of the patients with small intestinal disease, the terminal ileum (last part of the small intestine) is involved.
In 90% of the patients, Crohn’s Disease affects in a segmental pattern, i.e. some areas of the intestines are normal while some are diseased. Perirectal fistulas, fissures, abscesses and anal stenosis (narrowing) are present in 1/3 of patients with Crohn’s Disease, particularly those with large intestine involvement.
Causes of Crohn’s Disease
The peak age of the onset of this disease is between 15 and 30 years. A second peak occurs between the age of 60 and 80 years.
Smoking is associated with a two-fold increased risk of this disease.
Oral contraceptives are also linked to Crohn’s Disease – the relative risk of this disease for oral contraceptive users is about 1.9 times that of normal individuals.
Genetic factors may play a role in Crohn’s Disease. In normal individuals, the immune system in the inner layer of the gastrointestinal tract is inhibited to lumenal contents. In Crohn’s disease, this tightly regulated state of suppression of inflammation (a protective tissue response to injury or destruction of tissues) is altered, leading to uncontrolled inflammation. In Crohn’s Disease, activated CD4+Tcells (cells of the immune system) in the inner layer of the intestine and blood secrete inflammatory cytokines (constituents of the immune system), which lead to inflammatory cascade and the flare up of the disease.
A role of the measles virus or paramyxoviruses in the development of this disease has also been suggested.
Psychosocial factors can contribute to the clinical exacerbation of symptoms. Major life events such as illness or death in the family, divorce or separation, interpersonal conflicts, or some other major loss are associated with an increase in symptoms such as pain, bowel dysfunction and bleeding.
Acute stress can exacerbate bowel symptoms, even after the major life events are under control.
Symptoms of Crohn’s disease
Patients may have chronic history of recurrent episodes of right lower abdominal pain and diarrhea. Pain is usually colicky (spasm like); it precedes and is relieved by passing stools. Diarrhea is characteristic of active disease.
Patients may have nausea and vomiting.
Low grade fever is usually noted. High grade fever suggests abscess (pus) formation inside the abdomen.
Weight loss is common and develops as a consequence of diarrhea, anorexia (loss of appetite for food), and fear of eating.
A mass may be felt in the right lower side of the abdomen.
As the disease progresses, diarrhea decreases, and it eventually leads to chronic obstruction of the intestines and intractable constipation.
There may be malabsorption and steatorrhea (stools containing excess fat).
Intestines do not absorb nutrients and proteins well, hence leading to nutritional deficiencies.
Patients may have backbone fractures due to vitamin D deficiency and decreased calcium uptake.
Patients may have anemia (decreased amount of hemoglobin in blood) due to vitamin B12 deficiency.
Patients may develop narrowing of the large intestine lumen, leading to symptoms of bowel obstruction.
Patients may develop incontinence of stools (involuntary passing of stools), large hemorrhoids (piles), anal strictures (narrowing of the anus), anorectal fistula and perirectal abscess.
Diagnosis of Crohn’s disease
Diagnosis is made on the basis of symptoms given by the patient, clinical examination done by the physician and laboratory, and endoscopic and radiographic findings.
Blood tests reveal increased ESR (Erythrocyte Sedimentation Rate) and increased C- reactive protein. In severe cases, patients have hypoalbuminaemia [decreased albumin (protein) in blood], anemia and leucocytosis (increase in white blood cells).
Endoscopic findings of Crohn’s Disease include rectal sparing, aphthous ulceration, fistulas and skin lesions. Endoscopic appearance correlates poorly with clinical remission of the disease, thus, repeated endoscopies are not used to monitor the inflammation.
Early radiographic findings of the small intestine include thickened folds and aphthous ulceration. The segmental nature of this disease results in wide gaps of normal or dilated bowel between involved segments.
CT scan findings include mural thickening > 2 cm, homogenous wall density, mesenteric fat stranding, perianal disease and adenopathy.
MRI (Magnetic Resonance Imaging) may prove superior for demonstrating pelvic lesions such as ischiorectal abscesses.
Complications Associated with Crohn’s Disease
- Perforation of the intestine is seen in 1 to 2% of patients
- Peritonitis (inflammation of the inner layer of the abdomen)
- Intra-abdominal abscess
- Fistula formation
- Intestinal obstruction is seen in 40% of patients
- Massive hemorrhage
- Mal absorption
- Severe perianal disease
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