Intestinal thickening, also known as bowel wall thickening, is a finding on abdominal imaging tests, such as computed tomography (CT) scans or ultrasound. It is not a diagnosis itself but a sign that the layers of the intestinal wall are swelling, inflamed, or physically infiltrated. The normal small bowel wall should not exceed about three millimeters when distended, and the colon wall is typically five millimeters or less. The causes of thickening are generally categorized based on whether they result from chronic inflammation, acute infection, restricted blood flow, or physical infiltration by abnormal tissue.
Chronic Inflammatory Bowel Diseases
The most recognized chronic causes of intestinal wall thickening are the inflammatory bowel diseases (IBD), which include Crohn’s disease and ulcerative colitis. These conditions involve a misguided, long-term immune response that targets the digestive tract, leading to persistent inflammation. Over time, this chronic inflammation causes irreversible changes within the bowel structure, notably involving the buildup of scar tissue and the enlargement of muscle layers.
Crohn’s disease is characterized by inflammation that extends through the entire thickness of the bowel wall, a feature known as transmural inflammation. This deep involvement can affect any part of the gastrointestinal tract, but it most commonly targets the end of the small intestine, the ileum, and the beginning of the colon. The full-thickness inflammation results in severe thickening, which often leads to the formation of strictures, or narrowed segments, that can obstruct the passage of digestive contents. Crohn’s disease is also known for producing discontinuous involvement, where affected segments are interspersed with areas of healthy tissue, referred to as skip lesions.
Ulcerative colitis (UC), by contrast, is primarily confined to the large intestine and typically only affects the innermost layer, the mucosa. The inflammation usually begins in the rectum and spreads continuously backward through the colon. Although UC does not cause the same full-thickness damage as Crohn’s, chronic, severe cases can still result in thickening. This thickening is mostly due to inflammation and fluid accumulation (edema) in the submucosa, along with a compensatory overgrowth or hypertrophy of the muscle layer.
The structural differences in thickening help distinguish between Crohn’s disease and UC. The thickening seen in Crohn’s disease is typically deep, asymmetric, and segmental, often accompanied by surrounding fat inflammation. Conversely, UC thickening is generally more symmetrical and diffuse, affecting a continuous segment of the colon with inflammation largely restricted to the inner lining.
Acute Inflammatory and Infectious Causes
Many causes of intestinal thickening are acute and transient, resolving once the trigger is removed. Rapid-onset thickening frequently results from an infection causing acute inflammation and a sudden buildup of fluid within the bowel wall. This fluid accumulation, or edema, within the submucosal layer is the primary source of the increased thickness seen on imaging.
Common culprits include bacteria like Clostridium difficile, Salmonella, or E. coli, which cause rapid inflammation in the small or large intestine. Once the infection is treated or the body’s immune system clears the pathogen, the inflammation and associated edema subside. This process allows the bowel wall to return to its normal thickness.
Acute, localized inflammation of adjacent organs can also cause secondary, temporary thickening in the nearby bowel segment. For example, appendicitis may cause the adjacent terminal ileum or cecum to thicken. Similarly, diverticulitis, involving the inflammation of small pouches in the colon wall, leads to focal thickening of the affected colonic segment.
Thickening Caused by Blood Flow Restriction
Bowel wall thickening can also result from a lack of adequate blood flow, a condition known as ischemia. When the blood supply to a segment of the intestine is significantly restricted, the tissue is deprived of oxygen and nutrients, leading to damage and subsequent inflammation. This process forms the foundation of ischemic colitis or enteritis.
Ischemic colitis, the more common form, occurs when blood flow to the large intestine is temporarily reduced, often due to nonocclusive factors like a sudden drop in systemic blood pressure from shock or severe dehydration. The resulting oxygen deprivation causes injury to the inner lining, leading to inflammation and edema in the affected area. This damage manifests as segmental thickening of the bowel wall, often accompanied by a characteristic pattern of fluid accumulation in the submucosa.
This type of thickening is typically segmental, meaning it only affects the portion of the bowel that suffered the vascular compromise. The thickening seen on imaging is primarily due to the intense inflammatory response and submucosal edema that follow the initial ischemic event.
Thickening Due to Neoplasms and Systemic Conditions
Malignant neoplasms, such as primary colorectal carcinoma or lymphoma, cause bowel wall thickening by directly invading and replacing normal tissue. This form of thickening tends to be focal, meaning it is limited to a small area. It is often irregular or asymmetric in appearance.
Secondary cancers that have spread from other organs, such as melanoma or lung cancer, can also metastasize to the bowel wall, creating focal areas of thickening. These features distinguish physical infiltration from the more uniform swelling seen in inflammatory conditions.
Systemic diseases can also cause thickening by affecting the body’s fluid balance or circulation. Conditions like severe heart failure or cirrhosis cause widespread fluid retention and low levels of protein in the blood. This imbalance leads to fluid leakage and edema throughout the body, including the intestinal wall, causing diffuse, symmetric thickening. Similarly, rare infiltrative diseases like amyloidosis cause the deposition of abnormal proteins within the bowel wall layers, leading to structural thickening.