Correlation between the macroscopic severity of Crohn’s disease in resected intestine and bowel wall thickness evaluated by water-immersion ultrasonography

Abstract

Objectives: Transabdominal ultrasonography is a common and accurate tool for managing Crohn’s disease (CD); however, the significance of the resulting data is poorly understood. This study was performed to determine the association between bowel wall thickness evaluated by water-immersion ultrasonography and macroscopic severity, namely, refractory inflammation and subsequent fibrosis in CD surgical specimens.

Materials and methods: We retrospectively evaluated 100 segments of colon and small intestine from 27 patients with CD. The resected specimens were placed in saline postoperatively, and bowel wall thickness was measured by water-immersion ultrasonography and compared with macroscopic findings. Correlations between bowel wall thickness and macroscopic findings were assessed using analysis of variance and receiver operating characteristic curves.

Results: According to the progression of macroscopic severity, the mean bowel wall thickness was increased as follows: macroscopically intact: 4.1 mm, longitudinal ulcer scars: 5.4 mm, longitudinal open ulcers: 6.0 mm, large ulcers: 6.4 mm, cobblestone-like lesions: 7.1 mm, and fibrotic strictures: 7.4 mm. For all lesions except longitudinal ulcer scars, the bowel wall thickness was significantly thicker than that of macroscopically-intact areas (p < .001). According to receiver operating characteristic curves, bowel wall thickness >4.5 mm was associated with CD lesions, and thickness >5.5 mm was associated with more severe lesions.

Conclusions: The bowel wall thickness of CD lesions was evaluated by water-immersion ultrasonography correlated with macroscopic disease severity.

Keywords:

• Crohn’s disease
• transabdominal ultrasonography
• bowel wall thickness
• surgical specimen
• macroscopic findings
• water-immersion ultrasonography

Acknowledgment

The authors thank Dr Masanori Tanaka (Department of Pathology and Laboratory Medicine, Hirosaki City Hospital, Aomori, Japan) for advice regarding the pathology and Jane Charbonneau, DVM, from Edanz Group (www.edanzediting.com/ac), for editing a draft of this manuscript.

Disclosure statement

R. K. received personal fees and grants, scholarships, and funded research/collaborative research from Abbott Japan Co., Ltd.; AbbVie GK; AJINOMOTO Co., Inc.; Asahi Kasei Medical Co., Ltd.; Astrazeneca Co., Ltd.; Astellas Pharm Inc.; EA Pharma Co., Ltd.; Eisai Co., Ltd.; Janssen Pharmaceutical K.K.; JIMRO Co., Ltd.; Kissei Pharmaceutical Co., Ltd.; Kyorin Pharmaceutical Co., Ltd.; Kyowa Hakko Kirin Co., Ltd.; Otsuka Pharmaceutical Co., Ltd.; Nippon Kayaku Co., Ltd.; Mitsubishi Tanabe Pharma Corporation; Takeda Pharma Co., Ltd.; and Zeria Pharmaceutical Co., Ltd. H. K. received personal fees and grants, scholarships, and funded research/collaborative research from AbbVie GK; Astellas Pharma Inc.; EA Pharma Co., Ltd.; Janssen Pharmaceutical K.K.; JIMRO Co., Ltd.; Kissei Pharmaceutical Co., Ltd.; Kyorin Pharmaceutical Co., Ltd.; Kyowa Hakko Kirin Co., Ltd.; Medical View Co., Ltd.; Mitsubishi Tanabe Pharma Corporation; Mochida Pharmaceutical Co., Ltd.; Shire Japan K.K.; and Zeria Pharmaceutical Co., Ltd. S. M. received personal fees and grants, scholarships, and funded research/collaborative research from Grant-in-Aid for Scientific Research; Merck Serono Co., Ltd.; Zeria Pharmaceutical Co., Ltd.; Kissei Pharmaceutical Co., Ltd.; Chugai Pharmaceutical Co., Ltd.; Pfizer Inc.; Bristol-Myers Squibb K.K.; Astellas Pharma Inc.; Daiichi-Sankyo Co., Ltd.; Takeda Pharma Co., Ltd.; MSD K.K.; and Gilead Sciences. The other authors have no conflicts of interest.