Ischemic colitis is defined as a localized and reversible ischemic colonic lesion [1, 2] that usually occurs at the ileocecal junction and around the Griffith’s point and Sudeck’s point [3]. Ischemic proctitis occurs in only 2–5% of cases of ischemic coloproctitis because of the abundant collateral blood supply of the rectum [4, 5]. Moreover, ischemic proctitis after sigmoidectomy is rare [6]. There have been no reports on the prevalence of ischemic proctitis after sigmoidectomy. In general, the rectum is uncommonly affected by ischemia due to its relatively rich dual blood supply from both systemic and splanchnic circulation [7]. Bharucha et al. reported 328 ischemic colitis patients; of these, only 10 patients had isolated ischemic proctosigmoiditis [8]. In the present case, insufficient blood flow due to dissection of the inferior mesenteric artery may have contributed to the development of ischemic proctitis. Nelson et al. reported that an incidence of ischemic colitis after abdominal aortic surgery with inferior mesenteric artery resection is at least 0.5%, suggesting that ischemic proctitis is very rare [9]. Here, we presented a rare case of ischemic proctitis that occurred 6 months after laparoscopic sigmoidectomy. The pathophysiology of ischemic proctitis after sigmoidectomy remains unclear. However, it was assumed to be related to several factors, including arteriosclerosis [9,10,11,12], venous congestion [13, 14], and anatomically complicated areas such as the Sudeck’s point [3, 15,16,17,18]. Sudeck’s point is a watershed area and a weak blood supply point at the rectosigmoid junction [15, 17]. An incomplete vascular anastomosis at the Sudeck’s point would result in ischemic changes in the remaining rectosigmoid colon. This could cause anastomotic leakage after sigmoidectomy [18]. This patient's anastomotic site was at the sigmoid colon approximately 10 cm higher than the promontorium level with high ligation of the inferior mesenteric artery, which might be one of the causes of impaired vascular perfusion. However, the severest part of the ischemic lesion was not located at the anastomosis and the ulcers were spread extensively towards the anal canal. Additionally, the patient did not experience anastomotic leakage, which suggests that the Sudeck’s point was not the sole cause of this patient’s proctitis. We assume that the blood insufficiency was partial. Some inflammation in the underlying arteriosclerotic disease might have combined with the anatomical problem. Therefore, based on the present case, we believe that the blood backflow from the anal side should be considered more carefully, especially in patients with risk factors for ischemic proctitis such as arteriosclerotic disease. Evaluation of blood flow in the anastomotic bowel using indocyanine green is considered one of the methods for preventing bowel ischemia and anastomotic leakage [19]. Besides, since the ischemic proctitis occurred 6 months after sigmoidectomy in this case, intraoperative blood flow evaluation alone might not be sufficient as a preventive method. Considering the retrograde blood flow from the rectum, the most important thing is that the colon should not be resected distant from the anal verge in cases with redundant sigmoid colon.
The first-line treatment for ischemic colitis is non-surgical management, including withholding oral intake and administration of antibiotics. In severe cases, surgery including colostomy or abdominoperineal resection is indicated [20]. In general, O’Neill et al. reported that aggravating risk factors of ischemic colitis include lack of rectal bleeding, peritonism, renal dysfunction, and right-sided ischemic colitis [21]. The patient did not have any peritoneal signs or aggravating risk factors. Furthermore, the patient’s abdominal symptoms improved relatively fast with bowel rest, and surgical treatment was unnecessary. If the patient had abdominal discomfort with peritoneal signs or conservative treatment was unsuccessful, we would have performed the surgery. For non-surgical management, there have been reports of the use of HBO [22], vasodilators such as PGE1 [23], and NO [24]. The main aim of non-surgical management of ischemic proctitis is restoring tissue perfusion. Tissue perfusion is classified into three groups, namely, adequate perfusion, no perfusion, and marginal perfusion, called penumbra [25]. Ischemic-reperfusion injury induces leukocyte adherence to endothelial cells where they are activated. This activation results in the release of reactive oxygen species, which convert xanthine dehydrogenase into xanthine oxidase necessary for lipid peroxidation. This reaction induces tissue and organ injuries. In addition to tissue oxygenation and reducing edema via vasoconstriction [26], HBO inhibits β2 integrin-mediated leukocyte adherence to endothelial cells in the animal model and decreases ischemic-reperfusion injury; thus, HBO exerts its greatest influence in the penumbra [27]. In the present case, there was no mechanical vessel obstruction, and the anastomotic site was also considered to be the penumbra; therefore, HBO, which decreases the effect of ischemic-reperfusion injury, was effective in this case. Patients without aggravating risk factors are good candidates for non-surgical management, including HBO.
