LAUSR

To the Editor, We were very impressed by Ihnát et al, whose analysis examined both anorectal dysfunction after radiotherapy and damages related to internal anal sphincter. Nevertheless, we believe it is important to introduce our histological observations on this topic. We analyzed 25 surgical specimens of patients who underwent abdominoperineal resections 5 weeks after long‐term radiotherapy with 55 Gy and concurrent Folfox treatment. While rectal wall and internal anal sphincter displayed just minor edema and hyperemia, both external anal sphincter and muscles of the perineal floor showed more visible lesions. They mainly affected the striated muscle myofibrils through nuclear swelling and more serious pycnosis, karyolysis, and karyorrhexis. Corresponding cytoplasmatic lesions involved a widespread hyalinosis, showing disappearance of striated bands and reduced immune‐histochemical staining with anti‐ Sarcomeric actin antibodies. Newly generated fibroblasts and collagen fibrils were detected in the interstitial spaces between muscle fibers. Arterioles showed partially disrupted endothelium and media layer edema. Lymphatic capillaries appeared mildly dilated. Peripheral nervous fibers exhibited edema, and new collagen fibrils wrapped the single axons. As surgical specimens of patients who had received short‐term radiation therapy of only 25 Gy did not show similar lesions, we can assume that detected radiation toxicity is dose dependent, not ruling out chemotherapy as an aggravating factor. We estimate that detected lesions evolve following a series of events: direct radiation damage produces a local cytokines release that depresses cells replication and increases capillary permeability, leading to erythrocytes diapedesis, extravasation of serum proteins, and local edema. In the middle‐term, we did not record any proper remodeling of the striated muscles; we recorded just their partial repair, mainly provided by fibroblasts, which generate new collagen fibrils. This process involved also peripheral nervous fibers, with an induced functional damage. Therefore, we are allowed to suppose a real “vascular‐nervous myopathy” for perineal floor muscles and external anal sphincter. This justifies both hard perineal wound healing, which follows abdominoperineal resection and dysfunction of anal sphincter apparatus in the case of restorative rectal resection. In our opinion, improved radiation therapy protocols might lead to reduced secondary perineal damages, particularly in scheduled reconstructive surgery of upper or middle rectal cancers.