Hemorrhoidectomy creates an open perianal wound that is repeatedly exposed to contamination, mechanical irritation during defecation, and substantial postoperative discomfort. Moist wound management aims to maintain an appropriate wound interface that supports re-epithelialization while balancing hydration, exudate control, wound protection, and patient comfort. This narrative review evaluates the biological rationale, clinical evidence, dressing selection, adjunctive therapies, and practical implementation of moist wound management after hemorrhoidectomy. A structured literature search prioritized randomized controlled trials, systematic reviews, meta-analyses, clinical guidelines, and recent comparative studies directly involving hemorrhoidectomy, while broader wound-healing evidence was used when procedure-specific data were unavailable. Current evidence suggests that selected dressing strategies may shorten epithelialization time, although direct hemorrhoidectomy-specific comparative evidence remains limited. In contrast, dressing-specific effects on postoperative pain are less certain, whereas topical pharmacological and sphincter-targeted interventions have separate evidence supporting analgesic benefit. Available studies provide some reassurance regarding early safety outcomes but are generally insufficiently powered to exclude differences in uncommon complications. Formal cost-effectiveness evidence comparing postoperative dressing strategies is also lacking. Moist dressings should therefore be considered within a multimodal postoperative approach that also addresses pain, sphincter spasm, hygiene, bowel regulation, and defecation-related mechanical stress. Future multicenter randomized trials should use standardized pain, epithelialization, complication, patient-reported, and health-economic outcomes to define which dressing strategies benefit specific patient groups.

Pressure ulcers (PUs), also termed pressure injuries, are chronic inflammatory wounds associated with recurrent ischemia-reperfusion (I/R), impaired fibroblast repair, poor vascularization, and delayed extracellular matrix remodeling. We evaluated ferrous lactate in hypoxia/reoxygenation-injured human dermal fibroblasts (HDFs) and in a rabbit PU model generated by cyclic magnetic compression. In HDFs subjected to I/R-like stress, ferrous lactate increased viability, proliferation, and scratch migration, reduced TNF-α, IL-6, and IL-1β, and increased IL-10 and TGF-β. For in vivo treatment, ferrous lactate was delivered topically in sodium alginate vehicle and compared with untreated, vehicle, and commercial comparator groups. On day 14, wound closure reached 94.73 ± 2.49% in the 2 mM ferrous lactate group, compared with 44.80 ± 4.18% in untreated controls, 61.90 ± 1.29% in the vehicle group, and 71.50 ± 3.80% in the commercial comparator group. Wound closure in the 2 mM group was significantly greater than that in the commercial comparator group (P < 0.05). Ferrous lactate treatment was also associated with improved re-epithelialization, granulation tissue formation, collagen deposition, and Ki67-positive cell proliferation, together with increased VEGF expression and CD31-positive vascular staining. These findings provide preliminary preclinical evidence that topical ferrous lactate promotes pressure ulcer repair.