Postoperative Buttock Skin Injuries Not Explained by Electrosurgical Burns: Three Cases Suggesting an Ischemia–Reperfusion Mechanism
Summary: Published March 10, 2026 in the Journal of Clinical Medicine (MDPI), this case series from Tenri Hospital (Nara, Japan) presents three perioperative patients who developed painful buttock/sacral skin lesions on postoperative day 1 — a pattern traditionally attributed in the Japanese dermatological literature to stray electrosurgical burns. The authors challenge this attribution on both electrophysical and clinical grounds, arguing instead that these lesions represent ischemia–reperfusion-related deep tissue injury (DTI), consistent with NPIAP/EPUAP pressure injury classification. Case 1 was an 80-year-old woman following 8-hour coronary bypass surgery, in whom the mesh-pattern erythema precisely matched the intraoperative warm-water circulating blanket (a nonconductive device), with CK peaking at 2,448 U/L; histology showed no thermal necrosis, only mild capillary dilation. Case 2 was a 15-year-old girl after anterior cruciate ligament reconstruction using only bipolar electrocautery (not monopolar), who developed diffuse bilateral gluteal swelling with markedly elevated enzymes (CK 6,075 U/L; AST 321; LDH 511) and CT-confirmed bilateral gluteal muscle oedema. Case 3 was an 87-year-old woman after hip fracture fixation in which no electrosurgical device was used at all, yet she developed a 6×7.7 cm sacral erythema with central ulcerative necrosis, and ultrasound confirmed gluteal muscle oedema. The proposed mechanism — surgical mechanical loading → localized deep tissue ischemia → reperfusion-triggered oxidative stress, ROS generation, and inflammatory cascade → delayed subcutaneous and muscle injury — explains the characteristic 12–24 hour delay in lesion appearance that is inconsistent with immediate thermal injury. The authors also note that misattribution to electrosurgical burns has medico-legal and institutional implications, and call for multidisciplinary evaluation (dermatology, anaesthesiology, clinical engineering) of such events.
Key Highlights:
- Three cases: 80-year-old (8-h CABG), 15-year-old (ACL reconstruction with bipolar only), 87-year-old (hip fixation, no electrosurgery) — all developed painful buttock/sacral lesions on postoperative day 1 with intact skin at OR discharge
- Electrosurgical burn hypothesis refuted per case: (1) nonconductive warming device matched lesion morphology; (2) bipolar-only case excludes dispersed monopolar stray current; (3) no electrosurgery used — leaving ischemia-reperfusion as the only plausible mechanism
- Markedly elevated muscle enzymes in Cases 2 and 3 (CK, AST, LDH) and CT/ultrasound evidence of gluteal muscle oedema confirm deep tissue involvement beneath intact or minimally disrupted skin
- Ischemia–reperfusion DTI mechanism: prolonged perioperative pressure → ischemia → reperfusion triggers ROS, endothelial injury, inflammatory cascade → delayed subcutaneous/muscle damage → skin manifestation 12–24 h postoperatively
- Histology (Case 1): intact epidermis and dermis with no necrosis or inflammation — consistent with early DTI, not thermal burn
- Clinical implication: perioperative pressure injury prevention (intraoperative positioning, padding, pressure redistribution) rather than electrosurgical equipment management is the appropriate preventive response; misattribution may misdirect incident investigations and delay correct preventive action
Keywords: deep tissue injury perioperative, ischemia reperfusion pressure injury, postoperative pressure injury prevention, perioperative wound care, deep tissue pressure injury staging, surgical positioning skin injury
Hiroshi Tanabe Yoshinori Nakamura