Fracture blisters: clinical and pathological aspects
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Updated: Nov 8, 2026

Pseudofracture: An Acute Peripheral Tissue Trauma Model
Published on: April 18, 2011
C D Varela1, T K Vaughan, J B Carr
1Orthopaedic Surgery Service, 67th Evacuation Hospital, United States Army Medical Activity, Wuerzburg, Germany.
Abstract:
Fracture blisters are tense vesicles or bullae that arise on markedly swollen skin directly overlying a fracture. There is very little objective data in the literature detailing their characteristics and management. All fracture blisters that occurred over a 3 1/2-year period were studied retrospectively at four hospitals, of which three were level I trauma centers. A total of 53 blisters developed in 51 patients. They occurred in characteristic locations along the human musculoskeleton, most commonly overlying the tibia, ankle, and elbow. They arose within 24-48 h of acute injury in most instances. The timing of surgical intervention affected the occurrence of fracture blisters. Those patients with acute fractures who underwent open reduction internal fixation (ORIF) within 24 h of injury had the lowest incidence of fracture blisters (2.0%) compared with those delayed for > 24 h (8.0%) (p < 0.001). In those patients with fracture blisters present at time of surgery, patient care was affected in 10 of 13 cases (71%). Two of these were major complications occurring as postoperative wound infections. Other management problems consisted of delaying surgery, and changing in the operative plan. There were no adverse affects on patient care when the fracture blister developed postoperatively. Twenty-one fractures with blisters were treated by closed means, with the presence of fractures blisters delaying closed reduction and casting in two. Biopsy examination of 15 blisters supported the clinical impression that fracture blisters are subepidermal vesicles. The blister fluid was found to be a sterile transudate. Microbial evaluation of 11 ruptured fracture blisters demonstrated colonization (primarily with skin pathogens), occurred soon after blister rupture, and continued until reepithelialization.
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