Fracture blisters


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. They occurred in characteristic locations along the human musculoskeletal, 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. 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 sub epidermal vesicles. The blister fluid was found to be a sterile transudate. Microbial evaluation of 11 ruptured fracture blisters demonstrated colonization, occurred soon after blister rupture, and continued until reepithelialization.

Types of fracture blisters

Two types of fracture blisters have been identified: clear fluid-filled and blood-filled. The blood-filled blisters have been shown histological to have complete separation of the dermis from the epidermis, whereas the clear fluid-filled blisters demonstrate partial epidermal separation of the epidermis from the underlying dermis, with a few scattered areas of retained epithelial cells on the dermis. It is believed that blood-filled blisters are the result of injury to the papillary vasculature, allowing blood to escape into the blister. These represent a more significant injury histological and clinically. Due to detachment of the epidermis from the underlying dermis, eventual necrosis of the epidermis often ensues. Edema and venous stasis resulting from the injury induce collapse and thrombosis of affected blood and lymphatic vessels, thus adding to circulatory compromise.

Conclusion

Fracture blisters may appear as early as six hours after injury or as late as three weeks after trauma. These blisters signify underlying soft tissue damage and may result in increased infection rates for both operatively and no operatively treated fractures. Treatment recommendations have consisted of benign neglect, debridement, aspiration and surgical delay until reepithelialization occurs. Fracture blisters are defined as skin bullae and blisters representing areas of epidermal necrosis with separation of the stratified squamous cell layer by edema fluid. Fractures blisters contain sterile fluid but demonstrate colonization with multiple organisms once ruptured. Bacterial colonization was shown to be present until reepithelialization. This coupled with the resultant epidermal necrosis and hypoxia. It leads to an increased susceptibility to wound infection and dehiscence that is double the overall complication rate compared to fractures void of blistering.

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