IN THIS ARTICLE
- Care outcome
A 57-year-old horticulturist is working on a ladder leaned up against a tree trunk when the ladder slips, causing her to fall six feet onto concrete. Her right foot and ankle sustain the force of the fall; she is in excruciating pain and unable to bear weight on the foot. She is immediately transported to a local emergency department for evaluation.
Physical exam reveals a tearful middle-aged female in moderate distress and acute pain. There is moderate swelling of the right medial and lateral malleolus, as well as the midfoot, with blue and purple discoloration on the medial and lateral malleolus. Radiographs of the right ankle identify nondisplaced fractures of the distal fibula and tibia. Foot x-rays are unremarkable. A splint is ordered. The patient is given crutches (non-weight-bearing status), pain medication, and a referral to orthopedics.
On day 3, the patient presents to orthopedics, where the splint is removed. An irregular, 4 × 3–in (at largest diameter), serohemorrhagic blister is discovered on the medial aspect of the lower leg, above the right malleolus (see Figure 1). Multiple 1- to 3-mm vesicles surround much of the anterior border. Moderate edema is noted from the top of the lesion to the midfoot, concentrated around the lateral and medial malleolus. Extensive blue, purple, and black discoloration is seen below the malleolus. The patient is diagnosed with a fracture blister.
Fracture blisters are taut, bullous, subepidermal vesicles that can accompany fractures or severe twisting injuries. They overlie markedly edematous soft tissue and histologically resemble a second-degree burn.1,2
Physiologically, blisters are caused by increased interstitial pressure due to swelling, with subsequent increased filtration pressure and colloid osmotic pressure in the epidermal gap.3 This causes a disruption that allows fluid to move into the weakened area.3 Areas most at risk for fracture blister formation are those with tight, closely adhered skin without muscle or enveloping fascia, where there is less soft tissue between the skin and bone prominences (eg, ankle, elbow, foot, distal tibia).2-4
Approximately 3% of all patients with acute fractures requiring hospitalization develop a fracture blister.4 Any condition that predisposes a patient to poor wound healing (eg, peripheral vascular disease, diabetes, hypertension) increases risk for a fracture blister.2 Recognizing which patients are at greatest risk is vital, as implementing prevention strategies and intervening when fracture blisters do form can help decrease complications—including infection and delayed surgery—and improve fracture resolution. In this patient’s case, the extent of the injury and force of the fall caused the fracture blister to form.
Diagnosis of a fracture blister is based on clinical presentation. There are two types: hemorrhagic blisters and clear fluid-filled blisters. Hemorrhagic blisters indicate more severe injury and longer healing time (approximately 16 d), while clear fluid-filled blisters demonstrate minimal injury and therefore are quicker to heal.2,4
The differential diagnosis for fracture blisters includes friction blisters and disorders such as epidermolysis bullosa and bullous pemphigoid. Friction blisters form when the epidermis is subjected to repeated friction or shear forces (eg, from a cast or splint).5,6 These forces mechanically separate epidermal cells at the stratum spinosum layer.7 The pressure that moves across the skin forces fluid into the deeper open spaces, filling them but leaving the surface layer intact.1
Epidermolysis bullosa (EB) is a group of rare inherited cutaneous and mucus membrane disorders. EB involves fragility and detachment of subepithelial tissues, which results in blistering and erosions.8,9 The blisters tend to develop in areas subject to minor trauma, such as the extensor aspects of the elbows and the dorsal aspects of the hands and feet.9 They can also be triggered by exposure to heat, friction, scratching, and adhesive tape.10
Bullous pemphigoid, a chronic autoimmune skin disorder, is characterized by pruritic, bullous lesions. When IgG autoantibodies bind to certain hemidesmosomal antigens, complement activation causes a subepidermal blister.11While bullous pemphigoid most commonly affects those older than 60, it can also occur in children. Diagnosis is confirmed by skin biopsy and immunofluorescence testing.11
Treatment and management
Although several recommendations have been published, there is no gold standard and treatment of fracture blisters remains controversial. Early surgical intervention for fractures could decrease the incidence of fracture blisters.1,3
The goal of treatment is to achieve re-epithelialization of the dermis.3,12,13 Once a blister forms, management techniques vary. Some recommend keeping closed blisters covered with a dry dressing to protect them from damage.3 Strauss et al recommend unroofing to avoid traumatic rupture; however, this does increase risk for infection.12 Recommendations differ depending on provider preference and each patient’s individual situation.
Elective unroofing of a blister is typically followed with one of several treatment options. These include covering the open blister with a topical antibiotic cream (eg, silver sulfadiazine 2%); applying a nonadherent, occlusive bismuth-tribromophenate-petroleum gauze dressing; or elevating and immobilizing the affected extremity.12,13