Wound Clinic Case Study: Fracture Blister

CASE STUDY INTRODUCTION
Often times, patients will present to the outpatient wound clinic with blisters. Typically, the blisters originate from a burn or friction, or may be associated with other medical conditions, such as bullous pemphigoid, epidermolysis bullosa, or herpes, to name a few. The presentation of these blisters may be very unusual and create confusion for the clinician. Patients may also be concerned with their appearance, and the presence of comorbid conditions may impair healing. This case study chronicles the care of a recent blister presentation in the outpatient setting.

PATIENT
52-year-old female involved in an all-terrain vehicle (ATV) accident in December 2017. The ATV flipped, causing a traumatic orthopedic event to her right foot. An MRI confirmed a comminuted fracture of the proximal shaft of the 2nd metatarsal, nondisplaced fracture of the base of the 3rd metatarsal, and bone bruising of the cuboid. Orthopedics immobilized the patient with a cast boot. She was unable to wear the boot secondary to excessive pain after blisters were present. The patient continued to smoke extensively and maintained her work schedule. Blisters formed by Day 3 post-injury, with skin deterioration developing with eschar in March 2018. The primary care
physician referred the patient to the wound clinic in early April.

PATIENT'S HISTORY & FACTORS AFFECTING HEALING

• Labs:

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white blood cell (WBC) count = elevated (initial wound clinic visit)

• Lower extremity circulation:

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normal ankle-brachial index (ABI)

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normal transcutaneous oximetry (TCOM)

• Edema:

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+ edema 3 months post-injury

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patient continued to work post-injury with restrictions

• Nutrition:

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vitamin D deficiency (noted during initial wound clinic visit = 7ng/mL)

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cholesterol and low-density lipoproteins = high (noted during initial wound clinic visit)

-
decreased transportation of oxygen¹ and nutrients due to increased diffusion distance (swelling)

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body mass index = 26.6

• Other:

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+ pain

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+ heavy smoking

CONCLUSION
Fracture blisters occur in about 2.9% of all fractures (typically high-energy traumas), with higher occurrences among ankle and calcaneus fractures.² Fracture blisters are also known as trauma blisters, epidermal necrosis, epidermolysis, and avascular necrosis of the skin. The true etiology is unknown and there is no universal consensus on how to treat them or their impact on subsequent surgery. The skin may suffer a mechanical shear, separating the epidermal and dermal layers to an extent. Injuring the epidermal-dermal layer and excess tissue pressure from post-traumatic edema allows for fluid to fill this space of tissue separation.

Fracture blisters have been defined as “skin bullae and blisters representing areas of epidermal necrosis with separation of the stratified squamous cell layer from the underlying vascular dermal layer by edema fluid.”³ They may also appear in low-energy trauma, can be seen in open fractures, and, to a lesser degree, can occur with elective foot and ankle surgery. Typically, the blister may appear 2.5 days later, but as early as six hours or as late as three weeks post-surgery. Their location is not necessarily over the fracture, but is typically seen on distal extremities. 

There are two types of fracture blisters: fluid-filled and blood-filled. Both may be seen together. Fluid-filled blisters have a partial epidermal/dermal separation while blood-filled blisters have complete separation. The roof of the blood blister is the entire epidermis; the base is the dermis. The papillary dermal vessels are damaged, thus leaking blood into this space. Fluid blisters may resolve faster than those filled with blood. One particular concern with fracture blisters is that skin compromise may be encountered with surgical incision and lead to infection. As the skin circulation is compromised, the risk for infection and dehiscence increases. Due to the type of trauma, where rapid onset edema and increased tissue pressure occurs, signs of compartment syndrome should be ruled out and monitoring of involved extremity neurovascular status is warranted. 

In this case study, based on data collected, it is thought that the wound was not in a positive healing trajectory due to persistent edema and a smoking habit. These two factors decreased the amount of needed oxygen to the injured area, prolonging and aggravating inflammation, and creating the right environment for bacteria to proliferate. Once these factors were successfully addressed and advanced modalities were introduced, the wound began to significantly decrease in size and eventually healed. 

1. Aviles F, Whitten-Byles D. Oxygen & wound healing: going beyond hyperbaric therapy. TWC. 2018;12(11):14-21.

2. Varela CD, Vaughan TK, Carr JB, Slemmons BK. Fracture blisters: clinical and pathological aspects. J Orthrop Trauma. 1993;7(5):417-27.

3. Shelton ML, Anderson RL. Complications of fractures and dislocations of the ankle. In: Epps CH, Complications of Orthopaedic Surgery. 3rd ed. Philadelphia, PA: JB Lippincott; 1988:599-648.