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When a Patient Presents With Pedal Skin Changes After Knee Injury
An 18-year-old male presented to the office with a chief complaint of pain, swelling, and difficulty bearing weight on his right foot. The patient was treated at an emergency room locally within the past week following a fall from his Moped in which he suffered a fractured right patella.
The patient was being treated conservatively with splintage and bracing to the right knee. Crutches were being utilized to avoid weight-bearing, bending, and pressure to the knee. Prior radiographs taken at the time of the injury revealed no foot or ankle pathology, nor were there any foot or ankle signs or symptoms at that initial injury presentation. The pain and swelling increased over the course of a few days after his discharge from the emergency department, while having the lower extremity dependent. Past medical and surgical history were negative. The patient was not taking any medications for chronic conditions, and only took pain medication dispensed after injury. The patient had no allergies. His remaining history was unremarkable.
When evaluated in the office, hemorrhagic bullae were present to the dorsum of the foot, with fluctuance and surrounding edema (Figure 1). The largest bulla measured approximately 7 by 5 cm, with smaller bullae measuring up to approximately 3 by 2 cm. The bullae were tense, blood-filled, with surrounding erythema, edema and pain. No streaking cellulitis was evident. Incision and drainage was performed to evacuate the largest bulla. The macerated tissue was de-roofed exposing a full-thickness ulceration down to the tendon layer (Figure 2). Copious irrigation was performed utilizing normal saline, and wound cultures were taken. Empiric antibiotics were dispensed, and the area was packed with iodoform. A triple antibiotic ointment, as well as a non-adherent moist-dry sterile dressing and a compressive elastic bandage, were then applied.
Repeat radiographs confirmed no evidence of fracture, and insurance coverage limited further diagnostics. Results of the wound culture confirmed infection and the antibiotics were re-evaluated and continued. The patient was unable to perform dressing changes at home secondary to cost. Instead, he presented to the office 2–3 times weekly for local wound care and dressing changes. Luckily having no systemic comorbidities, the wound granulated within approximately 4–6 weeks (Figure 3). He remained non-weight-bearing during treatments and healed uneventfully (Figure 4).
Key Questions to Consider
1. What injuries can be associated with this condition?
2. What are the recommended treatment protocols?
3. What are the side effects associated with this condition?
Answering The Key Diagnostic Questions
1. Fracture or associated trauma
2. Aspiration, deroofing bullae, non-adherent dressings
3. Scarring, pain, reflex sympathetic dystrophy, skin grafts, prolonged healing, infection
What You Should Know About Hemorrhagic Bullae
Dermatologic complaints are common presentations in the emergency room. Hemorrhagic bullae, as presented in this case, are a manifestation caused by variable etiologies, including infection, trauma, drugs, hypersensitivity, autoimmune, and vascular complications. Comorbidities like diabetes mellitus can complicate the treatment and outcomes associated with hemorrhagic bullae.
Early recognition of serious underlying disease accounting for hemorrhagic bullae is therefore important. Bullae may be single or multiple on evaluation, and although patients may appear ill, patients who present in the early course of illness may appear well but can deteriorate rapidly.1 Swelling is usually the most common clinical complaint; however, patients can present with erythema, leukocytosis, soft tissue infection, necrotizing fasciitis, associated wound and/or fracture, pain, fever, and hypotension. High-velocity trauma, such as motor vehicle accidents, pedestrian strikes, calcaneal, ankle, and pilon fractures can be associated with bullae (both clear and/or hemorrhagic). These may delay potential surgical intervention and incision placement. Infected hemorrhagic bullae may be polymicrobial, and common pathogens have been found to be Vibrio species, and Streptococcus.1
The cascade of events that take place in closed soft-tissue injuries can be divided into three phases: inflammatory, proliferative, and reparative.2 The inflammatory phase of the cascade mainly refers to changes in microcirculation, which is disrupted due to soft tissue breakdown at the time of injury. Bullae formation is directed by two parameters during the inflammatory phase. First, soft tissue edema leads to an increase of interstitial pressure. As a result, filtration pressure increases and leads to diminished cohesion between epidermal cells. This results in the transport of fluid into the blister.
The second scenario, and one that is more likely, is increased colloid pressure in an epidermal or subepidermal cleft, which leads to fluid transfer into the cleft. When a critical level of stress is reached, separation of the dermal-epidermal junction occurs due to the differing elasticity and viscoelastic properties of the two layers. There is impaired dermal and epidermal nutrition from traumatic rupture of venous plexi, causing obstruction, hemorrhage, and arterial spasm with subsequent epidermal necrosis.3 The potential space fills with fluid creating a bulla. The degree of involvement depends on the severity of the inciting injury causing the increase in osmotic pressure at the dermal-epidermal junction.3
Blisters may appear within a few days of injury or as late as 3 weeks after trauma and can be clear or hemorrhagic filled vesicles. The two differ in their histological appearance. In hemorrhagic bullae the dermis is completely free of epidermal cells, which may lead to increased re-epithelialization time and associated morbidity.4 Re-epithelialization occurs within 6 to 21 days.3 It is considered clinically complete when a moist dermal layer or granulation-type tissue is covered by an epithelial layer, and the blister bed is no longer sensitive to touch.4 Alternatively, superficial wound care may allow spontaneous healing within 2 weeks.3 Patients need to be monitored for wound and/or skin complications, and infection. If surgery is scheduled, it is best to wait until the blisters resolve.
A Closer Look at Treatment Options
Currently, there is no universal consensus on the appropriate treatment of this soft-tissue injury. Much of the uncertainty is related to the paucity of scientific investigation into this clinical problem. Successful management of soft tissue injury is of paramount importance for a favorable clinical outcome. Otherwise, complications such as soft tissue loss, protracted course of treatment, deep infection, pain, stiffness, reflex sympathetic dystrophy, amputation, and skin grafting may occur.4
While there is no distinct plan for bullae treatment, various options have been discussed. These include aspiration, unroofing, and non-adherent sterile dressings while leaving bullae intact. The preferred method of treatment in the literature review was removing the roof of the bullae and dressing the wound. Preparation for deroofing can be done under Betadine preparation with subsequent use of silver sulfadiazine (Silvadene) cream applied twice daily, covered by a dry sterile dressing. Silvadene is a topical sulfonamide that acts as an inhibitor of bacterial folic acid synthesis. By preventing folate synthesis, Silvadene deprives bacterial cells of essential cofactors for purine, pyrimidine, and amino acid synthesis. This minimizes soft-tissue complications by promoting re-epithelialization and diminishes local bacterial counts in the blister bed.
In one study, patients who presented with hemorrhagic bullae had a higher rate of scarring versus those patients with clear fluid–filled bullae.4 However, no patient reported avoidance of wearing specific clothing because of the cosmetic appearance of their lower extremities. Residual pain in the region of the previous blisters has also been reported but did not seem to limit function for the study’s participants.
In Conclusion
Hemorrhagic bullae have a higher risk of complications, presumably because they represent more severe tissue disruption. They can lead to an increased risk of scarring and limit function. They can be associated with major illnesses and comorbidities, such as diabetes mellitus. It is imperative to understand the patient’s full medical history so proper treatment can be performed, and complications can be avoided.
Dr. DeLauro is a Diplomate of the American Board of Podiatric Medicine and the American Board of Foot and Ankle Surgery. She is in private practice in New York and New Jersey.
References
1. Hsiao CT, Lin LJ, Shiao CJ, Hsiao KY, Chen IC. Hemorrhagic bullae are not only skin deep. Am J Emerg Med. 2008 Mar;26(3):316-9. doi: 10.1016/j.ajem.2007.07.014. PMID: 18358943.
2. Tosounidis TH, Daskalakis II, Giannoudis PV. Fracture blisters: pathophysiology and management. Injury. 2020 Dec;51(12):2786-2792. doi: 10.1016/j.injury.2020.11.059. PMID: 33308645.
3. Ballo F, Maroon M, Millon SJ. Fracture blisters. J Am Acad Dermatol. 1994 Jun;30(6):1033-4. doi: 10.1016/s0190-9622(09)80152-7. PMID: 8188872.
4. Strauss EJ, Petrucelli G, Bong M, Koval KJ, Egol KA. Blisters associated with lower-extremity fracture: results of a prospective treatment protocol. J Orthop Trauma. 2006 Oct;20(9):618-22. doi: 10.1097/01.bot.0000249420.30736.91. PMID: 17088664.
5. Bork K. Physical forces in blister formation. The role of colloid osmotic pressure and of total osmolality in fluid migration into the rising blister. J Invest Dermatol. 1978 Sep;71(3):209-12. doi: 10.1111/1523-1747.ep12547271. PMID: 690485.
