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fracture blister

Fracture blister

Fracture blister is skin blistering and significant soft tissue swelling near fracture such as the ankle, wrist elbow and foot, where skin adheres tightly to bone with little subcutaneous fat cushioning 1. Fracture blister that results resembles that of a second degree burn. Clinically, 2 fracture blister types were identified: (1) clear fluid filled, and (2) blood filled 2. Histologically, both blister types demonstrated a cleavage injury at the dermo-epidermal junction. However, the dermis of the clear fluid filled blister retained occasional epithelial cells, while the dermis of blood filled blisters was completely devoid of epidermis. Minimal to no evidence of dermal injury was found in histologic sections from the blister beds or from the skin in close proximity to blisters. The blood filled blister appears to represent a slightly deeper injury than the clear fluid blister and had a higher risk of poor healing of surgical incisions 2.

Fracture blisters are a relatively uncommon complication of fractures, occurring in about 2.9% of all acute fractures requiring hospitalization 3. Fracture blisters significantly alter treatment, making it difficult to splint or cast and often overlying ideal surgical incision sites.

Currently no uniform consensus regarding the optimal management of fracture blisters exists 4. This represents an area of need for further research. While most agree that fracture blisters should not be directly operated through, recommendations have varied. These include observation and surgical delay, to deroofment and topical antibiotics 5.

Fracture blisters are likely best left intact to preserve the sterile environment 1. If possible, early surgical intervention should be accomplished to prevent blister formation, but if already present, blisters should be allowed to resolve prior to surgery 1.

Fracture blisters cause

Fracture blisters are hypothesized to result from large strains applied to the skin during the initial fracture deformation 6, causing a cleavage injury at the dermo-epidermal junction. Anatomic areas where tight, closely adhered skin without a muscle or enveloping fascia is present appear to be the sites most predisposed to this type of injury 3. The blister formation is proposed to result from the increased interstitial pressure of post-traumatic edema, which acts to decrease cohesion between epidermal cells and facilitate fluid transport into a blister cavity. Venous stasis due to thrombosis of injured vessels and fragile lymphatics also contribute to local tissue hypoxia leading to epidermal necrosis and blister formation 3. These forces combine to cause an injury which resembles a second-degree burn rather than a friction blister. Blisters can form as early as six hours post fracture and the majority within 24–48 hours 3.

Risk factors for development of fracture blisters include anatomical sites with thinner skin without the underlying protection of muscle or adipose (ankle, wrist, elbow, foot, and distal tibia) and any conditions that predispose to poor wound healing, such as peripheral vascular disease, collagen vascular disease, hypertension, smoking, alcoholism, diabetes mellitus, and lymphatic obstruction 1. High energy injury, such as falls of an average of 18 feet, motor vehicle accidents, pedestrian vs. motor vehicle accidents and grade 1 and 2 open tibia fractures also predispose to fracture blister formation. Studies by Varela 3 and Strauss 7 provide detailed data regarding fracture blisters based on location, the results of which are compiled in Table 1. Varela 3 conducted a three and a half year study characterizing all fracture blisters presenting to four different hospitals in a major metropolitan area from 1986 –1989. Strauss conducted a similar four year study at a major Level 1 trauma center from 1999–2003.

Two types of fracture blisters are commonly seen: clear fluid-filled and hemorrhagic blisters. Hemorrhagic blisters represent a more severe injury where the dermis is completely stripped of epidermal cells, taking approximately 16 days to heal. The clear fluid-filled blisters have minimal injury to the dermis with some epidermal cells remaining attached, healing in approximately 12 days. The frequency of these types of blisters, based on whether clear or liquid, is noted in Table 2.

Table 1. Fracture location and blister frequency

LocationNumber of fracturesNumber of blistersPercentage of blisters at each fracture site
Pilon54916.7%
Distal humerus10220%
Elbow dislocation18316.7%
Calcaneus1021514.7%
Tibial plateau195178.7%
Ankle412276.6%
Tibial shaft416143.4%
Humeral shaft3412.9%
Radius (shaft and distal)11521.7%
Total1356906.6%

Table 2. Blister type and frequency

Blister TypeOccurrencePercentage
Blood Filled3939%
Clear Filled4141%
Combination2020%
Total100100%

Complications fracture blisters

Strauss et al. 5 reported a 13% wound complication rate in their study of 45 patients with lower extremity fracture blisters. In this study, all patients received blister deroofment followed by twice daily silver sulfadiazine (Silvadene) application to the blister bed. Two major wound complications were noted in patients with a history of non-insulin dependent diabetes mellitus. This included a deep infection requiring revision surgery and ultimate ankle fusion, and a persistent medial wound breakdown requiring hardware removal. It is also important to note that their overall average surgical delay was seven days. Furthermore, a significant difference in surgical delay was found between ankle and tibial plateau fractures, which averaged six and 11 days each, respectively.

Fracture blister treatment

Management of fracture blister is the most controversial at this point in time. Some authors advocate leaving blisters intact and awaiting resolution prior to surgical stabilization 3. Others recommend early surgical correction to prevent blister formation, and if blisters are already present, then to incise without regard to blister location even if the incision would be through a blister 7. Yet some have seen more complications from intentional incision through or deliberate unroofing of the blister 3.

In a prospective analysis, Giordano and Koval compared various treatment modalities including blister aspiration, deroofment plus silvadene application, and leaving the blister intact 8. No significant difference in blister healing was found between the different modalities. Eighty-seven percent had reepithelialized their blister beds at an average of three months while 13% suffered wound complications requiring subsequent skin grafting in all but one. It is important to note that all wound complications were associated with a blood-filled blister type. Additionally, in two of these cases the surgical incision was made directly through a blood-filled blister bed. Both of these cases experienced wound complications requiring split thickness skin grafting. No wound complications were noted when incisions were made through clear fluid-filled blister beds. The authors’ final recommendation was to leave all blisters untreated unless spontaneous rupture occurs 8.

Varela et al. 9 also found no significant difference in fracture blister healing between those treated with dry dressings, silvadene application, or whirlpool debridements plus silvadene application. In this study all blisters were left to rupture spontaneously. More importantly, these authors performed a histologic and microbial analysis on 15 of the fracture blisters. Their analysis confirmed that fracture blisters are subepidermal vesicles filled with sterile transudate. Furthermore, their microbial analysis indicated rapid colonization of the blister bed with opportunistic skin flora, namely Staphylococcus epidermidis and Staphylococcus aureus, shortly following blister rupture.

In contrast to the findings of Strauss et al. 5 and Giordano and Koval 8, Hasegawa et al 4 did not observe any post-operative wound complications despite operating through blood-filled blister beds in patients with a history of non-insulin dependent diabetes. It is possible that this may be due to our small sample size and shorter follow-up period. However, given the near complete reepithelialized blister beds and limited soft tissue swelling at the time of surgery, we were likely operating through soft tissue that had adequately recovered from the initial trauma. Additionally, the absence of post-operative wound complications, including further blister development, may be attributed to our post-surgical application of a circumferential PREVENA Plus wound vacuum.

Multiple studies demonstrate increased tissue perfusion, decreased wound edema, and stimulation of granulation tissue following negative pressure wound therapy. When comparing traditional negative pressure wound therapy with negative pressure wound therapy with instillation and dwell, Omar et al. 10 found faster wound healing times when negative pressure wound therapy was combined with sterile saline instillation. Together, these factors likely accounted for our faster reepithelialization time, significant reduction in soft tissue swelling, and consequently shorter delay to surgery. It is also possible that the circumferential application of wound vacuums may have enhanced these responses given the larger regional surface area covered. However, this has not been tested in the literature yet and as such remains theoretical only.

As suggested by Varela et al. 9, the high rate of wound complications previously noted may in part be due to the rapid colonization of blister beds with staph species. In a study by Hasegawa et al 4, they demonstrated no wound complications at any time point despite the intentional rupture of all fracture blisters. Hasegawa et al 4 believe this to be due to their use of sterile saline instillation. It is well established that negative pressure wound therapy without instillation does not play a large role in reducing bacterial load in wounds. However, several recent studies demonstrated a significant reduction in bioburden in chronic wounds after seven days of negative pressure wound therapy with instillation and dwell 11. While these studies instilled an antimicrobial solution, Hasegawa et al 4 chose to instill sterile saline given the relatively clean appearance of the skin prior to wound vacuum application, as well as the well-established efficacy of normal saline irrigation on traumatic and chronic wounds. Still, further research is required to determine the true efficacy of negative pressure wound therapy with saline instillation on bioburden reduction.

It is also important to point out that in both cases, VeraFlo sponge was applied directly over intact skin that surrounded the fracture blisters. Specifically, in case one, this represented a relatively large area anteriorly and over the lateral malleolus. Interestingly, this resulted in very mild skin maceration. Thus, while Hasegawa et al 4 do not believe that the use of negative pressure wound therapy with instillation and dwell over intact skin was necessary to achieve their results, they do believe that one week of negative pressure wound therapy with instillation and dwell with short dwell times can be used safely over intact skin. It is possible that their one minute saline soak times prevented further skin injury that is typically expected when traditional wound vacuum sponge is applied directly to intact skin with continuous suction. However, to their knowledge this has not yet been tested. As such, future research should include a larger sample size, longer follow-up, and comparison trials. For instance, comparing negative pressure wound therapy versus negative pressure wound therapy with instillation and dwell versus PREVENA plus, as well as negative pressure wound therapy with instillation and dwell with sterile saline versus an antimicrobial solution to more accurately determine the efficacy of negative pressure wound therapy with sterile saline instillation on fracture blister management.

While consensus among these authors has not been reached, it is clear that the presence of fracture blisters complicates and delays definitive repair. Fracture blisters, and the skin breakdown associated with them, may result in chronic ulcers, infection and prolonged hospital stays. A study by Strauss 7 illustrates these complications further (Table 3). In a population with these risk factors, identification and early treatment is crucial to preventing these poor outcomes.

Table 3. Delay in definitive care

Fracture LocationDelay in definitive care (days)
Ankle6
Tibial plateau11
Tibial shaft3.5
Calcaneal12
Pilon6.75
Mean7.7
[Source 7 ] References
  1. Uebbing CM, Walsh M, Miller JB, Abraham M, Arnold C. Fracture blisters. West J Emerg Med. 2011;12(1):131–133. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3088393
  2. Giordano CP, Koval KJ, Zuckerman JD, Desai P. Fracture blisters. Clin Orthop Relat Res. 1994;(307):214–221.
  3. Varela C, Vaughan TK, Carr J, et al. Fracture Blisters: Clinical and Pathologic Aspects. J of Orthopedic Trauma. 1993;7(5):417–27.
  4. Hasegawa IG, Livingstone JP, Murray P. A Novel Method for Fracture Blister Management Using Circumferential Negative Pressure Wound Therapy with Instillation and Dwell. Cureus. 2018;10(10):e3509. Published 2018 Oct 29. doi:10.7759/cureus.3509 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6314796
  5. Blisters associated with lower-extremity fracture: results of a prospective treatment protocol. Strauss EJ, Petrucelli G, Bong M, Koval KJ, Egol KA. J Orthop Trauma. 2006;20:618–622.
  6. Giordano C, Scott D, Koval K, et al. Fracture Blister Formation: A Laboratory Study. J of Trauma-Injury, Infection, and Critical Care. 1995 Jun;38(6):907–9.
  7. Strauss E, Petrucelli G, Bong M, Koval K, Egol K. Blisters Associated with Lower Extremity Fracture: Results of a Prospective Treatment Protocol. J of Orthopedic Trauma. 2006 Oct;20(9):618–622.
  8. Treatment of fracture blisters: a prospective study of 53 cases. Giordano CP, Koval KJ. J Orthop Trauma. 1995;9:171–176.
  9. Fracture blisters: clinical and pathological aspects. Varela CD, Vaughan TK, Carr JB, Slemmons BK. J Orthop Trauma. 1993;7:417–427.
  10. A comparative study of negative pressure wound therapy with and without instillation of saline on wound healing. Omar M, Gathen M, Liodakis E, Suero EM, Krettek C, Zeckey C, Petri M. J Wound Care. 2016;25:475–478.
  11. Yang C, Goss SG, Alcantara S, Schultz G, Lantis Ii JC. Effect of Negative Pressure Wound Therapy With Instillation on Bioburden in Chronically Infected Wounds. Wounds. 2017;29(8):240–246. https://www.woundsresearch.com/article/effect-negative-pressure-wound-therapy-instillation-bioburden-chronically-infected-wounds
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