fracture blisters

2
Journal of the American Academy of Dermatology Volume 30, Number 6 Brief communications 1033 Fracture blisters Fig. 1. Lateral view ofleft foot 1 day after injury dem- onstrating marked edema, ecchymoses, and hemorrhagic bullae. decompresses the soft tissue and prevents blister formation. Similarly, rapid surgical decompression at the time of open reduction and internal fixation may prevent their development. 5 Bullae may also develop under casts; these may be true fracture blis- ters or friction blisters from cast-induced shear stresses. Histologically, fracture blisters are subepidermal and represent separation of the necrotic epidermis from the dermis by edema fluid. The degree of involvement depends on the severity of the inciting injury causing the increase in osmotic pressure at the dermoepidermal junction. 5 Fracture blisters are a reflection in the skin of the same trauma that caused the fracture. They are From the Departments of Dermatology- and Or thopedics." Geisinger Medical Center. Reprints not available. JAM ACAD DERMATOL 1994;30:1033-4. Copyright @ 1994 by the American Academy of Dermatology, Inc. 0190-9622/94 $3.00 + 0 16/54/52500 Frances Ballo, MD,a Michele Maroon, MD,a and S. John Millon, MDb Danville, Pennsylvania Fracture blisters occur ncar fractures adjacent to joints or areas of limited skin mobility. They may also result from high-energy trauma. I These blisters have been associated with fractures of the ankle, knee.? and supracondylar part of the humerus.' The bullae resolvespontaneously within 10to 14 days but result in delay of surgical reduction. Alternatively, aggressive surgical debridement may produce reso- lution within 5 to 10 days. I We report the first case of fracture blisters seen by our department. CASE REPORT A 75-year-old white man noticed left foot pain after falling off a ladder the preceding day. Examination showed marked edema of the dorsum of the left foot and ankle and serous and hemorrhagic bullae (Fig. 1). A roentgenogram showed a comminuted calcaneal fracture withou t significant in traart icular displacement. The foot was sterilely prepared and wrapped in a soft cotton ster- ile dressing. Ten days later blisters and ecchymoses were still present but no erythema was seen. A sterile dressing and short leg cast were applied and reapplied 3 weeks later. Final examination at 7 weeks showed complete res- olution of the fracture blisters and only a trace of residual edema. A short removable leg splint was applied, and the patient tolerated gradual weight-bearing. DISCUSSION Fracture blisters may appear within a few days of injury! or as late as 3 weeks after trauma." Bulla formation is caused by impaired dermal and epider- mal nutrition with subsequent epidermal necrosis. . This results from traumatic rupture of venousplexi, causing obstruction, hemorrhage, and arterial spasm.Theankleis particularlyvulnerabletotrauma resulting in skin breakdown , because of flatter epi- dermal papillae, sparse subcutaneous tissue, and ex- tensive arborizing veins. Fracture blisters rarely oc- cur with open fractures because the open wound

Upload: s-john

Post on 02-Jan-2017

216 views

Category:

Documents


0 download

TRANSCRIPT

Page 1: Fracture blisters

Journal of the American Academy of DermatologyVolume 30, Number 6 Briefcommunications 1033

Fracture blisters

Fig. 1. Lateral view ofleft foot 1 day after injury dem­onstrating marked edema, ecchymoses, and hemorrhagicbullae.

decompresses the soft tissue and prevents blisterformation. Similarly, rapid surgical decompressionat the time of open reduction and internal fixationmay prevent their development.5 Bullae may alsodevelop under casts; these may be true fracture blis­ters or friction blisters from cast-induced shearstresses.

Histologically, fracture blisters are subepidermaland represent separation of the necrotic epidermisfrom the dermis by edema fluid. The degree ofinvolvement depends on the severity of the incitinginjury causing the increase in osmotic pressure at thedermoepidermal junction.5

Fracture blisters are a reflection in the skin of thesame trauma that caused the fracture. They are

From the Departments of Dermatology- and Or thopedics." GeisingerMedical Center.

Reprints not available.

JAM ACAD DERMATOL 1994;30:1033-4.

Copyright @ 1994 by the American Academy of Dermatology, Inc.

0190-9622/94 $3.00 + 0 16/54/52500

Frances Ballo, MD,a Michele Maroon, MD,a and S. John Millon, MDbDanville, Pennsylvania

Fracture blisters occur ncar fractures adjacent tojoints or areas of limited skin mobility. They mayalso result from high-energy trauma. I These blistershave been associated with fractures of the ankle,knee.? and supracondylar part of the humerus.' Thebullae resolvespontaneously within 10to 14days butresult in delay of surgical reduction. Alternatively,aggressive surgical debridement may produce reso­lution within 5 to 10 days.I We report the first caseof fracture blisters seen by our department.

CASE REPORT

A 75-year-old white man noticed left foot pain afterfalling off a ladder the preceding day. Examinationshowed marked edema of the dorsum of the left foot andankle and serous and hemorrhagic bullae (Fig. 1). Aroentgenogram showed a comminuted calcaneal fracturewithou t significant intraarticular displacement. The footwas sterilely prepared and wrapped in a soft cotton ster­ile dressing. Ten days later blisters and ecchymoses werestill present but no erythema was seen. A sterile dressingand short leg cast were applied and reapplied 3 weekslater. Final examination at 7 weeks showed complete res­olution of the fracture blisters and only a trace of residualedema. A short removable leg splint was applied, and thepatient tolerated gradual weight-bearing.

DISCUSSION

Fracture blisters may appear within a few days ofinjury! or as late as 3 weeks after trauma." Bullaformation is caused by impaired dermal and epider­mal nutrition with subsequent epidermal necrosis.

. This results from traumatic rupture of venousplexi,causing obstruction, hemorrhage, and arterialspasm.Theankleis particularlyvulnerabletotraumaresulting in skin breakdown , because of flatter epi­dermal papillae, sparse subcutaneous tissue, and ex­tensive arborizing veins. Fracture blisters rarely oc­cur with open fractures because the open wound

Page 2: Fracture blisters

1034 BriefcommunicationsJournal of the American Academy of Dermatology

June 1994

viewed by the orthopedic surgeon as an indication ofcompromised skin circulation and a relative con­traindication to immediate open reduction and in­ternal fixation.f Shelton and Anderson' noted thatalthough one or two blisters on an edematous anklemay appear harmless, they are "the tip of an icebergof diminished epidermal-dermal viability." Devel­opment of an infected fracture is the risk of operat­ing through damaged skin, and it may be necessaryto delay surgery for several weeks. 7 In a study of 121surgically treated closed ankle fractures, those inju­ries associated with fracture blisters or abrasions hadmore than twice the overall complication rate,including increased infections and other woundproblems.f It has also been noted that the develop­ment of fracture blisters in the vicinity of a supra­condylar fracture early in the course of treatmentmay portend impending Volkmann's ischemic con­tracture."

When a fracture with soft tissue injuries is beingtreated, it is critical to prevent the formation offracture blisters. The limb should be elevated andthe fracture reduced. Ifblisters occur, various treat­ment options exist. This could involve removing theroof of the blister and dressing the wound. Reepi­thelialization takes 6 to 21 days. Alternatively,superficial wound care may allow spontaneous heal­ing within 2 weeks. Open surgery is best avoidedduring this period, but closed manipulation can beattempted.' If a plaster cast is to be applied, evacu­ation of bullae and use of an antibiotic aerosol sprayto the area have been recommended before applica-

tion.!? Although many authors recommend com­pression to minimize edema and blood formation,impaired venous return and local perfusion defectsmay result. One author advises the use of compres­sion only immediately after injury before swellingoccurs.f Traction may be indicated in fractures withintraarticular extension complicated by blister for­mation.!'

REFERENCES

I. Russell TA. General principles of fracture treatment. In :Crenshaw AH, ed. Campbell's operative orthopaedics. StLouis: Mosby-Year Book, 1992:778.

2. Dabezies EJ, D'Ambrosia R. Fracture treatment for themultiply injured patient. Instr Course Lec t 1986;35: I3-21.

3. La1 GM, Bahn S. Delayed open reduction for supracondy­lar fractures of the humerus. Int Orthop 1991;15:189-91.

4. Conwell HE, Reynolds Fe, eds. Management of fractures,dislocations, and sprains. St Louis: CV Mosby, 1961:I 19­20.

5. Shelton ML, Anderson RL. Complications of fractures anddislocations of the ankle. In: Epps CH, ed. Complicationsand orthopedic surgery. Philadelphia: JB Lippincott, 1978:535-77.

6. Wilson IN, ed. Watson-Jones: fractures and joint injuries .Edinburgh: Churchill Livingstone, 1982:8.

7. Wilson IN, ed. Watson-Jones: fractures and joint injuries.Edinburgh: Churchill Livingstone, 1982:365.

8. Carragee EJ , CsongradiJJ, Bleck EE. Early complicationsin the operative treatment of ankle fractures: influence ofdelay before operation. J Bone Joint Surg [Br] 1991;73:79-82.

9. Hartman JT, ed . Fracture management: a practical ap­proach. Philadelphia: Lea & Febiger, 1978:169-70.

10. Wilson IN, ed. Watson-Jones: fractures and joint injuries.Edinburgh: Churchill Livingstone, 1982:294.

1[. Rockwood CA, Green DP , Bucholz RW, eds. Fractures inadults. Philadelphia: JB Lippincott, [991:1925-31.

Werner's syndrome associated with myelofibrosis

a chromosome instability disorder because it dis­plays multiple stable chromosome rearrangementsand, apparently to a lesser extent, chromosomebreakage. 1 Like other similar syndromes, WS is as­sociated with a high frequency of malignancy, pre­dominantly mesenchymal tumors.s 3 Salk4 reviewedcases of neoplasia in patients with WS and under­lined the absence ofprostatic and pancreatic cancers(common among elderly patients) and the high fre­quency of noncarcinomatous tumors. Three cases ofleukemia were also reported . Ten cases of WS havebeen documented in Sardinia, a prevalence of

From the Institute of Derm atology, University of Sassari"; Institute ofGeneral Biology and Med ical Genetics, University of Paviab;a nd theInstitute of Medical Pathology, University of S assari.?

Reprint requests: Francesca Cottoni, MD, Istituto di C!inica Derrnato-logica, Viale Mancini 5, 07100 Sass ari, Italy.

JAM ACAD DERMATOL 1994;30:1034-6.

Copyright @ 1994 by the American Ac ademy of Dermatology, [ncoOL 90-9622/94 $3.00 + 0 t6/54/52347

Francesca Cottoni, MD, a Susi Scapaticci, BD,b Rosanna Faedda, MD,c Elena Capra, BD,band Agostina Murgia, MDa Sassari, Italy

Werner's syndrome ( WS ) is a ra re autosomal re­cessive disease characterized by the precocious ap­pearance of many alterations that otherwise wouldappear only in old age. WS may also be classified as