Management of the Morel-Lavallée Lesion

Management of the Morel-Lavallée Lesion

Management of the More l- Lavalle´ e Le s i o n Dustin Greenhill, MD*, Christopher Haydel, MD, Saqib Rehman, MD KEYWORDS  Closed degloving injury  M...

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Management of the More l- Lavalle´ e Le s i o n Dustin Greenhill, MD*, Christopher Haydel, MD, Saqib Rehman, MD KEYWORDS  Closed degloving injury  Morel Lavalle´e lesion  Soft tissue injury  Hematoma  Sclerodesis

KEY POINTS    

Diagnosis of Morel-Lavalle´e lesions is often missed or delayed. The presence of a lesion over operative fractures increases the risk of postoperative infection. Advanced imaging may help determine the best methods of treatment. Treatment options include compression, aspiration, percutaneous or open surgical treatment, and sclerotherapy. Additionally, postoperative management plays an equal role in treatment success.  Specific treatment should be individualized for each patient based on a surgeon’s thorough understanding of Morel-Lavalle´e lesions.

In 1863, a French physician named Maurice MorelLavalle´e1 first described a unique posttraumatic fluid collection that developed in a patient who fell from a moving train. More than a century later, while Letournel and Judet2 compiled their wellknown series of acetabular fractures, they also witnessed the same characteristic lesions develop over the greater trochanter and named them Morel-Lavalle´e (ML) lesions. Such lesions have been described by other terms in the literature, such as ML effusion or hematoma, posttraumatic pseudocyst, posttraumatic soft tissue cyst, closed degloving injury, or chronic expanding hematoma.2,3 If a lesion occurs, it is almost always after direct trauma to the pelvis, thigh, or knee. A hypovascular suprafascial space develops in which fluid easily accumulates. Posttraumatic hematoma formation increases the risk of infection, and a unique combination of physical properties inhibits physiologic dead space closure.4 Such lesions are rare, and diagnosis is often delayed or missed. As a result, their natural history is

not yet clearly established. In a series of approximately 1100 consecutive pelvic fractures, Tseng and Tornetta5 reported that 19 (1.7%) patients developed ML lesions. However, the actual incidence is higher because lesions can occur without an underlying fracture and a small portion likely persist subclinically.6 Letournel and Judet2 published an incidence of 8.3% after trauma to the greater trochanter.2 Consequently, the true incidence is unknown. The current body of available literature consists entirely of case series composed of heterogeneous groups of patients. Therefore, no standard treatment algorithms exist. This article helps physicians understand the currently accepted surgical indications, techniques, and controversies when managing patients with an ML lesion.

CAUSE Individuals are at risk for developing an ML lesion after sustaining a significant blow or sudden shearing force to any area with strong underlying fascia, most often around the pelvis or lower

The authors have nothing to disclose. Department of Orthopaedic Surgery & Sports Medicine, Temple University Hospital, 3401 North Broad Street, Zone B 5th Floor, Philadelphia, PA 19140, USA * Corresponding author. E-mail address: [email protected] Orthop Clin N Am 47 (2016) 115–125 http://dx.doi.org/10.1016/j.ocl.2015.08.012 0030-5898/16/$ – see front matter Ó 2016 Elsevier Inc. All rights reserved.

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INTRODUCTION

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Greenhill et al limb. Motor vehicle collisions tend to be responsible for most of these lesions, and more than 50% are due to high-energy mechanisms.7,8 However, a low-energy mechanism does not rule out the possibility. ML lesions have been reported to occur after sports injuries or, very rarely, less violent mechanisms.9–11 The lower limb is involved in greater than 60% of cases, with most involving the greater trochanter.12 This area of the body is predisposed given the increased mobility of soft tissue, limited anterolateral perforator vessels to the subdermal vascular plexus originating from the lateral femoral circumflex vessels, subcutaneous nature of bone, and strength of the fascia lata as it attaches to the iliotibial band.13–15 A substantial number of these lesions will occur with underlying osseous fractures and injuries to other organ systems.14 Female sex and a body mass index of 25 or greater are proposed risk factors, presumably because of the increased fat in predisposed regions.12,16 However, more recent studies have brought these risk factors into question.8

Fig. 1. Clinical appearance of an ML lesion 7 days after the patient sustained a shearing force to the greater trochanter while snowboarding. After the initial injury, the patient resumed sporting activities until a discolored, fluctuant area developed 4 days later.

PATHOGENESIS As a result of violent shear, a thick layer of subcutaneous fat and skin is ripped from its underlying, firmly secured fascia. During this process, lymphatic channels and perforating vessels from underlying muscle are torn and release their contents into the newly created cavity. The fluid mixture now contains blood, fat, and necrotic debris within a relatively hypovascular space that is ill equipped to drain internally because of the intact underlying fascia. As lesions progress beyond the acute phase, blood is reabsorbed and replaced by serosanguineous and lymphatic fluid, which has low coagulation ability and high molecular weight.17 A sustained inflammatory reaction eventually leads to a cystic mass surrounded by a fibrous capsule that forms as a result of peripheral deposition of hemosiderin, granulation tissue, and fibrin.3,18 Exact timing of the aforementioned mechanisms is unknown, but MRI classifications detecting lesions in various phases suggest that lesions are altered with age.19

CLINICAL MANIFESTATIONS A large swollen bruised area whereby a hematoma develops in a delayed fashion should alert practitioners to the possibility of a closed degloving injury (Fig. 1). Clinical manifestations of ML lesions include soft tissue swelling with or without ecchymosis, skin contour asymmetry and hypermobility, and soft fluctuance with minimal or absent tenderness. Lesions can occur anywhere but are most

often located around the peritrochanteric or peripelvic region. Skin will often have decreased sensation and may appear dry, cracked, or discolored in more chronic lesions (Fig. 2). Lesions may not be apparent at the time of initial trauma. Either they are masked by more serious injuries or it takes some time for the hematoma to develop. Reported delays to diagnosis occur in approximately one-third of patients.12 Depending on the study, the average time to diagnosis ranges between 3 days and 2 weeks.8,12,20 Patients have even presented complaining of chronic contour deformities up to 13 years after injury.12 Because ML lesions are a result of trauma, they can present at any age. The youngest documented case was in a child aged 28 months.21 Those caring for pediatric trauma patients should be especially vigilant when managing soft tissue wounds given the decreased clarity with which children communicate their symptoms.

IMAGING Standard radiographs can confirm the presence of a soft tissue mass without calcifications.22 They can also be used to determine whether or not the lesion has underlying fractures, which may significantly affect further management. Ultrasound is useful as both a diagnostic and therapeutic modality. Neal and colleagues23 observed ultrasound characteristics in 21 ML lesions. Acute lesions are heterogeneous and lobular with irregular margins. Lesions older than 8 months

Management of the Morel-Lavalle´e Lesion (T2W) images. Days to weeks after injury, oxidation of iron within heme to its ferric state results in lesions appearing hyperintense on both T1W and T2W images. In more chronic lesions, a peripheral capsule containing hemosiderin appears hypointense on T1W and T2W images.25 Furthermore, fibrous septations and calcified fat nodules may be present within the lesion (Fig. 4).

CLASSIFICATION No standard classification system exists for ML lesions. Carlson and colleagues16 classified lesions as acute (<3 weeks old) or chronic (>3 weeks old). However, the choice of 3 weeks was arbitrary and not consistent with the remaining available literature. Multiple investigators have defined acute versus chronic based on the presence or absence of a capsule, and this method does have limited ability to guide treatment.26,27 Mellado and Bencardino19 created a classification based on MRI appearance, which does help determine the age of the lesion but has not been used to guide treatment. Fig. 2. Clinical appearance of a chronic ML lesion. This 16-year-old boy first presented as an outpatient with a painless slow-growing mass 3 months after sustaining a blow to his inner thigh on the handlebar of a motocross bike.

are homogeneous and flat. Lesions greater than 18 months old have smooth margins. All lesions were compressible and none had vascularity. All lesions were either hypoechoic or anechoic, and there was no relationship between echogenicity and age. This finding was presumed to be a result of repeat hemorrhage or fatty remnants. However, fat can appear as hyperechoic nodules.24 Computed tomography is often obtained in trauma patients with ML lesions. Lesions are often differentiated from hematomas by fluid-fluid levels due to sedimentation of blood components.24 Lesions less than 1 month old will have irregular margins (Fig. 3). More chronic lesions will be homogenous and have smooth margins, and a capsule may be appreciated.21 The average Hounsfield unit for a hematoma is 75, whereas it is 17 for an ML lesion.17 MRI is considered the preferred method of imaging to determine lesion characteristics and chronicity.18 Findings correlate with classic hemorrhage and magnetic properties of blood breakdown products. Within hours of injury, oxygen-rich hemoglobin yields a homogeneous collection that is hypointense on T1-weighted (T1W) images and hyperintense on T2-weighted

DIFFERENTIAL DIAGNOSIS An extensive list of differential diagnoses exists for ML lesions, especially when they present as chronic lesions with an unclear cause. MRI and physical exam can be used to differentiate almost all confounding diagnoses. Abscess, contusion, or hematoma can be differentiated from ML lesions based on tenderness, firmness, cutaneous sensation, and the condition of the overlying skin. Contusions will have increased skin tension and less fluctuance.9 In the knee, ML lesions have been misdiagnosed as prepatellar bursitis for as long as 7 months.28 Extension of fluctuance beyond the anatomic boundaries of the prepatellar bursa is the main distinguishing characteristics of ML lesions of the knee. Prepatellar bursae have been shown to terminate before the midthigh proximally and before the midcoronal plane medially and laterally.9 Furthermore, ML lesions (as opposed to prepatellar bursitis) do not respond to steroid injections because they lack a synovial lining.3 ML lesions may also be easily mistaken for soft tissue tumors, especially when they present in the subacute to chronic phase as a painless slow-growing mass. MRI can distinguish benign lesions from sarcomas if contrast reveals internal enhancement of the tumor.18

PRINCIPLES OF MANAGEMENT There is currently no universally accepted treatment algorithm for the management of ML lesions.

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Greenhill et al Fig. 3. Computed tomography scan obtained during an initial trauma evaluation identified an acute ML lesion of the right medial thigh. This patient also sustained severe visceral injuries, a closed acetabular fracture, and an open tibia fracture.

However, the available literature does establish the following guidelines. For acute lesions, some form of treatment should be initiated as early as possible. Benign neglect of an acute lesion may predispose patients to develop a chronic hematoma without any reduction in dead space. Theoretically, this further compromises the blood supply to the skin and increases the likelihood of recurrence. Furthermore, hematoma formation in polytrauma patients predisposes the wound to bacterial colonization.29 In lesions overlying a planned surgical approach to displaced fractures, the potential for bacterial colonization justifies prophylactic surgical debridement. Uncomplicated subacute or chronic lesions should undergo imaging in order to determine the extent and characteristics of the lesion. Presence of a fibrous capsule implies that the lesion will likely recur without surgical intervention. Absolute indications for surgical intervention include deep infection, severe skin necrosis, or association of a lesion with an open fracture. Relative indications for surgical management include unsuccessful nonsurgical treatment, symptomatic lesions, and those overlying a planned surgical approach for acute fixation of a closed fracture.

Conservative management options include compression dressings and aspiration. Surgical options include debridement of necrotic material through either small percutaneous or large open incisions. Large incisions were originally recommended in order to adequately debride necrotic components. They improve visualization and allow intraoperative dead space closure at the risk of further impairing subdermal vascularity. Furthermore, they allow complete capsular resection in more chronic lesions. More recently, less invasive treatment has been described with superior outcomes. The decision to perform less invasive treatment depends on several factors to include lesion characteristics, approach to underlying fractures, and need for capsular resection. Adjuncts to surgical debridement include sclerodesis and drain placement. Investigators have used the aforementioned treatment options in various combinations. A thorough understanding of lesion pathophysiology and specific lesion characteristics (such as acuity, location, size, symptoms, and absence or presence of underlying operative fracture) will allow surgeons to individualize treatment plans. Fig. 5 provides the authors’ recommended treatment

Fig. 4. (A, B) Short tau inversion recovery sequence MRI depicting a chronic ML lesion measuring 8.2  6.8  3.2 cm with characteristic internal septations, calcified fat globules, and a fibrous capsule. (C) T2weighted fast spin echo sequence MRI depicting an ML lesion in the gluteal region in a patient who presented 3 years after initial injury with a painless contour deformity.

Management of the Morel-Lavalle´e Lesion

Fig. 5. Recommended treatment algorithm.

algorithm based on a thorough review of the literature.

PREOPERATIVE PLANNING Timing of definitive fixation for fractures with associated ML lesions is an important aspect of preoperative planning. Both immediate and staged treatment have been described with varied success. Investigators uniformly agree that surgical debridement before internal fixation is necessary to avoid postoperative hematoma.2,4 Additionally, the increased prevalence of bacterial colonization in acute lesions among trauma patients may indicate staged treatment. In opposition, fractures that undergo delayed open reduction are at risk for increased operative time, blood loss, and difficulty obtaining anatomic reduction. Whether or not to delay definitive fixation should depend on the factors discussed earlier. Also, external fixator pins through the lesion should be avoided if possible.30 Hak and colleagues6 treated 15 pelvic fractures at the time of initial debridement with concerning results, but this may have resulted from incisions being left open to heal by secondary intention. By contrast, Carlson and colleagues16 emphasized strict dead space closure during initial debridement while performing fracture osteosynthesis directly through 6 lesions and had no postoperative infections. These investigators warned that any signs of clinical infection during the index procedure should warrant staged treatment. Tseng and Tornetta5 delayed definitive fixation until 24 hours after drain removal following percutaneous debridement with excellent results. Surgeons should use their best clinical judgment when scheduling definitive fixation of underlying fractures.

CONSERVATIVE TREATMENT Nonoperative treatment methods mainly consist of compression bandaging with or without fluid aspiration. In general, investigators suggest that small lesions are more amenable to conservative treatment methods.28,31 Conservative management was estimated by Shen and colleagues27 to be successful less than 50% of the time, but this statistic may actually be much higher or lower depending on lesion characteristics. Compression bandaging is a well-documented, necessary adjunct to both conservative and postsurgical treatment in order to allow fibrous adhesions within the preexisting lesion. As expected, its efficacy may depend on lesion location. Among 13 lesions identified in a systematic review that were treated conservatively, all those not receiving compression failed conservative measures, whereas 62.5% of those receiving compression healed successfully.27 Harma and colleagues31 reported 5 acute lesions of which 4 healed with conservative management alone after an average of 6.8  3.96 weeks. Those investigators did not mention the size of the lesions and only aspirated one of them. Parra and colleagues7 treated 2 out of 3 large thigh lesions successfully with compression alone. Multiple investigators have attributed their treatment failures to inadequate compression bandaging.12,31 Risk of iatrogenic inoculation via simple aspiration is also a common concern given the increased prevalence of these closed lesions to be culture positive. However, data from some of the larger case series suggest that aspiration under sterile conditions carries an acceptable risk and should be performed when indicated. Among

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Greenhill et al the reported cases of sclerodesis, almost all included patients had at least one aspiration without developing infection.18,32 The 16 patients reported by Bansal and colleagues33 averaged 3.4 aspirations before doxycycline sclerodesis within at least a 6-month period and remained free of infection. Zero of 13 uncomplicated knee lesions averaged 2.7 aspiration attempts without any subsequent infections.9 In a series of 87 lesions whereby 25 underwent simple aspiration, there was one infection in the aspiration group.8 This finding was not statistically different than the nonoperative and operative group infection rates. One case report describes the clinical course of a patient who underwent 10 aspirations over a 7-month period without developing infection.28 Another case report describes a patient who underwent multiple repeated aspirations for 10 months without developing infection.34

SURGICAL TREATMENT: TECHNIQUES AND OUTCOMES Open Debridement In 1976, Ronceray26 described the first formal open surgical technique aimed at preventing lesion recurrence whereby aponeurotic fenestrations were created deep to the lesion in order to allow internal drainage and healing. This method was primarily applied to abdominal lesions, and the results with respect to injured extremities are not reported. Coulibaly and colleagues35 reported success rates with this method as low as 40%. Currently described open treatment includes a longitudinal incision across the lesion along a palpable midpoint, removal of necrotic fat, irrigation and debridement of the deep fascial layer (using a plastic brush or electrocautery scratch pad) to encourage revascularization, and dead space closure by sealing healthy fat to fascia with an absorbable suture. If the lesion is chronic and a capsule is present, complete removal of the fibrous capsular tissue should be performed (Fig. 6). Additionally, a sclerosing agent may be added at the surgeon’s discretion. Outcomes after open treatment have been reported with variable results. In a landmark article, Hak and colleagues6 emphasized the challenges of managing an ML lesion over a fractured pelvis. In hopes of preventing hematoma formation over a planned surgical approach, closed degloving lesions in 24 hospitalized polytrauma patients were treated with open surgical debridement before or during internal fixation of pelvic fractures. The duration between injury and initial debridement averaged 13.1 days (range 2–60 days). Fascia was closed but the

Fig. 6. Specimens obtained during open capsular resection of a chronic ML lesion. The pathology report confirmed fragments of nodular, benign adipose tissue with necrosis, fibrin, and chronic inflammation.

degloved portion was left open to drain and heal by secondary intention. Intraoperative fluid from 11 lesions (46%) yielded positive cultures, although patients did not necessarily exhibit symptoms of infection. Culture results did not correlate with the time between injury and surgical debridement. All wounds eventually healed, but the postoperative course for some patients was alarming. Three patients developed deep bone infections; 2 patients required split-thickness skin grafting; one patient developed a chronic soft tissue infection that needed a posterior thigh flap; 2 patients underwent elective cosmetic surgery after their wounds healed. The aforementioned outcomes led to subsequent modifications of open surgical technique to encourage meticulous dead space closure by sealing healthy fat to fascia with an absorbable suture.16,36 If minimal fat remains after debridement, a nonabsorbable suture can be used to join the skin and fascia. Carlson and colleagues16 reported zero postoperative infections in their series of 24 lesions treated with open debridement and dead space closure. It is presumed that circulating bacteria in polytrauma patients predisposed acute lesions to have positive cultures. Most patients in the series reported by Hak and colleagues6 had significant injuries to include 4 open pelvic fractures, numerous visceral organ injuries, and injuries to the peripheral and central nervous system. Of note, only 2 of 9 lesions in this series cultured after 2 weeks had positive cultures. Therefore, clinicians should interpret the aforementioned results with respect to the acuity of the lesion and the trauma patient population that was studied. The likelihood of bacterial colonization in an isolated closed wound may not be as high as that of acutely injured patients with polytrauma. Carlson

Management of the Morel-Lavalle´e Lesion and colleagues16 included details for 13 of 14 closed degloving injuries of which zero were clinically infected before initial debridement. Furthermore, Bansal and colleagues33 cultured fluid from 16 chronic lesions after excluding those with prior surgery or underlying fractures. None of their lesions produced positive cultures.

Limited Incision Concerns about infection risk and flap survival following open treatment led to the description of minimally invasive techniques as the current gold standard for appropriate lesions. The first mention in the English literature that specifically addressed treatment of closed degloving injuries via a limited incision occurred in 1991. Hudson12 reported 16 patients who underwent irrigation and debridement through a small incision, appropriately sized to allow evacuation of necrotic products. If displaced fat created a contour deformity, the incision was extended across the entire lesion. All lesions healed successfully except one extensive gluteal lesion over a fractured pelvis in which compression could not be maintained. No lesions within their series occurred over a displaced fracture. In order to address the treatment of acute lesions over displaced pelvic fractures, Tseng and Tornetta5 described a new technique using small percutaneous incisions. They reported encouraging results among a series of 19 consecutive patients. Their technique included irrigation and drainage of hematoma through two small 2-cm incisions (one each at the proximal and distal extent of the lesion). The proximal incision was placed posterosuperiorly to ensure the entire cavity was influenced. A plastic brush was used to debride necrotic fat before the lesion was again irrigated with pulse lavage until exiting fluid was clear. Finally, a suction drain was left within the lesion until output was less than 30 mL per day. Intravenous antibiotics were discontinued 24 hours after drain removal. All lesions were debrided within 3 days of injury, and drain removal took place between 3 and 8 days after debridement. The injury profile of these polytrauma patients was similar to that of the series reported by Hak and colleagues.6 However, only 3 of 16 (19%) of patients had positive fluid cultures at the time of initial debridement. Fifteen patients underwent surgical fixation of displaced pelvic or acetabular fractures. Percutaneous fixation of the posterior pelvic ring was performed immediately following initial debridement (during the same procedure) in 7 patients. One of these patients had a positive fluid culture but no

sequelae. Open reduction and internal fixation in the remaining 8 patients was delayed until 24 hours after drain removal. Three open reductions were performed directly through the lesion without infectious complications. Subsequent investigators have reproduced similar satisfactory results after percutaneous debridement. Zhong and colleagues20 performed the procedure described by Tseng and Tornetta5 on 8 lesions after an average time to diagnosis of 11.9 days. Lesions healed in an average time of 3.25 weeks after debridement without recurrence or infection, although 2 patients required skin grafting for associated flap necrosis. Additionally, Matava and colleagues37 performed the aforementioned procedure on an extensive peritrochanteric lesion whereby 500 mL of fluid was aspirated. The patient returned to playing professional football without recurrence 22 days after debridement.

Sclerodesis Introduction of various sclerosing agents into more chronic lesions has been successfully described as an adjunct to percutaneous surgical treatment. A systematic review reports a success rate for percutaneous sclerodesis of chronic lesions to be 95.7%.27 Once inside the lesion, sclerosing agents activate an inflammatory cascade that encourages scar formation and fusion of subdermal membranes. Especially in the presence of a chronic or recurring lesion, sclerodesis potentially avoids the need for a more extensive and painful surgical incision wide enough to allow capsular resection and dead space closure. If necessary, sclerodesis can be repeated and does not interfere with future surgical options. The concept of injecting a sclerosing agent into an ML lesion was derived from its application in malignant pleural effusions, whereby talc and doxycycline are commonly used.38 In 2006, Luria and colleagues17 were the first to use sclerodesis in 4 ML lesions that failed prior aspiration. After defining the cavity with contrast fluid under fluoroscopic guidance, they evacuated all contents and instilled 5 g of sterile talc diluted in 50 mL sterile saline, removed the mixture after 5 minutes, and left a drain in until the output was less than 30 mL per day. Three patients had drains removed after 1 week and enjoyed an uncomplicated postprocedural course. One patient with a nonoperative pelvic fracture and bilateral lesions developed subsequent infection treated with only antibiotics and simple drainage. In 2013, Bansal and colleagues33 reported their results after using doxycycline as a sclerosing

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Greenhill et al agent in 16 chronic lesions. All lesions were present more than 6 months and failed prior intervention. They inserted 21-gauge needles into the proximal and distal extent of the lesion, drained all fluid from the cavity, instilled 500 mg of doxycycline powder (obtained from 100-mg capsules and mixed with 25 mL of saline solution), had the patients maneuver themselves once every 10 minutes for 1 hour, aspirated the mixture, then applied a compression dressing for 4 weeks. No drains were used. The average volume aspirated was 387 mL (range 150–700 mL). All lesions resolved without recurrence in an average time of 5 weeks and were followed for more than 2 years. Subsequent investigators have also described their use of doxycycline for recurrent lesions with similar success.9 Other sclerosing agents proposed for use include alcohol, bleomycin, and tetracycline. Penaud and colleagues32 described 5 chronic lesions treated with pure ethanol, all of which had confirmation of a capsule via MRI. Postprocedural imaging 6 months later confirmed complete absence of a capsule in 4 patients and a small asymptomatic cavity in one patient. Bleomycin has been used in malignant pleural and pericardial effusions but is less popular because of higher costs.39 The low postoperative infection rates after sclerodesis have been anecdotally attributed to the antibacterial effects of sclerosing agents.

POSTOPERATIVE CARE Drains are almost universally described as part of all surgical procedures. In general, surgeons leave them in until the output is less than 30 mL per day. Postoperative drains were generally removed within 1 week for acute lesions and up to several weeks for more chronic lesions.5,6,16,17,20 Compression is also of utmost importance, and investigators have directly blamed its absence for treatment failure.33 For patients with acute lesions managed as inpatients, antibiotics were also used until 24 hours after drain removal.5,16

COMPLICATIONS Postoperative Infection Treating displaced fractures through ML lesions at the time of initial debridement may increase the risk of infection. The study by Hak and colleagues,6 whereby 46% of closed lesions were culture positive during initial debridement, made the orthopedic community distressingly aware of the potential disaster that might exist within these lesions. Fifteen of 24 patients underwent open reduction and internal fixation at the time of initial

debridement, after which the skin was left to heal by secondary intention. Three patients subsequently developed deep bone infections, and several others had wound complications. There is further concerning evidence that acute ML lesions harbor infectious potential if opened. In a series of 20 patients with vertically unstable sacral fractures, 2 of 5 patients with ML lesions became infected postoperatively. However, none of the 15 patients without an ML lesion developed a postoperative infection.40 In a case series of 4 patients with spinopelvic dissociation and lesions overlying the approach used for internal fixation, 2 patients developed postoperative infections and one patient developed skin necrosis that led to infection and extensive soft tissue reconstruction.41 Most literature highlights the potential risk of bacterial colonization within planned surgical incisions for underlying displaced fractures. However, this risk is not to be confused with that of nonoperative or surgically decompressed lesions. In the series of 19 patients by Tseng and Tornetta,5 internal fixation was delayed until 24 hours after percutaneous debridement and no patients developed postoperative infections. In 2007, Carlson and colleagues16 highlighted 6 fractures treated directly through ML lesions after thorough debridement and meticulous dead space closure with no subsequent infections. When sclerodesis is used, the infection risk seems to be low. Doxycycline sclerodesis in 16 patients and alcohol sclerodesis in 5 patients did not result in any postoperative infections.32,33 Talc sclerodesis in 5 lesions led to one postoperative infection.17 Conservative management via aspiration and compression dressings in 4 patients by Harma and colleagues31 led to one sacral ulcer that became infected. In a systematic review by Shen and colleagues,27 almost all postoperative infections were managed with antibiotics alone. In summary, surgeons should not allow the risk of bacterial colonization in trauma patients to prohibit appropriately staged surgical debridement when necessary.

Recurrence Lesion recurrence is a primary concern when treating ML lesions. It is thought to occur because of the decreased capability of lesions to evacuate fluid combined, the persistent introduction of blood and lymph, and squamous cells within a more chronic lesion’s serosal lining.17 Persistent fluid collection is a cosmetic and symptomatic nuisance for patients; allows time for a pseudocapsule to develop, thus, making definitive treatment more detailed; and places the overlying soft tissue at

Management of the Morel-Lavalle´e Lesion risk for ulceration and subsequent infection. Methods used to prevent recurrence aim to enhance fluid drainage and close dead space. Recurrence rates are different with regard to conservative versus operative management. Actual rates of lesion recurrence are unknown. A recent systematic review reports that open treatment exhibited a 4.2% rate of recurrence, whereas less invasive drainage yielded a recurrence rate of 17.4%; but those figures had no statistically significant difference.27 Given the widely heterogeneous lesion characteristics within the available literature, it is difficult to determine which lesions have the highest risk of recurrence. The most obvious risk factor for recurrence is the presence of a fibrous capsule. After simple aspiration of an encapsulated lesion, fluid collections are almost guaranteed to recur without capsular resection or sclerodesis. Lesion location has also been suggested as a risk factor for recurrence, as compression bandaging around the hip or buttock region is more difficult to maintain than around the knee and distal thigh.33 Surgical technique similarly affects recurrence rates. For example, among the 24 patients reported by Carlson and colleagues16 in which meticulous dead space closure was a main priority, zero lesions recurred. Lesion size may be a risk factor for recurrence after conservative treatment, and some investigators even modify their surgical indications based on this belief. However, establishing a numerical cutoff value to differentiate small from large lesions is controversial. Ronceray26 suggested in 1976 that small lesions are more amenable to conservative treatment, whereas operative management should be considered for larger lesions. Nonetheless, he did not define what constitutes a small versus large lesion. Nickerson and colleagues8 retrospectively reviewed their treatment of 87 lesions and recommended that aspirating more than 50 mL indicates operative intervention because of a statistically higher risk of recurrence. Several statistical flaws confound their conclusion. First, the aspiration group in this study consisted of 25 patients with significantly larger lesions (P 5 .006) and longer diagnostic delays (P 5 .001) than the operatively treated group. Secondly, aspirated lesions were not categorized by location. This point is important because subsequent compression therapy in certain locations, such as the gluteal folds, is more difficult to maintain. Lastly, 75% of the lesions that recurred after aspiration were a result of highenergy trauma. These confounders suggest that other factors may have been responsible for the increased rate of recurrence noted in lesions whereby an initial aspiration yielded greater than 50 mL of fluid. Tejwani and colleagues9 reported

good results after 27 knee lesions were treated with nonoperative measures. Their reported aspirated quantities were relatively low compared with other studies, averaging between 46 and 77 mL (range 12–300 mL).

Skin Necrosis Soft tissue compromise remains a concern before and after operative management. Limited blood supply to the skin during hematoma formation, combined with increased mechanical friction and shear, predispose these lesions to ulceration and subsequent skin necrosis or infection. Operative intervention with larger incisions may place the skin at more risk for necrosis than less invasive techniques.5 Skin necrosis should be subsequently managed with further debridement and skin grafting or soft tissue flaps as necessary.

Contour Deformity Displacement of fat during the initial injury often leads to asymptomatic, asymmetric, and nonfluctuant displacement of the skin when compared with the contralateral extremity.3 This displacement is primarily a cosmetic concern. Slight skin hypermobility may also be present. By contrast, sclerodesis of chronic lesions leads to skin immobility in a subset of patients that is only symptomatic during persistent high-level athletic activity.9,33

SUMMARY ML lesions represent a serious soft tissue injury, although their diagnosis is often missed or delayed. These lesions are known to be associated with high rates of recurrence, skin necrosis, and infection. In the case of underlying pelvic fractures, lesions have the ability to create treacherous outcomes after open treatment of underlying displaced fractures. Clinicians should remain suspicious when managing patients after shearing injuries or direct blows to the greater trochanter. Early recognition and optimal management can save patients from undesirable morbidity and consequent need for more complex surgical management.

ACKNOWLEDGMENTS We wish to thank Dr. Alison Gattuso, St. Christopher’s Hospital for Children, Philadelphia, PA for her contributions to this article.

REFERENCES 1. Morel-Lavallee M. Decollements traumatiques de la peau et des couches sous-jacentes. Arch Gen Med 1863;1:20–38, 172-200, 300-332.

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Greenhill et al 2. Letournel E, Judet R. Fractures of the acetabulum. 2nd edition. Berlin: Springer; 1993. 3. Li H, Zhang F, Lei G. Morel-Lavallee lesion. Chin Med J (Engl) 2014;127(7):1351–6. 4. Helfet DL, Schmeling GJ. Complications. In: Tile M, editor. Fractures of the pelvis and acetabulum. 2nd edition. Baltimore (MD): Williams and Wilkins; 1995. p. 451–67. 5. Tseng S, Tornetta P. Percutaneous management of Morel-Lavallee lesions. J Bone Joint Surg Am 2006;88(1):92–6. 6. Hak DJ, Olson SA, Matta JM. Diagnosis and management of closed internal degloving injuries associated with pelvic and acetabular fractures: the Morel-Lavalle´e lesion. J Trauma 1997;42(6): 1046–51. 7. Parra JA, Fernandez MA, Encinas B, et al. MorelLavalle´e effusions in the thigh. Skeletal Radiol 1997;26(4):239–41. 8. Nickerson TP, Zielinski MD, Jenkins DH, et al. The Mayo Clinic experience with Morel-Lavalle´e lesions: establishment of a practice management guideline. J Trauma Acute Care Surg 2014;76(2): 493–7. 9. Tejwani SG, Cohen SB, Bradley JP. Management of Morel-Lavallee lesion of the knee: twenty-seven cases in the national football league. Am J Sports Med 2007;35(7):1162–7. 10. Moriarty JM, Borrero CG, Kavanagh EC. A rare cause of calf swelling: the Morel–Lavallee lesion. Ir J Med Sci 2011;180(1):265–8. 11. Van Gennip S, Van Bokhoven SC, Van den Eede E. Pain at the knee: the Morel-Lavalle´e lesion, a case series. Clin J Sport Med 2012;22(2):163–6. 12. Hudson DA. Missed closed degloving injuries: late presentation as a contour deformity. Plast Reconstr Surg 1996;98(2):334–7. 13. Cormack GC, Lamberty BG. The blood supply of thigh skin. Plast Reconstr Surg 1985;75(3): 342–54. 14. Kottmeier SA, Wilson SC, Born CT, et al. Surgical management of soft tissue lesions associated with pelvic ring injury. Clin Orthop Relat Res 1996;(329):46–53. 15. Dawre S, Lamba S, Sreekar H, et al. The MorelLavallee lesion: a review and a proposed algorithmic approach. Eur J Plast Surg 2012;35:489–94. 16. Carlson DA, Simmons J, Sando W, et al. MorelLavale´e lesions treated with debridement and meticulous dead space closure: surgical technique. J Orthop Trauma 2007;21(2):140–4. 17. Luria S, Applbaum Y, Weil Y, et al. Talc sclerodhesis of persistent Morel-Lavalle´e lesions (posttraumatic pseudocysts): case report of 4 patients. J Orthop Trauma 2006;20(6):435–8. 18. Bonilla-Yoon I, Masih S, Patel DB, et al. The Morel-Lavalle´e lesion: pathophysiology, clinical presentation,

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