Morel-Lavallée lesions are closed degloving injuries sustained during violent soft tissue shear that separate the subdermal fat from its strong underlying fascia. Lesions most often occur in the peritrochanteric region, and patients may have concomitant polytrauma. As a result, a hematoma develops that has a high rate of acute bacterial colonization and chronic recurrence. Conservative treatment outcomes are best for those managed acutely. However, diagnosis is often delayed or missed. Furthermore, there is no universally accepted treatment algorithm. Diagnosis and treatment depend on a surgeon’s thorough understanding of the cause, pathophysiology, imaging characteristics, and treatment options of Morel-Lavallée lesions.
Key points
- •
Diagnosis of Morel-Lavallée 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-Lavallée lesions.
Introduction
In 1863, a French physician named Maurice Morel-Lavallée 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 Judet compiled their well-known series of acetabular fractures, they also witnessed the same characteristic lesions develop over the greater trochanter and named them Morel-Lavallée (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. 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.
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 Tornetta 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. Letournel and Judet published an incidence of 8.3% after trauma to the greater trochanter. 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.
Introduction
In 1863, a French physician named Maurice Morel-Lavallée 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 Judet compiled their well-known series of acetabular fractures, they also witnessed the same characteristic lesions develop over the greater trochanter and named them Morel-Lavallée (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. 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.
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 Tornetta 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. Letournel and Judet published an incidence of 8.3% after trauma to the greater trochanter. 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 limb. Motor vehicle collisions tend to be responsible for most of these lesions, and more than 50% are due to high-energy mechanisms. 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. The lower limb is involved in greater than 60% of cases, with most involving the greater trochanter. 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. A substantial number of these lesions will occur with underlying osseous fractures and injuries to other organ systems. Female sex and a body mass index of 25 or greater are proposed risk factors, presumably because of the increased fat in predisposed regions. However, more recent studies have brought these risk factors into question.
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. 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. Exact timing of the aforementioned mechanisms is unknown, but MRI classifications detecting lesions in various phases suggest that lesions are altered with age.
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. Depending on the study, the average time to diagnosis ranges between 3 days and 2 weeks. Patients have even presented complaining of chronic contour deformities up to 13 years after injury. 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. 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. 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 colleagues observed ultrasound characteristics in 21 ML lesions. Acute lesions are heterogeneous and lobular with irregular margins. Lesions older than 8 months 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.
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. 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. The average Hounsfield unit for a hematoma is 75, whereas it is 17 for an ML lesion.
MRI is considered the preferred method of imaging to determine lesion characteristics and chronicity. 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 (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. 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 colleagues 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. Mellado and Bencardino created a classification based on MRI appearance, which does help determine the age of the lesion but has not been used to guide treatment.
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. In the knee, ML lesions have been misdiagnosed as prepatellar bursitis for as long as 7 months. 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. Furthermore, ML lesions (as opposed to prepatellar bursitis) do not respond to steroid injections because they lack a synovial lining. 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.
Principles of management
There is currently no universally accepted treatment algorithm for the management of ML lesions. 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. 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 algorithm based on a thorough review of the literature.
Related posts:
Diagnosis of Periprosthetic Infection
Going Out with a Bang
Congenital Anomalies of the Hand—Principles of Management
Robotically Assisted Unicompartmental Knee Arthroplasty with a Handheld Image-Free Sculpting Tool
Congenital Anomalies of the Hand—Principles of Management
Scapholunate Advanced Collapse
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
