Introduction
Morel-Lavallée (ML) lesions occur when deforming forces of pressure and shear lead to an internal degloving injury. This injury involves the stripping of subcutaneous tissue from the deep fascia, causing hemolymphatic accumulation in dead space [1,2]. While acute ML lesions are often managed successfully with conservative compression therapy, severe disruption of the perforating blood vessels can result in delayed and localized complications within the subcutaneous layer [2]. If initial serosanguinous fluid collections are not properly evacuated, the persistent fluid can act as a chronic irritant. This localized vascular insufficiency, caused by the initial trauma and compounded by sustained inflammation, plays a key role in the development of delayed necrotic changes [3,4]. As a result, nodular cystic fat necrosis (NCFN) and encapsulated oil cysts may arise as rare, yet significant, consequences of these chronic ischemic events [3,5]. Clinically, these delayed lesions often present as palpable masses or noticeable contour deformities, which can pose a diagnostic challenge and typically require definitive surgical intervention [1,5].
In this report, we discuss a rare case of delayed NCFN and calcified oil cysts that developed from a conservatively treated ML lesion. We emphasize the macroscopic pathological findings, the value of ultrasonographic diagnostics, and the clinical benefits of appropriate surgical excision for optimal reconstruction. This case report was approved by the Institutional Review Board of Daejeon Eulji Medical Center (IRB No. 2026-03-004). Written informed consent was obtained from the patient for the publication of this report and any accompanying images, ensuring the protection of the patient’s human rights.
Case
A 35-year-old female patient presented to our clinic with a progressively bulging mass and an adjacent depressed scar on her left posterior proximal thigh, just below the gluteal fold. One year earlier, she had sustained a degloving injury in a motor vehicle accident, which was diagnosed as an ML lesion with no associated fractures. At that time, the patient underwent successful treatment with conservative compression therapy. Upon re-presentation to our clinic 1 year after the initial injury, physical examination revealed a localized, firm contour deformity measuring approximately 15.0×7.0 cm (Fig. 1). Ultrasound imaging exhibited multifocal hypoechoic lesions with prominent hyperechoic rims located in the deep subcutaneous layer, highly suggestive of chronic encapsulated fat necrosis (Fig. 2). The two largest fat necrosis lesions measured approximately 4.7×3.2 cm and 3.8×2.5 cm, respectively. Additionally, several calcified oil cysts ranging from 0.5×0.6 cm to 0.8×0.6 cm were observed (Fig. 2).
Surgical exploration revealed multiple discrete, firm masses embedded within the deep subcutaneous tissue and adherent to the underlying peripheral fascia (Fig. 3). Following meticulous en bloc excision, macroscopic examination yielded improved characterization of these specimens, identifying several smooth, pearl-like encapsulated oil cysts alongside irregular, yellowish nodules of NCFN surrounded by dense, calcified capsules (Fig. 4). Subsequent histopathological examination revealed anuclear adipocytes, lipid-filled macrophages, and multinucleated giant cells characteristic of fat necrosis, alongside focal areas of dystrophic calcification indicating chronic tissue ischemia. Additionally, a pseudocyst with mild chronic inflammation and thick collagenous fibrosis was observed, definitively confirming the diagnosis.
Fig. 1
Preoperative clinical photograph. The image reveals a bulging mass accompanied by an adjacent depressed scar on the left posterior proximal thigh, resulting in a noticeable contour deformity.
Fig. 2
Ultrasonographic findings. Multifocal hypoechoic cystic structures with distinct hyperechoic rims in the deep subcutaneous layer are visible, which are characteristic of encapsulated fat necrosis (yellow arrows). Discrete calcified oil cysts are also noted (red asterisks).
Fig. 3
Intraoperative photograph. The intraoperative image displays the gross appearance of the nodular cystic fat necrosis and encapsulated masses, which are firmly attached to the deep peripheral fascia during surgical exploration.
Fig. 4
Macroscopic gross specimens. The excised masses exhibit distinct pathological features, including completely encapsulated oil cysts (red asterisk) and areas of dense calcification surrounding the fat necrosis (yellow arrows).
Given the dense and calcified nature of the fibrous capsule, simple drainage was considered insufficient. Therefore, complete en bloc excision was performed to resect all masses entirely with their intact capsules. To obliterate the extensive dead space resulting from the excision, multiple layers of progressive-tension quilting sutures were meticulously placed to anchor the subcutaneous tissue flap to the underlying deep fascia, minimizing shear forces. This was followed by the insertion of a Penrose drain and primary repair of the dermal layers to resolve the contour deformity and correct the depressed scar (Fig. 5). Despite appropriate placement of the surgical drain, a seroma with an initial aspiration volume of 60 mL developed at the surgical site following drain removal. This is a recognized sequela owing to the persistent dead space inherent to the excision of chronic ML lesions. The seroma was successfully managed through a conservative approach, completely resolving after 2 months of serial aspirations performed at 2-week intervals, combined with intralesional injections of triamcinolone acetonide (40 mg) and sustained compressive dressings using elastic bandages, without the need for additional interventions. The patient experienced an otherwise uneventful recovery with optimal aesthetic results and no recurrence at the 6-month follow-up (Fig. 6).
Discussion
The pathophysiology of delayed fat necrosis following a degloving injury is primarily caused by the initial damage to perforating vessels [1,2]. This severe local trauma leads to a prolonged ischemic environment, which progresses through an inflammatory phase and ultimately results in fibrosis, NCFN, and lipid cyst formation [3,4]. Over time, these unresolved cysts can trigger chronic granulomatous reactions and distinctive calcification, as observed in our macroscopic surgical specimens [3,6]. Ultrasound plays a crucial role in diagnosing such delayed subcutaneous changes [7]. Classical ultrasound imaging reveals anechoic cystic structures containing mobile echogenic foci [3,7]. Furthermore, lipid cysts demonstrate a unique radiological progression [6]. These lesions most often present with a pathognomonic appearance: a lucent center surrounded by a smooth, thin rim [6]. In delayed presentations, the chronic inflammatory response gradually causes the rim to calcify [6].
Surgically, while small asymptomatic fat necrosis may be observed, symptomatic lesions causing aesthetic deformities often necessitate further intervention [5,8]. The macroscopic findings in our case—specifically, the thick, calcified capsule surrounding the oil cysts and necrotic fat nodules—suggest that prolonged conservative approaches or simple aspiration may be insufficient in the chronic stage [3,9]. Therefore, we propose that the identification of a distinct hyperechoic calcified rim on ultrasound can serve as a useful clinical indicator to consider surgical intervention. In such advanced stages, complete surgical removal of the calcified cysts, along with their intact fibrotic capsule, is an effective method to eradicate the chronic inflammatory source, prevent recurrence, and facilitate optimal soft-tissue remodeling [5,9].
Meticulous obliteration of the dead space and precise primary repair subsequently allow for adequate soft tissue remodeling and complete contour restoration [8,10]. However, managing the extensive dead space remains a clinical challenge, often leading to postoperative recurrent seroma formation [1,11]. Our case demonstrates that even with meticulous dead space obliteration and the intraoperative placement of a Penrose drain, the profound disruption of subcutaneous architecture can still result in fluid accumulation after the drain is removed. Recent literature highlights various interventions for post-traumatic seromas, including the use of surgically placed drains along with aggressive tissue debridement or percutaneous aspiration combined with sclerotherapy [11,12]. This case illustrates that continuous conservative management, involving serial aspirations and sustained compressive dressings, is a highly effective approach for resolving these fluid collections without resorting to complex flap surgeries or additional sclerosing agents [10,12]. Additionally, this case emphasizes the importance of clinicians remaining alert to the possibility of chronic encapsulated complications following conservative management of ML lesions. Thorough surgical excision and meticulous reconstruction can provide a definitive solution for optimal wound healing [2,5].
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