Lipomembranous Panniculitis with Ulceration and Secondary Calcinosis Cutis: Successful Treatment Using Carbon Dioxide Laser Exci

Lipomembranous panniculitis is a fibrotic process that usually occurs in the legs. This condition has also been referred to as lipodermatosclerosis, venous stasis panniculitis, or hypodermitis sclerodermiformis. The principal features are a sclerosing panniculitis with dermal and subcutaneous fibrosis and fat necrosis. Although the exact pathogenesis is uncertain, it is thought to occur as a result of ischemic changes.¹
The major physical finding is painful, woody thickening in the subcutaneum of the distal one-third of the lower leg. It is usually unilateral and noncircumferential and occasionally ulcerates. A history of deep vein thrombosis and other signs of venous disease may be present including hemosiderosis and/or pitting edema. However, venograms and Doppler investigations are usually normal.¹
Treatment of the condition is often difficult. The authors herein report a novel, previously unreported method of management—removal of the entire sclerotic mass using carbon dioxide laser with marsupialization and healing by secondary intention.

Case Report

An 83-year-old woman presented with a 1-year history of painful ulceration of the medial aspect of the right lower leg. The patient had been hospitalized for an episode of increased pain, redness, and swelling surrounding the ulcer, which the authors considered consistent with cellulitis. Two previous episodes of cellulitis had also occurred during the previous year; both required hospitalization and had responded to treatment with oral and systemic antibiotics and local wound management. Local wound care included saline wet-to-dry dressings and enzymatic debriding agents.
The patient noted mild swelling of the legs that was worse at the end of the day. Tenderness of the ulcer was worse with dependency. There was no history of previous trauma to the area, joint complaints, pancreatic disease, or other tender nodular lesions or ulcerations. After treatment with antibiotics, the patient developed significant diarrheal stools.
The patient had a history of mild hypertension, anemia, glaucoma, carcinoma of the bladder, and congestive heart failure. Previous medications included furosemide, isosorbide, metronidazole, and timolol ophthalmic.
On examination, the patient was thin and complained of moderate soreness of the medial aspect of the distal medial right lower leg. There was 2+ pitting edema of the right lower leg and 1+ pitting edema of the left lower leg. Pulses of the feet were 1+. The feet and legs were warm with good capillary fill bilaterally.
An ulcer measuring 1.5 cm was noted on the medial aspect of the distal right lower leg (Figure 1). Avascular material with focal, yellow, firm deposits was present within the ulcer. In addition, surrounding the ulcer was a palpable, firm, plate-like mass situated deep within the ulcer. The mass measured approximately 8.5 cm x 4.0 cm. Occasional fine vascular ectasias of the lower legs and feet were noted bilaterally.
On laboratory investigation, results of the following tests were either negative or normal: liver function tests, amylase, lipase, and antinuclear antibodies. Stool testing was positive for Clostridium difficile toxin. Culture from the right leg ulcer demonstrated methicillin-resistant Staphylococcus aureus. White blood cell count ranged between 8,800 and 54,500 with left shift during treatment with antibiotics. Total protein and albumin were 4.9 and 2.0. Blood urea nitrogen ranged between 8 and 55 with creatinine 0.7–2.2.
Skin biopsy from the edge of the ulcer demonstrated a thinned epidermis. The superficial dermis showed sclerosis with angioplasia, patchy, chronic inflammation, and pigment deposition. Fibroadipose tissue with broad bands of sclerosis and fibrosis and prominent lipomembranous change with shrunken fat lobules was present beneath the dermis. Some areas demonstrated prominent calcification within the sclerotic adipose tissue. In addition, other areas showed a lobular panniculitis with foamy macrophages and scattered lymphocytes and plasma cells. The biopsy was consistent with lipomembranous panniculitis.
The cellulitis was treated with intravenous vancomycin. After resolution of the cellulitis, the patient was given local anesthesia, and the large subcutaneous mass was removed with a CO₂ laser. The laser had a spot size of 0.22 mm and focused energy at 15 W. Using the laser in focused/cutting mode, the mass was dissected from the surrounding normal tissue. The mass was removed partly as a solid structure; however, in many areas curettage was also required to separate the devitalized tissue from healthy structures. The process extended to the level of the fascia and was intimately associated with the overlying dermis. Again, using the laser in focused mode, the skin overlying the mass was also removed (Figures 2 and 3). The final defect measured 8.5 cm x 4.5 cm x 2.0 cm. The patient tolerated the procedure well. The wound was allowed to heal by secondary intention. The patient subsequently had steady, gradual healing over 4 months without complications (Figure 4).

Discussion

Lipomembranous (sclerosing) panniculitis was first described in the French literature in 1955 as hypodermitis sclerodermaformis, a reference to the scleroderma-like qualities of the skin of the legs.² Recently, it has been most commonly referred to as sclerosing panniculitis, lipodermatosclerosis, or lipomembranous panniculitis.¹
In its clinical findings, lipomembranous panniculitis may resemble other inflammatory processes of the subcutaneum including erythema nodosum, erythema induratum, pancreatic fat necrosis, scleroderma, scleromyxedema, vasculitis, and cellulitis. However, it is distinguished by its solitary nature, the absence of other systemic features, and its frequent occurrence in individuals with venous disease including venous insufficiency or a history of thrombophlebitis.¹ Women are more often affected than men.¹
Pathogenesis is thought to revolve around the sustained venous hypertension noted in virtually all patients.³ Impaired fibrinolysis, or enhanced clot formation as may be seen in some patients with low plasma levels of proteins C and/or S, may contribute to the development of the process. Indeed, in one series of patients with lipodermatosclerosis, 4 of 19 (21%) affected patients were found to have low levels of either of these proteins.⁴
Histologically, there may be 3 phases. Early lesions may demonstrate a lymphocytic infiltrate within the subcutaneous septae accompanied by midlobular zones of necrosis with characteristic ghosts of adipocytes. These changes are not accompanied by vasculitis or venous occlusive findings, although features of venous disease, such as focal hemorrhage and/hemosiderosis, may be present. Intermediate lesions may show thickened fibrous septae and a mixed inflammatory infiltrate, hyalinized sclerosis that encases fat cells, and lipophagic fat necrosis. Advanced lesions will show more pronounced septal and peripheral sclerosis, accompanied by fat microcysts and focal membranous fat necrosis. Vascular changes may include endarteritis obliterans, hemorrhage, dilated veins, and capillary proliferation; these features suggest an ischemic etiology for the changes seen.⁵ Inflammation usually subsides in the late lesions.¹
Multiple therapies have been suggested for the process. Initial treatments have been directed at the cellulitis or venous obstruction, if present. Specific therapies reported as being helpful include graded stockings or elastic bandages,^3,6 ultrasound,⁷ and the anabolic steroid stanozolol.^3,6 Stanozolol has been thought to work through its action as a fibrinolytic agent.^6,8,9 However, hepatotoxicity has been reported to complicate this therapy.¹⁰ Other therapies, such as colchicine, hydroxychloroquine, saturated solution of potassium iodide, and steroids, have been only modestly successful in treating panniculitis.¹ Concerns regarding the fragile medical state of the patient in this case led the authors to consider a surgical rather than medical approach to her condition.
Management in this patient was directed at removal of the necrotic adipose and sclerotic tissue. Multiple episodes of cellulitis, nonhealing painful ulceration for greater than 1 year, and complicating C difficile enterocolitis were features that prompted the authors to initiate more aggressive therapy. It was reasoned that the avascular, necrotic tissue would be unable to support normal mechanisms of wound healing. The CO₂ laser was selected because of its ability to reduce bleeding, thereby allowing better surgical visualization and more precise removal of the necrotic tissue. Of note is the fact that the patient had previously failed to respond to more conservative surgical and medical debridement.
Following removal of the necrotic and sclerotic material, the patient experienced almost complete and immediate relief of pain with gradual healing of the ulceration over a 4-month period. At 18 months follow-up, the wound remained healed, and no additional areas of dermatosclerosis appeared.

Conclusion

Carbon dioxide laser removal of the necrotic and sclerotic area of dermatosclerosis and secondary intention healing appears to be a safe and effective means of treating patients in whom medical management has failed or may not be appropriate.