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Lipodermatosclerosis

Lipodermatosclerosis is a chronic inflammatory disorder primarily affecting the skin and subcutaneous tissues of the lower extremities, characterized by fibrosis, induration, and hardening that often results in a distinctive "inverted champagne bottle" appearance of the legs.^[1] It is most commonly associated with chronic venous insufficiency, where venous hypertension leads to capillary leakage, leukocyte trapping, and subsequent tissue remodeling.^[1] This condition can manifest in acute, subacute, or chronic phases, with the acute form presenting as tender, erythematous plaques and the chronic form involving persistent pigmentation, pain, and potential progression to venous ulcers.^[2] The etiology of lipodermatosclerosis is predominantly linked to venous valvular incompetence, impaired calf muscle pump function, or prior deep vein thrombosis, exacerbated by risk factors such as obesity, advanced age, female sex, prolonged immobility, and smoking.^[1] Epidemiologically, it predominantly impacts middle-aged and older adults, with women comprising the majority of cases, and an estimated 50% of acute episodes progressing to the chronic stage without intervention.^[1] Pathophysiologically, sustained venous hypertension induces hypoxia, inflammation, and excessive collagen deposition in the dermis and subcutis, downregulating angiogenesis while promoting fibrosis.^[1] Clinically, patients often report leg heaviness, tightness, and tenderness, alongside visible signs like hyperpigmentation, edema, and bilateral involvement in up to 45% of cases.^[3] Diagnosis is primarily clinical, relying on characteristic physical findings and history of venous disease, though duplex ultrasound may confirm underlying venous insufficiency, and biopsy is reserved for atypical presentations to reveal lobular panniculitis with membrane formation.^[2] Management focuses on addressing the root cause through compression therapy (e.g., graduated stockings) and leg elevation as first-line interventions, which can alleviate symptoms and prevent ulceration.^[3] Adjunctive treatments include topical or intralesional corticosteroids for acute inflammation, pentoxifylline^[3] or anabolic steroids like danazol for chronic fibrosis, and in severe cases, surgical options such as vein ablation.^[1] Early and sustained therapy is crucial, as untreated lipodermatosclerosis can lead to debilitating pain, mobility limitations, and complications like ulceration in up to 20-30% of advanced cases.^[2]

Introduction

Definition and Overview

Lipodermatosclerosis is a chronic inflammatory disorder of the lower extremities characterized by subcutaneous fibrosis, skin induration, and panniculitis, which involves inflammation of the subcutaneous fat layer.^[1]^[3]^[4] It is classified as a form of lower extremity panniculitis, also referred to as sclerosing panniculitis or hypodermitis.^[4]^[5]^[6] This condition is strongly associated with chronic venous insufficiency, where sustained venous hypertension leads to tissue changes, often resulting in the classic "inverted champagne bottle" appearance of the leg in advanced cases due to narrowing of the distal lower limb from fibrosis.^[3]^[7]^[1] The condition was first described in 1955 by Huriez and colleagues, who termed it hypodermitis sclerodermiformis in the context of venous disease.^[1]^[7] Lipodermatosclerosis typically progresses from an acute inflammatory phase to a chronic fibrotic stage.^[6]

Epidemiology

Lipodermatosclerosis (LDS) primarily affects individuals with advanced chronic venous insufficiency (CVI), with approximately 10% of patients with chronic venous disease developing the condition.^[7] In the general population, the prevalence of CEAP class C4b, which encompasses LDS and related skin changes, ranges from 2.1% to 13.2%, varying by country and sex.^[7] The incidence of LDS increases with age, as chronic venous hypertension progresses over time.^[8] Demographically, LDS shows a strong predilection for women, with studies reporting ratios as high as 87% female patients in clinical cohorts.^[9] The condition peaks in middle-aged to older adults, with mean ages around 62 years and highest incidence in women aged 40-50 years and men aged 70-79 years.^[9]^[8] It is most commonly diagnosed in individuals over 40, though onset can occur up to age 75.^[1] Geographically and socioeconomically, LDS is more prevalent in Western countries with aging populations, such as the United States and Europe, where data from large-scale studies predominate.^[7] It occurs more frequently in populations with high rates of obesity and sedentary lifestyles, which exacerbate venous stasis, though no strong racial predisposition has been identified.^[1]

Pathophysiology

Underlying Mechanisms

Lipodermatosclerosis (LDS) primarily arises from chronic venous insufficiency (CVI), where venous hypertension leads to blood pooling in the lower extremities and increased hydrostatic pressure within the microvasculature.^[1] This elevated pressure disrupts the endothelial barrier of capillaries, causing leakage of plasma proteins, including fibrinogen, and extravasation of red blood cells into the surrounding dermal and subcutaneous tissues.^[1] The resulting accumulation of these components initiates a cascade of inflammatory and fibrotic responses that characterize the condition.^[1] The pathogenic sequence begins with leukocyte trapping in the slowed-flow microvasculature, where activated white blood cells adhere to the endothelium and migrate into the interstitium.^[1] These leukocytes release pro-inflammatory cytokines and growth factors, such as transforming growth factor-β (TGF-β), which stimulate fibroblast proliferation and excessive extracellular matrix production.^[10] Concurrently, leaked fibrinogen polymerizes into fibrin, forming perivascular "fibrin cuffs" that encase capillaries and impair oxygen diffusion to tissues, exacerbating hypoxia and perpetuating inflammation.^[1] This process, detailed in histopathological studies, underscores the shift from acute injury to chronic remodeling.^[11] LDS progresses through distinct phases: an acute inflammatory stage marked by edema, erythema, lymphocytic infiltration, and capillary hemorrhage, often with initial fat necrosis; and a chronic fibrotic phase involving persistent collagen deposition in the dermis and subcutis, leading to tissue hardening.^[1] During the chronic stage, upregulation of procollagen type I mRNA in fibroblasts drives septal sclerosis, while inflammation subsides but fibrosis dominates.^[12] Key tissue alterations include thickening of hypodermal septa, atrophy of subcutaneous fat lobules, and deposition of hemosiderin from degraded red blood cells, which contributes to the characteristic brownish pigmentation.^[1] These changes, observed in biopsy analyses, reflect the fibro-inflammatory interplay central to LDS pathogenesis.^[11]

Risk Factors

Lipodermatosclerosis is associated with several non-modifiable risk factors, including advanced age greater than 40 years, which contributes to progressive venous valve incompetence and reduced tissue elasticity.^[1] Female sex also predisposes individuals to the condition, likely due to hormonal influences on venous wall integrity and higher prevalence of multiparity.^[3] A history of deep vein thrombosis (DVT) further elevates risk by causing post-thrombotic damage to venous structures, leading to chronic reflux.^[1] Modifiable risk factors play a significant role in disease development and can be targeted for prevention. Obesity, defined as a body mass index greater than 30 kg/m², exerts mechanical pressure on lower extremity veins, exacerbating venous hypertension and inflammation.^[1] Prolonged immobility or standing impairs venous return, promoting stasis and endothelial dysfunction.^[3] Smoking accelerates vascular damage through nicotine-induced vasoconstriction and oxidative stress, compounding venous insufficiency.^[8] Pregnancy represents another modifiable factor, as it induces hypercoagulability, increased intra-abdominal pressure, and hormonal changes that strain the venous system.^[13] Additional contributors include previous leg trauma, which may scar venous valves or disrupt flow dynamics, and a family history of venous disease, indicating genetic predispositions to weaker vein walls or connective tissue.^[8] Occupations involving extended standing, such as those of nurses or teachers, heighten exposure to gravitational stress on the legs, thereby increasing susceptibility.^[1] Interaction effects among risk factors amplify disease likelihood; for instance, obesity combined with venous reflux has been shown in cohort studies to significantly increase the risk of lipodermatosclerosis compared to either factor alone.^[14] These factors collectively contribute to sustained venous hypertension, the core pathophysiological driver of the condition.^[1]

Clinical Features

Signs and Symptoms

Lipodermatosclerosis manifests through a spectrum of subjective symptoms that evolve across its acute, subacute, and chronic phases, primarily affecting the lower legs and often linked to underlying venous insufficiency.^[1] Patients typically report localized discomfort in the gaiter region, with symptoms progressing from acute inflammatory sensations to persistent chronic unease.^[3] In the acute phase, lasting less than one month, individuals experience sudden onset of severe, burning pain and tenderness in the lower legs, accompanied by a sensation of warmth, rapid swelling, itch, aching, and heaviness.^[1]^[3] This phase is characterized by intense local pain that can be debilitating, often prompting confusion with infectious processes due to the acute discomfort.^[7] During the subacute phase, spanning one month to one year, symptoms include a mix of acute and chronic features, such as ongoing aching, heaviness, and emerging hyperpigmentation with sclerotic changes.^[1]^[2] The chronic phase, exceeding one year, involves persistent dull, aching pain, leg fatigue, and reduced mobility, with possible progression to ulceration that exacerbates pain and limits function.^[3] Patients often describe a woody, indurated sensation correlating with altered leg contour, alongside ongoing edema that heightens fatigue.^[7] Symptom progression typically advances from erythematous, tender plaques to firm induration, with bilateral involvement occurring in approximately 45% of cases, most commonly around the medial malleolus.^[9]

Physical Examination Findings

Lipodermatosclerosis presents distinct physical examination findings that vary between its acute and chronic phases, primarily affecting the lower extremities. In the acute phase, clinicians observe tender, poorly demarcated erythematous plaques with induration and warmth, often localized to the medial aspect of the leg above the malleolus, which may mimic cellulitis due to the inflammatory edema.^[1]^[7] These changes reflect subcutaneous inflammation and fibrosis. In the chronic phase, the skin appears brawny and sclerotic with firm, woody induration and brownish hyperpigmentation from hemosiderin deposition, forming well-defined, circumferential plaques that are typically nontender.^[1]^[2] This pigmentation results from chronic venous stasis and extravasated red blood cells. Associated skin findings may include atrophie blanche, characterized by white, ivory-colored scars with telangiectasias, and stasis purpuric dermatitis.^[7] The leg often exhibits an "inverted champagne bottle" morphology, with atrophy of the calf muscles, constriction at the ankle, and relative sparing of the feet, contributing to a tapered, narrowed lower leg appearance.^[1]^[2] Pitting edema is common in early stages, particularly proximally, alongside visible varicose veins and scarring from prior ulcerations.^[1] These findings are primarily distributed in the bilateral lower third of the legs, with the medial gaiter region most affected, and tenderness on palpation may align with patient-reported pain in affected areas.^[7]^[2]

Diagnosis

Clinical Evaluation

The clinical evaluation of lipodermatosclerosis begins with a detailed history to assess the onset and progression of symptoms. Patients should be queried regarding the duration of leg pain, swelling, or skin changes, which helps differentiate acute episodes (typically lasting less than one month) from subacute (one month to one year) or chronic forms (more than one year).^[1] A thorough venous history is essential, including prior episodes of deep vein thrombosis, varicose veins, or venous ulcers, as lipodermatosclerosis commonly arises in the context of chronic venous insufficiency.^[1] Risk factors such as obesity, advanced age, family history of venous disease, tobacco use, prolonged immobility, or occupations involving extended standing should be explored, alongside any history of lower limb trauma, surgery, recurrent cellulitis, peripheral vascular disease, or diabetes.^[1]^[15] The impact on quality of life, including the nature of pain—often burning and intense in acute phases or aching in chronic stages—should also be evaluated to gauge functional limitations.^[1] Physical examination focuses on systematic inspection and palpation of the lower extremities, particularly the gaiter region around the medial ankle. Inspection reveals characteristic skin hyperpigmentation (often reddish-brown hemosiderin staining), an inverted champagne-bottle leg shape with calf hypertrophy and ankle narrowing, and surrounding edema.^[1]^[7] Palpation assesses for woody induration or firm fibrosis in the subcutaneous tissue, tenderness in acute cases, and the presence of varicose veins or atrophie blanche (pale, scarred patches).^[1]^[15] A bilateral presentation occurs in approximately 45% of cases, but unilateral involvement warrants further scrutiny.^[1] Staging of lipodermatosclerosis is based on clinical duration and features to guide management. Acute lipodermatosclerosis presents with sudden-onset tender, erythematous, warm plaques resembling inflammation, often without significant swelling.^[1]^[7] Subacute stages show a transitional mix of inflammatory erythema and emerging fibrosis, while chronic forms feature nontender, thickened, hyperpigmented, fibrotic plaques with skin tethering and potential ulceration.^[1] The underlying venous disease is classified using the CEAP system, where lipodermatosclerosis corresponds to class C4b (skin and subcutaneous changes including lipodermatosclerosis or atrophie blanche), indicating advanced chronic venous disease.^[16]^[7] Red flags during evaluation include unilateral presentation without clear venous risk factors, rapid progression beyond typical inflammatory patterns, or associated systemic symptoms such as fever or malaise, which may suggest alternative diagnoses like cellulitis, erythema nodosum, or vasculitis rather than primary lipodermatosclerosis.^[1]^[15] Lack of response to initial conservative measures or lymphadenopathy further prompts consideration of differentials.^[7]

Diagnostic Tests

The primary diagnostic test for lipodermatosclerosis is duplex ultrasound, a noninvasive imaging modality that evaluates venous reflux, obstruction, vein diameter, and blood flow in the lower extremities to confirm underlying chronic venous insufficiency.^[1] This examination identifies characteristic changes such as dermal thickening in the acute phase and subcutaneous fibrosis in the chronic phase, aiding in distinguishing lipodermatosclerosis from other conditions.^[17] Duplex ultrasound integrates with clinical history by providing objective evidence of venous pathology that correlates with the patient's symptoms and examination findings.^[7] Adjunctive testing includes the ankle-brachial index (ABI), which measures the ratio of ankle to brachial systolic blood pressure to exclude concomitant peripheral arterial disease before initiating compression therapy; a normal ABI value greater than 0.9 indicates adequate arterial perfusion.^[1] In cases of atypical presentation, such as unusual distribution or rapid progression, a skin biopsy may be performed, preferably via a 6- to 8-mm punch biopsy, revealing histopathological features like lobular panniculitis with septal fibrosis, fat lobule necrosis, and membrane formation.^[1] Biopsy is reserved for select scenarios due to the risk of nonhealing ulceration at the site.^[7] Adjunctive imaging, such as magnetic resonance imaging (MRI), may assess deep tissue involvement, demonstrating skin thickening and a "honeycomb" pattern of fibrous septa that may not be visible on ultrasound.^[18]

Treatment

Conservative Management

Conservative management forms the cornerstone of treatment for lipodermatosclerosis, focusing on mechanical and behavioral strategies to alleviate symptoms, reduce venous hypertension, and prevent disease progression.^[1] These approaches aim to improve venous return, minimize edema, and protect the skin from further damage, often serving as an adjunct to pharmacological interventions when required.^[3] Compression therapy is essential and typically involves the use of multi-layer bandages or graduated compression stockings with pressures of 30-40 mmHg to reduce edema, support venous flow, and relieve pain associated with induration.^[3] This mechanical intervention enhances calf muscle pump efficiency and is recommended as the first-line strategy, with adjustable garments or inelastic bandaging preferred in acute phases for higher interface pressures exceeding 40 mmHg.^[7] Leg elevation above heart level for 30 minutes, 3-4 times daily, promotes venous drainage and helps control swelling, particularly when combined with compression.^[3] Patients are advised to incorporate this into daily routines to counteract gravitational effects on venous pressure. Lifestyle modifications play a critical role in long-term management, including weight loss to decrease intra-abdominal pressure in obese individuals, regular exercise such as calf muscle pumps (e.g., tiptoe raises or foot flexions) to bolster venous return, smoking cessation to improve circulation, and avoidance of prolonged standing to prevent stasis.^[7]^[3] For associated venous ulcers, wound care emphasizes moist wound healing with nonadherent dressings (e.g., hydrocolloids or foams) under compression, alongside off-loading techniques like elevation to facilitate tissue repair and reduce infection risk.^[19] Management often requires involvement of a multidisciplinary team, including wound care specialists, to monitor healing and address complications promptly.^[1]

Pharmacological Interventions

Pharmacological interventions for lipodermatosclerosis primarily target inflammation, fibrosis, and associated venous insufficiency to alleviate symptoms and prevent progression. Anti-inflammatory agents, such as topical corticosteroids (e.g., clobetasol propionate), are employed for acute inflammatory flares to reduce erythema, pain, and edema, typically in short courses to minimize risks like skin atrophy.^[2] Intralesional corticosteroids, particularly triamcinolone acetonide (10-40 mg/mL injected into indurated areas), have demonstrated efficacy in early-stage disease by mitigating inflammation and halting progression to chronic induration, with patients reporting rapid pain relief within weeks.^[20] Venous modifiers like pentoxifylline, a methylxanthine derivative that improves microcirculation and inhibits fibrosis through hemorrheologic effects, are recommended at a dose of 400 mg three times daily. Randomized controlled trials (RCTs) have shown that pentoxifylline improves the rate of complete healing of venous ulcers—a common complication of lipodermatosclerosis—compared to placebo when used adjunctively, with a relative risk of approximately 1.5 in meta-analyses and benefits attributed to reduced tumor necrosis factor-alpha levels.^[21]^[22] For severe induration refractory to standard measures, anabolic steroids such as danazol (100 mg daily) may be considered due to their fibrinolytic and anti-inflammatory properties, with case reports indicating resolution of painful fibrosis and improved tolerability of compression therapy after 4-8 weeks.^[23] Diuretics, including furosemide, can address refractory edema in select cases but should be used cautiously to avoid exacerbating hypovolemia or electrolyte imbalances, as they do not target underlying venous pathology.^[24] These agents are most effective when combined with compression therapy to optimize outcomes.

Surgical Options

Surgical options for lipodermatosclerosis are considered when conservative management fails to control symptoms or prevent progression, particularly in cases of refractory venous hypertension or associated ulceration. These interventions primarily target the underlying venous insufficiency to alleviate chronic inflammation and fibrosis in the lower extremities. Referral to a vascular specialist is recommended for patients with confirmed superficial or deep venous reflux contributing to the condition.^[1] Endovenous ablation techniques, such as laser (EVLA) or radiofrequency ablation (RFA), are first-line invasive procedures for treating great saphenous vein incompetence in lipodermatosclerosis, especially in patients with advanced chronic venous insufficiency (CEAP class C4b or higher). These minimally invasive methods seal incompetent veins under ultrasound guidance, reducing ambulatory venous hypertension and improving tissue perfusion; thermal ablation is supported by strong evidence (Class I, Level A recommendation). Ultrasound-guided foam sclerotherapy (UGFS) serves as an alternative or adjunct for superficial venous reflux or incompetent perforator veins, particularly in patients unsuitable for thermal ablation, offering effective reflux elimination with minimal downtime (Class IIb, Level B). Both procedures demonstrate benefits in halting disease progression and mitigating skin changes when performed early in symptomatic cases.^[7]^[1]^[7] For lipodermatosclerosis complicated by non-healing venous ulcers, surgical debridement via shave therapy involves excision of necrotic tissue and surrounding fibrotic lipodermatosclerotic tissue using a grafting knife, followed by immediate meshed split-skin grafting. This approach is indicated for recalcitrant ulcers (often lasting over a year) due to deep venous incompetence or post-thrombotic changes, yielding long-term healing rates of approximately 67% after 2-3 years of follow-up. Percutaneous drainage techniques may also be employed to remove liquefied subcutaneous fat in inflammatory phases, enhancing microcirculation in CEAP C4-C6 stages.^[25]^[7]^[26] In select refractory cases with deep venous reflux, vein ligation procedures—such as subfascial endoscopic perforator surgery (SEPS) or saphenofemoral junction ligation—address incompetent perforating veins or proximal reflux to redirect blood flow and reduce hypertension. These are reserved for advanced disease unresponsive to endovenous methods, often combined with postoperative compression to sustain outcomes and prevent recurrence. Compression therapy remains mandatory following all surgical interventions to support venous return and optimize healing.^[27]^[28]^[7]

Prognosis and Complications

Prognosis

Lipodermatosclerosis typically follows a chronic and recurrent course, characterized by phases including acute (less than 1 month), subacute (1 month to 1 year), and chronic (more than 1 year). Without treatment, the condition often progresses, with approximately 50% of patients advancing to the chronic stage within 12 months of discontinuing compression therapy, based on a study of 30 patients.^[1] Early intervention with compression therapy significantly improves outcomes by alleviating symptoms and slowing disease progression. For instance, consistent use of graduated compression elastic stockings has been shown to reduce the area of lipodermatosclerosis significantly at 6 months (p=0.01) and 12 months (p=0.04) in a randomized controlled trial of 153 patients with healed venous ulcers. Factors such as patient compliance, obesity, immobility, and underlying chronic venous insufficiency strongly influence prognosis, with non-compliance or comorbidities linked to higher rates of progression and recurrence.^[1]^[29]^[1] In the long term, acute cases may achieve remission with prompt management, while chronic cases generally necessitate lifelong therapy, including compression and lifestyle modifications, to stabilize symptoms and prevent further deterioration. Recent data from cohort studies emphasize the benefits of multidisciplinary care; for example, compression therapy alone reduced ulcer recurrence from 46% to 21% at 6 months in one trial, highlighting the potential for substantial recurrence reduction through integrated approaches.^[1]^[29]

Complications

One of the primary complications of untreated or advanced lipodermatosclerosis is the development of venous ulcers, which occur in up to 20% of patients with advanced chronic venous insufficiency, a condition closely associated with lipodermatosclerosis. These ulcers typically appear in the medial malleolar region and exhibit slow healing due to fibrosis, impaired tissue perfusion, and recurrent trauma in the affected area.^[30]^[1] Infections, including cellulitis and abscess formation, frequently arise from skin breakdown in lipodermatosclerosis, with the risk exacerbated by persistent edema that compromises skin integrity. The acute inflammatory phase of the condition is often misdiagnosed as cellulitis, potentially delaying appropriate management.^[1]^[7] Additional complications encompass chronic pain, reported in approximately 43% of cases, which can result in immobility and muscle deconditioning, further worsening venous stasis. Lipodermatosclerosis may also lead to secondary lymphedema through lymphatic obstruction in advanced stages. Rarely, chronic ulcers in this context can progress to squamous cell carcinoma, necessitating vigilant surveillance.^[7]^[1]^[31] Early intervention to manage underlying venous disease is crucial for preventing these complications, while longstanding ulcers require regular monitoring for malignant transformation. These adverse outcomes contribute to a poorer overall prognosis by increasing morbidity and healthcare burden.^[1]

References

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