Tools
Dermatopathology Evaluation of Panniculitis
Introduction
Panniculitis encompasses a wide variety of skin diseases characterized primarily by inflammation of the subcutaneous fat. The condition is not an extension of dermatoses of the dermis, such as morphea, or fascia, such as eosinophilic fasciitis, into the subcutis.[1] Panniculitis typically presents clinically with tender subcutaneous erythematous nodules or plaques, most often on the lower extremities. Additional features, such as sclerosis, ulceration, or atrophy, may also be noted depending on the subtype.[2]
Panniculitis encompasses a heterogeneous group of rare disorders that may present with similar clinical features. Therefore, diagnosis can be difficult without histopathological correlation. Combining patient history, physical examination, and histopathological examination of a biopsy specimen is often necessary to diagnose panniculitides accurately and separate them from bruising and neoplasia.[3]
Issues of Concern
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Issues of Concern
Panniculitis can be challenging to diagnose because the presentation is often nonspecific, and laboratory findings alone can lead to misdiagnosis.[4] Panniculitis encompasses several subtypes requiring histopathologic evaluation due to their clinical similarities. Diagnostic challenges can arise from biopsy specimens with insufficient subcutaneous fat or are taken too late, producing nonspecific findings.[5]
A deep incisional biopsy should be performed after cleansing the skin surface with alcohol, which is allowed to evaporate. Punch biopsy specimens may fracture and leave valuable evidence of inflammation or necrosis. An electric rotary power punch may overcome this limitation.
If a punch biopsy is performed, it should be at least 6 mm in diameter to accommodate culture and hematoxylin and eosin staining. Including areas of necrosis in the biopsy is important for facilitating culture and special stains, such as fungal and acid-fast bacillus stains.[6]
Causes
Panniculitis is a broad term for conditions resulting from inflammation of the subcutaneous fat, which can be due to infection, trauma, enzymatic destruction, malignancy, or autoimmune factors. Achieving a precise diagnosis often requires a stepwise approach, including appropriate biopsies of deeper skin sections and thorough clinicopathologic correlation.[7][8] The condition has no universally accepted classification. However, many pathologists use the following stepwise approach:
- Determine whether the inflammation predominantly affects the fat lobules, such as the lobular, the septa between the lobules, such as the septal, or both. Most panniculitides have a mixture of both septal and lobular inflammation.
- Assess for vasculitis and, if present, evaluate the size and type of blood vessels involved, such as venules or arterioles of small vessels and veins and arteries of large vessels.
- Identify the type of cells in the inflammatory infiltrate, such as neutrophils, lymphocytes, histiocytes, and plasma cells.
- Recognize any additional histopathological features that may help lead to a final diagnosis, such as the presence or type of necrosis, sclerosis, or foreign bodies.
Although not necessary for diagnosis, special stains, polarized light microscopy, and culture may help further characterize the lesion. Polarized light microscopy helps rule out foreign material, whereas culture may identify inciting microbes such as bacteria or fungi.
Anatomical Pathology
Subcutaneous fat is organized into lobules and septa. The lobules are made up of energy-rich adipocytes, which are separated by thin septa composed of collagen and reticulin connective tissue.[9] The septa contain blood vessels, lymphatics, and nerves. Each lobule is supplied by its respective artery or arteriole, representing a terminal blood vessel where damage can lead to inflammation and necrosis of the adipocytes. Adipocytes appear empty on the hematoxylin-eosin staining with a signet-ring morphology. The nucleus is flattened and displaced to the side of the cell through a large, fat-containing vacuole.
Morphology
Histopathologically, panniculitis can be classified into predominantly septal or lobular panniculitis with or without vasculitis. The classification informs the treatment choice, helps predict the disease course and treatment response, and determines the need for additional interventions.
Predominantly Septal Panniculitides Without Vasculitis
Predominantly septal panniculitides without vasculitis are typically caused by damage to small venules. This category includes:
Erythema nodosum: Erythema nodosum is widely considered the most common form of panniculitis and is the prototype for septal panniculitis without vasculitis. The condition presents as an acute nodular eruption on the lower legs, possibly associated with systemic symptoms. The lesions are typically transient and can be associated with underlying infections or systemic conditions, including sarcoidosis; Behcet disease; celiac disease; Sweet syndrome; inflammatory bowel disease; reactions to drugs such as isotretinoin, sulfonamides, and ciprofloxacin; infection with bacteria such as staphylococcal and streptococcal infections; fungi such as dermatophyte and sporotrichosis; viruses such as HIV; mycobacteria; and malignancy, such as leukemia.
Histology shows thickened subcutaneous fat septa with inflammatory infiltrates of varying morphology, depending on the age of the lesion (see Image. Erythema Nodosum, Low Power). Early lesions present with edema, hemorrhage, neutrophils, and Miescher radial microgranulomas. These microgranulomas are the histopathological hallmark of erythema nodosum, consisting of small histiocytes aggregated around a central star-shaped cleft (see Image. Erythema Nodosum, High Power).[10][11] Fibrosis, lymphocytes, and multinucleated giant cells predominate in later stages.
Deep morphea/scleroderma: Histopathology reveals septal thickening with collagen bundles replacing subcutaneous fat surrounding eccrine ducts. In the early acute phase, a mixture of inflammatory lymphocytes and plasma cells may be present. In the later chronic phase, fibrosis and hyalinization are predominant. Granulomatous infiltrates are absent.[12] Systemic sclerosis exhibits this pathology.
Necrobiotic xanthogranuloma: Histopathology typically shows large areas of necrobiosis alternating with granulomatous inflammation, including foamy histiocytes, cholesterol clefts, and Touton giant cells, which are characterized by a wreath of nuclei surrounded by a peripheral rim of foamy cytoplasm (see Images. Necrobiotic Xanthogranuloma Pathology, Low Power and Necrobiotic Xanthogranuloma Pathology, High Power).[13]
Subcutaneous granuloma annulare: Subcutaneous granuloma annulare histopathology is characterized by infiltrates of palisading histiocytes surrounding mucin and basophilic degeneration of collagen bundles (see Images. Granuloma Annulare, Low Power and Granuloma Annulare, High Power).[14] The presence of mucin is considered a hallmark of subcutaneous granuloma annulare. Multinucleated giant cells, eosinophils, lymphocytes, and neutrophils may also be observed infiltrating the dermis.[15]
Rheumatoid nodule: Rheumatoid nodules appear in approximately 20% of patients with rheumatoid arthritis. Histopathology shows large areas of necrobiosis with eosinophilic material composed of fibrin, surrounded by palisading histiocytes within the dermis and subcutaneous fat (see Image. Rheumatoid Nodule Pathology).
Necrobiosis lipoidica: Histopathology typically shows layers of granulomatous inflammation, occasional multinucleated giant cells, histiocytes, plasma cells, and alternating zones of degenerated collagen without mucin (see Images. Low-Power Pathological Findings of Necrobiosis Lipoidica: Skin Biopsy and High-Power Pathological Findings of Necrobiosis Lipoidica: Skin Biopsy).[16]
Predominantly Septal Panniculitides With Vasculitis
Predominantly septal panniculitides with vasculitis may arise from etiologies, including malignancies and autoimmunity. This set of conditions includes the following:
Leukocytoclastic vasculitis: Histopathology of leukocytoclastic vasculitis reveals septal inflammation with necrosis of postcapillary venule walls, evident as necrotic endothelial cells, neutrophils, nuclear dust, and fibrin deposition in the vessel walls (see Image. Leukocytoclastic Vasculitis Pathology).
Superficial thrombophlebitis: Superficial thrombophlebitis predominantly affects larger veins in the deeper dermis and subcutaneous fat and presents with cord-like induration. Therefore, histopathology typically reveals vasculitis and thrombosis occluding the lamina (see Image. Thrombophlebitis Pathology).[17] The predominant inflammatory cell type in earlier lesions is mainly composed of neutrophils. Later stages may show lymphocytes, histiocytes, and giant cells. This condition is associated with pancreatic carcinoma, Behcet syndrome, and Buerger disease.
Cutaneous polyarteritis nodosa: Histopathology of cutaneous polyarteritis nodosa reveals the involvement of the septa's small-to-medium–sized arteries and arterioles. Lesions show prominent fibrinoid necrosis and fibrin deposition, with the destruction of the tunica intima (see Image. Polyarteritis Nodosa Pathology). Neutrophils make up most inflammatory cells in earlier stages. Lymphocytes and histiocytes later increase in proportion. This pathology is considered a benign polyarteritis nodosa unrelated to systemic vasculitis.
Other causes of septal panniculitis include factitial panniculitis, cellulitis, nephrogenic systemic fibrosis, hydroa vacciniforme, cytomegalovirus infection, microscopic polyangiitis, apomorphine infusion, cryoglobulinemia, Whipple disease, and α1-antitrypsin deficiency.
Predominantly Lobular Panniculitides Without Vasculitis
Conditions with predominantly lobular panniculitides without vasculitis arise from various causes. These conditions include the following:
Subcutaneous fat necrosis of the newborn: Subcutaneous fat necrosis of the newborn is a self-resolving panniculitis affecting the thighs, cheeks, and buttocks of neonates. The condition is related to hypothermia and hypercalcemia. The presence of needle-shaped clefts within adipocytes is a hallmark histopathological finding (see Image. Subcutaneous Fat Necrosis of the Newborn, Low Power).[18][19] Subcutaneous fat necrosis shows a dense lymphocytic infiltrate (see Image. Subcutaneous Fat Necrosis of the Newborn, High Power).[20] Electron microscopy shows needle-shaped crystals in parallel and macrophages surrounding necrotic fat cells.[21]
Sclerema neonatorum: Sclerema neonatorum presents with waxy, dry skin and is considered a diffuse form of subcutaneous fat necrosis of the newborn. However, this condition is less common, likely due to improved neonatal care.[22] Histopathology is similar to subcutaneous fat necrosis of the newborn with minimal inflammation, including the absence of histiocytes, and no calcification.[23]
Post-steroid panniculitis: Unlike subcutaneous fat necrosis of the newborn, post-steroid panniculitis has less inflammation and fewer needle-shaped clefts. By comparison, inflammation is scarce or absent in sclerema neonatorum (see Image. Post-steroid Panniculitis Pathology).
Cold panniculitis: Cold panniculitis can present with indurated plaques in severely cold conditions, typically in younger children. Histopathology reveals lymphocytes and histiocytes in the fat lobules, with marked edema and superficial and deep perivascular dermal infiltrate. The most significant changes are observed at the dermis-subcutis junction. This condition can overlap with deep perniosis in its presentation.
α1-Antitrypsin deficiency: This condition is characterized by low serum levels of α1-antitrypsin, most notably resulting in tender lesions that ulcerate with an oily discharge following an inciting event, such as trauma.[24][25] The acute phase presents with neutrophilic inflammation, followed by severe necrosis and destruction of fat lobules. A histopathological feature specific to this form of panniculitis includes the splaying of neutrophils between collagen bundles in the deep dermis in the early stages and floating fat in later stages.[26][27]
Cytophagic histiocytic panniculitis: Cytophagic histiocytic panniculitis presents as tender nodules with fever and liver dysfunction.[28] Histopathology shows fat necrosis and sheets of histiocytes phagocytosing erythrocytes, leukocytes, and nuclei, thus the term bean bag cells.[29] Some cases of cytophagic histiocytic panniculitis have been recharacterized as subcutaneous panniculitis-like T-cell lymphoma.[30]
Pancreatic panniculitis: Pancreatic panniculitis typically presents as tender nodules on the lower extremities and is often associated with acute pancreatitis.[31] Histopathology of pancreatic panniculitis shows fat necrosis with saponification of adipocytes and a predominance of neutrophils (see Image. Pancreatic Panniculitis Pathology). In contrast to other types of lobular panniculitides showing necrosis as a late finding, pancreatic panniculitis may show necrosis in the acute phase. Furthermore, aggregates of ghost adipocytes, which have lost their nuclei and developed thick shadowy walls, may be present.[32]
Lupus panniculitis: Lupus panniculitis, also known as lupus profundus, presents typically on the trunk or proximal extremities as a complication of systemic lupus erythematosus or chronic cutaneous lupus erythematosus.[33] Histopathology of lupus panniculitis shows predominantly lobular panniculitis, although a mixed lobular-septal pattern may also be observed. Characteristic features include lymphoid follicles containing germinal centers without fat necrosis.[34] Collagen bundles of the septa are often hyaline and sclerotic, with an infiltrate composed of lymphocytes and plasma cells. Lymphocytic infiltrates may contain nuclear dust. Immunofluorescence studies often show a linear deposition of immunoglobulin M and complement C3 along the dermo-epidermal junction.[35]
Connective tissue panniculitis: Connective tissue panniculitis is a rare condition that typically presents on the lower limbs in patients with a low antinuclear antibody titer.[36] The condition may result from medications or lipoatrophy. Histopathology shows lobular panniculitis similar to erythema induratum without vessel changes.[37]
Subcutaneous sarcoidosis: Subcutaneous sarcoidosis presents with flesh-colored tender nodules on the extremities of middle-aged women. Histopathology is consistent with sarcoidosis, including naked lobular granulomas with fibrosis and some central necrosis.[38]
Lipodystrophy: Lipodystrophy may be secondary to morphea, lupus panniculitis, or repeated insulin or steroid injections. However, primary lipodystrophy includes total, partial, and localized lipodystrophy.[39] Total lipodystrophy may be acquired, as in Lawrence syndrome, associated with metabolic dysfunction, or congenital, as in Beradinelli–Seip syndrome.
Congenital total lipodystrophy is classified into 3 types. Type 1 is due to a mutation in the 1-acylglycerol-3-phosphate O-acyltransferase-2 gene. Type 2 is due to a mutation in the seipin gene. Type 3 is due to a mutation in the caveolin-1 gene.[40][41] Partial lipodystrophy presents with a loss of facial fat symmetrically and may be familial, such as Dunnigan type, or acquired, such as Barraquer-Simons disease. Of the acquired form, the Weir-Mitchell type does not include the lower extremity, whereas the Laignel-Lavastine type includes lower body hypertrophy.[42][43][44]
Unilateral variants of partial lipodystrophy associated with facial hemiatrophy comprise Parry-Romberg syndrome.[45] Familial partial lipodystrophy is an autosomal dominant partial lipodystrophy associated with mutations in the LMNA gene, which is implicated in progeria.[46] Localized lipodystrophy typically occurs in injection sites and may be confused with morphea. The condition presents with solitary annular areas of atrophy.[47][48][49] Lipedema presents with fat deposition, typically in the buttocks, and appears clinically similar to lymphedema.[50]
Histopathology of lipedema shows fatty hypertrophy with thickened fibrous septa. In contrast, the other lipodystrophy types may show small lipocytes and myxoid connective tissue or lobular panniculitis with lymphocytes, lipophages, and plasma cells, which may show vasculitis in the dermis or immunoreactants on vessels on direct immunofluorescence.[51][52] Lipodystrophy may be associated with HIV, such as HIV-associated lipodystrophy, or aging and obesity, such as gynoid lipodystrophy and cellulite. Some cases exhibit membranous change, such as membranous lipodystrophy, with pseudomembranous fat necrosis.[53][54]
Lipodermatosclerosis: Sclerosing panniculitis, also known as lipodermatosclerosis, results from chronic venous insufficiency of the lower extremities. Histopathological findings vary by stage. Early stages present with ischemic necrosis of the lobule center, sparse lymphocytic infiltrate, and extravasation of erythrocytes and hemosiderin (see Image. Sclerosing Panniculitis, Low Power). Late-stage lesions show sclerosis of the septa, fat necrosis, and lipomembranous change, which is observed as an eosinophilic feathery lining composed of anuclear cystic adipocytes.[55] Lipomembranous change suggests lipodermatosclerosis (see Image. Sclerosing Panniculitis, High Power).
Factitial or traumatic panniculitis: Factitial or traumatic panniculitides, such as encapsulated fat necrosis, should be considered when histopathology shows unusual features without vasculitis or thrombosis. These conditions may result from self-inflicted injuries or iatrogenic causes, including cosmetic or therapeutic substances. They may arise from accidental or intentional blunt trauma.
Histopathology typically shows mostly lobular panniculitis with a predominantly neutrophilic inflammatory infiltrate in acute stages and a more granulomatous infiltrate in late stages. For example, cosmetic silicone injections may result in a granulomatous reaction in some patients, showing foamy histiocytes and multinucleated giant cells. Vitamin K injections may present on histopathology with sclerosis of collagen bundles in the septa and lymphocytic and plasma cell inflammatory infiltrates that may resemble deep morphea.[56]
Alternately, areas of fat necrosis in the subcutis with cystic spaces of variable size and shape within fat lobules and varying degrees of hemorrhage and fibrosis may be observed (see Image. Traumatic Panniculitis Pathology). The periphery of the lesions may have necrotic adipocytes without nuclei.[57]
Postirradiation pseudosclerodermatous panniculitis: This condition can occur following irradiation. Histopathology may show thickened, sclerotic septa and lobular panniculitis.[58][59]
Neutrophilic panniculitis: The erythematous, tender lesions of neutrophilic panniculitis may be associated with neutrophilic dermatoses, such as Behcet syndrome. Histopathology reveals heavy neutrophilic infiltrates within the fat lobules.[60][61]
Eosinophilic panniculitis: Eosinophilic panniculitis shows septal and lobular panniculitis with eosinophils and flame figures. Although not a specific diagnosis, this condition is a reaction pattern associated with infection, such as gnathostomiasis.[62][63]
Predominantly Lobular Panniculitides With Vasculitis
Predominantly lobular panniculitides with vasculitis may affect arteries and veins. This set of conditions includes the following:
Erythema induratum of Bazin: Erythema induratum of Bazin, also known as nodular vasculitis, is the most common type of lobular panniculitis with vasculitis and may affect both veins and arteries (see Image. Erythema Induratum of Bazin). Tuberculosis has been implicated as one of the possible causes of this syndrome. Histopathology in the early stages typically shows neutrophils with extensive necrosis of adipocytes, foamy histiocytes, and multinucleated giant cells. Caseous necrosis and liquefaction may appear when arteries are severely damaged.
Neutrophilic lobular panniculitis: Neutrophilic lobular panniculitis is an unusual and rare variant of panniculitis associated with rheumatoid arthritis. The condition presents histopathologically with lobule adipocyte necrosis, neutrophils, foamy histiocytes, and multinucleated giant cells.[64]
Lucio phenomenon: Lucio phenomenon is a variant of leprosy that presents with necrotizing vasculitis of the dermis and subcutis, mainly affecting the smaller vessels and venules. The predominant cell type relating to perivascular inflammation includes foamy histiocytes that contain acid-fast bacilli.[65]
Erythema nodosum leprosum: Erythema nodosum leprosum presents as a necrotizing vasculitis involving small-to-medium–sized vessels of the dermis and subcutis. The predominant cell type is the neutrophil.
Weber-Christian disease is sometimes considered a type of panniculitis characterized by numerous lipophages, but it is probably best described as idiopathic panniculitis. Some cases of Weber-Christian disease have later been discovered to fit with other entities. Thus, this term, along with Rothmann-Makai syndrome, is no longer used.[66][67]
Subcutaneous panniculitis-like T-cell lymphoma is a rare cutaneous lymphoma that should be distinguished from panniculitis.[68] Histopathology typically shows a lobular panniculitis pattern but with pleomorphic, neoplastic lymphocytes and histiocytes rimming adipocytes to form a lace- or net-like pattern.[69][70]
Other causes of lobular panniculitis include atheromatous emboli, Behcet disease, blind loop syndrome, chemotherapy recall reaction, Crohn disease, dermatomyositis, granuloma annulare, hydroa vacciniforme, jejunoileal bypass, lymphoma, Niemann-Pick disease, nutritional abnormalities, oxalosis, Sjogren syndrome, Sweet syndrome, gout, medications, and infections.[71]
Clinical Significance
Panniculitis is a relatively uncommon disorder characterized by various histopathological features and encompasses a range of subtypes linked to infection, trauma, malignancy, or inflammatory diseases.
Patients typically present with tender, erythematous, subcutaneous nodules or plaques, most often on the lower extremities. However, certain types of panniculitides develop preferentially in certain areas, such as the calf for erythema induratum, the pretibial region for erythema nodosum, and the upper arms, shoulders, and face for lupus panniculitis.[72] Depending on the etiology, panniculitis may also present with ulcers, atrophy, sclerosis, or livedo racemosa.[73] Additional systemic features may include fever, weight loss, malaise, and arthralgia.[74]
Panniculitis is diagnosed and classified using a combined approach, including clinical presentation and histopathological correlation based on biopsy findings. Diagnosis sometimes requires additional tests and studies, including microbiological cultures, lab tests, and polarized light microscopy.
Management focuses on panniculitis resolution and treatment of the underlying illness. The recommended measures include:
- Rest and elevation of affected areas
- Nonsteroidal anti-inflammatory drugs
- Supportive care
- Compression stockings
- Antibiotics
- Systemic steroids
- Immunosuppressants
- Biologics
- Surgical removal of nonhealing lesions
Panniculitis may last weeks to months, and the outcome depends on the underlying cause of inflammation. Lesions may resolve spontaneously and recur. Some forms of panniculitis heal without sequelae, but others may cause significant morbidity, resulting in scarring or disfigurement.
Panniculitis is a relatively uncommon disorder encountered in clinical practice. However, the condition is best managed by an interdisciplinary team that may include a variety of practitioners, as the specific etiologies and histopathological subtypes differ significantly. Dermatology, rheumatology, pediatrics, and primary care may coordinate with pathology in managing the various panniculitis subtypes. Systemic disease-associated types may also involve oncology, infectious disease, gastroenterology, nephrology, or pulmonology.
When initially presenting for evaluation, a trained clinician should perform the deep punch or incisional scalp biopsy to obtain a sufficient sample for the pathologist's evaluation. A shave biopsy is too superficial and should not be used for lesions suspected of panniculitis.
Coordination between primary care providers and specialists in dermatology and dermatopathology is crucial for optimal patient care. Identifying the etiology of panniculitis can be challenging, especially if the practitioner is not well-versed in the diverse range of potential underlying conditions or the appropriate biopsy techniques. Once a diagnosis is made through clinical and histopathologic correlation, managing panniculitis effectively involves addressing the underlying cause. Given that different organ systems may be affected depending on the etiology, an interprofessional team approach is essential to improving outcomes.
Media
(Click Image to Enlarge)
Pancreatic Panniculitis Pathology. Histopathology of pancreatic panniculitis shows fat necrosis with saponification of adipocytes and a predominance of neutrophils.
Contributed by N Sathe, MD
(Click Image to Enlarge)
Erythema Induratum of Bazin. Histopathology in the early stages shows neutrophils with extensive necrosis of adipocytes, foamy histiocytes, and multinucleated giant cells. Caseous necrosis and liquefaction may appear when arteries are severely damaged.
Contributed by P Chu, MD
(Click Image to Enlarge)
Erythema Nodosum, Low Power. The low-power histology image shows thickened subcutaneous fat septa with varying inflammatory infiltrates depending on the lesion's age.
Contributed by P Chu, MD
(Click Image to Enlarge)
Erythema Nodosum, High Power. The high-power image highlights Miescher radial microgranulomas, characterized by small histiocytes clustered around a central star-shaped cleft, a hallmark of erythema nodosum.
Contributed by P Chu, MD
(Click Image to Enlarge)
Leukocytoclastic Vasculitis Pathology. Histopathology of leukocytoclastic vasculitis reveals septal inflammation with necrosis of postcapillary venule walls, evident as necrotic endothelial cells, neutrophils, nuclear dust, and fibrin deposition in the vessel walls.
Contributed by P Chu, MD
(Click Image to Enlarge)
Low-Power Pathological Findings of Necrobiosis Lipoidica: Skin Biopsy. Histopathology shows layers of granulomatous inflammation, occasional multinucleated giant cells, histiocytes, plasma cells, and alternating zones of degenerated collagen without mucin.
Contributed by P Chu, MD
(Click Image to Enlarge)
High-Power Pathological Findings of Necrobiosis Lipoidica: Skin Biopsy. Histopathology shows layers of granulomatous inflammation, occasional multinucleated giant cells, histiocytes, plasma cells, and alternating zones of degenerated collagen without mucin.
Contributed by P Chu, MD
(Click Image to Enlarge)
Necrobiotic Xanthogranuloma Pathology, Low Power. Histopathology shows large areas of necrobiosis alternating with granulomatous inflammation, including foamy histiocytes, cholesterol clefts, and Touton giant cells, which are characterized by a wreath of nuclei surrounded by a peripheral rim of foamy cytoplasm.
Contributed by P Chu, MD
(Click Image to Enlarge)
Necrobiotic Xanthogranuloma Pathology, High Power. Histopathology shows large areas of necrobiosis alternating with granulomatous inflammation, including foamy histiocytes, cholesterol clefts, and Touton giant cells, which are characterized by a wreath of nuclei surrounded by a peripheral rim of foamy cytoplasm.
Contributed by P Chu, MD
(Click Image to Enlarge)
Rheumatoid Nodule Pathology. Histopathology shows large areas of necrobiosis with eosinophilic material composed of fibrin, surrounded by palisading histiocytes within the dermis and subcutaneous fat.
Contributed by P Chu, MD
(Click Image to Enlarge)
Sclerosing Panniculitis, Low Power. Histopathological findings vary by stage. Early stages show ischemic necrosis at the lobule center, sparse lymphocytic infiltrate, and extravasation of erythrocytes and hemosiderin.
Contributed by P Chu, MD
(Click Image to Enlarge)
Sclerosing Panniculitis, High Power. Late-stage lesions show sclerosis of the septa, fat necrosis, and lipomembranous change, which is observed as an eosinophilic feathery lining composed of anuclear cystic adipocytes. Lipomembranous change suggests lipodermatosclerosis.
Contributed by P Chu, MD
(Click Image to Enlarge)
Post-steroid Panniculitis Pathology. Histopathology shows less inflammation and fewer needle-shaped clefts.
Contributed by P Chu, MD
(Click Image to Enlarge)
Subcutaneous Fat Necrosis of the Newborn, Low Power. This image shows subcutaneous fat necrosis, a self-resolving panniculitis in neonates, typically affecting the thighs, cheeks, and buttocks. Key histopathological features include needle-shaped clefts within adipocytes, indicative of the condition's hallmark.
Contributed by P Chu, MD
(Click Image to Enlarge)
Subcutaneous Fat Necrosis of the Newborn, High Power. The high-power image reveals a dense lymphocytic infiltrate associated with subcutaneous fat necrosis. Electron microscopy shows needle-shaped crystals in parallel and macrophages surrounding necrotic fat cells.
Contributed by P Chu, MD
(Click Image to Enlarge)
Thrombophlebitis Pathology. The histopathology reveals vasculitis and thrombosis occluding the lamina.
Contributed by P Chu, MD
(Click Image to Enlarge)
Traumatic Panniculitis Pathology. The image shows areas of fat necrosis in the subcutis with cystic spaces of varying sizes and shapes within fat lobules, along with varying degrees of hemorrhage and fibrosis.
Contributed by P Chu, MD
(Click Image to Enlarge)
Polyarteritis Nodosa Pathology. Histopathology of cutaneous polyarteritis nodosa reveals the involvement of the septa's small-to-medium–sized arteries and arterioles. Lesions show prominent fibrinoid necrosis and fibrin deposition, with the destruction of the tunica intima.
Contributed by P Chu, MD
(Click Image to Enlarge)
Granuloma Annulare, Low Power. The low-power image shows subcutaneous granuloma annulare with infiltrates of palisading histiocytes surrounding mucin and areas of basophilic degeneration of collagen bundles.
Contributed by SR Zaidi, MD
(Click Image to Enlarge)
Granuloma Annulare, High Power. The high-power image shows subcutaneous granuloma annulare with infiltrates of palisading histiocytes surrounding mucin and areas of basophilic degeneration of collagen bundles.
Contributed by N Sathe, MD
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