Inflammatory Diseases of the Skin

Wortsman, Ximena; Carreño, Laura; Morales, Claudia

doi:10.1007/978-1-4614-7184-4_4

Ximena Wortsman MD²,
Laura Carreño MD³ &
Claudia Morales MD³

2075 Accesses
9 Citations

Abstract

This chapter reviews common inflammatory diseases of the skin that may undergo sonography. Fluid collections and fistulae, lipodermatosclerosis, panniculitis, psoriasis, morphea, warts, and hidradenitis suppurativa are among the several conditions that are covered in this chapter. A correlation of the clinical and sonographic findings is described and well illustrated using selected cases.

An insight into the world of sonography in psoriasis, morphea, lupus, dermatomyositis, and hidradenitis suppurativa, among others

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Ultrasound of the Subcutaneous Tissue

Dermatology and Pruritus Ani

Keywords

These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

1 Introduction

This chapter comprises several entities from different origins that can vary from trauma to viral infections or autoimmune diseases. Sonography has been proved useful for unmasking the anatomical changes that affect the skin layers and deeper structures during the inflammatory phases and also may show variable degrees of activity such as active, inactive, or atrophic stages in these conditions. In this chapter we will review the most common cutaneous inflammatory entities that may undergo ultrasonography.

The sonographer usually plays an active role in the assessment of the staging of inflammatory entities, sometimes having to extend the examination to other regions initially not previously requested by the referring physician. Thus, dealing with inflammatory conditions may also imply examining single or multiple lesions during the course of the same examination; therefore, baseline knowledge of the common sites of involvement in some of the entities may facilitate the process. Additionally, details such as sequential lighting of the examination room should be considered to properly place the probe when dealing with multiple locations.

2 Pathology

2.1 Hematomas-Seromas

Fluid collections secondary to trauma comprise one of the common causes of ultrasound requests in the soft tissues. The difference between hematomas and seromas is that hematomas contain a high presence of red blood cells, blot clots, and inflammatory cells in the acute phase that also show fibrin, granulation tissue, and debris in the late phases. In contrast, seromas (also called lymphoceles) are mainly composed of clear serous lymph fluid usually generated by leaks in the lymphatic network. Patients presenting with hemophilia, Ehler-Danlos syndrome, and sickle cell anemia may also easily have hematomas in the soft tissues. Thus, fluid hematic collections are frequently found in the cutaneous layers and can vary in their sonographic representation according to the main composition, phase of involvement, and presence of liquefaction that could also show a mixed pattern (sero-hematic collections). Hematomas may commonly present on sonography as anechoic collections that can turn to hypoechoic or heterogeneous within days or weeks. Seromas usually present as anechoic clean collections as a result of their serous component. At the beginning the fluid collections are usually compressible with the probe and at late stages, compression is hard to perform because the fluid has been replaced by fibrous tissue and scarring components. The size of the collection also varies over a short period of time (days) and the sonographic follow up could be an objective way to confirm the regression of the hematoma. The latter fact could be important when dealing with hemorrhagic soft-tissue tumors that can occasionally mimic hematomas, but these entities usually do not significantly regress over days. Hemorrhagic tumors commonly show a mixed echogenicity with hypoechoic-anechoic or heterogeneous echogenicity, and they present low or absent capability of compression with the probe. Color Doppler can show peripherical hypervascularity in hematomas at the initial stages and hypovascularity at the late phases [1–5] (Fig. 4.1).

2.2 Abscesses

Abscesses imply the presence of infection and/or pus within a fluid collection. Common causes of these organized collections are hematomas, ruptured epidermal cysts, inflamed pilonidal cysts, etc. Skin and soft-tissue infections are also the most common cause for hospital admission of injection drug users [6]. Abscesses present on ultrasound as distended anechoic or heterogeneous fluid collections, usually with multiple echoes or debris. They sometimes present anechoic communicating tracts to superficial (e.g., epidermal or subepidermal) or deep (e.g., muscular or articular) layers. Color Doppler usually demonstrates increase blood flow predominantly in the periphery of the collection [7]. Ultrasound-guided needle aspiration can be a useful technique for the identification of causative pathogens, and good results could be expected with ultrasound-guided gun biopsy culture from lesions without fluid collection [8] (Figs. 4.2 and 4.3).

2.3 Edema

The retention of fluid within the skin layers can be caused by various entities from trauma to inflammatory diseases. The venous and/or lymphatic systems usually fail to remove the excess of fluid that becomes stuck between the fatty lobules of the subcutaneous tissue. The incompetence of the lymphatic system is called lymphedema and differs from lipoedema, the latter being a different concept that implies an accumulation of fat abnormally distributed in the lower limbs [9]. Ultrasound has been reported to support the assessment of the changes in the thickness of the skin layers in post-thrombotic syndrome and the monitoring of the compression therapy in chronic venous disease [10]. Impairment of cutaneous microcirculation is a major predisposing factor in inflammation and ulceration in patients with chronic venous insufficiency (CVI). Increase of capillary filtration rate predisposes to the formation of edema. Local lymphedema is a complication of CVI and is often underdiagnosed [11]. On sonography, edema usually appears as anechoic fluid between the lobules of the subcutaneous tissue. In cases with lymphedema there is thickening of all the cutaneous layers, hypoechogenicity of the dermis, and increased echogenicity of the subcutaneous tissue in addition to the anechoic fluid between the fatty lobules of the hypodermis (Figs. 4.4 and 4.5).

2.4 Chronic Venous Insufficiency-Lipodermatosclerosis-Liposclerosis

This is the result of an impairment of the main superficial veins and their tributaries that elicit microvascular changes derived from venous ecstasy. Thus, veins and capillaries become dilated, elongated, and tortuous and their endothelium is injured generating an increased extravasation, leading to an enlarged pericapillary space, edema in the interstitial tissue, and to the clinical finding of swelling. Hemoglobin from extravasated erythrocytes in the pericapillary space is degraded to hemosiderin and is responsible for hyperpigmentation. Microthrombosis in the capillaries causes microinfarction and micronecrosis. Hence, skin areas with severe microangiopathy have reduced numbers of perfused nutritional capillaries. Furthermore, the increased blood flow in the deeper skin layers does not contribute to nutrition of the superficial skin layers. The microvascular ischemia is patchy and appears to be the main factor determining trophic changes and venous ulceration. The process of microinfarction and micronecrosis is followed by the formation of a granulation tissue, proliferation of capillaries and fibroblasts, and finally wound healing by formation of scar tissue destroying the microlymphatic network. Clinically this process leads to lipodermatosclerosis, also called liposclerosis (i.e., induration and hyperpigmentation), atrophy, and in its most extreme form, to ulceration where the compensating mechanisms are no longer able to repair the damage. Thus, incompetence of the superficial venous system can generate dilation and secondaryt edema in the skin layers. The most common affected veins are the saphenous venous system (greater and lesser saphenous veins), the perforans veins (i.e., drain superficial structures directly into the deep venous system, therefore, crossing the fascial plane), and communicating veins (i.e., connecting veins in the same fascial plane and venous system). The incompetent vessels and their venous reflux are detectable using sonography, the latter being a feature usually well demonstrated on color Doppler and spectral curve analysis, and mainly when performing the Valsalva maneuver, which is even more evident when the patient is in upright position. Clinically, the skin shows varicose veins (i.e., dilated, tortuous, and palpable veins), reticular veins (i.e., dilated but non-palpable veins), and/or telangiectasias (small reddish to purple non-palpable dilated venous tracts) [12, 13]. Ultrasound has been reported as useful for guiding treatments such as sclerotherapy supporting the localization of the insufficient venous tracts [14]. Lipodermatosclerosis is a consequence of deep venous insufficiency and a risk factor for the occurrence of venous leg ulceration. It is characterized by induration and hyperpigmentation of the skin involving one or both of the lower legs in a characteristic “inverted champagne bottle” appearance. Associated with venous insufficiency, chronic lipodermatosclerosis is most common in middle-aged women. In addition to the chronic form of presentation there is an acute form that exhibits symptoms of severe pain. On sonography, lipodermatosclerosis presents as a diffuse thickening and decreased echogenicity of the dermal layer commonly associated with superficial venous insufficiency signs [15–17] (Figs. 4.6, 4.7 and 4.8).

2.5 Panniculitis

Panniculitis implies the presence of inflammation in the adipose tissue of the subcutaneous layer. It can be associated with a wide range of systemic diseases or local injuries such as trauma or cold, among others.

Clinically, panniculitis is characterized by red, purplish, or skin-colored lumps. Nevertheless, the clinical features frequently show low specificity and can cause trouble with obtaining a diagnosis on the physical examination.

Panniculitis is usually somewhat mixed because the inflammatory infiltrate involves both the septa and lobules; however, histologically, panniculitis can be classified according to the main affected component in the subcutaneous tissue, hence it can be separated into two types: septal and lobular panniculitis, and then each subtype can be subdivided according to presence of vasculitis as follows:

1.
Septal panniculitis with vasculitis
2.
Septal panniculitis without vasculitis
3.
Lobular panniculitis with vasculitis
4.
Lobular panniculitis without vasculitis

Septal panniculitis with vasculitis includes leukocytoclastic vasculitis involving the small blood vessels of the septa; superficial thrombophlebitis resulting from inflammation and subsequent thrombosis of large veins of the septa; and cutaneous polyarteritis nodosa, which is a vasculitis that involves the arteries and arterioles of the septa of subcutaneous fat with few or no systemic manifestations. Often septal panniculitis without vasculitis is the consequence of dermal inflammatory processes extending to the subcutaneous fat, such as necrobiosis lipoidica, subcutaneous granuloma annulare, scleroderma, rheumatoid nodule, and necrobiotic xanthogranuloma. However, in other cases, the inflammatory process is primarily located in the fibrous septa of the subcutis with or without involvement of the overlying dermis such as in erythema nodosum, the most frequently seen septal panniculitis (without vasculitis). Erythema nodosum in fully developed lesions is characterized histopathologically by Miescher’s radial granulomas in the septa. On sonography, septal panniculitis (SP) shows prominent thickening and hypoechogenicity of the septa, in addition to the increased echogenicity of the fatty tissue. In contrast, lobular panniculitis primarily affects the lobules of the fatty subcutaneous tissue and can be observed in a wide spectrum of diseases such as erythema induratum of Bazin (nodular vasculitis), the most common variant of lobular panniculitis with vasculitis, or sclerosing panniculitis that results from chronic venous insufficiency of the lower extremities; calciphylaxis and oxalosis, which implies panniculitis with calcification of the vessel walls, sclerema neonatorum, an inflammatory disease with crystals within the adipocytes, subcutaneous fat necrosis of the newborn, and post-steroid panniculitis, among others. Lobular panniculitis may also be an expression of infections, trauma, or factitial causes involving subcutaneous fat. Lipodystrophies are common sequelae of panniculitis and can be separated in hypertrophic or atrophic, according to the increase or decrease in the fatty component [18–20]. On sonography, lobular panniculitis presents as marked blurriness and increased echogenicity of the fatty lobules of the subcutaneous tissue. Although the septa may present some degree of thickening and hypoechogenicity, these changes are less prominent compared with SP. In the presence of fat necrosis, anechoic or hypoechoic round-shaped pseudocystic structures have been reported as the result of fat liquefaction [21]. On color Doppler imaging, vascularity can be variable going from low to high although the hypovascularity in the subcutaneous tissue on the ultrasound examination does not detract the presence of vasculitis. Therefore, the primary role of ultrasound should be directed to assess the presence of panniculitis and ideally support the difference between mostly septal or lobular panniculitis (Figs. 4.9, 4.10, 4.11, 4.12 and 4.13).

2.6 Odontogenic Fistula

These fistulous tracts are commonly originated in dental inflammatory and infectious processes that drain into the soft tissues and open into the subepidermal or epidermal zones, commonly the maxillae or mandibular regions of the face. Clinically, these odontogenic fistulae may mimic a dermatologic origin, appearing as erythematous or bluish papulae that could drain viscous fluid. These lesions can also clinically mimic malignant skin tumors.

On sonography, the fistulous tracts usually appear as hypoechoic, sometimes slightly heterogeneous bands. The connection between the bony margin of the maxillae or mandible is usually assessed using sonography and commonly an erosion can be detected in the bony margin. With color Doppler imaging there is frequently hypervascularity in the periphery of the tracts [22, 23] (Figs. 4.14 and 4.15).

2.7 Mondor’s Disease

Mondor’s disease is a superficial vein thrombosis usually located in the subcutaneous tissue. The clinical sign is a cord-like palpable structure that tends to disappear over time. On sonography, the affected venous tract can be recognized as a tubular hypoechoic structure in correlation with the cord-like structure. Occasionally increased echogenicity of the subcutaneous tissue that surrounds the superficial vein can be found. On color Doppler imaging, no flow is detectable within the vessel in the acute phase. After a few weeks, the vascularity may return in concordance with the disappearance of the palpable cord-like structure and the ultrasound changes. Importantly, sonography may provide a tool to differentiate Mondor’s disease from linear morphea [24] (Fig. 4.16).

2.8 Warts

Warts are common entities caused by the infection with the human papilloma (HP) virus and can generate painful lesions that can clinically mimic a foreign body or Mortons’ neuroma when they are located in the plantar region. On physical examination, warts present as painful hyperkeratotic lesions frequently located in the soles of the feet. Warts can also affect other regions of the body, such as the hands. The HP virus causes an ingrown proliferation that usually shows an oval fusiform hypoechoic structure on sonography that affects the epidermis and dermis. Vascularity is variable and can go from hypo- to hypervascular in the sublesional dermis. Additionally, inflammatory changes in the vicinity of the wart that commonly affect the underlying plantar bursae can be detected. Painful warts (symptomatic) are usually associated with a higher presence of vascularity and bursitis [25, 26] (Figs. 4.17, 4.18, 4.19, 4.20 and 4.21).

2.9 Psoriasis

Psoriasis is an autoimmune inflammatory disease that affects the skin, nails, enthesis and joints. Clinically, typical psoriatic plaques are characterized by erythematous, itchy, and elevated areas with increased scaling. Commonly, patients may recognize that new lesions appear at sites of injury to the skin (Koebner’s phenomenon). These plaques commonly affect the extensor aspects and the scalp, but there are other forms of presentation that can also involve the flexor and intertriginous areas (i.e., axilla, groin, umbilical region, inframammary folds) with low or absent scaling. Less frequent types of psoriasis are guttate psoriasis, an acute form most commonly found in children after an upper respiratory infection and characterized by small droplike, salmon or pink papules, with fine scales; and pustular psoriasis (localized or generalized) that shows persistent pinhead-sized, sterile, sub-corneal pustules, persistent pustular eruptions of the hands and feet (localized) or affecting the skin in general. These pustules grow and merge into larger regions that can facilitate a secondary bacterial infection. The latter conditions can also affect the oral mucosa and the lips. Erythrodermic psoriasis, another rare and severe form of psoriasis, shows a widespread inflammation and erythroderma (i.e., exfoliative dermatitis) over most of the body surface. It can be accompanied by severe itching, swelling, and pain [27].

Nail involvement is extremely common in psoriasis and affects approximately 50 % of patients. In less than 5 % of the cases, the involvement of the nails can appear without cutaneous lesions. About 10–20 % of people with psoriasis also have psoriatic arthritis, and 80 % of patients with psoriatic arthritis (PsA) present nail psoriasis. Clinical manifestations of nail psoriasis are pitting, discoloration, onycholysis (i.e., separation of the nail plate from the nail bed), and subungual hyperkeratosis as well as nail plate crumbling and splinter hemorrhages [28].

Other types of inflammatory involvement in psoriasis include the joints, enthesis, and the bowel. PsA is a chronic inflammatory arthropathy associated with psoriasis, and is included among the seronegative spondyloarthropathies. The presence of cutaneous psoriasis is very important for correct and early diagnosis of PsA because the cutaneous lesions commonly precede the appearance of joint manifestations [29].

Histologically, psoriatic plaques show acanthosis (elongation of the rete ridges and corresponding dermal papillae), parakeratosis (presence of nucleated inmature keratinocytes in the stratum corneum), orthokeratosis (hypertrophy of the stratum corneum), loss of the granular cell layer, spongiform pustules, dermal mononuclear infiltrates, and parakeratotic microabscesses. At the nail, there is hyperkeratosis of the nail plates. Synovial proliferation is detected in the articular areas [30].

On sonography, psoriatic plaques show thickening of the epidermis and hypoechogenicity and thickening of the upper dermis. Occasionally, undulation of the epidermis can be detected. On color Doppler imaging, increased dermal blood flow is usually detected within the lesions. Ungual sonographic involvement varies according to the phase of activity of the disease, hence, going from early to late phases: thickening and decreased echogenicity of the ungual bed, focal hyperechoic spots in the ventral plates, and wavy plates and thickening of both plates (dorsal and ventral) can be found. Blood flow is usually increased in the proximal nail bed with low flow arterial vessels especially during the active phases of the disease. Joints can show prominent synovium, anechoic fluid, and periarticular erosions commonly in the interphalangeal joints. Tendinopathy that shows hypo- or heterogeneous echogenicity, usually at the insertion sites of the tendineous structures, has also been sonographically reported in patients with psoriasis even at subclinical stages. Increased blood flow may detected in the synovium on color Doppler imaging in active phases. Sonographic monitoring of treatment in psoriasis has been recently reported [31–33] (Fig. 4.22).

2.10 Morphea

Also known as localized scleroderma, morphea is a fibrosing disorder of the skin and underlying tissues. Morphea is differentiated from systemic sclerosis because of the absence of sclerodactyly, Raynaud phenomenon, and nail fold capillary changes. Nevertheless, patients with morphea commonly have systemic symptoms such as malaise, fatigue, arthralgias, and myalgias, as well as positive autoantibody serologies. However, morphea is almost uniformly limited to those tissues derived from the mesoderm. The underlying pathogenesis of morphea is not completely understood at this time, but ultimately it results in an imbalance of collagen production and destruction. Early morphea lesions present as erythematous to purple indurated lesions that turn into sclerotic, atrophic, hairless plaques with varying amounts of post-inflammatory hyperpigmentation. There are several clinical subtypes of morphea, the most common is the plaque type, also called circumscribed morphea, that presents as fewer that three discrete indurated plaques. The superficial variant is more frequent and localized and limited to the epidermis and dermis. The deep variant of plaque morphea is also called subcutaneous or deep; morphea can affect the subcutaneous tissue, fascia, and muscular layers. Some classifications included in the plaque-morphea variants are the guttate (drop-like) presentation, the atrophoderma of Pasini and Pierini, keloidal type, and the lichen sclerosis et atrophicus. Generalized morphea is defined as more than four indurated plaques larger than 3 cm and/or involving two or more corporal regions but sparing the face and hands. Linear morphea is the most common subtype in children and can present as “en coup de sabre” (ECDS), progressive hemifacial atrophy (Parry-Romberg syndrome [PRS]), or linear limb involvement. In these three subtypes the lesions progress rapidly to atrophy of the skin. ECDS can be associated with ocular and central nervous system involvement and usually presents on the paramedian forehead. Deep morphea involves the skin and deeper layers, such as muscle or bone. This type includes the morphea profunda that affect the subcutaneous tissue; eosinophilic fasciitis, which is a variant of deep morphea that affects the fascial plane; and pansclerotic morphea, that produces a circumferential involvement of the epidermis, dermis, subcutaneous tissue, muscle, and bone. The latter subtype elicits muscle atrophy, joint contractures, and non-healing ulcers. Patients with pansclerotic morphea and chronic wounds have been reported to present a high risk of squamous cell carcinoma of the skin. There is also a mixed variant of morphea composed by a combination of two or more subtypes [34, 35]. Histologically, the appearance of morphea can vary according with the phase of the disease. In the early stages, thickening of the collagen bundles, perivascular inflammatory infiltrates composed mainly of lymphocytes, plasma cells, and eosinophils can be detected. In the late stages, the inflammatory infiltrate regress and the dermal collagen bundles become more prominent and eosinophilic, and the eccrine glands, vessels, and subcutaneous fat become atrophic [34].

The activity of the disease can be monitored using sonography, therefore, the lesions can vary from hypoechogenicity and thickening of the dermis with hyperechogenicity of the subcutaneous tissue in the active phase, to thinning of the dermis and subcutaneous tissue in the atrophy phase. At the end stage (atrophy), a direct contact between the dermis and the muscle layer can be detected. Increased blood flow is commonly detected in the cutaneous layers during active phases. Nevertheless, the lesions become hypovascular on color Doppler imaging at the end stages. It is possible to detect the partial or full thickness involvement of the lesions and their asynchronic presentation using sonography (i.e., multiple lesions in different phases of activity). The most sensitive sonographic signs for detecting activity are cutaneous hypervascularity and increased echogenicity of the underlying subcutaneous tissue (100 % sensitivity and specificity for both). In patients that present with PRS (progressive hemifacial atrophy), the ipisilateral parotid gland has been reported to be affected with signs of inflammation [35–38] (Figs. 4.23, 4.24, 4.25, 4.26, 4.27, 4.28 and 4.29).

2.11 Cutaneous Lupus

Cutaneous lupus is the cutaneous form of lupus erythematous (LE) and may precede systemic involvement. The term ‘cutaneous lupus erythematosus’ (CLE) comprises several related autoimmune skin disorders, defined as ‘specific’ skin manifestations of LE. The spectrum of clinical presentation of CLE is wide, reaching from mild erythema to disseminated scarring skin lesions, all of them photosensitive dermatosis [39]. According to the phase of activity and presentation of the disease, there are three forms of cutaneous lupus: acute cutaneous lupus (classical malar erythematous eruption with a butterfly pattern in the midface and/or a generalized erythematous maculopapular eruption), subacute cutaneous lupus (non-scarring, non–atrophy-producing), and chronic cutaneous (discoid) lupus (scarring, atrophy producing) [40]. Nonspecific skin lesions such as generalized or acrolocalized (i.e., peripheral location such as limbs, fingers, or ears) vasculitis, livedo reticularis, and alopecia are frequently seen in patients with cutaneous lupus. Other typical cutaneous lupus subsets, such as lupus profundus/panniculitis, lupus tumidus, urticaria vasculitis, hypertrophic lupus, and bullous lupus are rather rare variants. Butterfly rash and/or macular exanthema are characteristic skin lesions of systemic LE rarely found in patients with cutaneous lupus [41]. It is the localized cutaneous form of lupus characterized by erythematous plaques or swellings that can evolve to atrophic or depigmented plaques at the end stage. Histologically, lupus presents mucin deposits, thick collagen, and inflammatory cells according to the stage of the disease.

On sonography, active cutaneous lupus shows hypoechogenicity and thickening of the dermis and increased echogenicity of the subcutaneous tissue. The hypoechogenicity of the dermis tends to adopt a fusiform shape. Lesional hypervascularity is commonly detected in active stages. Atrophy of the cutaneous layers and hypovascularity are common at the end stages (discoid lupus). Information about the involvement of vessels, such as the digital arteries, can be obtained. These vessels can present thrombotic and vasculitis phenomena, which can complicate the treatment and/or prognosis of the disease. These thromboses present as hypoechoic filling of the vessels using sonography. Absence of flow is demonstrated on the spectral curve analysis on color Doppler ultrasound [22, 42, 43] (Figs. 4.30, 4.31, 4.32, 4.33 and 4.34).

2.12 Dermatomyositis

Dermatomyositis is a systemic autoimmune disease that primarily affects skeletal muscle, skin, and the lungs. Although the disorder is rare, with a prevalence of one to ten cases per million in adults and one to 3.2 cases per million in children, early recognition and treatment are important ways to decrease the morbidity of systemic complications. Dermatomyositis is characterized by autoantibodies, tissue inflammation, parenchymal cell damage and death, and vasculopathy. Clinically, these patients present with “Gottron’s papules” (erythematous, usually symmetric and keratotic macules located over the methacarpal and interphalangeal joints that can mimic psoriasis), “heliotrope rash” (violaceous eruption on the upper eyelids and rarely on the lower eyelids), the shawl sign (erythematous, poikilodermatous macules distributed in a “shawl” pattern over the shoulders, arms, and upper back), the V-sign (erythematous eruption in a V-shaped distribution over the anterior neck and chest), and periungual telangiectasias. Calcinosis is usually subclinical, although when the deposits are large, they can be palpable as an induration and associated to hyperpigmentation. Proximal muscle weakness or pain (upper or lower extremity and trunk) and elevated serum creatine kinase or aldolase levels are common. The diagnosis is confirmed by histology that shows a mixed B- and T-cell perivascular inflammatory infiltrate and perifascicular muscular fiber atrophy on the muscle biopsy.

Increased echogenicity of the muscle secondary to edema can be detected on sonography. Contrast-enhanced ultrasound with its capability of measuring perfusion has been reported as a useful tool for diagnosing acute inflammation in poly- and dermatomyositis. Calcinosis can be also detected on sonography and presents as hyperechoic spots, usually with posterior acoustic shadowing. Increased echogenicity of the subcutaneous tissue secondary to panniculitis has also been reported [22, 44–47] (Figs. 4.35 and 4.36).

2.13 Hidradenitis Suppurativa

Hidradenitis suppurativa (HS), also called acne inversa, is a chronic and recurrent inflammatory disease affecting the skin that bears prominent hair follicles and apocrine glands. The exact cause is still controversial but seems to present an autoimmune origin. Clinically, HS shows painful, deep seated inflamed lesions including nodules, sinus tracts, and abscesses with scarring and inflammation in the axillae and groin regions. This disease can less commonly affect the buttock, vulvar, or inframammary regions. The severity of the disease can be clinically assessed using Hurley’s classification that separates the stages in: I mild, II moderate and III severe [48]. Histology shows follicular occlusion and inflammatory involvement of the apocrine glands with dense lymphocytic infiltrates around the hair follicle, and acute and chronic inflammatory cells around the apocrine glands. The inflamed sinus tracts frequently contain desquamated keratin, histiocytes, giant cells, and hair shafts within dense fibrosis. Squamous epithelium lined cyst or sinuses in the dermis all containing keratin and containing half hair shafts are usually observed [49]. On sonography, anechoic fluid collections with echoes (debris) and fragments of hair shafts, hypoechoic fistulous tracts in the dermis and subcutaneous tissue, thickening and hypoechogenicity of the dermis, and enlargement of the hair follicles can be detected. Frequently increased vascularity is observed in the periphery of the collections and regional lymph nodes seem to conserve the size, although they may present some cortical thickening during the inflammatory phases. Additionally, anechoic or hypoechoic dermal pseudocystic subclinical lesions in the dermis can be seen [50, 51]. Sonography may support the diagnosis and the assessment of severity in this recurrent disease [52] (Figs. 4.37, 4.38, 4.39, 4.40, 4.41, 4.42, 4.43 and 4.44).

2.14 Foreign Bodies

Foreign bodies are exogenous components that can be retained in the skin through many mechanisms commonly related to trauma. Occasionally, patients are not aware of the retained material but clinically they present with induration, erythema, and scarring. There are two main types of foreign bodies according to origin: organic (derived from living structures) such as splinters of wood or thorns of roses, or inert, also called synthetic, such as pieces of glass or metal.

Histology shows giant cells, macrophages, and inflammatory cells. Some foreign bodies such as wood, suture material, or glass are birefringent and can be identified using polarized light.

On sonography, foreign bodies appear as hyperechoic linear or band-like structures. Inert materials such as glass or metal usually show a posterior reverberance artifact. Commonly, there is hypoechoic granulomatous tissue surrounding the foreign body. Fluid collections in the vicinity such as hematomas or abscesses, or the involvement of deeper structures, can be ruled out. Occasionally, these foreign bodies may migrate and/or can be found far from the puncture wound level; therefore, it is suggested to examine a wide range of tissue. Sonography may prove their existence, assess the exact axis, location and measurements and also guide the removal. In an acute setting, the sonographer should avoid the contamination of the open wound with gel, therefore, the usage of sterile gel is recommended. In the presence of soft-tissue emphysema, a lateral approach to the wound or a water bath (when the lesional area is located in the distal arm or leg) can help [53–55] (Figs. 4.45, 4.46 and 4.47).

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Department of Radiology and Dermatology, Institute for Diagnostic Imaging and Research of the Skin and Soft Tissues, Clinica Servet, University of Chile, Faculty of Medicine, Almirante Pastene 150, Providencia, Santiago, Chile
Ximena Wortsman MD
Department of Pathology, Dermopathology Section, Hospital Clinico Universidad de Chile, Faculty of Medicine, University of Chile, Santiago, Chile
Laura Carreño MD & Claudia Morales MD

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Ximena Wortsman MD
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Laura Carreño MD
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Claudia Morales MD
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Correspondence to Ximena Wortsman MD .

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Clinica Servet, Faculty of Medicine, University of Chile, Almirante Pastene 150, Santiago, 7500551, Chile
Ximena Wortsman

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Wortsman, X., Carreño, L., Morales, C. (2013). Inflammatory Diseases of the Skin. In: Wortsman, X. (eds) Dermatologic Ultrasound with Clinical and Histologic Correlations. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-7184-4_4

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DOI: https://doi.org/10.1007/978-1-4614-7184-4_4
Published: 17 May 2013
Publisher Name: Springer, New York, NY
Print ISBN: 978-1-4614-7183-7
Online ISBN: 978-1-4614-7184-4
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Inflammatory Diseases of the Skin

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