Skin manifestations

This study addresses the elevated prevalence of skin and soft tissue infections (SSTIs) within the pediatric demographic, necessitating a comprehensive inquiry into their varied clinical manifestations. The primary objectives involve the assessment of clinical and laboratory characteristics of SSTIs in children and an exploration of their correlation with treatment efficacy.

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Clinical Manifestations Infection is acquired as the result of a break in the epithelium during sexual contact with an infected individual. After an incubation period of 4–7 days, the initial lesion—a papule with surrounding erythema—appears. In 2 or 3 days, the papule evolves into a pustule, which spontaneously ruptures and forms a sharply circumscribed ulcer that is generally not indurated (Fig. 139-2). The ulcers are painful and bleed easily; little or no inflammation of the surrounding skin is evident.

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The clinical manifestations of DGI have sometimes been classified into two stages: a bacteremic stage, which is less common today, and a joint-localized stage with suppurative arthritis. A clear-cut progression usually is not evident. Patients in the bacteremic stage have higher temperatures, and their fever is more frequently accompanied by chills. Painful joints are common and often occur in conjunction with tenosynovitis and skin lesions. Polyarthralgias usually include the knees, elbows, and more distal joints; the axial skeleton is generally spared.

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Harrison's Internal Medicine Chapter 137. Gonococcal Infections Definition Gonorrhea is a sexually transmitted infection (STI) of epithelium and commonly manifests as cervicitis, urethritis, proctitis, and conjunctivitis. If untreated, infections at these sites can lead to local complications such as endometritis, salpingitis, tuboovarian abscess, bartholinitis, peritonitis, and perihepatitis in female patients; periurethritis and epididymitis in male patients; and ophthalmia neonatorum in newborns.

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Association of Virulence Mechanisms with Specific Meningococcal Infections Specific disease manifestations of meningococcal infections have specific virulence and pathogenic mechanisms, as described below for fulminant meningococcemia and meningitis. Fulminant Meningococcemia Purpura Fulminans Fulminant meningococcemia is perhaps the most rapidly lethal form of septic shock experienced by humans. It differs from most other forms of septic shock by the prominence of hemorrhagic skin lesions (petechiae, purpura; see Fig. 52-5) and the consistent development of DIC.

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Sepsis with Skin Manifestations (See also Chap. 18) Maculopapular rashes may reflect early meningococcal or rickettsial disease but are usually associated with nonemergent infections. Exanthems are usually viral. Primary HIV infection commonly presents with a rash that is typically maculopapular and involves the upper part of the body but can spread to the palms and soles. The patient is usually febrile and can have lymphadenopathy, severe headache, dysphagia, diarrhea, myalgias, and arthralgias.

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Rare patients with localized early stage mycosis fungoides can be cured with radiotherapy, often total-skin electron beam irradiation. More advanced disease has been treated with topical glucocorticoids, topical nitrogen mustard, phototherapy, psoralen with ultraviolet A (PUVA), electron beam radiation, interferon, antibodies, fusion toxins, and systemic cytotoxic therapy. Unfortunately, these treatments are palliative. Adult T Cell Lymphoma/Leukemia Adult T cell lymphoma/leukemia is one manifestation of infection by the HTLV-I retrovirus.

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Polymorphous Light Eruption After sunburn, the most common type of photosensitivity disease is polymorphous light eruption (PLE), the mechanism of which is unknown. Many affected individuals never seek medical attention because the condition is often transient, becoming manifest each spring with initial sun exposure but then subsiding spontaneously with continuing exposure, a phenomenon known as "hardening.

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Dermatomyositis The cutaneous manifestations of dermatomyositis (Chap. 383) are often distinctive but at times may resemble those of systemic lupus erythematosus (SLE) (Chap. 313), scleroderma (Chap. 316), or other overlapping connective tissue diseases (Chap. 316). The extent and severity of cutaneous disease may or may not correlate with the extent and severity of the myositis.

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Lupus Erythematosus The cutaneous manifestations of lupus erythematosus (LE) (Chap. 313) can be divided into acute, subacute, and chronic types. Acute cutaneous LE is characterized by erythema of the nose and malar eminences in a "butterfly" distribution (Fig. 55-5). The erythema is often sudden in onset, accompanied by edema and fine scale, and correlated with systemic involvement. Patients may have widespread involvement of the face as well as erythema and scaling of the extensor surfaces of the extremities and upper chest.

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Harrison's Internal Medicine Chapter 55. Immunologically Mediated Skin Diseases Immunologically Mediated Skin Diseases: Introduction A number of immunologically mediated skin diseases and immunologically mediated systemic disorders with cutaneous manifestations are now recognized as distinct entities with consistent clinical, histologic, and immunopathologic findings. Many of these disorders are due to autoimmune mechanisms.

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Also associated with systemic diseases. b Reviewed in section on Purpura. cReviewed in section on Papulonodular Skin Lesions. d Favors plantar surface of the foot. Note: TEN, toxic epidermal necrolysis. Livedoid vasculopathy (livedoid vasculitis; atrophie blanche) represents a combination of a vasculopathy plus intravascular thrombosis. Purpuric lesions and livedo reticularis are found in association with painful ulcerations of the lower extremities. These ulcers are often slow to heal, but when they do, irregularly shaped white scars are formed.

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Palpable purpura are further subdivided into vasculitic and embolic. In the group of vasculitic disorders, cutaneous small-vessel vasculitis, also known as leukocytoclastic vasculitis (LCV), is the one most commonly associated with palpable purpura (Chap. 319). Underlying etiologies include drugs (e.g., antibiotics), infections (e.g., hepatitis C virus), and autoimmune connective tissue diseases. Henoch-Schönlein purpura is a subtype of acute LCV that is seen primarily in children and adolescents following an upper respiratory infection.

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Systemic causes of nonpalpable purpura fall into several categories, and those secondary to clotting disturbances and vascular fragility will be discussed first. The former group includes thrombocytopenia (Chap. 109), abnormal platelet function as is seen in uremia, and clotting factor defects. The initial site of presentation for thrombocytopenia-induced petechiae is the distal lower extremity.

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Blue Lesions Lesions that are blue in color are the result of either vascular ectasias and tumors or melanin pigment in the dermis. Venous lakes (ectasias) are compressible dark-blue lesions that are found commonly in the head and neck region. Venous malformations are also compressible blue papulonodules and plaques that can occur anywhere on the body, including the oral mucosa. When there are multiple rather than single congenital lesions, the patient may have the blue rubber bleb syndrome or Mafucci's syndrome.

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White Lesions In calcinosis cutis there are firm white to white-yellow papules with an irregular surface. When the contents are expressed, a chalky white material is seen. Dystrophic calcification is seen at sites of previous inflammation or damage to the skin. It develops in acne scars as well as on the distal extremities of patients with scleroderma and in the subcutaneous tissue and intermuscular fascial planes in DM. The latter is more extensive and is more commonly seen in children.

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Pink Lesions The cutaneous lesions associated with primary systemic amyloidosis are often pink in color and translucent. Common locations are the face, especially the periorbital and perioral regions, and flexural areas. On biopsy, homogeneous deposits of amyloid are seen in the dermis and in the walls of blood vessels; the latter lead to an increase in vessel wall fragility. As a result, petechiae and purpura develop in clinically normal skin as well as in lesional skin following minor trauma, hence the term pinch purpura.

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Common causes of erythematous subcutaneous nodules include inflamed epidermoid inclusion cysts, acne cysts, and furuncles. Panniculitis, an inflammation of the fat, also presents as subcutaneous nodules and is frequently a sign of systemic disease. There are several forms of panniculitis, including erythema nodosum, erythema induratum/nodular vasculitis, lupus profundus, lipodermatosclerosis, α1-antitrypsin deficiency, factitial, and fat necrosis secondary to pancreatic disease. Except for erythema nodosum, these lesions may break down and ulcerate or heal with a scar.

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Red Lesions Cutaneous lesions that are red in color have a wide variety of etiologies; in an attempt to simplify their identification, they will be subdivided into papules, papules/plaques, and subcutaneous nodules. Common red papules include arthropod bites and cherry hemangiomas; the latter are small, bright-red, domeshaped papules that represent benign proliferation of capillaries.

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Several metabolic disorders are associated with blister formation, including diabetes mellitus, renal failure, and porphyria. Local hypoxia secondary to decreased cutaneous blood flow can also produce blisters, which explains the presence of bullae over pressure points in comatose patients (coma bullae). In diabetes mellitus, tense bullae with clear viscous fluid arise on normal skin. The lesions can be as large as 6 cm in diameter and are located on the distal extremities. There are several types of porphyria, but the most common form with cutaneous findings is PCT.

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