Chapter 054. Skin Manifestations of Internal Disease (Part 14)

Also systemic.fIn adults, associated with renal failure and immunocompromised state.Vesicles and bullae are also seen in contact dermatitis, both allergic and irritant forms (Chap. 53). When there is a linear arrangement of vesicular lesions, an exogenous cause should be suspected. Bullous disease secondary to the ingestion of drugs can take one of several forms, including phototoxic eruptions, isolated bullae, Stevens-Johnson syndrome (SJS), and toxic epidermal necrolysis (TEN) (Chap. 56). Clinically, phototoxic eruptions resemble an exaggerated sunburn with diffuse erythema and bullae in sun-exposed areas. The most commonly associated drugs are doxycycline, sulfonamides, thiazides, NSAIDs,and psoralens. The development of a...
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Chapter 054. Skin Manifestations of Internal Disease (Part 14) Chapter 054. Skin Manifestations of Internal Disease (Part 14) e Also systemic. f In adults, associated with renal failure and immunocompromised state. Vesicles and bullae are also seen in contact dermatitis, both allergic andirritant forms (Chap. 53). When there is a linear arrangement of vesicular lesions,an exogenous cause should be suspected. Bullous disease secondary to theingestion of drugs can take one of several forms, including phototoxic eruptions,isolated bullae, Stevens-Johnson syndrome (SJS), and toxic epidermal necrolysis(TEN) (Chap. 56). Clinically, phototoxic eruptions resemble an exaggeratedsunburn with diffuse erythema and bullae in sun-exposed areas. The mostcommonly associated drugs are doxycycline, sulfonamides, thiazides, NSAIDs,and psoralens. The development of a phototoxic eruption is dependent on thedoses of both the drug and ultraviolet (UV)-A irradiation. Toxic epidermal necrolysis is characterized by bullae that arise onwidespread areas of erythema and then slough. This results in large areas ofdenuded skin. The associated morbidity, such as sepsis, and mortality arerelatively high and are a function of the extent of epidermal necrosis. In addition,these patients may also have involvement of the mucous membranes and intestinaltract. Drugs are the primary cause of TEN, and the most common offenders arephenytoin, barbiturates, carbamazepine, sulfonamides, penicillins, and NSAIDs.Severe acute graft-versus-host disease (grade 4) can also resemble TEN. In erythema multiforme (EM), the primary lesions are pink-red macules andedematous papules, the centers of which may become vesicular. The clue to thediagnosis of EM, as opposed to a morbilliform exanthem, is the development of adusky violet color or petechiae in the center of the lesions. Target or iris lesionsare also characteristic of EM and arise as a result of active centers and borders incombination with centrifugal spread. However, iris lesions need not be present tomake the diagnosis of EM. EM has been subdivided into two major groups: (1) EM minor due toherpes simplex virus (HSV); and (2) EM major due to HSV, Mycoplasmapneumoniae, or rarely drugs. Involvement of the mucous membranes (oral, nasal,ocular, and genital) is seen more commonly in the latter form. Hemorrhagic crustsof the lips are characteristic of EM major and SJS as well as herpes simplex,pemphigus vulgaris, and paraneoplastic pemphigus. Fever, malaise, myalgias, sorethroat, and cough may precede or accompany the eruption. The lesions of EMusually resolve over 3–6 weeks but may be recurrent, especially when due toHSV. In addition to HSV (in which lesions appear 7–12 days after the viraleruption), EM can also follow vaccinations, radiation therapy, and exposure toenvironmental toxins. Induction of SJS is most often due to drugs, especially sulfonamides,phenytoin, barbiturates, penicillins, and carbamazepine. Widespread duskymacules and significant mucosal involvement are characteristic of SJS, and thecutaneous lesions may or may not develop epidermal detachment. If the latteroccurs, by definition, it is limited to 30% BSA). In addition to primary blistering disorders and hypersensitivity reactions,bacterial and viral infections can lead to vesicles and bullae. The most commoninfectious agents are HSV (Chap. 172), varicella-zoster virus (Chap. 173), and S.aureus (Chap. 129). Staphylococcal scalded-skin syndrome (SSSS) and bullous impetigo aretwo blistering disorders associated with staphylococcal (phage group II) infection.In SSSS, the initial findings are redness and tenderness of the central face, neck,trunk, and intertriginous zones. This is followed by short-lived flaccid bullae and aslough or exfoliation of the superficial epidermis. Crusted areas then develop,characteristically around the mouth. SSSS is distinguished from TEN by thefollowing features: younger age group (primarily infants), more superficial site ofblister formation, no oral lesions, shorter course, less morbidity and mortality, andan association with staphylococcal exfoliative toxin (exfoliatin), not drugs. Arapid diagnosis of SSSS versus TEN can be made by a frozen section of the blisterroof or exfoliative cytology of the blister contents. In SSSS the site ofstaphylococcal infection is usually extracutaneous (conjunctivitis, rhinorrhea,otitis media, pharyngitis, tonsillitis), and the cutaneous lesions are sterile, whereasin bullous impetigo the skin lesions are the site of infection. Impetigo is morelocalized than SSSS and usually presents with honey-colored crusts. Occasionally,superficial purulent blisters also form. Cu ...