Skin bulla

Annobil SH. 1988. Skin bullae following kerosene poisoning. Ann Trop Pediatr 8(l) 45-47. 

Estimated prevalence of clinically overt disease in the United Kingdom. Skin lesions and neurovisceral crises may occur alone or together. Fragile skin, bullae. 

Acute photosensitivity without fragile skin, bullae. 

IV. Diagnosis is usually based on a history of ingestion and should be suspected in any epileptic patient with stupor or coma. Although skin bullae are sometimes seen with barbiturate overdose, these are not specific for barbiturates. Other causes of coma should also be considered (see p 19). 

Intermediate (within 24 AH hours) Blisters and bullae indicate severe skin and tissue ischemia. 

Late The skin becomes violaceous and progressively gangrenous hemorrhagic bullae may be present. Septic shock may ensue. 

In the OECD test guideline for skin sensitization (OECD TG 406), the following definition is given Skin sensitization (allergic contact dermatitis) is an immunologically mediated cutaneous reaction to a substance. In the human, the responses may be characterized by pruritis, erythema, edema, papules, vesicles, bullae, or a combination of these. In other species, the reactions may differ and only erythema and edema may be seen. ... 

Kerosene on the skin for 20 minutes in a 45-year-old man produced erythema, bullae, burning, and itching. In another case study, three boys (2-15 years old) and 1 girl (2 years old) exhibited blisters, erythema, fiaccid bullae, pustules, soreness, burning, and denudation of skin after dermal exposure. "... 

Skin sensitization Allergic contact dermatitis. An immunologically modulated cutaneous reaction to a substance or chemical by the animal. Response by humans to skin sensitization are observed in the form of erythema, edema, papules, pruritis, bullae, and vesicles. 

Skin Irritation and redness with delayed production of wheals, vesicles, or bullae, followed later by areas of necrosis (see Table 25.7). 

Photo 27.3 Twenty days after exposure. Note rupture of the bulla, with dead skin becoming whitish and the surrounding epidermis showing areas of dry desquamation. (Oliveira et al., 1991. Reproduced with permission of the Health Physics Society.)... 

The skin initially pales and then becomes erythematous within a few hours of exposure (Requena et al, 1988). Erythema, blisters, bulla, and small vesicles form over 2 to 24 h. The blisters can progress for several more days. Erythema resolves over 3 to 7 days, while ulcers take 6 to 8 weeks to heal (Garigan, 1996 Sidell et al, 1997). Discoloration (brown or black hyperpigmentation) commonly occurs after resolution of the bums, especially in areas with thinner skin (Requena et al, 1988). 

The skin, which is unlikely to react unfavorably to topical boric acid, can react strongly if it is absorbed systemically resultant redness can mimic scarlet fever, and psoriasiform lesions, bullae, and alopecia can occur. 

A 67-year-old man presented with an acute bullous eruption 6 weeks after starting bumetanide. He had numerous large tense bullae on erythematous skin, with superficial ulceration on the thighs, arms, and anterior trunk. Pruritus was severe. Routine laboratory tests were normal, except for blood eosinophilia. Biopsy of a blister showed subepidermal bullae associated with dermal infiltrates of neutrophils and eosinophils. Direct immunofluorescence showed continuous linear deposits of C3 and IgG at the basement membrane zone, confirmed by immunoelectron microscopy. Circulating IgG antibasement membrane antibodies were localized in the roof of the blister. Compete clinical heahng and normalization of immunology occurred within 2 months of withdrawal of bumetanide. 

Bullous pemphigoid has been reported in an 84-year-old man after topical therapy with fluorouracil 1% solution daily over several days for actinic keratosis. All treated lesions became bullous, with the development of a few bullae on untreated areas of normal skin. Bullous lesions were pruritic and sore and some contained hemorrhagic fluid. There was a leukocytosis (11.7 x 10 /1). The blister fluid contained predominantly eosinophils, and immuno-fluorescent studies of the serum and blister fluid showed anti-basement membrane antibody titers of 1 640 and 1 160 respectively. Fluorouracil was discontinued and the patient was treated with steroids and saline compresses, with abatement of symptoms (119). 

A 75-year-old man with prostatic carcinoma took flutamide for 18 months and developed blisters on the back of the hands and fingers after exposure to the sun (4). The bullae were associated with skin fragility and atrophic scarring. Histopathology and direct immunofluorescence showed ultrastructural features similar to those described in porphyria cutanea tarda. However, porphyrin concentrations in the urine and blood were normal. Flutamide was withdrawn and the lesions healed, without relapse after 11 months. 

Maculopapular rash, urticaria, and itching have been reported itching may be more common with mefloquine than with chloroquine. However, there are isolated case reports concerning more serious skin conditions exfoliative dermatitis (36) cutaneous vascuhtis (SEDA-17, 3) and a bilateral facial rash, comprising raised red lesions and flat bullae (SEDA-17, 329). 

A 65-year-old Caucasian woman developed a localized skin eruption within hours of using ketoprofen gel on her knees to relieve arthralgia (187). The lesions were pruritic, well-demarcated, and erythematous, and later became studded with vesicles and small bullae. Histology and immunopathology suggested autoimmune pemphigus. 

A 32-year-old HIV-positive man, who had been treated with didanosine and lamivudine, added saquinavir (600 mg tds) because of a rising plasma HIV-1 RNA viral load. Five days later he presented with a generalized maculopapular skin eruption, the lesions being centered on a bulla, and erosive lesions on the palate. Histological examination was compatible with erythema multiforme. Saquinavir was discontinued and all the mucocutaneous lesions healed within 15 days. RechaUenge was not attempted. 

There have been several cases of tiopronin-induced pemphigus, characterized by intra-epidermal bullae with acantholysis and epidermal intercellular deposition of IgG and C3 (17,18). The eruption can present as multiple red crusted macules. One patient first had pemphigus in association with penicillamine and later had a relapse while taking tiopronin (19). In skin explant cultures, tiopronin can cause acantholysis with intra-epidermal splits and bulla formation (20). 

A 52-year-old woman was given vancomycin 1 g intravenously bd and within 12 hours developed a generalized pruritic maculopapular rash (83). Over the next few days, the lesions progressively worsened and transformed into hemorrhagic and non-hemorrhagic vesicles and bullae. Mucosal surfaces, palms, and soles were spared. The skin lesions completely healed without scarring within 2 weeks of vancomycin withdrawal. There was no recurrence 5 months later. 

Characterized by thin-walled, easily ruptured, flaccid bullae that are seen to arise on normal or erythematous skin and over mucous membranes, the lesions of PV appear initially in the mouth (in about 60% of the cases) and then spread, after weeks or months, to involve the axillae and groin, scalp, face and neck. The lesions may become generalized. 

Lesions on sun-exposed skin, particularly the backs of the hands, forearm, and face, are present in all patients. These lesions are identical to those seen in the other bullous porphyrias (Table 32-4). Increased mechanical fragility of the skin, with trivial trauma leading to erosions, is present in virtually aU patients. Subepidermal bullae, hypertrichosis of the face, and patchy pigmentation are also common. Erosions and bullae heal slowly to leave atrophic scars, milia, and depigmented areas. Patchy or diffuse sclerodermatous changes are less common and, unlike the other skin lesions, may affect areas of the trunk that are not exposed to sun. 

EPP is characterized by life-long acute photosensitivity caused by accumulation of protoporphyrin-IX in the skin. The absence of fragile skin, subepidermal bullae, and hypertrichosis distinguishes it clinically from all other cutaneous porphyrias. 

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