Epidermal necrosis

Toxic epidermal necrolysis Epidermal necrosis with skin detachment Present As above Supportive0... 

Exposure to high concentrations may cause tracheobronchitis and pulmonary edema. The irritation threshold in humans is 0.2 5-0.5 ppm, and concentrations above Ippm are extremely irritating to all mucous membranes within 5 minutes. Fatalities have been reported at levels as low as 10ppm, and 150 ppm was lethal after 10 minutes. The violent irritant effect usually prevents chronic toxicity in humans. Skin contact causes irritation, burns, and epidermal necrosis." Eye splashes cause corneal damage, palpebral edema, blepharoconjunctivitis, and fibrinous or purulent discharge. ... 

Ethyl acrylate applied to the skin of mice three times per week for life caused dermatitis, dermal fibrosis, epidermal necrosis, and hyperkeratosis neoplastic changes were not observed. ... 

Idiosyncratic dmg reactions (IDRs) are most commonly characterized by a reaction involving fever or rash, with or without internal organ involvement. The spectrum of responses ranges from a minor rash, to potentially fatal toxic epidermal necrosis and Stevens-Johnson syndrome. Immunoglobulin E (IgE)-mediated anaphylactic shock, occasional joint pain, hepatotoxicity or nephrotoxicity are also well documented [24]. The frequency of such reactions are unknown but estimated to be between 1 1000 and 1 10000 exposures and may be enhanced on re-challenging susceptible individuals with the same dmg. 

Dermal/Ocular Effects. Schonning (1966) described a case of a 57- year-old man who accidentally spilled acrolein over his genital area. Swelling of the penis and scrotum occurred, and after 15 days the genital area was deeply ulcerated and gangrenous. No follow-up information was provided. Lacroix et al. (1976) applied a solution of 10% acrolein in ethanol to 12 volunteers the skin was biopsied 48 hours later. All subjects exhibited irritation and had papillary edema, and 11 had polymorphonuclear infiltrates. In addition, five cases of epidermal necrosis occurred. No further information was provided. 

Cases of accidental dermal contact with acrolein and studies with volunteers clearly indicate that acrolein is a strong dermal irritant, causing skin burns. A 10% solution in ethanol applied to the skin caused epidermal necrosis. 

Liquid splashes to the eye can cause corneal damage and exposures to concentrations of 0.25 ppm may cause eye irritation, lacrimation, conjunctivitis, lid edema, fibrinous or purulent discharge, and corneal injury. Splashes to the skin can result in dermal irritation, edema, and, in some cases, epidermal necrosis. 

In severe injuries (e.g., corrosions), extensive epidermal necrosis, with accompanying damage to the... 

Level 2 The skin is left to dry for 4-5 minutes between two successive coats. The second and third coats trigger more pronounced erythema and cloudy white frosting, as well as some pain and discomfort. The discomfort will last around quarter of an hour. Trauchessec " applies the solution once a week until results are achieved. The first treatment consists of only one coat, the second of two, and the third of three coats of solution. After level 2, the patient s skin feels dry and tight. The top layers of the epidermis, dried out by the solution, appear transparent but still stick to the underlying cells. Flaking occurs within 4-5 days. Locally, some areas may turn a brownish color where Jessner s solution has penetrated more deeply than anticipated. After three coats, the stratum corneum separates from the skin, there is no blistering or epidermal necrosis, and the dermis is not directly affected. 

Skin. The potential to cause skin irritation was investigated in rats, guinea pigs and mice who had 0.1 ml 12.5% CS in either com oil or acetone applied unoccluded to the shaven dorsal trunk skin for 6 h, and the area subsequently and periodically inspected up to 21 days for local reactions. Erythema was more marked than oedema, and both resolved by 7 days post-application. Histological examination of skin biopsies taken from a few animals at 3 days after CS application showed foci of epidermal necrosis in the contaminated area with spongiosis and acute inflammatory infiltration of the outer dermis (Ballantyne and Swanston, 1978). 

Often, less intense reactions are encountered. The epidermolytic, exfoliative toxins A and B attack the epidermidis causing epidermal necrosis (e.g., Sap/tytococcMX-scalded skin syndrome) [9]. Membrane-damaging toxins at infection sites (e.g., a-toxin, a-hemolysin) are a major factor in tissue damage after bacterial adherence has occurred. Other exoproteins, such as proteases, collage-nase, hyaluronidase, and lipase, act as virulence enhancers but do not actively destroy host tissues. 

If pure CA is applied to the nipple or to the flank of an unsensitized guinea pig, an erythema and edema appear at the site of the test. After 14 hours the histological examination shows epidermal lesions (vesicles, detachement of the epidermis, epidermal necrosis) and a dermal infiltrate which is partially composed of eosinophils which invade the epidermis. 

If pure PA is applied to the flank and nipple of unsensitized guinea pigs, a light redness is observed after 14 hours. Under histological examination the lesions of the flank and nipple are numerous intra-epidermal vesicles, epidermal detachment, epidermal necrosis, dermal infiltrate with numerous eosinophils which also invade the epidermis. 

In some sections more or less extended epidermal necrosis and detachment of the epidermis are seen, in others intra-epidermal abcesses may be observed. In the upper dermis, the small vessels are dilated and there are extravasations. The infiltrate is very extensive, being composed of small round cells, connective tissue cells, and eosinophils. The eosinophils are intra- and perivascular. We cannot say, as we did in the sensitization with CA, that the infiltrate is largely composed of eosinophils, but we can affirm that these are much more numerous than in the sensitization with DNCB. 

Fig. 20. Guinea pig sensitized to PA. Flank 14 hours after a single application of 25% PA in dioxane epidermal necrosis, infiltrate...

Achromasia, superficial necrosis, karyopyknosis, possibly acantholysis and superficial vesicles/bullae Acantholysis, karyopyknosis, complete epidermal necrosis, intraepidermal vesicles/bullae... 

Achromasia, superficial or complete epidermal necrosis, subepidermal vesicles/bullae... 

Serious events - meloxicam has been implicated in the following serious adverse events GI bleeding, MI, stroke, GI ulceration and perforation, anaphylactoid reactions, HTN, CHF, bronchospasm, nephrotoxicity, renal papillary necrosis, hepatotoxicity, exfoliative dermatitis, blood dyscrasias, anemia, toxic epidermal necrosis, Stevens-Johnson syndrome, thromboembolism [1,5]. 

There were no cases of osteonecrosis of the jaw, toxic epidermal necrosis, Ste-vens-Johnson syndrome, or drug rash with eosinophilia and systemic symptoms (DRESS). 

Skin A serious cutaneous adverse reaction was recently linked to tranexamic acid in a patient with liver cirrhosis and acute rectal bleeding. A 67-year-old male was prescribed oral tranexamic acid, which partially resolved his symptoms. However, 10 days after treatment began a purplish rash appeared on the patient s trunk, which became confluent with blisters and epidermal necrosis over the following days. Tranexamic acid was suspended and a skin biopsy was found to be consistent with toxic epidermal necrosis (TEN). Resolution of the skin lesions was favourable with fluid replacement, oral prednisone and N-acetylcysteine, but after 2 weeks the patient died secondary to acute renal failure, respiratory infection and multiorgan failure. This is the first report of TEN that occurred in a patient being treated with oral tranexamic acid [66 ]. 

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