When A Patient Has A Post-Op Bullous Reaction
- Volume 26 - Issue 4 - April 2013
- 6840 reads
- 5 comments
Cutaneous drug eruptions are a common cause of rash, itching and blistering of skin. Typically, drug eruptions occur seven to 10 days following administration of a drug. It can, however, take up to three weeks for a rash to develop. Medications that patients have taken for many years are less likely to be a source of the drug eruption. In some cases, a drug eruption can occur up to three weeks after discontinuing drug use (i.e. penicillin). The most common drugs that are associated with cutaneous drug eruptions include: antibiotics (especially penicillin-based drugs), NSAIDs, sulfa-based medications and anti-convulsants such as phenytoin (Dilantin, Pfizer). The classification of drug eruptions includes erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis, erythroderma and exanthematous pustulosis.
Life-threatening reactions include Stevens-Johnson syndrome, toxic epidermal necrolysis, erythroderma and angioedema.
The classic appearance of erythema multiforme is a target or bull’s eye lesion. Patients with erythema multiforme generally have a prodromal period of flu-like symptoms before developing the cutaneous reaction. The most common area for erythema multiforme is on the hands and feet.
Stevens-Johnson syndrome is typically associated with fever, malaise, myalgia, arthralgia and extensive erythema multiforme lesions on the trunk and face. Blistering may affect up to 10 percent of the patient’s body surface.
Toxic epidermal necrolysis, which is the most severe reaction, can lead to bullous lesions comprising up to 30 percent of the patient’s body surface area. There is a high mortality rate approaching 40 percent.1 Typically, there is a prodromal period of nausea, chest pain, fever, malaise, sore throat and conjunctivitis. In about half the cases, there is oral involvement.
Contact dermatitis is a dermatologic condition in which an inflammatory reaction occurs due to direct contact of a substance. There are two types of contact dermatitis. Irritant dermatitis is the most common type and is typically caused by acids, alkalies, fabric softeners and solvents. Clinically, irritant contact dermatitis generally looks like a sunburn.
What You Should Know About Allergic Contact Dermatitis
Allergic contact dermatitis is caused by exposure to a substance to which the body has sensitivity or allergic reaction. The common culprits causing allergic contact dermatitis include tape and adhesives; topical antibiotics (especially neomycin); fabrics; metals (nickel); rubber/latex gloves; plants (poison ivy) and fragrances in perfumes, soaps and lotions.
The typical rash that occurs from allergic contact dermatitis includes redness of the skin as well as vesicles that weep and crust. Conversely, irritant dermatitis often appears as red, dry, cracking of skin (fissures).
The case presented was a classic example of allergic contact dermatitis to Mastisol. Clinically, the patient developed a flaccid bulla and vesicles on an erythematous base. The erythema was well demarcated not from the Steri-Strips but rather the surface area that had an application of Mastisol. Even though I was concerned about cellulitis and possible abscess, the patient had a component of pruritus, which is not a symptom of infection. Furthermore, when I drained the bulla, there was no purulence and the underlying dermis appeared healthy.
Most of the autoimmune bullous skin eruptions occur in older adults with associated oral lesions. This patient did not have any systemic manifestations of fever, chills, malaise or flu-like symptoms, which ruled out many of the cutaneous drug reactions.
This patient developed an allergic contact dermatitis from Mastisol, which I treated successfully with a tapered dose of oral prednisone 60/40/20/10/5 mg x three days each. Local treatment included topical betadyne to dry out the weeping bulla/vesicles. Once the lesions were dry, I had her use triamcinolone (Kenalog, Bristol-Myers Squibb) 0.1% ointment on the rash. She ultimately responded very quickly to this treatment and all evidence of the rash was gone in two weeks. Luckily, she did not develop a keloid on her surgical scar, which was my main concern while planning surgery.