Treating The Acute Onset Of An Asymptomatic Solitary Blister
- Volume 25 - Issue 12 - December 2012
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A biopsy of the involved skin showed a subepidermal bulla without any inflammatory infiltrate. A direct immunofluorescence test was negative.
Within two weeks, the patient recovered uneventfully with slight residual hyperpigmentation but no scarring. Based on the clinical, histopathological and immunofluorescence pattern, I diagnosed the patient with bullosis diabeticorum.
What You Should Know About Bullosis Diabeticorum
Bullosis diabeticorum, also known as diabetic bullous dermopathy, bullous disease of diabetes and diabetic bullae, is a rare, distinct, spontaneous, noninflammatory, blistering condition of unknown etiology occurring in patients with diabetes mellitus.1 Clinical history and location raise the index of suspicion.
In most cases, bullosis diabeticorum manifests as an abrupt, spontaneous development of blisters on the lower extremity (toes, feet and shins). This patient did not have a history of antecedent trauma or infection. The blisters have a propensity to be large and often have an asymmetrical shape as I saw with this patient. The blisters are painless and not pruritic.2 Histopathology of the bullae show cleavage at both the intra-epidermal and subepidermal levels. The only serious complication is secondary infection if the bulla ruptures go untreated. Some do recommend de-roofing the blister and treating it with antibiotics, but no studies have occurred because it is such a rare occurrence.
There is no reference in the existing literature about the relationship of the occurrence of diabetic bullae and the degree of metabolic derangement or glycemic control.3 The condition reportedly affects approximately 0.5 percent of patients with diabetes in the U.S. population.4 One study found a higher incidence of bullosis diabeticorum in patients with skin of color. Researchers found that bullosis diabeticorum occurs in 334 out of 1,000 Hispanics, 296 out of 1,000 African-Americans, 243 out of 1,000 Asians and 184 out of 1,000 Caucasians.5
A Closer Look At The Differential Diagnosis
Blister beetle dermatitis. Beetles do not bite or sting, but they do release a vesicating agent called cantharidin (the same agent that doctors use to place on a wart to cause a blistering effect). The beetles exude this blistering fluid if they are pressed or crushed on the skin, but the patient needs to be in contact with the insect. Treatment of these blisters mimics the treatment of other blisters: drainage of the bullae and application of cold, wet compresses and topical antibiotics. Treatment of this blister also requires cleansing with acetone, ether, soap or alcohol to remove the cantharidin.2
Friction blister (mechanical trauma). Low intensity pressure on friction leads to lichenification and hyperpigmentation whereas heavier and persistent friction leads to hyperkeratosis and callus formation. Sudden shearing forces may lead to friction blisters, erosions or ulcers. Mid-epidermal necrosis, heat, sweating and maceration increase the risk of blistering. The use of acrylic or polypropylene socks as well as the newer toe socks with individual space for each toe has lessened the incidence of blisters, particularly in between the toes. One should perform biomechanical evaluation of the foot to assess if there are signs of previous rubbing (callus, hyperpigmentation, thickening of skin). Evaluation of the foot for bunions and hammertoes can help in making the diagnosis.
Contact dermatitis (poison ivy). Bullae and vesicles occur in a linear configuration. It is rare to see a solitary lesion. It is common for patients to have a history of being out in the yard or woods. This is a form of delayed hypersensitivity. The time between the exposure causing the eruption and the onset of symptoms is between one day and two weeks.