A 39-year-old female presented to my office with a chief complaint of pain surrounding both great toe joints. She had symptoms for five to six years. Prior treatment measures included wearing wider shoes and bunion pads. Her main area of pain was on the medial bony prominence at the great toe joint.
Her past medical history was remarkable for depression. Daily medications included sertraline (Zoloft, Pfizer), fish oil, vitamin B12 and vitamin D. Allergies included an allergy to penicillin, which caused a rash but not anaphylaxis. Past surgical history included two Caesarean sections and excision of keloids. The patient was married, unemployed, a non-smoker and a mild drinker of alcohol.
The podiatric exam revealed strong pedal pulses of 2/4 for the dorsalis pedis and posterior tibial arteries bilaterally. The capillary refill was less than three seconds to the toes. Her skin was warm and pink. The neurologic exam revealed symmetric deep tendon reflexes and epicritic sensation was intact to the level of the toes. There was no clonus or Babinski reflex.
The dermatologic exam revealed skin temperature, texture and turgor within normal limits. There was no evidence of rash, edema, varicosities or a break in the integument. Her toenails were healthy. The orthopedic exam revealed symmetric, pain-free range of motion of the ankle and hindfoot. Gross visualization of her feet revealed mild to moderate bunion deformities with lateral deviation of the great toes. The range of the motion of the great toe joints was not painful. The dorsomedial eminence of the great toe joint was painful to palpate.
Radiographs of her feet revealed a moderate underlying metatarsus adductus with mild to moderate bunion deformity. No acute fracture was visible. No underlying arthropathy was present.
The patient elected to have surgery to address the chronic pain and deformity of her feet. She wanted to have surgery on the right foot first. Abnormal preoperative labs were remarkable for a mean corpuscular volume of 76.3 (normal values 81.0 FL-97.4 FL), a mean corpuscular hemoglobin of 24.8 (normal values 37.0 PG- 34.0 PG) and a red blood cell distribution width of 16.2 (normal values 11.7%-14.4%). Her remaining complete blood counts and chemistry profile were normal.
I performed a traditional Austin bunionectomy with single screw fixation in a standard fashion. Due to the patient’s history of keloids, I used a minimal reactive suture. I closed the skin with a 5-0 Prolene suture in a running intradermal stitch, using Mastisol (Eloquest Healthcare) and Steri-Strips (3M) to reinforce the skin. Her surgery progressed without any technical difficulty or complications.
The patient followed up in one week for her first postoperative appointment. She had been in moderate pain and described some itching on her foot. She self treated with diphenhydramine (Benadryl, McNeil Consumer Healthcare) and that did help. Clinically, her foot was very swollen and red. I was concerned about infection due to the bright red appearance of her dorsal foot. I cleansed the foot, wrapped it in an elastic compression bandage and instructed her to continue to elevate and ice the foot. She wore a pneumatic fracture boot for weightbearing as tolerated. I gave her a prescription for clindamycin (Cleocin, Pfizer) 300 mg #21, i PO TID. I advised her to return to the office in two weeks.
I received a phone call from the patient two days after her initial postoperative visit. She noted that she was developing a blister on the top of her foot and having more itching and pain. I instructed her to return to the office the following day for evaluation.
A large bulla was present in the interspace between the big toe and the second toe. I removed her Steri-Strips to inspect the rest of the surgical wound and found multiple small vesicles in the region of the Steri-Strips and to the periphery of the incision line. There was no evidence of purulence. I drained the bulla, which was flaccid and contained a serosanguineous fluid, but I left the roof of the blister intact. The area of erythema was localized to the surgical site. No ascending lymphangitis was present.
Key Questions To Consider
1. What are the differential diagnoses?
2. What is the diagnosis?
3. What features of this condition differentiate it from other conditions?
4. What is the appropriate treatment?
Answering The Key Diagnostic Questions
1. Cellulitis/abscess, pemphigus vulgaris, bullous pemphigoid, stasis bulla, cutaneous drug eruption and contact dermatitis
2. Allergic contact dermatitis
3. The erythema was well demarcated from the surface area in which I had applied Mastisol. The patient had a component of pruritus, which is not a symptom of infection. After drainage, the bulla did not have any purulence and the underlying dermis appeared healthy.
4. A tapered dose of oral prednisone (60/40/20/10/5 mg x three days each) and local treatment with topical Betadine (Purdue Products) to dry out the weeping bulla/vesicles, and triamcinolone (Kenalog, Bristol-Myers Squibb) 0.1% ointment on the rash.
A Closer Look At The Differential Diagnoses
This case illustrates a bullous reaction following podiatric surgery. The common differential diagnoses include cellulitis/abscess, pemphigus vulgaris, bullous pemphigoid, stasis bulla, cutaneous drug eruption and contact dermatitis.
Pemphigus vulgaris is a dermatologic condition characterized by flaccid bullae of the skin and mucous membranes. The lesions are rarely pruritic and can be painful. The disease is an autoimmune disorder caused by antibodies attacking desmoglein 1 and 3 antibodies. The mean age of onset is typically between 50 and 60 years of age. The most common areas of predilection include the trunk, intertriginous areas, neck and head.
Bullous pemphigoid is a condition that yields tense blisters. These blisters are usually on the upper arms and thighs, but are also visible on the hands and feet. The autoimmune disorder occurs in older people, who are usually in their 70s or older. The condition can be precipitated by medications including non-steroidal anti-inflammatory drugs (NSAIDs), antibiotics, furosemide (Lasix, Sanofi-Aventis), captopril (Capoten, Bristol-Myers Squibb) and penicillamine (Cuprimine, Valeant Pharmaceuticals).
Stasis bullae are caused by prolonged swelling in an extremity. Oftentimes, there is associated stasis dermatitis, which will cause redness and scaling of skin. Stasis bullae are caused by excessive fluid pushing toward the surface of the skin, creating a pocket that manifests as vesicles or bullae. This condition typically occurs in patients who retain fluids due to congestive heart failure, kidney disease, liver disease, post-phlebitic syndrome of the leg, venous insufficiency or hypoalbuminemia.
Cellulitis and/or abscess can occur after surgery. Even though the incident rate of postoperative infection is low, this is the most critical diagnosis to rule out. With abscess, blistering of skin can occur where infectious material (purulence) is trying to extrude from the body. Cellulitis is a common finding with infection causing redness and potential streaks along a lymphatic channel (lymphangitis). Patients with cellulitis/abscess would typically encounter more pain than one would expect after surgery. There may be accompanied systemic effects such as fever, chills and/or malaise. Itching is not a common element of infection. If you suspect an abscess, institute antibiotics for treatment and perform incision and drainage with lavage immediately.
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.
Dr. Fishco is board-certified in foot surgery and reconstructive rearfoot and ankle surgery by the American Board of Podiatric Surgery. He is in private practice in Phoenix. He is also a faculty member of the Podiatry Institute.
Dr. Fishco pens a monthly blog for Podiatry Today. For more info, visit www.podiatrytoday.com/blogs/william-fishco-dpm-facfas .
1. Halevy S, Ghislain PD, Mockenhaupt M, Fagot JP, Bouwes Bavinck JN, Sidoroff A. Allopurinol is the most common cause of Stevens-Johnson syndrome and toxic epidermal necrolysis in Europe and Israel. J Am Acad Dermatol. 2008; 58(1):25-32.