Are You Confident of the Diagnosis?

What you should be alert for in the history

Friction blisters are typically painful blisters, developing in areas of, and following, recent repetitive mechanical stressors. As such, they are most commonly seen on the hands and feet following occupational or recreation-related activities that may be new or more intense than the patient’s routine endeavors.

Characteristic findings on physical examination

The characteristic finding is an intact or recently ruptured discrete bullous lesion on areas of thick stratum corneum (plantar more commonly than palmar), following recent new or intense frictional trauma. Tips of fingers and toes, palms, balls of feet, and the posterior heel are common sites (Figure 1, Figure 2). There is sometimes mild and localized macular erythema at the peripheral edge. The blister fluid is clear, occasionally blood tinged, serous fluid.

Expected results of diagnostic studies

While biopsy is rarely required for diagnosis, it is fairly characteristic. Typically on acral skin, there is an intraepidermal split just below the stratum granulosum. At the somewhat shaggy periphery of the blister are pale-staining, amorphous keratinocytes (Figure 3). The basal layer is typically normal and the underlying dermis shows only paucicellular perivascular inflammation.

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Diagnosis confirmation

Reasonable considerations in the differential diagnosis would include:


This condition is distinguished by medication history, and the presence of hyperpigmentation and/or violaceous hue; biopsy shows a subepidermal split from basal cell hydropic degeneration, with individual keratinocyte necrosis, and a superficial and deep mixed dermal infiltrate, often with conspicuous pigment incontinence.


This condition is distinguished by multiple lesions (bullae, scarring, milia) at various sites of trauma; biopsy shows typically paucicellular subepidermal split from Type VII collagen antibodies (highlighted by direct immunofluorescence).


This condition would be expected clinically if there is a family or personal history of repeated/excessive blistering after minor frictional activities; biopsy would also be paucicellular and intraepidermal but the split is in the intrabasal layer versus the subgranular layer; immunofluorescence antigenic mapping or transmission electron microscopy are also diagnostic.


This condition is often accompanied by adjacent scaling and/or interdigital maceration; potassium hydroxide (KOH) and/or fungal culture would be positive; biopsy would show septate hyphae in the stratum corneum, with an intraepidermal blister and associated spongiosis with lymphocytes and neutrophils.


In this clinical setting of diabetes (Type I or Type II), there would be spontaneous development, with minimal or no history of an inciting event, and the lesions would be relatively less symptomatic. Biopsy shows a predominantly subepidermal blister and negative direct immunofluorescence.


These lesions are typically located at the dorsal foot or ankle of relatively immobile and older patients. There is background pitting edema, with or without stasis dermatitis.


While rare, bullous malignant melanoma can mimic a hemorrhagic blister; therefore, suspicion is warranted and biopsy appropriate if there is clinical suspicion of an associated pigmented lesion. Dermoscopy can be of help in identifying signs such as a pigment network and branching pigment streaks.

Who is at Risk for Developing this Disease?

At risk include those participating in repetitive, new, and/or strenuous activities, whether they be occupationally related or recreational. Runners, hikers, musicians, and military personnel are frequently affected.

What is the Cause of the Disease?

Repetitive shear frictional force (Ff) of a material or object against thick epidermis causes keratinocytes at the level of the stratum spinosum to separate. The resultant space then fills with serous fluid, observed as a blister.


Those factors that increase the shear Ff exacerbate blister development, namely, moisture and perpendicular (plantar) pressure such as might be encountered on the feet of a marching soldier carrying a heavy load. Moisture increases frictional forces, in part, through keratinocyte swelling, thereby increasing the contact surface area.

Systemic Implications and Complications

While there is no evidence that antibiotics influence blister healing, secondary impetigo with resultant cellulitis and even sepsis are possible, especially in those with diabetes or peripheral vascular disease. Of note, staphylococcal toxic shock syndrome, manifesting with a scarlatiniform rash and systemic symptoms, has been reported in two children, following blister formation from new football/soccer shoes.

Treatment Options

Treatment options include:

  • Prevention

  • Astringents

  • Sterile drainage

  • Antiseptic wound care

Optimal Therapeutic Approach for this Disease


Prevention is the cornerstone of therapy. “Weekend warriors” might benefit from easing into new endeavors, as initial repeated low-intensity Ff encourages cellular proliferation and thickening, which may reduce development of blisters. Similarly, well-fitted footwear, or breaking in a new pair of heels or work boots before wearing, can better distribute frictional force contact points, decreasing blister formation. Hands can be protected by wearing work gloves.

Evidence suggests that because moisture increases Ff, the use of antiperspirants decreases blister formation, although their use may be limited by irritant contact dermatitis. In a group of West Point cadets (plebs) using 20% aluminum chloride solution for approximately 3 consecutive nights prior to a 21km hike, there was a 21% versus 48% blister incidence.

Wearing dry, adequately padded socks is important. Synthetic (acrylic, polypropylene, CoolMax) socks may have a somewhat better ability to wick moisture away from the skin-sock interface than their natural (cotton) counterparts.

Anecdotal reports of mild astringents, such as 10% tannic acid (tea soaks) and acetic acid (pickle juice), used to “harden” blister-prone skin appear dubious. It is said, however, that Hall of Fame blister-prone pitcher Nolan Ryan used pickle brine soaks on the middle finger of his throwing hand.


Friction blisters heal spontaneously; it takes 2-5 days for new stratum granulosum and stratum corneum to form at the blister base. Evidence suggests that sterile drainage, while maintaining the blister roof, allows quicker functional improvement and less discomfort, while protecting from secondary infection. Should the blister roof be removed or torn, antiseptic wound care and bandage is appropriate.

If it is necessary to continue the blister-inciting activity, hydrocolloid or moleskin dressings can decrease pain and provide an added barrier. Additonally, cyanoacrylate and compound tincture of benzoin have been used at the blister base for pain relief and to lessen further abrasion.

Patient Management

The patient should know that escalating pain and redness around the blister may indicate infection, and this should prompt topical antibiotic use and evaluation by a healthcare specialist to consider systemic treatment (as cellulitis and sepsis can develop).

Unusual Clinical Scenarios to Consider in Patient Management

Secondary infection has resulted in cellulitis and staphylococcal toxic shock syndrome.

What is the Evidence?

Cortese, T, Fukuyama, K, Epstein, W, Sulzberger, M. “Treatment of friction blisters”. Arch Dermatol. vol. 97. 1968. pp. 717-22. (After being given experimentally produced blisters, patients were evaluated during the natural healing course of untreated friction blisters, fluid-removed blisters, and top-removed blisters. The authors found that fluid removal does not slow healing and that a maintained blister top is superior.)

Akers, W, Leonard, F, Ousterhout, D, Cortese, T. “Treating friction blisters with alkyl-a-cyanoacrylates”. Arch Dermatol. vol. 107. 1973. pp. 544-7. (Evaluated sensitivity, acceptability, application techniques, inflammation, and infection associated with the use of cyanoacrylate for blisters. Cyanoacrylate proved superior to Neosporin cream and moleskin treatment.)

Heymann, W. “Dermatologic problems of the endurance athlete”. J Am Acad Dermatol. vol. 52. 2005. pp. 345-6. (A topic summary based on dialogue between Drs. Scott Phillips and Gary Brauner for “Dialogues in Dermatology” . An insightful brief summary on the topic of friction blisters.)

Knapik, J, Reynolds, K, Barson, J. “Influence of an antiperspirant on foot blister incidence during cross-country hiking”. J Am Acad Dermatol. vol. 39. 1998. pp. 202-6. (A double-blind study demonstrating that antiperspirants can reduce foot blisters, but carry a significant incidence of irritant dermatitis [57%].)

Reynolds, K, Darrigrand, A, Roberts, D, Knapik, J, Pollard, J, Duplantis, K. “Effects of an antiperspirant with emollients on foot-sweat accumulation and blister formation while walking in the heat”. J Am Acad Dermatol. vol. 33. 1995. pp. 626-30. (A randomized trial evaluating an antiperspirant with emollient for blister prevention and irritant dermatitis. The emollient reduced dermatitis but failed to reduce blister or “hot spot” development.)

Gerhardt, L, Strassle, V, Lenz, A, Spencer, N, Derler, S. ” Influence of epidermal hydration on the friction of human skin against textiles”. J R Soc Interface. vol. 5. 2008. pp. 1317-28. (Using corneometry and suction chamber technology with human subjects, the authors found a highly positive linear correlation between skin moisture and friction coefficient, as a result of skin softening and increased real contact area and adhesion.)

Vogt, T, Brunnberg, S, Hohenleutner, U, Landthaler, M. “Bullous malignant melanoma: an unusual differential diagnosis of a hemorrhagic friction blister”. Dermatol Surg. vol. 29. 2003. pp. 102-4. (Case report of a 66-year-old female, presenting with an asymptomatic hemorrhagic translucent bulla between the 1st and 2nd toe at the site of sandal strap contact. It proved to be a 2.2mm acrolentiginous malignant melanoma.)

Taylor, C, Riordan, F, Graham, C. “New football boots and toxic shock syndrome”. BMJ. 2006. pp. 1376-8. (Two similar case reports of adolescents developing a friction blister over the achilles tendon, and then becoming febrile and lethargic, with vomiting and scarletiform rash. Both patients’ blisters grew S. aureus, while blood cultures were negative. In one patient, polymerase chain reaction isolated the TSST gene.)