INTRODUCTION — Friction blisters are intraepidermal blisters caused by the skin repeatedly rubbing on another object. This type of blister most commonly occurs on the hands, fingers, feet, and toes (picture 1A-B).
The causes, clinical features, and management of friction blisters will be reviewed here. An overview of the approach to the diagnosis of cutaneous blistering is provided separately. (See "Approach to the patient with cutaneous blisters".)
EPIDEMIOLOGY — Friction blisters are a common occurrence in both children and adults. Populations most at risk include individuals whose recreational or occupational activities require prolonged walking or running, such as endurance athletes, hikers, and soldiers [1,2]. (See "Heel pain in the active child or skeletally immature adolescent: Overview of causes", section on 'Friction blister' and "Overview of running injuries of the lower extremity", section on 'Friction blisters'.)
PATHOPHYSIOLOGY — Friction blisters result from shearing forces within the epidermis. The shearing forces produce necrosis and dissociation of keratinocytes, leading to an intraepidermal split in the stratum spinosum. Hydrostatic pressure causes the area of separation to fill with fluid similar in composition to plasma but with lower protein levels [3].
The magnitude of the frictional force and the number of passes of an object on the skin determine the likelihood for blister formation [3]. Moist skin produces higher frictional forces than dry or wet skin, increasing the risk for blistering [4].
Blisters are most likely to occur in skin areas that have a thick stratum corneum held tightly to underlying structures, such as the palms of the hands or soles of the feet. On the feet, friction blisters can occur in the setting of poorly fitting shoes. Vigorous activity and bearing heavy loads both appear to increase risk for foot blisters [3].
Friction injury in sites of very thin skin (eg, atrophic or sun-damaged skin) is less likely to result in blistering. Rather, the overlying epithelium may be sloughed, and an erosion may result immediately.
PREDISPOSING DISORDERS — Underlying conditions can increase risk for friction-induced blistering. Epidermolysis bullosa, a group of inherited disorders characterized by mechanical fragility of epithelial and basement membrane zone tissues, presents with blister, erosion, or ulcer formation in sites of minor skin trauma. Acquired diseases that cause skin fragility, such as epidermolysis bullosa acquisita, porphyria cutanea tarda, and pseudoporphyria, also can predispose to friction-induced blisters [5]. (See "Epidermolysis bullosa acquisita" and "Porphyria cutanea tarda and hepatoerythropoietic porphyria: Pathogenesis, clinical manifestations, and diagnosis" and "Pseudoporphyria".)
CLINICAL MANIFESTATIONS — Friction blisters are usually preceded by erythema and a sense of pain or burning at the site of skin trauma. Progression to vesicles or bullae generally occurs within hours. The vesicles and bullae are often tense and filled with clear fluid (picture 1A). However, excessive trauma may damage the underlying vasculature resulting in a hemorrhagic vesicle or bulla (picture 1B) [6]. Pressure associated with the accumulation of fluid within blisters can cause discomfort.
Friction blisters generally occur in linear or oval configurations. Underlying disorders can influence sites of predilection. As an example, patients with localized epidermolysis bullosa simplex, the most common variant of epidermolysis bullosa, primarily develop blisters on the feet or hands (picture 2A-B). More extensive friction or trauma-induced blistering may occur in other epidermolysis bullosa variants. (See 'Predisposing disorders' above and 'Additional evaluation' below.)
Friction blisters may rupture soon after formation or persist for hours to several days depending on the thickness of the overlying stratum corneum. Compared with blisters on skin sites with a thinner stratum corneum, blisters in sites with a thick stratum corneum, such as the palms or soles, tend to persist for longer periods. The re-epithelialization occurs in 7 to 10 days, if there is no further trauma to the area. In the absence of an underlying blistering disorder, blisters generally resolve without scarring.
HISTOPATHOLOGY — The friction blister forms with a split in the stratum spinosum below the stratum granulosum (figure 1). Midepidermal necrosis is evident. The blister roof consists of normal and necrotic keratinocytes. The blister floor consists of normal, edematous, and pale degenerating keratinocytes. The deeper layers of the epidermis appear normal.
Within 24 hours after blister formation, there is evidence of the process of re-epithelialization. High mitotic activity is present in basal cells. After 48 to 120 hours, a new stratum granulosum and stratum corneum are present.
Changes in the dermis are minor. Typically, there is only a sparse perivascular infiltrate in the upper dermis. A significant inflammatory infiltrate is not observed provided secondary infection is absent [3,6].
The histopathologic appearance of friction-induced blisters varies in patients with disorders that predispose to blistering. In epidermolysis bullosa simplex, the separation may be suprabasilar or within basal keratinocytes. Friction-induced blisters in porphyria cutanea tarda and pseudoporphyria occur at the basement membrane within the lamina lucida. (See 'Predisposing disorders' above.)
DIAGNOSIS — The diagnosis of friction blisters can be made based upon the patient history and physical examination. A skin biopsy is not usually necessary and is typically reserved for patients in whom the diagnosis is in question or for patients in whom an underlying disorder is suspected. (See 'Additional evaluation' below.)
The patient history is critical for diagnosis. Patients should be asked about recent rubbing trauma in the affected area and preceding symptoms. Pain or a burning sensation often precedes friction blister formation. A supportive history for foot blisters may include new shoes or recent vigorous physical activity.
The physical examination should involve assessment of the blister site and surrounding skin. Prominent inflammation (eg, erythematous papules or plaques) is not typical and suggests an alternative diagnosis or secondary infection. (See 'Differential diagnosis' below.)
If the diagnosis remains uncertain after the patient history and physical examination, a skin biopsy may help to confirm the diagnosis. Ideally, the biopsy specimen should include the blister edge and adjacent skin. The differential diagnosis determines whether additional testing is necessary. (See 'Differential diagnosis' below.)
ADDITIONAL EVALUATION — Suspicion for an underlying disorder that predisposes to blistering should arise when blistering is more frequent or severe than expected based upon the patient history or exhibits impaired healing. Knowledge of the duration of the problem and the family history may be helpful. Patients with epidermolysis bullosa often have onset of blistering in infancy or childhood and a chronic course. Patients with epidermolysis bullosa simplex, which is most often transmitted in an autosomal dominant fashion, may report similar blistering in other family members. A drug history is useful for the diagnosis of pseudoporphyria. (See 'Predisposing disorders' above.)
Patients with presentations concerning for an underlying disorder should also be examined for suggestive physical signs. Blisters primarily involving the dorsal hands can be a sign of porphyria cutanea tarda or pseudoporphyria (picture 3A-B). Other physical findings of porphyria cutanea tarda include hyperpigmentation, hypertrichosis, and localized sclerodermoid plaques. Also, unlike classic friction blisters, blisters related to porphyria cutanea tarda, pseudoporphyria, and epidermolysis bullosa acquisita tend to heal with scarring or milia formation (picture 4A-B). Patients with epidermolysis bullosa may also have mucosal erosions or adhesions.
The diagnosis of epidermolysis bullosa, epidermolysis bullosa acquisita, porphyria cutanea tarda, and pseudoporphyria is reviewed separately. (See "Diagnosis of epidermolysis bullosa" and "Epidermolysis bullosa acquisita", section on 'Diagnosis' and "Porphyria cutanea tarda and hepatoerythropoietic porphyria: Pathogenesis, clinical manifestations, and diagnosis", section on 'Diagnostic evaluation' and "Pseudoporphyria", section on 'Diagnosis'.)
DIFFERENTIAL DIAGNOSIS — The differential diagnosis of friction blisters includes other causes of localized blisters. In particular, other potential causes of blistering on the hands and feet, such as acute palmoplantar (dyshidrotic) eczema, bullous tinea pedis, and allergic contact dermatitis, may be in the differential diagnosis. Attention to the patient history and additional findings, such as pruritus and erythema, aid with diagnosis. For patients with a history of rubbing trauma, minimal inflammation at the blister site, and a lack of pruritus, friction blister is the most likely diagnosis:
●Acute palmoplantar (dyshidrotic) eczema – Acute palmoplantar eczema presents with recurrent, intensely pruritic vesicles or bullae on the hands or feet (picture 5A-B). Common sites of blistering are the palms, soles, and sides of the fingers or toes. In contrast, friction blisters are not typically associated with pruritus. (See "Acute palmoplantar eczema (dyshidrotic eczema)".)
●Allergic contact dermatitis – Allergic contact dermatitis is a pruritic eruption following contact with an allergen. Erythematous papules or plaques in skin areas that come in contact with the allergen are typical findings. Vesicles and bullae occur in severe cases (picture 6). (See "Clinical features and diagnosis of allergic contact dermatitis".)
●Vesicobullous tinea pedis – Vesicobullous tinea pedis is a variant of tinea pedis that presents with vesicles on the feet (picture 7). A potassium hydroxide preparation demonstrating septate hyphae distinguishes this diagnosis from friction blisters. (See "Dermatophyte (tinea) infections", section on 'Tinea pedis'.)
A broader differential diagnosis of localized skin blisters is provided separately. (See "Approach to the patient with cutaneous blisters", section on 'Localized distribution'.)
COMPLICATIONS — Blisters may become secondarily infected, manifesting as increasing redness, worsening pain, and purulent drainage. Progression to cellulitis can occur [7]. Staphylococcus aureus infection of friction blisters resulting in toxic shock syndrome has been reported [8].
MANAGEMENT — Friction blisters can heal spontaneously when the frictional forces are removed. Interventions are focused on reducing symptoms and minimizing risk for infection.
Symptomatic blisters — Drainage is suggested for painful blisters and blisters that cause functional limitations. Clinical experience suggests that a drainage procedure that maintains the blister roof minimizes discomfort and may also reduce risk for secondary infection.
Blister drainage is a relatively simple procedure that may be performed by a clinician or the patient at home. The blister surface should be cleansed with alcohol. A sterile needle is used to puncture the blister. For large blisters, performing more than one puncture helps to remove blister fluid easily. Light pressure can be applied to aid with removal of the fluid. The blister roof should be allowed to collapse over the blister site to serve as a biologic dressing. Topical or oral antibiotic therapy is not necessary in the absence of infection.
Asymptomatic blisters — Nonpainful, nonexpanding blisters that do not cause functional limitations may be left intact and allowed to resolve spontaneously. The advantage of an intact blister is maintenance of a sterile environment during re-epithelialization, minimizing the risk for infection. A bandage or other protective dressing can help to protect blisters located in sites where additional trauma cannot be avoided during healing.
Wound care — Ruptured blister sites should be gently cleansed daily and covered with a clean, dry dressing to protect the healing area from trauma and infection. Blister roofs should only be debrided if there is sign of infection.
Patients with clinical signs of infection (eg, worsening erythema and purulence) should receive appropriate topical or systemic antibiotic therapy. A culture can be performed prior to treatment to identify the causative organism.
When patients must continue physical activity that will irritate the blister site, application of a hydrocolloid dressing can provide a cushioning effect and may help to reduce discomfort during activity. Benefit of 2-octyl cyanoacrylate has not been proven [9].
PREVENTION — Measures that reduce frictional forces on the skin are the mainstay of prevention. Factors contributing to blister formation should be reviewed to identify helpful interventions, including the inciting activity, potential exacerbating factors (eg, moisture, sweating, heat), and the objects that were in contact with the skin. Preventive measures are particularly important for individuals whose occupations or athletic activities are associated with high risk for recurrent episodes of friction blisters.
Examples of measures to minimize skin friction include:
●Alter the inciting activity (eg, adjust technique, discontinue activity)
●Ensure proper fit of shoes or other gear that contact skin during the inciting activity (eg, foot does not slide within the shoe during activity)
●Reduce moisture in the affected area during activity (eg, treatment of hyperhidrosis, use of absorptive socks or clothing)
Despite the common occurrence of friction blisters, high-quality trials are lacking, and the value of products to reduce frictional force on the skin and protect from blistering remain uncertain. There is some support in the literature for interventions such as paper tape, thick-padded acrylic socks, padded wool socks combined with a synthetic inner liner, antiperspirants, and special insoles that provide cushioning that reduces shear forces on the skin [3]; however, conclusions on efficacy are complicated by study methodologic flaws and conflicting data [10]. In addition, antiperspirant use is associated with high risk for skin irritation.
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Blisters (The Basics)")
SUMMARY AND RECOMMENDATIONS
●The friction blister is a common disorder that occurs when frictional forces repeatedly applied to the skin lead to separation within the epidermis. Friction blisters are most likely to occur on the hands and feet. (See 'Epidemiology' above and 'Pathophysiology' above.)
●Friction blisters generally present as vesicles or bullae in linear or oval configurations (picture 1A-B). The blister cavity typically contains clear fluid. Hemorrhagic vesicles or bullae may also occur. Discomfort is common. (See 'Clinical manifestations' above.)
●Friction blisters can be diagnosed based upon a history of rubbing trauma in the affected area and consistent physical examination findings. Skin biopsies usually are not necessary. (See 'Diagnosis' above.)
●Infrequently, disorders associated with skin fragility are associated with friction blisters. Examples include epidermolysis bullosa, epidermolysis bullosa acquisita, porphyria cutanea tarda, and pseudoporphyria. Such disorders should be suspected when blistering is more frequent or severe than expected or exhibits impaired healing. (See 'Predisposing disorders' above.)
●Friction blisters can heal spontaneously provided the causative frictional force is removed. Treatment is focused on reducing symptoms and minimizing risk for secondary infection. (See 'Management' above.)
●Patients with painful blisters or blisters that cause functional limitations often have improvement in symptoms with blister drainage. A drainage technique that leaves the blister roof may help to reduce risk for secondary infection after drainage. Ruptured blister sites should be cleansed daily and covered with a clean, dry dressing. (See 'Symptomatic blisters' above and 'Wound care' above.)
●Asymptomatic blisters can be left intact and allowed to resolve spontaneously. (See 'Asymptomatic blisters' above.)
●Measures to reduce blister recurrence are aimed at reducing frictional forces on the skin. Factors contributing to blister formation should be reviewed, including the inciting activity, potential exacerbating factors (eg, moisture, sweating, heat), and the objects that were in contact with the skin. (See 'Prevention' above.)
