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Friction blisters

Friction blisters
Literature review current through: May 2024.
This topic last updated: Nov 03, 2023.

INTRODUCTION — Friction blisters are intraepidermal blisters that occur when epidermal injury results from repetitive shearing forces in the skin. The most common sites of involvement are the hands, fingers, feet, and toes (picture 1A-B). Prolonged walking or running is a common inciting activity for friction blisters on the foot. Unusually severe or frequent friction blisters may occur in the setting of underlying disorders of skin fragility (algorithm 1).

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".)

PATHOPHYSIOLOGY — Friction blisters result from shearing forces within the epidermis rather than simple rubbing of the epidermis [1]. The fundamental components of the mechanism of blister formation are moving bone, high friction force (the force opposing the movement of one surface against another), and repetition of the resulting shear events [1].

Effects of shearing forces on the epidermis – The shearing forces produce necrosis and dissociation of keratinocytes, leading to an intraepidermal split in the stratum spinosum (figure 1). Hydrostatic pressure causes the area of separation to fill with fluid similar in composition to plasma but with lower protein levels [2].

Factors influencing the likelihood of blister formation – The magnitude of the frictional force and the number of passes of an object on the skin determine the likelihood of blister formation [2]. Moist skin produces higher frictional forces than dry or wet skin, increasing the risk for blistering [3].

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. 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.

Experimental studies support large variability in the susceptibility to friction blister formation among individuals [4]. The reasons for differences in susceptibility to blistering after exposure to similar shearing forces are unclear.

RISK FACTORS — Friction blisters are a common occurrence in both children and adults.

Physical activity — Populations most at risk include individuals whose recreational or occupational activities require prolonged walking or running, such as endurance athletes, hikers, and soldiers [5,6]. 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 [2]. (See "Heel pain in the active child or skeletally immature adolescent: Overview of causes", section on 'Friction blister' and "Running injuries of the lower extremities: Patient evaluation and common conditions", section on 'Friction blisters'.)

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. (See "Epidermolysis bullosa: Epidemiology, pathogenesis, classification, and clinical features".)

Acquired diseases that cause skin fragility, such as epidermolysis bullosa acquisita, porphyria cutanea tarda, and pseudoporphyria, can also predispose to friction-induced blisters [7]. (See 'Recognition of predisposing disorders' below.)

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 typically occurs within hours.

Blister morphology – Friction blisters generally occur in linear or oval configurations. The vesicles and bullae are often tense and filled with clear fluid (picture 1A). Excessive trauma may damage the underlying vasculature, resulting in a hemorrhagic vesicle or bulla (picture 1B) [8].

Location – Friction blisters most commonly occur on the hands, fingers, feet, and toes (picture 1A-B). (See 'Pathophysiology' above.)

Underlying disorders can influence sites of predilection. For example, although 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 'Recognition of predisposing disorders' below.)

Symptoms – Pressure associated with the accumulation of fluid within blisters can cause discomfort. Pruritus is usually absent.

Course – 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.

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

Epidermis – Friction blisters form with a split in the stratum spinosum below the stratum granulosum (figure 1).

Additional findings include:

Midepidermal necrosis

Normal and necrotic keratinocytes in the blister roof

Normal, edematous, and pale degenerating keratinocytes in the blister floor

Normal-appearing deeper layers of the epidermis

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.

Dermis – 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 [2,8].

Impact of predisposing disorders – The histopathologic appearance of friction-induced blisters can vary 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 'Recognition of predisposing disorders' below.)

DIAGNOSIS — The diagnostic evaluation of friction blisters involves the recognition of consistent clinical findings. Atypical features should prompt consideration of underlying disorders of skin fragility or alternative diagnoses (algorithm 1). (See 'Recognition of predisposing disorders' below and 'Differential diagnosis' below.)

Diagnostic approach — The diagnosis of friction blisters can almost always 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 'Recognition of predisposing disorders' below.)

Patient history – 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. (See 'Risk factors' above.)

Physical examination – 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 and 'Complications' below.)

Role of biopsy – Although rarely needed, if the diagnosis remains uncertain after the patient history and physical examination, a skin biopsy may help to confirm the diagnosis. Skin biopsies may also be appropriate for the diagnosis of associated disorders of skin fragility. The differential diagnosis determines the type of biopsy indicated and the need for supplemental pathologic tests or other tests. The general approach to the diagnosis of skin blistering is reviewed separately. (See 'Differential diagnosis' below and 'Recognition of predisposing disorders' below and "Approach to the patient with cutaneous blisters", section on 'Diagnostic tests'.)

Recognition of predisposing disorders — Further evaluation is indicated for patients presenting with features that suggest an underlying predisposing disorder. Suspicion for such disorders should arise when blistering is more frequent or severe than expected based upon the patient history or when there is evidence for impaired healing, milia formation, or scarring (algorithm 1). Blisters related to porphyria cutanea tarda, rarer forms of porphyria (congenital erythropoietic porphyria and variegate porphyria), pseudoporphyria, epidermolysis bullosa acquisita, and some presentations of epidermolysis bullosa tend to heal with scarring or milia formation (picture 3A-B).

Blister location may also be helpful. For example, blisters primarily involving the dorsal hands can be a sign of porphyria cutanea tarda, pseudoporphyria, congenital erythropoietic porphyria, or variegate porphyria (picture 4A-B). Patients with epidermolysis bullosa or epidermolysis bullosa acquisita may also have mucosal erosions or adhesions (algorithm 1).

Epidermolysis bullosa – Epidermolysis bullosa is a clinically and genetically heterogeneous inherited skin fragility disorder. Although the typical clinical findings differ based upon the subtype of epidermolysis bullosa, characteristic features include blisters, erosions, nonhealing ulcers, and scars following minor trauma. In localized epidermolysis bullosa simplex (the most common variant of epidermolysis bullosa), blisters primarily develop on the feet or hands (picture 2A-B). However, more extensive friction or trauma-induced blistering may occur in other epidermolysis bullosa variants.

Patients with epidermolysis bullosa often have onset of blistering in infancy or childhood and report a chronic course. Patients with epidermolysis bullosa simplex, which is most often transmitted in an autosomal dominant fashion, may report similar blistering in family members.

The diagnosis of epidermolysis bullosa is usually managed by specialists experienced with the condition and may involve skin biopsy for immunofluorescence mapping and mutational analysis. (See "Diagnosis of epidermolysis bullosa".)

Epidermolysis bullosa acquisita – Epidermolysis bullosa acquisita is a rare acquired mucocutaneous blistering disease that usually occurs in adults. Classic clinical features include skin fragility, noninflammatory tense bullae, milia formation, and scarring (picture 3B). Patients may also have mucosal involvement. The diagnosis of epidermolysis bullosa acquisita generally involves a skin biopsy and immunofluorescence microscopy. (See "Epidermolysis bullosa acquisita", section on 'Diagnosis'.)

Porphyria cutanea tarda and other porphyrias – Porphyria cutanea tarda is a metabolic disorder caused by deficient activity of uroporphyrinogen decarboxylase in the liver. Classic clinical features include photosensitivity with noninflammatory blister formation, skin fragility, scarring, milia formation, hyperpigmentation, pruritus, hirsutism, and hair loss. Common sites for skin changes are the dorsal hands, forearms, ears, neck, and feet (picture 5). The diagnosis of porphyria cutanea tarda usually begins with measurement of serum or urine porphyrins. Similar skin lesions can occur in congenital erythropoietic porphyria and variegate porphyria, rarer forms of porphyria. (See "Porphyria cutanea tarda and hepatoerythropoietic porphyria: Pathogenesis, clinical manifestations, and diagnosis", section on 'Diagnostic evaluation' and "Congenital erythropoietic porphyria" and "Variegate porphyria".)

Pseudoporphyria – Pseudoporphyria is a bullous photodermatosis that may occur in association with medications, chronic renal failure and hemodialysis, or tanning bed exposure. Classic clinical features include skin fragility; noninflammatory bullae; milia formation; and scarring on the dorsal hands, forearms, face, or other sun-exposed areas (picture 4B). The diagnosis usually involves review of the patient's medication and disease history and testing to exclude porphyria cutanea tarda and other blistering diseases. (See "Pseudoporphyria".)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of friction blisters includes other causes of localized blisters, such as acute palmoplantar (dyshidrotic) eczema, allergic contact dermatitis, or vesicobullous tinea pedis. 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. (See 'Diagnosis' above.)

Acute palmoplantar (dyshidrotic) eczema – Acute palmoplantar eczema presents with recurrent, intensely pruritic vesicles or bullae on the hands or feet (picture 6A-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 7). (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 8). 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 erythema, worsening pain, and purulent drainage. Progression to cellulitis can occur [9]. Staphylococcus aureus infection of friction blisters resulting in toxic shock syndrome has been reported [10].

MANAGEMENT — Friction blisters typically heal spontaneously when the frictional forces are removed. Interventions are focused on reducing symptoms and minimizing risk for infection.

Asymptomatic, nondisabling 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.

Painful or disabling 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 postprocedure 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, ideally at or around the edge or base of the blister to keep the roof of the blister intact. 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.

Ruptured blisters — 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.

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 [11].

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 to identify the causative organism.

PREVENTION — Measures that reduce shear forces on the skin are the mainstay of prevention. Factors contributing to blister formation should be reviewed to identify potentially helpful interventions, including the inciting activity, potential exacerbating factors (eg, moisture), and the objects that were in contact with the skin. Preventive measures may be particularly helpful for individuals whose occupations or athletic activities are associated with high risk for recurrent episodes of friction blisters.

We typically counsel patients on the following measures:

Reduced repetition of shearing forces on the skin – If the inciting activity must be continued, this can involve reducing the duration of the inciting activity or adjusting technique, when feasible.

Gradual initiation of the potential inciting activity – Gradual exposure to activities likely to lead to friction blister formation rather than abrupt, intense initiation of such activities may allow for adaptative changes in the skin that increase resistance to mechanical damage and reduce the risk for blister formation [4]. In support of this approach, some studies have found blistering more likely to occur during the earliest weeks of exposure to an inciting activity than during later weeks [12,13].

Gradual introduction of new equipment or gear – Prior exposure to shoes or other gear that will be in contact with skin in at-risk sites might reduce risk for blister formation (eg, avoiding use of brand new shoes for a potentially inciting walking or running activity) [13,14]. In one study of 2617 individuals in a military training program, rates of friction blisters were lower among individuals who wore their training boots for more than 20 hours per week in the two weeks preceding the training period than individuals who wore their boots less frequently [13].

Implementation of measures to reduce frictional force (reduce surface factors contributing to increased friction and the force compressing two surfaces together) and shearing effects – Measures to reduce contributory skin trauma may include reducing skin moisture, changing the surfaces in contact with the skin, and addressing biomechanical factors (eg, orthopedic or gait abnormalities) that may increase shear forces on the skin [4].

Despite the common occurrence of friction blisters, high-quality trials are lacking, and the value of products to reduce frictional and shearing forces on the skin and protect from blistering remain uncertain. Examples of proposed interventions include paper tape [15]; thick-padded acrylic socks rather than cotton socks [16]; padded wool socks combined with a synthetic inner liner [12]; 20% aluminum chloride hexahydrate (an antiperspirant) [17]; and special neoprene insoles that provide cushioning, which reduces shear forces on the skin [18,19]. However, conclusions on efficacy are complicated by study methodologic flaws and conflicting data [2,4,20]. In addition, antiperspirant use is associated with high risk for skin irritation.

Our typical approach for foot friction blisters is to advise routine wearing of socks with shoes during physical activity (as opposed to no socks) to reduce moisture at the skin surface and reduce friction; we also address obvious physical abnormalities that may contribute to increased shear forces on the skin [4]. We approach use of other interventions, such as specific socks, shoe insoles, paper tape, orthotic devices, or physical therapy, on a case-by-case, trial-and-error basis.

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

Overview – The friction blister is a common disorder that occurs when shearing 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 'Risk factors' above and 'Pathophysiology' above.)

Clinical manifestations – 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.)

Diagnosis – Friction blisters can be diagnosed based upon a history of rubbing trauma in the affected area and consistent physical examination findings (algorithm 1). Skin biopsies are not usually necessary. (See 'Diagnosis' above.)

Recognition of predisposing disorders – Infrequently, friction blisters are a manifestation of disorders associated with skin fragility (algorithm 1). 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.)

Management – 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.)

Asymptomatic, nondisabling blisters – For patients with asymptomatic or minimally symptomatic blisters that are not causing functional limitations, we suggest leaving blisters intact rather than deliberate drainage (Grade 2C). (See 'Asymptomatic, nondisabling blisters' above.)

Painful or disabling blisters – For patients with painful blisters or blisters that cause functional limitations, we suggest deliberate blister drainage (Grade 2C). In our experience, patients 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. (See 'Painful or disabling blisters' above.)

Ruptured blisters – Ruptured blister sites should be cleansed daily and covered with a clean, dry dressing. 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. (See 'Ruptured blisters' above.)

Prevention – Measures to reduce blister recurrence are aimed at reducing frictional and shear forces on the skin. Potential measures to reduce exposure to factors that may contribute to blister formation should be reviewed, such as adjusting the inciting activity and allowing gradual introduction of activities and gear that may contribute to friction blisters.

Efficacy data for products to reduce risk for blistering are limited. We advise that individuals planning to participate in activities associated with risk for foot blisters (eg, prolonged walking, hiking, or running) wear socks during these activities. We approach use of other interventions, such as specific socks, shoe insoles, paper tape, orthotic devices, or physical therapy, on a case-by-case, trial-and-error basis. (See 'Prevention' above.)

  1. Rushton R, Richie D. Friction Blisters of the Feet: A New Paradigm to Explain Causation. J Athl Train 2024; 59:1.
  2. Knapik JJ, Reynolds KL, Duplantis KL, Jones BH. Friction blisters. Pathophysiology, prevention and treatment. Sports Med 1995; 20:136.
  3. Kirkham S, Lam S, Nester C, Hashmi F. The effect of hydration on the risk of friction blister formation on the heel of the foot. Skin Res Technol 2014; 20:246.
  4. Rushton R, Richie D. Friction Blisters of the Feet: A Critical Assessment of Current Prevention Strategies. J Athl Train 2024; 59:8.
  5. Scheer BV, Reljic D, Murray A, Costa RJ. The enemy of the feet: blisters in ultraendurance runners. J Am Podiatr Med Assoc 2014; 104:473.
  6. Brennan FH Jr, Jackson CR, Olsen C, Wilson C. Blisters on the battlefield: the prevalence of and factors associated with foot friction blisters during Operation Iraqi Freedom I. Mil Med 2012; 177:157.
  7. Thiers BH. The mechanobullous diseases. Hereditary epidermolysis bullosa and epidermolysis bullosa acquisita. J Am Acad Dermatol 1981; 5:745.
  8. Akers WA. Sulzberger on friction blistering. Int J Dermatol 1977; 16:369.
  9. Hoeffler DF. Friction blisters and cellulitis in a navy recruit population. Mil Med 1975; 140:333.
  10. Taylor CM, Riordan FA, Graham C. New football boots and toxic shock syndrome. BMJ 2006; 332:1376.
  11. Levy PD, Hile DC, Hile LM, Miller MA. A prospective analysis of the treatment of friction blisters with 2-octylcyanoacrylate. J Am Podiatr Med Assoc 2006; 96:232.
  12. Knapik JJ, Hamlet MP, Thompson KJ, Jones BH. Influence of boot-sock systems on frequency and severity of foot blisters. Mil Med 1996; 161:594.
  13. Patterson HS, Woolley TW, Lednar WM. Foot blister risk factors in an ROTC summer camp population. Mil Med 1994; 159:130.
  14. Gardner TB, Hill DR. Illness and injury among long-distance hikers on the Long Trail, Vermont. Wilderness Environ Med 2002; 13:131.
  15. Lipman GS, Sharp LJ, Christensen M, et al. Paper Tape Prevents Foot Blisters: A Randomized Prevention Trial Assessing Paper Tape in Endurance Distances II (Pre-TAPED II). Clin J Sport Med 2016; 26:362.
  16. Herring KM, Richie DH Jr. Friction blisters and sock fiber composition. A double-blind study. J Am Podiatr Med Assoc 1990; 80:63.
  17. Knapik JJ, Reynolds K, Barson J. Influence of an antiperspirant on foot blister incidence during cross-country hiking. J Am Acad Dermatol 1998; 39:202.
  18. Spence WR, Shields MN. New insole for prevention of athletic blisters. J Sports Med Phys Fitness 1968; 8:177.
  19. Smith W, Walter J Jr, Bailey M. Effects of insoles in Coast Guard basic training footwear. J Am Podiatr Med Assoc 1985; 75:644.
  20. Worthing RM, Percy RL, Joslin JD. Prevention of Friction Blisters in Outdoor Pursuits: A Systematic Review. Wilderness Environ Med 2017; 28:139.
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