What causes blisters?

Causes of Blisters

Blisters are primarily caused by friction, autoimmune conditions, infections, burns, or drug reactions, with the specific mechanism varying based on the underlying cause.

Types of Blisters and Their Causes

Friction Blisters

• Result from repetitive shear deformation involving three fundamental elements 1:
  1. Motion of bone
  2. High friction force
  3. Repetition of resulting shear events
• Commonly occur in areas with thick horny layer tightly attached to underlying structures (palms, soles) 2
• More likely to form in moist environments 2, 3
• Mechanical separation occurs at the level of the stratum spinosum, with hydrostatic pressure filling the area with plasma-like fluid 3

Autoimmune Blisters

• Bullous pemphigoid (BP) is the most common immunobullous disease in Western Europe 4
  • Caused by autoantibodies (primarily IgG) attacking components of the basement membrane zone
  • Main autoantigens are BP230 (BPAg1) and BP180 (BPAg2, collagen XVII)
  • Results in subepidermal blistering
  • Typically affects elderly patients
  • Presents as tense blisters on erythematous or normal-looking skin

Drug-Induced Blisters

• Can manifest as drug hypersensitivity syndromes 4:
  • Exanthema (skin rash) without systemic symptoms
  • Drug reaction with eosinophilia and systemic symptoms (DRESS)
  • Severe reactions like Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN)
• HIV medications commonly associated with blistering reactions 4:
  • NNRTIs (efavirenz, nevirapine, etravirine)
  • Certain protease inhibitors
  • Some NRTIs

Infection-Related Blisters

• Impetigo causes honey-colored crusted lesions with underlying blisters 5
  • Caused by Staphylococcus aureus or Streptococcus pyogenes
  • Highly contagious bacterial skin infection
  • Common in children

Other Causes

• Burns (thermal, chemical, electrical)
• Contact dermatitis
• Insect bites
• Edema
• Cellulitis
• Erythema multiforme 4

Pathophysiology of Blister Formation

Friction Blisters

1. Repetitive shear forces cause mechanical separation of epidermal cells
2. Hydrostatic pressure fills the space with fluid similar to plasma (lower protein content)
3. Healing begins within 6 hours with cellular activity at the blister base
4. New stratum granulosum forms at 48 hours and stratum corneum at 120 hours 3

Autoimmune Blisters

1. Autoantibodies target specific components of skin adhesion structures
2. Immune attack leads to separation at specific skin layers
3. In bullous pemphigoid, separation occurs at the basement membrane zone 4

Drug-Induced Blisters

1. Hypersensitivity reactions to medications
2. Can range from mild exanthema to severe blistering with mucosal involvement
3. Severe forms like SJS/TEN involve extensive epidermal detachment 4

Clinical Considerations

Risk Factors

• For friction blisters: vigorous activity, carrying heavy loads, poorly fitting footwear 3
• For bullous pemphigoid: advanced age, neurological diseases (dementia, stroke, Parkinson's) 4
• For drug reactions: certain medications (especially HIV medications), genetic predisposition 4

Management Approach

• Treatment depends on blister type, location, and symptoms 6:
  • Uncomplicated blisters without pain: leave intact
  • Painful blisters on palms/soles: puncture blister but leave roof intact
  • Ruptured blisters without infection: leave remnants of blister roof
  • Ruptured blisters with infection: remove remnants of blister roof
  • Burn blisters (grade 2a or higher): remove blister roof

Prevention Strategies

• For friction blisters 2, 3:
  • Properly fitting shoes broken in gradually
  • Protective padding over blister-prone areas
  • Drying foot powders
  • Non-slip insoles
  • Acrylic or polyester-wool combination socks
  • Gradual skin adaptation to friction through controlled exposure

The specific cause of blisters must be identified for appropriate management, as treatment approaches vary significantly based on etiology.