Epidemiology & Risk Factors

  • Pathophysiology: Prolonged sustained pressure over bony prominences exceeding capillary perfusion pressure (>32 mmHg) local tissue ischemia cell death and tissue necrosis. Shear and friction aggravate tissue breakdown.
  • Predisposing Factors:
    • Immobility: Spinal cord injury (SCI), stroke, ICU admission, dementia, hip fractures.
    • Incontinence: Fecal/urinary incontinence causes skin moisture and maceration loss of protective stratum corneum.
    • Malnutrition: Hypoalbuminemia, low BMI, vitamin/zinc deficiencies impair collagen synthesis and wound healing.
    • Impaired Sensation: Peripheral neuropathy (e.g., DM), encephalopathy.
    • Microvascular Disease: PVD, DM, smoking.
  • Common Anatomical Sites:
    • Sacrum and ischial tuberosities (most common).
    • Greater trochanters (lateral decubitus position).
    • Calcaneus (heels) and lateral malleoli.
    • Occiput (infants and long-term bedbound/intubated pts).

Clinical Features

  • Classification / Staging System (NPUAP/EPUAP):
    • Stage 1: Intact skin with non-blanchable erythema, usually over a bony prominence. May exhibit local warmth, edema, or induration.
    • Stage 2: Partial-thickness skin loss involving epidermis and/or dermis. Presents as a shallow open ulcer with a red-pink wound bed or an intact/ruptured serum-filled blister. No slough or subQ fat visible.
    • Stage 3: Full-thickness skin loss. Subcutaneous fat visible, but bone, tendon, or muscle is not exposed. Slough or eschar may be present. Undermining and tunneling may occur.
    • Stage 4: Full-thickness skin and tissue loss with exposed bone, tendon, or muscle. Slough/eschar often present; high risk of osteomyelitis. Palpable bone often present.
    • Unstageable: Full-thickness tissue loss where base is obscured by slough (yellow, tan, gray) and/or eschar (tan, brown, black). True depth cannot be determined until slough/eschar is removed.
    • Deep Tissue Pressure Injury (DTPI): Persistent non-blanchable deep red, maroon, or purple discoloration or epidermal separation revealing a dark wound bed or blood-filled blister.

Diagnosis

  • Initial/Screening:
    • Clinical inspection, measurement, and anatomical staging.
    • Probe-to-bone test: Palpating hard, gritty bone with a sterile metal probe at the ulcer base has high positive predictive value for underlying osteomyelitis.
  • Key Labs:
    • Nutritional markers: Prealbumin, albumin, transferrin.
    • Inflammatory markers: ESR and CRP (markedly elevated if osteomyelitis or deep space infection is present).
    • CBC: Leukocytosis indicates systemic infection or local soft tissue invasion.
  • Imaging:
    • Initial: Plain radiograph (X-ray) of the underlying bone (evaluates for cortical lysis, periosteal reaction; low sensitivity early).
    • Confirmatory / Gold Standard Imaging: MRI without and with IV contrast (highest sensitivity and specificity for osteomyelitis, deep abscess, or sinus tracts).
  • Microbiology / Biopsy:
    • Superficial swab cultures are CONTRAINDICATED (identifies surface colonization, not true infection).
    • Definitive diagnosis of wound infection requires deep tissue biopsy or needle aspiration of the ulcer base after wound debridement.
    • Bone biopsy and culture: Gold standard for confirming osteomyelitis.

Differential Diagnostics

  • Venous Stasis Ulcers:
    • Diff by location (medial malleolus), irregular shaggy borders, copious exudate, and surrounding stasis dermatitis (erythema, hemosiderin hyperpigmentation, lipodermatosclerosis); peripheral pulses usually intact.
  • Arterial (Ischemic) Ulcers:
    • Diff by location at the distal tips of digits or lateral malleolus; characteristic “punched-out” clean margins, pale/necrotic base, loss of hair, thin shiny skin, cool extremities, diminished/absent distal pulses, and pain exacerbated by leg elevation.
  • Diabetic Neuropathic Ulcers (Mal Perforant):
    • Diff by location over pressure-bearing plantar surfaces (e.g., metatarsal heads, heels); painless due to peripheral sensory neuropathy; characteristically surrounded by a thick keratotic rim (callus).
  • Pyoderma Gangrenosum:
    • Diff by rapid progression, extreme pain out of proportion to exam, violaceous undermined border, association with IBD or rheumatoid arthritis, and pathergy (lesions worsen after debridement or surgical trauma).
  • Marjolin Ulcer:
    • Diff by non-healing chronic wound undergoing malignant transformation into squamous cell carcinoma (SCC); presents with everted borders, exuberant granulation tissue, or vegetative mass; diagnosed via biopsy of the ulcer margin.

Management

  • General Measures (Prevention & Pressure Relief - First-Line):
    • Repositioning: Turn bedbound pts every 2 hours; chairbound pts every 15 to 60 minutes.
    • Support Surfaces: Pressure-reducing dynamic or static foam/air/alternating-pressure mattresses and heel offloading boots.
    • Optimize Nutrition: Ensure adequate caloric intake (30–35 kcal/kg/day) and high protein (1.25–1.5 g/kg/day); correct vitamin C and zinc deficiencies.
    • Moisture Control: Barrier creams, incontinence protocols, urinary/fecal collection devices if necessary.
  • Wound Bed Preparation & Dressings (by Stage):
    • Stage 1: Transparent film or barrier ointment for friction protection; pressure offloading.
    • Stage 2: Occlusive or semi-occlusive dressings to maintain a moist wound environment (e.g., hydrocolloid, thin foam).
    • Stage 3 & 4:
      • Hydrogels for dry wounds to promote autolytic debridement.
      • Alginates or hydrofiber for highly exudative wounds.
      • Negative Pressure Wound Therapy (wound VAC): Promotes granulation tissue formation and reduces edema in clean, debrided Stage 3/4 ulcers.
  • Debridement:
    • Indicated for nonviable tissue, slough, eschar, or biofilm (converts chronic wound bed to acute healing state).
    • Modalities: Sharp surgical debridement (preferred for extensive necrosis/infection), enzymatic (collagenase), autolytic.
    • High-Yield Exception: Dry, intact, non-fluctuant eschar on the heel should NOT be debrided if there is no erythema, edema, or fluctuance; it serves as a natural physiologic barrier.
  • Antimicrobial Therapy:
    • Topical Abx: Generally not recommended due to contact dermatitis risk and bacterial resistance.
    • Systemic IV Abx: Reserved strictly for pts with systemic signs of infection (sepsis), advancing cellulitis, or confirmed osteomyelitis (empiric coverage with Vancomycin + Piperacillin-Tazobactam or Cefepime; narrow based on deep cultures).
  • Surgical Management (Refractory / Extensive):
    • Myocutaneous or fasciocutaneous rotation/transposition flap closure after infection is eradicated and healthy granulation base is established.

Complications

  • Infectious:
    • Osteomyelitis (most common serious deep complication).
    • Bacteremia and Sepsis / Septic shock.
    • Local cellulitis, deep tissue abscess, infectious tenosynovitis.
    • Necrotizing fasciitis (crepitus, bullae, rapid progression; requires emergency surgical debridement).
  • Malignant:
    • Marjolin ulcer (aggressive SCC arising within a chronic, non-healing ulcer bed).
  • Structural:
    • Joint contractures and heterotopic ossification.
    • Sinus tract or fistula formation into the rectum, bladder, or joint space.