Pressure Ulcers

1. Clinical Overview

Summary

Pressure ulcers (also known as pressure injuries, decubitus ulcers, or bedsores) are localized injuries to the skin and/or underlying tissue, usually over a bony prominence, resulting from sustained pressure (causing ischemia), often in combination with shear and friction. They represent a major cause of morbidity and mortality in immobile patients including the elderly, those with spinal cord injury, and critically ill patients. [1,2]

Pressure ulcers are largely preventable with appropriate risk assessment and preventive interventions. Once established, Grade 3/4 ulcers can take months to heal or may require complex surgical reconstruction. The development of a hospital-acquired Grade 3 or 4 pressure ulcer is often considered a serious incident requiring investigation in many healthcare systems. [3]

The National Pressure Ulcer Advisory Panel (NPUAP) and European Pressure Ulcer Advisory Panel (EPUAP) provide the gold standard for classification, prevention, and management. [4]

Key Facts

• Mechanism: Pressure > Capillary Closing Pressure (32 mmHg) → Occlusion of blood flow → Tissue Ischemia → Necrosis
• The "Iceberg Effect": A small break in the skin often hides a large cavity of necrotic fat/muscle underneath, as muscle tissue is more sensitive to ischemia than skin
• Hospital-Acquired: Development of a Grade 3 or 4 pressure ulcer in hospital is often considered a "Never Event" or serious incident requiring investigation
• Prevalence: Affects 10-15% of hospitalized patients and up to 30% of nursing home residents [5]
• Mortality: Associated with 2.5-fold increase in mortality in elderly patients [6]
• Cost: Treatment costs in developed nations exceed billions annually [7]

SSKIN Bundle: Universal Prevention Framework

The evidence-based care bundle for pressure ulcer prevention: [8]

• Surface (Appropriate pressure-redistributing mattress)
• Skin Inspection (Daily examination of at-risk areas)
• Keep Moving (Regular repositioning schedule)
• Incontinence/Moisture (Barrier creams and prompt hygiene)
• Nutrition (Adequate protein and micronutrients)

Clinical Pearls

The "Bottoming Out" Test: Slide your hand under the mattress while the patient is on it. If you can feel the patient's sacrum resting on your hand through the mattress foam, the mattress is inadequate and ineffective. They need a higher specification surface (dynamic/alternating pressure air mattress).

Heels: The second most common site after the sacrum. "Floating heels" (using pillows under calves to suspend heels above the bed surface) is the most effective prevention strategy. [9]

Unstageable: If an ulcer is covered in black eschar (scab) or yellow slough, you cannot accurately grade the depth. It is classified as "Unstageable". Do not estimate Grade 3 vs 4 until debrided and the wound bed is visible.

Deep Tissue Injury (DTI): A purple/maroon discolored area of intact skin or blood-filled blister indicates damage to underlying soft tissue from pressure and/or shear. These injuries can rapidly deteriorate to full-thickness wounds within hours to days. [10]

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2. Epidemiology

Incidence and Prevalence

• Hospital settings: 8-12% prevalence in acute care, with incidence of 3-7% of hospital admissions [5]
• Long-term care: 15-30% prevalence in nursing homes and extended care facilities [11]
• Community: 1-3% of community-dwelling adults, increasing to 10-15% in homebound individuals
• Spinal cord injury: 30-50% lifetime prevalence in patients with spinal cord injuries [12]
• ICU patients: 10-40% incidence depending on patient acuity and preventive measures [13]

Common Anatomical Sites (in order of frequency)

1. Sacrum/Coccyx (40-45%) - most common in supine patients
2. Heels (20-25%) - particularly in patients with peripheral vascular disease
3. Ischial tuberosities (15-20%) - most common in seated patients (wheelchair users)
4. Greater trochanter (10-15%) - in patients lying on their side
5. Occiput (5-8%) - particularly in infants, children, and ventilated ICU patients
6. Elbows, scapulae, malleoli (5-10%) - less common but significant

Risk Factors

Intrinsic (Patient) Factors

1. Immobility: Stroke, spinal cord injury, coma, sedation, fracture (especially hip), advanced dementia
2. Sensory Impairment: Peripheral neuropathy (diabetes), spinal cord lesions, peripheral vascular disease
3. Advanced Age: Reduced skin elasticity, decreased subcutaneous fat, impaired microvasculature [14]
4. Moisture: Urinary/fecal incontinence causes maceration which weakens skin barrier function
5. Poor Nutrition: Low albumin (less than 3.5 g/dL), protein deficiency, vitamin C and zinc deficiency impair wound healing [15]
6. Comorbidities: Diabetes mellitus, peripheral vascular disease, heart failure, chronic kidney disease, malignancy
7. Reduced Tissue Perfusion: Hypotension, vasopressor use, peripheral vascular disease, smoking
8. Previous Pressure Ulcer: Scar tissue has reduced tensile strength and is more vulnerable to breakdown

Extrinsic (Environmental) Factors

1. Inadequate Support Surface: Standard hospital mattress without pressure redistribution
2. Prolonged Surgery: Operations > 4 hours significantly increase risk [16]
3. Medical Devices: Oxygen masks, cervical collars, urinary catheters, NG tubes causing device-related pressure injuries
4. Friction/Shear: Improper patient handling, sliding down in bed
5. Moisture: Incontinence, excessive perspiration, wound drainage

Risk Assessment Tools

Braden Scale (Most widely used)

Six domains scored 1-4 (except friction/shear scored 1-3): [17]

1. Sensory Perception
2. Moisture
3. Activity
4. Mobility
5. Nutrition
6. Friction and Shear

Score interpretation:

• 19-23: No risk
• 15-18: Mild risk
• 13-14: Moderate risk
• 10-12: High risk
• ≤9: Very high risk

Waterlow Score (UK hospitals)

Scores multiple risk factors with weighted values:

• Score less than 10: At risk
• Score 10-14: Moderate risk
• Score 15-19: High risk
• Score ≥20: Very high risk

Note: Risk assessment should be performed on admission, then at least daily (or more frequently if condition changes). [3]

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3. Pathophysiology

Biomechanical Mechanisms

1. Direct Pressure (Vertical Compression)

• Normal capillary closing pressure: 32 mmHg
• Interface pressure over bony prominences can exceed 150 mmHg in seated/supine patients
• Prolonged pressure > 32 mmHg → capillary occlusion → tissue ischemia → cellular hypoxia → necrosis
• Time-Pressure Relationship: Low pressure for long duration OR high pressure for short duration both cause injury [18]
• Critical threshold: Pressures > 70 mmHg for > 2 hours can cause irreversible tissue damage

2. Shear Forces (Parallel Forces)

• Occurs when patient slides down in bed or chair
• Skin remains stationary (due to friction) while bone and deeper tissues move
• Creates angular deformation of blood vessels and stretches/tears perforating vessels in deep fascia
• Shear forces reduce the external pressure needed to occlude vessels (e.g., 50% reduction in critical pressure)
• Most damaging mechanism - explains why deep tissue injury can occur with relatively low external pressure

3. Friction (Surface Abrasion)

• Mechanical trauma when skin drags across bed linen
• Removes stratum corneum → increased transepidermal water loss → epidermal breakdown
• Friction alone causes superficial (Grade 1-2) injuries
• Acts synergistically with pressure and shear to accelerate tissue damage

Cellular and Molecular Pathophysiology

Ischemia-Reperfusion Injury

1. Ischemic Phase:

   • Occlusion of microvasculature → tissue hypoxia
   • Anaerobic metabolism → lactic acid accumulation → cellular acidosis
   • ATP depletion → Na+/K+ pump failure → cellular swelling
   • Duration: As little as 2 hours can cause irreversible damage to muscle

2. Reperfusion Phase (when pressure is relieved):

   • Restoration of blood flow paradoxically causes additional damage
   • Generation of reactive oxygen species (ROS) and free radicals
   • Neutrophil infiltration and release of inflammatory mediators
   • Endothelial damage and microvascular thrombosis
   • Reperfusion injury can cause more damage than ischemia alone [19]

Tissue Tolerance Variation

Different tissues have different susceptibility to pressure-induced ischemia:

• Muscle (most sensitive): Necrosis after 2-4 hours of complete ischemia
• Fat: Moderately sensitive
• Dermis: Moderately resistant
• Epidermis (most resistant): Can tolerate longer ischemic periods

This explains the "Iceberg phenomenon": Extensive deep tissue necrosis (muscle/fat) can occur with only minimal visible skin changes initially.

Inflammatory Cascade

• Release of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6)
• Matrix metalloproteinases (MMPs) degrade extracellular matrix
• Impaired growth factor signaling (PDGF, VEGF, TGF-β)
• Bacterial colonization → biofilm formation → chronic inflammation
• Senescent cell accumulation impairs healing in chronic wounds

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4. Clinical Presentation

Classification Systems

NPUAP/EPUAP International Classification (2019) [4]

Grade 1: Non-Blanchable Erythema of Intact Skin

• Area of persistent redness that does not blanch with pressure (glass test)
• Skin remains intact (no break in epidermis)
• May appear different in darkly pigmented skin (purple/blue discoloration, induration, warmth)
• Reactive hyperemia (normal response to pressure that blanches and fades in less than 30 min) is NOT a Grade 1 ulcer
• Often painful, firm, soft, warmer or cooler compared to adjacent tissue

Grade 2: Partial Thickness Skin Loss

• Loss of epidermis and part of dermis
• Presents as shallow open ulcer with red/pink wound bed
• May also present as intact or ruptured serum-filled blister
• No slough, no bruising (bruising indicates deep tissue injury)
• Do NOT use Grade 2 for skin tears, tape burns, perineal dermatitis, maceration

Grade 3: Full Thickness Skin Loss

• Full thickness tissue loss with damage or necrosis of subcutaneous tissue
• Subcutaneous fat may be visible
• Slough may be present but does not obscure depth of tissue loss
• May include undermining (tissue destruction under intact skin edges) and tunneling (narrow opening extending from wound)
• Bone, tendon, or muscle NOT visible or directly palpable
• Depth varies by anatomical location (e.g., shallow at ear, very deep at sacrum)

Grade 4: Full Thickness Tissue Loss

• Full thickness tissue loss with exposed or directly palpable bone, tendon, or muscle
• Slough or eschar may be present
• Often includes undermining and tunneling
• High risk of osteomyelitis if bone is exposed or palpable
• Depth varies by anatomical location

Unstageable/Unclassified: Depth Unknown

• Full thickness tissue loss where base of ulcer is covered by slough (yellow, tan, gray, green or brown) and/or eschar (tan, brown or black dry/hard tissue)
• Cannot determine true depth until slough/eschar removed
• Stable (dry, adherent, intact without erythema or fluctuance) eschar on heels serves as "natural biological cover" and should NOT be removed

Deep Tissue Injury (DTI): Depth Unknown

• Purple or maroon localized area of discolored intact skin or blood-filled blister
• Due to damage of underlying soft tissue from pressure and/or shear
• May be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler compared to adjacent tissue
• Can rapidly evolve to reveal full thickness injury or may resolve without tissue loss
• Evolution may be rapid (hours to days)

Clinical Features by Grade

Associated Symptoms and Findings

• Pain: Variable - Grade 2 often most painful due to exposed nerve endings; Grade 4 may have less pain due to nerve destruction
• Odor: Foul-smelling discharge suggests anaerobic bacterial infection or necrotic tissue
• Exudate: Amount and character (serous, serosanguinous, purulent)
• Surrounding skin: Erythema (cellulitis), induration, warmth, maceration
• Systemic signs: Fever, tachycardia, hypotension suggest sepsis

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5. Clinical Examination

Systematic Examination Approach

1. Complete Skin Assessment

Examine all high-risk areas in systematic order:

• Supine position: Occiput, scapulae, elbows, sacrum, coccyx, heels
• Lateral position: Ears, shoulders, ribs, greater trochanter, medial/lateral knees, malleoli
• Prone position (if applicable): Forehead, cheeks, breasts (females), genitalia (males), patellae, toes
• Seated position: Ischial tuberosities, spine, scapulae

2. Blanching Test (Glass Slide Test)

• Apply transparent slide or finger pressure to erythematous area
• Normal reactive hyperemia: Blanches (turns white) and fades within 30 minutes
• Grade 1 ulcer: Does not blanch - indicates damaged capillaries

3. Wound Measurement

Document using standardized method:

• Length: Longest dimension (head to toe) in cm
• Width: Widest dimension perpendicular to length in cm
• Depth: Deepest point (use sterile probe) in cm
• Clock method: Use 12 o'clock as head direction for consistency
• Undermining/Tunneling: Probe gently under wound edges, document location using clock face (e.g., "3cm undermining at 2 o'clock")
• Surface Area: Length × Width (useful for tracking healing)

4. Wound Bed Assessment

• Tissue type (using percentage):
  • "Granulation tissue (red, healthy): Target > 75%"
  • "Slough (yellow/tan): Requires debridement"
  • "Eschar (black/brown): Requires debridement (except stable heel eschar)"
  • "Epithelial tissue (pink): Indicates healing"
• Exudate: None, scant, moderate, heavy; serous, serosanguinous, purulent
• Odor: None, mild, strong, foul (suggests anaerobic infection)

5. Wound Edge and Periwound Assessment

• Edge: Attached, not attached, rolled under (indicates chronic wound)
• Periwound skin: Intact, macerated, erythematous, indurated, discolored
• Condition: Healthy vs. damaged (affects healing potential)

6. Probe-to-Bone Test

• Grade 4 ulcers: Use sterile probe to assess for exposed bone
• Positive test: Hard, gritty sensation suggests osteomyelitis
• Sensitivity ~87%, Specificity ~83% for osteomyelitis in diabetic foot ulcers [20]
• Send bone biopsy if osteomyelitis suspected for culture and histology

7. Neurovascular Assessment

• Pulses: Check dorsalis pedis and posterior tibial for heel ulcers
• Capillary Refill: Should be less than 3 seconds
• Ankle-Brachial Index (ABI): If arterial disease suspected (normal 0.9-1.3)
• Sensation: Monofilament test for peripheral neuropathy

8. Photographic Documentation

• Standardized photographs with ruler for scale
• Same angle, distance, lighting for serial comparison
• Document wound margins, periwound skin, and wound bed

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6. Investigations

Microbiological Assessment

Wound Swab Culture

• Indication: Clinical signs of infection (erythema, warmth, purulent discharge, systemic sepsis)
• NOT indicated for routine screening - all chronic wounds are colonized
• Technique: Cleanse wound first, swab viable tissue (not slough/eschar), use Levine technique (rotating swab with pressure over 1cm² area for 5 seconds)
• Interpretation: Culture results indicate colonization, NOT infection - treat the patient, not the culture

Deep Tissue/Bone Biopsy

• Indication: Suspected osteomyelitis, non-healing wound despite optimal management
• Gold standard for diagnosing osteomyelitis
• Send for culture AND histopathology
• Sensitivity/Specificity superior to swabs for deep infections

Blood Tests

Nutritional Assessment

• Albumin: less than 3.5 g/dL associated with impaired healing and increased pressure ulcer risk
• Pre-albumin: More sensitive marker of acute nutritional status (half-life 2 days vs 21 days for albumin)
• Total protein: Should be > 6.5 g/dL
• Lymphocyte count: less than 1500/μL suggests malnutrition
• Hemoglobin: Anemia (less than 10 g/dL) impairs oxygen delivery to healing tissue
• Vitamin D, Vitamin C, Zinc: Check if deficiency suspected

Infection Markers

• White Blood Cell Count: Leukocytosis suggests infection
• C-Reactive Protein (CRP): Elevated in infection/inflammation
• Erythrocyte Sedimentation Rate (ESR): > 70 mm/hr suggests osteomyelitis (low specificity)
• Blood Cultures: If systemic sepsis suspected

Metabolic Panel

• HbA1c: Assess diabetic control (target less than 7% for healing)
• Renal Function: Chronic kidney disease impairs healing
• Liver Function: Hypoalbuminemia from liver disease

Imaging

X-ray (Radiography)

• Indication: Suspected osteomyelitis, foreign body
• Findings: Bone erosion, periosteal reaction, sequestrum formation
• Limitation: Changes visible only after 40-50% bone destruction; lag time of 2-4 weeks after infection onset
• Sensitivity: 28-75% for osteomyelitis
• Specificity: 60-83%

MRI (Magnetic Resonance Imaging)

• Gold standard imaging for osteomyelitis
• Sensitivity: 90-100%
• Specificity: 80-90%
• Findings: Bone marrow edema (T1 hypointense, T2 hyperintense), abscess formation, soft tissue involvement
• Advantage: Visualizes extent of infection into soft tissues and bone marrow
• Contraindications: Pacemakers, certain metal implants

CT Scan

• Indication: When MRI contraindicated, assess bone destruction
• Less sensitive than MRI for early osteomyelitis
• Useful for surgical planning

Nuclear Medicine (Bone Scan)

• Technetium-99m bone scan: Sensitive but not specific (positive in any bone turnover)
• Indium-111 labeled WBC scan: More specific for infection
• PET scan: Emerging modality with high sensitivity/specificity
• Use: When MRI unavailable or contraindicated

Ultrasound

• Limited role in pressure ulcers
• Can assess fluid collections or abscess
• May help guide drainage procedures

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7. Management

Management Principles

Pressure ulcer management follows a structured hierarchy:

1. Assess and treat underlying risk factors (immobility, nutrition, moisture)
2. Eliminate causative pressure (offloading and repositioning)
3. Optimize wound healing environment (debridement, moisture balance, infection control)
4. Consider advanced therapies (negative pressure, growth factors, surgical reconstruction)

Management Algorithm

         PRESSURE ULCER IDENTIFIED
                    ↓
      ┌─────────────┴─────────────┐
      │     RISK ASSESSMENT       │
      │  (Braden/Waterlow Score)  │
      └─────────────┬─────────────┘
                    ↓
      ┌─────────────┴─────────────┐
      │    REMOVE PRESSURE         │
      │    - Repositioning q2-4h   │
      │    - Support surface       │
      │    - Offload heels         │
      └─────────────┬─────────────┘
                    ↓
      ┌─────────────┴─────────────┐
      │    OPTIMIZE HOST           │
      │    - Nutrition (protein)   │
      │    - Glycemic control      │
      │    - Perfusion/oxygenation │
      │    - Treat incontinence    │
      └─────────────┬─────────────┘
                    ↓
      ┌─────────────┴─────────────┐
    SUPERFICIAL              DEEP/NECROTIC
    (Grade 1-2)              (Grade 3-4)
      ↓                           ↓
    PROTECT SKIN            DEBRIDEMENT
    - Films                 - Sharp/surgical
    - Foams                 - Larval therapy
    - Hydrocolloids         - Autolytic
      ↓                           ↓
    MONITOR                 INFECTION CONTROL
    - Daily inspection      - Antibiotics if indicated
    - Measure weekly        - Treat osteomyelitis
                                  ↓
                            ADVANCED THERAPY
                            - NPWT/VAC
                            - Skin substitutes
                                  ↓
                            SURGICAL RECONSTRUCTION
                            - Flap coverage
                            - Reconstruction

1. Prevention (The Best Treatment)

A. Risk Assessment

• Use validated tool (Braden or Waterlow) on admission and daily
• Reassess when condition changes
• Document risk level and implement appropriate interventions

B. Repositioning and Movement

• Frequency: Every 2-4 hours (higher risk = more frequent)
• Technique:
  • 30-degree tilt in supine position (avoid 90-degree side-lying which increases trochanteric pressure)
  • Use lifting devices, avoid dragging across sheets (reduces shear)
  • Small shifts in body weight (micro-movements) every 15 minutes for seated patients
• "Keep moving": Encourage maximum mobility and independence
• Avoid head-of-bed elevation > 30 degrees unless medically necessary (reduces shear forces)

C. Support Surfaces (Mattresses and Cushions)

Evidence-based selection: [8,9]

Important: No support surface eliminates need for repositioning

Seat cushions: Foam, gel, or air-filled cushions for wheelchair users

D. Skin Care and Hygiene

• Cleanse promptly after soiling with pH-balanced cleanser (avoid harsh soaps)
• Moisturize dry skin with emollients (reduces friction)
• Barrier creams for incontinence (zinc oxide, dimethicone, Cavilon™)
• Avoid massage over bony prominences (may cause deep tissue trauma)

E. Moisture Management

• Incontinence: Scheduled toileting, absorbent pads (changed frequently), consider urinary catheter or fecal management system for severe cases
• Perspiration: Breathable bed linens, climate control
• Wound drainage: Contain and manage exudate appropriately

F. Nutritional Optimization

Evidence-based recommendations: [15]

• Protein: 1.25-1.5 g/kg/day (higher for active ulcers or malnutrition)
• Calories: 30-35 kcal/kg/day
• Hydration: 30 mL/kg/day (unless contraindicated)
• Micronutrients:
  • "Vitamin C: 500 mg twice daily (collagen synthesis)"
  • "Zinc: 15-20 mg daily if deficient (avoid excess)"
  • "Vitamin D: Maintain > 30 ng/mL"
  • "Arginine: May enhance healing (9-15 g/day)"
• Nutritional supplements: High-protein ONS (oral nutritional supplements) if unable to meet needs

2. Wound Management

A. Wound Cleansing

• Normal saline or clean water (evidence shows tap water is safe and cost-effective)
• Avoid antiseptics (povidone-iodine, hydrogen peroxide, acetic acid) - cytotoxic to granulation tissue
• Use irrigation pressure 4-15 psi (35 mL syringe with 19-gauge angiocatheter)

B. Debridement (Removal of Necrotic Tissue)

Necrotic tissue impairs healing by promoting bacterial growth and impeding granulation. [4]

Special case - Heel eschar: Stable, dry, adherent eschar on heels should NOT be debrided - serves as natural biological dressing. Offload and monitor. Debride only if signs of infection (erythema, fluctuance, drainage).

C. Wound Dressings

Select dressing based on wound characteristics:

Dressing frequency: Change when saturated, leaking, or per manufacturer guidelines (typically every 1-7 days depending on type)

D. Infection Management

Distinguish:

• Colonization: Bacteria present but no host response (all chronic wounds) - do NOT treat
• Local infection: Erythema, warmth, increased pain, purulent discharge - topical antimicrobials (silver, cadexomer iodine)
• Spreading infection: Cellulitis, lymphangitis - systemic antibiotics
• Systemic infection: Sepsis - IV antibiotics, source control

Antibiotic selection (if systemically infected):

• Empiric coverage: Broad-spectrum (e.g., piperacillin-tazobactam, vancomycin + ceftazidime)
• Tailor based on culture and sensitivity
• Osteomyelitis: 6 weeks IV antibiotics minimum (often 6-12 weeks), consider surgical debridement

E. Negative Pressure Wound Therapy (NPWT/VAC)

Mechanism: [10]

• Applies sub-atmospheric pressure (-50 to -125 mmHg)
• Removes edema and exudate
• Increases local blood flow
• Promotes granulation tissue formation
• Reduces bacterial load
• Mechanically draws wound edges together

Indications:

• Grade 3-4 pressure ulcers (post-debridement)
• Large cavity wounds
• Bridge to surgical closure
• Post-operative flap protection

Contraindications:

• Untreated osteomyelitis
• Malignancy in wound bed
• Exposed blood vessels or organs without protective barrier
• Non-enteric/unexplored fistulas
• Necrotic tissue with eschar (debride first)

Evidence: Cochrane review shows NPWT may increase healing rate compared to standard dressings for Grade 3-4 ulcers.

3. Surgical Management

Indications for Surgery

• Grade 3-4 ulcers that fail conservative management (3-6 months)
• Patient medically fit for surgery and prolonged rehabilitation
• Adequate nutrition (albumin > 3.0 g/dL ideally)
• Patient can comply with post-operative non-weight-bearing (weeks to months)
• Adequate home support

Pre-operative Optimization

• Treat osteomyelitis (minimum 2-4 weeks IV antibiotics before flap coverage)
• Achieve clean granulating wound bed
• Optimize nutrition (albumin > 3.0, consider pre-albumin > 15 mg/dL)
• Glycemic control (HbA1c less than 7-8%)
• Cessation of smoking
• Correction of anemia (Hb > 10 g/dL)

Surgical Options

1. Excision and Primary Closure

• Limited role
• Small, shallow ulcers with minimal tissue loss
• High recurrence rate

2. Skin Grafting

• Split-thickness skin graft (STSG)
• Requires healthy, granulating wound bed
• No exposed bone or tendon
• Limited role - high recurrence due to lack of padding over bony prominence

3. Flap Reconstruction (Gold Standard for Grade 3-4)

Brings well-vascularized, durable tissue to cover defect:

Surgical Technique Principles:

• Excise ulcer and underlying bursa
• Debride heterotopic ossification and osteomyelitis
• Ostectomy of bony prominence (reduce pressure point)
• Obliterate dead space
• Tension-free closure
• Padding over bony prominence with muscle or fascia
• Careful hemostasis (hematoma increases infection risk)

4. Post-operative Care

• Strict bed rest: 2-4 weeks non-weight bearing on flap
• Gradual mobilization: Progressive weight-bearing over 4-6 weeks
• Air-fluidized bed or low-air-loss mattress
• Drain management: Closed suction drains removed when output less than 30 mL/day
• Prophylactic antibiotics: Usually 24-48 hours peri-operatively
• Nutritional support: Continue high-protein diet

Complications of Surgery

• Flap necrosis (5-15%): Most common complication, often partial
• Infection/wound dehiscence (10-20%)
• Hematoma/seroma (5-10%)
• Recurrence (20-40% at same site, up to 80% at any site over 10 years)

Recurrence Prevention Post-Surgery

• Continued pressure relief (appropriate support surfaces)
• Patient education on repositioning
• Outpatient monitoring (especially first 2 years)
• Prompt treatment of Grade 1 changes

4. Adjunctive and Emerging Therapies

Electrical Stimulation

• Low-level electrical current to wound bed
• May enhance blood flow and cell proliferation
• Some evidence for accelerated healing in Grade 3-4 ulcers

Hyperbaric Oxygen Therapy (HBOT)

• Controversial for pressure ulcers
• Limited high-quality evidence
• May consider for non-healing ulcers with hypoxia or osteomyelitis refractory to antibiotics

Growth Factors

• Platelet-derived growth factor (PDGF)
• Limited evidence in pressure ulcers (better evidence in diabetic foot ulcers)
• Expensive, not routinely recommended

Skin Substitutes/Cellular Therapies

• Bioengineered skin equivalents (Apligraf, Dermagraft)
• Limited evidence for pressure ulcers specifically
• May consider for non-healing wounds after failure of standard care

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8. Complications

Infection

Local Wound Infection

• Presentation: Increased pain, erythema, warmth, purulent discharge, delayed healing
• Management: Topical antimicrobials (silver, iodine), consider systemic antibiotics if spreading

Cellulitis

• Presentation: Expanding erythema beyond wound margins, warmth, edema, systemic symptoms
• Management: Systemic antibiotics (e.g., flucloxacillin, cephalexin; vancomycin if MRSA risk)

Osteomyelitis

• Incidence: 17-32% of Grade 4 ulcers with exposed bone
• Presentation: Non-healing wound, exposed bone, purulent drainage, fever
• Diagnosis: Probe-to-bone test, MRI, bone biopsy (gold standard)
• Management:
  • "Medical: 6-12 weeks IV antibiotics (after bone biopsy/culture)"
  • "Surgical: Debridement of infected bone, removal of sequestra, possible flap reconstruction"
• Antibiotics: Tailor to culture (common organisms: Staph aureus, Strep, Enterococcus, gram-negatives, anaerobes)

Sepsis and Septic Shock

• Presentation: Fever, hypotension, altered mental status, tachycardia, elevated lactate
• Management: Sepsis protocol - fluid resuscitation, broad-spectrum IV antibiotics, source control (debridement/drainage)
• Mortality: High, especially in elderly with multiple comorbidities

Necrotizing Fasciitis

• Rare but life-threatening
• Presentation: Rapidly spreading erythema, crepitus, severe pain, systemic toxicity
• Management: Surgical emergency - urgent extensive debridement, IV antibiotics, ICU care
• Mortality: 20-40%

Other Complications

Marjolin's Ulcer (Squamous Cell Carcinoma)

• Incidence: Rare (less than 2%), occurs in chronic non-healing ulcers (> 10-20 years)
• Presentation: Irregular, raised, friable wound edges; failure to heal despite optimal management
• Diagnosis: Wound edge biopsy
• Management: Wide local excision with negative margins, possible lymph node dissection

Heterotopic Ossification

• Formation of bone in soft tissues around chronic ulcer
• Palpable hard masses
• May require excision during surgical reconstruction

Sinus Tracts and Fistulas

• Tunneling from ulcer to joint space (septic arthritis) or other structures
• May require imaging (MRI, fistulography)
• Surgical exploration and closure often required

Amyloidosis

• Rare, in very chronic wounds
• Deposition of amyloid protein
• Can affect kidneys, heart (systemic amyloidosis)

Anemia

• Chronic inflammation
• Blood loss from wound
• Impairs healing, worsens prognosis

Decreased Quality of Life

• Chronic pain
• Social isolation
• Depression
• Loss of independence
• Caregiver burden

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9. Prognosis and Outcomes

Healing Rates

Factors affecting healing:

• Age (elderly heal slower)
• Nutrition (low albumin significantly impairs healing)
• Comorbidities (diabetes, vascular disease, renal failure)
• Smoking
• Continued pressure (non-compliance with offloading)
• Infection

Surgical Outcomes

• Primary healing rate post-flap: 70-85%
• Recurrence rate:
  • "Same site: 20-40% over 5 years"
  • "Any site: Up to 80% over 10 years in high-risk patients (spinal cord injury)"
• Factors predicting recurrence: Non-compliance, continued immobility, malnutrition, smoking

Mortality

• Hospital-acquired Grade 3-4 ulcers: Associated with 2.5-4x increased mortality in hospitalized elderly [6]
• Likely represents marker of overall frailty and comorbidity rather than direct cause of death in many cases
• Sepsis from infected pressure ulcer is a direct cause of death in some cases (particularly osteomyelitis, necrotizing fasciitis)

Economic Impact

• Cost per ulcer: $5,000 - $60,000 depending on severity and treatment duration (US estimates)
• Total annual cost: Estimated $11 billion annually in the US
• Prevention is cost-effective: $1 spent on prevention saves $2.50 on treatment

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10. Evidence and Guidelines

Key Guidelines

Landmark Studies and Evidence

1. The "Debridement Rule"

• Cannot accurately stage a wound until necrotic tissue is removed
• Exception: Stable, dry eschar on heels should NOT be debrided - acts as natural biological cover
• Debride only if signs of infection (erythema, fluctuance, drainage)

2. Support Surface Evidence

• Cochrane Review (2015): High-specification foam mattresses reduce pressure ulcer incidence vs standard hospital mattresses
• Alternating pressure mattresses may be more effective than constant low-pressure for high-risk patients [9]
• No support surface eliminates need for repositioning

3. Repositioning Frequency

• Traditional "turn every 2 hours" based on Norton's 1962 study
• Optimal frequency depends on individual risk factors and support surface
• Range: Every 2-6 hours for at-risk patients on appropriate surfaces

4. Nutrition

• Cochrane Review: High-protein supplementation may reduce incidence in at-risk patients and improve healing [15]
• Target 1.25-1.5 g/kg/day protein
• No strong evidence for specific micronutrients beyond correcting deficiencies

5. NPWT Evidence

• Multiple RCTs show NPWT may accelerate healing compared to standard dressings for Grade 3-4 ulcers
• Cochrane Review: Low to moderate certainty evidence supporting use
• Cost-effectiveness unclear in many settings

6. Surgical Reconstruction Outcomes

• Multiple case series demonstrate 70-85% primary healing with flap reconstruction
• Recurrence remains high (20-80% depending on population and follow-up duration)
• Best outcomes in motivated patients with good support and ability to maintain pressure relief post-operatively

Quality Indicators

Healthcare systems often track:

• Prevalence of hospital-acquired pressure ulcers (HAPU)
• Incidence of Grade 3-4 HAPU (often considered "never events")
• Time to risk assessment
• Compliance with prevention bundle (SSKIN)
• Healing rates

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11. Patient and Layperson Explanation

What is a Pressure Ulcer (Bed Sore)?

A pressure ulcer, also called a bed sore or pressure sore, is a wound that develops when you stay in one position for too long. When you lie or sit without moving, your body weight presses your skin against the bone underneath. This squeezes the tiny blood vessels that bring oxygen and nutrients to your skin.

Think of it like a garden hose - if you step on a hose, water can't flow through. Similarly, when pressure squeezes your blood vessels, blood can't flow to your skin. Without blood flow, the skin and tissues underneath begin to die, creating a wound.

Where Do They Happen?

Pressure ulcers usually develop over bony areas of your body:

• Bottom/tailbone area (most common when lying on your back)
• Heels (very common)
• Hip bones (when lying on your side)
• Sitting bones (if you sit in a wheelchair)
• Back of the head, elbows, shoulders (less common)

How Do They Start?

Stage 1: The skin looks red and doesn't turn white when you press on it. The skin is still intact but damaged underneath.

Stage 2: The top layer of skin breaks open, like a blister or shallow scrape.

Stage 3: The wound is deeper - goes through the skin into the fat layer underneath.

Stage 4: Very deep wound - you can see muscle or even bone. This is serious and can take many months to heal.

Can They Be Prevented?

Yes! Prevention is much easier than treating a pressure ulcer. Here's how:

1. Keep Moving: Change position every 2-4 hours. Even small movements help. If you can't move yourself, ask for help to be repositioned.

2. Special Mattress: Air mattresses that constantly inflate and deflate help redistribute pressure and give your skin a break.

3. Protect Your Heels: Pillows under your calves to "float" your heels off the bed surface work very well.

4. Keep Skin Clean and Dry: Moisture weakens skin. Keep skin clean, use barrier creams if you have incontinence.

5. Eat Well: Your body needs protein (meat, fish, eggs, beans) and vitamins to keep skin healthy. Aim for high-protein foods and stay hydrated.

6. Check Your Skin Daily: Look for any red areas, especially over bony parts. Report them immediately - early treatment is easier.

How Are They Treated?

Shallow sores (Stage 1-2):

• Remove pressure (this is the most important thing!)
• Special dressings to protect the wound and keep it moist
• Usually heal in a few weeks with proper care

Deep sores (Stage 3-4):

• Remove dead tissue (debridement) - sometimes with special medical maggots that eat only dead tissue
• Special vacuum dressing (VAC) that sucks fluid out and brings blood flow in
• May need surgery to cover the wound with healthy muscle and skin from another part of your body
• Can take many months to heal

What If They're Not Treated?

Untreated pressure ulcers can:

• Get infected (red, warm, pus, fever)
• Spread infection to the bone (osteomyelitis) requiring months of antibiotics
• Cause serious blood infection (sepsis) which can be life-threatening
• Take months or years to heal, causing chronic pain and limiting your activities

Living with a Pressure Ulcer

If you have a pressure ulcer:

• Stay off it: This is the #1 most important thing. The wound cannot heal if you keep lying/sitting on it.
• Follow dressing changes: Keep appointments, let nurses change dressings as recommended
• Eat high-protein foods: Your body needs building blocks to heal
• Report changes: New pain, odor, drainage, fever - tell your doctor right away
• Be patient: Deep wounds take a long time to heal from the bottom up. It's like filling a hole - it takes time.

Key Message

Prevention is EVERYTHING. Moving regularly, using the right mattress, eating well, and checking your skin can prevent most pressure ulcers. If you're at risk, talk to your healthcare team about a prevention plan. If you already have one, strict pressure relief and good wound care give you the best chance of healing.

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12. References

Primary Sources

1. Edsberg LE, Black JM, Goldberg M, et al. Revised National Pressure Ulcer Advisory Panel Pressure Injury Staging System. J Wound Ostomy Continence Nurs. 2016;43(6):585-597. doi:10.1097/WON.0000000000000281 PMID: 27749790

2. Coleman S, Gorecki C, Nelson EA, et al. Patient risk factors for pressure ulcer development: systematic review. Int J Nurs Stud. 2013;50(7):974-1003. doi:10.1016/j.ijnurstu.2012.11.019 PMID: 23375662

3. National Institute for Health and Care Excellence (NICE). Pressure ulcers: prevention and management. Clinical Guideline CG179. 2014. Available at: https://www.nice.org.uk/guidance/cg179

4. European Pressure Ulcer Advisory Panel, National Pressure Injury Advisory Panel, Pan Pacific Pressure Injury Alliance. Prevention and Treatment of Pressure Ulcers/Injuries: Clinical Practice Guideline. The International Guideline. 2019. Available at: https://internationalguideline.com

5. Chaboyer WP, Thalib L, Harbeck EL, et al. Incidence and prevalence of pressure injuries in adult intensive care patients: a systematic review and meta-analysis. Crit Care Med. 2018;46(11):e1074-e1081. doi:10.1097/CCM.0000000000003366 PMID: 30153154

6. Lyder CH, Wang Y, Metersky M, et al. Hospital-acquired pressure ulcers: results from the national Medicare Patient Safety Monitoring System study. J Am Geriatr Soc. 2012;60(9):1603-1608. doi:10.1111/j.1532-5415.2012.04106.x PMID: 22985136

7. Demarré L, Van Lancker A, Van Hecke A, et al. The cost of prevention and treatment of pressure ulcers: a systematic review. Int J Nurs Stud. 2015;52(11):1754-1774. doi:10.1016/j.ijnurstu.2015.06.006 PMID: 26231007

8. Wound, Ostomy and Continence Nurses Society (WOCN). Guideline for Prevention and Management of Pressure Ulcers (Injuries). WOCN Clinical Practice Guideline Series 2. 2016. Mount Laurel, NJ.

9. McInnes E, Jammali-Blasi A, Bell-Syer SE, et al. Support surfaces for pressure ulcer prevention. Cochrane Database Syst Rev. 2015;(9):CD001735. doi:10.1002/14651858.CD001735.pub5 PMID: 26333288

10. Huang C, Leavitt T, Bayer LR, Orgill DP. Effect of negative pressure wound therapy on wound healing. Curr Probl Surg. 2014;51(7):301-331. doi:10.1067/j.cpsurg.2014.04.001 PMID: 24935079

11. Lahmann NA, Halfens RJ, Dassen T. Prevalence of pressure ulcers in Germany. J Clin Nurs. 2005;14(2):165-172. doi:10.1111/j.1365-2702.2004.01041.x PMID: 15669924

12. Mawson AR, Biundo JJ Jr, Neville P, et al. Risk factors for early occurring pressure ulcers following spinal cord injury. Am J Phys Med Rehabil. 1988;67(3):123-127. PMID: 3377890

13. Cox J. Predictors of pressure ulcers in adult critical care patients. Am J Crit Care. 2011;20(5):364-375. doi:10.4037/ajcc2011934 PMID: 21885457

14. Jaul E, Barron J, Rosenzweig JP, Menczel J. An overview of co-morbidities and the development of pressure ulcers among older adults. BMC Geriatr. 2018;18(1):305. doi:10.1186/s12877-018-0997-7 PMID: 30547761

15. Cereda E, Klersy C, Serioli M, et al. A nutritional formula enriched with arginine, zinc, and antioxidants for the healing of pressure ulcers: a randomized trial. Ann Intern Med. 2015;162(3):167-174. doi:10.7326/M14-0966 PMID: 25560712

16. Schoonhoven L, Defloor T, van der Tweel I, et al. Risk indicators for pressure ulcers during surgery. Appl Nurs Res. 2002;15(3):163-173. doi:10.1053/apnr.2002.34145 PMID: 12173168

17. Bergstrom N, Braden BJ, Laguzza A, Holman V. The Braden Scale for Predicting Pressure Sore Risk. Nurs Res. 1987;36(4):205-210. PMID: 3299278

18. Kosiak M. Etiology of decubitus ulcers. Arch Phys Med Rehabil. 1961;42:19-29. PMID: 13753341

19. Peirce SM, Skalak TC, Rodeheaver GT. Ischemia-reperfusion injury in chronic pressure ulcer formation: a skin model in the rat. Wound Repair Regen. 2000;8(1):68-76. doi:10.1046/j.1524-475x.2000.00068.x PMID: 10760216

20. Grayson ML, Gibbons GW, Balogh K, et al. Probing to bone in infected pedal ulcers. A clinical sign of underlying osteomyelitis in diabetic patients. JAMA. 1995;273(9):721-723. PMID: 7853630

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13. Examination Focus

Common Exam Questions

Written Exam (MCQ/SBA)

1. Grading/Staging

Q: A 78-year-old nursing home resident has a wound on the sacrum with visible subcutaneous fat but no exposed muscle or bone. There is some slough present. How should this be graded?

• A) Grade 2
• B) Grade 3
• C) Grade 4
• D) Unstageable

Answer: B) Grade 3 Explanation: Visible subcutaneous fat with no exposed bone/muscle/tendon = Grade 3. Presence of slough does not make it unstageable unless the slough completely obscures the depth.

2. Prevention

Q: Which of the following repositioning strategies is MOST effective for preventing sacral pressure ulcers in bed-bound patients?

• A) 90-degree side-lying position every 4 hours
• B) 30-degree tilt alternating sides every 2-4 hours
• C) Prone positioning every 6 hours
• D) Sitting upright at 60 degrees every 3 hours

Answer: B) 30-degree tilt alternating sides every 2-4 hours Explanation: 30-degree tilt reduces pressure on both sacrum and trochanter. 90-degree side-lying increases trochanteric pressure. Evidence supports 2-4 hour repositioning intervals.

3. Risk Assessment

Q: A patient has a Braden Scale score of 11. This indicates:

• A) No risk
• B) Mild risk
• C) Moderate risk
• D) High risk

Answer: D) High risk Explanation: Braden Scale: ≤9 = very high risk, 10-12 = high risk, 13-14 = moderate risk, 15-18 = mild risk, 19-23 = no risk.

4. Special Cases

Q: A patient has dry, black eschar on the heel with no surrounding erythema or drainage. What is the MOST appropriate management?

• A) Urgent sharp debridement
• B) Larval therapy
• C) Leave intact and offload the heel
• D) Apply wet-to-dry dressings

Answer: C) Leave intact and offload the heel Explanation: Stable, dry heel eschar should NOT be debrided - it acts as a natural biological cover. Offload and monitor. Debride only if signs of infection.

5. Nutrition

Q: What is the recommended daily protein intake for a patient with an existing Grade 3 pressure ulcer?

• A) 0.8 g/kg/day
• B) 1.0 g/kg/day
• C) 1.25-1.5 g/kg/day
• D) 2.0 g/kg/day

Answer: C) 1.25-1.5 g/kg/day Explanation: Enhanced protein intake (1.25-1.5 g/kg/day) is recommended for wound healing. Standard RDA is 0.8 g/kg/day.

Clinical/OSCE Scenarios

Scenario 1: Skin Inspection Station

• Examine standardized patient/manikin
• Identify high-risk areas
• Perform blanching test
• Document findings using correct staging
• Communicate findings to examiner

Key actions:

• Systematic examination of all bony prominences
• Demonstrate glass slide/blanching test
• Correct terminology (non-blanchable erythema = Grade 1)
• Emphasize need for offloading

Scenario 2: Pressure Ulcer Prevention Counseling

• Patient/family member asks about preventing bed sores
• Explain SSKIN bundle
• Demonstrate repositioning techniques
• Discuss support surfaces

Key communication points:

• Movement is key - "every 2-4 hours"
• Special mattresses help but don't replace repositioning
• Nutrition matters - high protein diet
• Check skin daily
• Early intervention for redness

Viva/Oral Exam Questions

1. Pathophysiology Viva

Examiner: "Explain the pathophysiology of pressure ulcer development."

Model Answer: "Pressure ulcers develop through a combination of mechanical forces - primarily pressure, shear, and friction. When external pressure exceeds capillary closing pressure of approximately 32 mmHg, blood flow is occluded, leading to tissue ischemia and hypoxia. This is compounded by shear forces when patients slide down in bed, which cause angular deformation of blood vessels and can reduce the critical external pressure needed by up to 50%.

At the cellular level, prolonged ischemia leads to anaerobic metabolism, lactate accumulation, and cellular acidosis. When pressure is relieved, reperfusion paradoxically causes additional damage through generation of reactive oxygen species and inflammatory mediators - this is ischemia-reperfusion injury.

Importantly, different tissues have varying tolerance to ischemia. Muscle is most sensitive and can undergo irreversible damage after just 2-4 hours, whereas skin is more resistant. This explains the 'iceberg phenomenon' where extensive deep tissue necrosis can occur with minimal superficial skin changes initially."

2. Management Viva

Examiner: "A 68-year-old stroke patient develops a Grade 3 sacral pressure ulcer. How would you manage this?"

Model Answer: "I would approach this systematically:

First, remove the pressure - this is the most critical intervention. I'd ensure the patient is on an appropriate support surface such as an alternating pressure air mattress, and implement a strict repositioning schedule every 2-4 hours using 30-degree tilt positioning. I'd offload the sacrum completely.

Second, optimize the host. I'd assess and optimize nutrition - target protein intake of 1.25-1.5 g/kg/day with high-protein supplements. Check albumin, pre-albumin, hemoglobin. Ensure adequate hydration. Optimize glycemic control if diabetic. Manage incontinence to keep skin dry.

Third, wound management. For a Grade 3 ulcer, I'd perform debridement of any necrotic tissue - either sharp debridement at bedside or in theatre, or consider larval therapy if primarily slough. Once clean, I'd consider negative pressure wound therapy to promote granulation. Select appropriate dressings based on exudate level - foams or alginates for moderate to heavy exudate.

Fourth, infection control. I'd monitor for signs of infection. If systemically infected, send wound cultures and start empiric antibiotics. If bone is exposed or probed, investigate for osteomyelitis with MRI and bone biopsy.

Finally, if the wound fails to progress despite 3-6 months of optimal conservative management, and the patient is medically fit, I'd consider surgical reconstruction with a flap procedure. However, this requires careful patient selection, pre-operative optimization, and the patient must be able to comply with prolonged post-operative non-weight bearing."

3. Classification Viva

Examiner: "What is Deep Tissue Injury and how does it differ from a Grade 1 ulcer?"

Model Answer: "Deep Tissue Injury, or DTI, is a distinct category in the NPUAP/EPUAP classification system. It presents as a purple or maroon localized area of discolored intact skin, or a blood-filled blister. This indicates damage to underlying soft tissue from pressure and/or shear.

The key difference from a Grade 1 ulcer is the color and the depth of injury. A Grade 1 ulcer shows non-blanchable erythema - redness that doesn't turn white when pressed. DTI shows purple or maroon discoloration, indicating that the damage has occurred in deeper tissues - typically muscle or subcutaneous fat - even though the skin surface is still intact.

DTI is particularly concerning because it can rapidly evolve and deteriorate. Within hours to days, the overlying skin may break down to reveal a full-thickness wound - essentially unmasking the deep damage that was already present. The tissue often feels boggy, mushy, or indurated compared to surrounding tissue, and is usually very painful.

This is clinically significant because DTI represents the 'tip of the iceberg' - significant deep tissue damage may already be present even though the skin appears intact. These patients need urgent and aggressive pressure relief to prevent further deterioration."

High-Yield Facts for Exams

"One-Liner" Answers:

• Blanching test: Press red skin - if stays red (doesn't turn white) = Grade 1
• Most common sites: Sacrum #1, Heels #2
• Braden score ≤12: High risk
• Capillary closing pressure: 32 mmHg
• Most sensitive tissue to ischemia: Muscle (can die in 2-4 hours)
• Heel eschar rule: If dry and stable, leave it alone
• SSKIN: Surface, Skin, Keep moving, Incontinence, Nutrition
• Repositioning: Every 2-4 hours with 30-degree tilt
• Protein target: 1.25-1.5 g/kg/day for healing
• Grade 3 vs 4: Grade 3 = see fat, Grade 4 = see bone/muscle
• Unstageable: Can't see wound bed due to eschar/slough
• DTI: Purple intact skin, deep damage, can rapidly worsen
• Osteomyelitis treatment: 6-12 weeks IV antibiotics minimum
• Probe-to-bone: If you feel hard/gritty = likely osteomyelitis
• NPWT pressure: -50 to -125 mmHg

Mnemonics:

• SSKIN (prevention bundle): Surface, Skin inspection, Keep moving, Incontinence, Nutrition
• Pressure ulcer risk factors: "IMMOBILE SKIN"
  • Immobility
  • Moisture
  • Malnutrition
  • Old age
  • Bony prominences
  • Illness (comorbidities)
  • Low albumin
  • Edema
  • Sensory loss
  • Kidney disease
  • Infection
  • Neuropathy

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Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists and follow local guidelines and protocols.