What is the pathophysiology and management of pressure ulcers?

Pathophysiology of Pressure Ulcers

Primary Mechanism

Pressure ulcers develop when unrelieved pressure over bony prominences causes microvascular collapse, leading to tissue ischemia, hypoxia, and ultimately cell death and tissue necrosis. 1, 2

Mechanical Injury Cascade

The pathophysiological process begins with direct mechanical forces that initiate a destructive cascade:

Initial Mechanical Insult

• Sustained pressure compresses tissue between bone and external surfaces, causing microvascular collapse and reducing blood volume fraction in the affected area 3
• Moderate pressure levels (60 kPa at skin surface) can decrease oxygen partial pressure from physiological levels of 65 mmHg to hypoxic levels of 31 mmHg 3
• Shear forces occur during inadequate mobilization, stretching and angulating blood vessels, which further compromises perfusion 4, 2
• Friction during position changes causes direct mechanical trauma to the epidermis and dermis 4, 2

Progressive Tissue Damage

• Direct cell deformation from sustained external strains causes immediate deformation-inflicted cell damage 5
• This mechanical injury triggers inflammatory edema, which paradoxically exacerbates the cell-scale mechanical loading state 5
• The edema creates a nonlinear, escalating damage pattern where inflammation worsens tissue deformation, which in turn amplifies inflammation 5

Ischemic and Metabolic Injury

Oxygen Deprivation

• Microvascular collapse leads to tissue ischemia, preventing oxygen and nutrient delivery to cells 1, 3
• Hypoxia develops rapidly when blood flow is interrupted, with oxygen concentration dropping to levels incompatible with cellular survival 3
• Reperfusion injury occurs when blood flow is restored, generating toxic metabolites and free radicals that compound existing tissue damage 6

Cellular Consequences

• Impaired lymphatic drainage prevents removal of metabolic waste products 6
• Impaired interstitial fluid flow disrupts the cellular microenvironment 6
• Cell distortion from mechanical forces directly damages cellular structures 6
• Accumulation of toxic metabolites accelerates cell death 6

Contributing Factors

Intrinsic Patient Factors

• Advanced age reduces tissue regeneration capacity and causes fragile skin with decreased thickness and stiffness; thinner, less stiff skin shows lower oxygen concentrations under equivalent pressure 4, 3
• Limited mobility prevents autonomous position changes and pressure relief 4, 1
• Nutritional deficiencies, particularly hypoalbuminemia and malnutrition, impair tissue integrity and healing capacity 4, 1
• Comorbidities such as diabetes and microcirculation alterations compromise tissue perfusion and healing 4, 1
• Cognitive impairment prevents patients from communicating discomfort or repositioning themselves 4

Extrinsic Environmental Factors

• Excessive moisture from incontinence, sweating, or drainage causes skin maceration, weakening the epidermal barrier 4, 2
• Prolonged pressure without adequate relief (beyond 2-4 hours) allows ischemic damage to progress 4
• Inadequate use of pressure-redistributing support surfaces fails to prevent microvascular collapse 4

Clinical Pitfalls

The pathophysiology reveals why certain clinical scenarios are particularly dangerous:

• Medical device-related pressure ulcers develop rapidly because devices create focal high-pressure zones with continuous contact, initiating the deformation-inflammation spiral almost immediately 5
• Heel and sacral ulcers are common because these bony prominences have minimal soft tissue cushioning, making microvascular collapse occur at lower applied pressures 4
• The damage cascade is nonlinear and self-amplifying—once initiated, inflammation and edema accelerate tissue destruction even if pressure is partially relieved 5
• Older adults are disproportionately vulnerable because age-related decreases in skin thickness and stiffness result in greater oxygen deprivation under equivalent loading conditions 3