What is pressure ulcer?

A pressure ulcer, also known as a pressure sore, bed sore, or decubitus ulcer, is a localized injury to the skin and underlying tissue caused by prolonged pressure, friction, or shearing forces. Pressure ulcers typically develop over bony prominences such as the sacrum, hips, heels, elbows, and back of the head, where pressure points are most susceptible to damage.


Pressure ulcers are a common problem, particularly among individuals with limited mobility or those who are bedridden, wheelchair-bound, or otherwise unable to change positions regularly. Prolonged pressure on the skin can impair blood flow to the affected area, leading to tissue ischemia (lack of oxygen and nutrients) and ultimately tissue damage and ulceration.


Several factors contribute to the development of pressure ulcers:


  • Pressure: Continuous pressure on the skin and underlying tissues reduces blood flow to the area, leading to tissue ischemia and breakdown. Pressure ulcers are more likely to occur in areas where pressure points are in contact with a surface for extended periods, such as when lying in bed or sitting in a wheelchair.


  • Friction and Shear: Friction and shear forces can further damage the skin and underlying tissues, particularly when the skin is moist or when the individual is moved or repositioned improperly.


  • Immobility: Immobility and inability to change positions regularly increase the risk of pressure ulcers, as prolonged pressure on the same area can lead to tissue breakdown.


  • Poor Nutrition: Inadequate nutrition, dehydration, and deficiencies in vitamins and minerals can impair tissue repair and increase susceptibility to pressure ulcers.


  • Decreased Sensation: Individuals with impaired sensation, such as those with spinal cord injuries or neurological disorders, may not feel discomfort or pain from prolonged pressure, leading to delayed detection and treatment of pressure ulcers.


Pressure ulcers are classified based on the extent of tissue damage and depth of the ulcer:


  • Stage I: Non-blanchable erythema (redness) of intact skin, indicating potential tissue damage.
  • Stage II: Partial-thickness skin loss involving the epidermis and/or dermis. The ulcer is superficial and may appear as an abrasion, blister, or shallow crater.
  • Stage III: Full-thickness skin loss involving damage to or necrosis (death) of subcutaneous tissue. The ulcer extends through the dermis and may appear as a deep crater with or without undermining of adjacent tissue.
  • Stage IV: Full-thickness skin loss with extensive tissue damage, including damage to muscle, bone, or supporting structures. The ulcer may involve deep tissue necrosis and may appear as a large, deep crater with significant undermining.


What is the relationship between pressure ulcer and oxidative stress?

The relationship between pressure ulcers and oxidative stress is multifaceted and involves several interconnected pathways. Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the body’s antioxidant defenses, leading to cellular damage. Several factors related to pressure ulcers can contribute to oxidative stress:


  • Ischemia-Reperfusion Injury: Prolonged pressure on the skin and underlying tissues reduces blood flow to the affected area, leading to tissue ischemia (lack of oxygen and nutrients). When pressure is relieved and blood flow is restored (reperfusion), it can lead to the generation of ROS and oxidative stress. This ischemia-reperfusion injury contributes to tissue damage and inflammation, exacerbating the progression of pressure ulcers.


  • Inflammatory Response: Pressure ulcers trigger an inflammatory response in the affected tissues, characterized by the release of pro-inflammatory cytokines and activation of immune cells. Inflammatory processes can generate ROS and promote oxidative stress, which further contribute to tissue damage and impaired wound healing.


  • Tissue Damage and Necrosis: Pressure ulcers cause mechanical damage to the skin and underlying tissues, resulting in cellular injury and necrosis (death of cells). Necrotic tissue releases ROS and inflammatory mediators, perpetuating oxidative stress and inflammation in the surrounding tissues.


  • Impaired Wound Healing: Oxidative stress can impair various stages of the wound healing process, including inflammation, tissue regeneration, and remodeling. Excessive ROS production can disrupt the balance between collagen synthesis and degradation, leading to delayed wound healing and formation of chronic wounds such as pressure ulcers.


  • Cellular Dysfunction: Oxidative stress can induce cellular dysfunction and apoptosis (programmed cell death) in the affected tissues, further compromising tissue viability and contributing to the pathogenesis of pressure ulcers.


  • Underlying Conditions: Individuals at risk of pressure ulcers often have underlying health conditions such as diabetes, vascular disease, and immobility, which are associated with increased oxidative stress. These underlying conditions can exacerbate oxidative damage and impair the body’s ability to cope with pressure-induced tissue injury.