Bedsore Care

Bedsores, also known as “decubitus” ulcers and pressure ulcers, result from compression of soft tissue between an external surface (furniture or bedding) and a bony prominence, long enough to result in tissue damage. They are the most common complications in hospitalized and long-term institutionalized care.

Causes of Bedsores

When pressure applied to skin is greater than the arterial pressure that vascularizes that skin (32 mmHg), blood flow ceases. Not only tissue hypoxia develops, but also the accumulation of metabolic waste products which can be toxic. Prolonged (2 hours) or higher pressures (70 mmHg) can cause irreversible tissue damage.

Pressures are greatest over bony prominences:

  • Lying on a mattress: 150 mmHg.

  • Sitting: up to 300 mmHg over the ischial tuberosities.

Tissue casualties of Bedsores

Muscle is the most susceptible to tissue damage. In decreasing order, the susceptibility to tissue damage is as follows:

  • Muscle.

  • Subcutaneous fat.

  • Dermis.

This susceptibility scale explains how a deeper injury (i.e., muscle) can have severe damage with no evidence seen on the overlying skin, only to have that injury progress to the surface later. The extent of the initial injury is always greater than what may be seen in a visible bedsore on the skin.

Risk factors

How are Bedsores diagnosed?

Diagnosis of bedsores is usually focused on the areas most associated with pressure-induced injuries: the bony prominences. Pressure against them can vary by body position.

Bony prominence areas at risk include the following position-related structures:

  • Lying flat on the back (supine): Occipital bone, scapula, vertebrae, sacrum, coccyx, and calcaneus (heel).

  • Lying prone: Frontal bone, mandible, humerus, sternum, pelvic tuberosity, patella, and tibia.

  • Lying the side: Scapula, ribs, iliac crest, greater trochanter of femur, lateral knee, ankle (lateral and medial).

In diagnosing bedsores, which are obvious on inspection, a staging system has been developed for consistency of documentation purposes:

  • Stage 1: Intact skin with localized nonblanchable erythema.

  • Stage 2: Partial-thickness loss of skin with exposed dermis.

  • Stage 3: Full-thickness loss of skin, exposing fat and granulation tissue.

  • Stage 4: Full-thickness loss of skin and tissue loss with exposed fascia, muscle, tendon, ligament, cartilage, or bone.

Any of the stages can be associated with deep tissue injury.

Specific testing for patients with bedsores includes those for identifying causes of ulceration, such as cardiovascular conditions, diabetes, and neuropathy:

  • Glucose measurements.

  • ECG, cardiac ultrasonography, peripheral vascular studies and imaging.

  • Cultures for infections of ulcer sites.

Management of Bedsores

Management and treatment of bedsores (pressure-induced skin and soft tissue injuries) must include an appraisal of the patient’s general health. The evaluation of the wound is also part of management, since it is also used to judge progress of treatment.

Nutritional assessment should be made and changes implemented by a dietitian/nutritionist if there is concern for malnutrition.

Close daily surveillance of the bedsore(s) is necessary, and attention to the dressing, surrounding skin, and investigations into possible occult deeper tissue injury should be made.

Adequate pain control is part of management.

Evidence of infection (weeping, foul odor, or treatment failure) should prompt microbial culture and sensitivity testing to drive antibiotic choice for aggressive antimicrobial therapy, and subsequent re-testing as a “test-of-cure” of the therapy.

According to the different stages of ulceration:

  • Stage 1 (intact skin with localized nonblanchable erythema): Preventative measures and wound protection with transparent film.

  • Stage 2 (partial-thickness loss of skin with exposed dermis): Dressings and maintenance of a moist wound environment.

  • Stage 3: (full-thickness loss of skin, exposing fat and granulation tissue): Treatment of any infection, debridement of non-vitalized tissue, and appropriate dressings.

  • Stage 4: (full-thickness loss of skin and tissue loss with exposed fascia, muscle, tendon, ligament, cartilage, or bone): Treatment of any infection, debridement of non-vitalized tissue, appropriate dressings, and surgery for some full-thickness wounds.

Procedures such as direct closure, skin grafting, musculocutaneous and free flaps can be considered to hasten the progress if rapid wound coverage is necessary for the best outcomes.

Prevention of Bedsores

Prevention of bedsores involves an approach that blends a frequent re-positioning strategy for immobile patents with infection control, nutrition, and general health maintenance, since pressure itself is not the sole cause but a combination of pressure and host factors.

General health

The best preventative is to have the best tissue integrity by maintenance of good health. Diabetes, peripheral vascular disease, sickle cell anemia, vasculitis, and autoimmune disease should be aggressively followed and treated to ensure the best possible tissue integrity for the individualized patient.

Exploring the extent of tissue damage

Since what is observed on the surface may be masking much more severe damage below it, investigating full-thickness tissues and their underlying musculoskeletal structures will prevent treatment failure. Use of CT, MRI, and ultrasound are useful in this preventive strategy.

Positioning

Patients should be positioned and repositioned at least every 2 hours to relieve constant pressure at any one site. Current bedsores can be spared altogether from pressure effects.

Nutrition

Vitamins and proteins are necessary for tissue integrity, and nutritional support can be established via consultation with a dietitian/nutritionist. Any anemia due to incapacitation, diet, or medical condition should be corrected since even adequate perfusion with anemic blood is simply another type of hypoperfusion.

Dressings

Dressing choice is based on the stage of healing and should be adjusted for prevention of further ulceration.

Wound Care to prevent Ulcer progression

Wounds with necrotic tissue should have the non-vitalized tissue removed so as not to be a nidus of infection. Debridement is via irrigation (hydrostatic force) enzymes, surgery, or biologic debridement (larvae of the Australian sheep blow fly or maggots which secrete enzymes that dissolve dead tissue). Any infections are addressed immediately and tenaciously.

Altering the physics of the pressure forces

Foam mattresses help diffuse the pressure, as do air and hydro circulating mattresses.