Pressure sores, also known as pressure ulcers and decubitus ulcers, are caused by long-term pressure on local tissues and the occurrence of continuous ischemia, hypoxia, and malnutrition, resulting in tissue ulceration and necrosis. Skin pressure sores are a common problem in rehabilitation and care. According to the relevant literature, about 60,000 people die from pressure sore comorbidities each year.
1. Pressure factors
(1) Vertical pressure is the most important cause of pressure sores because the local tissues are subjected to continuous vertical pressure, especially at the rough bony projections of the body. Pressure sores can be caused by prolonged bed rest or wheelchair use, improper placement of the liner in the splint, unevenness or crumbs in the cast, and prolonged local pressure in excess of normal capillary pressure (in general, the pressure that the blood vessels under the skin can withstand is about 32 mmHg; if the pressure exceeds this, the local blood vessels may be distorted and deformed, affecting the passage of blood flow, and there will be ischemia).
(2) Friction Friction acts on the skin and easily damages the skin’s stratum corneum. When the patient is moving around in bed or in a wheelchair, the skin can be rubbed by the retrograde resistance of bed sheets and wheelchair cushion surfaces, and pressure sores are likely to occur when the skin is impregnated with sweat, urine, stool, etc. after being abraded.
(3) shear force so-called shear force is a force applied to the object leads to the production of a parallel reverse direction of the plane of sliding, is made by the friction and vertical pressure summed up. It is closely related to body position. For example, if the body slides down when the head of the bed is raised while lying down, there is a parallel frictional force between the skin and the bed, which, together with the gravitational force in the vertical direction of the skin, leads to the generation of shear force, causing local skin blood circulation disorders and the occurrence of pressure sores.
2. Nutritional status
Systemic nutritional deficiency, muscle atrophy, and lack of protection at the pressure site, such as long-term fever and cachexia.
Systemic nutritional disorders, insufficient nutritional intake, reduced protein synthesis, negative nitrogen balance, reduced subcutaneous fat, and muscle atrophy. Once under pressure, the skin at the bony bulge has to withstand external pressure and the squeezing pressure of the bony bulge on the skin, and the lack of muscle and fat tissue protection at the pressure area causes blood circulation disorders and pressure sores.
3. Reduced skin resistance
The skin is often subjected to physical stimuli such as moisture and friction (e.g. improper use of plaster bandages and splints, urinary and fecal incontinence, uneven bed sheets, and debris on the bed), which reduces the skin’s resistance.
Clinical manifestations
1. Susceptible site
Most often occurs at the bone augmentation without muscle wrapping or thin muscle layer, lack of adipose tissue protection and often under pressure.
(1) Supine position is more likely to occur at the occipital ridge, scapula, elbow, vertebral bulge, sacrococcyge, and heel.
(2) Lateral position is more likely to occur at the ear, shoulder crest, elbow, rib cage, hip, medial and lateral knee joints, and inner and outer ankle.
(3) Prone position is more likely to be found in the ear, cheek, shoulder, female breast, male genitalia, iliac crest, knee, and toe.
2. Clinical staging
National Pressure Sore Advisory Panel 2007 Updated Classification
(1) Suspected deep tissue injury Subcutaneous soft tissue is damaged by pressure or shear forces, with localized skin intact but may show color changes such as purple or maroon, or blisters leading to congestion. These damaged areas of soft tissue may be painful, hard, with mucoid exudate, moist, warm or cold compared to the surrounding tissue.
(2) Phase I pressure ulcer bruising and erythema – “redness, swelling, heat, pain, or numbness that does not fade for 30 minutes” The skin at the bony bulge is intact with limited erythema that does not fade with pressure. The dark skin may not have significant pale changes, but its color may differ from the surrounding tissue.
(3) Phase II pressure ulcer with inflammatory infiltration – “purplish red, hard, painful, blistering” with partial loss of dermis, manifesting as a shallow open ulcer with a pink wound bed (trabeculae) and no decaying flesh, or as a complete or ruptured serous blister.
(4) Stage III pressure ulcer with superficial ulceration – epidermal breakage and ulcer formation. Typical features: total skin tissue loss, visible exposure of subcutaneous fat, but unexposed bone, tendons, and muscle, and the presence of decaying flesh, but the depth of tissue loss is unclear and may contain subterranean and tunneling.
(5) Stage IV pressure ulcer necrotic ulcer stage – invasion of the subdermis, muscle layer, bone surface, and extension of infection. Typical features: total tissue loss with exposed bone, tendon, or meat, rotting flesh or scorched crust in some parts of the wound bed, often with subterranean rows or tunnels.
(6) Typical features of unstageable pressure ulcers: total tissue loss with rotting flesh covering the base of the ulcer (yellow, yellow-brown, gray, green, or brown) or scorched crust adhering to the wound bed (carbon, brown, or black).
Diagnosis
In general, local inflammation with redness, swelling, heat and pain around the wound, and if there are also pus and foul-smelling symptoms, it can be recognized as a local infection sign, and with fever, it indicates a systemic reaction.
1. Most often seen in bedridden patients with paraplegia, chronic wasting disorders, massive burns and deep coma.
2. Most often occurs at the sacrum, sciatic tuberosity and other bony prominences.
3. Erythema, blistering and ulcerative pathological changes appear at the site of continuous pressure.
Treatment
Early pressure sores have red skin, which may improve after taking measures such as turning and pressure reduction. When superficial skin ulceration, ulcers and exudate are present, the skin should be treated in a timely manner at a hospital.
Stage 1: Avoiding pressure and using topical pressure sore patches can heal on its own.
Stage 2: It can heal on its own if treated properly.
External application of Chinese ointment: moist burn cream, Jingwanhong, vital cream, etc.
Western medicine: silver sulfadiazine, zinc, etc.
Biological agents: alkaline fibroblast growth factor, epidermal growth factor.
Stage 3: Small area, can heal by itself with topical medication or trauma closure negative pressure suction technique (VSD).
Large area, requires surgical treatment.
Stage 4: requires surgical repair.
Non-stageable: requires surgical debridement and flap repair.
Prevention
1. Assessment and cleaning of the skin
Patients at risk for pressure ulcers should have a daily skin assessment cleaning the skin with warm water and a mild cleanser.
2. Local protection
Minimize the environmental factors that dry the skin Dry skin application of wetting agents.
3.Control of humidity
Reduce skin moisture caused by skin drainage, incontinence and wound drainage.
4.Body position
Bedridden patients without contraindications, turn every 2 hours, avoid direct pressure on the bony bulge in the lateral position. Strengthen prevention for patients with strictly restricted posture and change the point of emphasis in a timely manner.
5.Nutrition
6.Psychological support and health education
7.Actively treat the underlying disease
8.Decompression devices
Air cushion, foam cushion, water bed, wedge-shaped cushion, etc.
9.Application of local protective dressings
Hydrocolloid dressing can reduce the shear force and friction force of skin
Application of foam dressing is better for bone protruding parts