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Pressure Ulcers One to three million people develop pressure ulcers in the U. S. each year. Pressure ulcers reduce overall quality of life through pain, suffering, morbidity, and mortality and are a major burden on the health care system increasing staff time and cost.
The skin is a waterproof protective physical barrier with a blood reservoir and bacterial defense. The skin absorbs light and synthesizes vitamin D. Dermal cells contain a precursor of vitamin D, which when activated by sunlight, facilitates Calcium and Phosphorous absorption from the gut via the liver and kidneys, which synthesize calcitriol. The skin also defends against bacteria, and contains sensory receptors for heat, cold, pain, touch, and pressure. The skin has mechanical, chemical, and thermal functions, which include excretion and immunity (macrophage presentation). Normal skin consists of two layers, the dermis and epidermis, or outer layer, ranging from squamous surface cells to a connective tissue base.
Normal skin is 0. 5 to 4. 0 mm deep. The epidermis is a stratified squamous epithelium with five stratum's, the corneum, lucidum (not apparent on hairy skin), granulosum, spinous, and base. The epidermis is a vascular tissue of keratinocytes, which germinate in the lowest layer and migrate to the surface. The Dermis, below the epidermis, contains free nerve endings, blood vessels, Meissners corpuscles of touch, sebaceous oil glands, actor pili muscle, excretory ducts of sudoriferous sweat glands and the glands themselves, sensory nerves with lamellate d Pacinian corpuscles, hair follicles with hair roots in the dermis.
Known risk factors for pressure ulcer development are compromised nutritional status, unintentional weight loss, protein energy malnutrition, dehydration, low body mass index, reduced food intake, or impaired ability to eat. Intervention by a registered dietitian is essential for preventing and / or treating pressure ulcers with kilocalories of protein, amino acids, fluids and micro-nutrients especially vitamin C and zinc.
A Stage I pressure ulcer is change in skin temperature, tissue consistency (firm or boggy) and / or pain or itching. The ulcer is red or red, blue, or purple if the skin is dark.
A stage 2 pressure ulcer it partial skin loss involving epidermis, dermis, or both The ulcer is a superficial abrasion, blister, or shallow crater. Stage 3 is a deep crater of full thickness skin loss with damage to, or necrosis of, subcutaneous tissue to or through the underlying fascia without undermining adjacent tissue. Pressure ulcers are pathological changes at cellular level with damage the epithelium and platelet activation causing tissue acidosis, and alteration in lymphatic flow. Pressure results in a capillary occlusion, which damages the blood vessel resulting in tissue hypoxia. If the pressure is relieved, reactive hyperthermia occurs and the hypoxia resolves. If the pressure continues, tissue ischemia occurs and nutrients and metabolic wastes accumulate, capillaries are damaged, and fluid leaks into the interstitial space (edema).
Tissue edema causes slower perfusion resulting in a pressure ulcer. Once pathology occurs in the skin that produces melanin, the color of the regenerated skin is permanently changed. Muscle damage is not initially evident. Pressure at the highest point of contact between a bony prominence and the muscle fascia is the greatest. Once muscle damage occurs the regenerated granulosum is never the same and pressure destruction is likely to occur again.
Deep pressure ulcers begin to form at the bone and extent to the skin.
The pressure at the bone is three to five times greater at the bone than at the skin. Nurses must understand the inverted cone pressure gradient when assessing a pressure ulcer. A triangle with its base at the bone and apex at the skin illustrates the pressure gradient from the bone to the muscle fascia through subcutaneous tissue to the dermis and epidermis. High intensity pressure for a short period of time is as dangerous as prolonged less intense pressure. Tissue tolerance is the amount of pressure the skin can tolerate. Low intensity pressure caused by prolonged immobility, decreased sensory perception, or inadequate nutrition over a period of time causes tissue injury as well.
It costs less to prevent pressure ulcers than it does to treat them.
References: Bader, D. , Boston, C. , Colin, D. , Opens, C. (2005). The Aetiopathology of pressure ulcers: A hierarchical approach. Heidelberg: Springer. Braden, B. & Bergstrom, N. (1988). Braden scale for predicting pressure sore risk.
retrieved on May 30, 2009 from web Done, B. & Post hauer, M. (1998). The Role of Nutrition in Pressure Ulcer Prevention and Treatment retrieved on May 29, 2009 from web and web National Institute of Health (2009). Progression of a decubitis ulcer retrieved on May 29, 2009 from web NPUAP (2009). The National Pressure Ulcer Advisory Board retrieved on May 29, 2009 from web National Institute of Health (2009). Anatomy and Physiology of Skin retrieved on May 31, 2009 from web
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