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Nursing Care Plan for Decubitus Ulcer / Pressure Sores

Decubitus Ulcer / Pressure Sores


Decubitus ulcer is a local tissue necrosis that tends to happen when the soft tissues between the bony prominences depressed, with the external surface in the long term. (National Pressure Ulcer Advisory Panel [NPUAP], 1989a, 1989b).

Decubitus ulcer is an area of dead tissue caused by lack of blood flow area concerned. Decubitus comes from the Latin that means lying. Lying does not always lead to bedsores. Therefore, some people prefer the term pressure sores because of pressures that is the main cause of decubitus ulcers (Wolf, Weitzel & Fuerst (1989: 354) in Fundamentals of Nursing)


Decubitus sores are caused by a combination of extrinsic and intrinsic factors in patients.

Extrinsic Factors
  • Pressure: stressed skin and underlying tissue between the bones with another hard surface, such as beds and operating tables. Light pressure for a long time as dangerous as great pressure in a short time. Local microcirculation disorders occur later lead to hypoxia and necrosis. (interface pressure). Interfacial pressure is force per unit area of the body with the mattress surface. If the interfacial tension is greater than the average capillary pressure, the capillaries will easily collapse, the area becomes easier to ischemia and necrotic. Average capillary pressure is about 32 mmHg.
  • Friction and shifts: repeated friction will cause abrasion, so that the damaged tissue integrity. The strained skin, the skin layer shifts, local microcirculation disturbances.
  • Humidity: will cause maceration, usually due to incontinence, drain and perspiration. Macerated tissue will be easily eroded. In addition, the moisture also lead to skin prone to friction and tearing of tissue (shear). Alvi incontinence is more significant in the development of pressure sores than urinary incontinence because of bacteria and enzymes in the stool can damage the surface of the skin.
  • Cleanliness of the beds, appliances weaving a tangled and dirty, or medical equipment that causes the client fixed on a certain attitude also facilitate the occurrence of pressure sores.

Intrinsic Factor
  • Age: the elderly will decrease the elasticity and vascularity. Older patients have a high risk of developing pressure sores because of skin and tissue will change with aging. Aging results in muscle loss, decreased levels of serum albumin, a decrease in inflammatory response, decreased skin elasticity, as well as a decrease in cohesion between the epidermis and dermis. These changes, combined with other aging factors will make your skin decreases tolerance to pressure, friction, and energy tearing. In addition, as a result of aging is the reduction of subcutaneous fat tissue, reduced collagen and elastin tissue. decreasing the efficiency of collateral capillaries in the skin so the skin becomes thinner and fragile.
  • Decrease in sensory perception: Patients with decreased sensory perception will be decreased to feel the sensation of pain due to pressure on the bone protruding. When this happens in a long duration, the patient will be susceptible to pressure sores. because pain is a sign that normally encourages a person to move. Nerve damage (eg due to injury, stroke, diabetes) and coma can cause a reduced ability to feel pain.
  • Loss of consciousness: a neurological disorder, trauma, narcotic analgesics.
  • Malnutrition: People who are malnourished (malnutrition) does not have a protective layer of fat, and skin does not undergo complete recovery due to shortage of nutrients that are important. Therefore, the client with malnutrition are also at high risk of suffering from decubitus ulcers. In addition, malnutrition can be impaired wound healing. Usually associated with hypo-albumin. Hypoalbuminemia, weight loss, and malnutrition is generally identified as a predisposing factor for the occurrence of pressure sores. According to research Guenter (2000) stages three and four of pressure sores in elderly people associated with weight loss, low levels of albumin, and inadequate food intake.
  • Mobility and activities: Mobility is the ability to change and control the position of the body, while the activity is the ability to move. Patients who lie constantly in bed without being able to change the position at high risk for developing pressure sores. People who can not move (eg paralyzed, very weak, deprived). Immobility is the most significant factor in the incidence of pressure sores.
  • Smoking: Nicotine found in cigarettes can reduce blood flow and have toxic effects on the endothelium of blood vessels. According to the research Suriadi (2002) there was a significant association between smoking and the development of the pressure sores.
  • Skin temperature: According to the research Sugama (1992) rise in temperature is a significant factor in the risk of pressure sores.
  • The ability of the cardiovascular system decreases, so that the skin perfusion decreased.
  • Anemia.
  • Hypoalbuminemia, high risk of pressure sores and slow down healing.
  • Diseases that damage blood vessels also facilitate exposed to pressure sores and pressure sores worsen.

Clinical Manifestations

Occur in patients with paraplegia, quadriplegia, spina bifida, multiple
sclerosis and prolonged immobilization in the hospital. In addition, other factors need to be known of the history of the patient, including; onset, duration, history of previous treatment, wound care, previous surgical history, nutritional status and changes in body weight, a history of allergies, alcohol consumption, smoking and socio-economic circumstances of the patient. Anamnesis systems including include fever, night sweats, spasm (rigid), paralysis, odor, pain (Arwaniku, 2007). According NPUAP (National Pressure Ulcer Advisory Panel).

Pressure sores is divided into four stages, namely:

Stage 1: ulceration limited to the epidermis and dermis with erythema on the skin. Patients with good sensibility will complain of pain, this stage is usually reversible and can be cured in 5-10 days.
Signs and Symptoms:
A change of the skin that can be observed. When compared with normal skin, it will appear as a sign of the following: changes in skin temperature (colder or warmer), changes the consistency of tissue (more hard or soft), changes in sensation (itching or pain), In people who have white skin, sores may appear as redness persist. Whereas in people with dark skin, the wound will appear as a persistent red, blue or purple.

Stage 2: ulceration of the dermis, epidermis and into broad to the adipose tissue visible erythema and induration, and partial damage to the skin (epidermis and dermis partially) characterized by blisters. This stage can be cured in 10-15 days.
Signs and Symptoms:
Loss of partial layers of the epidermis or dermis of the skin, or both. Character is a superficial wound, abrasion, blister, or forming a shallow pit.

Stage 3: ulceration extending into the layer of fat and muscle subshell has begun to interfere with the edema and inflammation, infection will disappear fibril structure. Damage to all layers of the skin to the subcutaneous, do not pass through the fascia. Usually heal in 3-8 weeks.
Signs and Symptoms: 
Loss of skin layers are complete, including damage or necrosis of subcutaneous tissue or deeper, but not to the fascia. The wound looks like a deep hole.

Stage 4: ulceration and necrosis extends the fascia, muscles and joints. Can be cured in 3-6 months.
Signs and symptoms :
The loss of skin layers complete with extensive damage, tissue necrosis, damage to the muscles, bones or tendons. The presence of a deep hole and sinus passages are also included in stage IV of pressure sores.

NCP for Pressure Sores / Decubitus Ulcer - Physical Examination, Assessment and 6 Nursing Diagnosis

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