Pressure ulcer

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Pressure ulcer

Classification and external resources

ICD-10

L89

ICD-9

707.0

DiseasesDB

10606

MedlinePlus

007071

eMedicine

med/2709

MeSH

D003668

Pressure ulcers, also known as decubitus ulcers or bedsores, are localized injuries to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure, or pressure in combination with shear and/or friction. Most commonly this will be the sacrum, coccyx, heels or the hips, but other sites such as the elbows, knees, ankles or the back of the cranium can be affected. The cause of pressure ulcers is pressure applied to soft tissue so that blood flow to the soft tissue is completely or partially obstructed. Shear is also a cause; shear pulls on blood vessels that feed the skin. Pressure ulcers most commonly develop in persons who are not moving about or confined to wheelchairs. It is widely believed that other factors can influence the tolerance of skin for pressure and shear thereby increasing the risk of pressure ulcer development. These factors are protein-calorie malnutrition, microclimate (skin wetness caused by sweating or incontinence), diseases that reduce blood flow to the skin, such as arteriosclerosis or diseases that reduce the feeling in the skin, such as paralysis or neuropathy. The healing of pressure ulcers may be slowed by the age of the person, medical conditions (such as arteriosclerosis,diabetes or infection), smoking or medications such as antiinflammatory drugs. Although often prevented and treatable if found early, pressure ulcers can be very difficult to prevent in critically ill patients, frail elders, wheelchair users (especially where spinal injury is involved) and terminally ill patients. Primary prevention is to redistribute pressure by turning the patient regularly. The benefit of turning to avoid further sores is well documented since at least the 19th century. In addition to turning and re-positioning the patient in bed or wheelchair, eating a balanced diet with adequate protein and keeping the skin free from exposure to urine and stool is very important. The prevalence of pressure ulcers in hospital settings is high, but improvements are being made. According to the 2010 IPUP (International Pressure Ulcer Prevalence Survey) conducted in Canada, there was a significant decrease in the overall facility-acquired prevalence of pressure ulcers from 2009-2010. Ulcers were most

commonly identified at the Sacral / Coccyx ulcer location, however, heel ulcers were the most common facilityacquired location in the survey.[1]
Borok, tekanan juga dikenal sebagai decubitus borok atau bedsores, adalah luka-luka lokal untuk kulit dan / atau jaringan yang mendasari biasanya atas menonjol kurus, sebagai akibat dari tekanan, atau tekanan dalam kombinasi dengan dan geser / atau gesekan. Paling sering ini akan menjadi sakrum, ekor, tumit atau pinggul, tapi situs lain seperti siku, lutut, pergelangan kaki atau kembali dari tempurung kepala dapat terpengaruh. Penyebabnya tekanan borok adalah tekanan yang diterapkan untuk jaringan lunak sehingga aliran darah ke jaringan lunak tersebut adalah benar-benar atau sebagian terhambat. Ini juga sebuah geser menyebabkan; menggunting bulu menarik pada pembuluh darah yang memberi makan kulit. Ulkus tekanan paling sering mengembangkan dalam orang-orang yang tidak bergerak tentang atau terbatas untuk kursi roda. Hal ini banyak percaya bahwa faktor-faktor lain dapat mempengaruhi toleransi tersebut dari kulit untuk tekanan dan menggunting bulu sehingga meningkatkan risiko ulkus tekanan pembangunan. Semua faktor tersebut protein-calorie gizi kurang, microclimate ( kulit basah yang disebabkan oleh berkeringat atau inkontinensia ), yang mengurangi penyakit

English to Indonesian

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Tekanan ulkus, juga dikenal sebagai decubitus ulkus atau bedsores, lokal cedera pada kulit dan / atau yang mendasari jaringan biasanya atas menonjol kurus, sebagai akibat dari tekanan, atau tekanan dalam kombinasi dengan geser dan / atau gesekan. Yang paling umum ini akan menjadi sakrum, ekor, tumit atau pinggul, namun situs lain seperti siku, lutut, kaki atau belakang kranium dapat terpengaruh. Yang menyebabkan tekanan ulkus adalah tekanan yang diterapkan untuk jaringan lunak sehingga aliran darah ke jaringan lunak benar-benar atau sebagian terhambat. Geser juga penyebab; geser menarik pada pembuluh darah yang memberi makan kulit. Tekanan ulkus paling sering mengembangkan pada orang yang tidak bergerak terbatas untuk kursi roda. Secara luas diduga bahwa lain faktor dapat mempengaruhi toleransi dari kulit untuk tekanan dan geser sehingga meningkatkan resiko tekanan ulkus pembangunan. Semua faktor tersebut protein-calorie malnutrisi, microclimate ( kulit basah yang disebabkan oleh tanyai atau inkontinensia ), yang mengurangi penyakit

Contents
[hide]

1 Classification 2 Etiology 3 Pathophysiology 4 Epidemiology 5 Determining Risk for Developing Pressure Ulcers 6 Prevention 7 Treatment of Pressure Ulcers

7.1 Debridement

8 Biofilm/Infection

8.1 Nutritional support

9 Support Surfaces

9.1 Pressure ulcer intervention

10 Complications

11 See also 12 References 13 External links

[edit]Classification
The definitions of the four pressure ulcer stages are revised periodically by the National Pressure Ulcer Advisory Panel (NPUAP) in the United States. Briefly, however, they are as follows:

Stage I: Intact skin with non-blanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. The area may be painful, firm, soft, warmer or cooler as compared to adjacent tissue. Stage I may be difficult to detect in individuals with dark skin tones. May indicate at risk persons (a heralding sign of risk).

Stage II: Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled blister. Presents as a shiny or dry shallow ulcer without slough or bruising. This stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration or excoriation.

Stage III: Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling. The depth of a stage III pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have (adipose) subcutaneous tissue and stage III ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep stage III pressure ulcers. Bone/tendon is not visible or directly palpable.

Stage IV: Full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present on some parts of the wound bed. Often include undermining and tunneling. The depth of a stage IV pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have (adipose) subcutaneous tissue and these ulcers can be shallow. Stage IV ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon or joint capsule) making osteomyelitis likely to occur. Exposed bone/tendon is visible or directly palpable. In 2012, the NPUAP stated that pressure ulcers with exposed cartilage are also classified as a stage IV.

Unstageable: Full thickness tissue loss in which actual depth of the ulcer is completely obscured by slough (yellow, tan, gray, green or brown) and/or eschar (tan, brown or black) in the wound bed. Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore

stage, cannot be determined. Stable (dry, adherent, intact without erythema or fluctuance) eschar on the heels serves as the bodys natural (biological) cover and should not be removed.

Suspected Deep Tissue Injury: A purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue. A deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid exposing additional layers of tissue even with optimal treatment.

With higher stages, healing time is prolonged. While about 75% of Stage II ulcers heal within eight weeks, only 62% of Stage IV pressure ulcers ever heal, and only 52% heal within one year.[2] It is important to note that pressure ulcers do not regress in stage as they heal. A pressure ulcer that is becoming shallower with healing is described in terms of its original deepest depth (e.g., healing Stage II pressure ulcer).

[edit]Etiology
Pressure ulcers are accepted to be caused by three different tissue forces: Pressure, or the compression of tissues and/or destruction of muscle cells. In most cases, this compression is caused by the force of bone against a surface, as when a patient remains in a single decubitus position for a lengthy period. After an extended amount of time with decreased tissue perfusion, ischemia occurs and can lead to tissue necrosis if left untreated. Pressure can also be exerted by external devices, such as medical devices, braces, wheelchairs, etc. Shearing, a force created when the skin of a patient stays in one place as the deep fascia and skeletal muscle slide down with gravity can also cause the pinching off of blood vessels which may lead to ischemia and tissue necrosis. Friction is related to shear but is considered less important in causing pressure ulcers. Microclimate, is temperature and moisture of the skin in contact with the surface of the bed or wheelchair. Moisture on the skin causes the skin to loose the dry outer layer and reduces the tolerance of the skin for pressure and shear. Aggravating the situation may be other conditions such as excess moisture from incontinence, perspiration or exudate. Over time, this excess moisture may cause the bonds between epithelial cells to weaken thus resulting in the maceration of the epidermis. Temperature is also a very important factor. The cutaneous metabolic demand rises by 13% for every 1C rise in cutaneous temperature. When supply can't meet demand, ischemia therefore occurs. There are currently two major theories about the development of pressure ulcers. The first and most accepted is the deep tissue injury theory which claims that the ulcers begin at the deepest level, around the bone, and move outward until they reach the epidermis. The second, less popular theory is the top-to-bottom model which says that skin first begins to deteriorate at the surface and then proceeds inward.[3]

Stage 4 decubitus displaying the tuberosity of the ischium protruding through the tissue and possible onset of osteomyelitis

[edit]Pathophysiology
Pressure ulcers may be caused by inadequate blood supply and resulting reperfusion injury when blood reenters tissue. A simple example of a mild pressure sore may be experienced by healthy individuals while sitting in the same position for extended periods of time: the dull ache experienced is indicative of impeded blood flow to affected areas. Within 2 hours, this shortage of blood supply, called ischemia, may lead to tissue damage and cell death. The sore will initially start as a red, painful area. The other process of pressure ulcer development is seen when pressure is high enough to damage the cell membrane of muscle cells. The muscle cells die as a result and skin fed through blood vessels coming through the muscle die. This is the deep tissue injury form of pressure ulcers and begins as purple intact skin.

[edit]Epidemiology
Each year, more than 2.5 million people in the United States develop pressure ulcers. [4]Within acute care in the United States, the incidence of bedsores is 0.4% to 38%; within long-term care, 2.2% to 23.9%; and in home care, 0% to 17%. There is the same wide variation in prevalence: 10% to 18% in acute care, 2.3% to 28% in long-term care, and 0% to 29% in home care. There is a much higher rate of bedsores in intensive care units because of immunocompromised individuals, with 8% to 40% of ICU patients developing bedsores.[5] However pressure ulcer prevalence is highly dependent on the methodology used to collect the data. Using the European Pressure Ulcer Advisory Panel (EPUAP) methodology there are similar figures for pressure ulcers in acute hospital patients. There are differences across countries, but in Europe (for example) using this methodology pressure ulcer prevalence was consistently high, from 8.3% (Italy) to 22.9% (Sweden). [6]A recent study in Jordan also showed a figure in this range.[7]

[edit]Determining

Risk for Developing Pressure Ulcers

Patients who are immobile are at highest risk of developing pressure ulcers. The risk of developing bedsores can be determined by using the Braden Scale for Predicting Pressure Ulcer Risk. The scale contains 6 areas of risk, cognitive-perceptual, immobility, inactivity, moisture, nutrition, friction/shear.

[edit]Prevention
The most important care for a patient at risk for pressure ulcers and those with bedsores is the redistribution of pressure so that no pressure is applied to the pressure ulcer. In the 1940s Ludwig Guttmann introduced a program of turning paraplegics every two hours thus allowing bedsores to heal. Previously such patients had a two year life-expectancy, normally succumbing to blood and skin infections. Guttmann had learned the technique from the work of Boston physician, Donald Munro.[8] The NPUAP in conjunction with the European Pressure Ulcer Advisory Panel (EPUAP) published a comprehensive guideline on the prevention and treatment of pressure ulcers in 2009.[9] Nursing homes and hospitals usually set programs in place to avoid the development of pressure ulcers in bedridden patients such as using a routine time frame for turning and repositioning to reduce pressure. The frequency of turning and repositioning depends on the level of risk in the patient. Turning patients every 2 hours has been a longstanding tradition, with little evidence to support its practice. Pressure-redistributive mattresses are used to reduce high values of pressure on prominent or bony areas of the body. There are several important terms used to describe how these support surfaces work. These terms were standardized through the Support Surface Standards Initiative of the NPUAP. See S3I at npuap.org Many support surfaces redistribute pressure by immersing and/or enveloping the body into the surface. Some support surfaces contain multiple air chambers that are alternately pumped.[10] Antidecubitus mattresses and cushions can contain multiple air chambers that are alternately pumped.[11] Methods to standardized the products and evaluate the efficacy of these products have only been developed in recent years through the work of the S3I within NPUAP. [12] For individuals with paralysis, pressure shifting on a regular basis and using a wheelchair cushion featuring pressure relief components can help prevent pressure wounds. Controlling the heat and moisture levels of the skin surface, known as skin microclimate management, also plays a significant role in the prevention and control of pressure ulcers.[13] In addition, adequate intake of protein and calories is important. Vitamin C has been shown to reduce the risk of pressure ulcers. People with higher intakes of Vitamin C have a lower frequency of bed sores in bed-ridden patients than those with lower intakes. Vitamin C supplements have also been shown to help the healing of bed sores or pressure sores in a double-blind study. Maintaining proper nutrition in newborns is also used to prevent pressure ulcers. If unable to maintain proper nutrition through protein and calorie intake, it is advised to use supplements to support the proper nutrition levels.[14] Skin care is also important because damaged skin does not tolerate pressure. However, skin that is damaged by exposure to urine or stool is not a pressure ulcer. These skin wounds should be classified as Incontinence Associated Dermatitis.

In the UK the Royal College of Nursing has published guidelines in 'Pressure ulcer risk assessment and prevention'.[15] It is important to identify those who are at risk and to intervene early with strategies for prevention, in the bed, wheelchair or chair, in the bath and on the commode - indeed, it is a requirement within the National Standards for Care Homes (UK) to do so: "Standard 8.3 Service users are assessed, by a person trained to do so, to identify those service users who have developed, or are at risk of developing, pressure sores and appropriate intervention is recorded in the plan of care. 8.4 The incidence of pressure sores, their treatment and outcome, are recorded in the service users individual plan of care and reviewed on a continuing basis. 8.5 Equipment necessary for the promotion of tissue viability and prevention or treatment of pressure sores is provided."[16] Certain types of patients with risk of pressure ulcers require additional, specialized methods for prevention. One example is bariatric patients. Preventative measures for pressure ulcers in bariatric patients include:

Holistic assessment: Nurses assessments should encompass and identify all high-risk breakdown areas for careful monitoring and include any comorbidities and their effects on the patient.

Hygiene: Patients skin folds must be kept clean and dry to minimize the amount of moisture. Specialist equipment and safe manual handling: In order to avoid pressure damage, weight shifting is essential.[17]

[edit]Treatment

of Pressure Ulcers

[edit]Debridement
Main article: Debridement Necrotic tissue should be removed in most pressure ulcers. The heel is an exception in many cases when the limb is poorly perfused. Necrotic tissue is an ideal area for bacterial growth, it has the ability to greatly compromise wound healing. There are at five ways to remove necrotic tissue. 1. Autolytic debridement is the use of moist dressings to promote autolysis with the body's own enzymes and white blood cells. It is a slow process, but mostly painless and is most effective in patients with good immune systems. 2. Biological debridement, or maggot debridement therapy, is the use of medical maggots to feed on necrotic tissue and therefore clean the wound of excess bacteria. Although this fell out of favour for many years, in January 2004, the FDA approved maggots as a live medical device. [18] 3. Chemical debridement, or enzymatic debridement, is the use of prescribed enzymes that promote the removal of necrotic tissue. 4. Mechanical debridement, is the use of debriding dressings, whirlpool or ultrasound for slough in a stable wound

5. Surgical debridement or Sharp Debridement is the fastest method, as it allows a surgeon to quickly remove dead tissue.

[edit]Biofilm/Infection
Biofilm is one of the most common reasons for delayed healing in pressure ulcers. Biofilm occurs rapidly in wounds and stalls healing by keeping the wound inflamed. Frequent debridement and antimicrobial dressings are needed to control the biofilm. Infection prevents healing of pressure ulcers. Symptoms of infection in a pressure ulcer include slow or stalling healing, pale granulation tissue. See International Institute of Wound Infection. Infection can become [systemic] Symptoms of systemic infection include fever, pain, redness, swelling, warmth of the area, and purulent discharge. Additionally, infected wounds may have a gangrenous smell, be discolored, and may eventually exude even more pus. In order to eliminate this problem, it is imperative to apply antiseptics at once. Hydrogen peroxide is not recommended for this task as it is difficult to balance the toxicity of the wound with this. Dressings with cadexomer iodine, silver or honey have been shown to penetrate biofilms. Systemic antibiotics are not recommended in treating local infection in a pressure ulcer, as it can lead to bacterial resistance. They are only recommended if there is evidence of advancing cellulitis, osteomyelitis, or bacteremia.[19]

[edit]Nutritional

support

Upon admission the patient should have a consultation with a dietitian to determine the best diet to support healing, as a malnourished person does not have the ability to synthesize enough protein to repair tissue. The dietitian should conduct a nutritional assessment that includes a battery of questions and a physical examination, especially current body weight and history of weight loss. If malnourishment is suspected, lab tests should be run to check serum prealbumin. Additionally, a bioelectrical impedance analysisshould be considered. If the patient is found to be at risk for malnutrition, it is imperative to begin nutritional intervention with adequate intake of protein and calories. There is anecdotal evidence that high protein diet helps healing of sores. High protein diet seems to be especially helpful in sores that do not heal in eight weeks. Dietary supplements and nutrients including, but not limited to, arginine, glutamine, vitamin A,vitamin B complex, vitamin E, vitamin C, magnesium, manganese, selenium and zinc should be considered if the patient is depleted of these substances. It is very important that intake of these vitamins and minerals be overseen by a physician, as many of them can be detrimental in incorrect dosages. Vitamin C supplements have also been shown to help the healing of bed sores or pressure sores in a double-blind study.[20]

[edit]Support

Surfaces

At times the support surface needs to be upgraded to one that provides a low-air loss surface or alterating pressure surface, especially if it is difficult to move the patient off of the pressure ulcer. Complex pressure

ulcers may require air-fluidized support surfaces. If the patient can be positioned off of the ulcer, the basic prevention support surface may suffice. If the patient has pressure ulcers on two or more turning surfaces, for example, the sacrum and one hip, an upgraded support surface should be used to avoid having to position the patient continuously on the remaining area of intact skin, the other hip in this example.

[edit]Pressure

ulcer intervention

Patients with pressure ulcers should not lie or sit on them. Continued pressure reduces the blood flow to a wound that is trying to heal. Specific wound care for pressure ulcers includes the following: Stage I pressure ulcers. Remove all pressure from the ulcer. No topical therapies have been shown to aid healing. Stage II pressure ulcers. Cover the wound bed with hydrocolloid or foam dressings. If the ulcer is on the buttocks, be certain the wound bed is clean before applying the dressings and replace the dressing if the wound bed becomes contaminated from urine or stool beneath the dressing. Skin care products that can be liberally applied to the ulcer are also an alternative to dressings and work well for the incontinent patient. For those with Stage III or IV ulcers, once the necrotic tissue has been removed, fill the wound bed with a moisture retentive dressing or gel product to facilitate healing. Apply a cover dressing to hold the dressing or gel in place. Negative pressure wound therapy applied to the wound bed may also be used to improve granulation tissue formation in the pressure ulcer especially following surgical debridement. This technique uses foam or gauze placed into the wound cavity which is then covered in a film which creates an airtight seal. Once this seal is established, the negative pressure removes exudate and edema from the wound and stimulates blood supply to producegranulation tissue, capillary buds that begin the healing process in fullthickness ulcers. There are, unfortunately, contraindications to the use of negative pressure therapy. Most deal with the unprepared patient, one who has not gone through the previous steps toward recovery, but there are also wound characteristics that bar a patient from participating: a wound with inadequate circulation, a raw debrided wound, a wound with necrotised tissue and eschar, and a fibrotic wound or signs of cancer in the wound. After negative pressure wound therapy the patient should be reevaluated every two weeks to determine future therapy. Clean full thickness pressure ulcers can be closed with surgery such as a tissue flap, free flap or other closure methods. Following these operations, no pressure or tension (pulling) can be applied to the flap while it is healing. Often the patient has to begin sitting up in short time increments to allow inspection of the flap for signs of pressure ulcer (unblanchable redness, pallor, incisional separation). Specialty low-air loss beds or airfluidized beds are often required to promote healing of the flap in a low pressure environment. Air Fluidized Therapy, often achieved with air fluidized therapy beds, can prevent further damage and salvage injured, yet viable tissue. Studies have been done to assess the benefit of Air Fluidized therapy on patients with suspected deep tissue injury. A recent study, Air Fluidized Therapy Use In Patients With Suspected Deep Tissue Injury - A Case Series has found positive results.

[edit]Complications
Pressure ulcers can trigger other ailments, cause patients considerable suffering, and be expensive to treat. Some complications include autonomic dysreflexia, bladder distension, osteomyelitis, pyarthroses, sepsis, amyloidosis, anemia, urethral fistula, gangreneand very rarely malignant transformation (Marjolin's ulcer - secondary carcinomas in chronic wounds). Sores often recur because patients do not follow recommended treatment or develop seromas, hematomas, infections, or dehiscence. Paralytic patients are the most likely people to have pressure sores recur. In some cases, complications from pressure sores can be life-threatening. The most common causes of fatality stem from renal failure and amyloidosis. Pressure ulcers are also painful. Patients of all ages and patients with all stages of pressure ulcers report pain.
Definisi dari empat tahap ulkus tekanan yang direvisi secara berkala oleh national tekanan ulkus panel penasehat ( npuap ) di amerika serikat. Sebentar, namun, mereka adalah sebagai berikut: panggung aku: utuh kulit dengan non-blanchable kemerahan daerah lokal kurus biasanya atas sebuah menonjol. Kulit berpigmen gelap mungkin tidak punya blanching terlihat; warnanya mungkin berbeda dari daerah sekitarnya. Daerah tersebut dapat menyakitkan, perusahaan, lembut, atau dingin yang lebih hangat seperti dibandingkan untuk jaringan yang berdekatan. Panggung aku dapat sulit untuk mendeteksi dalam individu dengan kulit gelap nada. Mungkin menunjukkan pada risiko orang ( a heralding tanda risiko ). Tahap ii: ketebalan parsial hilangnya dermis menyajikan sebagai sebuah dangkal ulkus terbuka dengan sebuah merah luka merah muda tidur, tanpa slough. Mungkin juga hadir sebagai sebuah utuh atau / terbuka pecah blister serum-filled. Menyajikan sebagai sebuah mengkilat atau kering ulkus dangkal tanpa slough atau memar. Tahap ini tidak harus digunakan untuk menggambarkan air mata, kulit tape luka bakar, dermatitis perineum, atau kritik pedas maserasi. Tahap iii:

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Definisi dari empat tekanan ulkus tahap yang direvisi secara berkala oleh national tekanan ulkus panel penasehat ( npuap ) di amerika serikat. Sebentar, namun, mereka adalah sebagai berikut: tahap i: utuh kulit dengan nonblanchable kemerahan pada daerah lokal biasanya atas menonjol kurus. Kulit berpigmen gelap mungkin tidak terlihat blanching; warna mungkin berbeda dari daerah sekitarnya. Daerah dapat menyakitkan, perusahaan, lembut, lebih hangat atau dingin dibandingkan untuk jaringan yang berdekatan. Tahap i akan menjadi sulit untuk mendeteksi di individu dengan kulit gelap nada. Mungkin menunjukkan pada risiko orang ( heralding tanda risiko ). tahap ii: sebagian ketebalan hilangnya dermis menyajikan sebagai dangkal terbuka ulkus dengan merah merah muda luka tidur, tanpa slough. Mungkin juga hadir sebagai sebuah utuh atau terbuka / pecah serum-filled blister. Menyajikan sebagai shiny atau kering shaiiow ulkus tanpa slough atau memar. Tahap ini tidak boleh digunakan untuk menggambarkan kulit air mata, tape membakar, perineal dermatitis, kelelahan atau kritik pedas. tahap iii:

Pressure Sores: Symptoms

Remember: Unrelieved pressure on a specific area of the body (eg the heels , the hips) will affect

the blood supply to the skin and underlying tissues causing that area to become damaged. Mild tissue damage results in skin discolouration, giving a brown or purple appearance. This may look darker if the skin is very fair. More severe pressure ulcers can expose muscle and even bone. The area around the dead tissue will look red and inflamed and may become infected. There are four recognised grades of pressure ulcers in the EPUAP Wound Classification system.

GRADE 1: Discolouration of intact skin not affected by light finger pressure (non blanching erythema) This may be difficult to identify in darkly pigmented skin .

GRADE 2: Partial-thickness skin loss or damage involving epidermis and/or dermis. The pressure ulcer is superficial and presents clinically as an abrasion, blister or shallow crater.

GRADE 3: Full thickness skin loss involving damage of subcutaneous tissue but not extending to the underlying fascia. The pressure ulcer presents clinically as a deep crater with or without undermining of adjacent tissue.

GRADE 4: Full thickness skin loss with extensive destruction and necrosis extending to underlying tissue.

Causes

- Symptoms - Treatment - Prevention

Spinal Cord Injury : Quadriplegic and Paraplegic Injuries

For a person who has been paralysed due to a spinal cord injury, paraplegic and quadriplegic (tetraplegic) are terms used to describe the resultant medical condition. The classification of spinal cord injury depends on thespinal cord injury level and severity of a persons paralysis, and how it affects their limbs.

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There are typically two types of lesions associated with a spinal cord injury, these are known as a complete spinal cord injury and an incomplete spinal cord injury. A complete type of injury means the person is completely paralysed below their lesion. Whereas an incomplete injury, means only part of the spinal cord is damaged. A person with an incomplete injury may have sensation below their lesion but no movement, or visa versa. There are many types in incomplete spinal cord injuries, and no two are the same. Such injuries are known as Brown Sequard Syndrome, Central Cord Syndrome, Anterior Cord Syndrome and Posterior Cord Syndrome.

What is Spinal Cord Injury Rehabilitation

Rehabilitation for individuals with a spinal cord injury combines physical therapies with skill-building activities. These activities will usually take place at a specialist center such as a spinal cord injury rehabilitation center orspinal injury center. A rehabilitation team will usually oversee activities and include a doctor specialising in spinal injuries, social workers, physical and occupational therapists, sports educators, rehabilitation nurses, rehabilitation psychologists, vocational counsellors and nutritionists. Generally, paraplegics will be in hospital for around 5 months, where as quadriplegics can be in hospital for around 6 - 8 months, whilst they undergo rehabilitation. Both paraplegics and quadriplegics should have some kind of rehabilitation and physiotherapy before they are discharged from hospital, to help maximise their potential, or help them get used to life in a wheelchair, and to help teach techniques which make everyday life easier. Disabled sports, and wheelchair based sports can be an excellent way to build stamina, and help in rehabilitation by giving confidence and better social skills. The ultimate reward for many disabled sportsmen and women, is to win at the paralympic games, which will be coming to London in 2012.

Spinal Cord Injury Cure and Treatment

A cure for long term paralysis is still some years in the future, but clinical trials are taking place with olfactory ensheathing glial (OEG) cells and embryonic stem cell based therapy.

Quadraplegic, Tetraplegic, Paraplegic and it's Definition

Quadraplegic is derived from two separate words from two different languages, Latin and Greek. The word Quadra, meaning four which is derived from Latin, relates to the number of limbs. Plegic, is derived from the Greek word Plegia, meaning paralysis. Put the two together, and you have Quadraplegia. Tetra is derived from the Greek word for Four. Para is derived from the Greek word for "two" Hence: Tetraplegic and Paraplegic. In Europe, the term for 4 limb paralysis has always been tetraplegia. The Europeans would never dream of combining a Latin and Greek root in one word. In 1991, when the American Spinal Cord Injury Classification system was being revised, the definition of names was discussed. The British are more aware of Greek versus Latin names. Since Plegia is a Greek word and quadri is Latin, the term quadriplegia mixes language sources. Upon review of the literature, it was recommended that the term

tetraplegia be used by the American Spinal Cord Association so that there are not two different words in English referring to the same thing.