Sunday, June 14, 2009

Pressure Sores - Bedsores

Cited in Wikipedia:

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Classification and external resources
ICD-10 L89.
ICD-9 707.0
DiseasesDB 10606
eMedicine med/2709
MeSH D003668

Bedsores, more properly known as pressure ulcers or decubitus ulcers, are lesions caused by many factors such as: unrelieved pressure; friction; humidity; shearing forces; temperature; age; continence and medication; to any part of the body, especially portions over bony or cartilaginous areas such as sacrum, elbows, knees, ankles etc. Although easily prevented and completely treatable if found early, bedsores are often fatal – even under the auspices of medical care – and are one of the leading iatrogenic causes of death reported in developed countries, second only to adverse drug reactions. Prior to the 1950s treatment was ineffective until Doreen Norton showed that the primary cure and treatment was to remove the pressure by turning the patient every two hours.[1]

* 1 Classification
* 2 Etiology
* 3 Pathophysiology
* 4 Epidemiology
* 5 Treatment
o 5.1 Debridement
o 5.2 Infection control
o 5.3 Nutritional support
o 5.4 Proper care
o 5.5 Educating the caregiver
o 5.6 Wound intervention
* 6 Complications
* 7 See also
* 8 References
* 9 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 is the most superficial, indicated by non blanchable redness that does not subside after pressure is relieved. This stage is visually similar to reactive hyperemia seen in skin after prolonged application of pressure. Stage I pressure ulcers can be distinguished from reactive hyperemia in two ways: a) reactive hyperemia resolves itself within 3/4 of the time pressure was applied, and b) reactive hyperemia blanches when pressure is applied, whereas a Stage I pressure ulcer does not. The skin may be hotter or cooler than normal, have an odd texture, or perhaps be painful to the patient. Although easy to identify on a light-skinned patient, ulcers on darker-skinned individuals may show up as shades of purple or blue in comparison to lighter skin tones.
* Stage II is damage to the epidermis extending into, but no deeper than, the dermis. In this stage, the ulcer may be referred to as a blister or abrasion.
* Stage III involves the full thickness of the skin and may extend into the subcutaneous tissue layer. This layer has a relatively poor blood supply and can be difficult to heal. At this stage, there may be undermining damage that makes the wound much larger than it may seem on the surface.
Stage IV pressure ulcer
* Stage IV is the deepest, extending into the muscle, tendon or even bone.
* Unstageable pressure ulcers are covered with dead cells, or eschar and wound exudate, so the depth cannot be determined.

Suspected Deep tissue injury: 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.

Further description: 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

Bedsores are accepted to be caused by three different tissue forces:

Pressure, or the compression of tissues. 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 in an immunocompromised patient.

Shear force, or a force created when the skin of a patient stays in one place as the deep fascia and skeletal muscle slide down with gravity. This can also cause the pinching off of blood vessels which may lead to ischemia and tissue necrosis.

Friction, or a force resisting the shearing of skin. This may cause excess shedding through layers of epidermis.

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. Other factors in the development of bedsores include age, nutrition, vascular disease, diabetes mellitus, and smoking, amongst others.

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 re-enters 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 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, which eventually turns purple. Left untreated, the skin may break open and become infected. Moist skin is more sensitive to tissue ischemia and necrosis and is also more likely to get infected.

[edit] Epidemiology

Within acute care, 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.[4]

The risk of developing bedsores can be determined by using the Braden Scale for Predicting Pressure Ulcer Risk. This scale is divided into six risk categories:

1. sensory perception
2. moisture
3. activity
4. mobility
5. nutrition
6. friction and shear

The best possible interpretation is a score of 23 whilst the worst is a 6. If the total score is below 11, the patient is at risk for developing bedsores.[5]

[edit] Treatment

The most important thing to keep in mind about the treatment of bedsores is that the most optimal outcomes find their roots in a multidisciplinary approach; by using a team of specialists, there is a better chance that all bases will be covered in treatment.

There are seven major contributors to healing.

[edit] Debridement

The removal of necrotic tissue is an absolute must in the treatment of pressure sores. Because dead tissue is an ideal area for bacterial growth, it has the ability to greatly compromise wound healing. There are at least seven ways to excise necrotic tissue.[3]

1. Autolytic debridement is the use of moist dressings to promote autolysis with the body's own enzymes. It is a slow process, but mostly painless.
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.[6]
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 outside force to remove dead tissue. A quite painful method, this involves the packing of a wound with wet dressings that are allowed to dry and then are removed. This is also unpopular because it has the ability to remove healthy tissue in addition to dead tissue. Lastly, with Stage IV ulcers, there is the chance that overdrying of the dressings can lead to bone fractures and ligament snaps.
5. Sharp debridement is the removal of necrotic tissue with a scalpel or similar instrument.
6. Surgical debridement is the most popular method, as it allows a surgeon to quickly remove dead tissue with little pain to the patient.
7. Ultrasound-assisted wound therapy is the use of ultrasound waves to separate necrotic and healthy tissue.

[edit] Infection control

Infection has one of the greatest effects on the healing of a wound. Purulent discharge provides a breeding ground for excess bacteria, a problem especially in the immunocompromised patient. Symptoms of systemic infection include fever, pain, erythema, oedema, and warmth of the area, not to mention purulent discharge. Additionally, infected wounds may have a gangrenous smell, be discoloured, and may eventually exude even more pus.

In order to eliminate this bioburden, it is imperative to apply antiseptics and antimicrobials at once. It is not recommended to use hydrogen peroxide for this task as it is difficult to balance the toxicity of the wound with this. New dressings have been developed that have cadexomer iodine and silver in them, and they are used to treat bad infections. Duoderm can be used on smaller wounds to both provide comfort and protect them from outside air and infections.

It is not recommended to use systemic antibiotics to treat infection of a bedsore, as it can lead to bacterial resistance.

[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. If malnourishment is suspected, lab tests should be run to check serum albumin and lymphocyte counts. Additionally, a bioelectrical impedance analysis should be considered.

If the patient is found to be at risk for malnutrition, it is imperative to begin nutritional intervention with 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. 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.

[edit] Proper care

The most important care for a patient with bedsores is the relief of pressure. Once a bedsore is found, pressure should immediately be lifted from the area and the patient turned at least every two hours to avoid aggravating the wound. Nursing homes and hospitals usually set programs to avoid the development of bedsores in bedridden patients such as using a standing frame to reduce pressure and ensuring dry sheets by using catheters or impermeable dressings. For individuals with paralysis, pressure shifting on a regular basis and using a cushion featuring pressure relief components can help prevent pressure wounds.

Pressure-distributive mattresses are used to reduce high values of pressure on prominent or bony areas of the body. However, methods to evaluate the efficacy of these products have only been developed in recent years.[7]

[edit] Educating the caregiver

In the case that the patient will be returning to home care, it is very important to educate the family about how to treat their loved one's pressure ulcers. The cross-specialisation wound team should train the caregiver in the proper way to turn the patient, how to properly dress the wound, how to properly nourish the patient, and how to deal with crisis, among other things.

As this is a very difficult undertaking, the caregiver may feel overburdened and depressed, so it may be best to bring in a psychological consult.

[edit] Wound intervention

Once the patient has reached the point that intervention is possible, there are many different options. For patients with Stages I and II ulcers, the wound care team should use guidelines established by the American Medical Directors Association (AMDA) for the treatment of these low-grade sores.

For those with Stage III or IV ulcers, most interventions will likely include surgery such as a tissue flap, skin graft or other closure methods. A more recent intervention is Negative Pressure Wound Therapy, which is the application of topical negative pressure to the wound. This technique, developed by scientists at Wake Forest University, uses foam placed into the wound cavity which is then covered in a film which creates an airtight seal. Once this seal is established, the technician is able to remove exudate and other infectious materials in addition to aiding the body produce granulation tissue, the best bed for the creation of new skin.

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 debridled wound, a wound with necrotised tissue and eschar, and a fibrotic wound.

After Negative Pressure Wound Therapy, the patient should be reevaluated every two weeks to determine future therapy.

[edit] Complications

Pressure sores can trigger other ailments, cause patients considerable suffering, and be expensive to treat.[8] Some complications include autonomic dysreflexia, bladder distension, osteomyelitis, pyarthroses, sepsis, amyloidosis, anemia, urethral fistula, gangrene and very rarely malignant transformation. 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.

[edit] See also

* Wound healing
* Gangrene
* Liquefactive necrosis
* Iatrogenesis

[edit] References

1. ^ Elliott, Jane (21 March 2009). "How one nurse helped stop killer bedsores" (web). News article. BBC News. Retrieved on 21 March 2009.
2. ^ Thomas DR, Diebold MR, Eggemeyer LM (2005). "A controlled, randomized, comparative study of a radiant heat bandage on the healing of stage 3-4 pressure ulcers: a pilot study". J Am Med Dir Assoc 6 (1): 46–9. doi:10.1016/j.jamda.2004.12.007. PMID 15871870.
3. ^ a b Niezgoda JA, Mendez-Eastman S (2006). "The effective management of pressure ulcers". Adv Skin Wound Care 19 Suppl 1: 3–15. doi:10.1097/00129334-200601001-00001. PMID 16565615.
4. ^ "Pressure ulcers in America: prevalence, incidence, and implications for the future. An executive summary of the National Pressure Ulcer Advisory Panel monograph". Adv Skin Wound Care 14 (4): 208–15. 2001. PMID 11902346.
5. ^ Jiricka MK, Ryan P, Carvalho MA, Bukvich J (1995). "Pressure ulcer risk factors in an ICU population". Am. J. Crit. Care 4 (5): 361–7. PMID 7489039.
6. ^ "510(k)s Final Decisions Rendered for January 2004: DEVICE: MEDICAL MAGGOTS". FDA.
7. ^ Bain DS, Ferguson-Pell M (2002). "Remote monitoring of sitting behavior of people with spinal cord injury". J Rehabil Res Dev 39 (4): 513–20. PMID 17638148.
8. ^ Brem H, Kirsner RS, Falanga V (2004). "Protocol for the successful treatment of venous ulcers". Am. J. Surg. 188 (1A Suppl): 1–8. doi:10.1016/S0002-9610(03)00284-8. PMID 15223495.

Alexander's Care of the Patient in Surgery by Jane C Rothrock, Thirteenth Edition, 2007. Mosby

[edit] External links

* Decubitus Ulcer Prevention
* Bed Sores and Pressure Ulcers
* CNN article
* USA today article

v • d • e
Diseases of the skin and subcutaneous tissue (integumentary system) (L, 680-709)
skin disease

Staphylococcus (Staphylococcal scalded skin syndrome, Impetigo, Boil, Carbuncle) · Strep (Impetigo) · Corynebacterium (Erythrasma)
skin disease

Wart · Molluscum contagiosum · Erythema infectiosum · Exanthema subitum · Herpes simplex (Herpetic whitlow)

Cellulitis (Paronychia) · Acute lymphadenitis · Pilonidal cyst · Pimple (Pustule)
acantholysis (Pemphigus, Transient acantholytic dermatosis) · Pemphigoid (Bullous, Cicatricial, Gestational) · Dermatitis herpetiformis
and eczema

Atopic dermatitis · Seborrhoeic dermatitis (Dandruff, Cradle cap) · Contact dermatitis (Diaper rash, Urushiol-induced contact dermatitis) · Erythroderma · Lichen simplex chronicus/Prurigo nodularis · Itch (Pruritus ani, Pruritus scroti, Pruritus vulvae) · Nummular dermatitis · Dyshidrosis · Pityriasis alba

Psoriasis (Psoriatic arthritis) · Parapsoriasis (Pityriasis lichenoides et varioliformis acuta, Pityriasis lichenoides chronica, Lymphomatoid papulosis) · other pityriasis (Pityriasis rosea, Pityriasis rubra pilaris) · other lichenoid (Lichen planus, Lichen nitidus)

Dermatographic urticaria · Cold urticaria · Cholinergic urticaria · Solar urticaria

Erythema multiforme/drug eruptions: Stevens-Johnson syndrome · Toxic epidermal necrolysis · Erythema nodosum
Other erythema: Erythema annulare centrifugum · Erythema marginatum · Keratolytic winter erythema · Necrolytic migratory erythema · Erythema toxicum
Sunburn · actinic rays (Actinic keratosis, Actinic cheilitis) · Polymorphous light eruption (Acne aestivalis) · Radiodermatitis · Erythema ab igne
hypopigmentation (Albinism, Vitiligo) · hyperpigmentation (Melasma, Freckle, CafĂ© au lait spot, Lentigo/Liver spot, Acanthosis nigricans, Acral acanthotic anomaly)
Other skin
keratosis/hyperkeratosis (Seborrheic keratosis, Callus) · other epidermal thickening (Ichthyosis acquisita, Palmoplantar keratoderma)

skin ulcer (Pyoderma gangrenosum, Bedsore)

Cutaneous Markers of Internal Malignancy (Florid cutaneous papillomatosis, acanthosis nigricans, sign of Leser-Trelat)

atrophic (Lichen sclerosus, Acrodermatitis chronica atrophicans)

necrobiosis (Granuloma annulare, Necrobiosis lipoidica) · other granuloma (Granuloma faciale, Pyogenic granuloma)
cutaneous vasculitis (Livedoid vasculitis, Erythema elevatum diutinum)
collagen disease: Keloid
localized connective tissue disorders: Lupus erythematosus (Discoid lupus erythematosus, Subacute cutaneous lupus erythematosus) · Scleroderma/Morphea · Linear scleroderma · Calcinosis cutis · Sclerodactyly · Ainhum
see also congenital, neoplasia
Retrieved from ""
Categories: Skin conditions resulting from physical factors | Traumatology

Powered by MediaWiki
Wikimedia Foundation

* This page was last modified on 10 June 2009 at 09:41.
* All text is available under the terms of the GNU Free Documentation License. (See Copyrights for details.)
Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc., a U.S. registered 501(c)(3) tax-deductible nonprofit charity.

No comments:

Post a Comment