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Apr04
Bed Sores: Newer Issues
Bedsores - A comprehensive review.

Gurvinder Singh Sandhu*, Gourishankar Patnaik**

Introduction: One of the most nagging and frustrating problems in long term patient care is decubitus ulcer or commonly referred as Bed Sores. The problem becomes more compounded in cases of Diabetes Mellitus where there are problems ranging from delayed tissue healing to various biochemical changes that virtually frustrates every attempt to treat these patients. Proper Nursing Care is what is stressed up on.

According to www.medterms.com , Bed sore is defined as a painful often reddened area of degenerating, ulcerated skin caused by pressure and lack of movement, and worsened by exposure to urine or other irritating substances on the skin. Untreated bed sores can become seriously infected or gangrenous. Bed sores are a major problem for patients who are confined to bed or a wheelchair. They can be prevented by moving the patient frequently, changing bedding, and keeping the skin clean and dry. Synonyms include pressure sore, decubitus sore, or decubitus ulcer.



In a study conduced by the Healthcare Cost and Utilization Project (HCUP-USA) titled Hospitalizations Related to Pressure Ulcers among Adults 18 Years and Older in the year 2006 it was found that there were a total of 503,300 hospitalization with pressure ulcers noted as a diagnosis which is an increase in 78.9% since 1993 when there were about 281,300 hospitalization due to the same. Adult hospital stays bearing a diagnosis of pressure sores totaled up in 11.0 billion US Dollars in hospital bills in the year 2006 alone. (2)

Amongst others “highlighted” in the published report were: (2)

• Of the total admission, more than 90% of patient (among adults) with pressure ulcer related hospitalization were actually intended for other medical conditions like septicemia, pneumonia, and urinary tract infection to name a few.
• In comparison to hospital stays due to other medical conditions, pressure ulcers patients were more often discharged to a long-term care facility and are more likely to result in death in coming years.
• Almost every three out of four adult patients hospitalized with a secondary pressure ulcer diagnosis 72% were 65 years and older. On the contrary, adult patients with a principal diagnosis of pressures ulcers 56.5% of them are 65 or older.
• Moreover, the younger adults that are hospitalized primarily due to pressure ulcers often go hand in hand with paralysis and spinal cord injury.





Risk-factors

There are numerous risk factors listed below in development of pressure sores. (3)

• Prolong immobility :
Paraplegia
Arthritis
Operation and postoperative states
Plaster casts
Intensive care
• Decrease sensation :
Coma
Neurological disease or deficits
Diabetes Mellitus
Drug Induced Sleep
• Vascular Disease :
Atherosclerosis
Diabetes Mellitus
Scleroderma
Vasculitis
• Poor Nutrition :
Anaemia
Hypoalbuminemia
Vitamin C or Zinc deficiency




As the saying goes prevention is better than cure, after years of study on the topic per-say, several risk assessment tools have been devised for the immobile patient based on the known risk factor such as the “Norton scale”, and “Waterlow Pressure Sore Risk Assessment” are 2 validated systems which produce a numerical sore I while enabling staff to identify those at most risk. The table below depicts “Norton Scale”.


In recent days “Brandon Scale” for predicting risk for pressure ulcers is being used by many health care set-ups. Brandon’s scale is divided into six risk categories: sensory perception, moisture, activity, mobility, nutrition, 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.
The patho-physiology & staging
Bedsores are predisposed by 5 main factors: pressure, injury, anaemia, malnutrition and moisture. (6) There are 3 main etiology for pressure ulcers to develop are namely:
1. Compression between bony prominences and contact surfaces, as when a patient remains in a single decubitus position for a prolonged period of time which will lead to decreased tissue perfusion, ischemia occurs and resulting in tissue necrosis
2. Friction  rubbing against bed linen or patient’s gown.
3. Shearing forces. It’s the force that is created when skin of a patient stays in one place as the deep fascia and skeletal muscle slide down with gravity leading to pinching off of blood vessels which eventually ends up with tissue necrosis.
Infuriating the situation may be other conditions such as excess moisture from incontinence, perspiration or exudates where in elapse of time this excess moisture may deteriorate the bonds between epithelial cells resulting in the maceration of the epidermis.
At present there are 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 that says that skin first begins to deteriorate at the surface and then proceeds inward.
The results of all this will eventually lead to erosion, tissue ischemia, and finally infarction over the site. The most common sites where bed sores most frequently build up is over the sacrum, ischial tuberosities, trochanters, malleoli, and last but non the least the heels. It is not necessarily for the ulcers to only develop at these areas but they can develop elsewhere, including behind the ears when nasal cannulae are used for prolonged periods. Poorly fitting prosthetic devices are also grounds for pressure ulcers to develop over bony prominences. Increased force and duration of pressure directly influence risk and severity.
Pressure sores can as little as 3 to 4 hours to develope in some settings (for example trauma patients who are immobilized on rigid spine-immobilization boards) and these ulcers worsen when skin is overly moist and macerated (e.g., from perspiration or incontinence).
In February 2007 the National Pressure Ulcer Advisory Panel (NPUAP) added unstageable pressure ulcers on to the list of the already existing original 4 stages which are further described below.
Stage I: Intact skin, non-blanchable redness of a localized area usually over a bony prominence. The area may be painful, firm, and soft, with local temperature change as compared to adjacent tissue. It may be difficult to detect this stage in individuals with darker skin tones.
Stage II: Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. Patient in this stage may also present as an intact or open/ruptured serum-filled blister. Presentation is of a shiny / dry shallow ulcer without slough or with bruising which may very well be deep tissue injury. Conditions like skin tears, tape burns, perineal dermatitis, maceration or excoriation should not be mistaken and described in this stage.
Stage III: In this stage pressure ulcer varies by anatomical location. There is full thickness tissue loss with visible subcutaneous fat but bone, tendon or muscles are not exposed or palpable. Slough may be present but does not obscure the depth of tissue loss with possibility of undermining and tunneling. Areas that do not have subcutaneous tissue namely the nose-bridge, ear, occiput and malleolus shows shallow ulcer. On the contrary areas with significant adipose tissue can develop extremely deep stage III pressure ulcers.
Stage IV: In this stage there is full thickness tissue loss with exposed bone (visible and palpable), tendon or muscle with presence of slough over the wound bed with significant undermining and tunneling. Osteomyelitis may transpire in tandem of this stage as ulcers can extend into muscle and/or supporting structures namely fascia, tendon or joint capsule.
Unstageable: Full thickness tissue loss in which the base of the ulcer is covered by slough and/or eschar in the wound bed if and until the debris are removed to expose the base of the wound, the true depth, and therefore stage, cannot be determined.



Prevention
One must bear in mind that bedsores are easier to thwart than to treat. A task is never easily achievable even if it’s the smallest of task need work, the same goes here although wounds can develop in spite of the most scrupulous care, it's possible to prevent them in many cases. First and foremost, the treating physician needs to devise a plan that is comprehendible and easy to follow by caregivers. The cornerstones of such a plan include position changes along with supportive devices, daily skin inspections and a maximally nutritious diet further explained below.
Position changes:  As mentioned before it takes a mere 2-3 hours for a sore to develop over immobilized area hence changing of posture has to be frequent (experts claims to shift position every 15 minutes) and consistent as it’s crucial to prevent bedsores. If one is wheelchair bounded he/she should reposition 2 hourly. When night falls a caregiver should be there to assist a bed ridden patient to change position. Some guidelines that are readily available by some physician on position change are as listed:
• Lie at a 30-degree angle so to avoid lying directly on hipbones..
• When in supine position a head size sleeping pillow should be kept from below knee onwards supporting calf and up to the heel.
• Try to avoid contact between knees and ankle using a foam pad or pillow..
• A higher incline head of the bed makes it more prone that one will slide down, where in there will be friction and shearing injuries.
• A pressure-reducing mattress / bed should be used as there are many options readily available in market stores including foam, air, gel or water mattresses.
• Pressure-release wheelchairs have recently been introduced in the market where in it functions to redistribute pressure hence making sitting for long periods easier and more comfortable. All wheelchairs need cushions in order to reduce pressure and provide maximum support and comfort.
Skin inspection  Skin should be inspected thoroughly at least once a day for pressure sores as its fundamental part of prevention. Inspect your skin thoroughly at least once a day, using a mirror if necessary. Special attention are to be paid to these areas hips, spine and lower back, shoulder blades, elbows and heels if a patient is bed ridden. When in a wheelchair, look especially for sores over the buttocks and tailbone, lower back, legs, heels and feet If an area of your skin is red or discolored but not broken, keep pressure off the sore, wash it gently with mild soap and water, dry thoroughly, and apply a protective wound dressing. If there is visible skin damage or any sign of infection such as drainage from a sore, a foul odor, and increased tenderness, redness and warmth in the surrounding skin, get medical help immediately.
Nutrition  Malnourished populaces are the ones highly predisposed to bed sores. It's crucial to get enough calories, protein, vitamins and minerals in preventing skin breakdown and in aiding wound healing. Markers of under nutrition include albumin < 3.5 mg/dL or weight < 80% of ideal. Protein intake of 1.25 to 1.5 g/kg/day is desirable for optimal healing. Zinc supplementation supports wound healing, and replacement at a dose of 50 mg thrice daily may be useful. Supplemental vitamin C 1 g/day may be provided. Providing a drink of water to patients at each repositioning may be useful to aid hydration.
Lifestyle changes including cessation of smoking as tobacco use damages skin and slows wound healing as on the other hand exercise improves circulation, helps builds up vital muscle tissue strengthen the body overall.

Treatment
The 1994 consensus guidelines provide a brilliant approach to the rational treatment of pressure ulcers. Listed below are the general summaries indicating steps necessary in management of this important issue.
Debridement of necrotic tissue can be done through a variety of potential techniques, which aids in healing of the wound. Several different debridement techniques are available.
• Sharp debridement is used in critical situations like cellulitis where in devitalized tissue are removed..
• Mechanical debridement where Hydrotherapy (whirlpool baths), ultrasound, medical maggots, wound irrigation, or dextranomers are to be used to remove thick exudates and loose necrotic tissue. Urgent debridement is indicated in advancing cellulitis or sepsis. Wounds with very loose exudates- debridement with wet-to-dry dressings can be done but only with utmost care as it is often painful and it may remove healthy tissue.
• Enzymatic debridement involves applying topical debriding agents to remove devitalized tissue using collagenase, papain, fibrinolysin, or streptokinase.
• Autolytic debridement requires the use of synthetic dressings that allow devitalized tissue to self-digest from enzymes present in wound fluids. DuoDERM or Contreet (which is impregnated with silver and thus offers antimicrobial effects) are commonly applied.
Wound cleansing using a 30 ml syringe and a 18 gauge angiocatheter will provide sufficient force to remove eschar, bacteria, and other debris from the wound site. Initially wound should be cleansed with normal saline and not using solutions that are cytotoxic in nature, such as povidone iodine, sodium hypochlorite solution and hydrogen peroxide, should be avoided to avoid further damage to tissue.
Treatment of Infected sites following the procurement of swabs from the area which are immediately sent for culture n sensitivity test. Conventionally first line therapy should cover gram-positive skin organisms, such as the use of a first-generation cephalosporin (e.g. Cephalexin 250-500 mg po qid). If the clinical picture is suggestive and/or swab results are confirmatory, consideration for antipseudomonal coverage should be made. Broader coverage should be emperically instituted in diabetic patients.
Dressing selection should be based on its ability to keep ulcer tissue moist and the surrounding intact skin, dry. Multiple types of dressings are available, and the choice should be based on clinical judgement. Objectives are to keep the ulcer bed moist to retain tissue growth factors while allowing some evaporation and inflow of oxygen, to keep surrounding skin dry, to facilitate autolytic debridement, and to establish a barrier to infection. Adjuvant therapy and /or operative repair are made on a case-by-case basis. Modes of operation include electrical stimulation, hyperbaric oxygen and laser irrigation. Electrical stimulation is only recommended for stage III and IV pressure ulcers. The table below tabulates the different options of dressing available for pressure ulcers.





Conclusion
Pressure ulcers are a preventable and treatable medical problem. Proper management of this problem can result in significantly improved quality of life and shorter hospital stays for elderly patients. When ulcers do develop, a multidisciplinary approach to treatment is recommended.

*Final year Medical student
**Professor of Orthopedics ,Melaka Manipal Medical College, Melaka

N.B.This article is a product of a project given to one of the final year medical student as an exercise to make medical students and future doctors aware of their responsibility to treat preventable conditions like bed sores.
It comprehensively deals with the types, pathophysiology and necessary treatment regimens of this condition which is an indicator of nursing standards in a given setting.

References
1. Bedsores definition. http://www.medterms.com/script/main/art.asp?articlekey=11035
2. Russo C.A., Steiner C., Spector W. Statistical Brief # 64 Healthcare Cost and Utilization Project “Hospitalizations Related to Pressure Ulcers among Adults 18 Years and Older, 2006.” http://www.hcup-us.ahrq.gov/reports/statbriefs/sb64.jsp
3. Kumar P., Clark M. Kumar & Clark Clinical Medicine Textbook 6th edition. Elsevier Saunders 2005
4. Russel R.C.G., William N.S., Bulstrode C.J.K. Bailey & Love Short Practice of Surgery 24th Edition. Hodder Arnold 2004.
5. Wolff K., Goldsmith L. A., Katz S.I., Gilchrest B.A., Paller A.S., Leffell D.J., Fitzpatrick's Dermatology in General Medicine, 7th edition McGraw-Hill Professional 2008.
6. 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. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?an=00129334-200601001-00001
7. Support surfaces for pressure ulcer prevention by McInnes E, Cullum NA, Bell-Syer SEM, Dumville JC. http://www.cochrane.org/reviews/en/ab001735.html
8. Cervo FA, Cruz AC, Poscillico JA. Pressure ulcers: Analysis of guideline for treatment and management. Geriatrics. Mar 2000;55:55-60.
9. Pieper B. Mechanical Forces: Pressure, shear, and friction. In: Bryant RA. Acute and Chronic Wounds: Nursing Management, Second Edition. Mosby, Inc., 2000
10. Bergstrom N, Bennet MA, Carlson CE et al. Treatment of Pressure Ulcers. Clinical Practice Guideline, No 15. Rockville, MD. US Department of Health and Human Services. Public Health Service, Agency for Health Care Policy and Research. AHCPR Publication No. 95-0652. December, 1994.
11. Malone J.R., McInnes E. Pressure Ulcer Risk Assessment and Prevention. Royal College Of Nursing U.K. April 2001
12. Bedsores. Mayo Clinic. http://www.mayoclinic.com/health/bedsores/DS00570/DSECTION=symptoms
13. Encyclopedia for surgery. Bedsores. http://www.surgeryencyclopedia.com/A-Ce/Bedsores.html


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