what is good to cover and protect a pressure wound
Pressure Ulcers: Prevention, Evaluation, and Management
Am Fam Dr.. 2008 Nov 15;78(10):1186-1194.
The online version of this article includes supplemental content.
A more contempo article on pressure ulcers is available.
Patient information: See related handout on preventing bedsores, written by the authors of this article.
Article Sections
- Abstruse
- Etiology
- Prevention
- Assessment
- Nutritional Evaluation
- Management
- Complications
- References
A pressure ulcer is a localized injury to the pare or underlying tissue, normally over a bony prominence, as a result of unrelieved force per unit area. Predisposing factors are classified as intrinsic (e.thousand., limited mobility, poor nutrition, comorbidities, aging peel) or extrinsic (eastward.thousand., pressure level, friction, shear, moisture). Prevention includes identifying at-risk persons and implementing specific prevention measures, such as following a patient repositioning schedule; keeping the head of the bed at the everyman condom meridian to foreclose shear; using force per unit area-reducing surfaces; and assessing nutrition and providing supplementation, if needed. When an ulcer occurs, documentation of each ulcer (i.e., size, location, eschar and granulation tissue, exudate, odor, sinus tracts, undermining, and infection) and appropriate staging (I through IV) are essential to the wound assessment. Treatment involves management of local and afar infections, removal of necrotic tissue, maintenance of a moist environment for wound healing, and possibly surgery. Debridement is indicated when necrotic tissue is nowadays. Urgent sharp debridement should exist performed if advancing cellulitis or sepsis occurs. Mechanical, enzymatic, and autolytic debridement methods are nonurgent treatments. Wound cleansing, preferably with normal saline and appropriate dressings, is a mainstay of treatment for clean ulcers and afterwards debridement. Bacterial load can be managed with cleansing. Topical antibiotics should be considered if in that location is no comeback in healing after 14 days. Systemic antibiotics are used in patients with advancing cellulitis, osteomyelitis, or systemic infection.
Pressure ulcers, likewise called decubitus ulcers, bedsores, or pressure sores, range in severity from reddening of the pare to severe, deep craters with exposed muscle or bone. Force per unit area ulcers significantly threaten the well-existence of patients with limited mobility. Although lxx per centum of ulcers occur in persons older than 65 years,i younger patients with neurologic impairment or severe affliction are too susceptible. Prevalence rates range from 4.7 to 32.ane pct in hospital settings2 and from 8.5 to 22 percent in nursing homes.3
SORT: KEY RECOMMENDATIONS FOR PRACTICE
| Clinical recommendation | Evidence rating | References |
|---|---|---|
| Compared with standard infirmary mattresses, pressure-reducing devices subtract the incidence of pressure ulcers. | A | 10, 14 |
| At that place is no evidence to support the routine use of nutritional supplementation (vitamin C, zinc) and a high-protein nutrition to promote the healing of pressure ulcers. | C | xix |
| Heel ulcers with stable, dry out eschar exercise not need debridement if at that place is no edema, erythema, fluctuance, or drainage. | C | 8, sixteen |
| Ulcer wounds should not exist cleaned with skin cleansers or clarified agents (e.g., povidone-iodine [Betadine], hydrogen peroxide, acetic acid) because they destroy granulation tissue. | B | 8, 27, 28 |
Etiology
- Abstruse
- Etiology
- Prevention
- Assessment
- Nutritional Evaluation
- Management
- Complications
- References
Pressure ulcers are caused past unrelieved pressure, applied with corking force over a short menses (or with less strength over a longer period), that disrupts claret supply to the capillary network, impeding blood menses and depriving tissues of oxygen and nutrients. This external force per unit area must exist greater than arterial capillary force per unit area to lead to inflow impairment and resultant local ischemia and tissue damage. The about common sites for pressure ulcers are the sacrum, heels, ischial tuberosities, greater trochanters, and lateral malleoli.
Prevention
- Abstract
- Etiology
- Prevention
- Cess
- Nutritional Evaluation
- Management
- Complications
- References
RISK ASSESSMENT
Hazard assessment begins by identifying gamble factors and inspecting the skin. Risk factors for pressure ulcers are classified as intrinsic or extrinsic (Table one).4 Caregivers should be educated virtually take chances assessment and prevention and should inspect patients often to prevent pressure ulcers or identify them at early stages. Run a risk assessment scales may further heighten awareness, just have limited predictive ability and no proven effect on pressure ulcer prevention.5 The Braden Calibration ( Online Figure A) is the most normally used tool for predicting force per unit area ulcer risk6 (http://www.bradenscale.com/bradenscale.htm).
Table 1
Risk Factors for Pressure Ulcers
| Intrinsic | |
| Limited mobility | |
| Spinal string injury | |
| Cerebrovascular accident | |
| Progressive neurologic disorders (Parkinson illness, Alzheimer disease, multiple sclerosis) | |
| Hurting | |
| Fractures | |
| Postsurgical procedures | |
| Blackout or sedation | |
| Arthropathies | |
| Poor diet | |
| Anorexia | |
| Aridity | |
| Poor dentition | |
| Dietary restriction | |
| Weak sense of scent or taste | |
| Poverty or lack of admission to food | |
| Comorbidities | |
| Diabetes mellitus | |
| Depression or psychosis | |
| Vasculitis or other collagen vascular disorders | |
| Peripheral vascular disease | |
| Decreased hurting sensation | |
| Immunodeficiency or use of corticosteroid therapy | |
| Congestive middle failure | |
| Malignancies | |
| Finish-stage renal disease | |
| Chronic obstructive pulmonary disease | |
| Dementia | |
| Aging pare | |
| Loss of elasticity | |
| Decreased cutaneous blood flow | |
| Changes in dermal pH | |
| Flattening of rete ridges | |
| Loss of subcutaneous fat | |
| Decreased dermal-epidermal blood flow | |
| Extrinsic | |
| Pressure from any hard surface (e.g., bed, wheelchair, stretcher) | |
| Friction from patient's inability to motion well in bed | |
| Shear from involuntary muscle movements | |
| Moisture | |
| Bowel or float incontinence | |
| Excessive perspiration | |
| Wound drainage | |
INTERVENTIONS
Preventive measures should be used in at-risk patients. Pressure level reduction to preserve microcirculation is a mainstay of preventive therapy. In that location is no evidence to determine an optimal patient repositioning schedule, and schedules may need to be determined empirically.7 According to recommendations from the Agency for Health Intendance Policy and Enquiry, patients who are crippled should be repositioned every two hours.8 To minimize shear, the head of the bed should non exist elevated more than 30 degrees and should be maintained at the lowest degree of top needed to forbid other medical complications, such equally aspiration and worsening congestive heart failure symptoms.vii Some patients can reduce pressure past repositioning themselves using manual aids, such as a trapeze bar.
Pressure-reducing devices tin can reduce pressure or relieve pressure (i.e., lower tissue pressure to less than the capillary closing force per unit area of 32 mm Hg) and are classified as static (stationary) or dynamic.9 Static devices include foam, water, gel, and air mattresses or mattress overlays. Dynamic devices, such as alternating pressure devices and low–air-loss and air-fluidized surfaces, utilize a power source to redistribute localized pressure. Dynamic devices are mostly noisy and more than expensive than static devices. Pressure level-reducing surfaces lower ulcer incidence by 60 percent compared with standard hospital mattresses, although there is no clear deviation among pressure level-reducing devices.10,11 The benefit of dynamic versus static surfaces is unclear. Dynamic surfaces should be considered if a patient cannot reposition him- or herself independently or if the patient has a poorly healing ulcer.seven If in that location is less than i inch of material between the bed and pressure ulcer when feeling beneath the static surface, the device may not be effective and an alternative should be considered.7 Other pressure-reducing devices include chair cushions and pillows, foam wedges, and materials that are placed between the knees or used to relieve heel pressure. Ring cushions tin can cause pressure points and should not exist used.
Other preventive interventions include nutritional and pare care assessments. Although poor nutrition is associated with pressure ulcers, a causal relationship has not been established.12 1 large trial has shown that oral nutritional supplementation reduces risk, only several other trials have not.13 A Cochrane review concluded that there is insufficient bear witness on the relationship betwixt nutrition and force per unit area ulcer prevention.14 A more than contempo meta-analysis concluded that dietitian consultation and the use of skin moisturizers are reasonable preventive measures.xi However, the part of bactericidal and growth factor preparations is unclear. Continence care programs take non proved successful.fifteen Despite proper risk cess and preventive interventions, some force per unit area ulcers are unavoidable.
Assessment
- Abstruse
- Etiology
- Prevention
- Cess
- Nutritional Evaluation
- Management
- Complications
- References
Assessment of an established pressure ulcer involves a complete medical evaluation of the patient. A comprehensive history includes the onset and elapsing of ulcers, previous wound care, hazard factors, and a list of wellness issues and medications. Other factors such as psychological health, behavioral and cognitive status, social and fiscal resources, and access to caregivers are critical in the initial assessment and may influence handling plans. The presence of a pressure ulcer may indicate that the patient does not have access to adequate services or support. The patient may need more than intensive support services, or intendance-givers may demand more than grooming, respite, or assistance with lifting and turning the patient. Patients with communication or sensory disorders are particularly vulnerable to force per unit area ulcers because they may not experience discomfort or may express discomfort in singular means.
The physician should annotation the number, location, and size (length, width, and depth) of ulcers and assess for the presence of exudate, scent, sinus tracts, necrosis or eschar formation, tunneling, undermining, infection, healing (granulation and epithelialization), and wound margins. Most importantly, the physician should determine the phase of each ulcer (Figures 1 through 4).
Effigy i.
Phase I pressure ulcer. Intact skin with not-blanching redness.
Figure 2.
Stage II pressure level ulcer. Shallow, open up ulcer with blood-red-pink wound bed.
Effigy 3.
Phase III pressure level ulcer. Full-thickness tissue loss with visible subcutaneous fatty.
Figure four.
Stage 4 pressure ulcer. Full-thickness tissue loss with exposed muscle and os.
Table 2 presents the National Force per unit area Ulcer Advisory Panel'south staging system for pressure ulcers.16 In a person with dark skin pigmentation, a stage I ulcer may announced as a persistent red, blue, or majestic discoloration. The stage of an ulcer cannot be determined until enough slough or eschar is removed to expose the base of operations of the wound. Ulcers do not progress through stages in formation or healing. The Pressure Ulcer Calibration for Healing tool (Figure 5) can be used to monitor healing progress.17
Table ii
NPUAP Staging System for Pressure Ulcers
| Stage | Description |
|---|---|
| Suspected deep-tissue injury | Purple or maroon localized surface area of discolored, intact pare or claret-filled blister caused by harm to underlying soft tissue from force per unit area or shear; the discoloration may exist preceded past tissue that is painful, business firm, mushy, boggy, or warmer or libation compared with adjacent tissue |
| I | Intact skin with nonblanchable redness of a localized area, commonly over a bony prominence; night pigmented skin may not have visible blanching, and the afflicted area may differ from the surrounding area; the affected tissue may be painful, firm, soft, or warmer or libation compared with next tissue |
| II | Partial-thickness loss of dermis appearing as a shallow, open ulcer with a cherry-red-pink wound bed, without slough; may also appear every bit an intact or open/ruptured serum-filled blister; this stage should not be used to describe skin tears, tape burns, perineal dermatitis, macerations, or excoriations |
| III | Full-thickness tissue loss; subcutaneous fat may be visible, simply bone, tendon, or muscle is not exposed; slough may be present, but does non obscure the depth of tissue loss; may include undermining and tunneling* |
| 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 includes undermining and tunneling* |
| Unstageable | Full-thickness tissue loss with the base of the ulcer covered past slough (yellow, tan, gray, green, or brown) or eschar (tan, brownish, or black) in the wound bed |
Button Tool
Figure 5.
Force per unit area Ulcer Scale for Healing (Button) tool for monitoring the healing of force per unit area ulcers.
Adjusted with permission from Stotts NA, Rodeheaver G, Thomas DR, et al. An musical instrument to measure healing in pressure ulcers: development and validation of the Pressure Ulcer Scale for Healing (PUSH). J Gerontol A Biol Sci Med Sci. 2001;56(12):M795.
Nutritional Evaluation
- Abstract
- Etiology
- Prevention
- Assessment
- Nutritional Evaluation
- Direction
- Complications
- References
Despite the consensus that adequate diet is important in wound healing, documentation of its effect on ulcer healing is limited; recommendations are based on observational testify and expert opinion. Nutritional screening is function of the general evaluation of patients with pressure ulcers. Table 3 presents markers for identifying protein-calorie malnutrition.18 In patients who are malnourished, dietary consultation is recommended and a swallowing evaluation should be considered. Intervention should include encouraging adequate dietary intake using the patient's favorite foods, mealtime assistance, and snacks throughout the twenty-four hour period. High-calorie foods and supplements should exist used to prevent malnutrition. If oral dietary intake is inadequate or impractical, enteral or parenteral feeding should be considered, if compatible with the patient'due south wishes, to achieve positive nitrogen balance (approximately 30 to 35 calories per kg per day and 1.25 to 1.5 yard of protein per kg per 24-hour interval). Protein, vitamin C, and zinc supplements should exist considered if intake is insufficient and deficiency is present, although data supporting their effectiveness in accelerating healing have been inconsistent.nineteen
Table iii
Markers for Identifying Protein-Calorie Malnutrition in Patients with Pressure level Ulcers
| Unintentional weight loss of 5 percent or more in the previous 30 days or of 10 percent or more in the previous 180 days |
| Weight less than lxxx per centum of ideal |
| Serum albumin level less than 3.5 thousand per dL (35 g per L)* |
| Prealbumin level less than 15 mg per dL (150 mg per L)* |
| Transferrin level less than 200 mg per dL (2 one thousand per L) |
| Total lymphocyte count less than 1,500 per mm3 (1.50 × 10nine per L) |
Management
- Abstract
- Etiology
- Prevention
- Assessment
- Nutritional Evaluation
- Management
- Complications
- References
The management of pressure level ulcers is interdisciplinary, including primary care physicians, dermatologists, infectious affliction consultants, social workers, psychologists, dietitians, podiatrists, home and wound-care nurses, rehabilitation professionals, and surgeons. The basic components of pressure ulcer management are reducing or relieving pressure on the skin, debriding necrotic tissue, cleansing the wound, managing bacterial load and colonization, and selecting a wound dressing. Figure 6 is a brief overview of these key components.eighteen
Management of Pressure Ulcers
Figure half dozen.
Algorithm for the management of force per unit area ulcers.
Adapted with permission from Hess CT. Wound Care. 4th ed. Springhouse, Penn.: Springhouse; 2002:54–55.
The pressure-reducing devices used in preventive care also employ to handling. Static devices are useful in a patient who tin can modify positions independently. A depression–air-loss or air-fluidized bed may be necessary for patients with multiple large ulcers or a nonhealing ulcer, afterward flap surgeries, or when static devices are non effective. No one device is preferred.
Pain assessment should be completed, especially during repositioning, dressing changes, and debridement. Patients at the highest risk of pressure ulcers may not take total sensation or may require alternate pain assessment tools to aid in advice. The goal is to eliminate pain by covering the wound, adjusting pressure level-reducing surfaces, repositioning the patient, and providing topical or systemic analgesia. Small randomized controlled trials show that topical opioid (diamorphine gel; not bachelor in the United states of america) and nonopioid (lidocaine/prilocaine [EMLA]) preparations reduce pain during dressing changes and debridement.20,21
Necrotic tissue promotes bacterial growth and impairs wound healing, and information technology should exist debrided until eschar is removed and granulation tissue is present. Debridement, nevertheless, is not recommended for heel ulcers that have stable, dry eschar without edema, erythema, fluctuance, or drainage.8,sixteen Debridement methods include precipitous, mechanical, enzymatic, and autolytic. Abrupt debridement using a sterile scalpel or scissors may be performed at bedside, although more all-encompassing debridement should be performed in the operating room. Abrupt debridement is needed if infection occurs or to remove thick and all-encompassing eschar. Healing after sharp debridement requires adequate vascularization; thus, vascular cess for lower extremity ulcers is recommended.22 Anticoagulation is a relative contraindication for sharp debridement.
Mechanical debridement includes moisture-to-dry dressings, hydrotherapy, wound irrigation, and whirlpool bath debridement.23 Wet-to-dry dressings adhere to devitalized tissue, which is removed with dressing changes (dry dressings should not be moistened before removal). However, viable tissue may as well be removed and the procedure may be painful.24 Hydrotherapy via whirlpool bath debridement or irrigation may loosen debris. Enzymatic debridement is useful in the long-term care of patients who cannot tolerate sharp debridement; however, information technology takes longer to be effective and should not exist used when infection is nowadays.25,26
Wounds should exist apple-pie initially and with each dressing alter. Use of a 35-mL syringe and nineteen-gauge angiocatheter provides a degree of forcefulness that is effective yet rubber; use of normal saline is preferred. Wound cleansing with clarified agents (eastward.grand., povidone-iodine [Betadine], hydrogen peroxide, acetic acid) should be avoided because they destroy granulation tissue.27
Dressings that maintain a moist wound environment facilitate healing and tin can be used for autolytic debridement.28 Synthetic dressings (Table 4) reduce caregiver fourth dimension, cause less discomfort, and potentially provide more consequent moisture.xviii These dressings include transparent films, hydrogels, alginates, foams, and hydrocolloids. Transparent films effectively retain wet, and may be used alone for partial-thickness ulcers or combined with hydrogels or hydrocolloids for full-thickness wounds. Hydrogels tin can be used for deep wounds with light exudate. Alginates and foams are highly absorbent and are useful for wounds with moderate to heavy exudate. Hydrocolloids retain moisture and are useful for promoting autolytic debridement. Dressing choice is dictated by clinical judgment and wound characteristics; no moist dressing (including saline-moistened gauze) is superior.29 A wet-to-dry dressing should but be used for debridement and is not a substitute for a wound dressing. Because in that location are numerous dressing options, physicians should exist familiar with i or two products in each category or should obtain recommendations from a wound care consultant.
Table four
Overview of Different Dressings for Pressure Ulcers
| Dressing type | Description | Indication | Advantages | Disadvantages | Example (make names) |
|---|---|---|---|---|---|
| Transparent film | Agglutinative, semipermeable, polyurethane membrane that allows h2o to vaporize and cross the barrier | Management of phase I and 2 pressure ulcers with light or no exudates May be used with hydrogel or hydrocolloid dressings for total-thickness wounds | Retains moisture Impermeable to leaner and other contaminants Facilitates autolytic debridement Allows for wound observation Does not require secondary dressing (eastward.thousand., tape, wrap) | Not recommended for infected wounds or wounds with drainage Requires border of intact skin for adhesion May dislodge in high-friction areas Non recommended on fragile peel | Bioclusive, Carrafilm, Dermaview, Mefilm, Opsite, Polyskin, Suresite, 3M Tegaderm, Uniflex |
| Hydrogel | Water- or glycerin-based amorphous gels, impregnated gauze, or canvas dressings Amorphous and impregnated gauze fill the dead space tissue and can exist used for deep wounds | Direction of stages Two, 3, and IV ulcers; deep wounds; and wounds with necrosis or slough | Soothing, reduces hurting Rehydrates wound bed Facilitates autolytic debridement Fills expressionless tissue space Easy to apply and remove Can be used in infected wounds or to pack deep wounds | Not recommended for wounds with heavy exudate Dehydrates easily if non covered Difficult to secure (amorphous and impregnated gauze need secondary dressing) May cause maceration | Acryderm, Aquaflo, Aquagauze, Carradres, Carraguaze, Carrasmart, Carrasyn, Dermagauze, Dermasyn, Felxigel, SAF-Gel, Solosite, 3M Tegagel, Transigel |
| Alginate | Derived from brownish seaweed; composed of soft, nonwoven fibers shaped into ropes or pads | May be used as primary dressing for stages 3 and 4 ulcers, wounds with moderate to heavy exudate or tunneling, and infected or noninfected wounds | Absorbs up to xx times its weight Forms a gel within the wound Conforms to the shape of the wound Facilitates autolytic debridement Fills in dead tissue space Easy to employ and remove | Non recommended with light exudate or dry out scarring or for superficial wounds May dehydrate the wound bed Requires secondary dressing | Algicell, Algisite Yard, Carboflex, Carraginate, Dermaginate, Kalginate, Kaltostat, Melgisorb, Restore Calcicare, Sorbsan, 3M Tegagen |
| Foam | Provides a moist environment and thermal insulation; available as pads, sheets, and pillow dressings | May be used equally primary dressing (to provide absorption and Insulation) or as secondary dressing (for wounds with packing) for stages II to Iv ulcers with variable drainage | Nonadherent, although some have adherent borders Repels contaminants Easy to apply and remove Absorbs light to heavy exudate May exist used nether pinch Recommended for fragile skin | Non effective for wounds with dry eschar May require a secondary dressing | Allevyn, Biatain, Carrasmart, Curafoam, Dermalevin, Epigard, Hydrocell, Lyofoam, Mepilex, Optifoam, Polyderm, Polymem, SOF-foam, Tielle, Vigifoam |
| Hydrocolloid | Occlusive or semiocclusive dressings composed of materials such as gelatin and pectin; available in diverse forms (e.g., wafers, pastes, powders) | May be used as primary or secondary dressing for stages II to IV ulcers, wounds with slough and necrosis, or wounds with light to moderate exudates Some may be used for stage I ulcers | Impermeable to bacteria and other contaminants Facilitates autolytic debridement Self-adherent, molds well Allows observation, if transparent May be used nether compression products (compression stockings, wraps, Unna kick) May exist applied over alginate dressing to command drainage | Non recommended for wounds with heavy exudate, sinus tracts, or infection May roll at edges May injure frail skin upon removal Contraindicated for wounds with packing | Carrasmart, Combiderm, Comfeel, Dermafilm, Duoderm, Exuderm, Hyperion, MPM Excel, Nuderm, Primacol, RepliCare, Restore, Sorbex, 3M Tegaderm, Ultec |
| Moistened gauze | two × 2- or four × iv-inch square of gauze soaked in saline for packing | May exist used for stages III and Iv ulcers and for deep wounds, especially those with tunneling or undermining | Accessible | Must be remoistened oft Time-consuming to apply | Fluffed Kerlix, Patently Nugauze |
Urinary catheters or rectal tubes may be needed to forbid bacterial infection from feces or urine. Pressure ulcers are invariably colonized with bacteria; yet, wound cleansing and debridement minimize bacterial load. A trial of topical antibiotics, such equally silver sulfadiazine cream (Silvadene), should be used for up to 2 weeks for make clean ulcers that are not healing properly afterwards ii to four weeks of optimal wound care. Quantitative bacteria tissue cultures should exist performed for nonhealing ulcers after a trial of topical antibiotics or if at that place are signs of infection (e.m., increased drainage, olfactory property, surrounding erythema, hurting, warmth). A superficial swab specimen may be used; however, a needle aspiration or ulcer biopsy (preferred) is more than clinically significant.30 Systemic antibiotics are not recommended unless there is evidence of advancing cellulitis, osteomyelitis, and bacteremia.
Ulcers are difficult to resolve. Although more than 70 per centum of phase II ulcers heal after half dozen months of appropriate treatment, only fifty percent of stage Three ulcers and xxx pct of stage Iv ulcers heal within this period. Surgical consultation should exist obtained for patients with clean phase Three or IV ulcers that do not respond to optimal patient intendance or when quality of life would be improved with rapid wound closure. Surgical approaches include directly closure; peel grafts; and skin, musculocutaneous, and free flaps. Withal, randomized controlled trials of surgical repair are lacking and recurrence rates are loftier.
Growth factors (e.g., platelet-derived growth cistron becaplermin [Regranex])31,32 and vacuum-assisted closure for recalcitrant stage Iii and Iv ulcers are emerging direction options.33 The part of electromagnetic therapy,34 ultrasound,35 and hyperbaric oxygen therapy is unclear.36
Complications
- Abstract
- Etiology
- Prevention
- Assessment
- Nutritional Evaluation
- Direction
- Complications
- References
Although noninfectious complications of pressure ulcers occur, systemic infections are the virtually prevalent. Noninfectious complications include amyloidosis, heterotopic bone formation, perinealurethral fistula, pseudoaneurysm, Marjolin ulcer, and systemic complications of topical treatment. Infectious complications include bacteremia and sepsis, cellulitis, endocarditis, meningitis, osteomyelitis, septic arthritis, and sinus tracts or abscesses.8 Osteomyelitis has been reported in 17 to 32 percentage of infected ulcers and may pb to nonhealing ulcers with or without systemic manifestations.37 Plain radiographs and bone scans are often unreliable. Magnetic resonance imaging has a 98 percent sensitivity and 89 percent specificity for osteomyelitis in patients with pressure ulcers38; still, needle biopsy of the os (via orthopedic consultation) is recommended and can guide antibody therapy. Bacteremia may occur with or without osteomyelitis, causing unexplained fever, tachycardia, hypotension, or altered mental status.39 Overall bloodshed is high with both conditions,xl and empirical antibiotics pending civilisation results should cover methicillin-resistant Staphylococcus aureus, anaerobes, enterococci, and gram-negative organisms, such as Pseudomonas, Proteus, and Providencia species.41
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REFERENCES
testify all references
1. Whittington K, Patrick One thousand, Roberts JL. A national study of pressure level ulcer prevalence and incidence in acute care hospitals. J Wound Ostomy Continence Nurs. 2000;27(4):209–215. ...
two. Kaltenthaler E, Whitfield Medico, Walters SJ, Akehurst RL, Paisley S. U.k., USA and Canada: how exercise their pressure ulcer prevalence and incidence data compare? J Wound Intendance. 2001;10(i):530–535.
3. Coleman EA, Martau JM, Lin MK, Kramer AM. Pressure ulcer prevalence in long-term nursing domicile residents since the implementation of OBRA ′87. Double-decker Upkeep Reconciliation Act. J Am Geriatr Soc. 2002;50(4):728–732.
four. Garcia AD, Thomas DR. Cess and direction of chronic pressure ulcers in the elderly. Med Clin North Am. 2006;xc(5):925–944.
5. Schoonhoven L, Haalboom JR, Bousema MT, et al., for the prePURSE Report Group. Prospective cohort study of routine use of run a risk assessment scales for prediction of pressure level ulcers. BMJ. 2002;325(7368):797.
six. Pancorbo-Hidalgo PL, Garcia-Fernandez FP, Lopez-Medina IM, Alvarez-Nieto C. Take chances assessment scales for pressure level ulcer prevention: a systematic review. J Adv Nurs. 2006;54(ane):94–110.
seven. Whitney J, Phillips L, Aslam R, et al. Guidelines for the treatment of force per unit area ulcers. Wound Repair Regen. 2006;xiv(6):663–679.
8. Agency for Health Care Policy and Research. Treatment of pressure ulcers. Rockville, Dr..: U.S. Section of Wellness and Human being Services; 1994. AHCPR Publication No. 95-0652. http://world wide web.ncbi.nlm.nih.gov/books/bv.fcgi?rid=hstat2.chapter.5124. Accessed December 17, 2007.
9. Thomas DR. Prevention and treatment of pressure ulcers. J Am Med Dir Assoc. 2006;vii(1):46–59.
10. Cullum N, McInnes East, Bong-Syer SE, Legood R. Support surfaces for pressure ulcer prevention. Cochrane Database Syst Rev. 2004;(3):CD001735.
xi. Reddy M, Gill SS, Rochon PA. Preventing pressure level ulcers: a systematic review. JAMA. 2006;296(viii):974–984.
12. Thomas DR. Improving outcome of pressure level ulcers with nutritional interventions: a review of the prove. Diet. 2001;17(2):121–125.
13. Bourdel-Marchasson I, Barateau Thou, Rondeau V, et al. A multi-eye trial of the effects of oral nutritional supplementation in critically ill older inpatients. GAGE Group. Nutrition. 2000;16(1):1–5.
14. Langer 1000, Schloemer G, Knerr A, Kuss O, Behrens J. Nutritional interventions for preventing and treating pressure ulcers. Cochrane Database Syst Rev. 2003;(4):CD003216.
xv. Bates-Jensen BM, Alessi CA, Al-Samarrai NR, Schnelle JF. The furnishings of an exercise and incontinence intervention on pare wellness outcomes in nursing abode residents. J Am Geriatr Soc. 2003;51(iii):348–355.
xvi. National Pressure level Ulcer Advisory Console. Updated staging system. http://www.npuap.org/pr2.htm. Accessed December 17, 2007.
17. Stotts NA, Rodeheaver Chiliad, Thomas DR, et al. An instrument to measure out healing in pressure ulcers: evolution and validation of the Pressure Ulcer Scale for Healing (Push). J Gerontol A Biol Sci Med Sci. 2001;56(12):M795–M799.
18. Hess CT. Wound Intendance. fourth ed. Springhouse, Penn.: Springhouse; 2002.
19. Royal College of Nursing. The management of force per unit area ulcers in chief and secondary care. September 2005. http://www.prissy.org.uk/nicemedia/pdf/CG029fullguideline.pdf. Accessed December 17, 2007.
twenty. Flock P. Pilot study to determine the effectiveness of diamorphine gel to control force per unit area ulcer pain. J Pain Symptom Manage. 2003;25(vi):547–554.
21. Rosenthal D, Murphy F, Gottschalk R, Baxter M, Lycka B, Nevin Chiliad. Using a topical anaesthetic foam to reduce hurting during sharp debridement of chronic leg ulcers. J Wound Care. 2001;x(1):503–505.
22. Registered Nurses' Clan of Ontario. Cess and management of phase I to Iv pressure level ulcers. 2007. http://guidelines.gov/summary/summary.aspx?ss=15&doc_id=11013&nbr=5793. Accessed July 1, 2008.
23. Singhal A, Reis ED, Kerstein MD. Options for nonsurgical debridement of necrotic wounds. Adv Skin Wound Care. 2001;fourteen(2):96–100.
24. Ovington LG. Hanging moisture-to-dry dressings out to dry. Home Healthc Nurse. 2001;19(eight):477–483.
25. Püllen R, Popp R, Volkers P, Füsgen I. Prospective randomized double-blind study of the wound-debriding furnishings of collagenase and fibrinolysin/deoxyribonuclease in pressure ulcers. Historic period Ageing. 2002;31(2):126–130.
26. Bradley M, Cullum N, Nelson EA, Petticrew M, Sheldon T, Torgerson D. Systematic reviews of wound care management: (2). Dressings and topical agents used in the healing of chronic wounds. Health Technol Appraise. 1999;3(17 pt 2):1–35.
27. Rodeheaver GT. Pressure ulcer debridement and cleansing: a review of current literature. Ostomy Wound Manage. 1999;45(1A suppl):80S–85S.
28. Kerstein MD, Gemmen Due east, van Rijswijk L, et al. Cost and cost effectiveness of venous and pressure ulcer protocols of care. Dis Manage Health Outcomes. 2001;ix(xi):651–663.
29. Bouza C, Saz Z, Muñoz A, Amate JM. Efficacy of advanced dressings in the treatment of force per unit area ulcers: a systematic review. J Wound Care. 2005;fourteen(five):193–199.
xxx. Rudensky B, Lipschits Thousand, Isaacsohn Grand, Sonnenblick Thousand. Infected pressure level sores: comparison of methods for bacterial identification. S Med J. 1992;85(9):901–903.
31. Thomas DR. The promise of topical growth factors in healing pressure ulcers. Ann Intern Med. 2003;139(viii):694–695.
32. Robson MC, Phillips LG, Thomason A, Robson LE, Pierce GF. Platelet-derived growth factor BB for the treatment of chronic pressure level ulcers. Lancet. 1992;339(8784):23–25.
33. Argenta LC, Morykwas MJ. Vacuum-assisted closure: a new method for wound control and handling: clinical experience. Ann Plast Surg. 1997;38(vi):563–576.
34. Olyaee Manesh A, Flemming Yard, Cullum NA, Ravaghi H. Electromagnetic therapy for treating pressure ulcers. Cochrane Database Syst Rev. 2006;(2):CD002930.
35. Baba-Akbari Sari A, Flemming K, Cullum NA, Wollina U. Therapeutic ultrasound for pressure level ulcers. Cochrane Database Syst Rev. 2006;(3):CD001275.
36. Kranke P, Bennett M, Roeckl-Wiedmann I, Debus S. Hyperbaric oxygen therapy for chronic wounds. Cochrane Database Syst Rev. 2004;(2):CD004123.
37. Darouiche RO, Landon GC, Klima 1000, Musher DM, Markowski J. Osteomyelitis associated with pressure level sores. Curvation Intern Med. 1994;154(seven):753–758.
38. Huang AB, Schweitzer ME, Hume E, Batte WG. Osteomyelitis of the pelvis/hips in paralyzed patients: accuracy and clinical utility of MRI. J Comput Assist Tomogr. 1998;22(iii):437–443.
39. Bryan CS, Dew CE, Reynolds KL. Bacteremia associated with decubitus ulcers. Arch Intern Med. 1983;143(11):2093–2095.
40. Wall BM, Mangold T, Huch KM, Corbett C, Cooke CR. Bacteremia in the chronic spinal cord injury population: risk factors for mortality. J Spinal String Med. 2003;26(3):248–253.
41. Livesley NJ, Chow AW. Infected pressure ulcers in elderly individuals. Clin Infect Dis. 2002;35(xi):1390–1396.
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