REVIEW ARTICLE

Drugs Aging 2010; 27 (4): 311-325 1170-229X/10/0004-0311/$49.95/0

2010 Adis Data Information BV. All rights reserved.

Assessment and Management of Pressure Ulcers in the Elderly

Current Strategies
Efraim Jaul1,2
1 Skilled Geriatric Nursing Department, Herzog Hospital, Jerusalem, Israel 2 Hebrew University Hadassah Medical School, Jerusalem, Israel

Contents
Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1. Risk Factor Assessment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.1 Aging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.2 Co-Morbidities. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.3 Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.4 Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.5 Social, Family and Emotional Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2. Wound Assessment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.1 Site . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.2 Staging. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.3 Surface Appearance. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.4 Infection. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.5 Odour . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.6 Exudate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.7 Pain. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.8 Undermining . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.9 Surrounding Area . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3. Pathogenesis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.1 Extrinsic (External) Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.2 Intrinsic (Internal) Factors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4. Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.1 Stabilization and Cure of Reversible Medical Conditions and Treatment of Irreversible Conditions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.2 Preventing and Minimizing Complications of the Dysfunctional Status. . . . . . . . . . . . . . . . . . . . . . 4.3 Provision of Food and Fluids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4 Local Wound Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4.1 Debridement and Cleaning. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4.2 Dressings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4.3 Pressure Relief Devices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4.4 Local Agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4.5 Surgical Intervention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4.6 Complementary Treatments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.5 Family Support. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 312 313 313 314 314 315 316 316 316 317 317 317 317 317 317 317 318 318 318 318 319 319 319 320 321 321 321 322 322 322 322 322 323

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Abstract

Pressure ulcers (pressure sores) continue to be a common health problem, particularly among the physically limited or bedridden elderly. The problem exists within the entire health framework, including hospitals, clinics, longterm care facilities and private homes. For many elderly patients, pressure ulcers may become chronic for no apparent reason and remain so for prolonged periods, even for the remainder of the patients lifetime. A large number of grade 3 and 4 pressure ulcers become chronic wounds, and the afflicted patient may even die from an ulcer complication (sepsis or osteomyelitis). The presence of a pressure ulcer constitutes a geriatric syndrome consisting of multifactorial pathological conditions. The accumulated effects of impairment due to immobility, nutritional deficiency and chronic diseases involving multiple systems predispose the aging skin of the elderly person to increasing vulnerability. The assessment and management of a pressure ulcer requires a comprehensive and multidisciplinary approach in order to understand the patient with the ulcer. Factors to consider include the patients underlying pathologies (such as obstructive lung disease or peripheral vascular disease), severity of his or her primary illness (such as an infection or hip fracture), co-morbidities (such as dementia or diabetes mellitus), functional state (activities of daily living), nutritional status (swallowing difficulties), and degree of social and emotional support; focusing on just the wound itself is not enough. An understanding of the physiological and pathological processes of aging skin throws light on the aetiology and pathogenesis of the development of pressure ulcers in the elderly. Each health discipline (nursing staff, aides, physician, dietitian, occupational and physical therapists, and social worker) has its own role to play in the assessment and management of the patient with a pressure ulcer. The goals of treating a pressure ulcer include avoiding any preventable contributing circumstances, such as immobilization after a hip fracture or acute infection. Once a pressure ulcer has developed, however, the goal is to heal it by optimizing regional blood flow (by use of a stent or vascular bypass surgery), managing underlying illnesses (such as diabetes, hypothyroidism or congestive heart failure) and providing adequate caloric and protein intake (whether through use of dietary supplements by mouth or by use of tube feeding). If the ulcer has become chronic, the ultimate goal changes from healing the wound to controlling symptoms (such as foul odour, pain, discomfort and infection) and preventing complications, thereby contributing to the patients overall well-being; providing support for the patients family is also important. Recent advances in wound dressings allow for greater control of symptoms and prevention of complications, and have also enabled the affected patient to be integrated more readily into the family setting and in the community at large. Ethical and end-of-life issues must also be addressed soon after the wound has become chronic. This article discusses the pathogenesis of pressure ulcer development in the elderly in relation to concomitant diseases, risk factor assessment and the management of such ulcers.

Pressure ulcers (pressure sores, bedsores) are a common problem among the elderly in hospitals, long-term healthcare facilities and at home. They reduce quality of life and can even be life threatening.[1-3]
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There has been an increase in the prevalence of pressure ulcers in recent years.[4,5] Increased life expectancy in the overall population has resulted from solutions being found for many geriatric
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illnesses but has also exposed other dormant medical problems, especially in the old-old.[6] Advancing chronological age increases exposure to pathological factors that develop as a result of biological aging. Modern medicine has transformed many acute diseases to chronic conditions, allowing patients to live longer even when these chronic conditions are severe.[7] As a consequence, debilitated patients with severely limited daily functioning are living increasingly prolonged lives, sometimes by artificial means.[8] Early intervention is emphasized as a preventative procedure for bedsores. When elderly patients are confined to bed at the onset of an acute illness and shortly after hospital admission, pressure ulcers are prone to develop as a result of a lack of repositioning or failure to use pressurereducing devices.[9-11] In one study, 30% of elderly patients with hip fracture developed pressure ulcers shortly after hospital admission.[12] The natural course of a pressure ulcer in an elderly patient is difficult to predict. For no apparent reason, many patients become stuck with a pressure ulcer at a certain stage for prolonged periods and sometimes for the remainder of their lives. A large number of grade 3 and 4 pressure ulcers become chronic wounds.[13,14] An elderly patient may live for a long time with a bedsore, and may even die from a complication of the ulcer (sepsis or osteomyelitis).[15] Even in the best of circumstances, when the wound has been cured, it may recur if the underlying contributing risk factors, such as immobility, persist. Many factors act synergistically to cause pressure ulcers. The first potential risk factor is the process of aging of the patients skin.[16,17] The second risk factor is the pathology and structural impairment associated with a disease that is undermining the physiological infrastructure of the skin. The third contributing factor is malnutrition as part of a chronic disease that reduces muscle mass, thins the skin and reduces immunocompetence.[18] However, the most significant risk factor is the functional outcome of disease, including immobility, incontinence and impaired cognition. These functional impairments, particularly immobility, increase the vulnerability of the skin to extrinsic factors, such as pressure, shearing forces, friction and wetness, that
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reduce the integrity of the skin tissue and result in development of pressure ulcers.[19] Pressure ulcers reflect a geriatric syndrome in which multifactorial pathological conditions are present and the accumulated effects of impairment of multiple systems aggravate the vulnerability of the older person to development of these ulcers. Multiple aetiological factors interacting in pathogenetic pathways cause a single manifestation, e.g. a pressure ulcer.[20] Assessment and management of pressure ulcers require a comprehensive and multidisciplinary approach in order to understand the patient behind the ulcer. Such an assessment should take into account the patients underlying pathology and severity of primary illness, co-morbidities, functional state (activities of daily living), nutritional status, and social and emotional support, rather than focus on the wound alone. Each health discipline (nursing staff, aides, physician, dietitian, occupational and physical therapists, and social worker) has its own role to play in helping patients overcome pressure ulcers.[21] Therefore, the comprehensive geriatric approach focuses on symptom control, prevention of complications, emotional support, family involvement and the patients overall well-being, as well as on healing the ulcer. This review discusses the pathogenesis of pressure ulcer development in the elderly, the importance of considering concomitant diseases and other risk factors, and the management of pressure ulcers. Connecting the pressure ulcer to the person as a whole is emphasized throughout the review. 1. Risk Factor Assessment Assessment of pressure ulcers should comprise both a local evaluation of the wound and a systemic assessment of the patient. The status of a pressure ulcer reflects the patients overall physical and functional status; the appearance of pressure ulcers in a frail elderly person often indicates a poor prognosis.[22,23]
1.1 Aging

The potential risk of developing a pressure ulcer in the elderly population increases exponentially
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with age:[24] 70% of pressure ulcers occur in people aged >70 years.[25] The aging process and environmental factors damage the skin and increase the likelihood of developing pressure ulcers. Age-related skin changes are indicated by flattening of the dermo-epidermal junction and slow turnover of skin cells, loss of elasticity, thinning of subcutaneous layers, reduction of overall muscle mass (sarcopenia), and decreased intradermal vascular perfusion and oxygenation.[26,27] The physiological healing process of wounds consists of four dynamic, well defined, overlapping stages: haemostasis, inflammation, proliferation and remodelling.[28] In aging individuals, the healing process might be arrested at any of these stages, and particularly at the inflammatory or proliferative stage. The mediators of this arrest can include impairment of inflammatory cells, growth factors, proteases, cellular and/or extracellular elements.[29] A low level of activity of the inflammatory cells and growth factors, with resultant slowing of the migration of macrophages, may result in arrest at the inflammatory stage.[30] The levels of platelet-derived growth factor and transforming growth factor are also significantly reduced. Angiogenesis in the wound is significantly delayed and re-epithelialization is slower than in younger patients. On the other hand, the level of activity of the matrix metalloproteinases, which break down intercellular structural proteins, is greatly increased in the elderly and may result in arrest at the proliferative stage.[31]
1.2 Co-Morbidities

may not be sufficient awareness of the risks associated with temporary immobility, e.g. deconditioning of the muscle, which occurs commonly after falls, hip fracture, surgery and infection.[33] These conditions increase the likelihood of development of pressure ulcers as a result of patients not being able to reposition themselves.[34,35] The high prevalence of many systemic chronic illnesses or disease states in the elderly contributes to pressure ulcers.[35] Arterial insufficiency may cause ischaemia by arteriosclerosis, the watershed effect and vascular steal syndrome. Venous insufficiency and chronic lymphoedema impair fluid return from the lower limbs. Multiple sclerosis, diabetes mellitus and stroke can cause sensory deprivation. Congestive heart, liver or kidney failure may cause chronic oedema. Neurological disease of the CNS such as dementia or Alzheimers disease may cause agitation and friction. Cancer and other terminal conditions impair immunocompetence. Parkinsons disease, antipsychotic drugs and dementia increase the risk of spasticity. Dehydration can cause skin dryness; high temperature, fever and urinary incontinence cause skin wetness. Medications used to treat chronic diseases may have adverse effects such as bladder dysfunction, reduced blood pressure, rigidity, sedation, confusion, drowsiness and constipation. All of these systemic diseases or states make the skin more vulnerable to becoming ulcerated and, thereby, more prone to developing a pressure ulcer.[36]
1.3 Function

Physiological changes in older people lead to a decrease in bodily reserves, making the body vulnerable to disease. Superimposed on normal aging are pathological processes that impel the individual into acute illness, which in turn results in the collapse of diverse systems such as skin tissue. This collapse is similar to a domino effect, leading to the development of pressure ulcers and potentially to multisystem failure.[32] Acute disease often demands a period of bed rest that may well predispose to and increase the risk of developing pressure ulcers. However, there
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The outcomes of advancing disease may be severe disability, including immobility, incontinence and impaired cognition.[37] These disabilities contribute to the development and persistence of pressure ulcers, notably when combined with an underlying co-morbidity. Immobility is the most significant risk factor for the formation of pressure ulcers.[38] Other risk factors evaluated as part of the functional assessment of patients with pressure ulcers include extrinsic causes such as shearing and direct pressure forces and intrinsic factors resulting from co-morbid diseases.[39]
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Immobility in the elderly is the inability to change the position of the body, or part of it, without help. It may be caused by depression of the CNS, as in the case of the vegetative state, extensive stroke or end-stage dementia, and may be complicated by an accompanying sensory impairment. Mild stroke, advanced diabetes and spinal injury affecting part of the body, such as hand paralysis whereby the patient is unable to grasp the bed side-rails and turn him- or herself, may give rise to pressure ulcers because of a lack of movement. Physical or chemical restraints sometimes used in delirious elderly patients can cause motor or sensory impairment. Chemical restraints may lead to sensory deficiencies as a result of sedative and hypnotic medication use, resulting in sleepiness and loss of awareness. Physical restraints may lead to motor limitations, resulting in abrasions, injuries and breakdown of the skin. In addition, other functional impairments such as urinary or faecal incontinence or cognitive impairment disrupt the integrity of the skin by causing wetness and lack of awareness, respectively.[40] At the onset of an acute illness and at the time of admission to a hospital or other medical facility, every elderly patient requires risk assessment to identify the risk of pressure ulcers. The most widely used and recognized risk assessment scales are the Norton, Braden and Waterlow scales, all of which measure risk quantitatively.[41-43] The Norton scale score ranges from 5 to 20 points.[41] It assesses five risk-based items: physical condition, mental condition, activity, mobility and continence. A score of 14 is considered high risk. The Braden scale score ranges from 6 to 23 points and assesses risk according to six factors: sensory perception, skin moisture, activity levels, mobility, observed nutritional intake, and friction and shearing forces.[42] A score of 16 is considered high risk. The Waterlow scale assesses eight items: body build (weight and height), visual evaluation of the skin, sex and age, continence, mobility, appetite, medication and special risk.[43] The potential for risk occurs with a score between 10 and 14 points. Of these scales, the Braden scale was found to have the best sensitivity and specificity, i.e.
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57.1% and 67.5%, respectively, with a risk ratio of 4.08.[44] The Norton scale had 46.8% sensitivity and 61.8% specificity, with a risk ratio of 2.16. The Waterlow scale had 82.4% sensitivity and 27.4% specificity, with a risk ratio of 2.05. Nurses clinical judgment had 50.6% sensitivity and 60.1% specificity, with a risk ratio of 1.69. Although high in sensitivity and specificity, the scales taken together had a modest positive predictive value of 37%, but this was still greater than nurses clinical judgement.[44]
1.4 Nutrition

Pressure ulcers and impaired nutrition often co-exist in the frail elderly, whether hospitalized or living in a long-term care setting.[45] There is a strong correlation between poor nutritional status and the development of pressure ulcers.[46] The appearance of pressure ulcers reflects a catabolic state accompanied by protein consumption, resulting in muscle wasting and tissue destruction.[47] Every elderly patient should be regarded as at risk for malnutrition because of physical, social or mental conditions. Malnutrition often begins with protein energy malnutrition, a condition that is frequently seen in elderly persons in nursing home facilities and hospitals as well as at home.[48] Nutritional assessment involves taking a history from the patient or the family regarding food intake, particularly with regard to protein and total calorie consumption and weight loss. A history of digestive problems (e.g. nausea, constipation, diarrhoea and/or vomiting) should be noted. The state of dentition should be evaluated, including chewing and swallowing ability. Impaired functional ambulation and hand and finger skills should be identified. Other important contributing factors include social isolation, lack of nearby family accessibility and poverty.[49] Awareness on the part of the physician of all medications being taken, particularly those that can cause digestive problems, reduce appetite, cause constipation and bring about dryness of the mouth, is of primary importance.[50] Dietary restrictions on eggs and meats, which are good
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sources of protein, should be abandoned in these cases. Depression and dementia and other neurological disorders require mental and neurological examination. Bedside assessment of swallowing ability is an examination that is too often overlooked by the physician and nurse and its importance must be emphasized. A speech therapist can be valuable in recommending a given food texture or fluid density in situations where either eating or drinking ability is limited.[51] The Subjective Global Assessment (SGA) scale is an effective clinical nutrition assessment tool.[52] The SGA measures four items: the percentage of weight lost in the previous 6 months; gastrointestinal complaints; loss of subcutaneous fat; and reductions in muscle tissue. Another malnutrition risk assessment tool used for elderly patients is the Mini Nutritional Assessment (MNA) Short Form, which measures body mass index, involuntary loss of weight in the previous 3 months, acute disease in the previous 3 months, mobility, the presence of neuropsychological diseases and loss of appetite in the previous 3 months.[53] Anthropometric measurement as part of nutritional assessment focuses on the triceps skin fold, mid-arm circumference, atrophy of muscles and presence of oedema. Accompanying these assessments are measurements of laboratory markers (albumin, haemoglobin, cholesterol and total lymphocyte count) that reflect the existing nutritional status and often tend to highlight the acute physical state.[54]
1.5 Social, Family and Emotional Factors

comfort, diminution of quality life, cognitive impairment and reduced competence, that require periodic assessment. End-of-life issues may arise, such as the advisability of amputation or extensive surgical debridement, admission to a nursing home or the declaration of the patient as DNR (do not resuscitate). Thus, the family should be provided with realistic expectations about the situation. The familys wishes should be respected whenever possible, especially when the patient is no longer competent to make decisions on his or her own behalf.[56] 2. Wound Assessment Wound assessment comprises evaluation of a number of parameters: site, staging (depth), surface appearance (colour), infection, odour, exudate, pain, undermining (of the soft tissue) and the condition of the area surrounding the wound.[57,58]
2.1 Site

It is possible for a pressure ulcer to not heal and become chronic. This unanticipated clinical course of the ulcer leads to frustration for patients and their families, and increases emotional upset. Social workers need to assess the family support networks and community resources of the patient and family. The accompanying economic burden resulting from the pressure ulcers also has to be assessed.[55] The chronicity of a pressure ulcer results in symptoms and other sequelae, such as pain, dis 2010 Adis Data Information BV. All rights reserved.

The typical hot spots for pressure ulcers are where bony prominences underlie soft tissues. The majority of bedsores occur in the lower trunk, over the sacrum and coccyx (tailbone), ischium, gluteal muscles (buttocks) and greater trochanters (hips). The location of pressure ulcers may provide insight into their cause. For example, excessively prolonged sitting and lack of repositioning should be suspected if the wound is located overlying the ischial tuberosities. Heel ulcers occur in sedentary patients and indicate a possible component of arterial insufficiency. There are also atypical locations for pressure ulcers that may point to underlying bony malformations, such as winged scapula or kyphosis. Another unusual causative factor for pressure sores is insertion of tubes into the patient for therapeutic reasons. Indeed, pressure ulcers may be caused by tubes either at the point of insertion or anywhere along the course of the tube. A pressure ulcer in the nostril at the point of entry of a nasogastric tube is commonly seen. Another common example is an ulcer of the glans penis next to an indwelling urinary
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catheter, at the urethral opening. The tape that binds a tracheostomy tube to a patient also can cause a bedsore on the back of the neck. Wrinkles in bed sheets or clothing may also cause pressure ulcers.
2.2 Staging

2.4 Infection

There are four stages of bedsores:[59]  Stage I consists of intact skin with nonblanching erythema.  Stage II is marked by partial skin-thickness damage or loss, involving epidermis and/or dermis, including blisters and abrasions.  Stage III is described by a full-thickness skin loss with damage to subcutaneous tissue, but not deeper than the underlying fascia.  Stage IV includes extensive destruction of underlying tissue, including muscle and possibly bone and supporting structures. A recent official revision of the staging system by the National Pressure Ulcer Advisory Panel (NPUAP) added the categories of an unstageable state and deep tissue injury.[60] The unstageable category is identified as a surface covering of necrotic tissue, slough or eschar, with depth obscuration. Deep tissue injury is defined by injury to subcutaneous tissues under intact skin. It initially appears as a discolouration or bruising of the skin, later progressing to a deep pressure ulcer.
2.3 Surface Appearance

The classic manifestations of infection, such as redness (rubor), pain (dolor), heat (calor) and swelling (turgor), apply also to bedsores, as do foul odour, bleeding and purulent exudates. Any or all of these features may be found, particularly in a non-healing pressure ulcer. Every bedsore is colonized by bacteria and, therefore, needs routine cleaning. However, there is no justification for bacterial culture of the surface except when the bedsore involves bone, has formed an abscess or is a non-healing wound. Systemic administration of antibacterials, selected on the basis of antibacterial susceptibility, is then warranted.
2.5 Odour

The presence of necrotic tissue or a severe infection is often accompanied by a foul odour, particularly in the presence of anaerobic bacteria. These foul odours may disturb the patient and those in the immediate vicinity. The proper treatment includes surgical (sharp) debridement, thorough cleaning and appropriate application of dressings containing absorbent and charcoal ingredients.
2.6 Exudate

The surface of a pressure ulcer may be described as viable, with a bright red colour; this reflects granulation and proliferation of new vessels (neovascularization), leading to healing. A dark red colour may be indicative of local infection or bleeding. Pieces of bone may be extractable from deeper bedsores. Over-granulation may be due to infection and non-healing. Necrotic tissue is a non-viable tissue; slough is dead tissue, usually cream-coloured or yellow; and eschar is a black, hard crust overlying the wound. It is difficult to determine the stage (depth) of a wound with overlying eschar, slough and necrotic tissue, and this presentation is therefore termed unstageable (see section 2.2).
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Pressure ulcers often exude (secrete) serous, bloody or purulent liquid in varying amounts. In the case of excessive secretion, an active infection should be suspected. These exudates, particularly if serous, may accompany the oedema surrounding a bedsore and predispose to superimposed infections.
2.7 Pain

A pressure ulcer may cause pain continuously or intermittently. Intermittent pain may occur during local treatment and dressing changes. Continuous pain is characteristic of neuropathy, ischaemia, oedema and/or infection.
2.8 Undermining

Undermining of the soft tissue underlying a pressure ulcer is often manifested by pockets of
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pus (abscesses). These pockets must be opened and drained in order to facilitate healing. There is no justification for administering systemic antibacterials without first properly draining these abscesses. The importance of bluntly probing an abscess, whether with a (gloved) finger or mechanical probe, cannot be overemphasized.
2.9 Surrounding Area

The skin area surrounding a pressure ulcer may be either macerated or infected. It may be macerated because of excessive wound exudates and the relative inability of the dressing to absorb the secretion. In addition, cellulitis and eczematous or callosities should be identified and treated. 3. Pathogenesis The pathogenesis of pressure ulcers is traditionally divided into local and systemic factors. Geriatricians view these risk factors in terms of intrinsic (internal) and extrinsic (external) factors. Local factors relating to the wound, such as hypoxia, inadequate vascular supply and infection, reflect systemic, intrinsic processes that affect pressure ulcers.[61]
3.1 Extrinsic (External) Factors

The four most common extrinsic (external) physical forces that cause pressure ulcers are interface (axial) pressure, shearing (tangential) pressure, friction and excessive moisture.[62,63] Interface (axial) pressure causes a decrease in capillary blood flow and occlusion of blood perfusion to the local territory, which is followed by tissue ischaemia. The average intravascular capillary pressure is 32 mmHg; sitting on a hard surface results in a local pressure of 300500 mmHg (dependent on weight and surface area). Lying in bed causes a local pressure of 5094 mmHg on the heels, sacrum and scapula. A pressure ulcer is a product of both the intensity and duration of such pressure. There is an inverse correlation between the duration of sitting and the intensity of pressure, that is, a pressure ulcer may develop in less sitting time with strong intensity or in response to a longer duration of sit 2010 Adis Data Information BV. All rights reserved.

ting with low intensity.[64] Therefore, reducing the intensity of the pressure through use of a pressure-relieving surface is as important as frequently repositioning the patient in order to reduce the duration of pressure on any particular area of the skin. Physiological changes in the aging skin include progressive atrophy of the vasculature and deterioration of the supporting dermis, such that collagen and elastin become sparse; all of these changes increase the susceptibility to pressure-induced damage.[16] Shearing (tangential) pressure occurs when bone and the subcutaneous layer move against the skin block in opposite directions to each other. The capacity to maintain a stable position while sitting or lying is impaired with age. Elderly persons tend to slide down while sitting on a chair or even from a lying position when the head of the bed is raised more than 30. As a result, the dermal vessels become twisted, impairing blood perfusion and favouring the development of ischaemia. Aging skin is affected by shearing forces because of a reduction in elasticity which increases local torsion.[65] Friction is caused by two forces moving in opposite directions, in this case the surface of an external object against the skin. Frequently, agitated elderly persons rub their heels or elbows and cause the formation of intra-epidermal blisters, thereby damaging the skin and accelerating the formation of pressure ulcers. This effect of friction on developing pressure ulcers is increased 5-fold with accompanying moisture excess. Moisture causes maceration of the skin, which facilitates injury to the skin even with light pressure. Moisture may be due not only to urinary or faecal secretions but also to any other body fluids, such as perspiration caused by fever or a hot environment, drainage of a fistula or excessive secretion from a wound, or wetness after bathing.[66] There is a synergetic interaction between moisture and axial pressure.
3.2 Intrinsic (Internal) Factors

The intrinsic (internal) factors focus on the patients pathology, including the various facets of multiple diseases that contribute to the development
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of pressure ulcers. The mechanism through which these intrinsic factors work can be explained on the basis of vascular, degenerative, inflammatory or metabolic changes. Some of the principal factors promoting pressure ulcers include impairment of the level of consciousness, limitation of mobility, diminution of the sensory system, occlusion of the arterial vessels and blockage of the venous/lymphatic vessels. Other factors are incontinence and wetness formation, agitation and involuntary movement, and increased spasticity. Oedema formation, maceration of the skin, dehydration, immunosuppression, reduced oxygenation and lack of adequate red and white blood cell components are also factors. Medications for other diseases may produce adverse effects on the skin, including lowered perfusion due to antihypertensive drugs, a cholinergic effect and increased spasticity. Finally, other pathological conditions of the skin that predispose to bedsores, such as dry skin (xerosis) and skin trauma, should also be noted.[37,67] 4. Management Management of pressure ulcers in the elderly is not limited to local wound treatment alone; rather, the full pathology of the patient should be taken into account. The responsibility for treating pressure ulcers should be shared by a multidisciplinary team. The focus of treatment is prevention and remedial actions. Medical management includes stabilizing and curing all reversible medical conditions, treating all irreversible conditions, and preventing and minimizing complications of the patients dysfunctional status. Other facets of treatment involve the provision of food and fluids, local wound treatment and family support.
4.1 Stabilization and Cure of Reversible Medical Conditions and Treatment of Irreversible Conditions

lizing medical effects that are damaging to the skin. For instance, congestive heart failure with associated leg oedema may be reversed by giving intensive diuretic treatment. Hypothyroidism with associated oedema may be corrected with Lthyroxine (levothyroxine sodium). Occlusion of blood vessels is treated by angioplasty and insertion of a stent or by performing a bypass grafting procedure. If these procedures cannot be implemented, anticoagulation may be achieved with warfarin, aspirin (acetylsalicylic acid) or clopidrogel. Antibacterial drugs are the preferred treatment for systemic infections. Treatment for contracture and spasticity in multiple sclerosis, Alzheimers disease and other degenerative diseases involves the use of antispastic medications such as baclofen, botulinum toxin or physiotherapy. Levodopa/carbidopa is given to release rigidity in Parkinsons disease. Parkinsonism caused by anticholinergic adverse effects of antipsychotic drugs should be stopped by withdrawal of these drugs. Severe and painful arthritis causing immobility should be treated by antiinflammatory or analgesic drugs. It is important to review the patients entire medication list, particularly noting medications with adverse effects such as dryness of the skin, swallowing difficulties, sleepiness, lowered blood pressure, bladder dysfunction or constipation.
4.2 Preventing and Minimizing Complications of the Dysfunctional Status

Where possible, the physician should stabilize or cure all reversible medical conditions. Treatment of irreversible conditions focuses on stabi 2010 Adis Data Information BV. All rights reserved.

Immobility is a major risk factor associated with pressure ulcers and is the focus of preventative and remedial treatment. The inability to change position without help creates a wide range of complications such as deep venous thrombosis, pulmonary embolism, osteoporosis, muscular atrophy, constipation, faecal impaction and pressure ulcers. All of these phenomena should be prevented. If the cause of the immobility is reversible or temporary, it is imperative to start and develop treatment rapidly. For instance, an elderly person affected by pneumonia should not rest in bed, but be encouraged to sit or even walk. Elderly patients recovering from surgery for hip fracture can be
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rapidly mobilized. It is important to remember that a pressure ulcer may appear within hours but take years to heal. In the initial stages of immobility, use of pressure relief devices such as mattresses and overlays, cushions, and ankle or heel protectors should be encouraged. Usage can be dynamic or static, depending on the potential for developing pressure ulcers or on the current stage of the ulcers. Repositioning is a key factor in the prevention and treatment of pressure ulcers. It is recommended that recumbent patients should be repositioned every 2 hours and seated patients every 1530 minutes. A stable sitting position should be maintained and slipping prevented by elevating the posterior seat wedge. For recumbent patients, the head of the bed should be kept at less than 30. Appropriate lifting devices should be used rather than manual transfer. Ulcers caused by spasticity can be prevented by putting a cushion between direct contact points of bony prominences such as knees and ankles. The rehabilitation team (occupational and physical therapists) should exercise the patients joints through a range of passive motions, thus preventing the formation of contractures. They should also instruct orderlies and caregivers on how to position the patient in bed or in a wheelchair through the proper use of pillows and cushions. Orderlies are often the first members of the clinical staff to discover a new wound because they bathe, dress and reposition patients frequently during each shift. The moisture from urinary incontinence can be reduced by regularly taking the patient to the bathroom, changing diapers frequently and applying cream to the skin. Inserting an external urinary catheter for the night and changing the administration time for diuretic medication for congestive heart failure from day to night is helpful for the patient and often allows for a restful sleep. Administering a-adrenoceptor antagonist drugs to ease hypertrophy of the prostate and utilizing anticholinergic drugs to prevent bladder contraction helps prevent urinary incontinence. In other cases of urinary retention, inserting an indwelling urine catheter is indicated, but this strategy is debatable as a method for redu 2010 Adis Data Information BV. All rights reserved.

cing wetness as a part of the treatment of pressure ulcers because of high associated infection rates.
4.3 Provision of Food and Fluids

Despite a strong association between poor nutritional status and development of pressure ulcers, a causal relationship has not been established.[18] Several studies[38,68-70] have indicated that impairment of nutritional intake, diminution in dietary protein intake, reduction in the ability to feed oneself and recent weight loss are risk factors for development of pressure ulcers. Early detection of these nutritional and dietary factors by the treating physician may prevent dehydration and malnutrition. Early nutritional supplementation with additional calories and protein, either orally or through use of tube (enteral) feeding (via a nasogastric tube or a percutaneous endoscopic gastrostomy), may reduce the risk of developing pressure ulcers.[71,72] With the use of a feeding gastrostomy it is possible to feed patients orally with food of adequate texture to preserve their sense of taste, thereby providing a source of pleasure while relieving the burden on the part of the family to feed the patient orally. However, it is generally agreed that it is not possible to draw any firm conclusions regarding the effect of enteral nutrition on the prevention and treatment of pressure ulcers.[73] Many elderly patients with pressure ulcers also suffer from severe dementia and the subject of tube feeding in this context is a topic of ongoing clinical and ethical debate.[74] There are those who maintain that nutritional support via tube feeding fails to improve patients nutritional status or even alleviate pressure ulcers.[75] It must also be taken into account that tube feeding carries the risk of early and late complications such as aspiration pneumonia and self-extubation.[76] In this authors experience, tube feeding extends patient median survival time significantly,[77,78] although there was no support for this view in a systematic review.[79] Families should be encouraged to discuss the advantages of tube feeding with the multidisciplinary team and agreement to use a gastrostomy should be based on informed consent. Inserting a
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gastrostomy implies a prior assessment of the patients competence to give consent or alternatively requires the appointment of a proxy or guardian to give assent. After inserting a gastrostomy tube, the dietitian should be consulted regarding the energy and protein intake required in relation to the severity of pressure ulcers. Caution is advised in order to prevent the refeeding syndrome in cases where the patient has not eaten for a few days. Therefore, moderation should be exercized with respect to the initial feeding rate and intake should be increased gradually.[80] The recommendations for required feeding set out by the European Pressure Ulcers Advisory Panel (EPUAP 2003) are for an energy intake of 3035 calories/kg of bodyweight/day, 11.5 g of protein/kg of bodyweight/day and 30 mL of liquids/kg of bodyweight/day.[81]
4.4 Local Wound Treatment

Local wound treatment has advanced rapidly in recent years. In particular, significant advances have been made in wound dressing. The traditional passive dressings designed to protect the wound are being replaced by dressings that can absorb secretions, maintain moisture and encourage granulation and re-epithelialization. Some modern dressings utilize silver ions for antibacterial action, while others contain analgesics or activated charcoal for its odour-neutralizing properties. Such dressings simplify the local treatment of wounds while maintaining a reasonable quality of life for the patient. Certain dressings may be left in place for a number of days (as long as there is neither excessive secretion nor local discomfort), thus obviating the need for frequent visits to the nurse or doctors office. Thus, the patient enjoys the relative freedom to maintain a regular lifestyle.[82] Strategies for local wound treatment in the elderly are discussed in the following sections.
4.4.1 Debridement and Cleaning

formed to remove necrotic tissue, slough and other nonviable components of the ulcer, to promote healing[62] and to facilitate staging. There are several methods of debridement: surgical (sharp), enzymatic, chemical, autolytic (permitting the body to perform self-debridement beneath an occlusive dressing), biological (maggot) and mechanical (dry on wet, drip or friction). These methods may be used in combinations or sequentially. A common practice for extensive grade 3 and 4 pressure ulcers is to use an initial sharp debridement in combination with a mechanical procedure, followed by autolytic methods.[83] There is little trial evidence and no firm recommendations to support the use of any particular wound cleansing solution or technique for pressure ulcers in clinical practice.[84] Furthermore, some controversial preparations are still in use for local treatment of pressure ulcers, including antiseptic preparations such as povidone-iodine, sodium hypochlorite and hydrogen peroxide solutions. Some of these antiseptic preparations damage healing tissue (granulation) and poison fibroblasts. No improvement in healing has been found with the use of topical antibacterial creams over placebo.[85]
4.4.2 Dressings

Debridement is the cornerstone for treating contaminated pressure ulcers (and every ulcer starts out as contaminated). Debridement is per 2010 Adis Data Information BV. All rights reserved.

Once a wound is clean, it is essential to preserve local humidity in order to prevent dressinginduced desiccation. A variety of dressings is available: low-adherent dressings, transparent (film) dressings, hydrocolloid dressings, hydrogel dressings, foam, alginate and antimicrobial dressings.[86] The choice of optimal dressing depends on the state of the wound, i.e. its stage, the amount of secretion, its odour and its site. For example, a stage 3 or 4 ulcer with a large volume of secretion requires a primary absorbent dressing, such as alginate, and a secondary dressing, such as hydrocolloid or foam. A dry wound may require a primary moisture-preserving primary dressing such as hydrogel, and a secondary dressing such as film for stage 2 ulcers and hydrocolloid or foam for stage 3 or 4 ulcers. A malodorous wound requires application of activated charcoal
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for its odour-neutralizing properties.[87] Nurses serve as the first line in detecting changes in the patients wound status, and the nurses who carry out the local treatment of the wounds often determine which type of dressing should be applied. In the treatment of chronic pressure ulcers, alternative procedures include the use of a local agent (see section 4.4.4), surgical intervention and/or complementary treatment (see section 4.4.6). These methods are rarely used in the elderly because intrinsic (see section 3.2) and extrinsic factors (see section 3.1) have not been resolved.
4.4.3 Pressure Relief Devices

advantages when used to treat pressure ulcers but their usage may provide benefit to some individuals. Systematic reviews of these treatment choices have rarely been performed and usage is left to the choice of the practitioner.
4.4.5 Surgical Intervention

Surgery for pressure ulcers is rarely required in the elderly. Extensive debridement or excision of a bony prominence is rare and not advisable for patients in a poor medical condition. Closure of a clean wound with a fasciocutaneous or myocutaneous flap is rarely performed as the principal factor causing the pressure sore, i.e. immobility, is still present.
4.4.6 Complementary Treatments

Pressure relief devices may be either static or dynamic. Static support surfaces such as mattresses or overlays are filled with air, water, gel or foam, or various combinations of these. Dynamic support surfaces include alternating-pressure mattresses, low-air-loss beds and air-fluidized mattresses. When a specialized foam overlay was compared with a standard operating table mattress, the former was found to significantly decrease the incidence of postoperative pressure ulcers.[88] Specialized foam and sheepskin overlays were also consistently superior to standard hospital mattresses in reducing the incidence of pressure ulcers.[89,90] When the difference in pressure ulcer incidence between dynamic and static support surfaces was evaluated, no clear differences were seen[91] but both were superior to the standard surface.[92] No difference was found in the incidence of pressure ulcers when dynamic surface overlays were used compared with dynamic surface mattresses.[67]
4.4.4 Local Agents

Complementary treatments comprise a group of interventions, both mechanical and physical, such as gas (hyperbaric oxygen or ozone), light, sound and electrical stimulation, magnetic fields, water immersion and negative pressure wound therapy procedures. All of these modalities have undergone systematic review and none has been shown to be of benefit in the treatment of pressure ulcers.[95-100]
4.5 Family Support

Local agents include an extensive spectrum of dissimilar products such as solutions, creams, blood products and skin substitutes. Choices of treatment are broad, diverse, and usually depend on practice, personal preference and local medical customs. The options vary from traditional ointments, such as sugar, urea and balsam of Peru, to treatments developed in recent years, such as genetic engineering and advanced biotechnology.[93,94] These agents may have minimal
2010 Adis Data Information BV. All rights reserved.

The social worker and the doctor should work together to help patients and their families make informed decisions based on realistic expectations. The social worker can assist in obtaining medical devices and also in identifying and using community resources. Problems associated with amputation, insertion of a gastrostomy and placing the patient in an institution require healthcare professional support as well as an awareness of cultural beliefs and preferences. The major decisions should ultimately be made by the patient and his or her family. It is important to avoid threatening that the patient will die if these procedures are not carried out. Palliative treatment, such as symptom control in relation to pain, constipation, secretions, odour and infection of the wound, should be provided in terminal cases. The primary aim underlying patient and family support is to optimize the patients quality of life.
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5. Conclusions The primary principle underlying management of pressure ulcers is to prevent their occurrence taking into consideration the physical and pathological condition of the patient. The multidisciplinary management team must take a broad approach, not only with respect to the wounds, but also to the needs of the patient and family. In some temporary circumstances, such as postoperatively or after an acute illness, it will be possible to mobilize the patient rapidly and initiate use of early pressure-relieving devices and frequent repositioning strategies. Nevertheless, should a pressure ulcer develop, the goal of the treating physician should be to heal the ulcer by addressing and stabilizing underlying illnesses, augmenting caloric and protein intake, and instituting strategies for pressure relief and frequent repositioning. In cases where the pressure ulcer becomes chronic, the physicians goal changes from that of healing to one of optimizing the patients quality of life, controlling the symptoms (pain, discomfort, foul odour, infection), supporting the family, and dealing with ethical and end-of-life issues. Acknowledgements
No sources of funding were used to assist in the preparation of this review. The author has no conflicts of interest that are directly relevant to the content of this review. The author would like to thank Dr Sheva Mann, Professor Arnold Rosin and Iris Arad for their help in editing the article.
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Correspondence: Efraim Jaul, Director, Skilled Geriatric Nursing Department, Herzog Hospital, PO Box 3900, Jerusalem 91035, Israel. E-mail: jaul@zahav.net.il

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Drugs Aging 2010; 27 (4)

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