Chronic Wounds: Palliative Management for the Frail Population—PART II

Oscar M. Alvarez, PhD;1 Marge Meehan, RN, MIM;2 William Ennis, DO;3 David R. Thomas, MD, FACP;4 Frank D. Ferris, MD;5 Karen Lou Kennedy, RN, CS, FNP;6 Roisin Rogers, RN, MSN, CWCN;7 Marianne Bradley, RN, MS, CWOCN;8 Judith J. Baker, PhD;9 Adolfo Fernandez-Obregon, MD;10 George Rodeheaver, PhD;11

Chronic Wounds in the Frail Population

This section will review specific wounds most often seen among frail elderly that may have gradually become recalcitrant and nonresponsive to treatment regimes.

Pressure ulcers. Definition. Of all the chronic wound categories included in this document, pressure ulcers have the least satisfactory definition, which may account for the broad application of this term to ulcers having different etiologic factors. The definition of a pressure ulcer, according to the Pressure Ulcers in Adults: Prediction and Prevention is “…any lesion caused by unrelieved pressure resulting in damage of underlying tissue.”21 These ulcers usually occur over bony prominences and are classified based on depth of penetration through soft tissue layers to bone. Pressure ulcers are virtually the only type of wound that are solely attributed to external forces: pressure, shear, friction, and maceration.

Assessment. The presence of a pressure ulcer on a frail elderly person demands a comprehensive assessment of the entire patient to determine what factors and underlying diseases may have contributed to that ulcer’s occurrence. Pressure ulcers, theoretically, should always be considered healable, since external forces can generally be controlled. However, pressure ulcers among the frail population present some unique challenges.

The relationship between frailty and pressure ulcers is linked by significant commonalities in the core definition of frailty and key etiologic influences for pressure ulcers. Impaired mobility and abnormal nutrition form the cornerstone that defines frailty. Not surprisingly, these same factors are associated with the development of pressure ulcers.

Physical appearance. Pressure ulcers have a wide range of shapes and depth but can generally be confined to breakdown observed over bony prominences that have been exposed to some degree of pressure and probably other physical forces. The wound’s edges and its shape provide clues as to the influencing factors that initiated the skin breakdown. An oblong wound with a pocket of undermined tissue is most likely caused by a combination of pressure and shearing forces. This type of pressure ulcer is found most commonly over the sacral and ischial prominences. Wounds that form from blisters, with immune system or chemical irritant etiologies ruled out, are most likely caused by pressure and friction forces. Pressure ulcers that present with only a small opening to the skin and may drain foul smelling exudates are referred to as closed ulcers. These ulcers are formed through exposure to excessive pressure that has damaged the deep soft tissue before the epidermal layer. Another common pressure ulcer is one that is completely covered with eschar, often found on the heel. It is important to rule out other etiologic influences, such as peripheral vascular disease, before making the determination a wound is solely caused by pressure.

The wound bed of a pressure ulcer is also subject to a wide range of appearances. Exposure to excessive amounts of moisture and chemical irritation, such urine and/or fecal matter, will cause a pressure ulcer’s wound bed to become heavily contaminated while also weakening the surrounding intact skin.

Comorbidities. The occurrence of pressure ulcers is often accompanied by underlying medical conditions that predispose a patient to this type of ulcer. Clinical conditions that are the primary risk factors for developing pressure ulcers include continuous urinary incontinence or chronic voiding dysfunction, chronic bowel incontinence, paraplegia, quadriplegia, sepsis, and the illnesses and conditions listed above under Nonhealing Chronic Wounds.

Disease management treatments that contribute to pressure ulcer risk include steroid therapy, radiation therapy, chemotherapy, renal dialysis, and head elevation the majority of the day.

Venous ulcers. Definition. The venous system returns blood to the cardiopulmonary system. Injury as well as disease can prevent veins from effectively performing this job. There are four major disruptive mechanisms that prevent the vascular system from performing optimally: thrombus, embolism, dilation or varicosity, and hemorrhage.

Microcirculatory changes associated with chronic ulcers, diabetes, and repeated bouts of previous vessel damage lead to fibrin cuffs, causing a stained ring around the gator or ankle region of the lower extremity. The fibrin cuff is seen histologically around dermal vessels, which result in impaired cutaneous nutrition and, ultimately, ulceration.22 The action of neutrophils adhering to tissue damaged by ambulatory venous hypertension releases highly reactive substances generating free radicals and subsequent tissue injury.23

The degree to which any of these mechanisms lead to significant dysfunction or resultant ulceration depends mostly on the location of the involved vein. Obstruction of superficial veins rarely cause serious problems. However, if deep veins become occluded or obstructed, major peripheral problems can result.24

Once the venous system is impaired in its ability to return blood to the cardiopulmonary system, skin and subcutaneous tissues near the involved vein(s) are no longer receiving adequate oxygenation and nutrition. While it is widely accepted that venous insufficiency ulcers can result, the exact mechanism by which oxygenation and nutrition becomes compromised remains a constant debate.

Venous ulcers account for 90 percent of all chronic wounds found on the lower leg.25 The exact incidence among immobile patients, the population that is most likely to be frail, is unknown. Epidemiological studies from Western Australia suggest a prevalence of 0.62 per 1000 individuals with 90 percent of patients being 60 years or older. This group comprises 16.7 percent of the population with a relative prevalence of 3.3 per 1000 persons.26

Immobile patients offer a therapeutic challenge most notably because of their debilitated states and predictable recurrences of their ulcers. Although the pathophysiology of venous ulcers has been widely studied, the exact mechanisms that cause venous ulceration is the subject of widespread speculation. Gay27 and Homans28 made a connection between deep vein damage and ulceration. Under normal ambulatory conditions, the calf muscles serve to pump the blood back up to the heart. Without adequate use of calf muscles, blood that collects in the saphenous venous system and its tributaries cannot make its way swiftly to the deep veins to be compressed by the action of musculofascial compartment to make its way back up to the heart. The absence of competent one-way valves shifts the high venous pressure generated from the calf muscle contraction to the cutaneous vasculature. This all leads to chronic venous hypertension.29–31

Assessment. Physical evaluation of a patient with a chronic lower-extremity ulcer in which a vascular etiology is suspected begins with the same documentation of a comprehensive clinical history as is done to work up any chronic wound. For the frail patient, who probably has some degree of significant activity limitation, the examination becomes somewhat more complex. The frail patient requires a complete evaluation of clinical history, which must sometimes be obtained from family members, past physicians, and nursing staff responsible for the care of the patient. Aside from inquiring about possible causal trauma, which is not always readily recalled, many other areas deserve investigation.

It is also important to note the use of medications that may impair wound healing. Sensitizers like ethylene diamine, neomycin, and lanolin, among others, can produce a contact dermatitis. Systemic corticosteroids have direct impact by impairing the physiologic process of wound healing. Nicotine and alcohol use can have profound impacts on wound healing. Many of these patients have lived alone for prolonged periods prior to being placed in a nursing facility. These periods have often been times where medical problems have not been properly addressed, allowing for progressive deterioration of their health, which leads to chronic institutional care.32,33

The first element of a clinical examination is the determination of the history of immobility leading to the inactivity of the calf-muscle pump. This is usually the trigger event that culminates in venous ulceration. A medical history of associated disorders, such as deep vein thrombosis and arterial disease, is important. Previous history of nutritional deficiencies, metabolic disorders, diabetes, collagen vascular disease, antiphospholipid syndrome, periarteritis nodosa, pyoderma gangrenosum, family history of sickle cell disease, thalassemia, hereditary spherocytosis, or any autoimmune disorder should be determined. Time of onset of ulceration may be rapid or slow.

Physical appearance. Venous ulcers are most commonly found on the lower extremities, especially around the malleolus. The wound bed of a venous ulcer exudes copious drainage; a greenish-yellowish, fibrinopurulent, adherent exudate may be seen at the base of the ulcer, which may be highly irregular in shape. Superinfection, pain, and malodorous drainage may ensue. Chronic lower-extremity swelling, often mistaken for originating in cardiac, hepatic, and renal disease, leads to varicosities.

Erythrocytes extravasate into the dermis under pressure and leave behind hemosiderin deposits in the skin or cayenne pepper purpura. A pruritic rash often appears, leading to excoriations and further dermal staining with melanophages as a post-inflammatory event. The topical agents used to keep it under check often aggravate stasis dermatitis. Further acute inflammation produces panniculitis, which becomes more sclerosed with time leading to lipodermatosclerosis. Dystrophic calcium deposits develop sometimes. The exact mechanism by which ulcers result from this long series of events is unknown. It is believed that the capillary fibrin cuff around the vessels and the activity of inflammatory mediators in part derived from white cell entrapment within the cuff all lead to microvascular ischemia. It is possible that minor trauma may also play a role in the ulceration process.

Comorbidities. Venous ulcers are often complicated by comorbidities that include lymphatic obstruction, lymphedema, stasis dermatitis, arthritis, skin rashes, interstitial edema, including bullae microvaricosities, deep vein thromboses, and skin infections (e.g., ecthyma, cellulites). Patients presenting with venous ulcers may have a history of lower-extremity injury, such as a fracture or severe crush injury. Obesity may also accompany the occurrence of venous ulcers, as well as gait abnormalities and arthritis.

Arterial ulcers. Definition. Peripheral arterial occlusive disease (PAOD), which affects the large- and medium-sized vessels, is the most common atherosclerosis disorder of the lower extremities associated with impaired wound healing.34 Patients who develop ulcers or gangrene have impaired circulation to the skin. Arterial stenosis or occlusion impairs blood flow to the extent that despite compensatory mechanisms, the nutritive requirements of peripheral microcirculation cannot be met.35 Ischemia results in tissue necrosis and subsequent ulceration.

The underlying pathology of ischemic ulcers that causes the clinical symptoms observed includes plaque deposits that become calcified, damage to the vessel from chronic hypertension,36,37 and increased platelet aggregation causing formation of microthrombi.

These sequelae of peripheral arterial disease result in the narrowing of the vessel lumen leading to the reduction of blood flow, loss of vessel elasticity, and a loss of vessel ability to self regulate blood flow in response to metabolic needs.

Assessment. Trauma is the precipitating event for arterial ulcers. Ischemia and infarction of local tissue occur with tissue loss and gangrene. As with all patients suspected of having arterial disease as the etiologic basis for a chronic wound, a complete clinical history and examination must be completed to confirm and then determine severity of the contributing disease.
Evaluation should accomplish the following objectives: objective confirmation of the diagnosis; assessment of hemodynamic requirements for successful intervention (revascularization); assessment of patient operative risk; assessment of atherosclerotic risk factors; and assessment of atherosclerosis in other body systems.

The examination will assess both the coronary and cerebral circulation, basic hematological and biochemical tests, resting ECG, ankle or toe pressure measurement, or other objective measures of severity of the ischemia. Additionally, the exam should include imaging of lower-limb arteries in patients if vascular surgery is assessed to be a realistic option. Duplex scan of the carotid arteries should be done in selected patients at high risk as well as a more detailed coronary assessment in selected patients.

Although the above clinical examinations would provide the ideal diagnostic information necessary to assess the severity of arterial damage, not all the listed tests are feasible for the frail elderly. Alternatively, a simple test at the bedside can confirm whether the patient has dependent rubor, which is indicative of severe ischemia. Arterial to brachial index (ABI) is the standard noninvasive examination used to assess the lower-extremity macrovascular status.38 Noninvasive studies, such as ABI, using ultrasonic Doppler will identify claudication if it is less 0.7mmHg and severe ischemia if it is less than 0.4mmHg. Also, measuring segmental pressure or pulse volumes at different levels can determine where the arterial occlusion is located. Noninvasive vascular testing, including segmental pressures, toe pressures, Doppler waveform analysis, and duplex scanning, can be helpful and should be done in patients for whom surgery is a viable option.39–42

Transcutaneous oxygen measurement (TcpO2) is used to determine the degree of microvascular perfusion. TcpO2 measures the diffusion of oxygen into the periwound tissue and is indirectly measured via transcutaneous oxygen monitoring.43 A TcpO2 greater than 30mmHg suggests the patient has adequate perfusion to heal. This measurement is valuable if the ABI is low and can aid in the decision to perform surgical revascularization, which should be avoided if possible.44,45 However, the practical application of this technology may be limited because the instrumentation is costly and requires temperature control. Additionally, the testing process is lengthy, limiting its usefulness among a frail patient population.

Physical appearance. Arterial ulcers are located on the distal lower extremity because of inadequate perfusion of the skin and subcutaneous tissue at rest.46,47 This type of ulcer has a “punched out” appearance that follows some form of trauma to the leg. The wound bed is dull pink, indicating poor perfusion, and the base will be granular. The patient will display dependent rubor and have minimal or absent pulses. The affected limb will have a waxy appearance, no hair, and the patient, if able to communicate, will report claudication pain.

Comorbidities. Patients that present with arterial ulcers will often have additional chronic illnesses that complicate the potential for healing. They include diabetes, hypertension, and a family history of arterial disease. Arterial ulcers can also present with varying degrees of neuropathy. Spinal cord injuries that resulted in either paraplegia or quadriplegia with associated disturbances to arterial blood flow predispose patients to arterial ulcers of the lower extremities.

Diabetic/neuropathic ulcers. Definition. Diabetic neuropathy refers to various types of nerve damage, a common sequelae of diabetes. Nerve damage is the etiologic basis for diabetic ulcers. Neuropathy leads to loss of protective sensation, setting the stage for skin breakdown. How the nerves are injured is not entirely clear, but research suggests that high blood glucose changes the metabolism of nerve cells and causes reduced blood flow to the nerve. In a study of diabetic patients with foot ulcers, 60 to 70 percent were related to neuropathy, 15 to 20 percent were related to peripheral vascular disease (PVD), and 15 to 20 percent related to PVD combined with neuropathy.48 Peripheral neuropathy is a major contributing factor in more than 90 percent of foot ulcers and, ultimately, amputation.49,50

There are different types of nerves and, therefore, different types of possible diabetic neuropathy. These can be grouped as sensory (ability to detect heat, cold, and pain sensation), motor (ability to contract muscles to control movement), and autonomic (ability to regulate heart rate and

The most common type of diabetic neuropathy affects the sensory nerves in the legs and is usually known as peripheral neuropathy. The motor and autonomic nerves can also be involved, which will adversely impact the patient’s mobility and control over normal bodily functions. Patients with neuropathy were found to have seven-fold increased risk of ulceration when compared with diabetic patients without this complication.51

Neuropathy can result in two sets of seemingly contradictory problems. The first is the loss of ability to feel pain and other sensations, which leads to neuropathic ulceration. The second problem is symptoms of pain, burning, a sensation of pins and needles, or numbness. These sensations cause varying degrees of discomfort and pain. Most patients with neuropathy have only one of these problems, while others can be affected by both.

While there are changes in microvascular function in the diabetic foot, neuropathic ulcers are the result of alterations in nerve cell transmissions that cause a loss or complete absence of sensitivity to pressure and pain. This observation is strengthened by the similarity found between foot ulcers in diabetic patients and those patients with Hansen’s disease where there is no vascular compromise, only sensory loss.52 The fact that foot ulceration does not occur among diabetic patients during enforced bed rest demonstrates the major role played by direct mechanical load in the development of neuropathic foot ulceration.52

Assessment. The first step in assessing a suspected diabetic/neuropathic ulcer is to confirm the presence of one or more types of neuropathy. There are many different methods of diagnosing and grading diabetic neuropathy. The most important aspect of grading diabetic neuropathy is the assessment of potential and degree of loss of sensation in the feet. Diabetic neuropathic ulcers are primarily a consequence of loss of protective sensation (LOPS), which is a significant change caused by neuropathy.49 Tests are conducted that determine if the patient can feel the pain of a pin prick, the touch of cotton gauze, or the vibration of a tuning fork. However, the problem with testing sensation with a pin prick, cotton gauze, or tuning fork is that these tests cannot be standardized and, therefore, results will vary among different users. Standardized tests used to measure neuropathy include testing vibration sensation and measuring touch sensation using a monofilament. The limitation of all these tests that measure pain, touch, or vibration sensation is that they depend upon the patient’s ability to communicate his or her response to the test’s measure of sensory acuity. For the frail elderly patient, measurement of neuropathy may be impractical. In these cases, determination of neuropathic origin for a chronic wound will depend heavily on physical assessment and medical history, particularly serial blood glucose levels, hemoglobin, and A1C (glycohemoglobin).

Physical appearance. A typical neuropathic ulcer is found on the plantar surface of the diabetic foot. Patients with sensory loss neuropathy are unaware of any potential pressure they are causing to the bottom surfaces of their feet. The usual initiating factor for breakdown is injury from excessive repetitive pressure on a specific area of the foot.53–55

Among frail elderly adults, neuropathic or diabetic ulcers may be seen on the heels, particularly in those patients who either occasionally use wheelchairs to facilitate efficient movement or are wheelchair bound. These ulcers may also occur when therapeutic footwear or splints are utilized.

Examination of the feet will also reveal variations in shape that may be responsible for exerting excessive pressure on specific areas of the foot. These pressure areas can initiate skin breakdown. Sometimes, the foot shape abnormality is part of the diabetic neuropathy or other disease processes. Abnormalities include clawed toes, rocker bottoms, and abnormal toe nails. Clawed toes occur as a result of imbalance of the muscles in the feet due to diabetic neuropathy. This increases pressure at the tip or apex of the toes. In the presence of neuropathy, these sites become ulcer prone. Rocker-bottom deformity occurs due to Charcot’s joint, which is a complication of diabetic neuropathy. Toe nails can become infected, thickened, and deformed.

Comorbidities. Wounds located on the lower extremities of patients with diabetes diagnosed with some form of neuropathy must be assessed to determine contributing factors. It is imperative that the role of mechanical forces, potential circulatory diseases, and type of neuropathy be distinguished in order to establish the basis of treatment. As reviewed above, controlling the underlying disease processes and/or mechanical forces, when possible, can begin only after a thorough assessment is completed.

Diabetic ulcers must be evaluated to determine if there are any circulatory deficits that may have contributed to the onset of the breakdown. Physical examination of the feet will also yield clues as to the circulatory condition of the lower extremities. Feet that appear purplish in color and feel cold may have impaired circulation. If pulses in the foot can be clearly felt, the risk of foot ulceration due to vascular disease is small. Alternatively, if a person has claudication or rest pain (especially the latter), there is sufficient peripheral vascular disease to consider skin breakdown to be associated with that disease.

When the foot pulses are very weak or not palpable, then it is necessary to carry out noninvasive vascular tests to assess the risk. This is done by measuring the ABI. A simple hand-held Doppler machine is required for this test. The test requires a determination of the brachial artery blood pressure, which is compared to ankle pressure. For example, a patient with a brachial pressure of 120mmHg and an ankle pressure of 132mmHg has an ABI of 1.1 (132/120 = 1.1). ABI values of between 0.9 and 1.2 are considered normal and values between 0.6 and 0.8 indicates definite vascular disease.

Sometimes the arteries in the ankles are calcified due to diabetes. This makes measurement of blood pressure at the ankle unreliable. In this situation, more information is obtained by measuring the pressure at the toe. As a guide, a toe brachial index less than 0.5 indicates the presence of peripheral vascular disease. An additional means for ruling out peripheral arterial occlusive disease in diabetic patients with foot ulcers is by conducting pulse volume recording or segmental pressure oxymetry examination.

Other chronic ulcers. Definition. Although the types of wounds described previously account for the majority of chronic wounds, there are still other types of wounds to consider. Frail patients may present with ulcers that result from inflammatory origins. Some examples include vasculitis, sickle cell, pyoderma gangrenosum, or lupus. The presence or history of cancer can be accompanied by chronic wounds that may be directly associated with tumors or are the result of radiation injuries, such as burns, or abscesses.

Assessment. As with all chronic wounds, accurate assessment and determination of the likelihood of reversing the effects of the underlying disease or condition that contributed to the occurrence of the ulcer is the primary goal of assessment.

Physical appearance. The appearance of any chronic wound provides significant clues as to its origin. As with all the types of chronic wounds, those ulcers not fitting into the categories of ulcers listed previously must be examined for clues of their origins.

Comorbidities. The appearance of any chronic wound is usually accompanied by the presence of at least one significant disease or condition that impairs the circulatory, immune, or pulmonary systems. As described in the other wound types previously, complicating diseases will often either be directly associated with the incidence of the chronic wound or have exacerbated the condition of the patient, which makes breakdown likely.

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