Wound healing processes are complex and sensitive to internal and external environmental forces. In this section, we review internal (host) and external (environmental) factors as well as inappropriate management (iatrogenic) factors that need to be identifi ed and assessed that may interfere with wound healing.
We begin this section by looking at the patient and three groups of factors that infl uence whether a wound will go on to heal or become chronic or refractory:
• Underlying pathology (intrinsic factors)
• Environmental infl uences (extrinsic factors)
• Inappropriate management (iatrogenic factors)
These factors that affect wound healing are summarized in Table 3.1.
The Patient’s Health Status
We begin with the patient’s health status including his or her internal and external environment, to identify factors such as comorbidities that will aid in predicting the healing response.
Chronic wounds affect millions of people and are a particular problem of the elderly who are most likely to have comorbidi- ties assumed to impair healing. Few studies have identifi ed spe- cifi c comorbidities that can be attributed to effecting healing and nonhealing. Two retrospective reviews showed that patients with comorbid conditions of cerebral vascular accident (CVA), neuropathy, and dementia were statistically never likely to heal (p < .0001).1,2 Other important comorbidities identifi ed associ- ated with the never healing included malnutrition, infection,1 diabetes mellitus (DM), depression, dementia, and degenerative arthritis.2 Other statistically signifi cant factors identifi ed here as predictive of nonhealing were a high number of chronic ulcers and lower hemoglobin counts.2 Hypertension, cardiovascular/
respiratory diseases, senile dementia, and neurologic disease are conditions identifi ed as associated with development of pres- sure ulcers.3 The effects of chronic and comorbid illness on predicting wound healing must be considered as part of the holistic patient evaluation. From what we know, it is reasonable to say that early identifi cation of factors that predict wound healing response will help you triage cases, reduce variability in cost and care, and improve the prognosis and outcome for planned interventions.
Underlying Pathology (Intrinsic Factors)
Underlying pathology includes the intrinsic factors related to the patient’s health status that can affect skin integrity and/or healing. Intrinsic factors affecting health and wound healing considered here include age, body systems and asso- ciated chronic diseases, perfusion and oxygenation, immu- nosuppression, neurologically impaired skin, confusion and mental status wound extent and duration, and skin changes at the end of life.
At the completion of this chapter, the reader will be able to:
1. Identify patient-related factors that effect wound healing.
2. Perform tests and assess adjacent tissues and periwound status.
3. Perform tests and evaluate wound status.
4. Apply classifi cation systems to diagnose wound severity.
5. Explain and apply the concept of wound phase diagnosis, based on the status of the phase of wound healing.
Carrie Sussman
and Wound
3
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Intrinsic Related to Medical Status Extrinsic Related to Environment Iatrogenic Related to Wound Management
Age Medications Local ischemia
Chronic Disease Nutrition Inappropriate wound care
Perfusion and oxygenation Irradiation and chemotherapy Trauma
Immunosuppression Psychophysiologic stress Wound extent and duration
Neurologically impaired skin Wound bioburden and infection Factors Affecting Wound Healing
3.1
TABLE
Age
Infl ammation, cell migration, proliferation, and maturation responses slow with aging.4,5 A major skin change that occurs with aging is thinning of the epidermis, which increases the risk of injury from shearing and friction, resulting in skin tears and ulceration. The skin also loses its impenetrability to substances in the environment, so irritants and certain drugs are more readily absorbed. The reproductive function of epidermal and fi broblast cells diminishes with age, and replacement is slowed.
Elastin fi bers are lost, and the skin becomes less elastic. There is diminished vascularity of the dermis, and the dermis atro- phies, which slows wound contraction and increases the risk of wound dehiscence.6 Wound dehiscence is two to three times higher in patients over age 60, yet, as Eaglstein5 notes, the caus- ative factors may be infection, inadequate protein intake, and other medical complications—not solely age.
Aging and chronic disease states often go together, and both delay repair processes; this is due to delayed cellular response to the injury stimulus, delayed collagen deposition, and decreased tensile strength in the remodeled tissue. The regeneration pro- cess can be diminished as a result of impaired circulatory func- tion. Because chronic disease is more common in older adults, age is at least a marker for conditions that predispose to chronic wounds, and it is typically identifi ed as a cofactor in impaired healing.7 Despite these factors, aging alone is not a major fac- tor in chronic wound healing. Research now demonstrates that healing is only slightly retarded in healthy elderly individuals without chronic disease states, compared with that of a young population.1,2,8 Patient age does not signifi cantly affect the heal- ing time for leg ulcers associated with venous insuffi ciency9 or for neuropathic foot ulcers using total contact casting.10 However, age appears to affect the risk for skin breakdown in individuals who are older than 85 years; this group demon- strated a 30% risk of developing pressure ulcers.11
Chronic Diseases
Cardiopulmonary morbidities. Chronic diseases of all kinds affect the cardiopulmonary system and oxygen-transport pathway that delivers oxygen from the lungs to the tissues and removes carbon dioxide. Oxygenation and oxygen balance in the tissues are key requirements for healing. The cardiopul- monary system is affected by hematologic, neuromuscular, musculoskeletal, endocrine, and immunologic conditions.12 For example, in patients with chronic obstructive pulmonary disease, breathing functions are compromised. This reduces effi cient respiratory function, which affects lung volumes,
fl ow rates, and the delivery of oxygen to and removal of carbon dioxide from the tissues that are required for healing. Impaired cardiopulmonary function affects mobility that is considered a risk factor for skin ulceration.
Diabetes mellitus. Patients with DM are at risk for poor wound healing, due to the effects of high blood glucose levels on leukocyte function, predisposing them to increased risk of infection.13 The microvascular and neuropathic components of diabetes also place these patients at increased susceptibility to impaired healing.14 The rest of this section and Chapter 12 dis- cuss in more detail how DM infl uences multiple body systems associated with wound healing.
Immune suppression. In cases of immune suppression, such as is common in patients who have diabetes, cancer, human immunodefi ciency virus (HIV) infection, and acquired immune defi ciency syndrome, or those who are undergoing immunosuppressive therapy, the body lacks the ability to pro- duce an infl ammation phase that initiates the cascade of repair.
Absence or impairment of infl ammation at the onset of trauma will impair the healing cascade through all phases of healing.15 Perfusion and Oxygenation
All phases of wound healing require adequate perfusion to bring nutrients and oxygen to the tissues, thus the lack of perfu- sion is a signifi cant barrier to healing. Several factors infl uence perfusion including
Peripheral vascular impairment. Wound healing is depen- dent on a well-vascularized wound bed to sustain the growth of new tissue and immunological response of the tissues to counter infection, which means that adequate perfusion is required. Impaired peripheral vascular function such as chronic arterial hypertension secondary to peripheral arterial atheroma (hardening of the arteries) restricts blood fl ow and tissue perfusion because the blood vessels do not dilate but instead create blood fl ow resistance. A low fl ow state occurs that is usually located in the lower extremities, and the result is risk for arterial ulceration from severe tissue ischemia and the mechanisms of ischemic reperfusion injury, which were described in Chapter 2. Diabetes also leads to increased sus- ceptibility to peripheral arterial atheroma, which can progress to stenosis and occlusion, ischemia, and ulceration.16 Oxygen- free-radical activity, also described in Chapter 2, is elevated in individuals with DM and has been implicated in the etiology of vascular complications that may be related to ulceration and poor healing.16 Chronic venous hypertension leads to leukocyte accumulation in the skin and other tissues of the leg, which
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motor, and autonomic. Sensory neuropathy is the loss of the ability to recognize and react to sensations of touch, pain, pres- sure, and kinesthesia (position). It also frequently includes symptoms of burning and paresthesias. Other signs of PN are reports of gait and balance dysfunction. Motor neuropathy is the loss of the motor control of the muscles, and the results are the development of muscle atrophy and imbalance that con- tributes to structural changes and deformities. Neuropathy of the autonomic nervous system (ANS) impairs the function of the sweat and sebaceous glands located in the skin. When ANS function is impaired in the feet, the skin becomes dry and cracked, providing a portal of entry for infection. The skin acidity also changes, resulting in impairment of the ability to control surface bacteria. Because of an impaired immune sys- tem, another complication of diabetes, when infection occurs, these individuals are unable to generate an infl ammatory phase of repair and overcome the infection. Chapter 12 describes the examinations for testing for neuropathy, including photos of the consequences of polyneuropathy.
Spinal cord injury results in alteration of the functions of the same three nervous system components: sensory, motor, and autonomic and all may be affected at the same time depending on the extent and location of cord injury. In progressive condi- tions like PN, neuronal changes occur slowly and progressively over time. If the SCI lesion is above the 6th thoracic level, ANS function is impaired in the early stages postinjury, and the indi- vidual is often unable to maintain a constant body temperature.
This is due to loss of the ability to dissipate and retain heat from the interior of the body to the periphery via vasomotor responses to heating. Refl ex sweating is also lost with injury at these levels, which places the individual with an SCI at risk for overheating.22 Another complication of SCI is loss of vasomotor tone; this leads to dilation of the veins of the lower extremity, with resultant peripheral edema and frequent deep vein thrombosis.23
Neurologically impaired skin in persons with SCI undergoes metabolic changes that can take 3 to 5 years to stabilize follow- ing the SCI.22 These changes include the following:
• The rate of collagen catabolism increases immediately, and signifi cantly, and there is a rapid increase in the rate of col- lagen catabolism.
• Decreased enzyme activity related to defective collagen bio- synthesis in the skin below the level of injury decreases; the increased rate of catabolism of collagen, coupled with defec- tive collagen biosynthesis, produces fragile skin that is more subject to skin breakdown.
• Decrease in the proportion of type I collagen, allowing type III collagen greater prominence in the skin below the level of injury. Recall that properties of type III collagen include thin- ner, weaker, and has more widely spaced fi brils that contribute to the fragility of the neurologically impaired skin.
• Decrease in the density of adrenergic receptors in the skin below the level of injury could be the cause of abnormal vas- cular reactions.
• Large increase in the level of glycoaminoglycans (GAGs) excreted in the urine increases, robbing the skin of the elastic- ity necessary to adapt to mechanical insults.
Motor function loss, paralysis, produces muscle atrophy, which reduces muscle bulk over bony prominences and exposes the skin covering them to mechanical forces. It also limits initiate the damage that eventually leads to skin ulceration. In
addition to generating oxygen-free radicals, these cells replace proteolytic enzymes and infl ammatory cytokines that lead to skin ulceration.16 Thus, when reviewing the medical history, it is important to consider vascular changes such as these as intrinsic factors that will predict the development and healing of vascular ulcers. Perfusion assessment methods are described in Chapter 7. Chapter 11 covers the diagnosis and management of vascular ulcers.
Blood volume. Hypovolemia, the lack of adequate intravas- cular blood volume, has been shown to impair healing because there is insuffi cient volume to transport oxygen and nutrients to the tissues and remove waste products.17 Prolonged hypo- volemia impairs collagen production and diminishes leukocyte activities.8 There are no external signs of mild hypovolemia;
its diagnosis is made by measuring the transcutaneous partial pressure of oxygen in the blood (Chapter 6). Hypovolemia should be considered in situations that are common to the chronic wound population, such as the use of diuretics, renal dialysis, and blood loss.
Fluid administration can correct hypovolemia.8 Hartmann et al.18 reported that, according to measurements of subcutane- ous oxygen tension, fl uid replacement improved tissue perfu- sion19 and improved accumulation of collagen in healing wounds by day 7 in 29 patients after major abdominal surgery (p < .05).18 Fluid replacement thus can be used to improve tissue perfu- sion.19 When replacing fl uids, care must be taken to maximize intravascular volume without causing fl uid overload, as over hydration can lead to diffi culties related to edema. Thus, fl uid balance is the key principle to follow to promote wound heal- ing. For example, in anemia, there is reduced hemoglobin and thus reduced oxygen-carrying capacity of the blood. However, research data suggest that anemia does not impair wound heal- ing when there is adequate perfusion and blood volume.17 Immunosuppression
Wound healing is also delayed in patients with HIV or can- cer, in those undergoing immunosuppressive therapy, and in severely malnourished individuals.20 Immunosuppression retards or prevents the infl ammatory response and affects all phases of wound healing.15
Neurologically Impaired Skin
Neurologically impaired skin is related to several different pathologies. Two such conditions that are often associated with wounds are peripheral neuropathy (PN) and spinal cord injury (SCI).
Peripheral neuropathy is a complication associated with such conditions as chronic diabetes, alcoholism, and chemo- therapy and involves the loss of neuronal signaling and trans- mission. PN usually occurs fi rst in the feet and is progressive in the case of diabetes and other progressive conditions and with repeated series of chemotherapy and ongoing alcoholism.
Chemotherapy-induced sensory peripheral neuropathy (CIPN) is a relatively common side effect reported in 30% to 50% of patients who are treated with these agents. CIPN is underes- timated and underdiagnosed but is becoming more prevalent as survival rates and lifespan of cancer survivors increase.21 Therefore, the incidence of skin trauma due to insensitivity can also be expected to rise. Three types of PN can occur: sensory,
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was mentioned earlier as a requirement for adequate blood volume to perfuse tissues and deliver nutrients and oxygen to tissues as well as other important bodily activities. Chapter 7 discusses nutritional assessment and treatment in detail.
Wound Extent and Duration
Research supports that the extent of wound surface area, mul- tiple wounds, and wound depth are factors in time to healing1,2 since they impair the hosts’ ability to combat infection and to repair.6,8,28–31 Patients with venous ulcers that are initially large in size or who have moderate arterial insuffi ciency (ankle- brachial index [ABI] of 0.5–0.8, see Chapter 6) have associated delayed healing times.9 Injuries with large surface areas and multiple wounds, which increase the total body surface area to be repaired, increase the need for oxygen, nutrients, and adap- tive resources for healing because there is more damaged tissue to repair and therefore take longer to heal.
In addition to wound size, duration of ulceration is an important factor infl uencing wound healing. Researchers look- ing at factors that can be used to predict wound healing have identifi ed duration and size as two factors that are predictive of healing outcomes. Percentage of healing of ulcerated area at week 3 was a good predictor of 100% healing. Shorter duration of ulceration and smaller size were predictive of reduced time to heal.32 Ulcers that are large, long-standing, and slow to heal after 3 weeks of optimal therapy are unlikely to change their course.33 It is now possible to identify and diagnose correctly those ulcers that are unlikely to respond to standard care, and consideration should be given to introduce alternative thera- pies.33 Chapter 4 presents information about healing percent- age and size change predictors of healing.
Skin Changes at the Life’s End (SCALE)
In this section, we have reviewed systems and conditions that are predictive of problems with wound healing or nonhealing.
One system deserving special consideration is the skin. The skin is the largest organ in the body and it is subject to failure as are other organs. Kennedy observed that patients at the end of life may experience a skin failure phenomena that is a subset of pressure ulcers that she identifi ed as having the following char- acteristics: sudden onset; may be pear, butterfl y, or horseshoe shape; often located on the sacrum or coccyx but can appear in other areas, with irregular borders, showing colors of red, yellow, and black; and usually precedes death by a short period of time. This is now referred to as a Kennedy Terminal Ulcer (KTU)34,35 (Fig. 3.1).
Case studies have appeared in the literature that also docu- ment this phenomena.36 The pathogenesis of these ulcers has been attributed to hypoperfusion that occurs in conjunction with multiorgan system dysfunction or failures.37,38 However, at this time, this is only a suspicion. Research regarding the etiol- ogy and pathogenesis of this phenomena is under study.
Since KTU are considered a type of pressure ulcer, a persis- tent question in health care is whether all pressure ulcers are avoidable. To address this question, a panel of experts con- vened to consider this problem and the result is 10 consensus statements about skin changes at the end of life. The panel rec- ognized that at the end of life skin, the largest organ in the body, like any other organ undergoes “Physiological changes that occur as a result of the dying process (days or weeks) (that) may affect the skin and soft tissues and may manifest as observable ability to reposition and to be mobile. Sensory loss causes skin
insensitivity and loss of signaling of impending damage. The combination of these changes increases the vulnerability of the skin to ulceration as well as negatively affecting ulcer healing.22 Mental Status Changes (Dementia)
Changes in mental status often accompany aging. When there is obvious dementia, it is readily recognized; however, when there is mild cognitive impairment (MCI), it may be unob- served. When a patient with MCI has a wound, he or she may not be able to adhere to a wound management care plan. When you interview a patient, look for symptoms of MCI such as for- getfulness of recent events, inability to understand words, and diffi culty focusing on the interview or tasks. Ask a caregiver about personality changes.
Delirium, an acute confusional state, is characterized by reduced attention, changes in cognition, or perceptual dis- turbances.24 Delirium and depression may often coexist.
Development of delirium is often associated with the use of multiple medications to treat a variety of medical conditions and risk of infection. Delirium can have devastating conse- quences and in many cases is both preventable and treatable.
Suspicion of delirium requires an urgent referral to geriatric medicine or geriatric psychiatry.24
Depression is a common fi nding among elders. Elderly possess several factors that predispose them to depression.
Depression is correlated with a sedentary lifestyle, female gen- der, cigarette smoking, and alcohol consumption. The later behaviors increase as the depression increases. This population is dependent on others and has the presence of multiple dis- ease conditions and associated disabilities, which may include a wound. The occurrence of depression in community-dwelling older adults is reported to be as high as 20% to 37%. Patients who reside in nursing homes have a 15% to 25% prevalence of depression. Older adults also are embarrassed by these changes and often talk about somatic symptoms like aches and pains, and gastric problems diverting attention from the problems of depression. Subclinical depression often goes undetected and untreated due to the common misconception that depression is a part of normal aging or because of social taboos associated with depression or psychiatric care. Depression is character- ized by diminished appetite and signifi cant weight loss; loss of interest in activities of daily living; lack of sleep and lethargy;
restlessness; decreased capacity to concentrate, act, think, and do problem solving activities; feelings of worthlessness; loss of self-esteem; feelings of guilt; and suicidal or thoughts of death.
Major depression is characterized by fi ve or more of these symptoms.25 All of these factors are associated with impaired ability of wounds to heal.
Undernutrition (Malnutrition) and Dehydration
Undernutrition, formerly referred to as malnutrition, is defi ned as a state in which there is a nutritional defi ciency or an excess or imbalance of energy protein and other nutrients essential for support of bodily functions including healing.26 Undernutrition affects the hosts’ resistance to infection.27 The causal relation- ship between undernutrition and skin breakdown is at this point unclear, but it is clear that providing and consuming suffi cient kilocalories are necessary for tissue repair.26 In addi- tion, the patient must be able to chew, swallow, and consume enough nutrients to support tissue growth. Adequate hydration
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