The decubitus ulcer: many questions but few definitive answers

The decubitus ulcer: many questions but few definitive answers

Clinics in Dermatology (2007) 25, 101 – 108 The decubitus ulcer: many questions but few definitive answers Lawrence Charles Parish, MDa,*, Peter Lowt...

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Clinics in Dermatology (2007) 25, 101 – 108

The decubitus ulcer: many questions but few definitive answers Lawrence Charles Parish, MDa,*, Peter Lowthian, M.Phil, SRNb, Joseph A. Witkowski, MDc a

Department of Dermatology and Cutaneous Biology, Jefferson Medical College of Thomas Jefferson University, Philadelphia, PA 19107, USA b Retired Research Nurse, from the Royal National Orthopaedic Hospital, Stanmore, HA7 4LP, UK c Department of Dermatology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA

Abstract Decubitus ulcers appear to be associated with insidious trauma. Differential diagnosis can be tricky, and etiology is controversial with sustained localized pressure which plays a significant role. Sustained pressure can stretch soft tissues and blood vesels, causing multiple microthrombi around the point of maximum compression. This leads to prolonged ischemia and produces a plaque of dead tissue surrounded by microthrombi. Prevention often includes regular movement or supports that move the patient. Good nutrition is important, but the adverse effects of fever should not be overlooked. Antithrombotic agents should be considered. Occlusive dressings can be used for existing ulcers, while traditional treatments are less appropriate. Pressure and other stresses theoretically should be relieved. D 2007 Elsevier Inc. All rights reserved.

Introduction The decubitus ulcer has been the subject of our combined research interests for more than 3 decades, permitting us to watch and to participate in the evolution of various concepts and therapy.1-3 We have delved into various aspects of this perennial problem, raising a number of issues, but making little progress in resolving them.3-10 Among English-speaking people, bedsore is still the popular name for the decubitus ulcer. In the 1970s, when this somewhat neglected area of study was receiving

* Corresponding author. 1760 Market Street, Suite 301 Philadelphia, PA 19103, USA. Tel.: +1 215 563 8333; fax: +1 215 563 3044. E-mail address: [email protected] (L.C. Parish). 0738-081X/$ – see front matter D 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.clindermatol.2006.09.013

periodic attention, an international conference on the subject was organized in Glasgow. At this meeting, many speakers used the term decubitus ulcer, but others suggested that pressure sore was a more accurate name. Interestingly, however, the published report of the conference was called Bed Sore Biomechanics.11 This lack of agreement on even basic terminology has plagued the subject for many years. The current favorite names appear to be pressure ulcer and decubitus ulcer.12 Although there is still some uncertainty about the etiology of these lesions, many specialists prefer the term pressure ulcer. Yet, this strongly suggests that the etiology is cut and dried. On the other hand, decubitus denotes lying down which, in the case of lesions that start in chairs or internally (see below), is not particularly accurate.13 In this review, we use the older term decubitus ulcer for, as


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Shakespeare observed, changing the name does not change the smell.14 For those who prefer an euphemistic term, there is always torsion stress.15

What is a decubitus ulcer? The decubitus ulcer represents a defect that can extend from the epidermis through the underlying tissue, even reaching to bone. Frequently, it is found over bony prominences and often where the skin is firmly attached to bone.16-18 When infected, the decubitus ulcer can have an offensive smell, but not always, and not all decubitus ulcers become infected, which only compounds the question of etiology.6,19-21 The crucial aspect of these lesions is that they all appear to be initiated by insidious physical trauma in soft tissues. Traditionally, this has been attributed to prolonged bed rest on ordinary mattresses, which results in sustained high tissue pressures over bony prominences. Since the 1940s, when paraplegics began to live extended lives in wheelchairs, it became clear that prolonged pressures on the ischia and other prominences, when the patient is seated, could result in decubitus ulcers.22 Similarly, in the latter half of the 20th century, it became equally apparent that these lesions, when severe, were not necessarily associated with a terminal illness.23

Differential diagnosis Decubitus ulcers are not easily distinguished from other lesions such as contusions, friction burns, arterial ulcers, and iatrogenic ulcers associated with drug ingestion.24 Sacral and trochanteric ulcers can be accepted as decubitus ulcers (Fig. 1); however, an aortic aneurysm may also create a truncal ulcer. Scrotal ulcers are unlikely to be decubitus ulcers (Fig. 2).

Fig. 1 The patient developed a deep trochanteric ulcer, which, by staging schemes, might be labeled stage 4.

Fig. 2 A consult was requested for this 39-year-old man who had developed ulceration of the scrotum during the previous 10 days. He was thought to have a decubitus ulcer; however, the diagnosis is Fournier’s gangrene.

Ulcers on the foot provide opportunities for disagreement because peripheral vascular problems may be present and diabetes mellitus may also complicate the medical picture. Decubitus ulcers are generally found over bony prominences, but there are exceptions25 (Fig. 3). For example, there is the covert decubitus ulcer produced in the urinary tract because of prolonged traction on the catheter.26 Similarly, an intravenous apparatus can cause a decubitus ulcer when pressed firmly against the arm (Fig. 4). Although the arterial ulcer may give a punched out appearance on the leg or foot, more often than not, the ulcer also has a venous insufficiency component. To complicate the matter more, the diabetic foot ulcer can, arguably, be confused with a decubitus ulcer. The problem occurs in

Fig. 3 A 69-year-old man had had bilateral above-the-knee amputations 3 years prior because of uncontrolled diabetes mellitus. He was bedridden at home and developed numerous ulcerations on the back. Although vasculitis might be considered in the differential diagnosis, these skin defects represent decubitus ulcers.

The decubitus ulcer

103 superficial lesions, particularly when there is irritated or diseased skin. When the patient/support interface is damp, the friction can be high enough to cause the skin to adhere to the support surface.39 Typically, the dampness is created by sweating or by incontinence. If this develops in a paralyzed or similarly debilitated patient who is propped up in bed, his/her skeleton has the tendency to slide forward, but the skin is held back and adheres to the support. This makes the patient prone to the results of sustained angle forces, particularly at the sacrum and buttocks. Severe decubitus ulcers can result.40,41

Infected lesions and acute lesions

Fig. 4 An 82-year-old man with arteriosclerotic heart disease was hospitalized because of hypotensive episodes and arteriosclerotic heart disease. Not only did he develop a drug eruption to the sulfonamide-derived diuretic, but he also sustained a necrotic area where the intravenous canula was inadvertently pressed into his left arm.

trying to determine a single cause; it may not even be possible.27,28 Similarly, the neurotropic ulcer associated with leprosy can also cause diagnostic problems.

Etiology Pressure and pain loss The etiology and, for that matter, the pathogenesis of decubitus ulcers, is controversial. Experiments on healthy animals strongly suggest that decubitus ulcers are not necessarily directly attributable to ill health, as was once proposed by Charcot.29 They can be produced by sustained localized pressure on soft tissues and high-frequency repetitive pressures.30-34 The former situation occurs, for example, when a deeply unconscious patient is left undisturbed for many hours on an unpadded operating table, whereas the latter situation is sometimes found in ambulatory patients who have lost their peripheral pain receptors. Any minor trauma may go unnoticed so that with continued walking, an ulcer can develop.30,35 The loss of pain sensibility seems to be a highly significant factor in the etiology of decubitus ulcers.4 Comparatively healthy people also can develop decubitus ulcers when their pain sensibility is dulled for long periods by epidural anesthesia36 or by barbiturate overdosage.37,38

Decubitus ulcers produced experimentally can be considered to be acute ulcers.42 These lesions are normally without pathogenic bacteria, but often, they do become infected. A seemingly minor subcutaneous injury can become the locus for bacteria, either from bacteremia or from surface colonizers, thus producing an abscess that may be diagnosed as a closed decubitus ulcer.6,20 The pathogenesis of the acute ulcer becomes difficult to understand when it is attributed to sustained localized pressure, especially should healthy tissues be involved. Many clinicians have assumed that prolonged ischemia is the culprit; however, this fails to explain why higher tissue pressures can create ulcers after a short period of ischemia, whereas lower pressures, which still create an ischemic state, need longer periods to cause the identical lesion.32,43

Microthrombi Various ideas have been explored in attempting to solve this acute decubitus ulcer problem but, in the 1960s and 70s, Barton and Barton44 found that overt decubitus ulcers often exhibit a central cold spot on a thermographic camera. Such lesions are associated with multiple microvascular thrombi. Multiple microthrombi had previously been associated with

Friction It also seems clear that a sustained force applied to the skin at an angle can result in a decubitus ulcer. This is likely when the friction level between the patient and the support is elevated. Fairly high friction levels, as obtained by repeated rubbing against harsh bed sheets, can produce

Fig. 5 This paraplegic patient lay upon several coins in his pocket and did not comprehend the danger involved.


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decubitus ulcers by Reichel,41 and similar thrombi were later found by Dinsdale42 and by Witkowski and Parish45 when investigating established decubitus ulcers. These findings, and other considerations, lead us to conclude that acute decubitus ulcers, more often than not, are initiated by microvascular trauma.46 The rationale for this conclusion is based upon the following concept: when a mechanical force such as localized pressure (vertical or angled) is applied to the skin for a long period, it will slowly stretch the skin and subcutaneous tissue, including small blood vessels45: the higher the force, the more rapid the stretching or physical distraction as when hard objects press on the skin46 (Fig. 5). At the higher force level, as when a policeman’s baton (club) is used on a rioter’s back, a contusion is caused. This appears in 2 parallel lines with an unbruised central area. The explanation for this is based upon the fact that the central strip is mostly compressed, whereas the lateral areas are distracted—producing microvascular hemor-

Fig. 6

rhages. This further indicates that a spherically ended baton (a knobkerrie) would produce a ring-shaped contusion. Thus, a curved bony prominence (eg, the calcaneum) can, under sustained pressure, produce a ring-shaped area of microvascular trauma.46 Such microvascular trauma is not as easily noticed as a baton bruise because the bony prominence normally concentrates the tissue stresses close to itself.31,46 The lower pressures involved in the patient/support situation (usually about 100 to 500 mm Hg) mean that overt hemorrhage might not occur. Instead, many microvessels are sufficiently damaged to induce multiple microthrombi. If the tissue compression is unrelieved, these thrombi have time to mature, thereby causing anoxia and cellular death of the small area enclosed46 (Fig. 6). This small enclosed area is dehydrated and tightly compressed because it lies directly over the bony prominence.45 The tissues in the microthrombotic ring are stretched (by distraction), and because they are viscoelastic, they do not readily recover their normal shape, when the pressure

Postulated sections to show a microthrombotic ring while still under pressure.

The decubitus ulcer is relieved, even with the development of edema.33 This particularly applies when old age or disease reduces the elasticity of the skin and subcutaneous tissue.47 In these cases, short periods of pressure relief may fail to prevent ulcer formation, even if they do so for healthy young people.48 The concept of a ring of microthombi may explain why acute decubitus ulcers take 2 to 4 days to become overt, after the traumatizing force is relieved.32 The prolonged ischemia caused by the encircling thrombi produces the necrosis. Therefore, it is next to impossible to determine when the initial insult developed.

Evaluating, grading, and risk assessment Is there a way to define the ulcers under consideration and to grade them using a numerical and/or letter system, without relying on lengthy descriptions? There should be a way, but the severity of an overt decubitus ulcer is often debated, and this has allowed a variety of grading/ classification systems. The bStanmore Classification,Q which was developed in 1985, has given good service,49 but the better-known classifications today are those of the National Pressure Ulcer Advisory Panel (NPUAP grading system)50 and the European Pressure Ulcer Advisory Panel (EPUAP grading system).51 The fact remains that the ideal grading system has yet to be devised and generally accepted.19 Some nurses have used their own understanding of decubitus ulcer etiology to devise an early warning scheme to indicate which of their new patients are at risk for developing decubitus ulcers. Because this concerns preventative measures, such schemes are inappropriate for treatment planning. The best known of these risk-assessment schemes are probably the Norton Scale and the Braden Scale. These scales (or scores) are not meant to replace the observations of a seasoned clinician. Even so, some have been statistically validated with the aim of giving nurses more confidence in using them.52-56 Unfortunately, the popularity of any one scheme does not guarantee that it has been adequately evaluated.57,58

Prevention Care of the tissue The various additional factors, intrinsic and extrinsic, which are thought to influence the development of a decubitus ulcer, lend themselves to intense discussion.2,4,10,11,32,47,59 If we are to take seriously the above concepts, then we should direct our attention to anything that will strengthen the microvasculature7 or make for less thrombotic formation. There is some evidence that anti-

105 coagulants and antiplatelet aggregation agents can prevent the formation of decubitus ulcers.46,60 We also need to be aware of the role of fever or another rise in tissue temperature that might increase the risk of decubitus ulcer development due to increased metabolic demands.61 Such factors can decrease the time that tissues can survive without adequate oxygen and nutrients.62 Good nutrition with appropriate vitamins and minerals are obviously important to the maintenance of healthy tissue63; however, the question of absorption and appropriate use is raised. When patients are physiologically worn out from the multitude of diseases confronting them, the skin, just as any other organ system, can fail. In such cases, intervention with vitamins, minerals, or food supplements will be an exercise in futility.10,64,65

Movement and its effect In health, we all make regular subconscious movements and adjustments when walking, standing, sitting, and sleeping.30,66-68 Plausibly, these movements rely on pain receptors in the skin, which inform the brain when a compressed (or stretched) region needs some relief.47 For example, we are all familiar with the pain induced by ill-fitting shoes. When the pain is sufficient to reach the conscious level, we hopefully remove the shoe and rest. If such discomfort is allowed to continue intermittently, then the skin tends to hypertrophy with the development of clavi and callosities. This hypertrophy appears to result from repeated episodes of reactive hyperemia. Such episodes of hyperemia are actually used by plastic surgeons for skin expansion techniques.69 Similarly, on many new spinal-injured patients, nurses will use the reactive hyperemic flare to indicate when the patient should be moved. In time, this procedure appears to strengthen the panniculus adiposus so that many of these patients eventually rest up to 8 hours in one (sleeping) position without the need for turning.70

Turning Regular manual turning is a traditional, nursing, way of moving bed patients (onto different areas of the body) so as to avoid prolonged pressure on any one part. These schedules have a long history, dating back to mid Victorian times.71 There is no magic time interval. For example, American nurses tend to use a 2-hour scheme, whereas British nurses often use longer intervals. Turning may be combined with an occasional refreshing wash of the patient’s posterior, but the traditional bed rub has no place in modern nursing. Similarly, any attempt to harden the skin (eg, with methylated spirits) to prevent skin breakdown is unphysiologic.9,72 All turning or position changing should be accomplished in a planned, methodical way, but blanket rules for 2, 3, or

106 4-hour turning schedules are neither desirable nor practical. The schedules should be individualized to suit particular patients and change as the patient improves.73-75 Individual turning schemes are also required where special beds and nursing care are in short supply. Most nurses recognize that, in this situation, regular turning schemes are ideal, rather than practical. Some have even devised a scheme that involves every nurse giving his/her patient a bsmall shift of body weightQ each time the patient requires attention. This may obviate the need for 2 nurses to be involved but is patently a desperate bbetter-than-nothingQ measure.76

Special supports Preventing prolonged forces that compress or distort tissues should, theoretically, prevent acute decubitus ulcers. This can be accomplished by lowering the force level (ie, pressure or angled pressure) on the patient’s supported area. It can also be done by regularly moving the patient, his/her support, or both. The Low Air Loss Bed System is an example of lowering the force levels—by spreading the patient load evenly—over the support.77 A different kind of support is the Alternating Pressure Air Mattress, which allows the bed surface to regularly change its shape and, hence, the areas where the patient’s body is being supported.56 These, and similar methods, some of which apply to patients in wheelchairs, have been successful where they have been used appropriately. Yet, if not carefully tailored to nursing needs, special supports will not be used for very long.78 Providing that the patient’s support is reasonably compliant, it is generally best to rely on the regular movement methods.23 As well as imitating the normal, subconscious way that healthy people avoid decubitus ulcers, such methods also help prevent other hazards of immobility.68,79 In general, the modern development of specialized supports and their adoption by acute and extended care facilities have been extremely useful.

L.C. Parish et al. that are used on decubitus ulcers. The occlusive dressing is highly useful in promoting healing; however, if the skin is in a failing mode, then there is little, if any, healing that can occur. Indeed, it has been said that one can put almost anything on a decubitus ulcer, except the patient. This implies that clinicians and nurses can forget that pressure and other stresses should be relieved from a decubitus ulcer until it has healed. Unlikely as it seems, this does happen—sometimes because the nurses do not have the right equipment to relieve the pressure.82,84-86

Bureaucratic problems The restrictive formularies of many institutions make the clinician’s work more difficult. Appropriate dressings may not be available. Even worse, some institutions insist upon retaining in their manuals the use of treatments that vary from the unnecessary to the absurd. More to the point, evidencebased medicine may not even have been considered. Dakin’s solution (sodium hypochlorite) was fine for the gas gangrene of the trenches of World War I, but it has no place in the contemporary treatment of the decubitus ulcer. Similarly, antiseptics may be needed for the first few days of treatment, but after that, they can impede wound healing.9,72

Conclusions Much about the nomenclature, etiology, grading, prevention, and treatment of decubitus ulcers, is controversial. Disagreements about their pathogenesis would appear to be the fundamental problem. It is to be hoped that the new pathologic concepts mentioned in this review will help us make some progress toward a better understanding of these perennial lesions and that this will lead to a reduction in their incidence. The fact also remains that there is such a concept as skin failure and that all the king’s men can’t repair the extreme ravages of age and/or disease.64,65

References Treatment Debridement The treatment of existing (acute) decubitus ulcers is not substantially different from the treatment of any open wound. Initially, necrotic tissue may need to be medically or surgically debrided but not necessarily at the expense of the surrounding healthy tissue.80-82

Dressings The concept of moist healing has revolutionized the therapeutic approach.83 There are now, of course, a wide variety of commercial dressings, as well as traditional cures

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