221
CLINICAL PRACTICE Acute pressure area
care:
Sir James
Paget’s legacy
M. R. BLISS In 1862, Sir James Paget gave the address in surgery to the thirtieth annual meeting of the British Medical Association.1 Me now speak of some of /[the] that are not "Let me [the] things... things in the natural ( postoperative course; and chiefly that I may take occasion to point out the need of a much more minute record and analysis than has yet been made of the causes of danger and mortality after operataions. operations. Much has been done to ascertain the general mortality of each capital operation; and it has been done so well, and so laboriously, that it may seem ungracious to say that it is now time to do something more and better. Yet it is certain that we want to know what are, after each operation in each hospital, and in different modes of practice, not only the several total amounts but the several causes of danger or of death. In short, our tables of mortality after operations must be more minute in details, in order that, having better knowledge of the several dangers that are near, we may have better means of coping with them."
"Let
...
off the blood supply are greater in the region of a hard object such as a bone than in the skin. Consequently, deep pressure sores characteristically have overhanging edges, and apparently small skin lesions may interconnect by subcutaneous sinuses extending for many centimetres under intact skin (fig 2). As Paget observed, these sinuses result from breakdown of dead tissue produced during the original ischaemic episode; they are not, as is so commonly asserted, due to pressure or infection from a superficial sore spreading into the deeper layers. BODY WEIGHT
emphasise that causes of morbidity were important as causes of mortality in revealing just underlying abnormalities and suggesting remedies. He went
on to
as
"We have much to learn... in every case of erysipelas, pyaemia and the like, we ought to work until we can discover its probable origin ; we should have the strongest feeling that these diseases are not spontaneous and inevitable."
Paget did not specifically mention pressure sores in his list of postoperative complications, probably because patients undergoing surgery in the nineteenth century either did not survive long enough to get them, or were too young and otherwise healthy to be at risk. However, like Hunter and Charcot,3 he regarded management of pressure sores as essential to the practice of surgery. He included bedsores in the series of lectures given at St Bartholomew’s Hospital, London, and the Royal College of Surgeons that formed the basis of modem medical student teaching and led to the requirement of a medical degree for the practice of surgery in 1866. Having spent the first 7 years of his London career studying pathology, Paget began his lecture4 with a pathological definition of a bedsore as "the sloughing and mortification or death of a part produced by pressure". He identified certain "forerunners": "inflammation affecting prominent parts", usually the sacrum, the posterior superior spines of the ilium, the trochanters, and the ends of the spines of the vertebrae. That he did not mention the ischial tuberosities is probably because ill patients in his day did not sit in chairs. He described other signs of pressure damage as "pale or white patches" or "purple or yellow discoloration from the extravasation of blood or bloody fluid". "Sloughing follows these in the skin and subcutaneous tissue and fat. These latter die before the skin as sloughing proceeds faster in them, so when the skin comes away, the place formerly occupied by these tissues is empty." These careful observations anticipate later studies in animals5-7 and tissue viability measurements in man,8 which have shown that interstitial sores occur primarily in the deep tissues surrounding an underlying bony prominence (fig 1). Pressure differences which cause capillary distortion and cut
Fig 1-Diagram showing how tissue deformation under pressure may give rise to superficial and deep sores.
Fig 2--Interstitial pelvic
pressure sores (in a woman with multiple sclerosis) interconnected by subcutaneous sinuses.
Importance of illness Paget went on to talk about conditions that predispose to pressure sores: "the old, especially those with fractured neck of femur"; "the fattest and heaviest", but also "the thinnest"; "stages of fever". He mentioned typhus, in which "the whole system is so poor and degenerated that sloughing ADDRESS Department of Medicine for the Elderly, Hospital, London E9 6BE, UK (Dr M. R Bliss, MRCP).
Hackney
222
takes place without any pressure at all"-for example, "at the ends of the nose, ears, &c". Similar observations have recently been made of muscle necrosis in critically ill patients with multiorgan failure.9 Research interest is now focusing on the effects of free radicals and endothelial changes produced by bacterial and other toxins that precipitate microthrombi and tissue damage.10 Nevertheless, we should remember Paget’s observation: "as soon as the local disease is removed, the bedsores heal very
rapidly". No trophic
nerves
cautious about Charcot’s contention3that at least partly caused by the interruption of "trophic nerves" in patients with spinal cord injury and apoplexy. Charcot’s misapprehension was probably influenced by the appalling standards of surgery and nursing in French hospitals in his day.1 Most of the examples he gave were complicated by myelitis, and pressure necrosis in very ill patients may result from pressure so slight as not to seem like pressure at all. Most of Charcot’s patients were catheterised, and he himself noted the association of sores with "purulent urine". He was impressed by the rapid "muscular atrophy" that occurred in patients who got sores, and did not think that sensory loss was important. Paget disagreed: in another lecture," he discussed cases of corneal ulceration following section of the Vth nerve, noting the inconstant effect of nerve section on tissues. Like Brown-S6quard, 12 he found no impairment of nutrition and healing in paralysed limbs, but that they were much more vulnerable to injury. He observed that ulceration of the eye was usually worse when section was distal rather than proximal to the trigeminal ganglion, and wondered whether this might be due to interruption of sympathetic nerves from the superior cervical ganglion. This observation may be relevant to spinal injury practiceparaplegic patients with low spinal lesions are more vulnerable to pressure sores than quadriplegics with high lesions, a difference which cannot be explained solely by differences in nursing care.
Paget
pressure
was
sores-ie, tissue necrosis-were
An acute
injury
How quickly do pressure sores develop? According to Paget, "The risk of bed sores in the old with fractured neck of femur is chiefly in the first week; therefore treatment with a view to preventing them should commence immediately the patient takes to bed. After the first week, the risk is not nearly so great". This observation takes the breath away from Versluysen’s mid-1980 studies in the orthopaedic wards at St Bartholomew’s and Hackney Hospitals,13,14 in which she showed not only the very high frequency of sores in this condition (over 60% of patients in both hospitals) but also that 50% of the sores occurred, as Paget predicted, within the first week of injury. Versluysen concluded that the main factor was the poor physical condition of these frail patients after major trauma, and that methods of nursing care were only partly responsible. Her figures indicate, however, little progress in prevention, which suggests that early ambulation or chair-nursing are ineffective, if not injurious, methods of managing these acutely sick patients. In fracture of the spine, Paget noted that sores usually appear within 2 or 3 days. This observation likewise accords with modem studies. Thus, Richardson and Meyer15 found that 134 of 180 patients admitted to a spinal centre 72 hours after injury had sores, compared with none of 122 patients
Fig 3--Pelvic
in
young paraplegic patient. (a) Before surgery; (b) the best result that plastic surgery could achieve pressure
sores
admitted earlier. There
a
three main reasons why new such high risk. First, they often spinal injury patients have multiple injuries (eg, head or chest injuries, limb fractures) in addition to their spinal fracture/6 so they are likely to have hypoxia or reduced tissue oxygen uptake." Second, they are in a state of spinal shock.18 The cause of the vasomotor paralysis that occurs immediately after spinal cord injury and lasts for up to 3 months is still not clearly understood. However, it has profound effects, both on the deformability of the tissues, and hence the extent of capillary occlusion under pressure, and on the ability of the microcirculation to respond to the effects of ischaemia by reactive hyperaemia. Some patients with chronic spinal lesions have continuing abnormal vasomotor responses to repeated skin loading.19 The third reason why patients with spinal cord injury are at such high risk of pressure necrosis is the almost complete lack of medical training in acute pressure area care. By the time the patient is transferred to a specialist unit, it is too late (fig 3). About 35% of the work of modem spinal units is concerned with repairing the damage done to patients during acute or respite admissions to district general hospitals; the fact that it is no longer 100%, as it was when these centres were first established, is due entirely to their improved ability to admit patients immediately after injury, and not to better medical education. Spinal specialists themselves are to some extent responsible for this continuing neglect by their emphasis on the importance of direct admission rather than on improved training in medical schools. However, direct admission is not always possible-eg, in patients with multiple trauma who may require other specialist services-and cannot help patients are
are at
223
in other at-risk groups, such disease or the elderly.
as
those with
Remember to prevent
neurological
Medical training
Paget emphasised the need for training doctors in basic pressure area care, especially in prevention. Now let us look at the means of preventing bedsores, for ninetenths of your care must be devoted to this; for if once they appear, it is very difficult to get rid of them.... "First of all, look to the bed. Good bedmaking is an indispensable thing in the prevention of bed sores."
Unfortunately, the emphasis on chair-nursing to prevent bedsores that has dominated geriatric and general hospital practice for the past 40 years, in the mistaken belief that pressure sores are caused by immobility in bed rather than illness, has caused nurses to lose many of the bed-nursing skills evolved by their predecessors-eg, end-of-bed pleats and bedcradles to relieve pressure over the heels. Paget described a flotation water bed consisting of a deep chest covered with a waterproof sheet sufficiently loose to adapt itself to every part of the patient, noting that a patient "might lie on this for years and never have a sore". "Inferior to this, but still quite good", he says, is a bed on which the waterproof sheet is tight. "They will avert bedsores for a long time, but I would not say that a patient would never get a bedsore on them". However, he highlights the main disadvantage of flotation beds: "You cannot have these everywhere; you can’t take them about to everyone who may need them, and there are many cases in which they cannot be used at all, as in cases of fractured neck of femur, acute inflammation of the knee joint and many others". In lieu of anything better, he recommended an ordinary horsehair mattress, but noted that it should be placed on a firm surface, preferably on boards. He also "utterly condemns" feather beds. This should make us wonder what might be the results of a randomised controlled trial of the fibre overlays now in such widespread use. He discusses methods of "hardening the skin’ by means of nitrous ether-or whisky in Scotland or brandy in England. These methods probably worked because patients had to be turned over to apply them, and their wholesale condemnation, together with uncritical reliance on chairnursing, may be one of the reasons for the continuing high prevalence of pressure sores-affecting up to 10% of all patients in western hospitals.2O
Repositioning Are frequent changes of posture important? According to Paget, "If a patient can lie in 4 different positions during the day, bedsores may be prevented. He may lie on his back, each side, and on his face". This method, re-employed by Guttmann in the UK18 and by Munro2l and his colleagues in the USA for treating ex-servicemen with spinal injuries invalided home during the 1939-45 war, still forms the mainstay of management in paraplegia. The frequency of turning is reduced from 2 hourly to 4 hourly or less as the patient recovers from spinal shock, but is increased again whenever he gets any new illness or pressure marks on the skin. Nevertheless, as Paget observed, "You can’t make a stout person lie on his face; he would simply suffocate". He discussed the benefits of a divided mattress, but noted that this is likely to cause sores on the ilium and trochanters. "Large cushions made in the shape of a horseshoe may help." But, most important of all, he warned, "in speaking of the mode of curing bedsores already formed, let me remind you to continue your preventive treatment just as if there were none, lest they come on other parts".
How many patients undergo operations for repair of pressure sores today only to get new areas of tissue death elsewhere? Only a few years ago a case was presented at a grand round at a London teaching hospital as a triumph of plastic surgery. A young man had undergone repair of an ischial pressure sore and had been allowed to go to a wedding in a wheelchair in the early postoperative period. As a result, he got necrosis of the skin flap which necessitated amputation of his leg so that a muscle plication operation could be carried out to cover the new injured area. Pressure sores are a serious component of multiorgan failure in very sick or injured patients. As the numbers of elderly patients and those with chronic disease in the population increase, morbidity and mortality due to pressure sores must also increase-unless doctors stop thinking of these lesions as injuries unworthy of their attention and follow the example of Sir James Paget, for whom no observation was too trivial, no detail of management too menial, so long as it might improve the wellbeing of his patients. This article is based on a lecture to the 10th anniversary autumn conference of the Tissue Viability Society, Queen Mary and Westfield College, London,
Sept 19-20, 1991. I thank the Department of Medical Illustration, St Bartholomew’s Hospital for fig 1, Mr M. Johnson, medical photographer, Homerton Hospital, for fig 2, and Prof J. T. Scales, Mount Vernon and the Radium Institute, London, for fig 3.
REFERENCES
Paget J. The address in surgery read at the thirteenth annual meeting of the British Medical Association. Br Med J 1862; ii: 155-62. 2. Hunter J. Lectures on the principles of surgery: functions of nutrition and absorption. In: Palmer JF, ed. Works of John Hunter, vol 1. London: Longman, Rees, Orme, Brown, Green and Longman, 1835: 247-58. 3. Charcot JM. Lectures on diseases of the nervous system. Translated by Sigerson G. London: New Sydenham Society, 1877. 4. Paget J. Clinical lecture on bedsores. Students J Hosp Gazette (London) 1.
1873; 1: 144-46. 5. Husain T. An experimental study of some pressure effects on tissue with reference to the bedsore problem. J Pathol Bacteriol 1953; 66: 347-58. 6. Kosiak M. Aetiology of decubitus ulcers. Arch Phys Med 1961; 42: 19-29. 7. Le KM, Madsen BL, Barth PW, Ksander GA, Angell JB, Vistnes LM. An in-depth look at pressure sores using monolithic silicon pressure sensors. Plast Reconstruct Surg 1984; 74: 745-56. 8. Bader DL, Gant CA. Changes in transcutaneous oxygen tension as a result of prolonged pressures at the sacrum. Clin Phys Physiol Measure 1988; 9: 33-40. 9. Helliwell TR, Griffiths RD, Oakley JH, et al. Necrosis of muscle in critically ill patients. Br J Hosp Med 1989; 42: 140. 10. Sinclair AJ, Barnett AH, Lunec J. Free radicals and antioxidant systems in health and disease. Br J Hosp Med 1990; 43: 334-44. 11. Paget J. Lectures on surgical pathology: healthy nutrition. London: Longman, Green, Longman, Roberts and Green, 1863: 17-40. 12. Brown-Séquard E. Experimental researches applied to physiology and pathology. New York: Baillière, 1953: 12-17. 13. Versluysen M. Pressure sores in elderly patients: the epidemiology related to hip operations. J Bone Joint Surg 1985; 67B: 10-13. 14. Versluysen M. How elderly patients with femoral neck fracture develop pressure sores in hospital. Br Med J 1986; 292: 1311-13. 15. Richardson RR, Meyer PR. Prevalence and incidence of pressure sores in acute spinal cord injuries. Paraplegia 1981; 19: 235-47. 16. Silver JR. Spinal injury. In: Bader DL, ed. Pressure sores: clinical practice and scientific approach. Basingstoke: Macmillan, 1990: 97-115. 17. Faist E, Barre AE, Dittmer H, Heberer G. Multiple organ failure in polytrauma patients. J Trauma 1983; 23: 775-87. 18. Guttmann L. The problem of treatment of pressure sores in spinal paraplegics. Br J Plast Surg 1955; 8: 196-213. 19. Bader DL. Effects of compressive loading regimens on tissue viability. In: Bader DL, ed. Pressure sores: clinical practice and scientific approach. Basingstoke: Macmillan, 1990: 191-201. 20. Editorial. Preventing pressure sores. Lancet 1990; 335: 1311-12. 21. Munro D. Care of the back following spinal cord injuries: a consideration of bed sores. N Engl J Med 1940; 223: 391-98.
CLINICAL PRACTICE Acute pressure area
care:
Sir James
Paget’s legacy
M. R. BLISS In 1862, Sir James Paget gave the address in surgery to the thirtieth annual meeting of the British Medical Association.1 Me now speak of some of /[the] that are not "Let me [the] things... things in the natural ( postoperative course; and chiefly that I may take occasion to point out the need of a much more minute record and analysis than has yet been made of the causes of danger and mortality after operataions. operations. Much has been done to ascertain the general mortality of each capital operation; and it has been done so well, and so laboriously, that it may seem ungracious to say that it is now time to do something more and better. Yet it is certain that we want to know what are, after each operation in each hospital, and in different modes of practice, not only the several total amounts but the several causes of danger or of death. In short, our tables of mortality after operations must be more minute in details, in order that, having better knowledge of the several dangers that are near, we may have better means of coping with them."
"Let
...
off the blood supply are greater in the region of a hard object such as a bone than in the skin. Consequently, deep pressure sores characteristically have overhanging edges, and apparently small skin lesions may interconnect by subcutaneous sinuses extending for many centimetres under intact skin (fig 2). As Paget observed, these sinuses result from breakdown of dead tissue produced during the original ischaemic episode; they are not, as is so commonly asserted, due to pressure or infection from a superficial sore spreading into the deeper layers. BODY WEIGHT
emphasise that causes of morbidity were important as causes of mortality in revealing just underlying abnormalities and suggesting remedies. He went
on to
as
"We have much to learn... in every case of erysipelas, pyaemia and the like, we ought to work until we can discover its probable origin ; we should have the strongest feeling that these diseases are not spontaneous and inevitable."
Paget did not specifically mention pressure sores in his list of postoperative complications, probably because patients undergoing surgery in the nineteenth century either did not survive long enough to get them, or were too young and otherwise healthy to be at risk. However, like Hunter and Charcot,3 he regarded management of pressure sores as essential to the practice of surgery. He included bedsores in the series of lectures given at St Bartholomew’s Hospital, London, and the Royal College of Surgeons that formed the basis of modem medical student teaching and led to the requirement of a medical degree for the practice of surgery in 1866. Having spent the first 7 years of his London career studying pathology, Paget began his lecture4 with a pathological definition of a bedsore as "the sloughing and mortification or death of a part produced by pressure". He identified certain "forerunners": "inflammation affecting prominent parts", usually the sacrum, the posterior superior spines of the ilium, the trochanters, and the ends of the spines of the vertebrae. That he did not mention the ischial tuberosities is probably because ill patients in his day did not sit in chairs. He described other signs of pressure damage as "pale or white patches" or "purple or yellow discoloration from the extravasation of blood or bloody fluid". "Sloughing follows these in the skin and subcutaneous tissue and fat. These latter die before the skin as sloughing proceeds faster in them, so when the skin comes away, the place formerly occupied by these tissues is empty." These careful observations anticipate later studies in animals5-7 and tissue viability measurements in man,8 which have shown that interstitial sores occur primarily in the deep tissues surrounding an underlying bony prominence (fig 1). Pressure differences which cause capillary distortion and cut
Fig 1-Diagram showing how tissue deformation under pressure may give rise to superficial and deep sores.
Fig 2--Interstitial pelvic
pressure sores (in a woman with multiple sclerosis) interconnected by subcutaneous sinuses.
Importance of illness Paget went on to talk about conditions that predispose to pressure sores: "the old, especially those with fractured neck of femur"; "the fattest and heaviest", but also "the thinnest"; "stages of fever". He mentioned typhus, in which "the whole system is so poor and degenerated that sloughing ADDRESS Department of Medicine for the Elderly, Hospital, London E9 6BE, UK (Dr M. R Bliss, MRCP).
Hackney
222
takes place without any pressure at all"-for example, "at the ends of the nose, ears, &c". Similar observations have recently been made of muscle necrosis in critically ill patients with multiorgan failure.9 Research interest is now focusing on the effects of free radicals and endothelial changes produced by bacterial and other toxins that precipitate microthrombi and tissue damage.10 Nevertheless, we should remember Paget’s observation: "as soon as the local disease is removed, the bedsores heal very
rapidly". No trophic
nerves
cautious about Charcot’s contention3that at least partly caused by the interruption of "trophic nerves" in patients with spinal cord injury and apoplexy. Charcot’s misapprehension was probably influenced by the appalling standards of surgery and nursing in French hospitals in his day.1 Most of the examples he gave were complicated by myelitis, and pressure necrosis in very ill patients may result from pressure so slight as not to seem like pressure at all. Most of Charcot’s patients were catheterised, and he himself noted the association of sores with "purulent urine". He was impressed by the rapid "muscular atrophy" that occurred in patients who got sores, and did not think that sensory loss was important. Paget disagreed: in another lecture," he discussed cases of corneal ulceration following section of the Vth nerve, noting the inconstant effect of nerve section on tissues. Like Brown-S6quard, 12 he found no impairment of nutrition and healing in paralysed limbs, but that they were much more vulnerable to injury. He observed that ulceration of the eye was usually worse when section was distal rather than proximal to the trigeminal ganglion, and wondered whether this might be due to interruption of sympathetic nerves from the superior cervical ganglion. This observation may be relevant to spinal injury practiceparaplegic patients with low spinal lesions are more vulnerable to pressure sores than quadriplegics with high lesions, a difference which cannot be explained solely by differences in nursing care.
Paget
pressure
was
sores-ie, tissue necrosis-were
An acute
injury
How quickly do pressure sores develop? According to Paget, "The risk of bed sores in the old with fractured neck of femur is chiefly in the first week; therefore treatment with a view to preventing them should commence immediately the patient takes to bed. After the first week, the risk is not nearly so great". This observation takes the breath away from Versluysen’s mid-1980 studies in the orthopaedic wards at St Bartholomew’s and Hackney Hospitals,13,14 in which she showed not only the very high frequency of sores in this condition (over 60% of patients in both hospitals) but also that 50% of the sores occurred, as Paget predicted, within the first week of injury. Versluysen concluded that the main factor was the poor physical condition of these frail patients after major trauma, and that methods of nursing care were only partly responsible. Her figures indicate, however, little progress in prevention, which suggests that early ambulation or chair-nursing are ineffective, if not injurious, methods of managing these acutely sick patients. In fracture of the spine, Paget noted that sores usually appear within 2 or 3 days. This observation likewise accords with modem studies. Thus, Richardson and Meyer15 found that 134 of 180 patients admitted to a spinal centre 72 hours after injury had sores, compared with none of 122 patients
Fig 3--Pelvic
in
young paraplegic patient. (a) Before surgery; (b) the best result that plastic surgery could achieve pressure
sores
admitted earlier. There
a
three main reasons why new such high risk. First, they often spinal injury patients have multiple injuries (eg, head or chest injuries, limb fractures) in addition to their spinal fracture/6 so they are likely to have hypoxia or reduced tissue oxygen uptake." Second, they are in a state of spinal shock.18 The cause of the vasomotor paralysis that occurs immediately after spinal cord injury and lasts for up to 3 months is still not clearly understood. However, it has profound effects, both on the deformability of the tissues, and hence the extent of capillary occlusion under pressure, and on the ability of the microcirculation to respond to the effects of ischaemia by reactive hyperaemia. Some patients with chronic spinal lesions have continuing abnormal vasomotor responses to repeated skin loading.19 The third reason why patients with spinal cord injury are at such high risk of pressure necrosis is the almost complete lack of medical training in acute pressure area care. By the time the patient is transferred to a specialist unit, it is too late (fig 3). About 35% of the work of modem spinal units is concerned with repairing the damage done to patients during acute or respite admissions to district general hospitals; the fact that it is no longer 100%, as it was when these centres were first established, is due entirely to their improved ability to admit patients immediately after injury, and not to better medical education. Spinal specialists themselves are to some extent responsible for this continuing neglect by their emphasis on the importance of direct admission rather than on improved training in medical schools. However, direct admission is not always possible-eg, in patients with multiple trauma who may require other specialist services-and cannot help patients are
are at
223
in other at-risk groups, such disease or the elderly.
as
those with
Remember to prevent
neurological
Medical training
Paget emphasised the need for training doctors in basic pressure area care, especially in prevention. Now let us look at the means of preventing bedsores, for ninetenths of your care must be devoted to this; for if once they appear, it is very difficult to get rid of them.... "First of all, look to the bed. Good bedmaking is an indispensable thing in the prevention of bed sores."
Unfortunately, the emphasis on chair-nursing to prevent bedsores that has dominated geriatric and general hospital practice for the past 40 years, in the mistaken belief that pressure sores are caused by immobility in bed rather than illness, has caused nurses to lose many of the bed-nursing skills evolved by their predecessors-eg, end-of-bed pleats and bedcradles to relieve pressure over the heels. Paget described a flotation water bed consisting of a deep chest covered with a waterproof sheet sufficiently loose to adapt itself to every part of the patient, noting that a patient "might lie on this for years and never have a sore". "Inferior to this, but still quite good", he says, is a bed on which the waterproof sheet is tight. "They will avert bedsores for a long time, but I would not say that a patient would never get a bedsore on them". However, he highlights the main disadvantage of flotation beds: "You cannot have these everywhere; you can’t take them about to everyone who may need them, and there are many cases in which they cannot be used at all, as in cases of fractured neck of femur, acute inflammation of the knee joint and many others". In lieu of anything better, he recommended an ordinary horsehair mattress, but noted that it should be placed on a firm surface, preferably on boards. He also "utterly condemns" feather beds. This should make us wonder what might be the results of a randomised controlled trial of the fibre overlays now in such widespread use. He discusses methods of "hardening the skin’ by means of nitrous ether-or whisky in Scotland or brandy in England. These methods probably worked because patients had to be turned over to apply them, and their wholesale condemnation, together with uncritical reliance on chairnursing, may be one of the reasons for the continuing high prevalence of pressure sores-affecting up to 10% of all patients in western hospitals.2O
Repositioning Are frequent changes of posture important? According to Paget, "If a patient can lie in 4 different positions during the day, bedsores may be prevented. He may lie on his back, each side, and on his face". This method, re-employed by Guttmann in the UK18 and by Munro2l and his colleagues in the USA for treating ex-servicemen with spinal injuries invalided home during the 1939-45 war, still forms the mainstay of management in paraplegia. The frequency of turning is reduced from 2 hourly to 4 hourly or less as the patient recovers from spinal shock, but is increased again whenever he gets any new illness or pressure marks on the skin. Nevertheless, as Paget observed, "You can’t make a stout person lie on his face; he would simply suffocate". He discussed the benefits of a divided mattress, but noted that this is likely to cause sores on the ilium and trochanters. "Large cushions made in the shape of a horseshoe may help." But, most important of all, he warned, "in speaking of the mode of curing bedsores already formed, let me remind you to continue your preventive treatment just as if there were none, lest they come on other parts".
How many patients undergo operations for repair of pressure sores today only to get new areas of tissue death elsewhere? Only a few years ago a case was presented at a grand round at a London teaching hospital as a triumph of plastic surgery. A young man had undergone repair of an ischial pressure sore and had been allowed to go to a wedding in a wheelchair in the early postoperative period. As a result, he got necrosis of the skin flap which necessitated amputation of his leg so that a muscle plication operation could be carried out to cover the new injured area. Pressure sores are a serious component of multiorgan failure in very sick or injured patients. As the numbers of elderly patients and those with chronic disease in the population increase, morbidity and mortality due to pressure sores must also increase-unless doctors stop thinking of these lesions as injuries unworthy of their attention and follow the example of Sir James Paget, for whom no observation was too trivial, no detail of management too menial, so long as it might improve the wellbeing of his patients. This article is based on a lecture to the 10th anniversary autumn conference of the Tissue Viability Society, Queen Mary and Westfield College, London,
Sept 19-20, 1991. I thank the Department of Medical Illustration, St Bartholomew’s Hospital for fig 1, Mr M. Johnson, medical photographer, Homerton Hospital, for fig 2, and Prof J. T. Scales, Mount Vernon and the Radium Institute, London, for fig 3.
REFERENCES
Paget J. The address in surgery read at the thirteenth annual meeting of the British Medical Association. Br Med J 1862; ii: 155-62. 2. Hunter J. Lectures on the principles of surgery: functions of nutrition and absorption. In: Palmer JF, ed. Works of John Hunter, vol 1. London: Longman, Rees, Orme, Brown, Green and Longman, 1835: 247-58. 3. Charcot JM. Lectures on diseases of the nervous system. Translated by Sigerson G. London: New Sydenham Society, 1877. 4. Paget J. Clinical lecture on bedsores. Students J Hosp Gazette (London) 1.
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