Bums (1991) 17, (4), 329-334
Printedin Great Britain
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The evolution of burn treatment in the last 50 years* D. M. Jackson Formerly Surgeon in Charge, Bums Unit, Accident Hospital, Birmingham,
Introduction
The formation of burn research units
I have chosen to limit this review of bum treatment to the last 50 years because a great awakening of bum interest began in the decade centred on 1940; that is, between 1935 and 1945. This is not to belittle the studies of men like Underhill, Davidson and Pack in the USA in the 1920s and 1930s; there are always a few early risers before the bell goes for any general awakening. Before 1940, in Britain, a person with more than 30 per cent of the body surface area burned might well have been given a good dose of morphia by his general medical practitioner, and considerately left at home to die among his own relatives. Now, in contrast, such a patient is the object of keen, costly, multidisciplinary care in a well-ventilated, highly staffed specialist unit. This is my subject today: the contrast from bums being ‘nobody’s child’ fo having a privileged position in a special unit. What was the cause of this awakening! I believe it was threefold. First, between 1935 and 1940, sulphanilamide and penicillin and then plasma became available for clinical use. They were effective remedies against the two commonest killing complications of extensive bums, shock and infection. They offered new hope. The second factor was the prospect and then the reality of service and civilian casualties in World War II. The war concentrated minds, money and manpower powerfully on improving bum care. The third factor, I believe, was the timely invasion of clinical medicine and surgery by the scientific method. Clinicians were seeing more clearly the need for measurement, statistically controlled trials, and experiment. It was an idea whose time had come. Immense improvements have evolved since then, measurable by mortality, healing time and restored function, and I suggest to you that this progress has been due principally to three factors: I. The formation of bum research units. II. A better understanding of the bum wound. III. New and improved techniques. *Based on a Guest Lecture at the 8th International Injuries 1990, New Delhi, India 0 1991 Butterworth-Heinemann 0305-4179/91/040329-06
UK
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Congress
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What is a bums unit? First, a bums unit is a place, a building. It should be sited in or near a general hospital so that it can draw on the expertise of other disciplines. If that hospital is a teaching hospital, students and nurses will learn bum care as part of their training. A bums unit fits well into an accident hospital as they both work to the same emergency tempo; and it can be well linked to a plastic surgery unit that takes emergencies, making use of their special skin-grafting skills and experience. In Britain, a 30--40-bed bums unit, centrally placed in a big city, can meet the needs of a regional population of about five million people. A bums unit is also a centre where burns are collected. Burns are unsuitable for clean surgical wards. They are also a danger when scattered around the side wards of a general hospital where, too often, they are visited infrequently, are put last on the operating list, and in general are left to inexperienced junior staff. In a bums unit they cannot avoid being the centre of attention, the first consideration, the primary challenge - and this is what they need. Only when bums are collected for treatment is the stage set for research and advance. A well-run dressing clinic for outpatient bums should be part of the unit. Thirdly, a bums unit is a service - a 24-hour emergency service of expert medical and nursing care. For the team, the work is demanding and requires commitment and discipline. Emphasis must be placed on the prevention of ‘shock’ and infection, which means getting casualties very soon after burning. This in turn means teaching the public the urgency of treatment through the media, and ambulance and casualty teams must be taught not to touch exposed burns by hand but wrap them in sterile towels and sheets until they reach the bums unit. Agreement to by-pass a general hospital to reach the bums centre may have to be arranged. Basically, a bums unit needs admission and shock rooms, as clean as an operating theatre, where the patient can be undressed, recovered with sterile towels, transfused, catheterized and examined in a good light without disturbing other patients. A bums unit also needs a dressing room and a saline bathroom, each with clean positive-pressure ventilation to prevent air-borne infec-
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tion. Several separate cubicles are needed to isolate infected and noisy patients. Cotton sheets and blankets which can be sterilized should replace more usual woollen blankets. Mattresses should be covered with mackintosh so that they can be easily cleaned and sterilized between patients. Plates, cups and cutlery should be sterilized after use, and so should bedpans; but all this, and more, is useless without a strict discipline to prevent cross-infection between patients, by everyone. I have sketched an ideal. Disciplined habits to prevent infection cost nothing, but money for expensive buildings and equipment is hard to come by. I well remember my own arrival at the Birmingham Bums Unit in 1948. The hospital was over a hundred years old, and the building had been given up as unfit to be part of the Teaching Hospital, but a keen spirit of service was very much alive. An air-conditioned Dressing Station had been introduced by Leonard Colebrook, the first Director, and we were fortunately unlimited in supplies of plasma, blood and penicillin. On the negative side we had periods of understaffing and overcrowding, with overflow patients nursed in cold, dark, draughty, corridors. At first we had only one hand-basin in each X)-bedded ward, and no cubicles or curtains; but every few years small improvements were made. Some of you, I know, face much greater difficulties today - in old buildings, nursing patients on the floor, and without adequate blood, plasma, antibiotics and topical creams. If this is your situation, do not give up because you are not in an ivory bums unit. Pick out the best practices from the past for your particular situation and work for better times. 4. Lastly, a bums unit should be a research wit. One great advantage we had in Birmingham was a Medical Research Council team working in the same building. Four or five specialist research workers - in bacteriology, biochemistry, tissue culture, blood volume measurement and histology - played a major part in the clinical research of the Unit. They asked questions, offered help, and joined in running clinical controlled trials of promising new methods. Through their work we developed closer links with the Teaching Hospital, the Medical School and with industry. When many cases of a single condition are collected together - whether it be head injuries, spinal injuries or bums - it is too great an opportunity to miss. As well as upgrading the delivery of treatment to contemporary patients, controlled trials offer a priceless opportunity for gaining new knowledge and skills for patients in the future. Of course, isolated workers in the past have sometimes made big advances, but the most productive units have been those with one or more research specialists. However, even an isolated surgeon should measure his own results. He should know his bum mortality and morbidity: he needs a standard to beat next year.
II. The character of the burn wound If the greatest influence on bum treatment in the last SO years has been the setting up of bums units, the second has been growth in our understanding of the bum wound. Five characteristics of burns are detailed below. 1. A burn leaks like a sieve In the 1920s and 1930s the loss of fluid and protein from the circulation through a bum was well recognized (Underhill et
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al., 1930; Wilson et al., 1938), but plasma and serum for infusion were not available. Clinicians still treated the shock of extensive bums with one or two small, half-litre infusions of saline or gum-saline. This explains why, for instance, in 1937-41, in the Glasgow Royal Infirmary Bums Ward, 49 per cent, or a half of deaths, occurred within 24 hours of burning, and 72 per cent of deaths were within 3 days of burning (Colebrook et al., 1945). Shock was the commonest cause of death. Now, with adequate infusion, the mortality from shock is about 5 per cent of all burn deaths. What leaks from the bum? The loss of plasma from the circulation on the first day after, say, a 60 per cent bum, can amount to 7 litres. Even after the shock period water loss through such a bum can be 2-3 litres a day, but this can usually be replaced by oral fluids. This early exudate has a protein content of 3 g/dl, which means that the protein loss through the bum may be 60-90 g a day, or more than a man’s normal protein intake in health. Every litre of this exudate that evaporates from the actual body surface cools the body by about 600K calories. TO correct the consequent raised metabolic rate extensive burns are now usually nursed at about 80°F (27°C). Even a seemingly dry coagulated bum surface loses water vapour at 10 times the rate of that from normal skin. One more constituent which is lost in this ‘torrent’ of exudate is living leucocytes. These too escape through the burned tissue, some of them supplying the collagenase to digest and separate the slough. 2. A burn with its warm moist nutritious slough grows bacteria like a cooked-meat culture plate This has been appreciated at least since 1886, when doctors began to treat bums with antiseptics, such as carbolic oil (Dunbar, 1934). I well remember in 1939 a new 20 per cent bum was admitted against all the rules at my London Teaching Hospital. It produced a minor crisis. A bum could certainly not be admitted to a clean surgical ward, so this new clean wound was sent to the Septic Ward, where carbuncles and ischiorectal abscesses were drained, to have shock treatment; and then the patient was transfered to another hospital as soon as possible. That Teaching Hospital, I am glad to say, now has a well-known Bums Unit. Another feature of the extensive bum wound which must encourage invasive infection is the wide portal of entry for infection. However the likelihood of invasion and septicaemia seems to be linked more to the number of bacteria in the eschar, particularly if it is more than 10 to the power of 5 organisms/g in the tissues. 3. A burn is also a sheet of blotting paper While oedema fluid is flowing out through a recent bum under pressure, topical drugs can be absorbed into the body - against the tide as it were. This should make us very careful what topical substances we put on burns. Before 1940, topical tannic and pi& acids had been suspected of causing liver damage. In 1945, Colebrook described the absorption of sulphanilamide from a topical cream. In Birmingham in 1951, we found lactose in the urine after using penicillin in lactose powder on the bum surface. In 1966, Proctor reported fatal cases of coma and renal failure after dressing bums with 80 per cent hexylene glycol; and in another unit, 3 per cent hexachlorophene solution, used for cleaning bums before grafting, produced convulsions (Larson, 1967). The topical use of polybactrin powder for
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Jackson: Evolution of burn treatment bums, which contains neomycin sulphate, is now recognized as capable of causing permanent nerve deafness. This is not only a danger of hospital treatments. I remember a folk remedy near Bombay in the 1970s: a man’s bums had been painted with the local ink. His urine became bright green. Analysis of the ink showed a high concentration of the salts of heavy metals which could well have produced renal damage. Toxic absorption of industrial chemicals such as chromic acid and phenol through the skin is well documented, and some cases have proved fatal. If seen early, urgent tangential excision to remove remaining chemical in the burned skin may be indicated. 4. The difference between intensity and depth of burning A bum is a three-dimensional lesion; and, whether viewed from the surface or in section, there are typically three zones of intensity of burning - the zones of hyperaemia, stasis and coagulation. The surface of the intermediate ‘zone of stasis’ has a mottled pink colour at first which blanches on pressure, showing it has a capillary circulation. Then, after some minutes or hours, the pink areas cease to blanch on pressure because the dilated, leaking capillaries become stuffed with red cells and the flow becomes static. By 3 days postbum, the pink mottling of the zone of stasis disappears, and the now white slough liquefies and separates in the next 2-3 weeks. In 1942, it was still thought that this blanching on pressure in the zone of stasis was evidence of partial skin loss (National Research Council of Canada, 1942), but the sign has no sign(ticance regarding the depth of necrosis. In fact, all that the eye can see is the intensity of burning on the skin surface; whereas partial and full thickness skin loss depend on the viability of the epithelial elements on the undersurface of the skin, 0.5-0.7 mm deeper. For example, an electric flash bum can carbonize the skin surface but produce only a very shallow bum which will heal in 7-10 days. By 1949, Bull and Lennard-Jones (1949) published their studies on the reduced sensitivity to pin-prick after deep burning. The pin-prick test is a non-invasive way of diagnosing the viability of the deepest epithelial elements in the dermis. Its great advantage is that it needs no equipment except a sterile needle. It is most accurate on the day of burning, so one can understand that surgeons who receive their bums late are less impressed with the method. It should nof be used for bums of the face, scalp, palms and soles where epithelial elements extend more deeply; nor should it be used for chemical bums like phenol. The test should be interpreted in this way. Appreciation of firm pin-prick as sharp, and not just touch, signifies partial skin loss which will heal in 3 weeks. Analgesia (pin-prick felt as touch only) signifies either full thickness skin loss, or deep partial skin loss which will take 4 or more weeks to heal and may result in considerable scarring. This is sufficient information for a decision on whether to proceed with tangential excision and grafting. Our practice was to tangentially excise only analgesic bums. At operation, red dermis and red fat are further physical signs which show the depth of the zone of stasis. 5. The reversible nature of ‘zone of stasis burning’ As early as 1950, we were familiar with the pink ‘zone of stasis’ bum ceasing to blanche on pressure in the first day after burning, and becoming white by the third day. This
happened under a penicillin cream dressing or under tulle gras, and we regarded it as inevitable: necrosis, it seemed, was the result of progressive capillary stasis and ischaemia. By 1967-68, following Zora Janzekovic’s introduction of tangential excision, our practice was to excise to normal bleeding dermis or subcutaneous tissue before grafting. However, one day, during a deep excision of the front of a child’s fingers, we found that the digital nerves were only covered with a thin layer of red, ‘zone of stasis’ fat. A split skin autograft took well on this red fat, showing it was not essential to remove it all. No doubt others have discovered this too. However, it was Zawacki (1974a,b) who showed experimentally in guinea-pigs that a full skin thickness ‘zone of stasis’ bum was a reversible injury if the surface was covered with fresh porcine skin graft. Instead of capillary stasis proceeding to necrosis, the capillaries regained their circulation and much of the affected dermis survived. At first it seemed that this might be due to preventing drying, but keeping the bum surface wet with an oil-in-water cream did not reverse capillary stasis. To summarize this section, just as a carpenter must know the properties of the types of wood he works with, so we cannot know too much about the bum wound. There is much still to discover.
Development of techniques for treating shock, infection and the open wound
III.
This, I believe, is the third factor which has been responsible for the rapid evolution of bum treatment in these last 50 years. 1. Techniques in the treatment of bum shock 1940 was an important milestone in the prevention and treatment of bum shock - in Britain at least. Until then, bums were debrided and tanned under anaesthesia on admission. Intravenous therapy consisted of one or two small infusions of dextrose saline or gum-saline, often with transient improvements, but total volumes were completely inadequate by present standards. A systolic blood pressure down to 60mmHg was judged as only moderate shock, and another case of shock was described as corrected although the haemoglobin level remained at 112-130 per cent of normal for almost 3 days. It was this prolonged hypovolaemia that produced the generalized illness, which was called ‘toxaemia’. The jaundice and central lobular necrosis of the liver which were sometimes seen in these cases may have been due to prolonged liver anoxia or to absorption of tannic acid. It is interesting to note that both complications, the jaundice and the liver necrosis, ceased when adequate resuscitation with plasma was introduced and tanning was replaced by suphanilamide cream. In November 1940, Black advised giving half-strength plasma (which was just becoming available) to keep the burned patient’s haemoglobin below 110 per cent of normal. The infusion was to be started before general anaesthesia and tanning, and continued for 1-2 days, reviewing the patient’s condition every 2-3 h. The 3-4 litres he advised was S-10 times what would have been given as gum-saline a year before. This was the beginning of modem bum shock therapy in Britain. By the end of World War II the prevention of shock by early plasma infusion was well established, and deaths from shock in bums units were down to 5 per cent of all deaths. This was the first dramatic change in bum mortality.
332 During the 1950s, the measurement of blood volume and red cell destruction with radioactive isotopes gave precision to clinical treatment, and confirmed that colloid restored blood volume better than electrolyte solutions. Topley (1961) also showed that 20-40per cent of the red cell mass might be destroyed in the shock stage in extensive bums, requiring blood transfusion. This can be predicted: more than 2 per cent of microcytes at the head of the blood film in greater than 10 per cent bums will probably have 30 per cent or more of red cell loss later (Topley and Jackson, 195 7; Topley, I96 I). there has been a tendency, especially in Since the 196Os, the USA, to use more crystalloid solution, on the grounds that both leak freely from the circulation in the early hours after burning. Most surgeons in Britain, however, have continued to use considerable colloid, especially for children. Human plasma protein fraction, like 6 per cent Dextran in saline, is free from hepatitis risk. A good trend has been to break away from formulae for intravenous therapy except as a guide for the first hour, and to manage each patient by monitoring his/her haematocrit or haemoglobin, his/her urine output and concentration and other physiological responses to treatment. The goal is for the patient to reach 48 h without peripheral failure, renal failure or pulmonary oedema, and with the least risk of complications. Today the urgent global need is to make the effective treatment we already have available to the thousands who die without it in less fortunate situations. The difficulty often is to get the burned patient to medical care soon enough.
2. Techniques in the treatment of infection I have referred to the awakening of interest in the burned patient which followed Dunbar’s review in 1934. In that paper he stated that ‘A bum case when seen at once is sterile, but within 12 hours the streptococcus haemolyticus can be grown in 80 per cent of cases’ (p. 244). A year later, Dr Robert Cruickshank, a bacteriologist, writing about the same bum wards, reported that ‘66 per cent of the burned patients had haemolytic streptococci in their wounds 3-6 days after admission, compared with I1 per cent at the time of admission’. He also observed that haemolytic streptococci were frequently present in considerable numbers in the air of the bum wards, whereas they were found only in small numbers in the general surgical wards, and not at all (in his experience) in the medical wards of the hospital. To overcome the serious graft failure caused by streptococcal colonization at that time, pinch grafts were pushed into the infected granulation tissue with a blunt glass rod - a practice known as the ‘tunnelling of granulations’. So, in 1935, infection was being diagnosed and its incidence measured. Tannic acid, used by Dunlop in 1883 and soon abandoned, was popularized by Davidson (1926) and Wilson (1938) in the 1920sto decrease fluid loss, relieve pain and get a better eschar. It was easy to apply, and widely used for 15 or 20 years. Good results were obtained with shallow bums, but infection collected under the thick coagulated eschar of deep bums and there was no definite improvement in overall mortality. Tannic acid was also condemned by M&doe (1940) as a result of its use in treating the hands and faces of burned air crews in the Battle of Britain: he often found that fingers were fixed in flexion in hard crusts for weeks and became clawed and crippled, so he turned to saline soaks, sometimes
Bums (1991) Vol. 17/No.4 for as long as 4 hat a time. It is not surprising that tannic acid should have been followed by plain ‘exposure treatment’, and this was encouraged by Blocker in the States and by Wallace in Britain in the late 1940s. With exposure, there was nothing to prevent the bum being colonized with bacteria from the air or by contact, but relative dryness discouraged the growth of some dangerous bacteria such as pseudomonas. An opposing school led by Harvey Allen and in Chicago championed the treatment of bums Koch (1942) with paraffin gauze and a bulky cotton wool dressing and bandage, without topical antiseptics or antibiotics. I am not aware of any conclusive comparisons of these two methods. At this time Leonard Colebrook, a bacteriologist, entered the bum stage in Britain. He had been involved in the early successful trials of prontosil for puerperal sepsis, and had then studied war wound infections in France. He was convinced that infection in bums could be prevented and he proposed a triple approach, using a no-touch dressing technique (that is, using sterile instruments only), a topical antibacterial cream, and a dressing room air conditioned with filtered air under positive pressure. This concept, this triple combination, this seed, is still growing into a tree. Colebrook’s first choice of a topical agent, 1 per cent sulphanilamide cream, was not successful: the predominant streptococcal strain was very soon completely resistant, But by 1943, penicillin had become available, and he was able to report that 76 per cent of burns infected with haemolytic streptococci, when treated with penicillin cream (500units per g), lost their streptoccoci within 5 days (Colebrook et al., 1945). Later, in a controlled trial, only 2 per cent of bum sites treated with penicillin cream aquired Strep. pyogenes, in contrast to 38 per cent without penicillin (Jackson et al., zssrb). The next controlled trial we carried out assessed the prophylactic value of polymyxin cream (0.1per cent) in preventing colonization with Ps. pyocyunea (aemginosa). Only 7 per cent of bums treated with polymyxin cream acquired Ps. pyocyunea, compared with 24 per cent treated without polymyxin. Treatment with polymyxin cream also reduced the average healing time by 3 weeks, and improved graft take (Jackson et al., 195la). In the middle 196Os,several new antimicrobial substances were introduced to combat pseudomonas, which was still the commonest cause of fatal bum septicaemia. Carl Moyer, in 1965, introduced 0.5 per cent silver nitrate compresses: in our trial of this method only 3.1 per cent of silver nitrate cases grew pseudomonas, compared with 70 per cent of controls treated with penicillin cream - an impressive protection indeed (Moyer et al., 1965). In 1966,Moncrief, Lindberg and others introduced 10 per cent sulphamylon cream. Gentamicin next became available, and then carbenicillin; but carbenicillin-resistant pseudomonas organisms soon appeared, and we had to reserve this drug for septicaemias only. This outburst of effective new drugs against Gram-negative infection was the cause of the second big breakthrough in improving bum mortality in this half century - the first being adequate plasma infusion for shock in 1940. In 1968, 1 per cent silver sulphadiazine cream, or Flamazine, was introduced by Fox in the USA. It compared well with silver nitrate compresses and with silver nitrate and chlorhexidine cream in protecting against Ps. aemginosa and proteus but silver sulphadiazine was more effective against colifoxms (Lowbury et al., 1976). After about 6 months, however, resistance developed against silver sulphadiazine and we were glad to have silver nitrate and
Jackson: Evolution of burn treatment chlorhexidine cream to fall back on. The concept of having alternative barriers against infection which can be rotated in sequence is most helpful. As Lowbury has aptly put it. ‘The battle is between human wits and the ability of bacteria to develop resistance to previously effective antibiotics’. Every bum unit needs to monitor its own bacterial and resistance patterns continuously. 3. Techniques in early wound closure Before 1940, skin grafts for bums were usually applied to granulations 3-4 weeks after burning. Excision of full thickness bums on the day of injury was rarely performed. Surgeons were held back by uncertainty about the depth of burning and the fear of making a scar where there need not be one. By the mid 1940s, the experience of war wounds and the Pin-prick Test (in 1949) for the depth of bum necrosis made primary excision routine in bums units for small analgesic bums, except on the face and scalp, and palms and soles. In Birmingham, for instance, we frequently received bums on the feet of foundry workers from splashes of molten metal; there were usually several discrete, deep bums where molten metal had run into a caster’s protective boots. With excision and grafting on the same day, these men were healed and back at work in heavy boots a month sooner than previously. Inevitably, in the I~SOS, the size of bums treated by primary excision and grafting increased to 5 per cent, then 10 per cent, and even up to 25 per cent. There were two main problems - how to limit, measure and replace blood loss, and how to provide sufficient autograft to close the excised wound. At the end of the 1950s, to reduce bleeding during excision, we were limited to tipping the operating table and elevating the excision site. Tourniquets were used whenever possible, and coagulation diathermy. For safety, as excisions grew to 20-30 per cent, operation blood loss was monitored by swab-weighing and replaced as it occurred. The blood loss sometimes amounted to a litre in a 3 year old (or one blood volume), or to 3 litres in an adult. The patient’s blood volume was checked before and after surgery using radioactive isotopes, and corrected if necessary. My strong advice to those starting large excisions is to start small-say, with 5 per cent or less. In 1960, a controlled trial was completed, comparing primary excision and grafting of whole skin loss bums up to 25 per cent with grafting in the third week. The result was disappointing because the mean graft take was only 70 per cent in both groups due equally to subgraft haemorrhage and infection. Although we used alternate strips of autograft and homograft to extend the amount of permanent cover, we had no homograft bank from which to correct graft failure at once. By 1970, a decade later, the new antimicrobials had made bum excision on the day of injury less necessary, and it was accepted that excision at 72 h was both safer and easier. In 1968, Zora Janzekovic published her new method of tangential excision and grafting which she had been using for 8 years. This simple technique, requiring only a skin-graft knife, offered a visual method of confirming the depth of burning as repeated slices of necrotic bum were removed down to a viable surface which would take a graft. The method had a particular advantage in bums of mixed depth, One part of the bum could be excised down to deep fascia and autografted, while a contiguous partial thickness area
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could be tangentially excised and homografted. The important thing being that the whole wound was closed, greatly reducing the risk of postoperative infection. In the 196Os, too, Tanner introduced his method of mesh-grafting (Tanner et al., 1964). Clearly it was less perfect as complete skin cover, but by covering it with a finer mesh of homograft the wound was almost closed while still leaving opportunity for subgraft oozing to drain. The 1960s was also the decade when skin banks of cadaver homograft were developed in US bum centres, so that it was always possible to close excised or granulating bums without delay when sufficient autograft was not available (Shuck et al., 1969). Banked homograft was also used as a final preparation of the wound surface before autografting. Throughout the 1970s, enthusiasm for early excision continued, especially for large bums of more than 40 per cent of the body surface area to reduce the mortality rate. Great interest was aroused when Burke and his team (1975) in Boston succeeded in making homografts survive for many weeks in children by immunosuppression with azathioprine or antithymic globulin. The homograft was later excised and replaced with autograft as it became available. The children treated by Burke in this way had 80 per cent bums with no expected chance of survival from previous experience, but seven out of 11 survived and returned to school. Septic complications were successfully treated with antibiotics in spite of immunosuppression. Also in the 1970s, various instruments were evaluated for limiting blood loss during excision. Cutting diathermy, the carbon dioxide laser and the laser scalpel were compared with ordinary scalpel excision. Levine et al. (197.5) for example, using a 100-W American laser, found excision and haemostasis one and a half times faster than with scalpel excision. In contrast, using a 50-W laser, although we found laser blood loss was reduced to 73 per cent of scalpel blood loss, the laser speed of excision was appreciably slower (71 per cent of scalpel speed), making it a doubtful overall advantage (Jackson and Cason, 1977). It was not until the 1980s that early excision and grafting of extensive bums, without immunosuppression, was clearly shown to reduce mortality. Since the 194Os, it had been a way of securing more rapid healing and a better graft texture for smaller analgesic bums; that is, for bums that were deep partial or full thickness skin-loss. But as excisions increased in size, it became difficult to control blood loss and, even more, to close the excised wound completely at the same operation to prevent infection. The technique required considerable surgical experience, transfusion of large amounts of safe blood, adequate banks of fresh and frozen cadaver skin grafts and an instrument to mesh them. The problems are well discussed in an Intemational Round-Table Discussion entitled ‘Early Excision of Thermal Bums’, led by Dr David Heimbach in Geneva in 1987 (Heimbach et al., 1988). In 1989, Hemdon and his team in Galveston reported their comparison of early excision and conservative treatment. The patients in the trial were between 17 and 30 years of age, without inhalation injury, and their bums were between 30 and 98 per cent of the total body surface area. ‘Early excision’ was complete excision of all full skin thickness bum to the level of deep fascia within 72 h of admission. Excised wounds were covered immediately with expanded autograft (meshed 4 : 1) and overlaid with cadaver homograft (meshed 2 : 1). When all the autograft was used, the remaining raw area was covered with cadaver homo-
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graft, and this was replaced later with further meshed autograft and homograft overlay as autograft became available. ‘Conservative treatment’ involved daily washing, topical antimicrobial agents and grafting, when the wounds granulated, with less widely expanded autografts and without cadaver skin. The mortality rates of these two groups were 9 per cent and 45 per cent respectively. This might seem like the end of a chapter, but I am sure it is only the end of a paragraph. No mention has been made of the great progress in supportive treatment, the prevention of scarring and physical therapy.
References Allen H. S. and Koch S. L. (1942) The treatment of patients with severe burns. Sctrg. Gynecol. O&et. 79, 914. Black D. A. K. (1940) Treatment of bums shock with plasma and serum. Br. Med. J. 2, 693. Bull J. P. and Lennard-Jones J. E. (1949) The impairment of sensation in bums and its clinical application as a test of the depth of skin loss. Clin. Sci. 8, 155. Burke J. F., Quinby W. C., Bondoc C. C. et al. (1975) Immunosuppression and temporary skin tranplantation in the treatment of massive third degree bums. Ann. Surg. 182, 183. Colebrook L., Gibson T. and Todd J. P. (1945) St&es of Burns and Scab (Medical Research Council Special Report Series No. 249). London: HMSO. Davidson E. C. (1926) The prevention of toxaemia of bums. Treatment by tannic acid solution. Am. 1. Surg. 40, 114. Dunbar J. (1934) Review of the burn cases treated in the Glasgow Royal Infirmary during the past hundred years, with some observations on the present-day treatment. Ghgow Med. 1. 122,239. Fox C. L. (1968) Silver sulfadiazine - a new topical therapy for psudomonas in burns. Arch. Swg. 96, 184. Heimbach D., Hemdon D., Luterman A. et al. (1988) Early excision of thermal burns - an international round-table discussion. Geneva 1987.1. Bum Care R&&i!. 9, 549. Hemdon D. N., Barrow R. E., Rutan R. L. et al. (1989) A comparison of conservative versus early excision. Ann. Surg. 209,547. Jackson D. M. and Cason J. S. (1977) Bums excision by a carbon-dioxide laser. Lncel i, 1081. Jackson D. M., Lowbury E. J. L. and Topley E. (1951a) Pseudomonas pyocyanea in bums: its role as a pathogen and the value of local polymyxin therapy. Lancet ii, 137.
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Paper accepted
24 March
1991.
Correspondence should be addressed to: Mr D. M. Jackson, 17 Milford Court, Milford-on-Sea, Lymington, Hampshire SO41 OWF, UK.