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A Guide to the Treatment of Decubitus (Pressure) Ulcers in Paraplegia
Additional Article A Guide to the Treatment of Decubitus (Pressure) Ulcers in Paraplegia From the New York State Rehabilitation Hospital, West Haverstraw, New York
SIDNEY KAHN, M.D. Associate Clinical Professor of Plastic Surgery, Albert Einstein College of Medicine of Yeshiva University, New York City
IN PATIENTS with paraplegia, the continued presence of a decubitus ulcer is usually the most important factor delaying rehabilitation. In the treatment of these ulcers, reliance is too often laid upon the use of local medicaments, and too much time is wasted awaiting the promised magical result of a topical application which will remove necrotic tissue, sterilize the wound and produce epithelialization. When this train of events does not ensue, various regimens follow one another in confusing profusion, and the basic and generally simple principles of wound care are lost sight of. This paper is written to re-emphasize such basic principles.
DEFINITION
An ulcer is present when there is a loss of continuity of an internal or external body surface. A decubitus ulcer is such a wound caused by pressure associated with prolonged maintenance of a particular body posture. Such ulcers occur over bony prominences and are associated with necrosis of all the tissues from the surface to the underlying bone. The areas most
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conunonly involved are the sacral (from lying on the back), ischial (from sitting) and trochanteric (from lying on the side). Areas less frequently involved are the heel, malleolus, patella, iliac crest, elbow and occiput. ETIOLOGY
Nutritional Factors
Following closely upon the onset of paraplegia, there is a marked loss of appetite and weight; malnutrition commonly follows. The tissue wasting leads to the loss of subcutaneous fat and muscle bulk, decreasing the mechanical padding between skin and bone. Anorexia leads to avitaminosis; avitaminosis leads to an inability to maintain tissue integrity (particularly is this true of avitaminosis C). The negative nitrogen balance predisposes to edema of dependent parts. When the patient is recumbent, the edema fluid accumulates in the sacral area; this decreases the elasticity, resiliency and vitality of skin and underlying tissues, making them more susceptible to easy injury. Even minor injuries will not heal when a patient is in negative nitrogen balance. Once a wound is incurred, it will itself be an avenue for the further loss of essential body elements and will thus tend to perpetuate itself, making spontaneous restoration of body surface integrity less likely. Loss of Motor Power and Sensation
The paralysis of paraplegia removes normal motor stimuli to muscle. The lack of voluntary motor activity leads to the maintenance of one position with prolonged pressure upon vulnerable areas. Too, the relaxed atonic muscle cannot protect itself against such pressure as a normal muscle might do by reflex contraction. In addition, disuse atrophy occurs; this loss of muscle bulk (as opposed to the wasting of malnutrition) continues even after the patient's nutritional status improves. Muscle action aids blood flow; on the other hand, a paralyzed part exhibits a decreased venous return and tissue becomes deoxygenated; intravascular stasis thrombi further increase the damage and cause infarcts. The anesthesia of paraplegia removes warning symptoms of pressure from the patient's consciousness. Pressure
Pressure, superimposed upon the above factors, brings about necrosis and ulceration. Pressure is the sina qua non of decubitus ulceration. Prolonged pressure will cause such damage, even in a normal person with intact nutrition, motor power and sensation. Pressure produces direct damage by compressing tissue and secondary damage by decreasing blood flow and causing thrombosis. The seated posture causes pressure upon ischial areas far above the accepted mean capillary pressure. 1
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Wound Bacteriology
Once the skin is broken, a contaminated ulcer is present. There is no known medication which will rid a chronically open wound of bacteria. Seventy per cent of open wounds harbor hemolytic Staphylococcus aureus (coagulase-positive). Many other organisms are present. Such mixed infections feed and grow on the "wound pabulum" of dead tissues, blood serum, exposed tendons and fascia. 2 The effectiveness of an antibiotic in vitro against organisms cultured separately may be misleading when we are dealing with the mixed infections found in these wounds. Mixed infections are the rule; organisms not significant alone take on increased invasive or proteolytic properties in mixtures. The combined reactions of different bacteria may be more dangerous than a simple addition of their individual properties would indicate. However, surface bacterial contamination is not a problem; suppuration and invasive infection are. Suppuration will occur in the presence of necrotic material, and may then proceed to invasion. 3 PREVENTION
The prophylaxis of decubitus ulcers in paraplegia is essentially a nursing problem. Nutritional Factors
Order a high protein, high caloric, high vitamin diet, with vitamin and protein supplements if necessary. A patient's intake is not what he is offered, but what he eats. This truism is mentioned only because it is so often overlooked. Loss of appetite is common. Intake of the full diet ordered requires much urging and encouragement. Combat anemia and hypoproteinemia with foods of high quality and iron preparations; blood transfusions may be needed but are of only transient benefit unless oral intake is maintained. Male sex hormone often helps overcome the early negative nitrogen balance; 25 to 50 mg. of testosterone is given daily for a few weeks for its anabolic effect:' Mechanical and Physical Factors
Again the problem is one of nursing. Sheets must be smooth. Foam rubber rings, doughnuts, pillows and mattresses, or air mattresses are employed. Positioning to prevent pressure often requires ingenuity; ·a Stryker frame may be required. Patients are turned frequently. The head of the patient's bed should not be raised except for a very short period of time; the shearing force exerted between sacral tissues and the bed may abrade the skin, or, as shown by Reichel/ the skin and superficial fascia remain stationary because of friction, while the shearing force is transmitted to the area between the superficial and deep fascia as the torso
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Fig. 1. Spontaneous healing of sacral decubitus ulcer. A, Sacral ulcer containing necrotic fascia and granulations of poor quality. B, Three days after wound excision. C, Six weeks later. D, Eight weeks later, healed. Has remained stable during fourteen months' follow-up.
tends to slide toward the foot of the bed. It is preferable to use a footboard and then tilt the entire bed rather than elevate the upper half of the body. Observation of pressure points for the earliest sign of incipient ulceration is made at least daily. Local edema or a slight reddening or blanching of intact skin are danger signals; even then, preventive measures may be too late, since the tissue damage may occur simultaneously in all layers from skin to bone. 6 We have found silicone helpful for skin protection. It provides a water-repellent coating to the skin; it will not wash off with ordinary soap and water. Two per cent silicone in 95 per cent alcohol is applied daily as a spray. 7 It is for prevention, not treatment; it is not used directly on ulcers. Getting a patient up and to physical and social activities as soon as possible improves morale, appetite and blood circulation; it permits him to gain psychological encouragement from contact with others who are being rehabilitated. Unless there is an ischial ulcer, the patient may be permitted chair activities. The physiotherapist may give light massage to improve local circulation and tissue tone. Ultraviolet light will toughen skin and reduce the number of local bacteria.
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NONSURGICAL LOCAL TREATMENT OF ESTABLISHED ULCERS
Many decubitus ulcers will heal spontaneously if the preventive nutritional and mechanical principles just described are followed (Figs. 1, 9). Parts about the ulcer are protected with the silicone spray. The patient must not lie on the ulcerated part. Other areas are kept under continued observation; a patient kept off one pressure point will often neglect another. Dressings are changed at least once daily. Debridement of obviously dead tissue can be done during change of dressings with forceps and scissors. Getting rid of dead tissue removes the food upon which bacteria thrive; it shortens the lag phase of wound healing and permits underlying normal tissues to institute the proliferative phase. Ordinary wet dressings without medications will aid in spontaneous debridement. Normal saline is used, both as a wet dressing and for cleansing of secretions; daily saline irrigations are used for deeper wounds. A recent report describes the beneficial effects of brine baths, 8 but their effectiveness could not be evaluated from the report since the author employed them as part of the entire program (over a period of months) with full attention to nutritional, mechanical, topical and surgical aspects of a properly planned regimen. Medicated dressings are not ordinarily employed or recommended. The problem in decubitus ulcers is mechanical, nutritional and vascular, not chemical or bacterial; thus, surface applications are of little importance. "To cleanse the wound ... irrigation may be employed with normal saline, but never with a solution which would cause irritation if injected subcutaneously. This virtually rules out all antiseptics." 3 There is no known substance which will sterilize an open wound, or which will cause epithelium to grow. The locally acting agents discussed in the next three paragraphs have drawbacks which make their routine use inadvisable, particularly if such use leads to the neglect of more important factors. Antibacterial Substances
The best way to reduce the number of bacteria in a wound is to remove the devitalized tissue upon which they thrive. Antibacterial agents may be of some short-term value, but are generally not superior to saline dressings. If used, their choice should be guided by laboratory sensitivity tests, and even these may be misleading (see Wound Bacteriology). Moreover, many antibiotics cause local tissue sensitization, lose potency rapidly, must be freshly prepared, and often require refrigeration. The rapid replacement of vulnerable by resistant wound organisms under antibiotic therapy is commonplace. We restrict the use of local antibiotics to an occasional case, and then preoperatively only; they are not employed in wounds that are healing under a nonoperative regimen.
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Agents Said to Produce Debridement
Most wet dressings aid the removal of necrotic tissue by causing maceration of that tissue; the ingredient in the solution is generally of little importance. At any rate, a forceps and scissors can accomplish more debridement in a few seconds than can special medicaments in many hours. This applies to trypsin, vegetable enzymes (such as ficin and papain), phosphoric acid gel, pyruvic acid starch, salicylic acid and Dakin's solution. These may have other drawbacks as well, some injuring normal tissues or causing pain when the ulcer is not in an anesthetic area. Streptokinase-streptodornase enzymatic mixture dissolves fibrin and liquefies pus ;9 it may thus aid removal of coagula and purulent exudate, 10 but it does not cause the dissolution of necrotic tissue. The nonsurgical treatment of slough in a wound must await the development of an agent affecting collagen itself. A collagenase (derived from the Clostridium histolytica) has been developed; I have had no experience with it, but a recent report questions its ability to penetrate an eschar. Moreover, it may be toxic if absorbed from large areas upon which it may be applied. Fibrinolysin and deoxyribonuclease (from bovine pancreas) appear to have the same action as streptokinase-streptodornase (which brings about the formation of fibrinolysin from its precursor)/ 1 but the same drawbacks as well. It must be applied at least three times a day; it is of little effect when there is underlying arterial insufficiency; it will not affect large amounts of dead collagenous tissue. Its usefulness in the treatment of decubitus ulcers is thus questionable. Other Preparations
Other preparations recommended for use on wounds are mentioned in passing; almost all have had a very short-lived vogue: vitamin oils and ointments (e.g., cod liver oil ointment, vitamin C pastes, pantothenic acid or its alcohol analog panthenol), powdered red blood cells, dried blood plasma12 (in tissue culture, normal human serum and whole blood promoted epithelial outgrowth13), dyes (such as gentian violet), acetic acid, balsam of Peru, boric acid powder, granulated sugar, pectin/4 urea, 16 chlorophyll. 16 This list could be expanded almost indefinitely if we were to mention every substance said to sterilize or heal wounds or to be able to remove dead tissue from wounds without injuring viable tissues. Most are unnecessary, some are of very limited usefulness, others are harmful. None is recommended. SURGICAL TREATMENT OF ESTABLISHED ULCERS
Many decubitus ulcers are self-perpetuating. A thick fibrous bursa-like sac develops with heavy, grayish, dense, often calcified walls, and with contents of poor-quality chronically infected granulation tissue. This
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tissue effectively prevents healing or wound contracture. Once surgical repair has been done, the prompt primary union of sutured incisions indicates that it is the nature of the ulcer, not any continuing deficiency in the patient, that had prevented spontaneous healing previously. Thus, if after a trial period of nonsurgical therapy for a few weeks, a decubitus ulcer is not showing definite progress to healing, surgical repair is carried out. Other operative procedures required by the patient should be performed before the ulcer is attacked. Spasms and contracture deformities should be overcome or mitigated by the neurosurgeon or orthopedic surgeonP Spastic flexion contracture of hips and knees can be so severe that any position the patient assumes in bed causes pressure over bony prominences. Spasm can dislocate bones from their joints into the wound; it can disrupt suture lines. Abdominal spasm may cause the discharge of urine about a catheter and macerate operative sites. When return of voluntary motion is not expected, anterior rhizotomy is generally the operative procedure chosen by the neurosurgeon to relieve spasms. The operative sequence must be correlated with the urologist as well. Ordinarily, the repair of the decubitus ulcer is not undertaken until the urologist has removed urinary calcific deposits and controlled urinary tract infection. The purpose of the definitive surgery is to remove the ulcer, its contents, surrounding unsatisfactory tissues, infected bursae, and the underlying often devitalized bony prominence, 18 en bloc if possible (Fig. 7). Then, the defect is resurfaced with a transplanted pad of skin and fat. The transposed flap should have a broad pedicle which will permanently carry in a plentiful supply of blood. It must be of sufficient size to permit it to lie in its position loosely and without tension, and it must have sufficient bulk to-eliminate dead space and to stand up:under weight bearing and friction. Free skin grafts will generally "take" upon the granulations of a decubitus ulcer and may be employed as a temporary measure to close a wound while the patient's general condition improves. Even though such" free grafts will often hold up surprisingly well as a permanent surface, they are not to be used as a procedurerof choice. The safe rehabilitation of a paraplegic patient requires the provision of a supple, thick tissue cover to areas that have shown vulnerability to pressure. We almost invariably perform preliminary operative delays of flaps; that is, they are incised over only a portion of their borders, partially elevated and then resutured in their beds about three weeks before they are definitively transferred. Although some flaps may be of sufficient vascularity to permit immediate transfer, it is often difficult to determine this at the time; if an error of judgment is made-that is, if a flap is migrated and then is lost in whole or even in its distal part-this'" is catastrophic in that the loss is where the new tissue is needed most, the
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Fig. 2. A, Sacral decubitus ulcer. B, Ulcer closed with rotated flap. Donor area closed by approximation of wound margins.
decubitus ulcer is not cured, and the optimum source of new tissue has been made unsuitable for further use. Even if such an immediately transferred flap survives after a period of cyanosis, the saving of one operative stage may be paid for with a certain amount of fibrosis and rigidity of tissue; this is less satisfactory tissue in the long run than is a flap which displays normal color and vascularity from the outset. It is sometimes possible to close the defect left by the transfer of a flap by undermining and advancing adjacent tissues (Fig. 2). However, if this places any tension upon the flap, which ideally should lie loosely in its new position, resurfacing the donor bed with a free split thickness skin graft is preferable. Some authorities recommend permitting the donor bed to granulate for later reception of the free skin graft. However, an open wound is a source for bacterial contamination and subsequent infection which may insinuate itself under the adjacent flap. Moreover, immediate skin grafting of a surgically produced wound is preferable to grafting granulation tissue, in that all areas are closed primarily, the graft undergoes less secondary contraction and it becomes more quickly and satisfactorily naturalized. We have had no difficulty in the "take" of the immediately-placed skin grafts. '· Basic operative principles need not be detailed; they include the importance of careful hemostasis, gentle handling of flaps and grafts, the use of fine suture material, the use of drainage where a raw bone surface is oozing and the application of separate compression dressings for free graf(and ':flap so that they may be dressed individually. In paraplegic patients, most decubitus ulcers occur in anesthetic areas; however, an anesthesiologist is in attendance at operation since these patients require sedation and perhaps light anesthesia when bone is being resected. In addition, the anesthesiologist's attention to early signs of shock and its prevention is invaluable.
I
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Sacral Ulcers
The donor site of choice for the flap is the lumbar area above the ulcer (Figs. 3, 4, 5, 6). The flap is outlined transversely with its pedicle lateral. This provides an ample, easily rotated block of soft tissue, taken down to the deep fascia. The ultimate suture lines in the sacral area do not overlie the vulnerable midline. The skin graft that replaces the flap is not over a pressure area. Moreover, the level of anesthesia is frequently located just below the lumbar area; thus, sensitive tissue is brought down to a previously insensitive area. Buttock flaps are utilized only if the lumbar tissue has been rendered inadequate by previous scarring. If buttock is used, we prefer a unilateral flap, since bilateral flaps brought from either side will produce a suture line in the midline. Ischial Ulcers
After excision of wound, bursa and bone, ulcers over the ischial tuberosity may be repaired by primary closure19 • 20 (Fig. 7) or by use of local rotated flaps, from buttock above or thigh below (Fig. 8). The original suggestion for ostectomy in the treatment of decubitus ulcers was made by Kostrubala and Greeley; 18 the procedure evolved from a partial ischiectomy to a complete ostectomy of ischial tuberosity and rami. 21 We have generally not found it necessary to perform the latter radical procedure. Moreover, many of these patients require repair of bilateral ischial ulcers; it has been found that almost half of such patients develop urethral diverticula if bilateral ischiectomy is performed; they may then require permanent indwelling urethral catheters. 22
Fig. 3. Lumbar flap for recurrent sacral decubitus ulcer. A, Ulceration of previously applied graft. Demonstrates inadequacy of free skin graft as definitive surface. Note prepared lumbar flap ready for rotation into new position. B, Lumbar flap rotated. Free split-thickness skin graft to donor defect. Donor area for free graft seen on thigh.
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Fi . 5. acral decubitu ul r repair d with r tated flap. mon trate partia clo ure of donor defect by approximation of wound mar in , and partial clo ure with free graft. A, Preoperative. Note fascial slough. B, One week postoperative. C, Two months postoperative.
Treatm nt of Decubitus
Fig. 6.
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acral d cu itu ulcer repaired with lumbar flap. Demon trate stability of flap and free graft one year po toperative.
Fig. 7. Demon trate primary clo ure, the pro dure of choice in ischial decubitus ulcers. A, Right i chial decubitus ulcer. B, pecimen removed en bloc, with ulcer, "bur a" and portion of i chial tuberosity. C, Primary closure, four days postoperative. D, Three weeks postoperative.
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H
Fig. . Thr e decubitus ulcers repaired with flap (free kin graft applied to don r defects in each ca e). Right ischial tubero ity ulcer repaired with buttock flap, left i chial tub ro ity ulcer with posterior thigh flap, and sacral ulcer with lumbar flap.
Fig. 9. Healing of a trochanteric ulcer after wound exci ion without surgical repair. A, At time of wound excision. B, Spontan ou healing eight week later. C, Increasing naturalization of scar three months later.
Trochanteric Ulcers
In these ulcers, more than in any th r, the ul r orifi e may give little evidence of the extent of the und rlying \ und, \ hich i likely to be widely undermined and may lead into multiple burro\ ing inu e (Fig. 10). Mter wide wound exci ion and 0 te tomy, primary clo ure i usually possible (Figs. 10, 11). Closure of deep dead space is accomplished
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Fig. 10. Right trochanteric de ubitu ulcer. A, Burrowing inu. Applicator tick extend three inche beyond inferior margin of ulcer (on left). B, On operating tabl after wound excision. C, R ult of primary clo ure in lay r ; repair stable after nineteen months.
Fig. 11. A, Right trochanteric decubitus ulcer. B, On operating table; wound excision; ostectomy. C, Five months after primary closure in la.yers.
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Fig. 12. A, Trochanteric decubitus ulcer to be closed with lateral thigh flap. B, At close of operation: wound excision, resection of greater trochanter, advanced lateral thigh flap based anteriorly, free split thickness skin graft to defect left by advance· ment of flap. C, Three years later.
with pedicled muscle flaps, and more superficial closure is performed in layers by advancing subcutaneous and fascial tissues and skin; catgut is used for deep tissues, silk for the skin, and wide deep sutures of steel tied over bolsters or rubber catheter sections are used for retention. Where primary closure cannot be accomplished, rotation flaps are fashioned and utilized, with care that the donor site, upon which a free skin graft is placed, is not upon a pressure point (Figs. 12, 13, 14). Other Ulcers
Principles for closure of less common ulcers are the same as those which have been discussed. For patellar ulcers, patellectomy should be performed at the time of the repair with rotated flap. 23 • 24 Removal of a large portion of the iliac crest generally permits primary closure of anterior iliac spine ulcers (Fig. 15), although rotated flaps may be required (Fig. 16). The prolonged maintenance of a prone posture finds paraplegic patients supporting the upper half of their bodies on their elbows; ulcers occur here even when normal sensation exists. Here, too, bone removal permits repair in one stage. Malleolar, tibial crest and calcaneal ulcers
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ig. 13. Alt rnate ource of flap for trochanteric ulc r. A, Left tro hanteric ulcer. B, Patient is prone. Ulcer repaired with rotated flap from anterior thigh (flap is above in the photograph), free skin graft (below in the photograph) to donor area.
AHN
Fig. 14. Trochanteric decubitus ulcer repair d with lateral thigh flap. Demon trate degree to which flaps become naturalized and up pIe and retain tability. Tissue to right of flap is free skin graft used to resurface donor area of flap.
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Fig. 15. Primary clo ure of anterior iliac decubitu ulc r. A, Extent of ulcer. B, Height of convex iliac cre t. Removal of ulcer and bone yield ample tissue for primary closure. C, Eighteen day po toperative
Fig. 16. Iliac d cubitu ulcer clo ed with a flap wh re tis ues are inadequate for primary clo ure. A, lcer. B, Aft r exci ion of ul er and one; flap rotated from inguinal area; free graft to donor area. C, One month lat r. tability maintain d.
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can generally be treated by free skin grafting, although most will heal by secondary intention after wound excision. Postsurgical Therapy
The patient is moved frequently during the postoperative period, except on to the operative site. After repair of sacral and ischial ulcers, a constipating regimen is carried out for a week. If antibiotics were employed in the preoperative regimen, they are continued in the postoperative period as well. The flap is inspected on the second or third day, and the drain is removed; reinspection is performed every other day thereafter to discover any wound complications and to remove sutures. The dressing over the free skin graft (applied separately at the time of surgery) is not disturbed for eight to ten days, at which time sutures are removed. The patient is kept in bed for three weeks. Gradually increasing activities are begun at the end of that time so that the patient is on his full course of rehabilitiation and physiotherapy by the sixth week. All aspects of patient care described under Prevention are given continuing attention. A repaired ulcer is part of the patient and will be vulnerable to repeated damage; other areas, too, may undergo ulceration while attention is focused upon the area of repair.
CONCLUSION
A hospital which treats many paraplegic patients should have a standard procedure to follow in treating decubitus (pressure) ulcers. This routine is flexible and subject to variations in individual cases, but such variations should have the approval of a single supervising surgeon in order to avoid the random introduction of ineffectual procedures. Too often, impatience with)ack of progress toward healing leads to frequent changes in technique, often under the influence of a well advertised panacea which, it is implied, will sterilize a wound, remove slough and produce new epithelium. Many of these treatments, in addition to lacking merit and postponing definitive therapy, are expensive and very demanding in time of nursing personnel. The routine care of decubitus ulcers should encompass only simple principles of wound care and patient care. In this paper, these principles-nutritional, mechanical, biological and surgical-have been described. Stress has been laid upon prevention and simplicity in nonoperative therapy. If surgery is required, it aims at replacing the diseased tissue and underlying bony prominence with a thick skin and fat flap. The source of the flap is so chosen that the free skin graft which takes its place is not situated over a pressure point.
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REFERENCES 1. Kosiak, M., Kubicek, W. G., Olson, M., Danz, J. N. and Kottke, F. J.: Evaluation of Pressure as Factor in Production of Ischial meers. Arch. Phys. Med. 39: 623, 1958. 2. Lyons, C.: Chemotherapy in Management of Wounds. J.A.M.A. 133:215, 1947. 3. Wallace, A. B.: Thoughts on Wound Healing and Wound Care. Brit. J. Plast. Surg. 12: 150, 1959. 4. Langston, R. G.: Use of Testosterone in Debility States. Plast. & Reconstruct. Surg. 9: 543, 1952. 5. Reichel, S. M.: Shearing Force as Factor in Decubitus Ulcers in Paraplegics. J.A.M.A. 166: 762, 1958. 6. Kosiak, M.: Etiology and Pathology of Ischemic meers. Arch. Phys. Med. 40:62, 1959. 7. Brusca, D. D.: Use of Silicone Spray on Skin of Bedridden Patients. New York J. Med. 56: 894, 1956. 8. Nyquist, R. H.: Brine Bath Treatments for Decubitus meers. J.A.M.A. 169: 927, 1959. 9. Tillett, W. S., Sherry, S., Christensen, L. R., Johnson, A. J. and Hazelhurst, G.: Streptococcal Enzymatic Debridement. Ann. Surg. 131: 12, 1950. 10. Connell, J. F., Jr. and Rousselot, L. M.: Use of Enzymatic Agents in Debridement of Burn and Wound Sloughs. Surgery 30: 43, 1951. 11. Coon, W. W., Wolfman, E. F., Jr., Foote, J. A. and Hodgson, P. C.: Enzymatic Debridement with Bovine Fibrinolysin. Am. J. Surg. 98: 4, 1959. 12. Clark, A. B. and Rusk, H. A.: Decubitus Ulcers Treated with Dried Blood Plasma. J.A.M.A. 153: 787, 1953. 13. Allgower, M., Pomerat, C. M. and Blocker, T. G., Jr.: Influence of Normal Serum, Its Derivatives, and of "Wound Healing Agents" on Human Epidermis in Vitro. Ann. Surg. 135: 923, 1952. 14. Tompkins, G. A., Crook, G. W., Haynes, E. and Winters, M.: Pectin in Treatment of Various Types of Wounds. Surg., Gynec. & Obst. 72: 222, 1941. 15. Robinson. W.: Use of Urea to Stimulate Healing in Chronic Purulent Wounds. Am. J. Surg. 33: 192, 1936. 16. Smith, L. W. and Livingston, A. E.: Chlorophyll; An Experimental Study of Its Water Soluble Derivatives in Wound Healing. Am. J. Surg. 62: 358, 1943. 17. Cannon, B., O'Leary, J. J., O'Neil, J. W. and Steinsieck, R.: An Approach to Treatment of Pressure Sores. Ann. Surg. 132: 760, 1950. 18. Kostrubala, J. G. and Greeley, P. W.: Problem of Decubitus meers in Paraplegics. Plast. & Reconstruct. Surg. 2: 403, 1947. 19. Osborne, R.: Treatment of Pressure Sores in Paraplegic Patients. Brit. J. Plast. Surg. 8: 214, 1955. 20. Campbell, R. M. and Converse, J. M.: Saddle-Flap for Surgical Repair of Ischial Decubitus meers. Plast. & Reconstruct. Surg. 14: 442, 1954. 21. Blocksma, R., Kostrubala, J. G. and Greeley, P. W.: Surgical Repair of Decubitus Ulcer in Paraplegics. Plast. & Reconstruct. Surg. 4: 123, 1949. 22. Comarr, A. E. and Bors, E.: Perineal Urethral Diverticulum-Complication of Removal of Ischium. J.A.M.A. 168: 2000, 1958. 23. Gelb, J.: Plastic Surgical Closure of Decubitus Ulcers in Paraplegics as Result of Civilian Injuries. Plast. & Reconstruct. Surg. 9: 525, 1952. 24. Conway, H. and Griffith, B. H.: Plastic Surgical Closure of Decubitus meers in Patients with Paraplegia. Am. J. Surg. 91: 946, 1956. 102 East 78th Street New York 21, New York
SIDNEY KAHN, M.D. Associate Clinical Professor of Plastic Surgery, Albert Einstein College of Medicine of Yeshiva University, New York City
IN PATIENTS with paraplegia, the continued presence of a decubitus ulcer is usually the most important factor delaying rehabilitation. In the treatment of these ulcers, reliance is too often laid upon the use of local medicaments, and too much time is wasted awaiting the promised magical result of a topical application which will remove necrotic tissue, sterilize the wound and produce epithelialization. When this train of events does not ensue, various regimens follow one another in confusing profusion, and the basic and generally simple principles of wound care are lost sight of. This paper is written to re-emphasize such basic principles.
DEFINITION
An ulcer is present when there is a loss of continuity of an internal or external body surface. A decubitus ulcer is such a wound caused by pressure associated with prolonged maintenance of a particular body posture. Such ulcers occur over bony prominences and are associated with necrosis of all the tissues from the surface to the underlying bone. The areas most
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conunonly involved are the sacral (from lying on the back), ischial (from sitting) and trochanteric (from lying on the side). Areas less frequently involved are the heel, malleolus, patella, iliac crest, elbow and occiput. ETIOLOGY
Nutritional Factors
Following closely upon the onset of paraplegia, there is a marked loss of appetite and weight; malnutrition commonly follows. The tissue wasting leads to the loss of subcutaneous fat and muscle bulk, decreasing the mechanical padding between skin and bone. Anorexia leads to avitaminosis; avitaminosis leads to an inability to maintain tissue integrity (particularly is this true of avitaminosis C). The negative nitrogen balance predisposes to edema of dependent parts. When the patient is recumbent, the edema fluid accumulates in the sacral area; this decreases the elasticity, resiliency and vitality of skin and underlying tissues, making them more susceptible to easy injury. Even minor injuries will not heal when a patient is in negative nitrogen balance. Once a wound is incurred, it will itself be an avenue for the further loss of essential body elements and will thus tend to perpetuate itself, making spontaneous restoration of body surface integrity less likely. Loss of Motor Power and Sensation
The paralysis of paraplegia removes normal motor stimuli to muscle. The lack of voluntary motor activity leads to the maintenance of one position with prolonged pressure upon vulnerable areas. Too, the relaxed atonic muscle cannot protect itself against such pressure as a normal muscle might do by reflex contraction. In addition, disuse atrophy occurs; this loss of muscle bulk (as opposed to the wasting of malnutrition) continues even after the patient's nutritional status improves. Muscle action aids blood flow; on the other hand, a paralyzed part exhibits a decreased venous return and tissue becomes deoxygenated; intravascular stasis thrombi further increase the damage and cause infarcts. The anesthesia of paraplegia removes warning symptoms of pressure from the patient's consciousness. Pressure
Pressure, superimposed upon the above factors, brings about necrosis and ulceration. Pressure is the sina qua non of decubitus ulceration. Prolonged pressure will cause such damage, even in a normal person with intact nutrition, motor power and sensation. Pressure produces direct damage by compressing tissue and secondary damage by decreasing blood flow and causing thrombosis. The seated posture causes pressure upon ischial areas far above the accepted mean capillary pressure. 1
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Wound Bacteriology
Once the skin is broken, a contaminated ulcer is present. There is no known medication which will rid a chronically open wound of bacteria. Seventy per cent of open wounds harbor hemolytic Staphylococcus aureus (coagulase-positive). Many other organisms are present. Such mixed infections feed and grow on the "wound pabulum" of dead tissues, blood serum, exposed tendons and fascia. 2 The effectiveness of an antibiotic in vitro against organisms cultured separately may be misleading when we are dealing with the mixed infections found in these wounds. Mixed infections are the rule; organisms not significant alone take on increased invasive or proteolytic properties in mixtures. The combined reactions of different bacteria may be more dangerous than a simple addition of their individual properties would indicate. However, surface bacterial contamination is not a problem; suppuration and invasive infection are. Suppuration will occur in the presence of necrotic material, and may then proceed to invasion. 3 PREVENTION
The prophylaxis of decubitus ulcers in paraplegia is essentially a nursing problem. Nutritional Factors
Order a high protein, high caloric, high vitamin diet, with vitamin and protein supplements if necessary. A patient's intake is not what he is offered, but what he eats. This truism is mentioned only because it is so often overlooked. Loss of appetite is common. Intake of the full diet ordered requires much urging and encouragement. Combat anemia and hypoproteinemia with foods of high quality and iron preparations; blood transfusions may be needed but are of only transient benefit unless oral intake is maintained. Male sex hormone often helps overcome the early negative nitrogen balance; 25 to 50 mg. of testosterone is given daily for a few weeks for its anabolic effect:' Mechanical and Physical Factors
Again the problem is one of nursing. Sheets must be smooth. Foam rubber rings, doughnuts, pillows and mattresses, or air mattresses are employed. Positioning to prevent pressure often requires ingenuity; ·a Stryker frame may be required. Patients are turned frequently. The head of the patient's bed should not be raised except for a very short period of time; the shearing force exerted between sacral tissues and the bed may abrade the skin, or, as shown by Reichel/ the skin and superficial fascia remain stationary because of friction, while the shearing force is transmitted to the area between the superficial and deep fascia as the torso
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Fig. 1. Spontaneous healing of sacral decubitus ulcer. A, Sacral ulcer containing necrotic fascia and granulations of poor quality. B, Three days after wound excision. C, Six weeks later. D, Eight weeks later, healed. Has remained stable during fourteen months' follow-up.
tends to slide toward the foot of the bed. It is preferable to use a footboard and then tilt the entire bed rather than elevate the upper half of the body. Observation of pressure points for the earliest sign of incipient ulceration is made at least daily. Local edema or a slight reddening or blanching of intact skin are danger signals; even then, preventive measures may be too late, since the tissue damage may occur simultaneously in all layers from skin to bone. 6 We have found silicone helpful for skin protection. It provides a water-repellent coating to the skin; it will not wash off with ordinary soap and water. Two per cent silicone in 95 per cent alcohol is applied daily as a spray. 7 It is for prevention, not treatment; it is not used directly on ulcers. Getting a patient up and to physical and social activities as soon as possible improves morale, appetite and blood circulation; it permits him to gain psychological encouragement from contact with others who are being rehabilitated. Unless there is an ischial ulcer, the patient may be permitted chair activities. The physiotherapist may give light massage to improve local circulation and tissue tone. Ultraviolet light will toughen skin and reduce the number of local bacteria.
Treatment of Decubitus Ulcers in Paraplegia
1661
NONSURGICAL LOCAL TREATMENT OF ESTABLISHED ULCERS
Many decubitus ulcers will heal spontaneously if the preventive nutritional and mechanical principles just described are followed (Figs. 1, 9). Parts about the ulcer are protected with the silicone spray. The patient must not lie on the ulcerated part. Other areas are kept under continued observation; a patient kept off one pressure point will often neglect another. Dressings are changed at least once daily. Debridement of obviously dead tissue can be done during change of dressings with forceps and scissors. Getting rid of dead tissue removes the food upon which bacteria thrive; it shortens the lag phase of wound healing and permits underlying normal tissues to institute the proliferative phase. Ordinary wet dressings without medications will aid in spontaneous debridement. Normal saline is used, both as a wet dressing and for cleansing of secretions; daily saline irrigations are used for deeper wounds. A recent report describes the beneficial effects of brine baths, 8 but their effectiveness could not be evaluated from the report since the author employed them as part of the entire program (over a period of months) with full attention to nutritional, mechanical, topical and surgical aspects of a properly planned regimen. Medicated dressings are not ordinarily employed or recommended. The problem in decubitus ulcers is mechanical, nutritional and vascular, not chemical or bacterial; thus, surface applications are of little importance. "To cleanse the wound ... irrigation may be employed with normal saline, but never with a solution which would cause irritation if injected subcutaneously. This virtually rules out all antiseptics." 3 There is no known substance which will sterilize an open wound, or which will cause epithelium to grow. The locally acting agents discussed in the next three paragraphs have drawbacks which make their routine use inadvisable, particularly if such use leads to the neglect of more important factors. Antibacterial Substances
The best way to reduce the number of bacteria in a wound is to remove the devitalized tissue upon which they thrive. Antibacterial agents may be of some short-term value, but are generally not superior to saline dressings. If used, their choice should be guided by laboratory sensitivity tests, and even these may be misleading (see Wound Bacteriology). Moreover, many antibiotics cause local tissue sensitization, lose potency rapidly, must be freshly prepared, and often require refrigeration. The rapid replacement of vulnerable by resistant wound organisms under antibiotic therapy is commonplace. We restrict the use of local antibiotics to an occasional case, and then preoperatively only; they are not employed in wounds that are healing under a nonoperative regimen.
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Agents Said to Produce Debridement
Most wet dressings aid the removal of necrotic tissue by causing maceration of that tissue; the ingredient in the solution is generally of little importance. At any rate, a forceps and scissors can accomplish more debridement in a few seconds than can special medicaments in many hours. This applies to trypsin, vegetable enzymes (such as ficin and papain), phosphoric acid gel, pyruvic acid starch, salicylic acid and Dakin's solution. These may have other drawbacks as well, some injuring normal tissues or causing pain when the ulcer is not in an anesthetic area. Streptokinase-streptodornase enzymatic mixture dissolves fibrin and liquefies pus ;9 it may thus aid removal of coagula and purulent exudate, 10 but it does not cause the dissolution of necrotic tissue. The nonsurgical treatment of slough in a wound must await the development of an agent affecting collagen itself. A collagenase (derived from the Clostridium histolytica) has been developed; I have had no experience with it, but a recent report questions its ability to penetrate an eschar. Moreover, it may be toxic if absorbed from large areas upon which it may be applied. Fibrinolysin and deoxyribonuclease (from bovine pancreas) appear to have the same action as streptokinase-streptodornase (which brings about the formation of fibrinolysin from its precursor)/ 1 but the same drawbacks as well. It must be applied at least three times a day; it is of little effect when there is underlying arterial insufficiency; it will not affect large amounts of dead collagenous tissue. Its usefulness in the treatment of decubitus ulcers is thus questionable. Other Preparations
Other preparations recommended for use on wounds are mentioned in passing; almost all have had a very short-lived vogue: vitamin oils and ointments (e.g., cod liver oil ointment, vitamin C pastes, pantothenic acid or its alcohol analog panthenol), powdered red blood cells, dried blood plasma12 (in tissue culture, normal human serum and whole blood promoted epithelial outgrowth13), dyes (such as gentian violet), acetic acid, balsam of Peru, boric acid powder, granulated sugar, pectin/4 urea, 16 chlorophyll. 16 This list could be expanded almost indefinitely if we were to mention every substance said to sterilize or heal wounds or to be able to remove dead tissue from wounds without injuring viable tissues. Most are unnecessary, some are of very limited usefulness, others are harmful. None is recommended. SURGICAL TREATMENT OF ESTABLISHED ULCERS
Many decubitus ulcers are self-perpetuating. A thick fibrous bursa-like sac develops with heavy, grayish, dense, often calcified walls, and with contents of poor-quality chronically infected granulation tissue. This
Treatment of Decubitus Ulcers in Paraplegia
1663
tissue effectively prevents healing or wound contracture. Once surgical repair has been done, the prompt primary union of sutured incisions indicates that it is the nature of the ulcer, not any continuing deficiency in the patient, that had prevented spontaneous healing previously. Thus, if after a trial period of nonsurgical therapy for a few weeks, a decubitus ulcer is not showing definite progress to healing, surgical repair is carried out. Other operative procedures required by the patient should be performed before the ulcer is attacked. Spasms and contracture deformities should be overcome or mitigated by the neurosurgeon or orthopedic surgeonP Spastic flexion contracture of hips and knees can be so severe that any position the patient assumes in bed causes pressure over bony prominences. Spasm can dislocate bones from their joints into the wound; it can disrupt suture lines. Abdominal spasm may cause the discharge of urine about a catheter and macerate operative sites. When return of voluntary motion is not expected, anterior rhizotomy is generally the operative procedure chosen by the neurosurgeon to relieve spasms. The operative sequence must be correlated with the urologist as well. Ordinarily, the repair of the decubitus ulcer is not undertaken until the urologist has removed urinary calcific deposits and controlled urinary tract infection. The purpose of the definitive surgery is to remove the ulcer, its contents, surrounding unsatisfactory tissues, infected bursae, and the underlying often devitalized bony prominence, 18 en bloc if possible (Fig. 7). Then, the defect is resurfaced with a transplanted pad of skin and fat. The transposed flap should have a broad pedicle which will permanently carry in a plentiful supply of blood. It must be of sufficient size to permit it to lie in its position loosely and without tension, and it must have sufficient bulk to-eliminate dead space and to stand up:under weight bearing and friction. Free skin grafts will generally "take" upon the granulations of a decubitus ulcer and may be employed as a temporary measure to close a wound while the patient's general condition improves. Even though such" free grafts will often hold up surprisingly well as a permanent surface, they are not to be used as a procedurerof choice. The safe rehabilitation of a paraplegic patient requires the provision of a supple, thick tissue cover to areas that have shown vulnerability to pressure. We almost invariably perform preliminary operative delays of flaps; that is, they are incised over only a portion of their borders, partially elevated and then resutured in their beds about three weeks before they are definitively transferred. Although some flaps may be of sufficient vascularity to permit immediate transfer, it is often difficult to determine this at the time; if an error of judgment is made-that is, if a flap is migrated and then is lost in whole or even in its distal part-this'" is catastrophic in that the loss is where the new tissue is needed most, the
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SIDNEY KAHN
Fig. 2. A, Sacral decubitus ulcer. B, Ulcer closed with rotated flap. Donor area closed by approximation of wound margins.
decubitus ulcer is not cured, and the optimum source of new tissue has been made unsuitable for further use. Even if such an immediately transferred flap survives after a period of cyanosis, the saving of one operative stage may be paid for with a certain amount of fibrosis and rigidity of tissue; this is less satisfactory tissue in the long run than is a flap which displays normal color and vascularity from the outset. It is sometimes possible to close the defect left by the transfer of a flap by undermining and advancing adjacent tissues (Fig. 2). However, if this places any tension upon the flap, which ideally should lie loosely in its new position, resurfacing the donor bed with a free split thickness skin graft is preferable. Some authorities recommend permitting the donor bed to granulate for later reception of the free skin graft. However, an open wound is a source for bacterial contamination and subsequent infection which may insinuate itself under the adjacent flap. Moreover, immediate skin grafting of a surgically produced wound is preferable to grafting granulation tissue, in that all areas are closed primarily, the graft undergoes less secondary contraction and it becomes more quickly and satisfactorily naturalized. We have had no difficulty in the "take" of the immediately-placed skin grafts. '· Basic operative principles need not be detailed; they include the importance of careful hemostasis, gentle handling of flaps and grafts, the use of fine suture material, the use of drainage where a raw bone surface is oozing and the application of separate compression dressings for free graf(and ':flap so that they may be dressed individually. In paraplegic patients, most decubitus ulcers occur in anesthetic areas; however, an anesthesiologist is in attendance at operation since these patients require sedation and perhaps light anesthesia when bone is being resected. In addition, the anesthesiologist's attention to early signs of shock and its prevention is invaluable.
I
Treatment of Decubitus Ulcers in Paraplegia
1665
Sacral Ulcers
The donor site of choice for the flap is the lumbar area above the ulcer (Figs. 3, 4, 5, 6). The flap is outlined transversely with its pedicle lateral. This provides an ample, easily rotated block of soft tissue, taken down to the deep fascia. The ultimate suture lines in the sacral area do not overlie the vulnerable midline. The skin graft that replaces the flap is not over a pressure area. Moreover, the level of anesthesia is frequently located just below the lumbar area; thus, sensitive tissue is brought down to a previously insensitive area. Buttock flaps are utilized only if the lumbar tissue has been rendered inadequate by previous scarring. If buttock is used, we prefer a unilateral flap, since bilateral flaps brought from either side will produce a suture line in the midline. Ischial Ulcers
After excision of wound, bursa and bone, ulcers over the ischial tuberosity may be repaired by primary closure19 • 20 (Fig. 7) or by use of local rotated flaps, from buttock above or thigh below (Fig. 8). The original suggestion for ostectomy in the treatment of decubitus ulcers was made by Kostrubala and Greeley; 18 the procedure evolved from a partial ischiectomy to a complete ostectomy of ischial tuberosity and rami. 21 We have generally not found it necessary to perform the latter radical procedure. Moreover, many of these patients require repair of bilateral ischial ulcers; it has been found that almost half of such patients develop urethral diverticula if bilateral ischiectomy is performed; they may then require permanent indwelling urethral catheters. 22
Fig. 3. Lumbar flap for recurrent sacral decubitus ulcer. A, Ulceration of previously applied graft. Demonstrates inadequacy of free skin graft as definitive surface. Note prepared lumbar flap ready for rotation into new position. B, Lumbar flap rotated. Free split-thickness skin graft to donor defect. Donor area for free graft seen on thigh.
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ID EY KAH
Fi . 5. acral decubitu ul r repair d with r tated flap. mon trate partia clo ure of donor defect by approximation of wound mar in , and partial clo ure with free graft. A, Preoperative. Note fascial slough. B, One week postoperative. C, Two months postoperative.
Treatm nt of Decubitus
Fig. 6.
leer in Paraplegia
1 7
acral d cu itu ulcer repaired with lumbar flap. Demon trate stability of flap and free graft one year po toperative.
Fig. 7. Demon trate primary clo ure, the pro dure of choice in ischial decubitus ulcers. A, Right i chial decubitus ulcer. B, pecimen removed en bloc, with ulcer, "bur a" and portion of i chial tuberosity. C, Primary closure, four days postoperative. D, Three weeks postoperative.
1
ID EY
H
Fig. . Thr e decubitus ulcers repaired with flap (free kin graft applied to don r defects in each ca e). Right ischial tubero ity ulcer repaired with buttock flap, left i chial tub ro ity ulcer with posterior thigh flap, and sacral ulcer with lumbar flap.
Fig. 9. Healing of a trochanteric ulcer after wound exci ion without surgical repair. A, At time of wound excision. B, Spontan ou healing eight week later. C, Increasing naturalization of scar three months later.
Trochanteric Ulcers
In these ulcers, more than in any th r, the ul r orifi e may give little evidence of the extent of the und rlying \ und, \ hich i likely to be widely undermined and may lead into multiple burro\ ing inu e (Fig. 10). Mter wide wound exci ion and 0 te tomy, primary clo ure i usually possible (Figs. 10, 11). Closure of deep dead space is accomplished
Treatment of Decubitus Ulcer in Paraplegia
16 9
Fig. 10. Right trochanteric de ubitu ulcer. A, Burrowing inu. Applicator tick extend three inche beyond inferior margin of ulcer (on left). B, On operating tabl after wound excision. C, R ult of primary clo ure in lay r ; repair stable after nineteen months.
Fig. 11. A, Right trochanteric decubitus ulcer. B, On operating table; wound excision; ostectomy. C, Five months after primary closure in la.yers.
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Fig. 12. A, Trochanteric decubitus ulcer to be closed with lateral thigh flap. B, At close of operation: wound excision, resection of greater trochanter, advanced lateral thigh flap based anteriorly, free split thickness skin graft to defect left by advance· ment of flap. C, Three years later.
with pedicled muscle flaps, and more superficial closure is performed in layers by advancing subcutaneous and fascial tissues and skin; catgut is used for deep tissues, silk for the skin, and wide deep sutures of steel tied over bolsters or rubber catheter sections are used for retention. Where primary closure cannot be accomplished, rotation flaps are fashioned and utilized, with care that the donor site, upon which a free skin graft is placed, is not upon a pressure point (Figs. 12, 13, 14). Other Ulcers
Principles for closure of less common ulcers are the same as those which have been discussed. For patellar ulcers, patellectomy should be performed at the time of the repair with rotated flap. 23 • 24 Removal of a large portion of the iliac crest generally permits primary closure of anterior iliac spine ulcers (Fig. 15), although rotated flaps may be required (Fig. 16). The prolonged maintenance of a prone posture finds paraplegic patients supporting the upper half of their bodies on their elbows; ulcers occur here even when normal sensation exists. Here, too, bone removal permits repair in one stage. Malleolar, tibial crest and calcaneal ulcers
'1 r tment if D eubitu
leer in Paraplegia
1671
ig. 13. Alt rnate ource of flap for trochanteric ulc r. A, Left tro hanteric ulcer. B, Patient is prone. Ulcer repaired with rotated flap from anterior thigh (flap is above in the photograph), free skin graft (below in the photograph) to donor area.
AHN
Fig. 14. Trochanteric decubitus ulcer repair d with lateral thigh flap. Demon trate degree to which flaps become naturalized and up pIe and retain tability. Tissue to right of flap is free skin graft used to resurface donor area of flap.
Tr atrn nt oj Decubitu Ulcer in Paraplegia
1673
Fig. 15. Primary clo ure of anterior iliac decubitu ulc r. A, Extent of ulcer. B, Height of convex iliac cre t. Removal of ulcer and bone yield ample tissue for primary closure. C, Eighteen day po toperative
Fig. 16. Iliac d cubitu ulcer clo ed with a flap wh re tis ues are inadequate for primary clo ure. A, lcer. B, Aft r exci ion of ul er and one; flap rotated from inguinal area; free graft to donor area. C, One month lat r. tability maintain d.
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SIDNEY KAHN
can generally be treated by free skin grafting, although most will heal by secondary intention after wound excision. Postsurgical Therapy
The patient is moved frequently during the postoperative period, except on to the operative site. After repair of sacral and ischial ulcers, a constipating regimen is carried out for a week. If antibiotics were employed in the preoperative regimen, they are continued in the postoperative period as well. The flap is inspected on the second or third day, and the drain is removed; reinspection is performed every other day thereafter to discover any wound complications and to remove sutures. The dressing over the free skin graft (applied separately at the time of surgery) is not disturbed for eight to ten days, at which time sutures are removed. The patient is kept in bed for three weeks. Gradually increasing activities are begun at the end of that time so that the patient is on his full course of rehabilitiation and physiotherapy by the sixth week. All aspects of patient care described under Prevention are given continuing attention. A repaired ulcer is part of the patient and will be vulnerable to repeated damage; other areas, too, may undergo ulceration while attention is focused upon the area of repair.
CONCLUSION
A hospital which treats many paraplegic patients should have a standard procedure to follow in treating decubitus (pressure) ulcers. This routine is flexible and subject to variations in individual cases, but such variations should have the approval of a single supervising surgeon in order to avoid the random introduction of ineffectual procedures. Too often, impatience with)ack of progress toward healing leads to frequent changes in technique, often under the influence of a well advertised panacea which, it is implied, will sterilize a wound, remove slough and produce new epithelium. Many of these treatments, in addition to lacking merit and postponing definitive therapy, are expensive and very demanding in time of nursing personnel. The routine care of decubitus ulcers should encompass only simple principles of wound care and patient care. In this paper, these principles-nutritional, mechanical, biological and surgical-have been described. Stress has been laid upon prevention and simplicity in nonoperative therapy. If surgery is required, it aims at replacing the diseased tissue and underlying bony prominence with a thick skin and fat flap. The source of the flap is so chosen that the free skin graft which takes its place is not situated over a pressure point.
Treatment of Decubitus Ulcers in Paraplegia
1675
REFERENCES 1. Kosiak, M., Kubicek, W. G., Olson, M., Danz, J. N. and Kottke, F. J.: Evaluation of Pressure as Factor in Production of Ischial meers. Arch. Phys. Med. 39: 623, 1958. 2. Lyons, C.: Chemotherapy in Management of Wounds. J.A.M.A. 133:215, 1947. 3. Wallace, A. B.: Thoughts on Wound Healing and Wound Care. Brit. J. Plast. Surg. 12: 150, 1959. 4. Langston, R. G.: Use of Testosterone in Debility States. Plast. & Reconstruct. Surg. 9: 543, 1952. 5. Reichel, S. M.: Shearing Force as Factor in Decubitus Ulcers in Paraplegics. J.A.M.A. 166: 762, 1958. 6. Kosiak, M.: Etiology and Pathology of Ischemic meers. Arch. Phys. Med. 40:62, 1959. 7. Brusca, D. D.: Use of Silicone Spray on Skin of Bedridden Patients. New York J. Med. 56: 894, 1956. 8. Nyquist, R. H.: Brine Bath Treatments for Decubitus meers. J.A.M.A. 169: 927, 1959. 9. Tillett, W. S., Sherry, S., Christensen, L. R., Johnson, A. J. and Hazelhurst, G.: Streptococcal Enzymatic Debridement. Ann. Surg. 131: 12, 1950. 10. Connell, J. F., Jr. and Rousselot, L. M.: Use of Enzymatic Agents in Debridement of Burn and Wound Sloughs. Surgery 30: 43, 1951. 11. Coon, W. W., Wolfman, E. F., Jr., Foote, J. A. and Hodgson, P. C.: Enzymatic Debridement with Bovine Fibrinolysin. Am. J. Surg. 98: 4, 1959. 12. Clark, A. B. and Rusk, H. A.: Decubitus Ulcers Treated with Dried Blood Plasma. J.A.M.A. 153: 787, 1953. 13. Allgower, M., Pomerat, C. M. and Blocker, T. G., Jr.: Influence of Normal Serum, Its Derivatives, and of "Wound Healing Agents" on Human Epidermis in Vitro. Ann. Surg. 135: 923, 1952. 14. Tompkins, G. A., Crook, G. W., Haynes, E. and Winters, M.: Pectin in Treatment of Various Types of Wounds. Surg., Gynec. & Obst. 72: 222, 1941. 15. Robinson. W.: Use of Urea to Stimulate Healing in Chronic Purulent Wounds. Am. J. Surg. 33: 192, 1936. 16. Smith, L. W. and Livingston, A. E.: Chlorophyll; An Experimental Study of Its Water Soluble Derivatives in Wound Healing. Am. J. Surg. 62: 358, 1943. 17. Cannon, B., O'Leary, J. J., O'Neil, J. W. and Steinsieck, R.: An Approach to Treatment of Pressure Sores. Ann. Surg. 132: 760, 1950. 18. Kostrubala, J. G. and Greeley, P. W.: Problem of Decubitus meers in Paraplegics. Plast. & Reconstruct. Surg. 2: 403, 1947. 19. Osborne, R.: Treatment of Pressure Sores in Paraplegic Patients. Brit. J. Plast. Surg. 8: 214, 1955. 20. Campbell, R. M. and Converse, J. M.: Saddle-Flap for Surgical Repair of Ischial Decubitus meers. Plast. & Reconstruct. Surg. 14: 442, 1954. 21. Blocksma, R., Kostrubala, J. G. and Greeley, P. W.: Surgical Repair of Decubitus Ulcer in Paraplegics. Plast. & Reconstruct. Surg. 4: 123, 1949. 22. Comarr, A. E. and Bors, E.: Perineal Urethral Diverticulum-Complication of Removal of Ischium. J.A.M.A. 168: 2000, 1958. 23. Gelb, J.: Plastic Surgical Closure of Decubitus Ulcers in Paraplegics as Result of Civilian Injuries. Plast. & Reconstruct. Surg. 9: 525, 1952. 24. Conway, H. and Griffith, B. H.: Plastic Surgical Closure of Decubitus meers in Patients with Paraplegia. Am. J. Surg. 91: 946, 1956. 102 East 78th Street New York 21, New York