JOURNAL OF THE AMERICAN GERIATRICS SOCIETY Copyright 0 1976 by the American Geratrics Society

Vol. XXIV, No. 5 Printed in U.S.A

The Care of Decubitus Ulcers (Pressure Sores) ROBERT J. MICHOCKI, MS* and PETER P. LAMY, PhD, FCP**

University of Maryland HospitallSchool of Pharmacy, Baltimore, Maryland ABSTRACT: Despite a large volume of literature particularly directed toward treatment, pressure sores (including decubitus ulcers) remain a difficult problem, especially in the nursing home environment. The treatment of pressure sores is somewhat controversial and quite diversified. Selection of a successful therapeutic modality must be preceded by correct evaluation, i.e., whether the sore is superficial or deep, open or closed. The treatment of superficial sores is conservative and directed toward cleanliness, relief of pressure, and exposure to air. Surgical debridement may be indicated. Proteolytic enzymes often are employed as adjunctive therapy, although there are some major drawbacks to their use. The plethora of therapeutic agents suggested for the treatment of deep pressure sores probably is related to the difficulties in achieving success. Surgical debridement is indicated, and proteolytic enzymes are widely used. Possible interactions and factors leading to the inactivation of these enzymes are discussed, as is the use of various solutions, ointments, gold leaf, oxygen, dry heat, and other adjunctive devices. Of paramount importance in the management of pressure sores is the maintenance of cleanliness and dryness. Pharmaceutical services currently offered to nursing homes are expanding rapidly. In addition to the traditional drug distribution service, pharmacists are being called upon to provide internal staff development, in-service education, and drug information. A t present, the Medicare and Medicaid programs require the services of a pharmacist in an extended care facility and both programs have identical requirements and conditions for the pharmacist’s participation in five major areas (1): 1. Preparing, updating, and carrying out the policies and procedures for pharmaceutical services. These services include the control, accountability, labeling, storage, distribution and supervision of all drugs and biologicals. 2. Providing medication for the patient. * Instructor, Division of Clinical Pharmacy. * * Professor of Pharmacy and Director, Institutional Pharmacy Programs. Address for correspondence: Peter P. Lamy, PhD, University of Maryland Hospital/School of Pharmacy, 636 West Lombard Street, Baltimore, MD 21201.

3. Inspection of nursing-station drugs and physicians’ orders. 4. In-service education by the pharmacist for the staff of the facility. 5. Reporting of inspections and activities. In addition, a proposed standard (1)suggests that pharmacists will review the drug regimen for each patient at least monthly and report any irregularities to the attending physician. This proposed standard, as well as the areas of involvement previously outlined, may involve pharmacists in the provision of relevant information dealing with the therapeutic management of various disease states. An area of particular interest that pharmacists should become familiar with is the therapeutic management of pressure sores. In Howell’s study of 300 patients, aged 65 to 104 years, bedsores were the most common event associated with the terminal stages of life (2). Therefore, pharmacists providing service to nursing homes should develop a certain degree of knowledge and expertise in the field of pressure-sore management and treatment. The terms “bedsore” and “decubitus ulcer” are

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truly misnomers since “decubitus” means “lying down” and “bedsore” implies that these wounds occur in patients confined to bed. Many ulcers do result from the patient’s lying in one position too long, but others can arise from sitting, from prolonged standing on tilt boards or electric beds, or even from tight-fitting casts and dressings. All sores have one thing in common: they result from prolonged pressure, especially against a bony prominence. Therefore, the term pressure sore is a more accurate description of the process. When a patient is allowed to remain in the same position for an extended period, tissue anoxia and capillary thrombosis can occur; if the pressure is not relieved, this may result in death of tissues (3). The minimum pressure for keeping capillaries open is approximately 25 mm Hg, and the usual intracapillary pressure is about 40 mm Hg (3). Thus it follows that exogenous pressure in excess of these levels, exerted on susceptible bony areas (see Figure), will produce ischemia. The amount and the duration of the applied force are the most important etiologic factors in the development of pressure sores. The treatment of these sores is somewhat controversial and quite diversified. Over the past years, practitioners have employed an assortment of therapeutic modalities-solutions, dressings,

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soaps, enzymes, creams, ointments, gold leaf, honey, granulated sugar, oxygen therapy, and even the use of heat and cold. CLASSIFICATION Pressure sores may be classified arbitrarily into superficial or deep lesions (4-6). Deep sores, in turn, may be open or closed (7).

Superficial sores A superficial sore involves damage to the superficial layers of the skin; it does not extend into the subcutaneous tissue or muscle. Treatment is conservative and is directed towards cleanliness, relief of pressure and exposure to air. A superficial sore which is clean and not draining will heal quickly if those procedures are performed diligently (4,7-9). The decision to use a dressing depends, in part, upon the location of the sore (7). In an exposed area such as the knee or hip, it probably is best to let the sore dry without any dressing. In areas which are often in contact with bedclothes, such as buttocks or elbows, the patient may feel more comfortable and the new granulation tissue may be protected if the sore is covered with a single thin layer of gauze. Superfi-

Relative pressures (mm Hg) at significant pressure points in a recumbent patient.

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cia1 sores can deteriorate quickly if pressure is not relieved promptly. Weiss (8) recommends a wet physiologic-saline dressing to convert grayish unhealthy-appearing granulation tissue to healthylooking red tissue. If sloughs are present, they can be removed by using a 2 percent sodium chloride solution or a 20 percent sodium sulfate solution (4). If there is much debris, it can be liquefied by proteolytic enzymes. Most authors (7, 8, 10, 11)believe that surgical debridement is far superior to proteolytic enzymes in removing deep fibrotic tissue. The use of forceps and scissors can accomplish more debridement in a few seconds than can special medicaments in many hours. Proteolytic enzymes may aid in the dissolution of fibrin, liquefaction of pus and removal of coagula and purulent exudate, but they do not accomplish dissolution of necrotic tissue (11).Surgical debridement is the recommended therapy, but sometimes this method is not practicable. Nursing homes, because they lack the daily presence of a physician, may have to use enzymatic agents as an adjunct until surgical dhbridement can be performed. Most proteolytic enzymes belong to three main groups, i.e., originating from animal, vegetable or bacterial precursors. Some of the major drawbacks to using these agents include the frequent daily application, the inability to affect large amounts of dead collagenous tissue, and the expense. These enzymes may also cause excessive local irritation (12) and, because of their animal protein origin, allergic reactions (13).The routine use of these agents is inadvisable, especially if it leads to the neglect of more important factors. The accompanying Table provides a list of commercially available products.

Deep sores A deep sore is one in which all the layers of the skin, subcutaneous tissue or superficial fascia, and sometimes even muscle, have been damaged by pressure or subsequent infection (7). An open sore originates from the surface and extends downward through the various layers of tissue. A closed sore originates in the subcutaneous tissues and proceeds toward the surface, thus allowing degenerative changes to spread in all directions, possibly involving even bone (4). The surface of a closed deep sore may show only a small opening with a persistent discharge of pus. An open deep sore involves the necrosis of a great deal of tissue. The wound must be debrided

Enzymatic Debriding Agents in Common Use A. Vegetable Product: 1. Panafil ointment (Rystan Company, Inc.) a. Ingredients-Standardized papain 10%;urea U.S.P. 10%; water-soluble chlorophyl derivatives 0.5%. b. Application-once or twice daily. c. Precautions-Hydrogen peroxide may inactivate papain. B. Animal Products: 1. Biozyme ointment (Armour Pharmaceutical Company) a. Ingredients-Neomycin 0.35%; trypsin-chymotrypsin concentrate 10,OOO Armour Units per gm. b. Application-one to three times daily. c. Derivation-mammalian pancreas. 2. Elase ointment (Parke, Davis & Company) a. Ingredients-Fibrinolysin 30 units/30 gm; desoxyribonuclease 20,000 units/30 gm; thimerosal (mercury derivative) 0.12 mg/30 gm. b. Application-Two to three times daily. c. Derivation-Bovine plasma; bovine pancreas. d. Precautions-Mercury allergy; hypersensitivity to products of bovine origin. C. Bacterial Products: 1. Trauase ointment (Flint Laboratories) a. Ingredients-sutilains, 82,000 casein units of proteolytic activity per gm. b. Application-three to four times daily. c. Derivation-Bacillus subtilis. d. Precautions-Optimal pH 6.0-6.8; inactivation by: 1) detergents, 2) antiseptics, 3) germicides, 4) Burow’s solution (pH 3.6-4.4), 5) metallic ions (hexachlorophene, iodine, thimerosal, silver nitrate, nitrofurazone). 2. Collageme ABC Ointment (Advance Biofactures Corp.) Santyl Ointment (Knoll Pharm. Co.). a. Ingredients-Collagenase activity 250 units per gm. b. Application-Once daily or every other day. c. Derivation-Clostridium histolyticum. d. Precautions-Optimal pH 7-8; inactivation by: 1) detergents, 2) hexachlorophene, 3) heavy metals (mercury, silver), 4) Burow’s solution (aluminum acetate). .~

and the necrotic tissue removed. Getting rid of dead tissue removes the substance upon which bacteria thrive; it shortens the lag phase of wound healing and permits underlying normal tissues to start the proliferative phase (11). Surgical debridement is the method of choice. Once it has been performed, the clean wound can be maintained with physiologic-saline dressings applied four times a day (12). If the wound is a cavity, it should be loosely packed and the dressing allowed to dry for six hours. The dressing is then removed without re-wetting. The dry gauze will adhere to the necrotic material, removing it from the wound. Bliss and McLaren (7) recommend that the gauze be loosely packed; otherwise it may form a hard lump in the wound, seriously increasing local pressure. If the cavity is extremely “dirty” and a large amount of necrotic tissue is present, modified Dakin’s solution (diluted sodium hypochlorite solution, N.F. XIII) may be substituted for saline. After the wound has been thoroughly debrided, irrigation with a cleansing

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agent such as hydrogen peroxide can be performed (4). If extensive purulent drainage is present, Weiss (8) recommends a wet dressing of modified Dakin’s solution and 0.2 percent clorpactin solution (sodium oxychlorosene); when the purulent discharge has become serous, saline dressings may be substituted. Modified Dakin’s solution is very irritating and may dissolve clots or delay clotting in the same way it dissolves necrotic tissue. It should be used only when essential. Solutions must be freshly prepared, to avoid deterioration on exposure to air or elevated temperatures. If the color of the purulent discharge is blue-green or green, this may indicate contamination by Pseudomonas. In this particular circumstance, 4 percent boric acid solution can be used (4, 7) unless more vigorous therapy is indicated. Closed deep sores usually occur on the hips of patients who have been lying on their sides. Treatment is very difficult because only a small opening on the surface of the skin may be visible, yet extensive sinus tracking may be present. The removal of necrotic tissue and the treatment of infection become especially troublesome. Ribbon gauze soaked in modified Dakin’s solution or physiologic saline may be inserted deeply into the opening by means of a pair of sinus forceps (4,7). Harris (14) advocates daily care and believes that vigorous mechanical debridement, application of medicinal soaks (hydrogen peroxide or Epsom salt), and careful attention to the general nutritional state of the patient represent the key to successful therapy. For treatment of closed deep sores, he recommends the use of iodoform gauze or silver nitrate sticks introduced deeply into the sinus tracks. Usually the presence of a deep closed sore means a poor prognosis in relation to therapeutic management, and surgical intervention is often necessary. THERAPY

Proteolytic enzymes This form of treatment has been discussed in the section on “Classification.”

Gold leaf The use of gold leaf for the treatment of cutaneous lesions is not new. The first record of such treatment appeared in 1688 (15), when it was suggested that smallpox lesions be covered with

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beaten gold to prevent scarring. In 1964, Gallagher and Geschickter (16) noted that gold leaf could be used in surgery to seal vascular and membranous defects; when electrostatically charged, it exhibited a remarkable hemostatic effect on wounded arteries and veins, as well as on capillary bleeding. An electrostatic charge was imparted to gold leaf by stroking a camel-hair brush against a rubber comb and then touching the leaf with the charged brush. The gold leaf was then placed directly on the site of hemorrhage. When the charged leaf was touched to the tissue surface, it was immediately released from the brush and adhered tightly to the exposed tissue. Kanof (17) modified and simplified the procedure. His method consisted of the application of four to eight layers of autoclaved gold leaf (23 carat) to areas previously cleansed with ethyl alcohol. The sites were left uncovered and no other dressing or treatment was used. Ethyl alcohol eliminated the need for a brush and comb, since the alcohol increased the electromagnetic differential and attracted the leaf. Six patients with 11 non-healing ulcers were so treated. Six of the lesions healed, and a noticeable improvement occurred in the rest. However, the study lacked controls, and assessment of healing was based purely on subjective evaluations. In 1966, Wolf et a1 (18) treated 25 ischemic ulcers of various etiology; 20 were decubitus lesions and 3 of these served as controls. Gold leaf treatment was quite successful, except for 4 decubitus lesions which showed no improvement. Failure was attributed to excessive scar tissue, undermining, and prolonged friction. Healing during gold leaf treatment occurred only when hemoglobin values exceeded 12 gm/100 ml. In 1967, Smith et a1 (19) treated 44 patients (64 skin ulcers) with gold leaf and other occlusive agents, using an objective sign to monitor the effectiveness of each agent. The surface area of each ulcer was measured before and after treatment and progress was reported as the percentage re-epithelialized per day. The effect of gold leaf was compared to that of aluminum foil, flexible collodion, or a polyethylene film. The metal films were covered with an eye pad and secured with a bandage. Dressings were changed every five to seven days. The response rate with gold leaf was no better than that obtained with a simple dressing. Healing time was longer with gold leaf than with the simple dressing. Ulcers occluded with aluminum foil or polyethylene film failed to show re-epithelialization. The lesions treated with

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flexible collodion showed evidence of healing only

after heavy crust formation. This study differs from previous ones, in that the wounds were first surgically debrided and all signs of infection eliminated. Wounds were also covered with a dressing after application of the therapeutic agent. Dressings were changed every five to seven days in comparison to every forty-eight hours. Moreover, this study was partially controlled and an objective measure was used to monitor the patient’s progress. The results were also markedly different from those of previous reports. In 1969, Chick (20) reported a successful treatment program for decubitus ulcers, involving the use of gold leaf overlaid with a polyethylene film. Although this study was not controlled and results were not statistically significant, some important implications can be derived. The importance of a tight adherence between the gold leaf and the tissue being treated was crucial in assuring a successful outcome. This was accomplished by means of a foam-rubber pad similar to that used for padding a cast. The wound was then covered with a cling bandage. Treatment was repeated every three to four days. A polyethylene film placed over the gold leaf prevented the cracking and breaking which otherwise would have occurred, and reduced the number of layers needed. Chick (20) also recognized the importance of completely cleaning the wound and debriding it of any necrotic, fatty or crusty material before starting gold leaf therapy. Since the study lacked a control group, the possibility remains that the process of cleansing and debriding was all that was necessary to promote proper healing. In 1973, Risbrook et a1 (21) presented a case report of a 79-year-old woman with peripheral arteriosclerosis who suffered from a large (10 x 17.5 cm) raw painful ulcer on the left leg, of five years’ duration. Gold leaf was used in the standard fashion but no bandage or plastic wrap was employed. Treatment was administered every other day and the wound was debrided as necessary. After a two-year course of therapy, the ulcer healed. The length of time needed to complete healing points to the need for perseverance, which may well be a prerequisite for success. The therapeutic rationale for using gold leaf is that it causes epithelialization of cells (19), elicits a mild foreign-body reaction (16), and thus promotes healing (18). Despite the evidence presented, no definite conclusions can be drawn. Observations on a large series of patients under

controlled conditions would be necessary to determine the effectiveness of gold leaf. The reports reviewed here seem to indicate that stasis ulcers, secondary to peripheral vascular disease, may respond to gold therapy better than do pressure sores. However, this is only speculation and requires further documentation. Gold leaf can be purchased at any paint or art supply store. It is available in two forms - with or without an adhering backing of tissue paper. For the treatment of pressure sores, only plain sheets without the backing should be used because of easier handling of the leaf. The patient should be in positive nitrogen balance and the blood hemoglobin level should exceed 12 gm/100 ml. It is essential that a firm bond exist between the gold leaf and the tissues being treated. This requires electrostatic charging with ethyl alcohol. Adherence may also be promoted by using polyethylene film and a foam rubber pad. However, it must be remembered that the sores arise because of prolonged pressure. A tight-fitting dressing may exert substantial pressure and thus cause deterioration rather than improvement. During dressing changes, the gold leaf can be removed with warm water and hydrogen peroxide. The use of gold leaf is not without hazard. Malten and Mali (22) described 4 patients with contact dermatitis due to epicutaneous contact with metallic gold. In 3 of them, atopic dermatitis or contact dermatitis due to other agents preceded the gold sensitization. Therefore, patients should be thoroughly interviewed and screened for a history of atopic disease before starting gold leaf therapy. Oxygen

Another method of treating pressure sores involves the use of oxygen under pressure, to stimulate granulation tissue (23). The introduction of hyperbaric oxygen prompted Gorecki (24) to use oxygen to speed the healing of an accessible ulcer. The patient was an 86-year-old man under treatment for advanced pulmonary tuberculosis. Bedsores developed over the sacrum and right hip, measuring 1 x 1.5 and 1 x 2 inches, respectively. The patient was cooperative - lying on sheepskin, changing his position often, and walking as much as possible. General and local treatment cleared the infection, but for 9 months there was no healing to cover the areas of skin loss. Oxygen under pressure was carried directly from the tank through a tube and applied locally

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to the exposed wound by means of a plastic funnel anchored tightly to the tissue by a plastic sponge. The oxygen pressure achieved between the funnel and the wound was 15 rdm Hg with a flow rate of 12-15 liters per minute. Treatments (15 minutes each) were administered 3 to 4 times daily. After 4 weeks of therapy, the ulcers healed. Ursu (25) in Italy used ionized oxygen for the treatment of bedsores in 4 paraplegic patients. An apparatus was constructed which converted ordinary air into positive and negative oxygen ions. The positive ions were neutralized, leaving only the negative ions, which were then directed toward the sore. Treatments were administered daily for periods of 30 to 60 minutes. Healing occurred in 6 to 9 weeks. Ursu (25) claimed that the favorable effect of ionized oxygen was due to: 1) an antiseptic action (cf. oxygen in the treatment of anaerobic infections); 2) stimulation of granulation tissue; and 3) acceleration of the growth of epithelium. It is extremely difficult to assess the validity of this method of treatment. Adequate controlled trials are not available. Reported healing rates and progress are based upon subjective data and thus lack statistical significance. Nevertheless, oxygen is being used in the treatment of pressure sores. Sometimes this is accomplished by using an intranasal oxygen catheter to direct the flow to the site of the sore, usually for periods of 15 to 20 minutes, 3 or 4 times a day. No adverse effects have been reported, but proof of therapeutic effectiveness is also lacking. Oxygen therapy should not be viewed as a treatment entity. The wound must be debrided, cleansed and the external pressure relieved. Oxygen therapy may complement these measures, but it cannot replace them.

Dry heat Dry heat has also been exploited as a remedial measure in the treatment of pressure sores (26-28). It has been postulated that heat improves circulation and tissue oxygenation, and possibly retards infection. Dry heat usually is employed for superficial sores or early ulcers. Before starting therapy, the wound must be debrided of all sloughs and necrotic tissues. It is impossible to improve circulation in an area harboring necrosis without first removing the necrotic material. Electric lamp therapy consists of focusing a lighted 60-watt bulb on the designated body

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area(s) for 10 minutes, placed no closer than 18 inches and no farther away than 24 inches (26). The light must be directly beamed onto the lesion. The frequency of application varies, but treatment usually is given in the morning and at bedtime. Smigel and Russell (26) concluded that: “Electric lamp therapy (after debridement) shortens the treatment time by more than onethird in all stages of decubitus lesions of the skin and fascia. There is an added psychological factor because patients react well to the feeling of heat . . . therapy is inexpensive . . . available anywhere . . . and is easily adaptable to various sites, types and sizes of decubitus lesions.”

Sugar The treatment of pressure sores is not limited to advances in 20th Century Medicine; it also includes some methods developed in the early 1900’s. Magnus (29), in 1913, claimed that sugar had valuable antiseptic properties and recommended its use in the treatment of various wounds. A special formulation for “sugar paste” has been recommended for use on ulcerated lesions (30): Powdered cane sugar . . . . . . . . . . . . . . . . 30 gm Anhydrous lanolin . . . . . . . . . . . . . . . . . . 60 gm Compound tincture of benzoin.. . . . . . 2 ml Sucrose U.S.P. (cane sugar) is an inexpensive fermenting agent, negating the need for expensive enzymes (26). Sugar may also stimulate the growth of granulation tissue (26, 31). The crystals may serve as a matrix around which the new granulation tissue can form. Sugar may also enhance healing by retarding infection. An environment of high osmotic pressure may exert a bacteriostatic action by withdrawing water from microorganisms. However, a word of caution is necessary. Molds and fungi can act opportunistically as secondary invaders by taking advantage of an environment of high osmotic pressure in which they are capable of surviving. Comb honey (invert sugar, 50-90%, and water) has also been employed in the treatment of pressure sores (32). Its mode of action probably is identical to that of sugar. It is either spread on gauze for the more superficial sore or packed into the cavity of a deep sore. For deep sores, the entire area is covered with gauze and sealed with a waterproof spray (silicone). Another opinion on the subject of packing wounds with nutrients has been expressed by Walker (4) who states: “There are some who

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advocate packing of wounds with sugar . . . to “feed” sores. The logic of this packing of an unsterile, non-absorbable form of nutrient which is more liable to act as an irritant seems doubtful. It would appear better to feed such substances to the patient.” Miscellaneous Two very important but simple contributors to the management of pressure sores must not be neglected. It is of paramount importance that cleanliness and dryness be maintained in order to insure adequate healing or prevent further deterioration (4, 26). Cleanliness can be achieved by washing with soap and water. A mild non-irritating soap, such as Ivory, should be used. A soapless skin cleanser containing 3% hexachlorophene (pHisoHex) also can be used, since allergic reactions are rare (13). Walker (4) states that the pores of the skin must be kept clean in order to allow proper secretory function. Washing removes urine, excreta, and perspiration, and leaves the skin more absorbent. With this in mind, it is difficult to justify the application of pastes and ointments to ulcerated lesions, as these agents might encourage bacterial growth and impede the re-epithelialization process (31). The indiscriminate use of ointments and bandages may promote sweating and excoriating discharges, which irritate the ulcer, retard healing, and often induce extension of the ulceration (26). Alcohol removes essential fatty constituents from the skin, while rubbing may cause dryness, allergic inflammation, fissures, or desiccation and abrasion of the skin (4, 33). Witch hazel may also be harmful, in that it increases the incidence of sores (34). After cleansing of the sores with soap and water, Smigel and Russell (26) advocate the use of a nonalcoholic, antiseptic, mildly fatted lotion (Aloe-Rub). The problem of keeping patients clean and dry may seem to be straightforward, uncomplicated and easily solved. This may be true for cooperative, ambulant patients. However, patients being treated for pressure sores are chiefly those in a high-risk situation, unable or unwilling to cooperate, walk, or converse verbally. Furthermore, these patients often are incontinent of both feces and urine. Under these conditions, simple tasks can become major obstacles, of paramount importance. In nursing homes, where the staffhatient ratio

usually is less than ideal, urinary and fecal incontinence is a major problem in assuring a clean dry skin-no matter how good the nursing care. A methylbenzothonium chloride powder (Diaparene) dusted and rubbed into the texture of draw sheets helps to delay the decomposition of urine by ammonia-producing (urea-splitting) organisms (26), thereby delaying the onset of ammoniacal dermatitis. However, caution must be exercised in using powders because they may cake and cause additional irritation. The use of Diaparene cream to destroy urea-splitting organisms may be more practical in alleviating the problems of caking and irritation associated with the use of the powder. Smigel et a1 (35) claim that Diaparene is the most effective agent in the care of aged incontinent patients. Fecal incontinence can be controlled by inducing constipation to the point of obstipation. This is followed by the administration of a soapsuds enema at a predetermined time every second day (26). The sphincters then become habituated to a certain timing, thus preventing prolonged contact of fecal matter with the skin. Since its introduction in 1959 (36), the sheepskin has been used extensively in the prevention and treatment of bedsores. Bed linen, if not kept dry, clean and wrinkle-free may act as an abrasive or irritant. Conversely, sheepskin is soft and resilient, does not wrinkle, and distributes pressure evenly (36). It provides a smooth surface, reduces friction, and permits the free circulation of air. The dense cushion of wool also allows for the absorption and dissipation of moisture, thereby preventing it from remaining on the skin (4). If the sheepskin is to perform its functions properly, the patient must lie on it without any intervening material. Yet this simple and elementary fact is too often overlooked. Many patients are permitted to wear hospital gowns or pajamas, thus preventing direct contact; in this situation, any beneficial effect would be purely psychologic. Sheepskin is not without disadvantages (37). It soils easily, especially when used for the incontinent patient. One of the major disadvantages is the difficulty in laundering; moreover, repeated washings damage or abolish its initial properties. Sheepskins are not entirely uniform; and may be allergenic to some patients. They are available only in certain sizes. Because of these drawbacks, a synthetic product (Decubicare Pad) has been developed which has proved effective in the prevention and healing of decubitus lesions (37). A number of mechanical devices and specially

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designed mattresses are available, to reduce pressure by means of cyclical alteration or redistribution of weight (38-41). Among these are largecelled ripple mattresses, polyurethane foam, Stryker frames, rocking beds, water beds, air beds, and other aids. An excellent review of these appliances has been presented by Bliss (38).

COMMENT In the prevention and treatment of pressure sores, the pharmacist who provides service to nursing homes must not limit his expertise solely to drug therapy. He also must be knowledgeable concerning adjunctive and preventive measures useful in this special and troublesome field. Our review has attempted to highlight and describe some of the specific therapeutic modalities used in the treatment and prevention of these all-too-prevalent sores. We hope that this survey of the literature and of our personal experience will provide the pharmacist with some of the tools necessary for him to furnish the service needed by the medical and nursing staff for the benefit of patients in these increasingly numerous institutions.

REFERENCES 1. Gimon J: Pharmaceutical standards for participation in nursing homes, Md Pharm 50: 8, 1974. 2. Howell, TH: Some terminal aspects of disease in old age: a clinical study of 300 patients, J Am Geriatrics SOC17: 1034, 1969. 3. Dowling AS: Pressure sores - Their cause, prevention, and treatment, Md St Med J 19: 131, 1970. 4. Walker KA: Pressure Sores; Prevention and Treatment. London, Butterworth Company, 1971, pp 7-75. 5. Moolten SE: Bedsores in the chronically ill patient, Arch Phys Med Rehab 53: 430, 1972. 6. Binks FA: Pathogenesis and treatment of pressure sores, Physiotherapy 54: 281, 1968. 7. Bliss MR and McLaren R: Preventing pressure sores in geriatric patients, Nurs Mirr 123: 434, 1967. 8. Weiss A: Management of decubitus ulcers, New York State J Med 60: 79, 1960. 9. Edberg EL, Cerny K and Stauffer ES: Prevention and treatment of pressure sores, Phys Ther 53: 246, 1973. 10. Bailey BN: Bedsores. Baltimore, MD, Williams & Wilkins Company, 1967, p 75. 11. Kahn S: A guide to the treatment of decubitus (pressure) ulcers in paraplegia, Surg Clin N America 40: 1657, 1960. 12. G u t h i e RH and Goulian D: Decubitus ulcers: prevention and treatment, Geriatrics 28: 67, 1973. 13. Fisher AA: The role of topical medications in the management of stasis ulcers, Angiology 22: 206, 1971. 14. Harris Decubitus ulcers in the sick aged, J Geriatrics SOC13: 538, 1965.

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15. Robertson WG: Digby’s receipts, Ann Med Hist 7: 216, 1925. 16. Gallahger JP and Geschickter CF: The use of charged gold leaf in surgery, JAMA 189: 928, 1964. 17. Kanof NM: Treatment of cutaneous ulcers, J Invest Dermatol 43: 441, 1964. 18. Wolf N, Wheeler PC and Wolcott LE: Gold leaf treatment of ischemic skin ulcers, JAMA 196: 105, 1966. 19. Smith KW, Oden PW and Blaulock WK: A comparison of gold leaf and other occlusive therapy, Arch Dermatol96: 703, 1967. 20. Chick N: Treatment of ischemic and stasis ulcers with gold leaf and polyethylene film: preliminary report, J Am Geriatrics SOC17: 605, 1969. 21. Risbrook AT, Goodfriend SS and b i t e r JM: Gold leaf in the treatment of leg ulcers, J Am Geriatrics SOC21: 325, 1973. 22. Malten K E and Mali JW: Kontakt-Ekzem durch Goldverbindungen, Allerg Asthma 12: 31, 1966. 23. Rosenthal AM and Schurman A: Hyperbaric treatment of pressure sores, Arch Phys Med Rehab 52: 413, 1971. 24. Gorecki Z: Oxygen under pressure applied directly to bedsores: case report, J Am Geriatrics SOC12: 1147, 1964. 25. Ursu G: Bedsores treated with negative air-ions, Paraplegia 8: 182, 1970. 26. Smieel J O and Russell A: The do’s and don’t of therapy for dkcubitus lesions, with emphasis on use of the electric lamp, J Am Geriatrics SOC10: 975, 1962. 27. Nyquist RH: Brine bath treatments for decubitus ulcers, JAMA 169: 927, 1959. 28. Williams RW: Report on the W.C.P.T. investigation into the treatment of pressure sores, Physiotherapy 54: 288, 1968. 29. Magnus G: Wundbehandlung mit Zucker, Munchen Med Wchnschr 1: 406, 1913. 30. Rostenberg A, Medansky R and Wasserman E: Sugar paste in the treatment of leg ulcers, Arch Dermatol78: 94, 1958. 31. Adams LA and Bluefarb SM: How we treat decubitus ulcers, Postgrad Med 44: 269, 1968. 32. Hutton DJ: Treatment of pressure sores, Nurs Times 62: 1533, 1966. 33. Rudd TN: The pathogenesis of decubitus ulcers, J Am Geriatrics SOC10: 48, 1962. 34. Exton-Smith AN, Norton D and McLaren R An Investigation of Geriatric Nursing Problems in Hospital. London, National Corporation for the Care of Old People, 1962, pp 193-236. 35. Smigel JO, Murphy CM, Lowe K J et al: Care of the skin 5: 671, 1957. in the incontinent aged, J Am Geriatrics SOC 36. Davis L: Sheepskins and decubitus ulcers J Med A Alabama 29: 164, 1959. 37. Lieberman L, Panagis C and Neely MF: New method for prevention and treatment of decubitus lesions, J Am Geriatrics SOC10: 1028, 1962. 38. Bliss MR: A consideration of mechanical methods of preventing bedsores in elderly patients, Gerontol Clin 6: 10, 1964. 39. Brocklehurst JC: Pressure sores, Nurs Times 63: 1033, 1967.

40. Bliss MR, McLaren R and

Exton-Smith AN: Preventing

Pressure Sores in hospital: controlled trial of a large-celled ripple mattress, Brit Med J 1: 394, 1967. 41. Rowan NM: New system for supporting the patient in the management of decubitus ulcer: preliminary report, J Am Geriatrics SOC18: 421, 1970.

The care of decubitus ulcers pressure sores.

Despite a large volume of literature particularly directed toward treatment, pressure sores (including decubitus ulcers) remain a difficult problem, e...
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