You are in: eMedicine Specialties > Plastic Surgery > PRESSURE ULCERS Pressure Ulcers, Surgical Treatment and PrinciplesArticle Last Updated: Aug 5, 2008AUTHOR AND EDITOR INFORMATIONSection 1 of 12
  Author: Bradon J Wilhelmi, MD, Endowed Leonard Weiner, MD, Professor and Chief of Division of Plastic Surgery, Residency Program Director, University of Louisville School of Medicine Bradon J Wilhelmi is a member of the following medical societies: Alpha Omega Alpha, American Association for Hand Surgery, American Association of Clinical Anatomists, American Association of Plastic Surgeons, American Burn Association, American College of Surgeons, American Society for Aesthetic Plastic Surgery, American Society for Reconstructive Microsurgery, American Society for Surgery of the Hand, American Society of Plastic Surgeons, Association for Surgical Education, Plastic Surgery Research Council, and Wound Healing Society Coauthor(s): Michael Neumeister, MD, FRCSC, FACS, Program Director, Assistant Professor, Department of Surgery, Division of Plastic Surgery, Southern Illinois University School of Medicine Editors: Albert E Cram, MD, FACS, Professor Emeritus, Departments of Surgery, Otolaryngology Head & Neck Surgery and Orthopedic Surgery, University of Iowa College of Medicine; Consulting Staff, Iowa City Plastic Surgery; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Wayne Stadelmann, MD, Stadelmann Plastic Surgery, PC; Nicolas (Nick) G Slenkovich, MD, Practice Director, Colorado Plastic Surgery Center at Swedish Medical Center; Lars M Vistnes, MD, FRCSC, FACS, Professor of Surgery, Emeritus, Stanford University Medical Center Author and Editor Disclosure Synonyms and related keywords: pressure ulcer, decubitus ulcer, bed sore, pressure sore, nonhealing wound, non-healing wound, wound healing complication, wound-healing complication, pressure ischemia, paraplegia, quadriplegia, spina bifida, immobilization, multiple sclerosis, MS, Marjolin ulcers, pressure sore reconstruction, flap procedures, chronic wound, pressure sore carcinoma INTRODUCTIONSection 2 of 12
  Found during autopsies on Egyptian mummies, pressure sores are an ancient medical problem. The terms decubitus ulcer and pressure sore have been interchanged inappropriately over the years. Technically, the term decubitus ulcer refers to wounds developed over bony prominences while in the recumbent position (ie, sacrum, heel, occiput); the Latin decumbere means "to lie down." Therefore, semantically, wounds acquired from extended pressure in the seated or turned position (ie, ischial or trochanteric ulcers) are not decubitus ulcers. Therefore, in general, wounds acquired from pressure over bony prominences can always be called pressure sores. History of the ProcedureIn 1938, Davis was the first to suggest replacing the unstable scar of a healed pressure sore with a flap of tissue.1 In 1947, Kostrubala and Greeley recommended excising the bony prominence and adding padding for the exposed bone with local fascia or muscle-fascia flaps.2 ProblemOverall, patients with pressure sores are important users of medical resources. They require 50% more nursing time, remain hospitalized for significantly longer periods, and incur higher hospital charges. FrequencyPressure sores are common conditions among patients hospitalized in acute- and chronic-care facilities. Studies have suggested that, at any given time, 3-10% of hospitalized persons have pressure sores and 2.7% develop new pressure sores. Among a selected population, the incidence rate for the development of a new pressure sore has been demonstrated to be much higher, with a range of 7.7-26.9%. Two thirds of pressure sores that develop in hospitalized patients occur in patients older than 70 years.3 As elderly individuals become the fastest-growing segment of the population, with an estimated 1.5 million people living in extended-care facilities, the problem of pressure sores will have an even more profound influence on the American economy. Most studies found the prevalence rate of pressure sores in patients in nursing homes to be 3-6%. However, other studies reported prevalence rates as high as 25-33%. Pressure sores also occur with a higher frequency in young patients who are neurologically impaired. Immobility and lack of sensation make these patients susceptible to developing pressure sores. The incidence rate of pressure sores in these patients has been demonstrated to be approximately 5-8% annually, and 25-85% of these patients develop a pressure sore at some time. Once again, the treatment of pressure sores in this patient population represents a financial challenge, with an average cost per admission of a patient with a pressure sore of $78,000 at one hospital. EtiologySeveral theories exist on the etiology of pressure sores, mostly based on ischemia and hypoxia resulting in decreased oxygen delivery to the tissues. In 1879, Charcot suggested that injury to CNS trophic centers decreases tissue tolerance to local pressure and leads to skin necrosis. However, Brown Sequard demonstrated that pressure ulcers can heal equally well in paralyzed and nonparalyzed animals. The pressure ischemia theory maintains that pressure sores result from constant pressure sufficient to impair local blood flow to soft tissue for an extended period. This external pressure must be greater than arterial capillary pressure of 32 mm Hg to impair inflow and greater than venous capillary closing pressure of 8-12 mm Hg to impede the return of flow for an extended time. Constant external pressure for 2 hours or more produces irreversible changes in tissues in animal model studies. One study demonstrated no histologic changes with pressure release at 5-minute intervals. Lindan et al documented ranges of pressure applied to various anatomic points in certain positions.4 The points of greatest pressure with the patient supine included the sacrum, heel, and occiput, at 40-60 mm Hg. With the body in prone position, the chest and knees absorbed the greatest pressure, at 50 mm Hg. When the patient is sitting, the ischial tuberosities are under the most pressure, at 100 mm Hg. Obviously, these pressures are greater than end capillary pressure, indicating why these are the most common areas to develop pressure sores. Furthermore, studies have demonstrated the pathologic changes caused by pressure to be more severe in muscle than in skin and subcutaneous layers. These histologic studies revealed that early signs of damage occur in the upper dermis, with dilation of capillaries and venules and swelling and separation of endothelial cells. Then, perivascular infiltrates, platelet aggregates, and perivascular hemorrhage develop in the dermis. Additionally, subcutaneous fat demonstrates signs of necrosis along with early vascular changes. Interestingly, the epidermis shows no signs of necrosis until late because epidermal cells are able to withstand a prolonged absence of oxygen both in vivo and in vitro. Others have postulated that pressure ulcers result from metabolic deficits. Muscle has the highest nutritional demands, which helps explain this deeper tissue involvement preferential to skin. ClinicalPatient history In obtaining a history from the patient with a pressure sore, determine the associated medical cause for the ulcer (eg, paraplegia, quadriplegia, spina bifida, immobilization in hospital, multiple sclerosis). Other factors that should be elicited in the patient's history include onset, duration, other ulcers, prior medical treatment, wound care, and prior surgical treatment. (Click here to complete a Medscape CME activity on comorbidities and quality of life in patients with multiple sclerosis.) The patient's social situation also can impact treatment. Determine if the patient has a pressure-reducing mattress for the wheelchair and bed and an appropriate support system at home to minimize the risk of recurrence. Also, obtain a complete review of systems, including the presence of fevers, night sweats, rigors, weight loss, weakness, and loss of appetite. Click here to complete a Medscape CE activity on the care of patients with pressure sores. Physical examination In addition to the patient history, perform a physical examination. Describe the specific location of the pressure sore based on the underlying bony prominence (eg, sacral, ischial, trochanteric). Infection of the pressure sore is suggested by wound edge erythema, foul odor, purulent discharge, and necrotic bone. Determine the level of tissue injury (ie, to epidermis, dermis, subcutaneous fat, muscle, bone, joint). Several classification systems of pressure sores are available based on this level of injury. One widely accepted classification system has 4 stages. Pressure sore staging from Barczak et al5 is as follows:
Also, note the character of the wound base and if it has granulation tissue or necrotic tissue. Verrucous heaps of white tissue within or around the wound suggest malignant transformation, as is observed with Marjolin ulcers (see Images 1-2). Document the size of the wound, wound edge undermining, additional pockets, and sinus tract communication with the hip joint or urethra. Note existing scars and the presence of colostomy and cystostomy. Also assess the extent of associated spasm. INDICATIONSSection 3 of 12
Despite the susceptibility of muscle to early injury with pressure over bony prominences (see Relevant Anatomy), classification schematics recognize muscle involvement as a later stage in the process of wounding. The classification scheme is most useful in determining treatment. The decision to reconstruct a pressure ulcer is complex and based on several considerations. Stage 1 and 2 pressure sores are treated conservatively. In general, stage 3 and 4 pressure sores may require flap reconstruction, although some patients with stage 3 and 4 pressure sores must be treated conservatively because of coexisting medical problems. Wound reconstruction can be considered once the bacterial load has been minimized to fewer than 100,000 organisms to reduce the risk of infectious complications. Furthermore, the patient's social situation and nutritional status must be optimized (albumin level >3.5 g/mL) to reduce risk of an adverse outcome. RELEVANT ANATOMYSection 4 of 12
Pressure ulcers are described by location and the depth of involvement. Pressure sores can be found over the occiput, scapula, ischium, sacrum, trochanter, heels, and posterior iliac spine. These wounds can involve different levels of tissue. Muscle has been proven to be most susceptible to pressure. However, Daniel and Faibisoff found muscle to rarely interpose bone and skin in normal weightbearing positions in cadaver and clinical dissections.6 CONTRAINDICATIONSSection 5 of 12
Because the complication rate of pressure sore reconstruction can be extremely high, poor candidates for operations in general should not undergo pressure reconstruction. Patients without the proper support network and pressure-release bed at home are not good candidates for pressure sore reconstruction because of the risk for recurrence or other complications. Patients who are noncompliant with nonoperative measures used to promote healing by secondary intention are also poor candidates for reconstruction. Wound infections and osteomyelitis must first be aggressively debrided. Patients with significant fecal soiling into the pressure sore should be considered for diverting colostomy prior to reconstruction. Also, pressure sores with urethral fistulas should be diverted and healed prior to reconstruction. WORKUPSection 6 of 12
Lab Studies
Imaging Studies
Diagnostic Procedures
TREATMENTSection 7 of 12
Medical TherapyConservative treatment of pressure sores includes appropriate wound care, debridement of necrotic tissue, optimization of nutrition, release of pressure, and minimization of muscle spasticity to provide the patient with the best opportunity to heal by secondary intention. Stage 1 and 2 pressure sores are treated conservatively. Some patients with stage 3 and 4 pressure sores must be treated conservatively because of coexisting medical problems. For more information, please see Pressure Ulcers, Nonsurgical Treatment and Principles. Infection of pressure ulcer wounds can affect treatment. To optimize wound healing potential, the wound should be in bacteriologic balance. Pressure ulcer infection is suggested by the presence of necrotic tissue, wound edge erythema, purulent discharge, and a foul odor. The most common organisms found in pressure sores include Staphylococcus aureus, Proteus mirabilis, Pseudomonas aeruginosa, Bacteroides fragilis, and Bacteroides asaccharolyticus. When more than 100,000 organisms are growing on quantitative cultures obtained from the pressure sore wound, debridement and aggressive wound care are required before considering wound reconstruction. Wound infection can be confirmed by quantitative tissue culture with more than 100,000 organisms in culture (clostridial and group B streptococcal infections can occur at lower bacterial counts). For conservative treatment, remove all necrotic tissue. If necrotic tissue is minimal, moist-to-dry dressings can be used with modified Dakin solution or isotonic sodium chloride solution. More extensive necrosis may require surgical debridement at the bedside or in the operating room. Once the wound is clean, silver sulfadiazine (Silvadene) can be used to reduce the bacterial load, which has been demonstrated to hasten wound healing. Alternatively, a negative pressure dressing can be considered for deep wounds that are clean and in bacteriologic balance. The negative pressure dressing has been found to decrease healing time and bacteria. If the patient's nutritional status is deficient, as determined based on albumin level and caloric intake (energy intake), supplementation (either orally or enterically [tube feeding]) is required. In the short term, supplementation can be assessed by serum prealbumin level, which has a shorter half-life (2 d) than albumin (17 d) or urine nitrogen. Patients with gut dysfunction may require total parenteral nutrition. The pressure on the skin must be reduced by turning the patient in bed every 2 hours and by the use of a pressure-reducing mattress. Pressure-reducing mattresses include low–air loss beds, air-fluidized beds, and Roho cushion mattress seats for wheelchairs. Furthermore, sitting patients should shift their body weight every 15 minutes. Surgical TherapyIn general, stage 3 and 4 pressure sores require flap reconstruction. The choice of flap for reconstruction depends on the location of the ulcer (see Intraoperative details). Preoperative DetailsInvoluntary muscle spasms must be controlled preoperatively with baclofen or diazepam. Arrange for a pressure-reducing mattress (air-fluidized bed) for the postoperative period. Treat the patient for a urinary tract infection (UTI) if urinalysis and urinary culture findings (ie, nitrites, leukocyte esterase) confirm its presence. For more information on UTIs, see Urinary Tract Infection, Males; and Urinary Tract Infection, Females. Once the decision has been made to reconstruct, the wound is debrided. Debridement of a pressure sore that will be reconstructed is different from debridement of a pressure sore that will be treated conservatively (ie, allowed to heal by secondary intention). A radical bursectomy is performed by placing a methylene blue–moistened sponge in the bursa and excising the pressure sore circumferentially, removing all granulation tissue, even from the wound base (see Image 3). Intraoperative DetailsAfter the bursectomy, primary closure of the pressure sore is almost always under tension and is doomed to fail. Other technical points of pressure reconstruction include radically removing underlying necrotic bone, padding of the bone stump, filling the dead space with muscle, using a large flap, achieving adequate flap mobilization to avoid tension, and avoiding adjacent flap territories to preserve options to reconstruct other locations. The choice of flap for reconstruction depends on the location of the ulcer. Ischial pressure ulcers The ischial location is the most common location in individuals with paraplegia. When performing the excisional debridement in preparation for flap repair of ischial wounds, aggressive resection of the ischial tuberosity may risk a contralateral ischial pressure sore from increased contralateral pressure. Bilateral ischiectomy increases pressure on the perineum and increases the risk of perineal pressure sores. Pressure sore recurrence is common in the ischial location. Therefore, the first option for reconstruction of ischial wounds is the gluteal thigh rotation flap, which does not preclude the future use of the inferior portion of the gluteus maximus muscle. The gluteal thigh rotation flap is an axial flap based on the inferior gluteal artery. Both the biceps femoris and hamstring myocutaneous flaps transect the inferior gluteal artery. With the gluteal thigh flap, a superiorly based flap is elevated, with its axis being the inferior gluteal artery located between the greater trochanter and the ischial tuberosity (see Image 4). The gluteal thigh rotation flap is raised as a fasciocutaneous flap superiorly to the gluteal crease (see Image 5). The gluteal thigh flap may be raised to include the inferior portion of the gluteus maximus muscle, which increases the arc of rotation and also allows this flap to be used to reconstruct sacral defects (see Image 6). Another popular option for ischial reconstruction, the inferior gluteus maximus myocutaneous flap, limits options for reconstruction of sacral wounds. Bilateral V-Y advancement flaps, inferiorly based random flaps, and superior gluteal myocutaneous flaps are not options for sacral reconstruction if an inferior gluteal myocutaneous flap has been used (see Image 7). Other described options for ischial reconstruction include the hamstring myocutaneous flap, biceps femoris myocutaneous flap, tensor fascia lata (TFL) flap, gracilis myocutaneous flap, and medially based posterior thigh skin flap with or without biceps femoris. Sacral pressure ulcers Sacral ulcers are common in patients who have been on prolonged bed rest. Treatment involves complete ulcer excision, including the entire bursa, and conservative ostectomy. Small sacral ulcers can be reconstructed with an inferiorly based skin rotation flap with or without the superior gluteus maximus myocutaneous flap (see Images 8-10). The use of the random skin rotation flap does not preclude later use of the gluteus muscle. When using a random skin rotation flap, designing a large and wide flap with an axis of rotation that permits tension-free closure is essential. With the superior gluteal myocutaneous flap, a wide skin rotation flap is elevated with the superior portion of the gluteus maximus muscle. The landmarks for the superior gluteal artery on which the superior gluteus maximus muscle flap is based include the posterior superior iliac spine (PSIS) and the ischial tuberosity. The superior and inferior gluteal arteries branch from the internal iliac artery superior and inferior to the piriformis muscle approximately 5 cm from the medial edge of the origin of the gluteus maximus muscle from the sacrococcygeal line (from the PSIS to the coccyx; see Image 11). When using the superior portion of the gluteus maximus muscle as a flap, it is elevated in a lateral-to-medial direction to avoid injury to the superior gluteal artery, which can be difficult to identify from the medial direction because of the inflammation and scar of the sacral pressure sore. The insertion of the superior portion of the gluteus maximus muscle is the iliotibial; this insertion is released. The superior gluteal artery is only 4 cm long, which limits the rotation of the muscle. Thus, harvesting the entire length of the muscle may be necessary to allow for rotation or turnover into the defect without tension (see Images 12-13). Larger sacral ulcers require the use of bilateral flaps such as bilateral V-Y myocutaneous advancement flaps (see Image 14). V-Y flaps can be based on the superior, inferior, or whole gluteus maximus muscle depending on ulcer location. The V should be fashioned wide enough and long enough to close as a Y without tension. The medial edge of the origin of the gluteus maximus is elevated in a medial-to-lateral direction for approximately 4 cm because the superior and inferior gluteal arteries enter the gluteus muscle 5 cm from its origin. Release of the gluteal muscle insertion laterally is important for medial advancement and tension-free approximation of the muscles medially. Inflamed fibrous tissue along the medial muscle edge can be preserved and used to hold sutures for midline muscle approximation. Another option for sacral reconstruction is the transverse lumbosacral flap. Trochanteric pressure ulcers Trochanteric pressure sores are less common and are typically associated with minimal skin loss. Excisional debridement of trochanteric ulcers in preparation for flap repair involves resection of the entire bursa and greater trochanter of the femur. The TFL flap is the first option for reconstruction of trochanteric pressure sores. The TFL flap is a myocutaneous flap based on the lateral femoral circumflex artery. The TFL muscle is 13 cm long, 3 cm wide, and 2 cm thick, and it originates from the anterior superior iliac spine (ASIS) and the iliac crest and inserts into the iliotibial tract. The skin paddle is harvested 10 cm in width and designed over the muscle along an axis from the ASIS to the lateral tibial condyle (see Images 15-16). The inferior limit of the cutaneous territory can be extended to 6 cm above the knee and 25-35 cm in length. The lateral femoral circumflex artery can be found approximately 6-8 cm inferior to the ASIS. In patients with lumbar lesions, a sensate TFL flap can be designed to include the T12 dermatome by fashioning the flap to include the area 6 cm posterior to the ASIS. Other described modifications of the TFL flap include the retroposition V-Y flap and the bipedicled TFL. Other options for trochanteric reconstruction include the vastus lateralis myocutaneous flap, the gluteal thigh flap, and the anterior thigh flap. Multiple pressure ulcers Multiple pressure sores can be observed in the same patient. Reconstruction of multiple ulcers may require the use of a total thigh flap. The total thigh flap is a long and formidable operation necessitating the transfusion of 6-20 units of blood. It should be reserved as a salvage procedure when other attempts have been unsuccessful. Patients who have undergone a unilateral total thigh flap can sit a wheelchair (see Image 17). Postoperative DetailsPostoperative care of pressure sore reconstruction is extremely important to reduce the risk of complications. From the time of transfer from the operating table to the air-fluid bed, exercise care to prevent shearing and tension across the flap repair. Patients are positioned flat in the air-fluid bed for 4 weeks. After 4 weeks, the patient can be placed carefully into a semi-sitting position. Six weeks after surgery, sitting is begun initially for 10-minute intervals. After these sitting periods, evaluate the patient's flap for discoloration and wound edge separation. The sitting periods are increased at 10-minute intervals over 2 weeks for up to 2-hour periods. Patients are taught to lift themselves to relieve pressure for 10 seconds every 10 minutes. COMPLICATIONSSection 8 of 12
Pressure sores are associated with a number of adverse outcomes. Complications include autonomic dysreflexia, osteomyelitis, pyarthroses, sepsis, amyloidosis, anemia, recurrence, urethral fistula, and malignant transformation. Autonomic dysreflexia is a disordered autonomic response to specific stimuli. Patients with midthoracic spinal cord lesions are most prone to this response, which includes sweating, flushing, nasal congestion, headache, intermittent hypertension, piloerection, and bradytachycardia. The sweating and flushing occur proximal to the level of injury. Patients in whom autonomic dysreflexia is suggested are first positioned with their head up and are monitored for changes in heart rate and blood pressure. Then, the precipitating stimulus must be removed. The most common precipitating cause is bladder distension, which requires treatment with Foley catheter insertion or irrigation of an existing Foley catheter to remove blockage. Consider a rectal examination to evaluate for fecal impaction. Nifedipine, hydralazine, or topical nitroglycerin (Nitropaste) can be used to stabilize the blood pressure. Finally, spinal anesthesia may be required for autonomic dysreflexia refractory to the above measures. Foremost in the treatment of osteomyelitis is the removal of all nonviable bone, down to bone that bleeds bright red. When reconstructing pressure sores associated with osteomyelitis, use bone that is in the base flaps and has a muscle component. Place the muscle over this bone after appropriate bone debridement. The flap reconstruction can be performed at the same time as the bone debridement. Then, administer a 6-week course of intravenous antibiotics. Pyarthrosis of the hip joint can occur with communication of ischial or trochanteric ulcers. Often, the femur head contains osteomyelitis, which mandates its removal. The Girdlestone arthroplasty procedure has been described for this situation (ie, hip pyarthrosis), with removal of the femur head and reconstruction of this space with the vastus lateralis muscle flap (see Image 18).7 Recurrence rates for pressure sores can be high because of patient noncompliance, seromas, hematomas, wound infections, and dehiscence. Intraoperative measures that can minimize recurrence risk include tension-free flap reconstruction, suction catheter drainage, meticulous hemostasis, and aggressive debridement. Postoperatively, patients must use pressure-reducing mattresses and pressure-release techniques to decrease their risk of recurrence. Patients with paraplegia have the highest rate of recurrence (80%). Pressure sores can also erode into the urethra. Treatment of this complication (ie, urethral fistula) involves urinary diversion. Pressure sore reconstruction can be considered once the fistula has healed (see Images 19-20). Although Marjolin initially described malignant transformation of a chronic scar from a burn wound, the term Marjolin ulcer has been used interchangeably for malignant transformation of any chronic wound, including pressure sores, osteomyelitis, venous stasis ulcers, urethral fistulas, anal fistulas, and other traumatic wounds. This malignant transformation is, histologically, a well-differentiated squamous cell carcinoma; however, its behavior is very aggressive when it arises in pressure sores as compared to in burns or osteomyelitis. Pressure sore carcinoma is a highly lethal disease, with 12 of 18 patients reported in the literature dying within 2 years. Therefore, treatment of a pressure sore carcinoma must be aggressive. Wide local excision, amputation, and lymph node dissection have been described for Marjolin ulcers arising from burns or osteomyelitis. However, because pressure sore carcinoma is more aggressive, more radical treatment is required (eg, hemicorporectomy and regional node dissection) if a cure is to be effected. In a retrospective analysis at M.D. Anderson Cancer Center, in 3.4% of 1200 patients with squamous cell carcinoma, the carcinoma arose from thermal burns of irradiation dermatitis. The actual complication rate for malignant transformation of a pressure sore is not known but can be assumed to be low because only 18 cases are described in the literature. The most common causes of fatality for patients with chronic pressure sores are renal failure and amyloidosis. In general, mortality rates are higher for patients who develop a new sore and in whom the pressure sore fails to heal. OUTCOME AND PROGNOSISSection 9 of 12
With the highest complication rate of all procedures performed, pressure sore reconstruction is perhaps the most complex challenge to plastic surgeons. Treatment of patients with pressure sores involves several considerations to minimize the risk of adverse outcomes of the reconstruction. Patients must be meticulously and compulsively prepared preoperatively, with nutritional deficiency, anemia, spasms, and coexisting urinary infection corrected. Patients must have adequate social resources, including pressure-release beds, wheelchair mattresses, and a compliant attitude to prevent recurrence. Intraoperatively, technical points of pressure sore reconstruction must be followed stringently to minimize the risk of complications. The postoperative regimen for the transition from flat bed rest to sitting and from weight-shifting into and out of the wheelchair in the return to daily living must be strict and careful. Even with close adherence to the above stated guidelines, pressure sore recurrence rates are high. When caring for patients with chronic pressure sores, flap procedures must be planned carefully and social resources must be provided assiduously to reduce the high risk of adverse outcomes in this complication-prone population. FUTURE AND CONTROVERSIESSection 10 of 12
Wound healing factors that promote spontaneous wound closure of pressure ulcers have been identified. Platelets play an important role in the inflammatory phase of wound healing by providing hemostasis and releasing growth factors known to accelerate wound healing. Atri et al reported their success in augmenting spontaneous wound healing with platelet-derived growth factors for 23 subjects in whom initial treatment with Silvadene failed.8 Later, Robson et al and Mustoe and colleagues found recombinant platelet-derived growth factor BB in concentrations of 100 mcg/mL to effect clinical wound healing in a phase II study of stage 3 and 4 pressure ulcers.9, 10 The cost to treat patients with these growth factors is presently significant. However, in the future, these nonoperative measures may be involved in the treatment of pressure ulcers, especially for patients who are not suitable for surgery because of coexisting morbidities. MULTIMEDIASection 11 of 12
REFERENCESSection 12 of 12
Pressure Ulcers, Surgical Treatment and Principles excerpt Article Last Updated: Aug 5, 2008 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
