Plastic surgery

PART IX

TRUNK AND LOWER EXTREMITY

CHAPTER 98  PRESSURE SORES

KAREN L. POWERS AND LINDA G. PHILLIPS

INTRODUCTION

A pressure sore is localized soft-tissue injury resulting from unrelieved pressure, usually over a bony prominence. Because areas of tissue pressure depend on patient position, the term “pressure sore” is preferred, rather than bedsore or decubitus ulcer. Relieving the pressure caused by patient positioning is the key to prevention and healing. Factors contributing to the development of pressure sores include decreased mobility, decreased sensation, spasticity, shearing forces, friction, and moisture. With so many factors playing a part in pressure sore development, prevention and treatment frequently require a multidisciplinary approach, often with the plastic surgeon consulted for reconstruction of the soft-tissue defect.

The most widely accepted pressure sore staging system was revised by the National Pressure Ulcer Advisory Panel in 2007 to include the original four stages and an additional two stages regarding deep tissue injury and unstageable pressure sores (Table 98.1). Stage I includes intact skin with non-blanching erythema, stage II includes partial-thickness loss of dermis, stage III includes full-thickness tissue loss, and stage IV includes exposed bone, tendon, or muscle.1 Additional classification includes suspected deep tissue injury, usually characterized by maroon localized intact skin or blood-filled blister, and unstageable, which is a full-thickness ulcer with eschar at the base. Limitations exist in this system; signs like skin erythema can be present in more than one stage and dark skin pigmentation can actually obscure the presence of erythema, necessitating other diagnostic signs like increased skin temperature, edema, and induration, to accurately stage the wound. Long-standing wounds of the pelvic girdle warrant careful examination and possible imaging to evaluate for extension into deeper structures, such as the acetabulofemoral joint.

EPIDEMIOLOGY

The incidence of pressure sore formation is variable but the patient populations commonly studied include those in acute care settings, nursing home patients, and paraplegic populations. In general, pressure sores develop in approximately 9% of all hospitalized patients, affecting 2.5 million people annually.2 For acute and long-term care facilities, the overall reported prevalence ranges between 3.5% and 29.5%.3 In addition to causing pain, suffering, and disability, pressure sores contribute to over 60,000 deaths per year according to the National Pressure Ulcer Advisory Panel.1 Data from the National Pressure Ulcer Long Term Care Study suggest that up to 19% of new patients develop a pressure ulcer while in long-term care and 22% arrive with an existing pressure ulcer.4 Beginning in October 2008, The Centers for Medicare and Medicaid Services ended reimbursement of acute care facilities for the development of a hospital-acquired stage III or IV pressure sores, thereby compounding the challenge of pressure sore prevention with the essential task of documentation of pressure sores present on admission.

Multiple studies have demonstrated that age, moisture, immobility, and friction/shear are key risk factors.5 Impaired sensory perception is known to contribute to the development of pressure sores but the incidence in patients with spinal cord injuries varies greatly. The Braden Scale, incorporating factors such as mobility, can be used to predict an individual’s pressure sore risk. Stal et al.6 cited a 20% incidence in paraplegic patients and a 26% incidence in patients who were quadriplegic. For the majority of patients, wounds develop in either the supine or seated position. Up to 75% of all pressure sores are located around the pelvic girdle. This is not unexpected, as it mirrors the distribution of pressure in supine and sitting positions (Figures 98.1 and 98.2). A study of a large cohort from a statewide Arkansas registry cited significant risk factors in the spinal cord–injured patient, including being underweight, use of pain medications, smoking, suicidal behaviors, history of incarceration, and alcohol and drug use.7

PATHOPHYSIOLOGY

Compression of soft tissues results in ischemia and, if not relieved, it will progress to necrosis and ulceration, even in well-vascularized areas (Figure 98.3). What is seen on the surface is often merely thetip of the iceberg, as confirmed by pressure measurements taken over bony prominences8 (Figure 98.4). In susceptible patients, progression from excessive pressure to irreversible ischemia and tissue necrosis is accelerated by infection, inflammation, edema, and other factors that are not yet understood.

Pressure

Ischemia occurs when external pressure exceeds the capillary pressure, which was shown by Landis9,10 in the 1930s to be 12 mm Hg on the venous end and 32 mm Hg on the arterial end. If the external compressive force exceeds capillary bed pressure (32 mm Hg), capillary perfusion is impaired and ischemia will ensue. Original dog studies demonstrated an inverse parabolic relationship between the amount of pressure and duration of exposure (Figure 98.5). Early studies demonstrated that pressure of 70 mm Hg applied over 2 hours was sufficient to cause pathologic changes in dogs. Dinsdale11confirmed these results in a pig model; perhaps just as importantly, he was also able to demonstrate the absence of injury if pressure could be relieved for as little as 5 minutes, even with pressures as high as 450 mm Hg. Similarly, Daniel et al.12 demonstrated that pressure of 500 mm Hg applied for 2 hours, or pressure of 100 mm Hg for 10 hours, was sufficient to cause muscle necrosis. Interestingly, it was not until pressure of 600 mm Hg was applied for 11 hours that ulceration of the skin could be seen. Not only did these results confirm the relationship between pressure and time, but they also demonstrated that the initial pathologic changes occurred in the muscle overlying the bone, followed by the more superficial soft tissue, involving the skin last.13 Several classic studies investigated pressure and its effects as it relates to location, time, and intensity in humans (Figures 98.1 and 98.2). In the supine position, the maximal recorded pressures were 40 to 60 mm Hg near the heels, buttock, and sacrum. In the sitting position, pressures were greatest near the ischial tuberosities.

FIGURE 98.1. Distribution of pressures in a normal man. A. Prone. B. Sitting. (From Lindan O, Greenway RM. Piazza JM. Pressure distribution on the surface of the human body. I. Evaluation in lying and sitting positions using a “bed of springs and nails.” Arch Phys Med Rehabil. 1965;46:378.)

FIGURE 98.2. Distribution of pressures in a normal man, sitting. (From Lindan O, Greenway RM. Piazza JM. Pressure distribution on the surface of the human body. I. Evaluation in lying and sitting positions using a “bed of springs and nails.” Arch Phys Med Rehabil. 1965;46:378.)

FIGURE 98.3. Unusual pressure sore of lateral thorax.

Inflammation

Maintenance of soft-tissue integrity requires tightly regulated interactions between cells, growth factors, their receptors, extracellular matrix molecules, and a variety of proteases and their inhibitors. When tissue is injured by causes such as unrelieved pressure, there is a demargination and influx of cells responsible for inflammation. For injuries to heal, a series of events unfolds, including vasoconstriction/vasodilatation, coagulation, influx of proinflammatory cells like neutrophils and macrophages, and, finally, matrix formation/maturation. In chronic wounds, there is a breakdown in this sequence, leading to a non-healing wound. Altered immune function has been implicated in the development of pressure sores and molecular evidence points to an imbalance between matrix metalloproteases (MMPs) and tissue inhibitors of metalloproteases (TIMPs). MMPs, especially 1 and 9, are key to cell signaling and migration, whereas TIMPs, especially 1 and 2, bind to these proteases and presumably protect uninjured tissues. Numerous subsequent studies have documented the presence of elevated levels of various MMPs and decreased levels of TIMPs in chronic wounds, or an imbalance between the levels of MMPs and TIMPs.14 In patients with spinal cord injuries, the loss of sympathetic tone results in vasodilatation of denervated tissues, which further intensifies this problem.

FIGURE 98.4. Cone-shaped pattern of injury resulting from unrelieved pressure. The highest pressure and greatest injury is deep, adjacent to the bone. The cutaneous wound is only the “tip of the iceberg.”

FIGURE 98.5. Inverse relationship between time and pressure in the formation of pressure sores.

Edema

Approximately 80% of soft tissue mass is fluid. External pressure on soft tissue increases plasma extravasation, which leads to edema formation, a significant factor in pressure sore formation. Denervation contributes to pressure sore development through loss of blood vessel sympathetic tone and its subsequent vasodilatation, vessel engorgement, and edema. Circulatory deficiencies, such as heart failure, renal failure, and venous insufficiency, are risk factors for pressure sore formation in part due to their propensity to increase edema in dependent soft tissue. On a molecular level, inflammatory mediators such as prostaglandin E2 released in response to the trauma of compression increase leakage through the cell membranes and increase interstitial fluid accumulation.

PREOPERATIVE CARE

As Tchanque-Fossuo et al.5 noted in a 2011 review of evidence-based approaches to pressure sores, the goals of management for a patient with a pressure sore are (1) prevention of complications, particularly invasive infection, related to the existing sore; (2) preventing the existing sore from getting larger; (3) preventing sores in other locations; and, if possible, (4) closure of the wound. Most authors report high recurrence rates after surgical closure of pressure sores. Successful pressure sore coverage is multifactorial but key components include resolution of infection, the preoperative/postoperative relief of pressure, and, for cases of chronically non-ambulatory patients, the control of spasm and contractures.

Nutrition

The nutritional condition of the patient must be evaluated. Normal healing potential exists as long as serum albumin is maintained above 2.0 g/dL. In addition to an adequate supply of micronutrients such as zinc, calcium, iron, copper, and vitamins A and C, a diet with sufficient protein is required for optimal healing of pressure sores. The nutritional literature suggests a requirement of 1.5 to 3.0 g/kg/d of protein to restore lost lean body mass, and 25 to 35 cal/kg of non-protein calories should be delivered daily.15 Optimization of nutritional parameters must be balanced against practicality; some patients will never achieve normal albumin levels until their huge wounds are closed.

Infection

Compression of soft tissue impairs lymphatic drainage, leading to edema, ischemia, and other conditions favorable to colonization and infection by microorganisms. It is known that bacterial counts increase in compressed areas. Robson and Krizek16 quantified the effect of pressure on bacterial count, showing that incisions created in areas of applied pressure and inoculated with known concentrations of organisms allowed for a 100-fold greater bacterial growth than in areas not subjected to pressure. The proposed mechanisms include impaired immune function, ischemia, and impaired lymphatic function. Both pulmonary and urinary sources cause seeding and subsequent infection of pressure sores. Indwelling bladder catheters or self-catheterization programs can result in urinary sepsis in one-third of paraplegic patients. If left untreated, urinary infections can be a constant source of bacteremia.

Pressure sores may or may not present with local infection (deep or superficial). The removal of all nonviable tissue is the essential first step. After a soft-tissue debridement, a specimen should be sent to the microbiology laboratory to assess not only the bacterial types and sensitivities but also for quantitative culture. A result of more than 105 organisms per gram of tissue is diagnostic for invasive infection and is predictive of failure of surgical closure.17 Swab cultures are generally discouraged because they often represent only surface contaminants. Diagnosis of osteomyelitis depends on bone biopsy to identify the causative organism and magnetic resonance imaging to determine the extent of involvement. Surgical closure without eradication of bone infection through resection of devitalized bone is associated with a high recurrence rate. Osteomyelitis from a pressure sore requires a surgical solution, not a medical solution.

Appropriate intravenous antibiotics for cellulitis or osteomyelitis, along with topical antimicrobials, such as silver sulfadiazine, mafenide acetate, and buffered Dakin’s solution, should be used as adjuncts to surgery in the process of clearing infection. Although Dakin’s solution diluted to 0.025% has been shown to be bactericidal with preservation of fibroblasts, all topicals should be used for a limited time after debridement to avoid delayed wound healing.17

Relief of Pressure

The relief of pressure both preoperatively and postoperatively is the key to success, because healing will not occur in the presence of ischemia and/or necrosis. It is well known that relieving the pressure over a bony prominence for 5 minutes every 2 hours will allow adequate perfusion and prevent breakdown.11 Patient, family, and medical staff education is paramount in this goal, and it must be performed in both supine and sitting positions. Adjuncts include dynamic and static pressure-reducing support surfaces, such as foam, wheelchair cushions, specialized mattresses, cushions, and mattress overlays. Surgical staff should use all available means, such as “heel floating” and intermittent scalp massage by anesthesia staff, in addition to pressure point relief to minimize development of pressure sores during procedures in the operating room.

Spasm

Spasticity is common in patients with spinal cord injuries and is a key contributor in the development of pressure sores, especially as it relates to shear. In their review of long-term care patients in Germany, Lahmann et al.18 found that the presence of friction and shear had the strongest association with pressure sore formation. The incidence of pressure sores varies with the level of spinal cord injury. The more proximal the lesion, the higher the incidence of spasm: near 100% in the cervical region, 75% in the thoracic region, and 50% in the thoracolumbar region.13 Treatment of muscle spasticity should be implemented prior to surgery. The most common medical treatments for muscle spasms include baclofen, diazepam, and dantrolene. Botulinum toxin is an emerging treatment for spasticity and has been shown to be effective in reducing localized spasticity of the upper and lower limbs with minimal adverse effects.19 The lasting effects of the botulinum toxin treatment for muscle spasticity are approximately 3 months. If patients fail to respond to medical therapy, surgical intervention may be required, including peripheral nerve blocks, epidural stimulators, baclofen pumps, and rhizotomy. Rhizotomy, the interruption of spinal roots within the spinal canal, can be surgical or medical, the latter using subarachnoid blocks with phenol (phenol rhizotomy).

Contractures

Bedridden patients, especially those with long-standing denervation and/or altered sensorium, tend to develop joint contractures through tightening of both muscles and joint capsules. Contractures are common in hip flexors and contribute to the formation of trochanteric, knee, and ankle ulcers. Patients with significant hip and/or knee contractures should have every attempt made to treat the contractures prior to surgery to help prevent recurrence. If physical therapy is unsuccessful at relieving the contractures, tenotomies are performed. In mobile, wheelchair-bound patients, however, releasing the hip contractures can lead to a flail extremity, which may interfere with transfers.13

Comorbidities

Many chronic medical conditions—such as diabetes, smoking, peripheral vascular disease, and cardiovascular disease—are known to impair wound healing. In diabetics, glucose levels and hemoglobin A1c should be checked and optimized because hyperglycemia slows wound healing and increases the risk of wound dehiscence and infection. Recent work found that hemoglobin A1c greater than 6% was associated with both dehiscence and recurrence and that younger age and hypoalbuminemia were associated with early flap failure.20 Anemia can be an indicator of poor nutrition or chronic blood loss and should be worked up and corrected. In spinal cord injury patients, management of fecal soilage of the wound is necessary through alteration of the bowel routine or a diverting colostomy in selected patients.

SURGICAL TREATMENT PLANNING

When the challenges such as consistent pressure relief, adequate nutrition, eradication of infection, complete debridement, and reliable patient and family education have been accomplished, consideration can be given to surgical closure. Because the recurrence rate of pressure sores has been reported to be as high as 91%, the goal is to provide soft-tissue coverage of the pressure sore defect, while maintaining as many options as possible for future use. A number of strategies for closure have been attempted in the past and in general should be avoided. The temptation to perform a primary closure should be resisted even if the tissues seem to re-approximate easily. By definition, a pressure sore has an absolute tissue deficiency, and simply pulling the tissue together over a bony prominence will almost surely lead to tension and dehiscence. Skin grafting has been attempted with limited success because of the lack of bulk and poor durability in the face of the pressure and shearing forces. It is only successful in a patient where acute illness and immobility will be resolved. More successful strategies include the use of musculocutaneous and fasciocutaneous flaps, with each having its advantages. Flaps that include muscle have significant bulk and excellent blood supply. They, therefore, can be useful where a significant soft-tissue defect is present and also where a history of infection is a consideration. On the downside, muscle is not a good choice in ambulatory patients, as sacrificing muscle may lead to functional impairments.

Even if the patient is ambulatory, surgical planning for patients with pressure sores should include deep venous thrombosis risk stratification and appropriate prophylaxis. Non-ambulatory spinal cord injury patients have additional anesthetic risks when compared with non-spinal cord injury patients of a similar American Society of Anesthesiologists class. Autonomic dysreflexia can produce bradycardia and hypotension, or tachycardia and hypertension. This condition, plus the hyperkalemia that can be caused by the use of succinylcholine in spinal cord injury patients, must be discussed preoperatively with the anesthesia team.

For all patients in general and acute spinal cord injury patients in particular, prevention of pressure sores acquired in the operating room is paramount through intraoperative pressure relief, which can include such measures as “floating the heels.” Moving and positioning patients with pressure sores also requires coordination of the surgical, anesthesia, and support staff. Usually patients are anesthetized on their stretchers and transferred prone to the operating room bed. This process reversed at the completion of the case as patients are often positioned onto their freshly transferred tissue for extubation.

OPERATIVE MANAGEMENT

Debridement

Debridement of the pressure sore removes necrotic tissue, decreases the bacterial count and biofilm, and converts a chronic wound into an acute wound. The presence or absence of sensation in the tissues affected by pressure ulceration becomes an issue most often when sharp debridement is considered. The pain associated with the adequate removal of necrotic tissue in sensate patients makes bedside debridement impossible. In insensate patients, bedside debridement can be performed within reason, although the safety and extent is more often related to the control of hemorrhage. At the start of the debridement procedure, the cavity can be painted with a dilute solution of methylene blue and hydrogen peroxide to help define the cavity and leave a visual guide for excision. After the removal of the necrotic tissue, specimens of viable tissue should be sent for quantitative culture to aid in postoperative systemic and topical antibiotic coverage. Postoperatively, the wound is packed and dressings changed every 6 to 8 hours.

Ostectomy

Removal of the bony prominence is an integral but tricky part of the surgical treatment of pressure sores. Radical ostectomy should be avoided so as to prevent excessive bleeding, skeletal instability, and redistribution of pressure points to adjacent areas. Ischial ulcers best illustrate this as total ischiectomies often result in the formation of a contralateral ischial ulcer. Bilateral ischiectomy has also been proposed, but redistributed pressure has caused perineal ulceration and urethral fistulas. Therefore, removing the minimum amount of bone necessary when debriding ischial pressure ulcers is essential.13

Closure

When planning a surgical strategy, the surgeon should consider not only the present surgery but also the need for subsequent surgical procedures. The choice of closure strategy depends not only on the location, size, and depth of the ulcer but also on the previous surgeries performed. Primary closure, although tempting, is avoided. These wounds represent an absence of tissue and primary closure leads to tension, a scar over the original bony prominence, and dehiscence. Skin grafting has a low success rate, as grafting tends to provide unstable coverage. Musculocutaneous flaps provide blood supply and bulky padding and are effective in treating infected wounds. Disadvantages include sensitivity to external pressure, functional deformity in ambulatory patients, and lack of bulk in the elderly and in spinal cord patients. Fasciocutaneous flaps offer an adequate blood supply, durable coverage, and minimal potential for a functional deformity, and they more closely reconstruct the normal anatomic arrangement over bony prominences. The disadvantages include limited bulk for the treatment of large ulcers. In a recent review of 94 patients with sacral and ischial pressure wounds, there was no statistical difference in recurrence, complications, or morbidity between closure with fasciocutaneous flap and with myocutaneous flaps.21

Ischial Defects

Ischial pressure sores develop in patients who are seated, often in wheelchairs, for long periods of time. Because patients almost always return to sitting after repair of their ischial pressure sores, the recurrence rate traditionally has been high; Conway and Griffith reported a recurrence rate of 75% to 77%. Recent work cites recurrence rates as low as 19% to 33% that may be due in part to improved wheelchair cushions and other modalities.22 Ischial wound location, however, continues to correlate with late recurrence.20

FIGURE 98.6. Flaps for closure of ischial wounds.

FIGURE 98.7. Flaps for closure of sacral wounds.

Closure of an ischial defect is most commonly achieved with fasciocutaneous flaps or myocutaneous flaps. Perforator and free-flap reconstruction have been described but currently is not a mainstay of ischial pressure sore treatment. Some of the more commonly used closure strategies are featured in Figure 98.6. Given the high recurrence rate of pressure wounds, flap design should allow coverage of the ulcer but should not prevent the use of other flaps in the future. Important considerations for flap design include size and depth of the ulcer, quality and pliability of the surrounding skin, presence of previous surgical scars, and the ambulatory status of the patient. For example, the inferior gluteal musculocutaneous flap, based on the inferior gluteal artery, uses only the lower half of the gluteus maximus muscle. This rotation flap does not preclude later use of the posterior thigh flap and is less debilitating in ambulatory patients.

In the superiorly based gluteal flap (Figure 98.7), care is taken to avoid incisions over bony prominences when the patient is in the seated position. The biceps femoris, semimembranosus, and semitendinosus musculocutaneous flaps are said to be effective for ischial ulcers and they can be re-advanced. They are most reliably designed as a V-Y pattern, but do have several disadvantages, including closure is always under tension, the scar is directly over the maximal pressure point, and hip flexion tends to cause dehiscence. The tensor fascia lata (TFL) flap can occasionally be used to close ischial ulcers, although the distal aspect of the TFL flap is usually too thin to offer adequate padding, making the TFL flap, in general, not the best choice. For more complex, deeper, or larger wounds, a combination of flaps may need to be employed.

Sacral Defects

Sacral pressure sores occur in patients in the supine position, most of whom have had an acute illness. Musculocutaneous or fasciocutaneous flaps are the mainstays of surgical therapy but the use of perforator and free-flap reconstruction is increasing (Figure 98.7). Some groups have published that their first choice for reconstruction of ischial and sacral pressure sores is free tissue transfer with microvascular anastomosis to the gluteal vessels.23 Other surgeons using pedicled tissue transfer cite a 21% total recurrence rate after coverage with any flap of sacral wounds, with a lower (17%) recurrence rate after reconstruction with fasciocutaneous flap.24 The most commonly described musculocutaneous flaps are based on the gluteus maximus muscle. The gluteal flap can be based superiorly or inferiorly, part or all of the muscle or both muscles may be used; it can be constructed of muscle or muscle and skin; and it may be rotated, advanced, or turned over (Figure 98.8). Other flaps available include the transverse and vertical lumbosacral flaps, based on lumbar-perforating vessels, although these have significantly less bulk and, consequently, are less useful in deeper wounds.

FIGURE 98.8. Gluteal flap to sacral pressure sore. A. Sacral wound. B. Closure with gluteal fasciocutaneous flap.

FIGURE 98.9. Tensor fascia lata flap to ischial pressure sore. A. Flap design. B. Flap closure.

Trochanteric Defects

Trochanteric ulcers develop in patients who lie in the lateral position, especially in those who have significant hip flexion contractures. Perforator flap reconstruction of trochanteric pressure wounds is possible with a pedicled anterolateral thigh flap. However, the most commonly used flap for treatment of this location is the TFL flap. This highly reliable flap is based on the perforating vessels from the TFL muscle, although caution is advised as the distal aspect of the flap has a random blood supply that sometimes necessitates a delay procedure. Sensation from the nerve roots of L1, L2, and L3 by the lateral femoral cutaneous nerve makes this a potentially sensate flap in patients with spinal cord injury below L3. Rotation of the TFL flap results in a T-shaped junction between the flap and a primary closed donor site that is prone to dehiscence, often the donor site is skin grafted to avoid dehiscence (Figure 98.9).

Other Considerations

Only the most common pressure sores have been discussed in this chapter; however, if an anatomical location can serve as a pressure point, then it has the potential to develop a wound when subjected to unrelieved pressure (Figures 98.1 and 98.2). Some less common pressure sores, like those at the ear or scapula, often can be closed primarily or with local tissue rearrangement. Other pressure sores, such as those at the heels, are difficult to treat (Figure 98.10). In patients who have multiple pressure sores or who have undergone multiple previous procedures, there may not be any local options remaining. In extreme cases of pelvic girdle or lower extremity pressure sores, it may be necessary to consider total thigh flaps in which the femur is removed and the thigh tissue is used to close the wound (Figure 98.11).

POSTOPERATIVE CARE

Many of the preoperative care considerations (e.g., nutrition and management of chronic conditions such as spasm and diabetes) continue into the postoperative period. Careful nursing care is critical to postoperative success. An absorptive non-occlusive dressing is used in an effort to avoid macerating the wound. The control of urine and stool is important and in some cases colostomies are required pre-operatively. Drains are placed intraoperatively to remove serous fluid and to aid in apposition of the flaps to the wound bed. Because of probable intraoperative bacteremia, broad-spectrum antibiotic therapy is continued during the perioperative period. The antibiotics are modified to fit the sensitivity results of intraoperative cultures as these results become available. Pressure relief for the surgical site, usually involving bed rest and a pressure-relief bed, is of utmost importance. The patients are positioned to avoid pressure on the operative site, with turning every 2 hours, and use of low-air-loss mattresses when available. Patients are kept in the postoperative position, with no pressure allowed on the surgical site for 2 to 3 weeks. Before reseating after ischial pressure wound coverage, the patient’s wheelchair should be evaluated to ensure a proper fit and pressure distribution. There is no consensus on reseating protocols, but it is agreed that reseating must be gradual. A common protocol starts with 30 minutes the first day and then adds a 0.5-hour increment daily if tolerated without compromise of the surgical site.5

COMPLICATIONS

In addition to the acute complications related to treating pressure sores—hemorrhage, pulmonary and cardiac complications, and infection—a few long-term complications warrant discussion.

Recurrence

The reasons for high rates of recurrence are multifactorial. The underlying medical problems that contributed to ulcer formation still exist. The presence of spinal cord injury and/or altered mentation in the elderly persist. The labor-intensive nursing care issues (turning, local wound care, and avoidance of urine and fecal contamination) may not have changed from the preoperative setting. Social issues like the lack of financial resources, inadequate family and/or community support, and the use of drugs and alcohol may also be present. Many studies observed that the first 15 to 22 months are the most vulnerable time period for recurrence. A recent review by Keys et al.20 found a 39% recurrence rate of pressure sores after flap closure, with poor blood glucose control, younger age, and poor nutritional status (hypoalbuminemia) as significant risk factors. Patients with multiple risk factors had operative success rates that approached zero.

FIGURE 98.10. Heel pressure sore.

FIGURE 98.11. Total thigh flap. A. Large recurrent ischial wound. B. The distal lower extremity was amputated and the femur was removed with the specimen. C. The thigh tissue provides abundant tissue that can be folded over the wound. D. Closed wound.

Carcinoma

In 1828, Jean Nicholas Marjolin described a tumor that was present in a chronic wound. The term Marjolin ulcer is used to describe carcinoma arising in a chronic wound. The most common cell type is squamous cell carcinoma. In contrast to most other tumors of this type, these tumors tend to be aggressive with 2-year survival rates varying from 66% to 80%. Their metastatic rate, as compared with that of Marjolin ulcers arising in burn scars, is significantly higher at 61% versus 34%. The time interval of development is also reduced. The usual time to appearance is 25 years when compared with more than 30 years in burn-related carcinomas, but it can be as short as 2 years. Because of the aggressive nature of the disease, wide surgical excision to clear margins is recommended. Prophylactic lymph node dissection is not recommended, but therapeutic node dissection is indicated in the case of clinically involved nodes. Adjuvant radiation and/or chemotherapy may be indicated in cases of unresectable tumors or if the patient refuses surgery.

Nonsurgical Treatment

The ultimate treatment of pressure ulcers is not necessarily a surgical correction. If proper preoperative assessment and preparation are performed, there will usually be a period of time in which the ulcers can be observed. If during this time period the ulcer appears to be healing significantly, continuation of nonoperative treatment is indicated. Some patients may never be candidates for surgical correction because of significant medical problems. In these cases, avoidance of unrelieved pressure, control of infection (local and remote), control of incontinence, and improved nutrition may lead to successful ulcer closure, or at least may allow for a stable wound that does not progress.

Debridement of devitalized tissue and wound care remain the foundation of pressure sore management. Despite a plethora of available dressings, growth factors, and adjunctive therapies, there is no strong evidence to indicate that any given wound care regimen is superior, and as a consequence, none has become dominant.4 Enzymatic debridement ointments have been in use since the 1950s and continue to be a valuable tool. Negative pressure wound closure devices increasingly have been used for pressure sores. A recent Cochrane review, however, found that while the data do demonstrate a beneficial effect of wound healing, more quality research is needed before confirming it as a mainstay of pressure wound treatment.25

References

1.  National Pressure Sore Advisory Panel. Consensus Development Conference Staging System, February 2007. http://www.npuap.org/pr2.htm. Accessed August 7, 2011.

2.  Staas WE, Jr, Cioschi HM. Pressure sores—a multifaceted approach to prevention and treatment. West J Med. 1991;154:539-544.

3.  Lyder CH. Pressure ulcer prevention and management. JAMA. 2003;289: 223-226.

4.  Bergstrom N, Horn SD, Smout RJ, et al. The National Pressure Ulcer Long-Term Care Study: outcomes of pressure ulcer treatments in long-term care. J Am Geriatr Soc. 2005;53:1721-1729.

5.  Tchanque-Fossuo CN, Kuzon WM Jr. An evidence-based approach to pressure sores. Plast Reconstr Surg. 2011;127:932-939.

6.  Stal S, Serure A, Donovan W, et al. The perioperative management of the patient with pressure sores. Ann Plast Surg. 1983;11:347-356.

7.  Krause JS, Vines CL, Farley TL, et al. An exploratory study of pressure ulcers after spinal cord injury: relationship to protective behaviors and risk factors. Arch Phys Med Rehabil. 2001;82:107-113.

8.  Barth P, Le K, Madsen B, et al. Pressure profiles in deep tissue. Proceedings of the 37th Annual Conference in Engineering in Medicine and Biology. Los Angeles, CA, 1984.

9.  Landis EM. The capillary pressure in frog mesentery as determined by micro-injection methods. Am J Physiol. 1926;75:548-570.

10.  Landis EM. Micro-injection studies of capillary permeability. II. The relation between capillary pressure and the rate at which fluid passes through the walls of single capillaries. Am J Physiol. 1927;82:217-238.

11.  Dinsdale SM. Decubitus ulcers: role of pressure and friction in causation. Arch Phys Med Rehabil. 1974;55:147-152.

12.  Daniel RK, Wheatley D, Priest D. Pressure sores and paraplegia: an experimental model. Ann Plast Surg. 1985;15:41-49.

13.  Bauer JD, Mancoll JS, Phillips LG. Pressure sores. In: Thorne CH, ed. Grabb and Smith’s Plastic Surgery. 6th ed. Baltimore, MD: Williams & Wilkins; 2006:722-729.

14.  Schultz GS, Davidson JM, Kirsner RS, et al. Dynamic reciprocity in the wound microenvironment. Wound Repair Regen. 2011;19:134-148.

15.  Stratton RJ, Ek AC, Engfer M, et al. Enteral nutritional support in prevention and treatment of pressure ulcers: a systematic review and meta-analysis. Ageing Res Rev. 2005;4:422-450.

16.  Robson MC, Krizek TJ. The role of infection in chronic pressure ulcerations. In: Fredrick S, Brody GS, eds. Symposium on the Neurologic Aspects of Surgery. St. Louis, MO: C.V. Mosby, 1976:410-415.

17.  Bauer J, Phillips LG. MOC-PSSM CME article: pressure sores. Plast Reconstr Surg. 2008;121:1-10.

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