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The diverse nature of pressure sores requires a multidisciplinary approach to treatment. The surgeon cannot schedule the patient for surgery and expect a healed wound that will not reoccur. Without this cooperation, nursing home caregivers and primary care physicians should regularly evaluate their elderly and wheelchair-bound patients for the first signs of tissue necrosis. Internists can manage metabolic and physiologic diseases. Dietitians can determine energy requirements and suggest nutritional supplements to meet the patient’s caloric goals. Social workers should investigate the patient’s home for environmental hazards and help eliminate financial barriers to therapeutic intervention. The plastic surgeon examines the patient for severity of the wound and to determine the best surgical course of action, if indicated. The plastic surgeon can coordinate and mobilize the many team members. Case managers schedule appointments and coordinate transportation for routine checkups. If a surgical intervention is pursued, specially trained nurses can assist with postsurgical flap checks, dressing changes, and other nursing functions; they are an extension of the surgeon throughout the acute setting. Finally, physical and occupational therapists evaluate patient mobility and recommend custom equipment to help with healing and prevention of future pressure sore formation. These therapists can assist with range-of-motion exercises to help treat and prevent flexion contractures as well as activities of daily living. With a combined multidisciplinary team, patients receive the best prognosis for long-term pressure sore treatment and prevention.

The immobilized patient is at risk of developing breakdown of his or her skin and soft tissue. This breakdown is the necrosis of soft tissue described by the medical community as a pressure sore. Pressure sores are complex wounds that result from 1 or more contributing factors. Stress, time, spasticity, infection, edema, denervation, moisture, and poor nutrition are considered fundamental issues that result in or affect pressure sore development.

Position and contact with the environment is the critical component to the pressure sore injury. This contact is increased at particular points on the body that overlay underlying bony prominences. Prolonged contact between the human body and external objects compresses the flesh, resulting in ischemic necrosis and pressure sore formation of the intervening tissues. There is an inverse parabolic relationship between time and pressure in pressure sore formation. A high level of pressure induces tissue ulceration within a short time interval, and conversely, low levels of pressure require a prolonged timeframe to cause tissue damage. Spasticity of muscles contributes to pressure sore development by prolonging immobility and impeding surgical intervention.

Soiling of the skin can introduce microorganisms to the skin surface. This is especially of concern in the immobilized patient with a developing pressure sore. The presence of infectious microbes, which flourish in the media-like cellular breakdown products due to tissue necrosis, interfere with the healing of damaged tissues. The fluid environment of pressure sores contributes to both infection and necrosis. A contributing factor to edema is denervation of blood vessels. Moisture on pressure sores should be prevented by frequent dressing changes and the use of urinary catheters for incontinent patients.

Poor nutrition is a risk factor for the formation and exacerbation of pressure sores. The patient should be evaluated carefully by nutritional experts to determine the caloric needs and whether these demands are being met. The end goal is to meet nutritional requirements for normal wound healing. Clinical judgment should be applied in patients receiving nutritional therapy; the patient should be gaining strength and the wound site should be inspected regularly for signs of healing.

The vast majority of pressure sores result from contact between the patient and the posterior surface of the lower extremities. However, other locations are susceptible to pressure necrosis including arms leaning over bed rails, nasogastric and feeding tubes taped upward against the nasal ala, and the forehead area in prone patients. Almost two thirds of pressure sores occur while patients are in the hospital. Sacral, ischial, and trochanteric pressure sores are the most common sites.

The configuration of the pressure sore is that of a 3-dimensional cone. The majority of injury due to pressure necrosis is deeper and larger below the skin surface. This is due to vector forces that disperse high pin-point compression over a deep, wide area. In addition, the subcutaneous muscle has a higher metabolic activity and thus is more sensitive to prolonged anoxia. As objects trap the underlying muscle between the skin and the deeper bony prominence, the muscle’s vasculature is compromised.

There are 4 generally accepted stages of pressure sores. Stage I is exemplified by continued erythema of skin that cannot be blanched with a gloved finger. Stage II involves damage to the skin via ulceration, blistering, or abrasion, and is not really a pressure sore in the strict definition. Stage III lesions represent full-thickness destruction of the skin. Stage IV lesions include involvement of muscle, tendons, joints, nerves, and even bone. Stage III and IV lesions generally require surgical intervention.

Since the vast majority of pressure sores occur in the hospital, patients at risk must have routine skin inspection. Nurses are the eyes and ears of away physicians, and they must be attentive to the risk factors for pressure sore formation. Patients should be turned regularly every 2 hours for inspection for skin necrosis, particularly the pelvic area, and to shift the pressure points. Acute spinal cord injury patients are highly susceptible to pressure sore formation in the intervening days and should receive particular attention. Numerous bed technologies are available to assist nurses in these duties, but nurses turning and inspecting patients cannot be supplanted. The use of the many pressure-relieving devices often leads to complacency rather than prophylaxis of injury.

All patients admitted to the hospital should be continually evaluated for possible pressure sore formation. This begins with a clinical index of suspicion based on admitting diagnosis, current state of mobility, type of treatment being rendered to the patient, and the iatrogenic effect on the patient’s life. The usual method of pressure sore discovery comes from a thorough physical examination despite the absence of signs or symptoms.

Once a pressure sore is detected, a thorough clinical evaluation should be performed. Blood cultures are in order if the patient has signs and symptoms of sepsis: fever, elevated white blood cell count with a “left” shift (ie, elevated granulocytes), rigors, sweating, or change in mental status. Contributing factors must be addressed. This includes biopsies of the pressure sore itself to be sent for quantitative and qualitative wound cultures. Urine incontinence must be addressed to prevent maceration and soiling of the wound. Foley catheters should be placed in these patients. Stool incontinence warrants frequent dressing changes.

Obtaining consent from the pressure sore patient for surgical procedures sets the stage for what should be expected and possible outcomes. The patient needs full understanding of the large investment being made to treat this potentially lethal condition. Similarly, the clinician must carefully assess the patient’s ability to understand the acute cooperation and the long-term commitment of preventing recurrence. A meeting of the minds between clinician and patient serves to both educate the patient and provide an agreed clinical outline for the ensuing care.

Seven surgical goals can be identified for pressure sore treatment. These goals include total excisional debridement of the necrotic tissue, excision of infected or protuberant bone, acquiring hemostasis after debridement, obliteration of the anatomical dead space, coverage of the wound with vascularized flaps, flap placement to maximize blood flow, and restoring patients to their pre-injury state of independence. Some debilitated patients cannot tolerate a surgical procedure and should be considered for nonoperative therapeutic intervention. Topical therapy for the treatment of a pressure sore includes a spectrum of enzymes for debridement, elemental pastes, antimicrobials, and solutions. Spontaneous wound closure in small- to medium-sized pressure sores enhances as the bacterial counts decline. However, the finalized product is scar tissue with poorly developed skin covering, and the friable skin is subject to recurrent necrosis.

The patient and clinician are best served by performing pressure sore wound debridement in the operating room under general endotracheal anesthesia. Surgical equipment, lighting, patient positioning, and ability to obtain hemostasis are superior. The anesthesiologist can monitor the patient for signs of pain, excess blood loss, hypotension, and shock while the surgeon focuses on the wound. The surgical end result will be well-vascularized tissues with increased tissue oxygenation, and removal of all physical barriers to wound healing by whatever closure technique.

Surgical closure of the debrided pressure sore is best achieved with durable tissue using local rotation, fasciocutaneous, or musculocutaneous flaps. Small wounds in areas of excess skin can, theoretically, be excised and closed primarily. Such primary repairs place tension on the wound and a suture line directly over a pressure point. Skin grafting is another possible option, but the goal of healed skin grafts is to provide skin coverage and not padding.

Various flaps may be designed to cover the sacrum. The local buttock rotation flap is an excellent primary method to closure of the prepared sacral wound. A second design is the transverse lumbosacral flap. With both the local buttock rotation flap and the transverse lumbosacral flap, a deficit is created so that the primary wound can close the sacral wound. Closure of these iatrogenic, secondary wounds is performed with skin grafting. These secondary wounds are not located over bony prominences, so they are not subjected to the pressure and stress compared with the sacral area and will heal.

Ischial pressure sores are common to the wheelchair-bound seated patient as the ischium is a critical structure to pelvic stability in the seated position. Flap design depends on the size of the defect and previous closure methods for recurrent ischial pressure sores. Local random skin flaps are best used for small, shallow wounds. Other options include the tensor fascia lata flap, a reliable pedicle with a length advantage and that may restore sensate skin. The gluteal thigh flap is another option that provides bulk, reliability, and—interestingly—sensation to the ischial area. If muscle is not desired, an inferior gluteal artery perforator flap can be fashioned. Other described flaps include use of the hamstrings and total thigh flaps for multiple, recurrent pressure sores.

Skin and tissue breakdown over the greater trochanter—the lateral prominence of the proximal femur—is most associated with prolonged lateral decubitus positioning and large patients in narrow wheelchairs. The primary flap used to cover a debrided trochanter pressure sore wound is the tensor fascia lata musculocutaneous flap. The tensor fascia lata is a workhorse flap applicable to both ischial and trochanteric and sometimes sacral defects. Other options include the use of muscle flaps without skin, such as the gluteus and vastus lateralis; coverage is then achieved with a skin graft over the muscle belly.

Care for the postoperative patient is the same for the closure of pressure sore wounds as other flaps. The dressing is changed as necessary to keep the skin clean. Drains, if placed, are useful monitoring devices for excessive bleeding from underneath the flap. The operating physician should monitor the patient’s postoperative progress at regular intervals. However, the nursing staff is the crucial physician extender to keep an eye on the patient and report problems immediately. The majority of focus will be on the flap tissue, but other classic postoperative issues should not be ignored. Feeding should begin as tolerated by the patient to enhance tissue healing.

The last goal of surgical intervention is to restore the patient’s level of independence as before the pressure sore developed. This requires approximately 2 months of postoperative attention by the surgeon and a lifetime of care by the patient. Beginning at 2 or 3 weeks, the healing flap is sufficiently vascularized to support the patient’s sitting or lying on the flap for up to 10 minutes 3 times per day. This regimen is continued until 6 weeks postoperatively, at which point flap pressure time can increase to 2 hours. The exception to this is for ischial pressure sore repairs, which need a brief period of pressure relief every 10 minutes.

Several unresolved problems may prevent achievement of a healed, uncomplicated wound. The patient must be compliant and motivated to heal their injury despite their altered physical self. This requires good nutrition, rehabilitation and strengthening of their deconditioned state, and continence maintenance if necessary. Should recurrence of the wound develop, the physician must provide emotional support toward the patient’s frustrations, while determining and appreciating the raison d′être for the treatment failure. The patient, similar to other victims of chronic disease states, needs encouragement, support, and commitment from their caregivers.