Time
Changes
30 min
Hyperemia
2–6 h
Ischemia
6 h
Necrosis
2 weeks
Ulceration
Friction
Friction is the force resisting relative motion between two surfaces, which leads to shear. Friction develops between the patient’s skin and contact surfaces, such as clothes, bedding, transport equipment, orthotics, wheelchairs, and other appliances. When friction is excessive, superficial skin injuries such as blisters and abrasions develop [30, 31]. Skin breakdown leads to transepidermal water losses and ultimately allows moisture to accumulate. Moisture promotes skin adherence to sheets and other contact surfaces [32].
Shear
Subcutaneous tissue lacks tensile strength and is easily susceptible to shear stress [33, 34]. Patient transfers, sliding, dragging, and the boosting of patients in bed all cause significant shear. Positions such as the semi-Fowler’s or beach chair position as well as an individual sliding down a wheelchair create significant shear over the lower back and buttocks [35, 36].
Moisture
Excessive moisture leads to skin maceration and excoriation and is a risk factor for pressure sore development [37–39]. Incontinence is of particular concern in developing sores [40–42]. Urinary and fecal incontinence are common in the elderly, with even higher rates in institutionalized patients [43, 44].
Malnutrition
There is a strong correlation between malnutrition and pressure sores without any clear direct link [45]. Chronically ill patients with protein malnutrition typically have weight loss, poor wound healing, and immunosuppression, which correlate to increased susceptibility and definitive delayed healing of pressure sores [46–54].
Neurological Injury
Pressure sores are the most common complication and the second most common cause of hospitalization in spinal cord injury (SCI) patients [55–57]. Immobility in the bed or wheelchair causes increased pressure, friction, and shear with eventual pressure sore development. The lack of protective sensation in SCI patients leads to pressure sore development. Patients are unable to maneuver their bodies to off-load prolonged areas of direct pressure. Other causes frequent in this population for pressure sore development include incontinence, spasticity, and psychosocial issues [58, 59].
Prevention
As healthcare moves toward non-reimbursement for hospital-acquired pressure ulcers, there is increasing incentive to prevent these lesions. Although there have been numerous recommendations and studies, the overall incidence of pressure ulcers is unchanged [3, 60]. Although there is no strategy that reduces the incidence to zero, there are several interventions that are now part of standard care, which contribute to the prevention of pressure ulcers [44].
Skin Care
Optimal skin care includes cleaning, hydrating, and protecting. Both nurses and physicians tend to neglect this time and labor-intensive care modality [61]. Most recommendations involve utilizing soap and water followed by rubbing or drying. The surfactants found in soaps, while effective in removing debris, can have a negative effect due to the chemical irritants [62]. The skin has a natural protective acidity that is counteracted by the alkaline nature of most soaps; this can result in a disturbance of the skin flora balance. Multiple alternate cleansers have been marketed to address the problems with soap and water; however, little data exist at this time to recommend any particular product [63].
The benefits of proper skin hydration are established, yet few data recommend any one hydrating product over another [43, 64–66]. The typical method in obtaining skin hydration is through the use of emollients, which occlude the skin surface with a hydrophobic layer. In addition, humectants can be instituted, which act by attracting water from the surrounding environment.
Barrier products protect the skin in the setting of fistulas, stomas, wounds, or incontinence. Traditional products create a protective film over the skin due to the liquid emulsion component. There are recent advances in barrier preparations utilizing a polymer which forms a thin semipermeable membrane over the skin [67]. Despite the widespread use and the proliferation of products, there is scant data on their effectiveness [68]. Although the data on individual agents is lacking, there is evidence that a clear skin care protocol can benefit patients. Cole and Nesbitt found a reduction from 17.8 to 2 % over a 3-year period, whereas Lyder et al. noted an 87 % reduction in a nursing home setting [69, 70].
Incontinence
The relationship between urinary incontinence and pressure sore incidence is not clear, with limited evidence to demonstrate a causal relationship. The use of diapers and sanitary pads in conjunction with skin care is a better option when compared to the risks associated with extended use of a urinary catheter [71].
On the other hand, fecal incontinence is shown to be a risk factor for pressure sores. The etiology of fecal incontinence is sometimes difficult to correct, such as cognitive impairment, radiation injury, inflammatory bowel disease, or sphincter dysfunction. Conservative measures include diet modification and a wide variety of antimotility agents. Diarrhea may be due to infection, which should be ruled out and treated prior to using antidiarrheal agents. If medical management is unsuccessful, surgery may be considered, ranging from attempts at sphincteroplasty to elective colostomy [72, 73]. Although most patients are reluctant to consider an elective diverting colostomy, there is evidence of improved quality of life in patients with severe fecal incontinence [73].
Spasticity
The impact of spasticity on quality of life is not straightforward. Spasticity has been shown to increase the risk of pressure sores and impair the ability to perform activities of daily living (ADL) [74]. In contrast, some cases of spasticity may increase stability in positioning and even facilitate transfers and ADLs and prevent osteopenia [75, 76].
Physical therapy is the first intervention in treating spasticity. Pharmacologic modulation is the next step. The various agents (diazepam, baclofen, clonidine, gabapentin) each have potential for adverse effects [77]. The side effects include sedation, nausea, diarrhea, muscle weakness, and cognitive impairment. Baclofen may also be delivered directly into the central nervous system (intrathecal administration). This route reduces the systemic side effects but introduces possible complications such as pump malfunction [78]. Another method to control spasticity is injection with chemodenervation agents such as ethanol or botulinum. Although the effects are temporary, long-term use of chemodenervation agents will result in denervation atrophy [79, 80].
Surgical intervention may be considered in refractory cases. Local tenotomy or tendon transfer has had mixed results in the treatment of spasticity [81]. Rhizotomy has been complicated by both inadequate treatment of spasticity and severe atrophy, depending on the technique employed [82]. These neurosurgical techniques may be of benefit but usually don’t have prevention of pressure sores as their primary indication.
Pressure Relief
Extensive efforts have been made in pressure modulation, as this is the primary etiology of pressure ulcer pathogenesis. There are various surfaces and products, as well as protocols that direct patient positioning. The support surfaces and devices can be categorized as either constant low-pressure (CLP) devices or alternating-pressure (AP) devices. CLP devices distribute pressure over a large area to reduce the focal impact pressure in any specific area. They include static air, water, gel, bead, silicone, foam, and sheepskin supports. AP devices vary the pressure under the patient to avoid prolonged pressure at a specific anatomic point [83].
The two types of CLP devices that are most commonly used are low air loss (LAL) beds and air-fluidized (AF) beds. The LAL beds float the patient on air-filled cells that circulated warm air, which equalized the pressure and keeps the skin dry. These devices, when used properly, exert a maximum of 25 mmHg on any body part [84, 85]. AF devices work by circulating warm air through fine ceramic beads, creating a drying effect similar to LAL beds. The AF devices boast less than 20 mmHg pressure exerted on the patients; however, they are heavy and expensive [86].
Considerable evidence exists that the use of constant low-pressure overlays or sheepskin significantly decreases the incidence of pressure-related sores, when compared to standard hospital foam mattress [87–91]. Though several studies have compared CLP and AP devices, no clear advantage has been identified, despite attempts at pooled analysis [92].
Cushions for wheelchairs present a unique problem in that the typical wheelchair sling seat exerts a “hammocking” effect that can produce abnormal posture, leading to asymmetric pressure on the trochanter and ischium. Rigid-base cushions provide lumbar support and decrease ischial pressure by allowing wider weight distribution on the posterior thighs [93].
The development of pressure consciousness by the patient is essential in preventing pressure ulcers [94]. Release maneuvers should be performed every 15 min while the patient is seated.
Nutrition
Although limited evidence-based research is available, general consensus indicates that nutrition is an important aspect of a comprehensive care plan for prevention and treatment of pressure ulcers, and it is essential to address nutrition in every individual with pressure ulcers [95]. The body requires adequate calories, protein, fluids, vitamins, and minerals to maintain tissue integrity and prevent tissue breakdown. Little specific evidence exists related to medical nutrition therapy for preventing pressure ulcers [96, 97]. However, early nutrition screening and assessment are essential to identify risk of undernutrition and unintentional weight loss, which may precipitate pressure ulcer development and delay healing.
Diagnosis and Evaluation
Classification
The most commonly used system used for pressure sore classification is the NPUAP staging system [98]. Two recent additions to the staging classification are suspected deep tissue injury and unstageable [98, 99]. Pressure sores fall into one of the four stages based on their severity. The National Pressure Ulcer Advisory Panel (NPUAP), a professional organization that promotes the prevention and treatment of pressure ulcers, defines each stage as follows:
Stage I: The beginning stage of a pressure sore where the skin is not broken but appears discolored (non-blanching erythema of the skin).
Stage II: The outer layer of the skin (epidermis) and part of the underlying layer of the skin (dermis) are damaged or lost.
Stage III: The sore is a deep wound where the skin is lost with exposed fat and appears crater-like.
Stage IV: The sore shows large-scale loss of tissue with possible exposed muscle, bone, or tendons often with dead tissue at the bottom.
Patient Evaluation
A wide variety of factors must be considered when evaluating a new patient with a pressure sore. A thorough history and physical are imperative with meticulous examination of the wound and the patient. The wound history should include wound onset, duration, prior treatments, and current wound care regimens being used. The physical examination requires measurement in three dimensions, along with evaluating for tunneling or undermining [100]. The characteristics of the wound edges for eschar, slough, or necrotic tissue should be examined as well. If necrotic tissue is present, especially at the base, it should be debrided so accurate assessment of the base depth with exposed muscle, tendon, or bone can be determined.
In addition to a thorough history and physical, patient risk factors should also be assessed. The patient’s local environment can provide substantial insight into sources of friction, moisture, shear, and pressure. Spasticity if present, especially in the SCI patient, may need to be controlled medically or surgically. Nutrition should also be assessed with evaluation of serum albumin and prealbumin along with having a good understanding of the patient comorbidities such as diabetes, hypertension, or cardiac disease [101].
Osteomyelitis
Unrecognized osteomyelitis is a major source of morbidity and increased cost due to lengthier hospital stays [102, 103]. Erythrocyte sedimentation rate (ESR) and C-reactive protein levels along with a surgical bone biopsy can help in diagnosing and following progression of wound osteomyelitis [104–110]. MRI appears to be most accurate and is noninvasive while providing detailed anatomic information in regard to the ulcer [111, 112]. Bone biopsy also has consistent accuracy and assists in determining length of antibiotic therapy [113–115].
Surgical Management of Pressure Ulcers
The management of pressure ulcers is largely focused on preventative measures. Early identification and elimination of risk factors are paramount in arresting ulcer progression. Failure of nonoperative intervention is often associated with the development of large, advanced stage, recalcitrant ulcers [116]. It is at this stage that the plastic surgeon is often consulted to evaluate the patient for wound reconstruction.
The basic rules of pressure sore reconstruction are as follows. The ulcer, surrounding scar tissue, and encompassing bursa should be completely excised along with any associated calcified tissue. Underlying necrotic bone and associated heterotopic ossification should also be excised. During the reconstructive process, remaining bony appendages should be padded, and dead space should be resurfaced. The donor site should also be addressed, and occasionally additional grafts are required to ensure flap donor site healing. In general, the flaps should be comprised of a generous amount of tissue, and suture lines should be placed away from areas that are subject to high pressures. Some authors advocate for muscle-sparing flaps to preserve functionality in patients who remain ambulatory [116]. If possible, the initial flap harvest should not encroach on other potential donor sites, as recurrence rates are high despite even the most meticulous reconstruction [117].
Reconstructive Concepts
Surgical debridement is a quintessential step in the reconstructive process and, as such, deserves special recognition. Debridement begins with identifying the extent of the connective tissue bursa that encompasses the wound. This can be done simply by dissection and observation or with the assistance of methylene blue application. The wound appearance is often misleading as these connective tissue shells are frequently much larger than they appear on primary examination. Appropriate excision must include the entire bursa along with any other scar tissue or heterotopic ossification. Tissue should be excised down to a healthy, pliable bed, and when bony involvement is present, debridement should be carried down to healthy, hard, bleeding bone. The importance of adequate debridement cannot be stressed enough. It is the first step in creating a suitable recipient site for tissue transfer, and inadequate debridement is a common cause of flap failure [116].
After adequate debridement to healthy tissue, an appropriate operative approach must be selected. The analysis begins by exploring the different types of tissue transfer available. Isolated muscle flaps offer several theoretical advantages including increased bulk, rich vascular network, and the opportunity for a single-stage reconstructive procedure [117–119]. Animal model studies have also shown that the interposition of muscle between the skin and bone may disperse pressure and decrease the ulceration incidence [28]. However, other studies suggest that muscle flaps carry an increased risk of ischemic necrosis that may not be evident due to intact overlying skin [25, 120]. Despite these theoretical advantages, the success of muscle flaps is not largely proven in the scientific literature, and their indications remain poorly defined [121]. Musculocutaneous flaps, on the other hand, have shown promising results in preventing the vertical spread of underlying osteomyelitis when compared with random skin flaps and are commonly performed [122].
Perforator flaps are also commonly used for pressure sore reconstruction. These flaps generally involve isolating a fasciocutaneous segment and its associated vascular pedicle for transposition. These flaps maintain a rich vascular supply and also spare the underlying muscle, potentially preserving functionality in some patients while also preserving another possible donor site [123, 124]. Free flaps involve transposing a tissue unit and its associated vascular supply to a site distant from the initial harvest. They are not commonly used in pressure ulcer reconstruction [125–128]. The tensor fasciae latae flap (TFL) is frequently selected for free flap transfer. Surgeons have begun to explore the utility of the plantar free flap, which offers the advantage of being harvested from a purposed weight-bearing surface. This flap may prove useful especially in paraplegic patients who no longer bear weight on their lower extremities [116].
Another important concept in pressure sore reconstruction is tissue expansion. Expanders offer the advantage of increasing the size of sensate skin that can be advanced. This is particularly useful in spinal cord injury patients, with the hopes that sensate skin will prompt pressure avoidance behavior modifications [129–131]. Tensor fasciae latae and lumbosacral fasciocutaneous flaps are two types of flaps amenable to expansion, and their donor sites can often be closed primarily [132]. The disadvantages to tissue expansion involve placing a foreign body in a chronically infected wound, which theoretically creates a nidus for infection to continue to develop. As such, the primary indication for tissue expansion is to allow for sensate coverage of shallow ulcers that require minimal dead space filling, if any at all.
Reconstruction by Anatomic Region
Sacrum
There exists a multitude of options for sacral wound reconstruction, including but not limited to wide undermining and primary closure, random skin flaps, pedicle island flaps, free flaps, gluteus myoplasty, and selected advancement flaps [117, 123, 133]. The most frequently described techniques are the musculocutaneous rotation and advancement flaps, which are based on the gluteus maximus [134]. These flaps are often advanced using V-Y technique and harvest the superior aspect of the gluteus muscle in an attempt to preserve as much muscular function as possible (Fig. 14.1). Other reported techniques include gluteal artery perforator flaps, multi-island propeller flaps, and flaps harvested from the thoracolumbar region [135–138] (Figs. 14.2 and 14.3).
Fig. 14.1
Photographs depicting reconstruction of a superior gluteal cleft wound. Preoperative photo demonstrating the wound and the marked areas from which the flaps will be harvested (a). Postoperative photo demonstrating the end result of bilateral superior gluteal fasciocutaneous V-Y advancement flaps (b)
Fig. 14.2
Sacral ulcer reconstruction with rotational gluteal flap
Fig. 14.3
(a) Vascular supply to the gluteal musculocutaneous flap. (b) Superior gluteal artery is preserved and rotated with the flap. (c) The flap is elevated and rotated medially to cover the sacral wound
Midline Defects
Lumbar perforator flaps afford an easy transposition for low posterior midline defect coverage and spare the muscles of the lower extremities. Technical advantages include a large arc of rotation, and the donor site can be closed in primary fashion [139]. Studies report no recurrence and preserved sensation at 1.5 years using innervation-sparing bilateral fasciocutaneous and myocutaneous V-Y advancement perforator flaps for large sacral wounds [140].
Ischium
Ischial ulcers are frequently reconstructed by means of a posterior V-Y advancement flap based on the biceps femoris of hamstring muscles. The biceps advancement flap is preferred in ambulatory patients and has the most successful documented outcomes [141]. The hamstring-based flap is preferred in patients with spinal cord injury. Both can be readily advanced in the event of recurrence [116]. Other options include inferior gluteal rotation flaps, gluteal thigh flaps, perforator flaps, and free flaps [142–144]. Inferior gluteus maximus island flaps and inferior gluteal thigh flaps also have shown success rates of 94 % and 93 %, respectively [144]. Some authors have advocated the use of rectus abdominis flaps. However, others believe this muscle to be especially important in paraplegics as it initiates vertebral flexion, respiration, urination, defecation, and vomiting [145–147]. Sensate tensor fasciae latae flaps, innervated by the lateral femoral cutaneous nerve, also have been shown to assist in the sensation of rectal filling [125, 128, 148] (Figs. 14.4–14.6).
Fig. 14.4
Artist depiction of the gluteal thigh flap. The flap is based on the inferior gluteal artery and can be rotated to cover trochanteric, ischial and sacral ulcers. a. Anatomy of the posterior thigh including the dominant blood supply to the flap, the inferior gluteal artery.b. The axis of the flap is drawn showing the rotation point. The x marks the areas the flap can be rotated to cover (ischial and trochnateric ulcers)
Fig. 14.5
Marking and excision of the ischial ulcer a. The ulcer is shown b. Marking for proposed excision of the the ulcer c. Undermining of the ulcer is displayed. The marking is made at the edge of the undermined area d. The ulcer is packed with surgical tape e. The ulcer is excised just outside the dotted line f. The ulcer is completely excised including the undermined areas. The incision is outside the dotted line
Fig. 14.6
Reconstruction of the ischial ulcer with gluteal muscle flap and posterior thigh fasciocutaneous flap. g. Gluteal muscle flap covering ischium h. Quilting sutures to secure posterior thigh flap i. Posterior thigh flap has been rotated and secured j. Donor site defect k. Closure of donor site defect with skin graft
Trochanter
Trochanteric ulcers are generally reconstructed by flaps based on the tensor fasciae latae (TFL) or vastus lateralis [125, 128, 148–152]. The TFL is a versatile donor and offers many options for reconstruction. It can be transferred as muscle only, skin and muscle, and as an island or free flap. TFL V-Y advancement flaps have documented success rates of 93 % in this anatomical region [144]. However, if a Girdlestone procedure, or femoral head ostectomy, is also required, the vastus lateralis becomes the muscle of choice and can be transposed in a muscular or myocutaneous flap [153–155] (Fig. 14.7–14.10).
Fig. 14.7
Artist’s depiction of trochanteric ulcer reconstruction using the tensor fasciae latae flap. The flap is marked preoperatively (left) and raised as a pedicled musculocutaneous flap. The flap is rotated on its pedicle to cover the trochanteric defect, and the donor site is closed primarily (right)
Prophylactic Bone Resection
Another topic that warrants mention is that of prophylactic bone resection. Some surgeons recommend prophylactic resection of bony prominences beneath the area to be reconstructed [156]. Partial ischiectomy has been associated with recurrence rates of 38 %, while extension to total ischiectomy has reduced recurrence rates to only 3 % [117]. While the results are promising for total unilateral ischiectomy, these patients frequently develop ulcers on the contralateral side due to alterations to the bony geography that, in turn, reassign the points of maximum pressure [157]. With this in mind, some authors have begun to recommend prophylactic bilateral ischiectomy. However, such resection frequently increases the risk of developing perineal ulcers, urethrocutaneous fistulas, and ulcers in the distribution of the pubic rami. Therefore, bilateral prophylactic ischiectomy should be employed only during reconstruction of deep, extensive recurrent ischial wounds [158–160].
Postoperative Management
The main goal of postoperative management is the prevention of ulcer recurrence. Care should be focused on the management of incontinence and spasticity, as well as ensuring adequate nutritional support. Relief of pressure, shear forces, friction, and moisture are paramount, and these parameters should be constantly assessed [117, 161–165]. Quite possibly the most important adjunct to postoperative physical therapy is ensuring patient understanding and compliance [166–169]. With regard to postoperative care, the ongoing debate centers on the length that a patient should remain immobilized after surgery and timing of initiation of sitting protocols. Historically, patients were kept on bed rest 6–8 weeks postoperatively based on the theory that wounds reach maximal tensile strength by this point. However, more recent studies suggest that the period of immobilization can be shortened to 2–3 weeks or even 10–14 days without significant changes in outcomes [144, 170].
Regardless of the length of postoperative immobilization, active and passive range of motion exercises of the unaffected limb should begin almost immediately, and the affected limb should be ranged only just prior to the commencement of a sitting protocol [168]. Typical sitting regimens begin at 15 min intervals once or twice a day. Frequent pressure release maneuvers are of vital importance, and surgical sites are carefully monitored for any evidence of recurrence [168]. These intervals are gradually increased until discharge [170]. Prior to discharge, patients undergo seat mapping to evaluate support surfaces for potential areas of recurrence. Maximum allowable pressures are 35 mmHg for patients unable to perform pressure release maneuvers and 60 mmHg for those who can [171].
Outcomes and Complications
The principal metric of success regarding pressure sore reconstruction is the rate of recurrence. A wide range is reported in the literature, and it is therefore difficult to determine any true values [163, 165, 172–176]. In general, young, post-traumatic paraplegics and cerebrally compromised elderly patients have the highest recurrence rates at 79 % and 69 %, respectively. Given such high numbers, these preoperative conditions may preclude surgical reconstruction, as patient compliance is necessary and frequently an issue [165, 168]. As expected, children represent the other end of the spectrum and display considerably lower recurrence rates [177].
With respect to sacral wound management, success rates have been reported around 30 % for nonsurgical management and split-thickness skin grafting. However, ostectomy and ulcer excision with rotational flap reconstruction have resulted in success rates as high as 84 % [178]. Trochanteric ulcers have shown slightly higher success rates with nonsurgical management and split-thickness skin grafts, recorded at 41 % and 33 %, respectively. However, ulcer bursa resection and reconstruction with rotational flaps have reported success rates of up to 92 % [178]. In addition to nonsurgical and grafting of ischial ulcers, primary suturing has been reported with success rates around 50 %. Nevertheless, the best outcomes result from total ischiectomy with regional rotation flaps, which have reported recurrence rates of only 35 % [178]. Even with surgical reconstruction, the best outcomes are only achieved by collaboration between plastic surgeons and physical medicine and rehabilitation physicians [177].
Fig. 14.8
Excision and trochanteric wound reconstruction with rotational musculocutaneous flap. a. Excision of ulcer to healthy tissues b. Removal of ulcer c. Excision of involved bone d. Hemostasis of wound bed e. Reconstruction of wound with rotational musculocutaneous flap
Fig. 14.9
Artist depiction of anatomy of the TFL flap. The flap can be rotated to cover trochanteric and ischial ulcers
Fig. 14.10
Artist depiction of elevation of the TFL flap. The flap is elevated as a musculocutaneous flap with blood supply subfascial with the vastus lateralis. It is then rotated and donor site closed primarily
Complications of these procedures include hematoma, seroma, wound dehiscence, and, most importantly, ulcer recurrence. Suture line breakdown usually heals, and persistent slough from the wound is usually an indicator of inadequate preoperative debridement [111]. The same preoperative assessment for risk factors should be conducted once again, and patients should be nutritionally optimized before return to the operating room [115, 144]. Options for revision procedures include readvancing the initial flap, readvancement of a different plane of the initial flap, or harvesting a new flap from untouched territory, among others. Amputation and salvage flaps should be considered last resort options for critically ill patients with multiple confluent ulcers and/or acute life-threatening disease such as uncontrollable pelvic osteomyelitis [179, 180]. For any recurrent ulcer, biopsies should be sent for microscopic analysis to rule out malignant degeneration, also known as the development of a Marjolin’s ulcer. This transformation may be preceded by a change in symptoms not limited to increasing pain and/or discharge, a foul odor, or recurrent bleeding. Latency from the initial insult has been quoted at 20 years for pressure ulcers, and early recognition with proper staging and management offers the best chance for a cure [181].