International Wound Journal ISSN 1742-4801
INVITED REVIEW
A review of the surgical management of heel pressure ulcers in the 21st century David C Bosanquet1 , Ann M Wright2 , Richard D White1 & Ian M Williams1 1 Regional Vascular Unit, University Hospital of Wales, Cardiff, UK 2 Department of Surgery, Royal Gwent Hospital, Newport, UK
Key words Amputation; Angiosome; Calcanectomy; Heel ulcer; Pressure ulcer
Bosanquet DC, Wright AM, White RD, Williams IM. A review of the surgical management of heel pressure ulcers in the 21st century. Int Wound J 2015; doi: 10.1111/iwj.12416
Correspondence to Mr IM Williams Regional Vascular Unit University Hospital of Wales Heath Park Cardiff Wales CF14 4XW UK E-mail: [email protected]
Abstract Heel ulceration, most frequently the result of prolonged pressure because of patient immobility, can range from the trivial to the life threatening. Whilst the vast majority of heel pressure ulcers (PUs) are superficial and involve the skin (stages I and II) or underlying fat (stage III), between 10% and 20% will involve deeper tissues, either muscle, tendon or bone (stage IV). These stage IV heel PUs represent a major health and economic burden and can be difficult to treat. The worst outcomes are seen in those with large ulcers, compromised peripheral arterial supply, osteomyelitis and associated comorbidities. Whilst the mainstay of management of stage I-III heel pressure ulceration centres on offloading and appropriate wound care, successful healing in stage IV PUs is often only possible with surgical intervention. Such intervention includes simple debridement, partial or total calcanectomy, arterial revascularisation in the context of coexisting peripheral vascular disease or using free tissue flaps. Amputation may be required for failed surgical intervention, or as a definitive first-line procedure in certain high-risk or poor prognosis patient groups. This review provides an overview of heel PUs, alongside a comprehensive literature review detailing the surgical interventions available when managing such patients.
Introduction
A pressure ulcer (PU) is defined as a localised injury to the skin or underlying tissue, frequently occurring over bony prominences, arising as a result of pressure and/or shear forces (1). They are invariably the result of localised tissue ischaemia and failed wound healing (2). Macerated, injured and dry tissues contribute to PU development, as does systemic malnutrition, global limb ischaemia and physiological stress (3,4).
Anatomy and pathophysiology of heel PUs
The principal blood supply of the heel comprises the posterior tibial and peroneal arteries. Perforating branches of the peroneal artery supply the lateral aspect and skin of the heel, whilst the heel pad is supplied via the medial calcaneal branch of the posterior tibial artery (PTA). The heel is well designed to withstand forces incurred during standing and ambulation. The plantar surface of the heel comprises superficial and deep fascia, interspaced with tightly © 2015 Medicalhelplines.com Inc and John Wiley & Sons Ltd doi: 10.1111/iwj.12416
Key Messages
• a combination of marginal blood supply, thin skin and adipose tissue and bony prominences make the heel particularly prone to pressure ulceration when the leg rests supine • partial or total calcanectomy is an option for patients with osteomyelitis • revascularisation, which can be either open or endovascular, should be considered in patients with pressure ulcers and peripheral vascular disease • specialist institutions have reported using free flaps for complex heel wounds, with or without concomitant revascularisation • a small minority of patients are best served by timely amputations packed adipose tissue, and further cushioned by the attachments of abductor digiti minimi and flexor digitorum brevis muscles. 1
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Surgical management of heel pressure ulcers
Fibrous septa travel throughout the heel, connecting the underlying periosteum of the calcaneus with the overlying dermis (5). This tough elastic pad provides sufficient padding to withstand stress and shear forces. In contrast, the posterior aspect of the heel is particularly prone to ulceration due to its thin skin and lack of fat and muscle coverage. When supine, the entire weight of the lower limb rests on the heels. Weight is focused on a small area of the skin overlying the posterior tubercle of the calcaneus, creating a localised area of high pressure (6). The subcutaneous tissue has a marginal blood supply in this region, and early necrosis of the superficial adipose tissue has been demonstrated in PUs (7). Unsurprisingly, the strength of heel tissues has been shown to decrease with age (8).
Classification of PUs
PUs are classified by stage, from I to IV, depending on the depth of tissue loss (Table 1). Stage I is a non-blanching (i.e. non-resolving after removal of pressure) erythema of the skin, without any actual tissue loss. Stages II and III involve partial and total loss of the dermis, respectively, without involvement of deeper structures. Stage IV PUs are defined as full-thickness tissue loss through subcutaneous fat to the underlying tissues, with exposed bone, muscle or tendon. They may contain necrotic or sloughy material, and frequently undermine. Shear and friction are thought to account for more superficial ulceration, whilst pressure damage is predominantly accountable for deeper injury (7,9). Recently, the term ‘Deep Tissue Injury’ has been added as an unclassifiable type of PU. This term describes an area of intact skin covering the underlying damaged tissue, which may be ‘mushy’ or ‘boggy’ on palpation (1). Classification is only possible once the skin has been breached and the ulcer base examined. Table 1 Classification of pressure ulcers (PUs) Stage 1 Stage 2 Stage 3 Stage 4
Intact skin with non-blanching erythema in a localised area, typically over a bony prominence Partial thickness loss of dermis, with a shallow open ulcer Full-thickness tissue loss. Subcutaneous fat may show but not muscle, tendon or bone Full-thickness tissue loss with exposed muscle, tendon or bone
Derived from reference (27).
Site and severity of PUs
PUs can develop on any site of the body subject to prolonged external pressure. The heel and the sacrum are the most common areas affected. Incident data vary widely depending on the type of population examined, from the intensive care unit and acute medical care, to long-term rehabilitation facilities. The highest prevalence has been documented in those in ‘long-term acute care’ (up to 27⋅3%) (10), although incidence figures of 1⋅6–4⋅4% are more frequently reported in unselected inpatients (Table 2). Historical reports suggest that sacral PUs were twice as prevalent as heel PUs (11). Whilst a few recent studies continue to demonstrate an increased propensity towards sacral PUs (12,13), several others show that the incidence of heel PUs appears to be much closer to that of sacral PUs (14–16). Overall, the heel PUs account for up to a third of all documented PUs (Table 2). Data on the proportion of stage IV heel PUs specifically, and therefore likely to warrant surgical intervention, are more scanty. Data from 5947 university and general hospital patients from five countries showed that 11⋅4% of all heel PUs were grade IV (14). In another observational study from Sweden comprising 1192 hospitalised patients, 18% of all heel PUs were grade IV (15). Prognosis of heel PUs
Development of a PU, irrespective of its location, is associated with considerable mortality. Brown showed that development of a nosocomial full-thickness PU is associated with a 180-day mortality rate of almost 70% (17), similar to that reported by other authors (18,19). This striking mortality is often interpreted as a result of coexistent diseases that result in both PUs and high mortality rates, rather than attributing the mortality directly to PU (18,19). However, for outpatients attending specialist clinics, the prognosis for patients with heel PUs is more promising. In one prospective study of 157 heel PUs treated conservatively, 66% healed after a median of 200 days with 7% being resolved by a major amputation (20). A further 8% remained unhealed at the end of the study and 20% unhealed at the time of patient death. Numerous papers have shown that heel wounds in particular are associated with poorer outcomes when compared with tissue loss in the adjacent areas of the foot. Cevera et al. suggest limb salvage is 2–3 times less likely with heel ulceration compared with metatarsal ulceration, and is 1⋅5 times more expensive to manage (21). Pickwell et al. showed healing time
Table 2 Incidence of heel PUs in acute medical inpatients from recent observational studies; overall incidence and proportion of heel PU as a percentage of all PU
Study
Year
Location
No. of centres
Gallagher et al. (12) Gunningberg et al. (15) Jiang et al. (13) Vanderwee et al. (14)
2008 2011 2014 2007
Ireland Sweden China Multinational (five countries)
3 5 12 25
No. of patients
Overall incidence of heel PU (%)
Proportion of heel PU compared with all PU (%)
672 1192 39 952 5947
3⋅0 4⋅2 1⋅6 4⋅4
14⋅1 37 14⋅9 24⋅2
PU, pressure ulcer.
2
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to be prolonged in heel wounds compared with digital and plantar/midfoot wounds, although this may in be partly because of increased comorbidities in patients with heel wounds (22). Dosluoglu et al. compared revascularisation in 277 patients with heel or non-heel tissue loss (23). Whilst limb salvage rates were equivalent between the groups, survival rates were significantly worse in the heel ulceration group. Tukiainen et al. published a series of revascularisation and free flap tissue transfer for complex pedal wounds. The location of tissue loss on the heel (compared with elsewhere on the foot) was a significant independent predictor for subsequent amputation (24). Various ulcer-specific attributes are also known to predispose to poorer outcomes, including increasing size (20), longer wound duration (25) and the presence of osteomyelitis (26). Risk assessment for development of heel pressure ulceration
Primary prevention of PUs is of paramount importance, for which assessing an individual’s risk is the key. This involves careful skin assessment and clinical judgement using one of a number of assessment tools (27). The Waterlow PU risk assessment tool looks at a number of factors with several categories listed to provide an overall score for the risk of ulceration (28). Another scoring system for predicting PU risk is the Braden scale (29,30). This examines six criteria: sensory perception; moisture; activity; mobility; nutrition; and friction and shear. The Braden scale tends to be used in North America, whilst the Waterlow score is principally used in the UK and Europe. The importance of the initial assessment for the presence of risk factors cannot be stressed strongly enough. On the rare occasions when a PU develops in hospital, it might be considered negligent if stringent admission assessments have not been made and documented in the medical notes. Failure to identify and address risk factors when PUs develop makes any potential medicolegal claim difficult to defend. Patients who are at high risk for the development of PU as a result of specific medical states can also be identified. These include elderly patients (12) and patients with immobility [e.g. because of stroke or spinal cord injury (12,31)], peripheral sensory loss (32), renal disease (23), hypoalbuminaemia (12,23), peripheral vascular disease (PVD) (20,33) and diabetes (21,33) and with varying degrees of neuropathy. Patients undergoing surgery are also at increased risk (34). Treatment
Initial treatment for heel PUs must take into account the vascular state, presence of infection and pressure relief [i.e. VIP assessment (35)] prior to management of the wound. This requires input from a multidisciplinary team (MDT) involving vascular clinicians, podiatrists, tissue viability nurses, orthotists, dieticians, radiologists and diabetologists. There is evidence that local MDTs, for diabetic patients specifically, reduce the overall rate of major amputation and of recurrent ulceration (36,37). Non-surgical prevention and management of heel PUs, primarily by offloading and good skin/wound care, has been extensively reviewed elsewhere (27,38–40). Surgical intervention is often warranted in the context of extensive soft tissue infection, osteomyelitis or vascular insufficiency. © 2015 Medicalhelplines.com Inc and John Wiley & Sons Ltd
Surgical management of heel pressure ulcers
Debridement
With the exception of dry non-infected eschar, removal of devitalised tissue is mandatory for successful wound healing. Moist necrotic tissue will invariably become infected, promoting an inflammatory response, which impairs wound healing (41). Debridement can be achieved by a number of methods: autolytic debridement using the body’s own enzymes (typically under an occlusive dressing) to cleave necrotic tissue from healthy tissue; chemical/enzymatic debridement using various topical agents; mechanical debridement using specific dressings, which adhere to the necrotic tissue and ‘debride’ the wound when removed or using forceful saline lavage; biological debridement using maggots; or surgical debridement (42). Surgical debridement is the fastest method, and is appropriate in cases of extensive tissue loss/infection. Most of the time, surgical debridement can be performed easily at the bedside for small or superficial PUs. Occasionally, debridement in the operating room is often required for more extensive PUs (43). Schiffman et al. (44) describe the key steps in PU debridement: 1. expose any undermined areas by excising the overlying tissue 2. remove the callus from the wound edge 3. remove all non-viable and grossly infected tissue 4. obtain a deep tissue biopsy for microbiological culture and histological examination The outcomes after debridement alone for heel PU vary considerably depending on the size of ulceration, extent of infection, general health of the patient and numerous other factors. Repeated debridements are often required (44). Management of infection
Calcaneal osteomyelitis can occur if there is a communication between the overlying skin and the underlying bone. The most common microorganisms are Staphylococcus and Pseudomonas (45,46). The diagnosis is often made by a combination of plain radiographs and blood tests, which may be supplemented by more sensitive tests such as radionuclide bone scans and cross-sectional imaging (47). However, if a wound probes to bone in a diabetic patient, the likelihood of osteomyelitis is very high (48,49). Osteomyelitis is a difficult condition to adequately treat, and management will depend on numerous factors such as the overall health of the patient, the causative organism, the extent of the infection and the needs of the patient. First-line treatment is prolonged, often intravenous, antibiotic therapy after the identification of the relevant pathogen (26). This is often used in conjunction with topical antimicrobials, which may suffice when infection is limited to the wound or the surrounding soft tissues. Surgical treatment options for calcaneal osteomyelitis in the context of heel PU include partial calcanectomy (47,50), total calcanectomy (51,52) and (occasionally) total excision of the calcaneus and the talus (53). In general, these procedures are seen as limb saving and performed in individuals otherwise requiring trans-tibial or trans-femoral amputation. There is scant evidence as to the value of these surgical procedures, being limited to case series or reports. In Schade’s recent systematic review (2012), 16 series detailing 100 patients 3
Surgical management of heel pressure ulcers
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Figure 1 Operative management of a patient with large infected heel ulcer. (A) Debridement of the heel wound and creation of heel flap. (B) Daily debridement and irrigation of the wound. (C) Formation of granulation tissue. (D) Reconstructed heel created by suturing of heel flap to its bed (Reprinted with permission from reference 56).
undergoing either partial (n = 76) or total (n = 28) calcanectomy were identified (54). The underlying pathogenesis included diabetic ulceration as well as PU. After a weighted mean follow-up of 33 months, limb salvage rates were approximately 90%, with 85% improving their ambulatory status postoperatively. Major amputations were more likely in those undergoing total calcanectomy and in those with diabetes. These data show marked improvement from earlier series, in which there was a significant failure rate with more than 50% of patients requiring amputation or remaining unhealed at 2 years (55). Despite these promising results, these surgical interventions have not been subject to randomised trials, and should be only used in centres with local expertise (54). Occasionally, heel ulcers will present with extensive soft tissue infection in the absence of osteomyelitis, warranting debridement that can leave the calcaneal periosteum exposed. This is particularly problematic in an area where the skin is tight with little reserve to provide cover. Shojaiefard et al. have described managing such patients by raising a heel flap during the initial debridement procedure, using daily wound irrigation and debridement as required, before secondary closure of the heel flap over the calcaneus (Figure 1) (56). No wound recurrence occurred after 1 year follow-up. Revascularisation
Revascularisation provides increased arterial perfusion to allow PUs to heal in the presence of PVD. Despite an underlying aetiology of pressure, restoration of pulsatile arterial blood flow to the foot is seen as mandatory for successful wound healing in the context of PU with coexisting ischaemia. Revascularisation 4
to the foot may be achieved via surgical bypass (often to the pedal vessels) or by endovascular means. Successful revascularisation must be performed in conjunction with appropriate debridement, wound care, limb offloading, treatment with antimicrobials where appropriate and adequate nutritional intake, which often necessitates long hospital inpatient stays. A patent bypass graft does not guarantee that all ulcerated areas will necessarily heal: Carsten et al. identified heel ulceration as an independent risk factor for subsequent amputation in patients with functioning lower limb revascularisation (57). It should be noted that despite a wealth of published data on lower limb revascularisation in general, there are few reports specifically addressing the issue of revascularisation for PUs. The incidence of underlying PVD in patients with heel PU is considerable. A recent observational study of 506 patients with heel PUs showed that 83% of those patients imaged had evidence of PVD (58). Therefore, all patients with non-healing heel PUs who are considered fit enough to undergo revascularisation should be investigated by a combination of Duplex ultrasound and angiographic studies, whether magnetic resonance angiography (MRA), computed tomography (CTA) or catheter angiography. MRA is considered superior to CTA in assessing the arterial tree if significant calcification is present; a common scenario in patients with coexistent diabetes (59). Non-contrast MRA avoids the nephrotoxic problems associated with contrast in patients with renal dysfunction, and has been shown to be an accurate means of evaluating the lower limb vasculature in diabetic patients (60). It is possible to grade the radiological degree of pedal ischaemia using a system developed by Gentile © 2015 Medicalhelplines.com Inc and John Wiley & Sons Ltd
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Surgical management of heel pressure ulcers
Figure 2 Angiosomes of the foot and ankle, arising from the anterior tibial artery (ATA, one angiosome), posterior tibial artery (PTA, three angiosomes) and peroneal artery (PA, two angiosomes). The heel is supplied by branches of the posterior tibial and the peroneal arteries (Reprinted with permission from reference 78).
et al. for necrotic heel PUs, which highlights the importance of a patent PTA (61): • grade I: patent PTA • grade II: an occluded PTA with revascularisation via the peroneal artery • grade III: an occluded PTA with revascularisation via the dorsalis pedis artery • grade IV: no reconstitution but patent heel tributaries • grade V: an avascular heel. Revascularisation should be considered whenever technically possible. Open surgical revascularisation is considered the gold standard for patients with suitable anatomy, a good conduit, and life expectancy of greater than 2 years (62). Endovascular revascularisation can be attempted when the disease pattern is suitable, and is becoming increasingly popular as a first-line intervention. Whilst the long-term patency rates for angioplasty, especially of the tibial vessels, can be low (63), a temporary improvement in blood supply may permit wound healing (64). This is especially useful in the elderly, or those with significant comorbidities, when surgical bypass is deemed inappropriate (65,66). In deciding on target vessel revascularisation for those with crural disease, an increasing volume of evidence has highlighted the importance of considering the angiosome of the ischaemic lesion. An angiosome, first described by Taylor and Palmer, is a block of tissue comprising skin, subcutaneous tissue, fascia, muscle and bone, which is supplied by a specific artery and drained by its accompanying vein (67). The foot and ankle comprise six angiosomes (Figure 2) arising from the PTA (three), peroneal artery (two) and anterior tibial artery (one) (68). Revascularisation can be considered direct if the vessel revascularised directly supplies the area of tissue loss. For heel PUs, direct revascularisation is achieved by reperfusing the © 2015 Medicalhelplines.com Inc and John Wiley & Sons Ltd
peroneal and PTAs. Recent evidence has suggested that direct revascularisation results in improved wound healing and lower rates of amputation when compared with indirect revascularisation (69). However, indirect revascularisation may be adequate when sufficient collaterals are present (70), which explains why heel PUs can heal by reperfusing the anterior tibial artery. There is little evidence in the literature specifically examining the angiosome concept and healing of heel PUs; however it would appear sensible to perform a direct revascularisation wherever technically possible. Outcomes of surgical bypass are confined to case series, and inter-series comparisons are hampered by the heterogeneity of the patient population and the surgical procedures performed. Gentile et al. performed debridement and open revascularisation in 14 patients with necrotic heel PUs (61). Limb salvage was 91% at 24 months. Berceli et al. examined the outcomes of dorsalis pedis bypass in 432 patients, of whom 96 had heel ulceration (71). Eighty five percent of heel ulcers were healed at the end of the study period (mean ulcer healing time: 139 days), with a limb salvage rate of 90⋅7%. In a case series of heel ulcers by Treiman et al., revascularisation of 88 patients (of whom 85 had surgical procedures and 3 endovascular) yielded a healing rate of 73%, and a limb salvage rate of 89% at a mean follow-up of 21 months (72). However, many patients were excluded, having undergone primary amputation. Factors predictive for healing included a patent PTA and normal renal function. Goudie et al. retrospectively examined 21 diabetic patients with large (>4 cm2 ) heel ulcers undergoing open revascularisation with concurrent partial or total calcanectomy, followed by negative pressure therapy (73). Limb salvage at 48 months was 76%. Dosluoglu et al. examined 308 patients with tissue loss affecting either the heel or the foot, of whom 50 had heel ulceration and underwent endovascular (n = 38) or open surgical (n = 12) revascularisation. Limb salvage rates at 12 months were similar regardless of the revascularisation 5
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Surgical management of heel pressure ulcers
technique (endovascular 84%, open surgery 83%); however the presence of gangrene (compared with ulceration alone) significantly reduced limb salvage rates (61% versus 100%, respectively). Patients with heel ulceration were more likely to be non-ambulatory, have lower albumin levels and have gangrene, and whilst no difference in limb salvage was noted, heel ulcer patients had significantly worse mortality rates compared to those with foot ulceration.
Other surgical options for limb salvage
In 1985, Briggs et al. published their approach to managing complex pedal wounds, combining vascular reconstruction with a microvascular free flap (74). Since then, certain specialist centres have been performing either a combined or a two-stage procedure for patients with complex pedal wounds. Gentile et al. performed revascularisation with free flap transfer in five patients and free flap transfer alone in six, of whom all had necrotic heel PUs (61). Limb salvage rates were 60% and 81% at 24 months, respectively. Tukiainen et al. published their more recent series of 79 patients undergoing revascularisation and microvascular free flap procedures over a 14-year period, of which 18 were for heel wounds (24). Overall, limb salvage at 1 year was 73%, although reinterventions were required in most patients. Heel ulceration was associated with a significantly increased risk of amputation on multivariate regression. Whilst this is a technically feasible option, its use is confined to certain highly specialised centres with local expertise.
Primary Amputation
Despite the various surgical and non-surgical options available to treat patients with heel PUs, a significant number will require amputation. Certain clinical scenarios mandate amputation, such as extensive non-salvageable tissue loss in the context of acute sepsis. Some authors advocate primary amputation in those who are bed-bound with severe flexion contractures. Renal failure has been consistently shown to predict poorer outcomes after successful revascularisation of heel ulcers complicated by ischaemia (72,75). Certain authors caution against revascularisation in such patients because of the low rates of limb salvage and suggest that primary amputation is considered as the first-line treatment. Nehler et al. examined the issue of revascularisation for critical limb ischaemia and questioned whether it was always appropriate (76). They proposed that three factors should be considered: technical issues with bypass surgery; associated comorbidity; and the potential length of time for wound healing before revascularisation is considered. Their conclusions were quite circumspect in that many subgroups are best served by a timely primary amputation. Defining the proportion of patients that succumb to amputation is difficult because of the heterogeneity of cohorts. In two unselected series of diabetic patients with heel ulceration managed conservatively, 7–23% required major amputation (20,33). Marston et al. studied 32 heel ulcers in the context of limb ischaemia without revascularisation, of which 34% of the patients required an amputation (77). Amputation rates after attempted revascularisation range from 9% to 24%. 6
Conclusions
The heel is particularly prone to develop ulceration secondary to pressure. Adequate risk assessment and prevention are of paramount importance to those without ulceration, and failure to identify at-risk patients who subsequently develop ulceration could make medicolegal claims difficult to defend. Whilst the majority of heel PUs are superficial and can be managed conservatively, a significant subgroup has more extensive disease, which will require surgical intervention to aid healing. Limb-preserving interventions include debridement, partial or total calcanectomy, surgical or endovascular revascularisation and using tissue flaps. Outcomes vary depending on the stage of the disease, comorbidities (especially renal failure and diabetes) and the procedures performed, although a number of papers demonstrate that heel ulceration represents a more challenging clinical entity compared with other pedal ulcerations. Despite best surgical management, a number of patients will progress to amputation. Certain patients are best served by a timely definitive amputation, rather than a protracted course of interventions. Clinical expertise is essential in terms of careful case selection to ensure maximum limb salvage rates in this difficult-to-manage patient group. References 1. Black J, Baharestani MM, Cuddigan J, Dorner B, Edsberg L, Langemo D, Posthauer ME, Ratliff C, Taler G. National Pressure Ulcer Advisory Panel’s updated pressure ulcer staging system. Adv Skin Wound Care 2007;20:269–74. 2. Wong VK, Stotts NA. Physiology and prevention of heel ulcers: the state of science. J Wound Ostomy Continence Nurs 2003;30:191–8. 3. Grey JE, Harding KG, Enoch S. Pressure ulcers. BMJ 2006;332:472–5. 4. Mustoe TA, O’Shaughnessy K, Kloeters O. Chronic wound pathogenesis and current treatment strategies: a unifying hypothesis. Plast Reconstr Surg 2006;117:35–41. 5. Cichowitz A, Pan WR, Ashton M. The heel: anatomy, blood supply, and the pathophysiology of pressure ulcers. Ann Plast Surg 2009;62:423–9. 6. Gefen A. The biomechanics of heel ulcers. J Tissue Viability 2010;19:124–31. 7. Witkowski JA, Parish LC. Histopathology of the decubitus ulcer. J Am Acad Dermatol 1982;6:1014–21. 8. Kinoshita H, Francis PR, Murase T, Kawai S, Ogawa T. The mechanical properties of the heel pad in elderly adults. Eur J Appl Physiol Occup Physiol 1996;73:404–9. 9. Salcido R, Donofrio JC, Fisher SB, LeGrand EK, Dickey K, Carney JM, Schosser R, Liang R. Histopathology of pressure ulcers as a result of sequential computer-controlled pressure sessions in a fuzzy rat model. Adv Wound Care 1994;7:23–8. 10. Vangilder C, Macfarlane GD, Meyer S. Results of nine international pressure ulcer prevalence surveys: 1989 to 2005. Ostomy Wound Manage 2008;54:40–54. 11. Clark M, Cullum N. Matching patient need for pressure sore prevention with the supply of pressure redistributing mattresses. J Adv Nurs 1992;17:310–6. 12. Gallagher P, Barry P, Hartigan I, McCluskey P, O’Connor K, O’Connor M. Prevalence of pressure ulcers in three university teaching hospitals in Ireland. J Tissue Viability 2008;17:103–9. 13. Jiang Q, Li X, Qu X, Liu Y, Zhang L, Su C, Guo X, Chen Y, Zhu Y, Jia J, Bo S, Liu L, Zhang R, Xu L, Wu L, Wang H, Wang J. The incidence, risk factors and characteristics of pressure ulcers in hospitalized patients in China. Int J Clin Exp Pathol 2014;7:2587–94.
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14. Vanderwee K, Clark M, Dealey C, Gunningberg L, Defloor T. Pressure ulcer prevalence in Europe: a pilot study. J Eval Clin Pract 2007;13:227–35. 15. Gunningberg L, Stotts NA, Idvall E. Hospital-acquired pressure ulcers in two Swedish County Councils: cross-sectional data as the foundation for future quality improvement. Int Wound J 2011;8:465–73. 16. Whittington KT, Briones R. National Prevalence and Incidence Study: 6-year sequential acute care data. Adv Skin Wound Care 2004;17:490–4. 17. Brown G. Long-term outcomes of full-thickness pressure ulcers: healing and mortality. Ostomy Wound Manage 2003;49:42–50. 18. Berlowitz DR, Brandeis GH, Anderson J, Du W, Brand H. Effect of pressure ulcers on the survival of long-term care residents. J Gerontol A Biol Sci Med Sci 1997;52:106–10. 19. Thomas DR, Goode PS, Tarquine PH, Allman RM. Hospital-acquired pressure ulcers and risk of death. J Am Geriatr Soc 1996;44:1435–40. 20. Chipchase SY, Treece KA, Pound N, Game FL, Jeffcoate WJ. Heel ulcers don’t heal in diabetes. Or do they? Diabet Med 2005;22:1258–62. 21. Cevera JJ, Bolton LL, Kerstein MD. Options for diabetic patients with chronic heel ulcers. J Diabetes Complications 1997;11:358–66. 22. Pickwell KM, Siersma VD, Kars M, Holstein PE, Schaper NC. Diabetic foot disease: impact of ulcer location on ulcer healing. Diabetes Metab Res Rev 2013;29:377–83. 23. Dosluoglu HH, Attuwaybi B, Cherr GS, Harris LM, Dryjski ML. The management of ischemic heel ulcers and gangrene in the endovascular era. Am J Surg 2007;194:600–5. 24. Tukiainen E, Kallio M, Lepantalo M. Advanced leg salvage of the critically ischemic leg with major tissue loss by vascular and plastic surgeon teamwork: long-term outcome. Ann Surg 2006;244:949–57. 25. Bosanquet DC, Harding KG. Wound duration and healing rates: cause or effect? Wound Repair Regen 2014;22:143–50. 26. Lipsky BA, Berendt AR, Embil J, De Lalla F. Diagnosing and treating diabetic foot infections. Diabetes Metab Res Rev 2004;20:56–64. 27. Fowler E, Scott-Williams S, McGuire JB. Practice recommendations for preventing heel pressure ulcers. Ostomy Wound Manage 2008;54:42–57. 28. Waterlow J. Pressure sores: a risk assessment card. Nurs Times 1985;81:49–55. 29. Bergstrom N, Braden BJ, Laguzza A, Holman V. The braden scale for predicting pressure sore risk. Nurs Res 1987;36:205–10. 30. Braden BJ. The Braden Scale for predicting pressure sore risk: reflections after 25 years. Adv Skin Wound Care 2012;25:61. 31. Haisma JA, van der Woude LH, Stam HJ, Bergen MP, Sluis TA, Post MW, Bussmann JB. Complications following spinal cord injury: occurrence and risk factors in a longitudinal study during and after inpatient rehabilitation. J Rehabil Med 2007;39:393–8. 32. Gaubert-Dahan ML, Castro-Lionard K, Blanchon MA, Fromy B. Severe sensory neuropathy increases risk of heel pressure ulcer in older adults. J Am Geriatr Soc 2013;61:2050–2. 33. Bakheit HE, Mohamed MF, Mahadi SE, Widatalla AB, Shawer MA, Khamis AH, Ahmed ME. Diabetic heel ulcer in the Sudan: determinants of outcome. J Foot Ankle Surg 2012;51:152–5. 34. Uzun O, Tan M. A prospective, descriptive pressure ulcer risk factor and prevalence study at a university hospital in Turkey. Ostomy Wound Manage 2007;53:44–56. 35. Orsted HL, Searles GE, Trowell H, Shapera L, Miller P, Rahman J. Best practice recommendations for the prevention, diagnosis, and treatment of diabetic foot ulcers: update 2006. Adv Skin Wound Care 2007;20:655–69. 36. Larsson J, Apelqvist J, Agardh CD, Stenstrom A. Decreasing incidence of major amputation in diabetic patients: a consequence of a multidisciplinary foot care team approach? Diabet Med 1995; 12:770–6. 37. Dargis V, Pantelejeva O, Jonushaite A, Vileikyte L, Boulton AJ. Benefits of a multidisciplinary approach in the management of recurrent diabetic foot ulceration in Lithuania: a prospective study. Diabetes Care 1999;22:1428–31.
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Surgical management of heel pressure ulcers
38. McGinnis E, Stubbs N. Pressure-relieving devices for treating heel pressure ulcers. Cochrane Database Syst Rev 2014;2:CD005485. 39. Reddy M, Gill SS, Rochon PA. Preventing pressure ulcers: a systematic review. JAMA 2006;296:974–84. 40. Langemo D, Thompson P, Hunter S, Hanson D, Anderson J. Heel pressure ulcers: stand guard. Adv Skin Wound Care 2008;21:282–92. 41. Niezgoda JA, Mendez-Eastman S. The effective management of pressure ulcers. Adv Skin Wound Care 2006;19:3–15. 42. Steed DL. Debridement. Am J Surg 2004;187:71–4. 43. O’Neill DK, Tsui SM, Ayello EA, Cuff G, Brem H. Anesthesia protocol for heel pressure ulcer debridement. Adv Skin Wound Care 2012;25:209–19. 44. Schiffman J, Golinko MS, Yan A, Flattau A, Tomic-Canic M, Brem H. Operative debridement of pressure ulcers. World J Surg 2009;33:1396–402. 45. Wang EH, Simpson S, Bennet GC. Osteomyelitis of the calcaneum. J Bone Joint Surg 1992;74:906–9. 46. Merlet A, Cazanave C, Dauchy FA, Dutronc H, Casoli V, Chauveaux D, De Barbeyrac B, Dupon M. Prognostic factors of calcaneal osteomyelitis. Scand J Infect Dis 2014;46:555–60. 47. Walsh TP, Yates BJ. Calcanectomy: avoiding major amputation in the presence of calcaneal osteomyelitis-A case series. Foot 2013;23:130–5. 48. Grayson ML, Gibbons GW, Balogh K, Levin E, Karchmer AW. Probing to bone in infected pedal ulcers. A clinical sign of underlying osteomyelitis in diabetic patients. JAMA 1995;273:721–3. 49. Shone A, Burnside J, Chipchase S, Game F, Jeffcoate W. Probing the validity of the probe-to-bone test in the diagnosis of osteomyelitis of the foot in diabetes. Diabetes Care 2006;29:945. 50. Baumhauer JF, Fraga CJ, Gould JS, Johnson JE. Total calcanectomy for the treatment of chronic calcaneal osteomyelitis. Foot Ankle Int 1998;19:849–55. 51. Baravarian B, Menendez MM, Weinheimer DJ, Lowery C, Kosanovich R, Vidt L. Subtotal calcanectomy for the treatment of large heel ulceration and calcaneal osteomyelitis in the diabetic patient. J Foot Ankle Surg 1999;38:194–202. 52. Bollinger M, Thordarson DB. Partial calcanectomy: an alternative to below knee amputation. Foot Ankle Int 2002;23:927–32. 53. Han PY, Ezquerro R. Surgical treatment of pressure ulcers of the heel in skilled nursing facilities: a 12-year retrospective study of 57 patients. J Am Podiatr Med Assoc 2011;101:167–75. 54. Schade VL. Partial or total calcanectomy as an alternative to below-the-knee amputation for limb salvage: a systematic review. J Am Podiatr Med Assoc 2012;102:396–405. 55. Smith WJ, Jacobs RL, Fuchs MD. Salvage of the diabetic foot with exposed os calcis. Clin Orthop Relat Res 1993;296:71–7. 56. Shojaiefard A, Khorgami Z, Mohajeri-Tehrani MR, Larijani B. Large and deep diabetic heel ulcers need not lead to amputation. Foot Ankle Int 2013;34:215–21. 57. Carsten CG 3rd, Taylor SM, Langan EM 3rd, Crane MM. Factors associated with limb loss despite a patent infrainguinal bypass graft. Am Surg 1998;64:33–7. 58. Malik R, Pinto P, Bogaisky M, Ehrlich AR. Older adults with heel ulcers in the acute care setting: frequency of noninvasive vascular assessment, surgical intervention, and 1-year mortality. J Am Med Dir Assoc 2013;14:916–9. 59. Ouwendijk R, Kock MC, Visser K, Pattynama PM, de Haan MW, Hunink MG. Interobserver agreement for the interpretation of contrast-enhanced 3D MR angiography and MDCT angiography in peripheral arterial disease. Am J Roentgenol 2005;185:1261–7. 60. Hodnett PA, Ward EV, Davarpanah AH, Scanlon TG, Collins JD, Glielmi CB, Bi X, Koktzoglou I, Gupta N, Carr JC, Edelman RR. Peripheral arterial disease in a symptomatic diabetic population: prospective comparison of rapid unenhanced MR angiography (MRA) with contrast-enhanced MRA. Am J Roentgenol 2011;197:1466–73. 61. Gentile AT, Berman SS, Reinke KR, Demas CP, Ihnat DH, Hughes JD, Mills JL. A regional pedal ischemia scoring system for decision analysis in patients with heel ulceration. Am J Surg 1998;176:109–14. 7
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62. Bradbury AW, Adam DJ, Bell J, Forbes JF, Fowkes FG, Gillespie I, Ruckley CV, Raab GM. Bypass versus angioplasty in severe ischaemia of the Leg (BASIL) trial: a survival prediction model to facilitate clinical decision making. J Vasc Surg 2010;51:52–68. 63. Iida O, Soga Y, Kawasaki D, Hirano K, Yamaoka T, Suzuki K, Miyashita Y, Yokoi H, Takahara M, Uematsu M. Angiographic restenosis and its clinical impact after infrapopliteal angioplasty. Eur J Vasc Endovasc Surg 2012;44:425–31. 64. Romiti M, Albers M, Brochado-Neto FC, Durazzo AE, Pereira CA, De Luccia N. Meta-analysis of infrapopliteal angioplasty for chronic critical limb ischemia. J Vasc Surg 2008;47:975–81. 65. Soderstrom MI, Arvela EM, Korhonen M, Halmesmaki KH, Alback AN, Biancari F, Lepantalo MJ, Venermo MA. Infrapopliteal percutaneous transluminal angioplasty versus bypass surgery as first-line strategies in critical leg ischemia: a propensity score analysis. Ann Surg 2010;252:765–73. 66. Conrad MF, Crawford RS, Hackney LA, Paruchuri V, Abularrage CJ, Patel VI, Lamuraglia GM, Cambria RP. Endovascular management of patients with critical limb ischemia. J Vasc Surg 2011;53:1020–5. 67. Taylor GI, Palmer JH. The vascular territories (angiosomes) of the body: experimental study and clinical applications. Br J Plast Surg 1987;40:113–41. 68. Taylor GI, Pan WR. Angiosomes of the leg: anatomic study and clinical implications. Plast Reconstr Surg 1998;102:599–616 (discussion 7–8). 69. Bosanquet DC, Glasbey JC, Williams IM, Twine CP. Systematic review and meta-analysis of direct versus indirect angiosomal revascularisation of infrapopliteal arteries. Eur J Vasc Endovasc Surg 2014;48:88–97. 70. Varela C, Acin F, de Haro J, Bleda S, Esparza L, March JR. The role of foot collateral vessels on ulcer healing and limb salvage after
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successful endovascular and surgical distal procedures according to an angiosome model. Vasc Endovascular Surg 2010;44:654–60. Berceli SA, Chan AK, Pomposelli FB Jr, Gibbons GW, Campbell DR, Akbari CM, Brophy DT, LoGerfo FW. Efficacy of dorsal pedal artery bypass in limb salvage for ischemic heel ulcers. J Vasc Surg 1999;30:499–508. Treiman GS, Oderich GS, Ashrafi A, Schneider PA. Management of ischemic heel ulceration and gangrene: an evaluation of factors associated with successful healing. J Vasc Surg 2000;31:1110–8. Goudie EB, Gendics C, Lantis JC 2nd. Multimodal therapy as an algorithm to limb salvage in diabetic patients with large heel ulcers. Int Wound J 2012;9:132–8. Briggs SE, Banis JC Jr, Kaebnick H, Silverberg B, Acland RD. Distal revascularization and microvascular free tissue transfer: an alternative to amputation in ischemic lesions of the lower extremity. J Vasc Surg 1985;2:806–11. Edwards JM, Taylor LM Jr, Porter JM. Limb salvage in end-stage renal disease (ESRD). Comparison of modern results in patients with and without ESRD. Arch Surg 1988;123:1164–8. Nehler MR, Hiatt WR, Taylor LM Jr. Is revascularization and limb salvage always the best treatment for critical limb ischemia? J Vasc Surg 2003;37:704–8. Marston WA, Davies SW, Armstrong B, Farber MA, Mendes RC, Fulton JJ, Keagy BA. Natural history of limbs with arterial insufficiency and chronic ulceration treated without revascularization. J Vasc Surg 2006;44:108–14. Iida O, Soga Y, Hirano K, Kawasaki D, Suzuki K, Miyashita Y, Terashi H, Uematsu M. Long-term results of direct and indirect endovascular revascularization based on the angiosome concept in patients with critical limb ischemia presenting with isolated below-the-knee lesions. J Vasc Surg 2012;55:363–70.
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INVITED REVIEW
A review of the surgical management of heel pressure ulcers in the 21st century David C Bosanquet1 , Ann M Wright2 , Richard D White1 & Ian M Williams1 1 Regional Vascular Unit, University Hospital of Wales, Cardiff, UK 2 Department of Surgery, Royal Gwent Hospital, Newport, UK
Key words Amputation; Angiosome; Calcanectomy; Heel ulcer; Pressure ulcer
Bosanquet DC, Wright AM, White RD, Williams IM. A review of the surgical management of heel pressure ulcers in the 21st century. Int Wound J 2015; doi: 10.1111/iwj.12416
Correspondence to Mr IM Williams Regional Vascular Unit University Hospital of Wales Heath Park Cardiff Wales CF14 4XW UK E-mail: [email protected]
Abstract Heel ulceration, most frequently the result of prolonged pressure because of patient immobility, can range from the trivial to the life threatening. Whilst the vast majority of heel pressure ulcers (PUs) are superficial and involve the skin (stages I and II) or underlying fat (stage III), between 10% and 20% will involve deeper tissues, either muscle, tendon or bone (stage IV). These stage IV heel PUs represent a major health and economic burden and can be difficult to treat. The worst outcomes are seen in those with large ulcers, compromised peripheral arterial supply, osteomyelitis and associated comorbidities. Whilst the mainstay of management of stage I-III heel pressure ulceration centres on offloading and appropriate wound care, successful healing in stage IV PUs is often only possible with surgical intervention. Such intervention includes simple debridement, partial or total calcanectomy, arterial revascularisation in the context of coexisting peripheral vascular disease or using free tissue flaps. Amputation may be required for failed surgical intervention, or as a definitive first-line procedure in certain high-risk or poor prognosis patient groups. This review provides an overview of heel PUs, alongside a comprehensive literature review detailing the surgical interventions available when managing such patients.
Introduction
A pressure ulcer (PU) is defined as a localised injury to the skin or underlying tissue, frequently occurring over bony prominences, arising as a result of pressure and/or shear forces (1). They are invariably the result of localised tissue ischaemia and failed wound healing (2). Macerated, injured and dry tissues contribute to PU development, as does systemic malnutrition, global limb ischaemia and physiological stress (3,4).
Anatomy and pathophysiology of heel PUs
The principal blood supply of the heel comprises the posterior tibial and peroneal arteries. Perforating branches of the peroneal artery supply the lateral aspect and skin of the heel, whilst the heel pad is supplied via the medial calcaneal branch of the posterior tibial artery (PTA). The heel is well designed to withstand forces incurred during standing and ambulation. The plantar surface of the heel comprises superficial and deep fascia, interspaced with tightly © 2015 Medicalhelplines.com Inc and John Wiley & Sons Ltd doi: 10.1111/iwj.12416
Key Messages
• a combination of marginal blood supply, thin skin and adipose tissue and bony prominences make the heel particularly prone to pressure ulceration when the leg rests supine • partial or total calcanectomy is an option for patients with osteomyelitis • revascularisation, which can be either open or endovascular, should be considered in patients with pressure ulcers and peripheral vascular disease • specialist institutions have reported using free flaps for complex heel wounds, with or without concomitant revascularisation • a small minority of patients are best served by timely amputations packed adipose tissue, and further cushioned by the attachments of abductor digiti minimi and flexor digitorum brevis muscles. 1
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Fibrous septa travel throughout the heel, connecting the underlying periosteum of the calcaneus with the overlying dermis (5). This tough elastic pad provides sufficient padding to withstand stress and shear forces. In contrast, the posterior aspect of the heel is particularly prone to ulceration due to its thin skin and lack of fat and muscle coverage. When supine, the entire weight of the lower limb rests on the heels. Weight is focused on a small area of the skin overlying the posterior tubercle of the calcaneus, creating a localised area of high pressure (6). The subcutaneous tissue has a marginal blood supply in this region, and early necrosis of the superficial adipose tissue has been demonstrated in PUs (7). Unsurprisingly, the strength of heel tissues has been shown to decrease with age (8).
Classification of PUs
PUs are classified by stage, from I to IV, depending on the depth of tissue loss (Table 1). Stage I is a non-blanching (i.e. non-resolving after removal of pressure) erythema of the skin, without any actual tissue loss. Stages II and III involve partial and total loss of the dermis, respectively, without involvement of deeper structures. Stage IV PUs are defined as full-thickness tissue loss through subcutaneous fat to the underlying tissues, with exposed bone, muscle or tendon. They may contain necrotic or sloughy material, and frequently undermine. Shear and friction are thought to account for more superficial ulceration, whilst pressure damage is predominantly accountable for deeper injury (7,9). Recently, the term ‘Deep Tissue Injury’ has been added as an unclassifiable type of PU. This term describes an area of intact skin covering the underlying damaged tissue, which may be ‘mushy’ or ‘boggy’ on palpation (1). Classification is only possible once the skin has been breached and the ulcer base examined. Table 1 Classification of pressure ulcers (PUs) Stage 1 Stage 2 Stage 3 Stage 4
Intact skin with non-blanching erythema in a localised area, typically over a bony prominence Partial thickness loss of dermis, with a shallow open ulcer Full-thickness tissue loss. Subcutaneous fat may show but not muscle, tendon or bone Full-thickness tissue loss with exposed muscle, tendon or bone
Derived from reference (27).
Site and severity of PUs
PUs can develop on any site of the body subject to prolonged external pressure. The heel and the sacrum are the most common areas affected. Incident data vary widely depending on the type of population examined, from the intensive care unit and acute medical care, to long-term rehabilitation facilities. The highest prevalence has been documented in those in ‘long-term acute care’ (up to 27⋅3%) (10), although incidence figures of 1⋅6–4⋅4% are more frequently reported in unselected inpatients (Table 2). Historical reports suggest that sacral PUs were twice as prevalent as heel PUs (11). Whilst a few recent studies continue to demonstrate an increased propensity towards sacral PUs (12,13), several others show that the incidence of heel PUs appears to be much closer to that of sacral PUs (14–16). Overall, the heel PUs account for up to a third of all documented PUs (Table 2). Data on the proportion of stage IV heel PUs specifically, and therefore likely to warrant surgical intervention, are more scanty. Data from 5947 university and general hospital patients from five countries showed that 11⋅4% of all heel PUs were grade IV (14). In another observational study from Sweden comprising 1192 hospitalised patients, 18% of all heel PUs were grade IV (15). Prognosis of heel PUs
Development of a PU, irrespective of its location, is associated with considerable mortality. Brown showed that development of a nosocomial full-thickness PU is associated with a 180-day mortality rate of almost 70% (17), similar to that reported by other authors (18,19). This striking mortality is often interpreted as a result of coexistent diseases that result in both PUs and high mortality rates, rather than attributing the mortality directly to PU (18,19). However, for outpatients attending specialist clinics, the prognosis for patients with heel PUs is more promising. In one prospective study of 157 heel PUs treated conservatively, 66% healed after a median of 200 days with 7% being resolved by a major amputation (20). A further 8% remained unhealed at the end of the study and 20% unhealed at the time of patient death. Numerous papers have shown that heel wounds in particular are associated with poorer outcomes when compared with tissue loss in the adjacent areas of the foot. Cevera et al. suggest limb salvage is 2–3 times less likely with heel ulceration compared with metatarsal ulceration, and is 1⋅5 times more expensive to manage (21). Pickwell et al. showed healing time
Table 2 Incidence of heel PUs in acute medical inpatients from recent observational studies; overall incidence and proportion of heel PU as a percentage of all PU
Study
Year
Location
No. of centres
Gallagher et al. (12) Gunningberg et al. (15) Jiang et al. (13) Vanderwee et al. (14)
2008 2011 2014 2007
Ireland Sweden China Multinational (five countries)
3 5 12 25
No. of patients
Overall incidence of heel PU (%)
Proportion of heel PU compared with all PU (%)
672 1192 39 952 5947
3⋅0 4⋅2 1⋅6 4⋅4
14⋅1 37 14⋅9 24⋅2
PU, pressure ulcer.
2
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to be prolonged in heel wounds compared with digital and plantar/midfoot wounds, although this may in be partly because of increased comorbidities in patients with heel wounds (22). Dosluoglu et al. compared revascularisation in 277 patients with heel or non-heel tissue loss (23). Whilst limb salvage rates were equivalent between the groups, survival rates were significantly worse in the heel ulceration group. Tukiainen et al. published a series of revascularisation and free flap tissue transfer for complex pedal wounds. The location of tissue loss on the heel (compared with elsewhere on the foot) was a significant independent predictor for subsequent amputation (24). Various ulcer-specific attributes are also known to predispose to poorer outcomes, including increasing size (20), longer wound duration (25) and the presence of osteomyelitis (26). Risk assessment for development of heel pressure ulceration
Primary prevention of PUs is of paramount importance, for which assessing an individual’s risk is the key. This involves careful skin assessment and clinical judgement using one of a number of assessment tools (27). The Waterlow PU risk assessment tool looks at a number of factors with several categories listed to provide an overall score for the risk of ulceration (28). Another scoring system for predicting PU risk is the Braden scale (29,30). This examines six criteria: sensory perception; moisture; activity; mobility; nutrition; and friction and shear. The Braden scale tends to be used in North America, whilst the Waterlow score is principally used in the UK and Europe. The importance of the initial assessment for the presence of risk factors cannot be stressed strongly enough. On the rare occasions when a PU develops in hospital, it might be considered negligent if stringent admission assessments have not been made and documented in the medical notes. Failure to identify and address risk factors when PUs develop makes any potential medicolegal claim difficult to defend. Patients who are at high risk for the development of PU as a result of specific medical states can also be identified. These include elderly patients (12) and patients with immobility [e.g. because of stroke or spinal cord injury (12,31)], peripheral sensory loss (32), renal disease (23), hypoalbuminaemia (12,23), peripheral vascular disease (PVD) (20,33) and diabetes (21,33) and with varying degrees of neuropathy. Patients undergoing surgery are also at increased risk (34). Treatment
Initial treatment for heel PUs must take into account the vascular state, presence of infection and pressure relief [i.e. VIP assessment (35)] prior to management of the wound. This requires input from a multidisciplinary team (MDT) involving vascular clinicians, podiatrists, tissue viability nurses, orthotists, dieticians, radiologists and diabetologists. There is evidence that local MDTs, for diabetic patients specifically, reduce the overall rate of major amputation and of recurrent ulceration (36,37). Non-surgical prevention and management of heel PUs, primarily by offloading and good skin/wound care, has been extensively reviewed elsewhere (27,38–40). Surgical intervention is often warranted in the context of extensive soft tissue infection, osteomyelitis or vascular insufficiency. © 2015 Medicalhelplines.com Inc and John Wiley & Sons Ltd
Surgical management of heel pressure ulcers
Debridement
With the exception of dry non-infected eschar, removal of devitalised tissue is mandatory for successful wound healing. Moist necrotic tissue will invariably become infected, promoting an inflammatory response, which impairs wound healing (41). Debridement can be achieved by a number of methods: autolytic debridement using the body’s own enzymes (typically under an occlusive dressing) to cleave necrotic tissue from healthy tissue; chemical/enzymatic debridement using various topical agents; mechanical debridement using specific dressings, which adhere to the necrotic tissue and ‘debride’ the wound when removed or using forceful saline lavage; biological debridement using maggots; or surgical debridement (42). Surgical debridement is the fastest method, and is appropriate in cases of extensive tissue loss/infection. Most of the time, surgical debridement can be performed easily at the bedside for small or superficial PUs. Occasionally, debridement in the operating room is often required for more extensive PUs (43). Schiffman et al. (44) describe the key steps in PU debridement: 1. expose any undermined areas by excising the overlying tissue 2. remove the callus from the wound edge 3. remove all non-viable and grossly infected tissue 4. obtain a deep tissue biopsy for microbiological culture and histological examination The outcomes after debridement alone for heel PU vary considerably depending on the size of ulceration, extent of infection, general health of the patient and numerous other factors. Repeated debridements are often required (44). Management of infection
Calcaneal osteomyelitis can occur if there is a communication between the overlying skin and the underlying bone. The most common microorganisms are Staphylococcus and Pseudomonas (45,46). The diagnosis is often made by a combination of plain radiographs and blood tests, which may be supplemented by more sensitive tests such as radionuclide bone scans and cross-sectional imaging (47). However, if a wound probes to bone in a diabetic patient, the likelihood of osteomyelitis is very high (48,49). Osteomyelitis is a difficult condition to adequately treat, and management will depend on numerous factors such as the overall health of the patient, the causative organism, the extent of the infection and the needs of the patient. First-line treatment is prolonged, often intravenous, antibiotic therapy after the identification of the relevant pathogen (26). This is often used in conjunction with topical antimicrobials, which may suffice when infection is limited to the wound or the surrounding soft tissues. Surgical treatment options for calcaneal osteomyelitis in the context of heel PU include partial calcanectomy (47,50), total calcanectomy (51,52) and (occasionally) total excision of the calcaneus and the talus (53). In general, these procedures are seen as limb saving and performed in individuals otherwise requiring trans-tibial or trans-femoral amputation. There is scant evidence as to the value of these surgical procedures, being limited to case series or reports. In Schade’s recent systematic review (2012), 16 series detailing 100 patients 3
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Figure 1 Operative management of a patient with large infected heel ulcer. (A) Debridement of the heel wound and creation of heel flap. (B) Daily debridement and irrigation of the wound. (C) Formation of granulation tissue. (D) Reconstructed heel created by suturing of heel flap to its bed (Reprinted with permission from reference 56).
undergoing either partial (n = 76) or total (n = 28) calcanectomy were identified (54). The underlying pathogenesis included diabetic ulceration as well as PU. After a weighted mean follow-up of 33 months, limb salvage rates were approximately 90%, with 85% improving their ambulatory status postoperatively. Major amputations were more likely in those undergoing total calcanectomy and in those with diabetes. These data show marked improvement from earlier series, in which there was a significant failure rate with more than 50% of patients requiring amputation or remaining unhealed at 2 years (55). Despite these promising results, these surgical interventions have not been subject to randomised trials, and should be only used in centres with local expertise (54). Occasionally, heel ulcers will present with extensive soft tissue infection in the absence of osteomyelitis, warranting debridement that can leave the calcaneal periosteum exposed. This is particularly problematic in an area where the skin is tight with little reserve to provide cover. Shojaiefard et al. have described managing such patients by raising a heel flap during the initial debridement procedure, using daily wound irrigation and debridement as required, before secondary closure of the heel flap over the calcaneus (Figure 1) (56). No wound recurrence occurred after 1 year follow-up. Revascularisation
Revascularisation provides increased arterial perfusion to allow PUs to heal in the presence of PVD. Despite an underlying aetiology of pressure, restoration of pulsatile arterial blood flow to the foot is seen as mandatory for successful wound healing in the context of PU with coexisting ischaemia. Revascularisation 4
to the foot may be achieved via surgical bypass (often to the pedal vessels) or by endovascular means. Successful revascularisation must be performed in conjunction with appropriate debridement, wound care, limb offloading, treatment with antimicrobials where appropriate and adequate nutritional intake, which often necessitates long hospital inpatient stays. A patent bypass graft does not guarantee that all ulcerated areas will necessarily heal: Carsten et al. identified heel ulceration as an independent risk factor for subsequent amputation in patients with functioning lower limb revascularisation (57). It should be noted that despite a wealth of published data on lower limb revascularisation in general, there are few reports specifically addressing the issue of revascularisation for PUs. The incidence of underlying PVD in patients with heel PU is considerable. A recent observational study of 506 patients with heel PUs showed that 83% of those patients imaged had evidence of PVD (58). Therefore, all patients with non-healing heel PUs who are considered fit enough to undergo revascularisation should be investigated by a combination of Duplex ultrasound and angiographic studies, whether magnetic resonance angiography (MRA), computed tomography (CTA) or catheter angiography. MRA is considered superior to CTA in assessing the arterial tree if significant calcification is present; a common scenario in patients with coexistent diabetes (59). Non-contrast MRA avoids the nephrotoxic problems associated with contrast in patients with renal dysfunction, and has been shown to be an accurate means of evaluating the lower limb vasculature in diabetic patients (60). It is possible to grade the radiological degree of pedal ischaemia using a system developed by Gentile © 2015 Medicalhelplines.com Inc and John Wiley & Sons Ltd
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Figure 2 Angiosomes of the foot and ankle, arising from the anterior tibial artery (ATA, one angiosome), posterior tibial artery (PTA, three angiosomes) and peroneal artery (PA, two angiosomes). The heel is supplied by branches of the posterior tibial and the peroneal arteries (Reprinted with permission from reference 78).
et al. for necrotic heel PUs, which highlights the importance of a patent PTA (61): • grade I: patent PTA • grade II: an occluded PTA with revascularisation via the peroneal artery • grade III: an occluded PTA with revascularisation via the dorsalis pedis artery • grade IV: no reconstitution but patent heel tributaries • grade V: an avascular heel. Revascularisation should be considered whenever technically possible. Open surgical revascularisation is considered the gold standard for patients with suitable anatomy, a good conduit, and life expectancy of greater than 2 years (62). Endovascular revascularisation can be attempted when the disease pattern is suitable, and is becoming increasingly popular as a first-line intervention. Whilst the long-term patency rates for angioplasty, especially of the tibial vessels, can be low (63), a temporary improvement in blood supply may permit wound healing (64). This is especially useful in the elderly, or those with significant comorbidities, when surgical bypass is deemed inappropriate (65,66). In deciding on target vessel revascularisation for those with crural disease, an increasing volume of evidence has highlighted the importance of considering the angiosome of the ischaemic lesion. An angiosome, first described by Taylor and Palmer, is a block of tissue comprising skin, subcutaneous tissue, fascia, muscle and bone, which is supplied by a specific artery and drained by its accompanying vein (67). The foot and ankle comprise six angiosomes (Figure 2) arising from the PTA (three), peroneal artery (two) and anterior tibial artery (one) (68). Revascularisation can be considered direct if the vessel revascularised directly supplies the area of tissue loss. For heel PUs, direct revascularisation is achieved by reperfusing the © 2015 Medicalhelplines.com Inc and John Wiley & Sons Ltd
peroneal and PTAs. Recent evidence has suggested that direct revascularisation results in improved wound healing and lower rates of amputation when compared with indirect revascularisation (69). However, indirect revascularisation may be adequate when sufficient collaterals are present (70), which explains why heel PUs can heal by reperfusing the anterior tibial artery. There is little evidence in the literature specifically examining the angiosome concept and healing of heel PUs; however it would appear sensible to perform a direct revascularisation wherever technically possible. Outcomes of surgical bypass are confined to case series, and inter-series comparisons are hampered by the heterogeneity of the patient population and the surgical procedures performed. Gentile et al. performed debridement and open revascularisation in 14 patients with necrotic heel PUs (61). Limb salvage was 91% at 24 months. Berceli et al. examined the outcomes of dorsalis pedis bypass in 432 patients, of whom 96 had heel ulceration (71). Eighty five percent of heel ulcers were healed at the end of the study period (mean ulcer healing time: 139 days), with a limb salvage rate of 90⋅7%. In a case series of heel ulcers by Treiman et al., revascularisation of 88 patients (of whom 85 had surgical procedures and 3 endovascular) yielded a healing rate of 73%, and a limb salvage rate of 89% at a mean follow-up of 21 months (72). However, many patients were excluded, having undergone primary amputation. Factors predictive for healing included a patent PTA and normal renal function. Goudie et al. retrospectively examined 21 diabetic patients with large (>4 cm2 ) heel ulcers undergoing open revascularisation with concurrent partial or total calcanectomy, followed by negative pressure therapy (73). Limb salvage at 48 months was 76%. Dosluoglu et al. examined 308 patients with tissue loss affecting either the heel or the foot, of whom 50 had heel ulceration and underwent endovascular (n = 38) or open surgical (n = 12) revascularisation. Limb salvage rates at 12 months were similar regardless of the revascularisation 5
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technique (endovascular 84%, open surgery 83%); however the presence of gangrene (compared with ulceration alone) significantly reduced limb salvage rates (61% versus 100%, respectively). Patients with heel ulceration were more likely to be non-ambulatory, have lower albumin levels and have gangrene, and whilst no difference in limb salvage was noted, heel ulcer patients had significantly worse mortality rates compared to those with foot ulceration.
Other surgical options for limb salvage
In 1985, Briggs et al. published their approach to managing complex pedal wounds, combining vascular reconstruction with a microvascular free flap (74). Since then, certain specialist centres have been performing either a combined or a two-stage procedure for patients with complex pedal wounds. Gentile et al. performed revascularisation with free flap transfer in five patients and free flap transfer alone in six, of whom all had necrotic heel PUs (61). Limb salvage rates were 60% and 81% at 24 months, respectively. Tukiainen et al. published their more recent series of 79 patients undergoing revascularisation and microvascular free flap procedures over a 14-year period, of which 18 were for heel wounds (24). Overall, limb salvage at 1 year was 73%, although reinterventions were required in most patients. Heel ulceration was associated with a significantly increased risk of amputation on multivariate regression. Whilst this is a technically feasible option, its use is confined to certain highly specialised centres with local expertise.
Primary Amputation
Despite the various surgical and non-surgical options available to treat patients with heel PUs, a significant number will require amputation. Certain clinical scenarios mandate amputation, such as extensive non-salvageable tissue loss in the context of acute sepsis. Some authors advocate primary amputation in those who are bed-bound with severe flexion contractures. Renal failure has been consistently shown to predict poorer outcomes after successful revascularisation of heel ulcers complicated by ischaemia (72,75). Certain authors caution against revascularisation in such patients because of the low rates of limb salvage and suggest that primary amputation is considered as the first-line treatment. Nehler et al. examined the issue of revascularisation for critical limb ischaemia and questioned whether it was always appropriate (76). They proposed that three factors should be considered: technical issues with bypass surgery; associated comorbidity; and the potential length of time for wound healing before revascularisation is considered. Their conclusions were quite circumspect in that many subgroups are best served by a timely primary amputation. Defining the proportion of patients that succumb to amputation is difficult because of the heterogeneity of cohorts. In two unselected series of diabetic patients with heel ulceration managed conservatively, 7–23% required major amputation (20,33). Marston et al. studied 32 heel ulcers in the context of limb ischaemia without revascularisation, of which 34% of the patients required an amputation (77). Amputation rates after attempted revascularisation range from 9% to 24%. 6
Conclusions
The heel is particularly prone to develop ulceration secondary to pressure. Adequate risk assessment and prevention are of paramount importance to those without ulceration, and failure to identify at-risk patients who subsequently develop ulceration could make medicolegal claims difficult to defend. Whilst the majority of heel PUs are superficial and can be managed conservatively, a significant subgroup has more extensive disease, which will require surgical intervention to aid healing. Limb-preserving interventions include debridement, partial or total calcanectomy, surgical or endovascular revascularisation and using tissue flaps. Outcomes vary depending on the stage of the disease, comorbidities (especially renal failure and diabetes) and the procedures performed, although a number of papers demonstrate that heel ulceration represents a more challenging clinical entity compared with other pedal ulcerations. Despite best surgical management, a number of patients will progress to amputation. Certain patients are best served by a timely definitive amputation, rather than a protracted course of interventions. Clinical expertise is essential in terms of careful case selection to ensure maximum limb salvage rates in this difficult-to-manage patient group. References 1. Black J, Baharestani MM, Cuddigan J, Dorner B, Edsberg L, Langemo D, Posthauer ME, Ratliff C, Taler G. National Pressure Ulcer Advisory Panel’s updated pressure ulcer staging system. Adv Skin Wound Care 2007;20:269–74. 2. Wong VK, Stotts NA. Physiology and prevention of heel ulcers: the state of science. J Wound Ostomy Continence Nurs 2003;30:191–8. 3. Grey JE, Harding KG, Enoch S. Pressure ulcers. BMJ 2006;332:472–5. 4. Mustoe TA, O’Shaughnessy K, Kloeters O. Chronic wound pathogenesis and current treatment strategies: a unifying hypothesis. Plast Reconstr Surg 2006;117:35–41. 5. Cichowitz A, Pan WR, Ashton M. The heel: anatomy, blood supply, and the pathophysiology of pressure ulcers. Ann Plast Surg 2009;62:423–9. 6. Gefen A. The biomechanics of heel ulcers. J Tissue Viability 2010;19:124–31. 7. Witkowski JA, Parish LC. Histopathology of the decubitus ulcer. J Am Acad Dermatol 1982;6:1014–21. 8. Kinoshita H, Francis PR, Murase T, Kawai S, Ogawa T. The mechanical properties of the heel pad in elderly adults. Eur J Appl Physiol Occup Physiol 1996;73:404–9. 9. Salcido R, Donofrio JC, Fisher SB, LeGrand EK, Dickey K, Carney JM, Schosser R, Liang R. Histopathology of pressure ulcers as a result of sequential computer-controlled pressure sessions in a fuzzy rat model. Adv Wound Care 1994;7:23–8. 10. Vangilder C, Macfarlane GD, Meyer S. Results of nine international pressure ulcer prevalence surveys: 1989 to 2005. Ostomy Wound Manage 2008;54:40–54. 11. Clark M, Cullum N. Matching patient need for pressure sore prevention with the supply of pressure redistributing mattresses. J Adv Nurs 1992;17:310–6. 12. Gallagher P, Barry P, Hartigan I, McCluskey P, O’Connor K, O’Connor M. Prevalence of pressure ulcers in three university teaching hospitals in Ireland. J Tissue Viability 2008;17:103–9. 13. Jiang Q, Li X, Qu X, Liu Y, Zhang L, Su C, Guo X, Chen Y, Zhu Y, Jia J, Bo S, Liu L, Zhang R, Xu L, Wu L, Wang H, Wang J. The incidence, risk factors and characteristics of pressure ulcers in hospitalized patients in China. Int J Clin Exp Pathol 2014;7:2587–94.
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