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Managing The Recalcitrant Calcaneal Wound
August 2014
Although calcaneal ulcers complicated by osteomyelitis can seem destined for amputation, judicious multidisciplinary management can save a limb. These authors review key risk factors and potential complications, assess treatment options including the subtotal calcanectomy, and emphasize the merits of multidisciplinary care with a compelling limb salvage case study.
Recurrent ulcerations of the heel with osteomyelitis, diabetes and neuropathy present a challenge to the wound care specialist. Due to the poor nature of the soft tissue envelope with prolonged soft tissue inflammation and fibrosis complicated many times by neuropathy, osteomyelitis is often present in these patients.
Our patient population consists of many patients suffering from obesity with motor and sensory neuropathy, which allows quick transitions from a superficial dermal lesion to a deep tissue, limb-threatening infection. It has been our observation that wound care specialists do not refer these challenging patients to an experienced limb salvage surgeon in a timely manner. We feel that many times in spite of the best wound care, the plantar calcaneal ulcer will progress to an “emergency situation” consisting of septicemia and/or major amputations. The outlook for amputation of the contralateral limb and decreased survival rates as well as the increased energy requirements and inability to ambulate without the aid of assistive devices makes amputation an undesirable option for many patients.
Heel ulcers in patients with diabetes are usually difficult to treat and are a clinical challenge. Pressure in the heel area combined with neuropathy in patients with diabetes favors the development of extensive wounds. Weightbearing pressure and the paucity of vessels in the heel pad area delay the healing process when ulcers develop.
There are multiple studies that claim heel ulcers in diabetic feet often lead to amputations.1-3
The heel is the greatest weightbearing part of the foot and if one does not manage heel lesions properly, they can lead to sepsis, osteomyelitis, amputation and significant disability.
Recent studies have shown a lower amputation rate in patients with infected diabetic foot lesions by using multidisciplinary team approaches.4-5 There are few studies focused on the management of heel ulcers leading to limb preservation.6-7
The eventual goal is to preserve a limb that enables a patient to walk with or without a brace, and to live without imposing on caregivers.
The delayed identification, improper staging and certain risk factors of heel ulcers can lead to complications that will affect the patient’s way of life as well as increase the morbidity and mortality of the patient.
Patients with PAD are susceptible to the advancement of infected non-healing ulcers, which can potentially lead to below-knee amputations (BKA) and/or above-knee amputations (AKA). The pathophysiology of patients with PAD and the development of heel ulcers begin with increased pressure, shear forces and friction to the heel. These factors may subsequently lead to tissue hypoxia, reperfusion hyperemia, deep tissue injury and skin breakdown. One should evaluate patients with ischemic, non-healing ulcers using the Rutherford classification to allow for proper staging and appropriate intervention prior to the podiatric attempt of limb salvage (see “Understanding The Rutherford Ulcer Classification” at right).
In patients with PAD and a Rutherford score of 4, 5 or 6, it is essential that the patient achieve appropriate blood flow to allow for proper wound healing and/or appropriate healing potential following surgical intervention of the recalcitrant heel ulcer. Some of the traditional treatment options for restoration of blood flow to the lower extremity include the traditional open lower extremity bypass (i.e. femoral-popliteal bypass, posterior tibial bypass). However, recent refinement of endovascular intervention has played a pivotal role in limb salvage over the past 10 years. The advantage of endovascular intervention is that it allows for older, sicker patients to become surgical candidates for endovascular procedures.
In the patient with diabetic, ischemic heel ulcers, the most commonly affected stenosed vessels are the posterior tibial and peroneal arteries. These arteries supply the blood and nutrients to the posterior and plantar aspects of the heel. So if these vessels are occluded, it is easy to see why the healing potential of these ulcers is delayed. This is where endovascular intervention comes into effect.
Endovascular intervention focuses on the angiosome concept to provide proper blood flow to the appropriate angiosomal area of the foot.10 An angiosome is a three-dimensional block of tissue fed by source arteries. The blood supply is a reflection of the connective tissue framework of the body and consists of a continuous three-dimensional network of linked vascular territories throughout all tissues.
Once the patient has had successful endovascular intervention with patent vessels to the appropriate angiosome of the heel (posterior tibial/peroneal arteries), we recommend performing surgical intervention approximately 10-14 days after revascularization. Understand, however, that restenosis of these vessels is common. One should evaluate these patients closely and if restenosis occurs, prompt referral for revascularization is in order.
The post-op course is strict non-weightbearing to the surgical limb with the assistance of crutches, a walker, wheelchair or a Roll-A-Bout walker. Some patients benefit from offloading with external ring fixators. There should also be an intraoperative evaluation of whether the patient would benefit from primary closure of the open surgical wound or delayed primary closure. There is also the option of partial closure with a negative pressure wound therapy (NPWT) device. No matter what closure option the surgeon chooses, non-weightbearing of these surgical wounds is imperative for the success of healing these wounds and avoiding below-knee and/or above-knee amputations.
The diagnosis of osteomyelitis has been the subject of controversy.14-15 However, a bone biopsy is the gold standard. Due to the invasive nature of this method and the frailty of our patients with diabetes, we sometimes will use other tests to differentiate between osteomyelitis and Charcot neuroarthropathy. We also use both the “probe-to-bone test” and magnetic resonance imaging (MRI).
The best therapeutic approach is also a matter of debate.16-17 Some authors suggest wound care with antibiotic therapy.18-19
We feel that osteomyelitis in the heel poses a very high risk for BKA and suggest that treatment should consist of proper antibiotic therapy combined with surgery. A delay in treatment could allow the osteomyelitis to spread to the point where a partial calcanectomy is not indicated and a BKA would be necessary. Some of our patient observations indicated that because of prolonged ineffective treatment, much time elapsed between the occurrence of wounds and the diagnosis of osteomyelitis. An unsuccessful therapeutic approach has devastating consequences in patients with osteomyelitis of the heel. We strongly feel that prompt surgical treatment could change the devastating outcome of calcaneal osteomyelitis, leading to a BKA.
Surgical treatment of calcaneal osteomyelitis consists of partial or subtotal calcanectomy, total calcanectomy, flap coverage surgeries or below-knee amputation. We prefer an aggressive subtotal calcanectomy, which the literature supports.21-25
We prefer to reserve the total calcanectomy as a last resort due to the decreased strength of muscles and reduced ankle joint movement.25 Our patients are able to bear weight on their foot after a subtotal calcanectomy. This seems to be more stable than a total calcanectomy.23,26
She had insulin-dependent diabetes, was obese (275 pounds), and had hypertension, kidney failure, dyslipidemia, sensory and motor neuropathy and peripheral arterial disease. Her surgical history consisted of a left BKA approximately 11 years prior and multiple ulcer debridements.
She presented with an ulceration on the plantar aspect of the right heel that probed to the calcaneus. The tissues were not viable although she did not demonstrate gangrene. There was surrounding cellulitis without sepsis and she was on a repeat regimen of vancomycin.
The vascular exam demonstrated palpable dorsalis pedis pulses but the posterior tibial artery was not palpable. She demonstrated a cool right lower extremity with non-pitting edema and erythema. In spite of her neuropathy, she did have pain and cramping in her right calf. Utilizing a tuning fork and monofilament testing, we determined the patient had sensory neuropathy. She had minimal pain at the calcaneal ulcer site with weightbearing.
Osteomyelitis was evident on the radiologic exam. She had previous confirmation of osteomyelitis via bone biopsy. This was an extension from her plantar ulceration.
We referred her to endocrinology for blood sugar control, which was decreased and controlled with an insulin adjustment and dietary education. She then had endovascular intervention with a resulting two vessel runoff to perfuse the proper angiosome required for healing, correcting the partial occlusion of the posterior tibial artery.
After appropriate referrals and treatment, we felt that an aggressive attempt would be indicated to salvage her right lower extremity. Approximately five weeks after her endovascular procedure, she had surgery to correct her calcaneal defect. Our team felt that due to the possibility of restenosis of her endovascular procedure, she had the procedure in a timely manner.
We placed her in a lateral position without a tourniquet. After making two curvilinear incisions to ellipse the plantar ulcer, we deepened the incision to bone. After undermining the bone, we established full thickness tissue flaps. This allowed exposure of the calcaneus and demonstrated the spongy osteomyelitic bone, which we aggressively resected distal to the subtalar joint. We probed the surrounding soft tissues for pus pockets and sinus tracts. We debrided the distal superficial ulcer extension to healthy, viable tissue and used pulsed lavage for the remaining tissues. We placed vancomycin impregnated calcium sulfate beads and temporarily closed the wound with 0-nylon retention sutures, which allowed stretching of the skin for later final closure.
The patient returned to the OR four days later for deep wound inspection, further debridement, pulsed lavage and reinsertion of antibiotic beads. A drain helped facilitate skin closure. We placed an orthobiologic covering (Dermagraft, Organogenesis) over the distal subcutaneous defect and again debrided the defect. After discharge from the hospital, she went to a skilled nursing facility in a plantarflexed posterior splint. At nine weeks post-op, she had complete healing of all lesions. We subsequently fitted her with a patellar tendon bearing brace. She demonstrated adequate dorsiflexion and plantarflexion.
Recurrent ulcerations of the heel with osteomyelitis, diabetes and neuropathy present a challenge to the wound care specialist. Due to the poor nature of the soft tissue envelope with prolonged soft tissue inflammation and fibrosis complicated many times by neuropathy, osteomyelitis is often present in these patients.
Our patient population consists of many patients suffering from obesity with motor and sensory neuropathy, which allows quick transitions from a superficial dermal lesion to a deep tissue, limb-threatening infection. It has been our observation that wound care specialists do not refer these challenging patients to an experienced limb salvage surgeon in a timely manner. We feel that many times in spite of the best wound care, the plantar calcaneal ulcer will progress to an “emergency situation” consisting of septicemia and/or major amputations. The outlook for amputation of the contralateral limb and decreased survival rates as well as the increased energy requirements and inability to ambulate without the aid of assistive devices makes amputation an undesirable option for many patients.
Heel ulcers in patients with diabetes are usually difficult to treat and are a clinical challenge. Pressure in the heel area combined with neuropathy in patients with diabetes favors the development of extensive wounds. Weightbearing pressure and the paucity of vessels in the heel pad area delay the healing process when ulcers develop.
There are multiple studies that claim heel ulcers in diabetic feet often lead to amputations.1-3
The heel is the greatest weightbearing part of the foot and if one does not manage heel lesions properly, they can lead to sepsis, osteomyelitis, amputation and significant disability.
Recent studies have shown a lower amputation rate in patients with infected diabetic foot lesions by using multidisciplinary team approaches.4-5 There are few studies focused on the management of heel ulcers leading to limb preservation.6-7
The eventual goal is to preserve a limb that enables a patient to walk with or without a brace, and to live without imposing on caregivers.
What You Should Know About Heel Ulcer Complications
The incidence of heel ulcers is quite prevalent within the healthcare system. An estimated one in five patients who are hospitalized will develop decubitus heel ulcers.8-9 In fact, pressure ulcers of the heel are the second most common type of pressure ulcer behind the sacral decubitus ulcer and these decubitus heel ulcers comprise 19 to 32 percent of pressure ulcers. Sixty percent of these heel ulcers develop in an acute setting such as a hospital ICU. Detection of these heel ulcers is somewhat delayed with 54 percent detected at stage 2.8 The staging of these ulcers, along with any other type of ulcer, is critically important for the treatment regimen and in communication with other specialties that are incorporated in the team approach of healing the ulcers. Staging of ulcers helps guide the podiatric physician on the initial presentation as well as the progression or regression of the ulcers. The classification system currently recognized by the National Pressure Ulcer Advisory Panel (NPUAP) is below at left.
The delayed identification, improper staging and certain risk factors of heel ulcers can lead to complications that will affect the patient’s way of life as well as increase the morbidity and mortality of the patient.
What Are The Risk Factors For Heel Ulcers?
There are multiple risk factors for the development of heel ulcers as well as risk factors for delayed healing of the ulcers. We can classify these factors as intrinsic or extrinsic risk factors. We agree that the top two risk factors for non-healing and recalcitrant heel ulcers are associated with intrinsic risk factors, which come in the form of peripheral arterial disease (PAD) and neuropathy. Further intrinsic risk factors are limited mobility, poor nutrition, aging skin, loss of fat pad and bed rest. Extrinsic risk factors are those of constant pressure, friction or shear, and moisture.
Patients with PAD are susceptible to the advancement of infected non-healing ulcers, which can potentially lead to below-knee amputations (BKA) and/or above-knee amputations (AKA). The pathophysiology of patients with PAD and the development of heel ulcers begin with increased pressure, shear forces and friction to the heel. These factors may subsequently lead to tissue hypoxia, reperfusion hyperemia, deep tissue injury and skin breakdown. One should evaluate patients with ischemic, non-healing ulcers using the Rutherford classification to allow for proper staging and appropriate intervention prior to the podiatric attempt of limb salvage (see “Understanding The Rutherford Ulcer Classification” at right).
In patients with PAD and a Rutherford score of 4, 5 or 6, it is essential that the patient achieve appropriate blood flow to allow for proper wound healing and/or appropriate healing potential following surgical intervention of the recalcitrant heel ulcer. Some of the traditional treatment options for restoration of blood flow to the lower extremity include the traditional open lower extremity bypass (i.e. femoral-popliteal bypass, posterior tibial bypass). However, recent refinement of endovascular intervention has played a pivotal role in limb salvage over the past 10 years. The advantage of endovascular intervention is that it allows for older, sicker patients to become surgical candidates for endovascular procedures.
In the patient with diabetic, ischemic heel ulcers, the most commonly affected stenosed vessels are the posterior tibial and peroneal arteries. These arteries supply the blood and nutrients to the posterior and plantar aspects of the heel. So if these vessels are occluded, it is easy to see why the healing potential of these ulcers is delayed. This is where endovascular intervention comes into effect.
Endovascular intervention focuses on the angiosome concept to provide proper blood flow to the appropriate angiosomal area of the foot.10 An angiosome is a three-dimensional block of tissue fed by source arteries. The blood supply is a reflection of the connective tissue framework of the body and consists of a continuous three-dimensional network of linked vascular territories throughout all tissues.
Once the patient has had successful endovascular intervention with patent vessels to the appropriate angiosome of the heel (posterior tibial/peroneal arteries), we recommend performing surgical intervention approximately 10-14 days after revascularization. Understand, however, that restenosis of these vessels is common. One should evaluate these patients closely and if restenosis occurs, prompt referral for revascularization is in order.
Postoperative Considerations
Once the patient has had surgical intervention to the recalcitrant heel ulcer, post-op recovery is even more essential in the healing process. Some of these patients with chronic heel ulcers have had a BKA on the contralateral limb and the patients’ weight distribution and transfer weight depends on the condition of the limb that had surgery. This makes the postoperative recovery difficult in some patients.
The post-op course is strict non-weightbearing to the surgical limb with the assistance of crutches, a walker, wheelchair or a Roll-A-Bout walker. Some patients benefit from offloading with external ring fixators. There should also be an intraoperative evaluation of whether the patient would benefit from primary closure of the open surgical wound or delayed primary closure. There is also the option of partial closure with a negative pressure wound therapy (NPWT) device. No matter what closure option the surgeon chooses, non-weightbearing of these surgical wounds is imperative for the success of healing these wounds and avoiding below-knee and/or above-knee amputations.
What The Literature Reveals About Diagnostic And Therapeutic Timing
Nearly 20 percent of patients with an infected diabetic foot ulcer will develop osteomyelitis. According to some studies, osteomyelitis may occur in up to 66 percent of patients with diabetic foot ulcers.11 The majority of diabetic foot ulcers with underlying osteomyelitis are clinically unsuspected and infected and necrotic tissue often masks the osteomyelitis.12 Faglia and coworkers stated that there is a higher rate (52 percent) of BKAs when osteomyelitis is involved in the heel instead of the midfoot or forefoot.13
The diagnosis of osteomyelitis has been the subject of controversy.14-15 However, a bone biopsy is the gold standard. Due to the invasive nature of this method and the frailty of our patients with diabetes, we sometimes will use other tests to differentiate between osteomyelitis and Charcot neuroarthropathy. We also use both the “probe-to-bone test” and magnetic resonance imaging (MRI).
The best therapeutic approach is also a matter of debate.16-17 Some authors suggest wound care with antibiotic therapy.18-19
We feel that osteomyelitis in the heel poses a very high risk for BKA and suggest that treatment should consist of proper antibiotic therapy combined with surgery. A delay in treatment could allow the osteomyelitis to spread to the point where a partial calcanectomy is not indicated and a BKA would be necessary. Some of our patient observations indicated that because of prolonged ineffective treatment, much time elapsed between the occurrence of wounds and the diagnosis of osteomyelitis. An unsuccessful therapeutic approach has devastating consequences in patients with osteomyelitis of the heel. We strongly feel that prompt surgical treatment could change the devastating outcome of calcaneal osteomyelitis, leading to a BKA.
Current Insights On Treatment For Calcaneal Osteomyelitis And Calcaneal Ulcers
The calcaneus is covered by closely adhered periosteum over which muscles are attached. As a result of osteomyelitis, pus collected within the bone cannot strip the periosteum and collects underneath it. Accordingly, cortical bone does not get avascularized and the characteristic involucrum does not form. The periosteum is more commonly perforated than stripped off.20
Surgical treatment of calcaneal osteomyelitis consists of partial or subtotal calcanectomy, total calcanectomy, flap coverage surgeries or below-knee amputation. We prefer an aggressive subtotal calcanectomy, which the literature supports.21-25
We prefer to reserve the total calcanectomy as a last resort due to the decreased strength of muscles and reduced ankle joint movement.25 Our patients are able to bear weight on their foot after a subtotal calcanectomy. This seems to be more stable than a total calcanectomy.23,26
Should You Consider Flap Closure For Diabetic Heel Ulcers?
Coverage with flap closure is another consideration. This could include a free flap, which requires lengthy and costly hospitalization, microsurgery training, special instruments and a two team surgical approach. The second choice could be a lateral supramalleolar skin flap, which involves a more difficult dissection than the sural flap. The third choice is a sural flap, which is simple and the most reliable flap.27 The fourth choice is a posterior tibial perforator flap, which requires a more difficult dissection and a larger learning curve.28 Due to possible complications with healing in patients with diabetes associated with neuropathy and microvasculature pathology, we rarely utilize flap closures. In our experience with subtotal calcanectomy, we usually have adequate soft tissue for closure.Key Pearls For Performing A Subtotal Calcanectomy
Ensure prone or lateral positioning of the patient depending upon the placement of the incision and the health status of the patient. Incision planning is important as one should attempt to obtain complete closure of the ulcer while avoiding the medial neurovascular bundle. We do not utilize a tourniquet as we prefer to “read the tissues” to resect any non-viable portions. We attempt to utilize full thickness skin flaps to avoid any soft tissue damage. Resect the bone so there are no osseous prominences to pose difficulty later with shoe gear and weightbearing. We are aggressive and do not underestimate the osteomyelitic process, ensuring that we get a “clear zone” of healthy osseous tissue. This aggressive approach also allows for skin closure without tension. We have found that one can resect two-thirds to three-fourths of the calcaneal body with the patient experiencing stable ambulation post-op. We encourage the use of antibiotic beads with local delivery of antibiotics in conjunction with IV antibiosis. The majority of the time, we do not reattach the tendo-Achilles. Place the patient in a plantarflexed cast or splint for six to eight weeks. The Achilles tendon appears to reattach with fibrotic tissue with subsequent adequate motion and stability. These patients normally demonstrate an altered gait due to diabetic motor and sensory neuropathy but those who have had a subtotal calcanectomy do not seem to exhibit any significant gait changes leading to instability or falls.Case Study: Salvaging A Limb With Calcaneal Osteomyelitis
We did a consultation on a 69-year-old African-American female who was scheduled for a right below-knee amputation (BKA) due to osteomyelitis of the calcaneus. For 23 months, she had received treatment from numerous physicians who felt that conservative care had failed and there was no alternative other than major amputation. She had tried multiple treatment modalities including serial debridement, offloading with prescription shoes, multiple braces and casting. The patient had numerous wound care products including topical enzymes and orthobiologic wound coverings. She had concomitant hyperbaric oxygen therapy (HBOT) treatments for six weeks without healing and multiple regimens of IV antibiotics.
She had insulin-dependent diabetes, was obese (275 pounds), and had hypertension, kidney failure, dyslipidemia, sensory and motor neuropathy and peripheral arterial disease. Her surgical history consisted of a left BKA approximately 11 years prior and multiple ulcer debridements.
She presented with an ulceration on the plantar aspect of the right heel that probed to the calcaneus. The tissues were not viable although she did not demonstrate gangrene. There was surrounding cellulitis without sepsis and she was on a repeat regimen of vancomycin.
The vascular exam demonstrated palpable dorsalis pedis pulses but the posterior tibial artery was not palpable. She demonstrated a cool right lower extremity with non-pitting edema and erythema. In spite of her neuropathy, she did have pain and cramping in her right calf. Utilizing a tuning fork and monofilament testing, we determined the patient had sensory neuropathy. She had minimal pain at the calcaneal ulcer site with weightbearing.
Osteomyelitis was evident on the radiologic exam. She had previous confirmation of osteomyelitis via bone biopsy. This was an extension from her plantar ulceration.
We referred her to endocrinology for blood sugar control, which was decreased and controlled with an insulin adjustment and dietary education. She then had endovascular intervention with a resulting two vessel runoff to perfuse the proper angiosome required for healing, correcting the partial occlusion of the posterior tibial artery.
After appropriate referrals and treatment, we felt that an aggressive attempt would be indicated to salvage her right lower extremity. Approximately five weeks after her endovascular procedure, she had surgery to correct her calcaneal defect. Our team felt that due to the possibility of restenosis of her endovascular procedure, she had the procedure in a timely manner.
We placed her in a lateral position without a tourniquet. After making two curvilinear incisions to ellipse the plantar ulcer, we deepened the incision to bone. After undermining the bone, we established full thickness tissue flaps. This allowed exposure of the calcaneus and demonstrated the spongy osteomyelitic bone, which we aggressively resected distal to the subtalar joint. We probed the surrounding soft tissues for pus pockets and sinus tracts. We debrided the distal superficial ulcer extension to healthy, viable tissue and used pulsed lavage for the remaining tissues. We placed vancomycin impregnated calcium sulfate beads and temporarily closed the wound with 0-nylon retention sutures, which allowed stretching of the skin for later final closure.
The patient returned to the OR four days later for deep wound inspection, further debridement, pulsed lavage and reinsertion of antibiotic beads. A drain helped facilitate skin closure. We placed an orthobiologic covering (Dermagraft, Organogenesis) over the distal subcutaneous defect and again debrided the defect. After discharge from the hospital, she went to a skilled nursing facility in a plantarflexed posterior splint. At nine weeks post-op, she had complete healing of all lesions. We subsequently fitted her with a patellar tendon bearing brace. She demonstrated adequate dorsiflexion and plantarflexion.
In Conclusion
We have provided our insight into the management of patients with diabetic heel ulcers complicated by osteomyelitis. These difficult clinical entities require a multidisciplinary team approach due to multiple comorbidities associated with diabetic neuropathic ulcerations complicated by peripheral arterial disease. It is of utmost importance to understand the epidemiology, which encourages timely evaluation and aggressive surgical treatment to avoid sepsis and below-knee amputation. Dr. Pupp is the Program Director of the Podiatric Residency at Providence Hospital and Medical Center in Southfield, Mich. He is a Fellow of the American College of Foot and Ankle Surgeons, and is board certified in foot and ankle surgery by the American Board of Podiatric Surgery. He is the Chairman of the Board for the Save A Leg, Save A Life Foundation. Dr. LaLama is a third year podiatric surgery resident at Providence Hospital and Medical Center in Southfield, Michigan. References 1. Carsten C, Taylor S, Langan E, Crane M. Factors associated with limb loss despite a patent infrainguinal bypass graft. AM Surg. 1998;64(1):33-38. 2. Edwards J, Taylor L, Porter J. Limb salvage in end-stage renal disease (ESRD), comparison of modern results in patients with and without ESRD. Arch Surg. 1988;123(9):1164-1168. 3. Younes N, Albsoul A, Awad H. Diabetic heel ulcers: a major risk factor for lower extremity amputation. Ostomy Wound Manage. 2004;50(6):50-60. 4. Jung V. Foot salvage in diabetic gangrene. Zentrabl Chir. 1996;121(5):387-92; discussion: 392-393. 5. Rosenblum B, Pomposelli F, Giurini J, et al. Maximizing foot salvage by a combined approach to foot ischemia and neuropathic ulceration in patients with diabetes. A 5-year experience. Diabetes Care. 1994;17(9):983-987. 6. Chipchase S, Treece K, Pound N, Game F, Jeffcoate W. Heel ulcers don’t heal in diabetes. Or do they? Diabetic Medicine. 2005;22(9):1262-1258. 7. Treiman G, Oderich G, Ashrafi A, Schneider P. Management of ischemic heel ulceration an gangrene: an evaluation of factors associated with successful healing. J Vasc Surg. 2000;31(6):1110-1118. 8. Baumgarten M, Margolis DJ, Localio AR, et al. Extrinsic risk factors for pressure ulcers early in the hospital stay: a nested case-control study. J Gerontol A Biomed Sci. 2008;63(4):408-13. 9. Benbow M. Assessing the risk of pressure ulcer development. Br J Nurs. 2009;18(15):S26-9. 10. Taylor GI, Palmer JH. The vascular territories (angiosomes) of the body: experimental study and clinical applications. Br J Plast Surg. 1987; 40(2):113-141. 11. Butalia S, Palda V, Detsky AS, Mourad OL. Does this patient with diabetes have osteomyelitis of the lower extremity? JAMA. 2008;299(7):806-813. 12. Chen SL, Chen TM, Chou TD, Chang SC, Wang HJ. Distally based sural fasciomusculocutaneous flap for chronic calcaneal osteomyelitis in diabetic patients. Ann Plast Surg. 2005;54(1):44–48. 13. Faglia E, Clerici G, Caminiti M, et al. Influence of osteomyelitis location in the foot of diabetic patients with transtibial amputation. Foot Ankle Int. 2013 Feb;34(2):222-7. 14. Game F. Management of osteomyelitis of the foot in diabetes mellitus. Nat Rev Endocrinol. 2010;6(1):43-47. 15. Jeffcoate WJ, Lipsky BA. Controversies in diagnosing and managing osteomyelitis of the foot in diabetes. Clin Infect Dis. 2004;39(suppl 2):S115-S122. 16. Armstrong DG, Frykberg RG. Classifying diabetic foot surgery: toward a rational definition. Diabet Med. 2003;20(4):329-331. 17. Baravarian B, Menendez MM, Weinheimer DJ, Lowery C, Kosanovich R, Vidt L. Subtotal calcanectomy for the treatment of large heel ulceration and calcaneal osteomyeleitis in the diabetic patient. J Foot Ankle Surg. 1999;38(5):194-202. 18. Berendt AR, Peters EJ, Bakker K. Specific guidelines for treatment of diabetic foot osteomyelitis. Diabetes Metab Res Rev. 2009;24(suppl 1):S190-S191. 19. Lipsky BA, Berendt AR, Deery HG, et al; Infectious Diseases Society of America. Diagnosis and treatment of diabetic foot infections. Plast Reconstr Surg. 2006;117(7suppl):212S-238S. 20. Gaenslen FJ. Split-heel approach in osteomyelitis of os calcis. J Bone Joint Surg. 1931; 13(1):759-772. 21. WoII TS, Beals RK. Partial calcanectomy for the treatment of osteomyelitis of the calcaneus. Foot Ankle. 1991;12(1):31-34. 22. Crandall RC, Wagner FW Jr. Partial and total calcanectomy. A review of thirty-one consecutive cases over a ten-year period. J Bone Joint Surg. 1981; 63(1):152-155. 23. Horwitz T. Partial resection of the os calcis and primary closure in the treatment of resistant large ulcers of the heel with or without osteomyelitis of the os calcis. Clin Orthop. 1972; 84:149-153. 24. Martini M, Martini-Benkeddache Y, Bekhechi T, Daoud A. Treatment of chronic osteomyelitis of the calcaneus by resection of the calcaneus. A report of twenty cases. J Bone Joint Surg. 1974; 56(1):542-548. 25. Bragdon G, Baumhauer J. Total calcanectomy for the treatment of chronic osteomyelitis. Techniques Foot Ankle Surg. 2008; 7(1):52-55. 26. Wiltse LL, Bateman JG, Kase S. Resection of major portion of the calcaneus. Clin Orthop. 1959; 13:271-278. 27. Price MF, Capizzi PJ, Watterson PA, Lettieri S. Reverse sural artery flap: caveats for success. Ann Plast Surg. 2002;48(5):496–504. 28. Cavadas PC, Landin L. Reconstruction of chronic Achilles tendon defects with posterior tibial perforator flap and soleus tendon graft: clinical series. Plast Reconstruct Surg. 2006;117(1):266–71. Additional Reference 29. Frykberg RG, Veves A. Diabetic foot infections. Diabetes Metab Rev. 1996;12(3):255-270.
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