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Complications of Foot and Ankle Surgery in Patients With Diabetes

Marks, Richard M., MD

Clinical Orthopaedics and Related Research®: October 2001 - Volume 391 - Issue - p 153-161
SECTION I SYMPOSIUM: Complications in Foot and Ankle Surgeries
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Treatment of the foot and ankle in patients with diabetes often is fraught with complications, frequently multifactorial in nature. Because of the multidisciplinary approach to the patient with diabetes, it is imperative that the patient and all healthcare professionals who are treating the patient recognize the foot at risk, and the clinical hallmarks of Charcot neuroarthropathy. Failure to do so often leads to disastrous results, such as ulceration, destruction of normal foot architecture, and progressive deformity too severe to accommodate a brace, thereby necessitating surgical intervention. The surgical treatment of the foot in a patient with diabetes requires knowledge of the pathophysiology of the neuroarthropathic (Charcot) foot, so that the appropriate timing, extent of surgical intervention, and postoperative treatment in this unique population assures a higher success rate. One also must recognize associated factors that may be present in these patients, such as peripheral vascular compromise and poor nutritional status.

From the Division of Foot/Ankle Surgery, Medical College of Wisconsin, Department of Orthopaedic Surgery, Milwaukee, WI.

Reprint requests to Richard M. Marks, MD, 9200 West Wisconsin Avenue, PO Box 26099, Milwaukee, WI 53226-0099.

The treatment of foot and ankle disorders in patients with diabetes mellitus requires an organized multidisciplinary approach, which involves constant monitoring and followup of this enigmatic patient population.

It has been estimated that between 6% and 42% of patients with diabetes mellitus will have peripheral neuropathy develop, 1,5,6,15 and of those patients with neuropathy as many as 2.5% will have neuroarthropathic (Charcot) changes develop. The multisystemic nature of this disease, particularly concomitant peripheral vascular compromise and renal failure, creates a clinical entity that frequently is fraught with complications.

Complications in treatment of the foot and ankle in patients with diabetes involve delays in the diagnosis and recognition of neuropathic and neuroarthropathic states, failure to recognize the unique treatment protocol required for the neuroarthropathic injury, recognition of complications caused by associated medical conditions, failure to educate patients, and failure to institute preventative care.

Treatment of the foot in patients with diabetes depends on multiple factors, and is varied accordingly. One must determine whether neuropathy is present or absent. Additionally, one must determine whether there is evidence of an active or unresolved Charcot neuroarthropathic process. If deformity is present, is there associated instability? If ulceration is present, is there an associated deep infection, and is there adequate healing potential of the patient, or is there impaired vascular status and impaired nutritional status? All of these variables must be taken into consideration to minimize complications associated with the treatment of this patient population (Table 1).

TABLE 1

TABLE 1

Appropriate care of the foot in patients with diabetes additionally requires regular maintenance, evaluation, and education to guarantee patient compliance. Because of the multiple healthcare specialists that frequently are involved in the care of the patient with diabetes, it also is important to properly educate these providers as to the unique interventions that are required to avoid complications.

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Diagnosis and Recognition

The prompt recognition of the patient with diabetes who has peripheral neuropathy or a neuroarthropathic process is imperative to minimize the development of ulceration or joint destruction with concomitant deformity or both. All patients with diabetes should undergo monofilament evaluation to test for proprioceptive thresholds. This examination follows a seven-point evaluation in prescribed areas. The inability of a patient to feel the Semmes-Weinstein 5.07 monofilament (Hansens Disease Foundation, Carville, LA) is indicative of clinical peripheral neuropathy, and places the patient at risk for having ulceration develop because of the lack of protective sensation, and at risk for having a neuroarthropathic process develop. Such patients require the use of accommodative orthotics to protect the foot incapable of providing nociceptive and proprioceptive feedback. Without such protection, the patient with diabetes who has neuropathy is prone to ulceration under high pressure areas, particularly the metatarsal heads and sesamoids. These high pressure areas can lead to incipient ulceration, which in a sensate foot, typically would be painful, but is not recognized as noxious to the patient with neuropathy and is allowed to continue toward frank ulceration if appropriate intervention is not undertaken.

The diagnosis of the patient with diabetes who has an active neuroarthropathic (Charcot) process is essential for proper treatment, and the avoidance of progressive joint destruction, collapse, and the possible sequelae of dislocation and ulceration secondary to bony prominence and instability. Unfortunately, the diagnosis is delayed or missed in as many as 25% of patients. 7 Early recognition of the Charcot process helps avoid additional joint destruction.

The classification system of Eichenholtz 3 describes a three-stage disease process, which involves clinical and radiographic evaluation. In Stage I, the foot is warm, swollen, and red. This presentation frequently is confused with an infectious process, and it is not uncommon for a patient with diabetes to be subjected to intravenous antibiotics, bone scan, and biopsy for suspected osteomyelitis. Without antecedent ulceration, it is highly unlikely that this represents acute hematogenous osteomyelitis.

Unfortunately, many patients undergo triple phase bone scans, which will show intense activity in the region of involvement because of rapid bone turnover secondary to the Charcot process. Without a concomitant white blood cell scan, it virtually is impossible to diagnose an infectious process. Laboratory studies, such as an erythrocyte sedimentation rate and C-reactive protein can be helpful, yet are not conclusive, because many of these patients also may be immunocompromised because of the diabetes. Radiographs of the foot of patients with Stage I disease will reveal a destructive, fragmentive pattern which again, often is confused with osteomyelitis. Without knowledge of the Charcot process, many clinicians will underdiagnose neuroarthropathic disease.

When at all possible, radiographs with the patient standing should be obtained so that the integrity of the capsuloligamentous structures can be assessed accurately. It is not uncommon for patients with diabetes who have an incipient Charcot process to have nonweightbearing radiographs obtained that reveal no apparent joint subluxation, collapse or both only to have these processes rapidly progress with additional deformity in the ensuing days or weeks. When repeat radiographs are obtained with the patient weightbearing, the full severity of the Charcot process then is recognized, frequently too late.

When a patient with diabetes presents with an edematous, erythematous, hyperemic foot without a previous history of ulceration, a clinician’s first thought must be that of an active (Stage 1) Charcot process. Radiographs obtained with the patient weightbearing when possible, and appropriate laboratory tests also will help with the differential diagnosis. Perhaps the easiest test is to have the patient elevate his or her foot for several hours. Patients with Stage 1 Charcot disease will notice tremendous diminution of their symptoms, whereas the symptoms in a patient with an infection will be relatively unchanged. Stages 2 and 3 of the Charcot process involve resolution of the inflammatory response, with gradual bony consolidation. Patients who progress to Stage 2 disease will experience less redness, warmth, and swelling compared with patients with Stage 1 disease, but the foot will remain noticeably warmer and swollen versus the uninvolved side. Radiographs reveal no additional bone destruction, with incipient consolidation. In Stage 3, the clinical signs of inflammation have resolved completely, and radiographs show bone consolidation, perhaps with resultant deformity.

The recognition of these two latter phases has implications for continued treatment options as will be discussed later. The most common mistake made is not allowing sufficient time for the resolution of the inflammatory and destructive processes, thereby allowing progressive bony destruction and joint collapse. It is imperative, however, that the clinician recognize those patients with diabetes who are at risk for having neuroarthropathic changes develop. For this reason, the Eichenholtz classification has been modified to include a Stage 0, or at risk category. 12,13 This category of patients includes all patients with diabetes who have clinical neuropathy and patients with diabetes who have sustained an acute fracture or sprain (Fig 1). In patients with peripheral neuropathy, with or without previous trauma, who present with redness, warmth, and swelling of the foot without the concomitant radiographic changes seen in the Stage 1 Eichenholtz process, it must be assumed that this represents an incipient neuroarthropathic process, and the appropriate measures (as will be delineated later) must be undertaken. All patients with diabetes who sustain a sprain or fracture, particularly those with previously documented neuropathy, are considered at risk for having neuroarthropathic destruction develop. The initial clinical and radiographic presentations of these patients may appear similar to patients without diabetes and neuropathy; however, patients with diabetes are at significant risk of having neuroarthropathic changes develop. Therefore, the treatment protocol must be modified, as will be discussed later.

Fig 1A–B.

Fig 1A–B.

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Treatment Complications

Surgical treatment of the foot in a patient with diabetes seeks to preserve limb function by establishing a stable foot which is able to wear a shoe, able to be braced, or both. Such care must take into account the unique factors involved with the patient with diabetes, including the possible presence of neuropathy, the potential for having a neuroarthropathic process develop, and the unique factors that affect healing in the patient, thus necessitating a longer length of immobilization after surgery. Numerous patients are undertreated, particularly for acute fractures, out of the surgeon’s fear of a compromised outcome because of the patient’s disease. Additionally, the timing of surgical intervention in patients with acute fractures and in those with neuroarthropathic destruction is important to avoid loss of reduction and internal fixation, and to prevent additional neuroarthropathic collapse.

Frequently, orthopaedic surgeons tend to undertreat the patient with diabetes who has an acute foot or ankle fracture that requires surgical intervention. The same surgical criteria that is applied to the patient who does not have diabetes also should be applied to patients with diabetes. In a patient with an acute fracture without a concomitant active Charcot process who requires surgical intervention, one should attempt to achieve the most rigid internal fixation construct that will best ensure the maintenance of an adequate reduction. One should avoid a minimal treatment technique that can result in less than satisfactory fixation and incomplete reduction of fractures, out of fear of creating wound and bone healing problems.

Frequently, it is necessary to cross uninvolved joints with internal fixation devices to ensure a more rigid construct. For particularly unstable fractures such as periarticular fractures about the ankle, it is not uncommon to use a combination of internal and external fixation to establish a solid construct. 12,13 To avoid wound healing problems, surgeons also should attempt to establish full thickness flaps without undermining the subcutaneous tissues.

A second mistake commonly seen in the treatment of patients with acute fractures is that the length of immobilization of the fracture frequently is not of sufficient duration. A common scenario is to see a well-reduced fracture, with or without internal fixation, eventually develop loss of reduction, angular deformity, and perhaps joint destruction once the patient with diabetes is allowed to increase activities 4 (Fig 2). In general, fractures in patients with diabetes should be immobilized and unweighted at least two times longer than in fractures in patients who do not have diabetes.

Fig 2A–B.

Fig 2A–B.

Weightbearing is started as a slow, gradual process, at least two times greater than weightbearing in patients who do not have diabetes. During this period, it is necessary to use a removable boot brace or custom-molded brace to ensure maximal protection. Fractures about the ankle may require protection for as many as 6 to 8 months, frequently with the use of an ankle-foot orthosis, or custom-molded CROW (Charcot Restraint Orthotic Walker) boot. 10 It is imperative that radiographs be obtained on a regular basis, and that the patient’s clinical status be monitored very closely, checking for any signs of an incipient Charcot process.

Perhaps the most frustrating and enigmatic treatment is treating a patient with diabetes who has neuroarthropathic changes. For those patients with an active (Stage 1) Charcot process, it is imperative that the foot is mechanically unloaded with strict enforcement of elevation. The patient’s foot is placed in a total contact cast or a pneumatic boot brace to control peripheral edema and to provide bony and capsuloligamentous protection.

Surgical treatment in a patient with an active Charcot process should be undertaken only if there is the threat of eminent ulceration attributable to bony deformity. 8,12 If a patient with diabetes has sustained a fracture requiring surgical intervention that eventually had incipient Charcot changes develop, it is best to immobilize and elevate the limb initially to allow for resolution of the active inflammatory phase. Once this has resolved, it then is safe to undergo surgical intervention. Although this may necessitate delayed fixation of fractures with the possible necessity of correction osteotomy, early fusion, or both, this is preferable to operating on a patient with an active Charcot process. Although there is a recent report suggesting that such patients with midfoot injury and early Charcot changes can undergo successful surgical intervention, 14 it generally is thought that this is a risky proposition. 4,8,9,11–13

When consideration is given toward reconstruction of instability such as is seen in chronic Stage 2 neuroarthropathy, or reconstruction of a resultant Stage 3 deformity, the surgeon must take into account the patient’s activity requirements, ability to comply with a rigorous postoperative immobilization protocol, lower extremity perfusion, neurologic status, and the patient’s general medical condition. The goal of such surgery is to create a stable plantigrade foot which is able to be braced, able to wear a shoe, or both. Reconstructive procedures, therefore, are done to correct or prevent an ulcerative condition, to correct a deformity that otherwise is not able to be braced, and to improve ambulatory function.

It is important to recognize whether a patient is experiencing ongoing deformity, joint collapse, or both because of a chronic Stage 2 Charcot process, or whether the patient’s deformity represents an end stage (Stage 3) process that is stable. The surgical choices for these two clinical situations may be different, and unless the proper stage of the process is recognized, may lead to treatment complications.

Patients with a stable, Stage 3 Charcot process will not have signs of clinical inflammation such as warmth, swelling, and redness, and their radiographs will reveal no progressive bony changes. If the problem is ulceration caused by prominent bone, an exostectomy may be done, as long as the resultant exostectomy does not destabilize any joint. Exostectomy should not be done unless the patient has a stable (Stage 3) Charcot process. Complications resulting from plantar exostectomy include inadequate and excessive bone resection. Inadequate bone resection will lead to recurrent ulceration, although if an inordinately large amount of bone is removed resulting in gross bony instability, an active Charcot process will be created after surgery. Exostectomy done on a patient with a Stage 2 Charcot process, which by definition still is unstable, can result in additional instability and additional deformity after surgery.

Patients with ulceration or deformities that cannot be braced attributable to chronic instability (Stage 2 Charcot) will require a reconstructive fusion to properly realign the foot in a plantigrade position and relieve any high pressure areas. In this clinical scenario, the surgeon must obtain the most stable construct possible to ensure stability of the reconstructive procedure. Frequently, it is necessary to cross uninvolved joints to obtain good bony purchase for screws. 12 It has been shown that a plantar applied plate in midfoot fusions provides superior strength, 9 and it also may be necessary to reinforce a hindfoot or ankle reconstructive procedure with the use of an external fixator.

As mentioned for the surgical care of acute fractures, incisions must be done without undermining with dissection carried down directly to bone. Electrocautery also can be used for soft tissue dissection, because tissues and bone frequently are hyperemic. Sutures should be left in for a minimum of 3 to 4 weeks to ensure adequate soft tissue healing. Protected unweighting of the extremity also is necessary, at least twice that time necessary for the patient who does not have neuropathy. Weightbearing is allowed only in a controlled gradual fashion and only with the use of a protective device. All patients having a reconstructive procedure will require orthotics or braces after surgery. Radiographs must be obtained on a regular basis to ensure that adequate healing without an incipient Charcot process is being achieved.

Complications are encountered frequently during the treatment of ulcers in patients with diabetes. Most complications are attributable to improper mechanical unloading and immobilization, improper institution or lack of institution of shoe modifications once healing has been achieved, and not recognizing underlying causes for ulceration such as continued instability, or inadequate peripheral blood flow.

The most important principle for treatment of an ulcer in a patient with diabetes is to mechanically unload the affected area to diminish shear stresses, so that the ulcer can heal adequately. Patients require the use of a total contact cast, 11 boot brace, or shoe with appropriate modifications so that the ulcer can be unweighted maximally. In some patients, it is necessary to additionally unload this region with the use of a walker or crutches. Many patients express an unwillingness to comply with this treatment protocol, and this undoubtedly is complicated by peripheral neuropathy that fails to provide the appropriate proprioceptive feedback. In turn, many clinicians become frustrated by their patient’s inability to comply, and the arduous and labor intensive process of debridement, continual cast application, and frequent followup visits. There are numerous debridement and wound healing products now available on the market, and many healthcare professionals mistake these products as being adequate in their own right. It is absolutely necessary to unload mechanically the affected ulcerated site so that regranulation and healing can take effect. No wound healing medicine should be mistaken as an adequate alternative to unweighting of the ulcerated region.

Additionally, the clinician must recognize whether an ulcerated region is being created by a stable bony deformity, or whether this represents a smoldering Stage 2 Charcot process. As mentioned previously, the Stage 2 Charcot process will not heal in the long-term, because this represents an unstable clinical entity and the patient will require reconstructive surgery.

A third complication frequently seen during the treatment of ulceration in a patient with diabetes is that clinicians frequently do not determine whether there is sufficient peripheral circulation to allow for healing of an ulcer. In the patient with compromised vascular status, ulcers will have a poor healing rate. If these patients undergo surgical exostectomy or reconstruction, they more than likely will experience ongoing healing problems, frequently with disastrous results. Additionally, mechanical unloading of the ulcer and use of protective devices will be less effective because of impaired peripheral perfusion. Therefore, all patients with diabetes who have an ulcerative condition, or patients being considered for surgical intervention require evaluation of their peripheral vasculature.

Assessment of vascular status is done most reliably with the use of noninvasive arterial Doppler ultrasonography. Ankle-brachial indices should be obtained bilaterally. It also is imperative to obtain absolute toe pressures because the ankle-brachial indices may be elevated falsely because of small vessel calcification. Additionally, waveform recordings will help to determine the vascular status of the patient with diabetes. Although transcutaneous oximetry is a more site-specific measurement, these values can be unreliable if there is cellulitis or edema present, which are frequent in patients with diabetes who have neuropathy.

An ankle-brachial index greater than 0.45 is necessary to reliably heal foot ulcers in patients with diabetes, with an absolute toe pressure greater than 45 mm Hg. 15 As mentioned previously, the toe pressures are more reliable in the patient with diabetes. If vascular occlusive disease is present, the normal triphasic waveform will not be present. A biphasic waveform is indicative of peripheral vascular disease, whereas monophasic waveforms will be present if the vessels are incompressible, indicative of advanced vessel calcification.

Frequently, the vascular status of patients with diabetes either is not evaluated or inadequately assessed, which can result in protracted failed treatment of ulceration, or failure of surgical incision sites to heal. It is not uncommon to have patients undergo multiple procedures with progressively higher levels of amputation if the surgeon works on a dysvascular limb. If a vascular evaluation indicates peripheral vascular insufficiency, it is imperative to consult a vascular surgeon. Unless there is a life threatening infection, it is preferable to obtain adequate blood flow via bypass surgery before doing any reconstructive procedure.

Nutritional parameters also should be obtained to estimate the healing potential of a patient with diabetes. Laboratory studies obtained include albumin, total protein levels, and a total lymphocyte count. Positive predictors for successful wound healing include an albumin level of greater than 3.5 g/dL, total protein greater than 6.2 g/dL, and total lymphocyte count greater than 1500/mL. 2 If all three parameters are diminished, one can expect a 30% healing rate of wounds. In a nonemergent situation, it is preferable to maximize a patient’s nutritional status before doing surgical intervention.

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Patient Education and Preventative Care

The best way to avoid complications in the treatment of the foot and ankle in patients with diabetes is to ensure that patients do not put themselves at risk for having ulceration develop, and to allow them to recognize an incipient Charcot process so that additional progression can be avoided. All patients with diabetes should be tested for peripheral neuropathy, and if this is present, the patient should be prescribed accommodative orthotics to protect their nociceptive-impaired feet. Instructions must be given and reinforced on a regular basis pertaining to shoewear, avoidance of ambulating in bare feet, proper foot and nail care, and about the warning signs of an active Charcot process. If patients are unable to self examine and maintain their feet, then it is important to enlist the help of family members or healthcare providers to assist in such care. If advanced neuropathy or foot deformity is present, patients with diabetes must be educated concerning appropriate shoewear. Any episode of abnormal redness, warmth, or swelling, with or without antecedent trauma, requires prompt attention, and the patients must be sensitized as to the importance of seeking early intervention for a suspected Charcot process.

Foot and ankle care of the patient with diabetes requires patience, vigilance, and indefinite attention. It is important to not only recognize the difference between an acute, unstable and stable Charcot process, but also to recognize patients at risk for having a neuroarthropathic process develop.

The orthopaedic surgeon must recognize the appropriate treatment of patients with diabetes who have acute fractures or sprains, and recognize the development of an active Charcot process. One also must recognize the requirement for prolonged mechanical unloading and immobilization of these injuries.

The appropriate treatment of ulceration requires protection and mechanical unloading of the affected region. If surgical intervention is contemplated, the appropriate staging of the deformity and Charcot process is imperative to avoid treatment complications. Additionally, one must determine the healing potential of the patient through evaluation of the peripheral vascular status and the nutritional status of the patient. Patient education also is paramount for the appropriate treatment of this chronic, frequently progressive disease.

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References

1. Boulton AJ, Knight G, Drury J, et al: The prevalence of symptomatic, diabetic neuropathy in an insulin-treated population. Diabetes Care 8: 125–238, 1995.
2. Dickhaut S, DeLee J, Page C: Nutritional status: Importance in predicting wound-healing after amputation. J Bone Joint Surg 66A: 71–75, 1984.
3. Eichenholtz SN: Charcot Joints. Springfield IL, Charles C Thomas 1966.
4. Kristiansen B: Ankle and foot fractures in diabetics provoking neuropathic joint changes. Acta Orthp Scand 51: 975–979, 1980.
5. Kumar S, Ashe HA, Parnell LN, et al: The prevalence of foot ulceration and its correlation in type 2 diabetic patients: A population-based study. Diabetes Med 11: 480–484, 1994.
6. Lippmann HI, Perotto A, Farrar R: The neuropathic foot of the diabetic. Bull NY Acad Med 52: 1159–1178, 1976.
7. Lose G, Lindholm P: Transient painful osteoporosis of the hip in pregnancy. Int J Gynecol Obstet 24: 13–16, 1986.
8. Marks RM, Myerson MS: Neuroarthropathy. Foot 5: 185–192, 1995.
9. Marks RM, Parks BG, Schon LC: Midfoot fusion technique for neuroarthropathic feet: Biomechanical analysis and rationale. Foot Ankle Int 19: 507–510, 1998.
10. Morgan JM, Biehl III WC, Wagner Jr FW: Management of neuropathic arthropathy with the Charcot Restraint Orthotic Walker. Clin Orthop 296: 58–63, 1992.
11. Myerson M, Papa J, Eaton K, et al: The total-contact cast for management of neuropathic plantar ulceration of the foot. J Bone Joint Surg 74A: 261–269, 1992.
12. Sammarco GJ, Conti S: Surgical treatment of neuroarthropathic foot defomity. Foot Ankle Int 19: 102–9. 1998.
13. Schon LC, Marks RM: The management of neuroarthropathic fracture-dislocations in the diabetic patient. Orthop Clin North Am 26: 375–392, 1995.
14. Simon RS, Tejwani SG, Wilson DL: Arthrodesis as an early alternative to nonoperative management of Charcot arthropathy of the diabetic foot. J Bone Joint Surg 82A: 939–950, 2000.
15. Tesfaye S, Malik R, Ward JD: Vascular factors in diabetic neuropathy. Diabetologia 11: 480–484, 1994.

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Osaretin B. Idusuyi, MD; and G. James Sammarco, MD, Guest Editors

© 2001 Lippincott Williams & Wilkins, Inc.