Surgical Treatment of Charcot Neuroarthropathy THOMAS ZGONIS, DPM; JOHN J. STAPLETON, DPM; LUKE C. JEFFRIES, DPM; VALERIE A. GIRARD-POWELL, RN; LYNANNE J. FOSTER, MD
T
he Charcot foot was identified as early as 1703 by English physician William Musgrave and again by the American physician John Kearsley Mitchell in 1831, but it was Jean-Martin Charcot, a 19th century French neurologist, who first described the underlying pathology of the condition that now bears his name.1,2 It was not until 1936 that Charcot foot was linked to neuropathy as a result of diabetes mellitus.3 Identified variously as the neuropathic joint, Charcot joint, or Charcot neuroarthropathy, the condition refers to a chronic progressive destruction of joint integrity affecting one or more of the peripheral articulations. When Charcot neuroarthropathy affects the lower extremities, particularly the foot and ankle, severe fractures or dislocations with subsequent deformities can develop that pose great risk to to the chances for limb survival. Charcot foot is the greatest single relative risk factor for developing ulceration when compared with obesity, history of amputation, history of ulceration, or insensitivity to a Semmes-Weinstein 10-g (ie, 5.07-gauge) monofilament wire. The Semmes-Weinstein wire test is performed with the patient’s eyes closed. The clinician touches the wire on different areas of the plantar aspect of the patient’s foot that are free of scar tissue or previous ulcers. The patient confirms
indicates that continuing education contact hours are available for this activity. Earn the contact hours by reading this article and taking the examination on pages 987–988 and then completing the answer sheet and learner evaluation on pages 989–990. You also may access this article online at http://www.aornjournal.org.
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whether he or she feels the wire. This determines whether the patient’s protective sensation to the foot is intact. The pathway to amputation for a patient with diabetes who has a Charcot deformity is development of ulceration that progresses to a limb-threatening infection. This article describes the etiology, pathophysiology, classification, and common surgical treatment of Charcot neuroarthropathy. A knowledgeable and prepared multidisciplinary team must cooperatively formulate a plan of care that continues throughout the patient’s course of hospitalization.
PATHOPHYSIOLOGY The pathophysiology underlying the Charcot foot has been the subject of intense investigation, and a number of competing explanations attempt to account for the clinical and radiographic features of the neuropathic joint.1-6 The two standard theories put forward as the likeliest causes of the Charcot foot are the neurovascular
ABSTRACT CHARCOT NEUROARTHROPATHY, a chronic progressive destruction of joint integrity, is believed to result from a disturbance in pain and proprioceptive sensation. It is most commonly treated in patients with uncontrolled diabetes mellitus and dense peripheral neuropathy. PREVENTION, EARLY DIAGNOSIS, and early treatment are key to a patient’s successful outcome. Educating the patient is paramount to avoid further complications and subsequent amputations. THIS ARTICLE DESCRIBES the pathophysiology, staging, surgical treatment, and natural course of Charcot neuroarthropathy. AORN J 87 (May 2008) 971-986. © AORN, Inc, 2008.
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Trauma, even when not recalled by the patient, seems to be a precipitating factor in the development of many Charcot cases. Even a minor incident may set in motion a cascade of events resulting in the pathology seen in the Charcot foot.
or French theory and the neurotraumatic or German theory. The neurovascular theory, advocated by Charcot, maintains that increased peripheral circulation causes bone resorption and demineralization, subjecting weight-bearing extremities to pathologic fractures.1-3 This theory proposes that increased peripheral circulation is a function of the loss of vascular sympathetic tone associated with the autonomic neuropathy common among patients with diabetes. Autonomic sympathectomy accounts for the relative warmth, edema, and arteriovenous shunting characterizing the Charcot foot. The effect of peripheral neuropathy on overall bone density remains poorly understood, despite studies clearly showing that osteoclastic activity is favored over osteoblastic activity in acute and chronic Charcot.5 Recent attempts to validate the neurovascular theory on the basis of sympathetic activity have proved elusive, with investigations demonstrating an increase in osteoclastic activity as sympathetic tone increases, a finding which contradicts the French theory.6 In addition, the Charcot foot also is seen in conjunction with severe peripheral artery disease. The neurotraumatic theory, originally put forward by Volkman and Virchow, attributes the cause of Charcot foot to chronic, repetitive trauma to an insensate foot.1-3 This repetitive trauma, coupled with a loss of proprioceptive
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function, leads to the progressive destruction seen in the Charcot foot. Recent work has proposed that a prominent role is played by inflammatory molecules, describing a pathway involving cytokine-mediated insults. The proposed mechanism implicates interleukin-1, interleukin-6, and tumor necrosis factor alpha as likely mediators in the exaggerated expression of osteoclasts.7 Sensorimotor neuropathy is an absolute precondition to the development of the Charcot foot; however, the majority of patients with diabetic neuropathy do not develop neuroarthropathy. This has led some investigators to speculate that Charcot patients suffer from a unique form of neuropathy that predisposes them to neuroarthropathy. Some research has shown that Charcot patients have no ability to detect cold temperatures but remain sensitive to warmth and light touch.8 In this same study, all the patients with neuropathy who did not suffer from Charcot foot failed to demonstrate a similar sparing of sensory function.8 Other researchers suggest that chronic hyperglycemia induces changes in the tendinous insertions around the lower extremity, subjecting the foot to pathologic stresses.9 Clearly, the exact pathophysiology underlying the Charcot foot remains uncertain. Still, there is some consensus regarding the mechanisms involved in neuroarthropathy. Trauma, even when not recalled by the patient, seems to be a precipitating factor in the development of many Charcot cases. Even a minor incident may set in motion a cascade of events involving, to a greater or lesser degree, many of the mechanisms described above, with no one pathway accounting for all the pathology seen in the Charcot foot. It also has been reported that alterations in the biomechanics of the foot as a result of partial pedal amputations can result in increased pressures, induced microtrauma, and resultant Charcot deformity.10 Charcot foot is progressive in nature. The longer the trauma persists, even if it is microtrauma, the greater the destruction and resultant deformity. Minimizing progressive destruction and resultant deformities through early detection and immobilization is the initial goal in treating this severely debilitating disease process.11,12
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CLASSIFICATION Various attempts have been made to classify the Charcot foot. Each of the classification systems developed is based on either anatomic location or clinical and radiographic findings. Although other classification systems based on the anatomical location of foot and ankle collapse have been described in the literature, the most common classifications are the Eichenholtz classification and Brodsky’s classification. EICHENHOLTZ CLASSIFICATION. Perhaps the best known classification is the Eichenholtz classification.13 • Stage I is the acute or developmental phase. The patient typically presents with acute signs of inflammation characterized as calor (ie, heat), rubor (ie, redness), and edema. Radiographic findings demonstrate joint effusion, bone fragmentation, and joint subluxation or dislocations. • Stage II is the coalescent phase, in which the patient typically presents with decreased calor, rubor, and edema and radiographic evidence of bony consolidation or resorption of articular debris. • Stage III is known as the chronic or remodeling phase and is characterized by radiographic evidence of bone bridging and remodeling across affected fracture fragments and joints. It is important to note that no specific time periods are set within each stage and that each stage often depends on the severity of the initial presentation. Furthermore, a new Stage 0 was added to the original classification to increase clinical suspicion for the possible development of Charcot neuroarthropathy in the face of trauma and neuropathy. It represents a modification of the original system and is characterized simply as an incident of acute foot and ankle trauma in a setting of peripheral neuropathy with no radiographic findings.14,15 BRODSKY’S CLASSIFICATION. Brodsky’s classification is based on the anatomic location of the affected joints.16 • Type 1 affects the tarsometatarsal or “Lisfranc’s joint” and represents approximately 60% of cases. • Type 2 affects the hindfoot and is the second most common location for the development of Charcot neuroarthropathy.
The Eichenholtz classification, which is based on clinical and radiographic findings, does not specify time periods within each stage, and each stage often depends on the severity of the initial presentation.
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Type 3a involves of the ankle joint, and type 3b affects the posterior calcaneus. • Type 4 involves more than one region. • Type 5 affects the forefoot, which is the least common anatomic location for development of Charcot neuroarthropathy. According to Brodsky, each of these types may present in any of the stages described by Eichenholtz.17
CLINICAL PRESENTATION
AND
DIAGNOSIS
Clinically, the patient with Charcot foot presents in the acute stage (ie, Eichenholtz I or II) with a warm and edematous extremity, which may or may not be painful or deformed. Physical examination of the involved extremity during the acute stage demonstrates pronounced warmth, edema, and erythema when compared to the contralateral limb. This presentation often is confused with cellulitis and can make a definitive diagnosis difficult. Observing the extremity while it is elevated can help differentiate between Charcot neuroarthropathy and cellulitis. In Charcot neuroarthropathy, erythema, which is a result of arteriovenous shunting, often dissipates quickly when the extremity is elevated. On the other hand, in the presence of cellulitis, erythema persists despite the position of the extremity. The diagnosis becomes more challenging in the presence of an open wound or history of previous infections, which makes it difficult to differentiate an acute Charcot foot from a soft-tissue or bone infection. AORN JOURNAL •
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Given the aggressive nature of both an acute Alkaline phosphatase is a nonspecific serum Charcot foot and infection, the consequences of a marker for bone metabolism and may be inmissed diagnosis can lead to major limb complicreased in the patient with acute Charcot foot.5,18 cations. For this reason, further imaging in conIn addition, the patient’s overall nutritional status junction with radiographs, laboratory studies, can be measured with albumin or prealbumin and deep intraoperative cultures including a levels, total lymphocyte count, and transferrin bone biopsy may be used to help differentiate levels. Probable imaging studies include x-rays of Charcot neuroarthropathy from an infectious the foot, ankle, and lower extremity as well as process. A differential diagnosis also may inbone and bone marrow scans, magnetic resoclude the possibility of nance imaging scans, computed tomography (CT) scans, and diagnostic ultrasound. • underlying osteomyelitis, • deep vein thrombosis (DVT), SELECTION CRITERIA AND CONTRAINDICATIONS • septic arthritis, FOR RECONSTRUCTIVE SURGERY • acute trauma, and Some of the most common selection criteria • gout. In the chronic stages of Charcot neuroarthfor Charcot reconstruction include ropathy (ie, Eichenholtz III), deformity or ul• stable osseous deformities with recurrent ceration usually are present, whereas rubor, ulcerations or infections and hospital adcalor, and edema are not present (Figure 1). missions that are not amenable to conservaThe patient may report a history of trauma; tive treatments or however, the majority of patients have no • unstable deformities that cannot be controlled memory of an inciting event. Determining a sufficiently with a Charcot-restrained orthotic history of microtrauma should include asking walker or bracing and footwear. questions about changes in functional activity Additionally, or shoe gear and having recently undergone • there needs to be documented evidence of sufficient arterial perfusion, lower-extremity surgery. All these factors lead to increased pressure or biomechanical insta• there may not be evidence of erythema or edema and temperature changes (ie, tembility and may induce microtrauma resulting perature may be within 2° C (3.6° F) of the in the initiation of Charcot neuroarthropathy. contralateral foot), and “Rocker-bottom” foot is seen as collapse of the affected joints leading to skin breakdown with • underlying osteomyelitis may be medically and surgically treated before the final reconsubsequent ulceration and infection. structive procedure. In summary, having a high index of suspicion and ordering appropriate laboratory and imaging studies is paramount in making an early diagnosis. When differentiating between acute Charcot foot and an infectious process, laboratory tests may include, but are not limited to, the following: • complete blood count and differential, • comprehensive metabolic panel, • erythrocyte sedimentation rate and C-reactive protein, and Figure 1 • A preoperative picture of a severe Charcot foot and ankle fracture disloca• blood cultures and hemoglobin A1C. tion and a medial preulcerative lesion.
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In the presence of an ulceration or chronic open wound, staged reconstruction is necessary to convert a contaminated (ie, bacterial count > 105) or infected wound to a clean wound. Furthermore, to undergo limb-salvage or reconstructive surgery, the patient needs to • be medically stable with his or her comorbidities optimized as necessary by appropriate team members, • have been ambulatory before the Charcot event, • display compliance and the necessary cognitive function to understand the severity of the condition in order to prevent postoperative complications, and • have family and support groups available. Contraindications for surgery include, but are not limited to, • a patient’s being bedridden before the Charcot event, • arterial insufficiency, • untreated osteomyelitis, • severe soft tissue loss or infection, or • noncompliance. Relative contraindications also may include but are not limited to • end-stage renal disease; • morbid obesity; • poor nutritional status; • psychosocial issues (eg, self-neglect, depression); • retinopathy-induced blindness; • surgery during the acute Charcot stages; • tobacco use; and • venous insufficiency.19
TREATMENT OPTIONS The goal of limb salvage for Charcot deformity with or without ulceration is to achieve a functional, corrected foot that is resistant to skin breakdown when supported with custom footwear and orthotics. Prevention, early diagnosis, and early treatment are paramount to a patient’s successful outcome. Treatment options during the acute stages of Charcot disease include • complete bed rest, • immobilization, • the use of bracing or removable casting boots, and
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To undergo limb-salvage or reconstructive surgery, the patient needs to be medically stable, have been ambulatory before the Charcot event, be compliant with medical instructions, and have family and support groups available.
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total contact casting. These treatments may last several weeks to months and may be supported further by adjunctive therapies such as bone stimulation or administration of oral or IV bisphosphanates. The goal is to limit any predisposing factors (ie, further trauma) that may lead to a debilitating unstable deformity at the chronic Charcot stage. Some surgeons have advocated surgical reconstruction during the acute Charcot stages, but the actual decision between conservative or surgical intervention depends on • the size, anatomic location, and instability of the deformity; • the presence of infection; • the patient’s health status and compliance; • psychosocial issues (eg, depression, selfneglect); • the presence of obesity; • the patient’s ambulatory status; and • the patient’s life expectancy.20,21 As opposed to the acute Charcot foot, surgical reconstruction of the chronically deformed and unstable Charcot foot is well described and documented in the literature with less criticism and debate.22-25 Surgical reconstruction of these deformities includes • plantar exostectomies, • osteotomies, • single- or multiple-joint arthrodesis, and • staged distraction via external fixation AORN JOURNAL •
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followed by percutaneous or open arthrodesis procedures. Various fixation methods have been described in the literature for acute and chronic unstable Charcot deformities. These include, but are not limited to, • the use of internal locking plating; • the use of multiple screws or plates; • foot and ankle intermedullary nailing; • combined internal and external fixation; and • circular, multiplane-ring fixation.
THE ROLE OF EXTERNAL FIXATION IN CHARCOT FOOT AND ANKLE RECONSTRUCTION Patients with diabetes who suffer from Charcot neuroarthropathy often are challenging surgical candidates because of diabetesrelated complications. The presence of • ulceration, • severe osseous deformity, • poor bone quality, • neuropathy, • immune deficiency, • obesity, and • multiple comorbidities commonly seen in this patient population limit the use of traditional methods of internal fixation. The risk of surgical infection is increased in patients with diabetes mellitus secondary to their impaired immune system and peripheral vascular disease. If ulceration with an underlying bony prominence is present, the risk of infection and future amputation is high, and the ability to use internal fixation is limited. Charcot neuroarthropathy involving severe deformity, instability, ulceration, or infection of the foot or ankle makes successful limb salvage difficult. When the reconstructive foot and ankle surgeon is faced with this clinical scenario, limb salvage is plausible through a rational approach that incorporates • arthrodesis of affected joints to correct deformities; • plastic soft-tissue reconstruction for wound closure; and • application of a circular, external-fixation device. External fixation, specifically with the Ilizarov apparatus (ie, a circular external fixation frame) because of its diversity of applica-
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tions, provides a very efficient surgical method for treating complex Charcot deformities in conjunction with plastic surgery techniques. Ring fixation is a minimally invasive technique that provides adequate bone stabilization while respecting the soft tissue envelope. Distraction osteogenesis, bone transportation, gradual and acute deformity corrections, and arthrodesis can be accomplished with external fixation.
THE PREOPERATIVE CONSULTATION Often, the starting point in the presurgical consult with a patient who has a severe Charcot foot and ankle fracture dislocation begins with the choice between limb-salvage surgery, with all its attendant risks and potential complications, and amputation. Primary amputation may be a viable option in some situations, assuming the patient understands the risks and benefits associated with that choice. The longterm survival rate among diabetic patients who have undergone major limb amputation, however, especially in patients with end-stage kidney disease and other comorbidities, is quite poor. Depending on the level of amputation and presence of comorbidities, the one- and fiveyear survival rates are as low as 50% and 15%, respectively.26 In addition, the metabolic and cardiovascular demands for ambulation among amputees are substantially increased, adding to the morbidity associated with this choice.27,28 On the other hand, among relatively healthy patients, a definitive, primary amputation is associated with a comparatively short recovery period and early return to activities of daily living.29 If an amputation at a level compatible with healing and prosthetic fitting can be performed, the patient may pursue this route rather than the protracted course and associated morbidity of major lower-limb reconstruction. More studies need to be performed to evaluate the survival rates of limb salvage on this high-risk diabetic patient population. Diabetic limb salvage is fraught with potential complications, and a candid discussion with the patient about goals and expectations is mandatory before any surgical intervention is undertaken.30 Unrealistic patient expectations can represent a major obstacle to the long-term success of diabetic limb-salvage
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surgery. A concerted effort toward understanding what the patient expects of the surgical course and what the patient is prepared to do to realize these expectations must be dealt with in the preoperative period. Typically, this educational process is facilitated with pictures or a demonstration of the prebuilt external fixation frame to be used. The patient with diabetes mellitus, simply by virtue of his or her disease, is subject to depressive states, weakened immune function, and impaired wound healing ability, all of which conspire to complicate the postoperative course.31-33 The surgical candidate must understand these obstacles before undergoing limb-salvage surgery. A thorough history and physical examination is imperative for stratifying risk factors to help the surgeon identify patients who may benefit from reconstructive surgery. The surgeon reviews documentation, if available, regarding the initial Charcot event and prior treatments. Physical examination is extensive and includes close evaluation of • the deformity, • the temperature of the extremity, • ulcers if present, • vascular and neurological status, • previous scars, and • the soft tissue envelope. The surgeon orders weight-bearing x-rays (Figure 2) consisting of an anteroposterior, medial oblique, lateral oblique, long calcaneal axial, and lateral views of the patient’s foot as well as x-rays of the patient’s ankle and leg. The surgeon identifies the affected joints, joint malalignment, the apex of the deformity, the relationship of the deformity to the rearfoot and ankle, bone quality, and the stage of the Charcot process according to the Eichenholtz classification system. The surgical team makes templates of the x-rays to help the team plan for the necessary osteotomies or joint resections to achieve deformity correction. The surgeon may use CT scans to better visualize the deformity, particularly if the x-rays are distorted by overlap of bony architecture. The circulating nurse ensures that all available x-rays and other imaging scans are displayed in the OR to delineate the anatomy, which often is distorted in Charcot foot.
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Noninvasive vascular studies that should be performed before reconstructive limb-salvage surgery may include the ankle brachial index, pulse-volume recordings, transcutaneous oxygen pressure, and Doppler arterial ultrasound examination that will be used when evaluating adjunctive pedicle flaps if needed for soft tissue coverage. The reconstructive surgeon consults the vascular surgical team for further imaging and surgical clearance if the noninvasive study results are poor and the patient has had a history of wound healing complication after surgery. If an ulcer is present, the surgeon excises the ulcer and takes deep soft-tissue and bone cultures and quantitative bacterial counts three to five days before the definitive surgical procedure is performed. This prevents future surgical complications by ensuring that the wound is not infected or heavily contaminated. If osteomyelitis is questionable, indicated by the presence of a deep penetrating ulcer, the surgeon also may perform
Figure 2 • An anterior-posterior x-ray showing the severe instability, deformity, and dislocation at the talo-navicular and calcaneo-cuboid joints.
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a bone biopsy to differentiate Charcot neudetermines whether the patient is aware of his roarthropathy from osteomyelitis. If indicated, or her condition and has been educated about the surgeon performs the bone biopsy at the the proposed procedure. The nurse ensures that same time as the ulcer excision. Magnetic resothe patient was instructed on the type of externance imaging scans, CT scans, and three-phased nal fixation device that will be used so that the bone scans using technetium usually do not dispatient is not confused or scared when seeing tinguish Charcot neuroarthrothe apparatus after surgery. pathy from osteomyelitis. If imThe nurse also observes, asaging is needed to differentiate sesses, and documents the paosteomyelitis from Charcot tient’s psychosocial state. The neuroarthropathy, a combined nurse should report evidence evaluation using leukocyte of self-neglect, noncompliance, scintigraphy and bone marrow Modifications to the basic or depression to the surgeon imaging, such as a technetium because the patient may not be 99m sulfur colloid bone mara suitable candidate for this static external fixation row scan, is performed. This procedure. Patients undergocombination of tests is 92% sening reconstruction and appliframe can be made sitive and 100% specific.34 cation of a circular external The static circular external intraoperatively; however, fixator are required to be comfixation device usually is prepliant and show eagerness tobuilt outside the OR to save when the majority of the ward their recovery before valuable surgical time. The undergoing surgery. Anything most common Charcot foot less often leads to major postframe is prebuilt and and ankle frame is constructed operative complications. with two tibial rings, a foot After the surgeon has visitsterilized, surgical time is plate and a half-ring fastened ed with the patient and comto the foot plate and the distal pleted the informed consent reduced significantly. tibial ring. The static external and surgical site marking fixation frame should be fitted processes, the circulating nurse on the patient preoperatively arrives in the preoperative area to confirm the appropriate size. to assess the patient. While reThe frame should allow room viewing the patient’s medical for three finger widths on the record, the circulating nurse posterior aspect of the leg and two finger widths notes the results of any abnormal laboratory on the anterior aspect of the leg and around the studies. Reconstruction of a chronic Charcot defoot plate. This allows room for postoperative formity usually is not urgent, and the patient swelling while maintaining biomechanical staneeds to be medically optimized before underbility. Additional modifications from this basic going the selected procedure. In particular, if the static frame can be made intraoperatively; howpatient’s hemoglobin and hematocrit levels are ever, starting with the majority of the frame predecreased, the circulating nurse discusses this built and sterilized reduces the surgical time sigwith the surgeon and anesthesia care provider. nificantly. When gradual distraction and stabiliza- The nurse also confirms that blood units are tion are needed, the external fixation frame is not available and are administered before and durprebuilt and is assembled during the surgical pro- ing surgery as ordered. The nurse identifies cedure so it is easier to apply. whether the patient • is taking any medications, including overPREOPERATIVE PHASE the-counter medications; The preoperative nurse assesses the patient • has any medical or food allergies; and verifies the patient’s identity and accompa- • has undergone previous surgery; and nying history. During this assessment, the nurse • has ever experienced anesthesia complications.
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The nurse notes whether prophylactic antibiotics were administered preoperatively. The circulating nurse has the patient verbalize the planned procedure and ensures that the patient’s answers are consistent with the surgical consent and surgery schedule. The nurse then verifies that the surgeon and patient have marked the correct surgical lower extremity. After completing a history and physical examination, the circulating nurse documents all pertinent information and develops a nursing care plan. (See the general nursing care plan for all patients with diabetes who are undergoing surgery [page 940]). Table 1 provides additional nursing diagnoses, interventions, and outcomes for diabetic patients undergoing surgery for Charcot foot.
INTRAOPERATIVE PHASE The surgeon and circulating nurse discuss the specifics of surgical instrumentation, orthobiologics, suture supplies, and possible intraoperative imaging before the patient is
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transferred to the OR (Table 2). The circulating nurse and scrub person ensure that all equipment, instruments, and supplies needed for the procedure are available and in proper working condition before bringing the patient to the OR. The application of circular external fixation requires a vast amount of instrumentation and parts. Like any instrument-intense procedure, perioperative team members must be educated on the nomenclature of the procedurespecific equipment and parts. A common language then can be used by all surgical and nonsurgical team members to eliminate confusion during application of the devices. The circulating nurse and scrub person cooperatively prepare the OR suite for the planned procedure. They obtain • standard basic orthopedic instrument trays that include curved and straight osteotomes, flexible chisels, bone hooks, distractors, lamina spreaders, and large and small Steinman pins; • a sagittal saw and wire drivers for joint
TABLE 1
Nursing Care Plan for Patients Undergoing Surgical Repair of Charcot Neuroarthropathy Diagnosis Risk for ineffective individual or family coping
Nursing interventions
• • • • • • • •
Assesses the patient’s present coping status by questioning, listening carefully, and observing nonverbal signs of coping ability. Identifies individual values and wishes concerning care. Provides information to reinforce correct understanding of the disease process and need for surgery. Involves family members and support persons in perioperative teaching. Offers reassurance and emotional support to the patient and his or her family members throughout the perioperative period. Obtains an order for anti-anxiety medications and administers them as needed. Obtains consultation from appropriate health care providers for psychosocial support as needed. Evaluates the patient’s response to psychosocial support measures.
Interim outcome criteria
Outcome statement
The patient verbalizes understanding of perioperative care and expected outcomes.
The patient participates in decisions affecting his or her plan of care.
The patient exhibits decreased anxiety and appropriate coping behaviors.
The patient demonstrates knowledge of psychological responses to the invasive procedure.
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TABLE 2
Intraoperative Equipment and Supply Needs Equipment
• Bipolar electrosurgical unit (ESU) • External fixation device • Extra back table • Pacemaker magnet, if needed • Pneumatic tourniquet and cuff • Portable fluoroscopy unit • Radiolucent OR bed • Standard ESU and grounding pad Instrumentation
• Basic orthopedic instrument tray • Basic plastic or neurosurgery instrument tray • External fixation system • Internal fixation system, if needed • Pneumatic wire driver • Reciprocating sagittal saw • Steinman pins, large and small
Medications and solutions
• Antibiotic prophylaxis • Platelet-rich and platelet-poor plasma • Topical hemostatic agent Positioning aids
• Arm boards • Padding for extremities and bony prominences
• Hip roll • Kidney brace Supplies
• Absorbable and nonabsorbable sutures • Betadine solution • Bone and soft-tissue culture supplies • Orthobiologics (ie, autogenous and allogeneic bone graft, bone morphogenic proteins, cortical cancellous chips, human demineralized bone matrix) • Indwelling urinary catheter kit • Permanent marker • Postoperative dressings to be applied within the frame • Skin staples • Thromboembolic disease stocking and sequential compression device for the opposite lower extremity
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resections or osteotomies; and a basic plastic or neurosurgery instrument tray with fine and more delicate instrumentation, if a plastic surgery procedure is needed for soft tissue coverage in conjunction with the Charcot reconstruction. The scrub person prepares the standard sterile back table as well as an additional table for the circular external fixator equipment. In many instances, a extra Mayo stand for harvesting an autogenous iliac crest graft may be needed so that two surgical teams can work simultaneously. The circulating nurse ensures that a radiolucent OR bed is in the OR to facilitate intraoperative x-rays and fluoroscopy. The radiology technologist brings the fluoroscopy unit into the room for intraoperative imaging and positions it on the opposite side of the surgical extremity. The circulating nurse ensures that an electrosurgical unit (ESU) and grounding pad are immediately available. Often, diabetic patients undergoing Charcot reconstruction also are cardiac patients with pacemakers. If the patient has a pacemaker, the circulating nurse discusses this with the surgeon and the anesthesia care provider and ensures that a magnet or bipolar ESU is available to prevent cardiac complications. If orthobiologics (eg, allogeneic bone grafting, bone morphogenic proteins, platelet-rich and platelet-poor plasma) are to be used, the circulating nurse ensures that they are readily available in the room. The circulating nurse prepares the appropriate products in advance to reduce surgical time and allow for required exposure times for each product. The circulating nurse and anesthesia care provider transport the patient to the OR on a stretcher and assist the patient in moving to a supine position on the OR bed. The circulating nurse pads all nonsurgical extremities and secures them with safety straps. The perioperative nurse initiates a surgical time out to confirm the correct patient, procedure, surgical sites, and laterality and verify that required equipment is available. The circulating nurse remains with the patient and assists the anesthesia care provider during induction of anesthesia. The procedures
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for Charcot reconstructive surgery can be performed under either general or regional (eg, spinal, epidural) anesthesia as recommended by the anesthesia care provider. The circulating nurse evaluates and documents the patient’s baseline overall body skin integrity so that any changes in integrity can be identified postoperatively. If the patient has no signs of peripheral vascular disease or any other contraindications for the use of compression stockings, the nurse places a thromboembolic disease (ie, TED) stocking on the nonsurgical leg over which he or she places a pneumatic sequential compression device cuff to prevent DVT and pulmonary embolism in the postoperative period. If the procedure is expected to last longer than 180 minutes, the nurse may insert an indwelling urinary catheter, if requested by the anesthesia care provider. If a tourniquet will be used, the surgeon and circulating nurse wrap cast padding around the patient’s thigh and place an appropriately sized cuff around the thigh at its point of maximal circumference. For patients who are free of infection, a thigh tourniquet almost always is placed to minimize surgical time, prevent excessive bleeding, and allow better visualization of the affected joints. The tourniquet is deflated immediately after the surgical procedure and before the application of the static circular frame. According to AORN’s recommended practices on tourniquet use, When prolonged tourniquet time is desired, the tourniquet should be released for reperfusion of the limb every hour. The reperfusion time should be 15 minutes, after which the tourniquet may be reinflated for another full period.35(p488) The surgeon places a nonadherent drape over the tourniquet to prevent fluids from getting under the cuff. Typically, the nurse places a hip roll (eg, gel roll, rolled towel) under the patient’s ipsilateral hip to either • place the foot in a rectus position for midfoot corrections or • facilitate further internal rotation for lateral exposure during rearfoot and ankle corrections.
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If an autogenous iliac crest bone graft will be harvested by the orthopedic team, it typically is taken from the contralateral hip (opposite from the surgical extremity). In this case, the circulating nurse places the hip roll under the patient’s hip opposite of the surgical extremity. The circulating nurse then places the ESU grounding pad on a clean, intact area of skin on the thigh. Autogenous and allogeneic bone grafting commonly are needed in Charcot reconstructive surgery. The circulating nurse cleanses the surgical extremity to above the knee and the graft site, if applicable. The circulating nurse also cleanses the donor sites (eg, contralateral iliac crest). The surgeon and scrub person then apply the surgical drapes, ensuring that the knee is exposed to facilitate correct positioning during deformity correction and application of the circular external fixation apparatus.
SALVAGE SURGICAL TECHNIQUE If an ulcer is present, the surgeon excises and debrides it to adequately prepare the recipient wound for soft-tissue coverage. He or she then obtains intraoperative bone and soft-tissue cultures. This stage typically is performed three to five days before the definitive osseous reconstructive procedure to avoid surgical infection. The wound dressings are changed daily after surgery with moisture-retentive dressings or advanced wound care products. The final surgical osseous reconstruction begins with the surgeon marking the incision placements, keeping in mind the planned future plastic surgery procedures. Often the osseous anatomy and architecture are distorted by bone fragments and joint dislocations secondary to the Charcot process. Incisions that typically might be used in a foot with normal architecture may not be sufficient in the Charcot foot. It is important to plan incisions to allow adequate surgical exposure but still allow the incisions to be incorporated by eventual soft tissue coverage. After the surgeon has marked the planned incision sites, the pneumatic tourniquet is inflated. The surgeon creates direct dissection and full-thickness flaps, facilitating exposure of the affected joints while minimizing the degree AORN JOURNAL •
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of undermining to prevent tissue necrosis (Figure 3A). The surgeon removes bone fragments and debris that are not viable to prevent delayed unions or nonunions (Figure 3B). To correct the multiplane deformity and to achieve a plantigrade foot, the surgeon performs the joint resections with a sagittal saw or osteotome. He or she then packs the resected joints with autogenous or allogeneic bone graft (Figure 3C). If the surgeon is unable to dorsiflex the foot to neutral (ie, 90 degrees) from the lateral view, he or she may perform a percutaneous Achilles tendon lengthening or gastrocnemius recession. When joint alignment and deformity correction are obtained, the surgeon stabilizes the corrections with percutaneous Steinman pins or internal fixation (eg, screws, plates). The surgeon then closes the wound and performs soft-tissue coverage as needed. Before the surgeon applies the external fixator, the pneumatic thigh tourniquet, if still inflated, is released. At this point, the surgeon positions the prebuilt circular external fixation frame on the patient’s foot and lower extremity. The scrub person stacks opened towels under the patient’s posterior leg and heel until the surgeon can place two finger widths anterior and three finger widths posterior between the frame and the patient’s leg. The scrub person removes the towels after the patient’s foot and leg are suspended in the frame via the frontal plane
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Figure 3A • Intraoperative picture showing the talectomy procedure.
Figure 3B • Cartilage resection of the tibio-calcaneal-navicular joints.
Figure 3C • Insertion of a combined autogenous iliac crest bone graft (ICBG) and allogenic cortico-cancellous bone graft.
Zgonis — Stapleton — Jeffries — Girard -Powell — Foster
wires. To avoid rotational offset, the surgeon positions the frame so that the anterior crest of the tibia aligns with the anterior tabs of the tibia rings. The surgeon positions the frame laterally so that it is parallel with the foot in 90degree dorsiflexion. The scrub person maintains the patient’s foot and leg position until the surgeon tightens the wires to the frame. The surgeon achieves compression across the arthrodesis sites through manual tensioning of pre-bent wires. Typically, the surgeon obtains arthrodesis of the ankle and rearfoot with compression of the proximal tibial segment and the foot plate. The surgeon can insert additional wires as needed across the metatarsals to limit torque created around the forefoot. He or she also can place wires into the digits and attach the wires to the frame to prevent digital contractures (Figure 4). At the end of the procedure, the surgeon and scrub person cover the external fixator and wrap it with an elastic bandage. As the scrub person removes the drapes, the circulating nurse removes the tourniquet cuff and padding and examines the patient’s leg carefully for adverse reactions at the tourniquet site, such as venous congestion, bruising, pinching, or skin necrosis. Evidence of reperfusion to the extremity includes return of • capillary refill and color, • temperature, and • distal peripheral pulses.35 The circulating nurse reports any complications immediately to the surgeon and anesthesia care provider. The circulating nurse then calls the postanesthesia care unit (PACU) to provide an initial preparatory report, including the type of anesthesia administered and whether the patient will be intubated so the PACU nurse can prepare in advance to care for the patient. After transferring the patient to the postoperative bed or stretcher, the circulating nurse elevates the patient’s leg on two pillows with additional support under the knee.
POSTOPERATIVE PHASE The anesthesia care provider and circulating nurse transfer the patient to the PACU and provide report to the PACU nurse, including
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Figure 4 • Application of a static circular external fixation device.
• •
the patient’s latest blood glucose readings; whether the glucose readings remained consistent throughout the surgical procedure; • the type and amount, if any, of insulin administered intraoperatively; and • the type and timing of antibiotic administration. Antibiotics are continued for 24 hours postoperatively or longer in revisional procedures or for patient’s with a previous infection. The circulating nurse notes all pertinent facts on the patient’s electronic or written nursing notes in the medical record. Typically, the patient is hospitalized for five to seven days for pain management, antibiotic therapy, edema control, and medical management. During this period, medical/surgical unit nurses keep the patient’s surgical limb elevated and perform frequent vascular checks. Deep vein thrombosis prophylaxis is started on the first postoperative day. Initially, the physical therapist instructs the patient on how AORN JOURNAL •
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and when to perform exercises in bed. Shortly thereafter, the therapist teaches the patient how to use a walker or crutches to maintain strict non-weight bearing. This can involve a lot of effort and time by the patient and the therapist because the circular external fixation device can be heavy and bulky. On postoperative day three or four, the clinician performs the first dressing change. If needed, the surgeon then transfers the patient to the rehabilitation service for further physical medicine care before being discharged home. The surgical team examines the patient every two weeks postoperatively. The clinician instructs the patient to maintain strict non-weight bearing for three to four months. Early weight bearing is not advocated for the diabetic patient with neuropathy because he or she may accidentally cause trauma to the surgical site without any warning signs of pain and increase the risk of postoperative complications. After adequate bone consolidation and fu-
Zgonis — Stapleton — Jeffries — Girard-Powell — Foster
sion (Figure 5), the surgeon removes the external fixation frame in the OR with the patient under IV sedation and local anesthesia between weeks 12 and 16. The patient remains non-weight bearing for an additional four weeks using a short-leg cast. The clinician progresses the patient to partial and full weight bearing during the next month, with either a walking pneumatic device or walking cast. At this point, the pedorthotist fits the patient for a therapeutic shoe and bracing as needed. A pedorthotist is a physical therapist trained in the design, manufacture, and application of footwear and foot orthotics who has extensive biomechanical knowledge about how the body is supposed to move. The patient returns to the clinician for postoperative visits every two months for the next six months, then every three to four months unless complications arise. The clinician examines the contralateral foot at every postoperative visit to monitor for increased plantar pressures and the incidence of a Charcot event.
SUCCESSFUL MANAGEMENT OF CHARCOT NEUROARTHROPATHY
Figure 5 • Final six month clinical pictures showing the anatomic realignment and deformity correction.
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The reconstructive foot and ankle surgeon must have a vast knowledge of all available conservative and surgical treatment options. The etiology, pathophysiology, and natural progression of this debilitating disorder need to be further studied and better understood to improve early diagnosis and selection of appropriate treatment. These difficult-to-manage deformities require a multidisciplinary team approach and a tremendous effort from the patient’s family and social services. Prevention and patient education are crucial elements of successful management of Charcot neuroarthropathy.
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REFERENCES 1. Frykberg RG, Zgonis T, Armstrong DG, et al. Diabetic foot disorders: a clinical practice guideline (2006 revision). J Foot Ankle Surg. 2006;45 (5):S1-S66. 2. Jolly GP, Zgonis T, Polyzois V. External fixation in the management of Charcot neuroarthropathy. Clin Podiatr Med Surg. 2003;20(4):741-756. 3. Jordan WR. Neuritic manifestations in diabetes mellitus. Arch Intern Med. 1936;57:307-358. 4. Edmonds ME, Clarke MB, Newton S, et al. Increased uptake of bone radiopharmaceuticals in diabetic neuropathy. Q J Med. 1985;57(224):843-855. 5. Gough A, Abraha H, Li F, et al. Measurement of markers of osteoclastic and osteoblastic activity in patients with acute and chronic diabetic Charcot neuroarthropathy. Diabet Med. 1997;14(7): 527-531. 6. Chantelau E, Onvlee GJ. Charcot foot in diabetes: farewell to the neurotrophic theory. Horm Metab Res. 2006;38(6):361-367. 7. Baumahauer JF, O’Keefe RJ, Schon LC, Pinzur MS. Cytokine-induced osteoclastic bone resorption in Charcot arthropathy: an immunohistochemical study. Foot Ankle Int. 2006;27(10):797-800. 8. Stevens MJ, Edmonds ME, Foster AV, Watkins PJ. Selective neuropathy and preserved vascular responses in the diabetic Charcot foot. Diabetologia. 1992;35(2):148-154. 9. Grant WP, Sullivan R, Sonenshine DE, et al. Electron microscopic investigation of the effects of diabetes mellitus on the Achilles tendon. J Foot Ankle Surg. 1997;36(4):272-278. 10. Zgonis T, Stapleton JJ, Shibuya N, et al. Surgically induced Charcot neuroarthropathy following partial forefoot amputation in diabetes. J Wound Care. 2007;16(2):57-59. 11. Zgonis T, Roukis TS, Lamm BM. Charcot foot and ankle reconstruction: current thinking and surgical approaches. Clin Podiatr Med Surg. 2007;24(3): 505-517. 12. Roukis TS, Zgonis T. The management of acute Charcot fracture-dislocations with the Taylor spatial external fixation system. Clin Podiatr Med Surg. 2006; 23(2):467-483. 13. Eichenholtz SN. Charcot Joints. Springfield, MO: CC Thomas; 1966:1-20. 14. Sella EJ, Barrette C. Staging of Charcot neuroarthropathy along the medial column of the foot in the diabetic patient. J Foot Ankle Surg. 1999; 38(1):34-40. 15. Yu GV, Hudson JR. Evaluation and treatment of stage 0 Charcot’s neuroarthropathy of the foot and ankle. J Am Podiatr Med Assoc. 2002;92(4):210-220. 16. Brodsky JW. The diabetic foot. In: Surgery of the Foot and Ankle. Mann RA, Coughlin M, eds. St Louis, MO: CV Mosby, 1993: 877-958. 17. Sanders LJ, Frykberg RG. Diabetic neuropathic osteoarthropathy: the Charcot foot. In: The High Risk Foot in Diabetes Mellitus. Frykberg RG, ed. New
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York, NY: Churchill Livingstone; 1991:325-333. 18. Jude EB, Selby Pl, Burgess J, et al. Bisphosphonates in the treatment of Charcot neuroarthropathy: a double-blind randomised controlled trial. Diabetologia. 2002;44(11):2032-2037. 19. Zgonis T. Surgical correction of severe Charcot foot and ankle deformities with external fixation. Foot Ankle Qtly. 2006;18(4):149-157. 20. Zgonis T, Roukis TS, Frykberg RG, Landsman AS. Unstable acute and chronic Charcot’s deformity: staged skeletal and soft-tissue reconstruction. J Wound Care. 2006;15(6):276-280. 21. Zgonis T, Roukis TS, Polyzois V, Wukich DK. Surgical management of the unstable diabetic Charcot deformity using the Taylor spatial frame. Op Tech Orth. 2006;16(1):10-17. 22. Cooper PS. Application of external fixators for management of Charcot deformities of the foot and ankle. Foot Ankle Clin. 2002;7(1):207-254. 23. Fabrin J, Larsen K, Holstein PE. Arthrodesis with external fixation in the unstable or misaligned Charcot ankle in patients with diabetes mellitus. Int J Low Extrem Wounds. 2007;6(2):102-107. 24. Wang JC. Use of external fixation in the reconstruction of the Charcot foot and ankle. Clin Podiatr Med Surg. 2003;20(1):97-117. 25. Farber DC, Juliano PJ, Cavanagh PR, Ulbrecht J, Caputo G. Single stage correction with external fixation of the ulcerated foot in individuals with Charcot neuroarthropathy. Foot Ankle Int. 2002; 23(2):130-134. 26. Cutson TM, Bongiorni DR. Rehabilitation of the older lower limb amputee: a brief review. J Am Geriatr Soc. 1996;44(11):1388-1393. 27. Waters RL, Perry J, Antonelli D, Hislop H. Energy cost of walking of amputees: the influence of level of amputation. J Bone Joint Surg Am. 1976; 58(1):42-46. 28. Waters RL, Mulroy S. The energy expenditure of normal and pathological gait. Gait Posture. 1999; 9(3):207-231. 29. Davis BL, Kuznicki J, Praveen SS, Sferra JJ. Lower-extremity amputations in patients with diabetes: pre- and post-surgical decisions related to successful rehabilitation. Diabetes Metab Res Rev. 2004;20(Suppl 1):S45-S50. 30. Roukis TS, Stapleton JJ, Zgonis T. Addressing psychosocial aspects of care for patients with diabetes undergoing limb salvage surgery. Clin Podiatr Med Surg. 2007;24(3):601-610. 31. McIntyre RS, Soczynska JK, Konarski JZ, et al. Should depressive syndromes be reclassified as “metabolic syndrome type II”? Ann Clin Psychiatry. 2007;19(4):257-264. 32. Godbout JP, Glaser R. Stress-induced immune dysregulation: implications for wound healing, infectious disease and cancer. J Neuroimmune Pharmacol. 2006;1(4):421-427. 33. Sacco WP, Wells KJ, Friedman A, et al. Adherence, body mass index, and depression in adults AORN JOURNAL •
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with type 2 diabetes: the mediatational role of diabetes symptoms and self-efficacy. Health Psychol. 2007;26(6):693-700. 34. Palestro CJ, Love C, Tronco GC, Tomas MB, Rini JN. Combined labeled leukocyte and technetium 99m sulfur colloid bone marrow imaging for diag-
nosing musculoskeletal infection. Radiographics. 2006;26(3):859-870. 35. Recommended practices for the use of the pneumatic tourniquet in the perioperative practice setting. In: Perioperative Standards and Recommended Practices. Denver, CO: AORN, Inc; 2008:483-495.
Thomas Zgonis, DPM, is an assistant professor in the Department of Orthopaedics, Podiatry Division, and the director of the Reconstructive Foot and Ankle Fellowship at the University of Texas Health Science Center at San Antonio. Dr Zgonis has no declared affiliation that could be perceived as a potential conflict of interest in publishing this article.
ment of Orthopaedics, Podiatry Division, at the University of Texas Health Science Center at San Antonio. Dr Jeffries has no declared affiliation that could be perceived as a potential conflict of interest in publishing this article.
John J. Stapleton, DPM, is an associate of foot and ankle surgery at VSAS Orthopaedics, Allentown, PA, and clinical assistant professor of surgery at Penn State College of Medicine, Hershey, PA. Dr Stapleton has no declared affiliation that could be perceived as a potential conflict of interest in publishing this article. Luke C. Jeffries, DPM, is a reconstructive fellow and clinical instructor in the Depart-
Valerie A. Girard-Powell, RN, is a perioperative nurse at the University Hospital, San Antonio, TX. Ms Girard-Powell has no declared affiliation that could be perceived as a potential conflict of interest in publishing this article. Lynanne J. Foster, MD, is an assistant professor and deputy residency program director in the Department of Orthopaedics at the University of Texas Health Science Center at San Antonio. Dr Foster has no declared affiliation that could be perceived as a potential conflict of interest in publishing this article.
Victims of Childhood Abuse Spend More on Health Care
W
omen in their late 40s who were physically or sexually abused as children may spend up to 36% more on health care, according to a February 19, 2008, news release from The Ohio State University, Columbus. After accounting for other factors (eg, age, education), researchers concluded that childhood abuse correlated with increased spending on health care later in life. In a long-term study, researchers investigated 3,333 women living in the Pacific Northwest, 34% of whom reported some type of childhood abuse. Compared with women who were not abused as children, • women who were sexually abused as children paid an average of $382 (16%) more per year on health care, • women who were physically abused as children paid an average of $502 (22%) more per year on health care, and • women who were both sexually and physically
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abused as children paid an average of $790 (36%) more per year on health care. Women who experienced childhood abuse were more likely to be diagnosed with depression, report additional physical symptoms, and have a higher body mass index. Women who suffered both physical and sexual abuse as children also had higher rates of health service use in the following areas: • mental health, • hospital outpatient visits, • emergency department visits, • primary care, • specialty care, and • prescribed medications. Women who suffered child abuse spend more on health care [news release]. Columbus, OH: The Ohio State University; February 19, 2008. http://researchnews.osu.edu /archive/chldabus.htm. Accessed March 10, 2008.
Examination
3.6
Surgical Treatment of Charcot Neuroarthropathy PURPOSE/GOAL To educate perioperative nurses about surgical treatment of Charcot neuroarthropathy (ie, Charcot foot).
BEHAVIORAL OBJECTIVES After reading and studying the article on surgical treatment of Charcot foot, nurses will be able to
1. describe the symptoms of Charcot foot, 2. identify precipitating factors in the development of Charcot foot, 3. discuss options for surgical reconstruction of Charcot foot, and 4. describe perioperative nursing care of the patient undergoing surgical reconstruction of Charcot foot.
QUESTIONS 1. Charcot neuroarthropathy (ie, Charcot foot) is characterized by 1. arteriovenous shunting. 2. cyanotic discoloration. 3. edema. 4. relative warmth. a. 1 and 3 b. 2 and 4 c. 1, 3, and 4 d. 1, 2, 3, and 4 2. Although the exact pathophysiology is uncertain, many clinicians agree that ________________ is a precipitating factor in the development of many cases of Charcot foot. a. sedentary lifestyle b. trauma c. advanced age d. syphillus 3. As the affected joints collapse, the foot assumes a characteristic shape called a. equinus-bottom foot. b. rocker-bottom foot. c. flat foot. d. broken-arch foot.
© AORN, Inc, 2008
4. Surgical reconstruction of Charcot foot deformities include 1. osteotomies. 2. plantar exostectomies. 3. open or percutaneous arthrodesis. 4. single- or multiple-joint arthrodesis. 5. staged distraction via external fixation. a. 1 and 3 b. 2, 4, and 5 c. 1, 3, 4, and 5 d. 1, 2, 3, 4, and 5 5. During the preoperative assessment, the nurse notes any indications that the patient may not be a suitable candidate for this procedure, such as evidence of 1. depression. 2. noncompliance. 3. self-neglect. 4. visual impairment. a. 1 and 3 b. 2 and 4 c. 1, 2, and 3 d. 1, 2, 3, and 4 6. Reconstruction of a chronic Charcot
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deformity usually is not urgent. a. true b. false 7. Appropriate nursing interventions for a patient undergoing surgical reconstruction of Charcot foot include 1. assessing the patient’s present coping status. 2. identifying individual values and wishes concerning care. 3. involving family members and support persons in perioperative teaching 4. obtaining an order for anti-anxiety medications and administering the medication as needed. a. 1 and 3 b. 2 and 4 c. 1, 2, and 3 d. 1, 2, 3, and 4 8. The circulating nurse ensures that orthobiologics are available and prepared in advance. These may include 1. allogeneic bone graft. 2. bone morphogenic proteins.
The behavioral objectives and examination for this program were prepared by Rebecca Holm, RN, MSN, CNOR, clinical editor, with consultation from Susan Bakewell, RN, MS, BC, director, Center for Perioperative Education. Ms Holm and Ms Bakewell have no declared affiliations that could be perceived as potential conflicts of interest in publishing this article.
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3. platelet-poor plasma. 4. platelet-rich plasma. a. 1 and 3 b. 2 and 4 c. 1, 2, and 3 d. 1, 2, 3, and 4 9. If an autogenous bone graft will be harvested for a major rearfoot or ankle arthrodesis, it typically is taken from the a. contralateral iliac crest. b. cranium. c. ipisilateral iliac crest. d. tibia. 10. Postoperative care includes 1. antibiotic therapy. 2. deep vein thrombosis prophylaxis. 3. edema control. 3. medical management. 4. pain management. 6. physical therapy. a. 1, 3, and 5 b. 2, 4, and 6 c. 1, 3, 4, 5, and 6 d. 1, 2, 3, 4, 5, and 6
This program meets criteria for CNOR and CRNFA recertification, as well as other continuing education requirements. AORN is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation. AORN is provider-approved by the California Board of Registered Nursing, Provider Number CEP 13019. Check with your state board of nursing for acceptance of this activity for relicensure.
Answer Sheet Surgical Treatment of Charcot Neuroarthropathy
3.6 Event #08037 Session #1903
lease fill out the application and answer form on this page and the evaluation form on the back of this page. Tear the page out of the Journal or make photocopies and mail with appropriate fee to:
P
AORN Customer Service c/o AORN Journal Continuing Education 2170 S Parker Rd, Suite 300 Denver, CO 80231-5711 or fax with credit card information to (303) 750-3212. Additionally, please verify by signature that you have reviewed the objectives and read the article, or you will not receive credit.
Signature ______________________________________ 1. Record your AORN member identification number in the appropriate section below. (See your member card.) 2. Completely darken the spaces that indicate your answers to examination questions 1 through 10. Use blue or black ink only. 3. Our accrediting body requires that we verify the time you needed to complete this 3.6 continuing education contact hour (216-minute) program. ______ 4. Enclose fee if information is mailed. AORN (ID) #____________________________________________ Name__________________________________________________ Address ________________________________________________ City ___________________________________________________
State __________ Zip __________
Phone number __________________________________________ RN license #____________________________________________
State __________
Fee enclosed ___________________________________________ or bill the credit card indicated
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Expiration date _____________________
Signature _______________________________________________________________ (for credit card authorization) Fee: Members $18 Nonmembers $36
A score of 70% correct on the examination is required for credit.
Program offered May 2008
Each applicant who successfully completes this program will receive a certificate of completion.
The deadline for this program is May 31, 2011 © AORN, Inc, 2008
Participants receive feedback on incorrect answers.
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3.6
Learner Evaluation
Surgical Treatment of Charcot Neuroarthropathy his evaluation is used to determine the extent to which this continuing education program met your learning needs. Rate these items on a scale of 1 to 5.
T
PURPOSE/GOAL To educate perioperative nurses about surgical treatment of Charcot neuroarthropathy (ie, Charcot foot).
OBJECTIVES To what extent were the following objectives of this continuing education program achieved? 1. Describe the symptoms of Charcot foot. 2. Identify precipitating factors in the development of Charcot foot. 3. Discuss options for surgical reconstruction of Charcot foot. 4. Describe perioperative nursing care of the patient undergoing surgical reconstruction of Charcot foot.
CONTENT To what extent 5. did this article increase your knowledge of the subject matter? 6. was the content clear and organized? 7. did this article facilitate learning? 8. were your individual objectives met? 9. did the objectives relate to the overall purpose/goal?
TEST QUESTIONS/ANSWERS To what extent 10. were they reflective of the content? 11. were they easy to understand? 12. did they address important points?
LEARNER INPUT 13. Will you be able to use the information from this article in your work setting? 1. yes 2. no 14. I learned of this article via 1. the Journal I receive as an AORN member. 2. a Journal I obtained elsewhere.
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3. the AORN Journal web site. 15. What factor most affects whether you take an AORN Journal continuing education examination? 1. need for continuing education contact hours 2. price 3. subject matter relevant to current position 4. number of continuing education contact hours offered What other topics would you like to see addressed in a future continuing education article? Would you be interested or do you know someone who would be interested in writing an article on this topic? Topic(s): __________________________________ __________________________________________ Author names and addresses: _______________ __________________________________________ __________________________________________ __________________________________________ © AORN, Inc, 2008