Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_896_Библиотеки_им_академика_М_И_Перельмана

The initial presentation for active Charcot arthropathy is usually quite distinct in that a patient will seek attention for a profoundly swollen foot that is difcult to t into a shoe (Fig. 26.3). Although classically described as painless, 75% of these patients will complain of pain or aching in an otherwise insensate foot [17]. Frequently, an antecedent history of some type of injury can be elicited from the patient [34]. When no such history is available, the precipi­tating event might simply have gone unrecognized in the neuropathic limb.

The diagnosis of active Charcot foot is primarily based on history and clinical ndings. Standard radiographs should always be performed. Weight-bearing X-rays are most help­ful in evaluating subluxations and angular deformities. Contralateral X-rays (or previous X-rays) for comparison might make subtle subluxations more evident. Advanced imaging can help conrm diagnosis in complicated scenarios or when the index of suspicion for the disorder is high in the presence of an ostensibly normal X-ray. Inammation plays a key role in the pathophysiology and is the earliest exam nding [53, 59]. When presented with a warm, swollen, insensate foot, plain radiographs are invaluable in ascertain­ing the presence of osteoarthropathy and the degree [28, 60]. In most cases, no further imaging studies will be required to make the correct diagnosis. However, in the active, prodro­mal “stage 0” of Charcot foot, there may be primarily soft tissue changes noted without X-ray evidence of distinct bone or joint pathology [61, 62]. Further investigation with MRI, serial radiographs, or scintigraphy should be considered when suspicion is high for osteoarthropathy or concomitant wound to investigate for osteomyelitis [63–67]. Admittedly, differentiating between acute Charcot arthropathy, acute gout, and osteomyelitis solely based on plain radiographs can be difcult [68]. Additional laboratory studies may prove useful in determining the appropriate diagnosis. Leukocytosis can often suggest acute osteomyelitis; however, this normal response to infection can be blunted in persons with diabetes or autoimmune disorders [68, 69]. While the erythrocyte sedimentation rate (ESR) may also be elevated in the case of gout or acute infection, it often responds similarly to any inammatory process and is therefore nonspecic. Similarly, C-reactive protein (CRP) is an inammatory marker but rises in hours and thus can be trended in an acute window directly monitoring for inammation or infection and can be utilized to monitor therapy response as it is often elevated for only 3–7days [70]. Neither lab tests have been determined to be superior and are likely to yield concordant results [70]. Comparably, procalcitonin is a biologic serum marker also detectable within hours and peaks earlier than ESR and CRP, within 1day, and is not elevated in noninfectious inamma­tory conditions. Procalcitonin can be helpful in trending bac­terial infections or sepsis and in a systematic review was noted to be more sensitive, more specic, and more accurate in differentiating inammation due to infection versus non-

infectious cases and furthermore differentiating bacterial versus viral causes [71, 72]. All three inammatory markers can predict severity of infection and anticipated hospital duration [71–74].

When a foot ulcer probes to the bone, a bone biopsy is recommended to formally diagnose osteomyelitis [28, 75,

Pattern I encompasses atrophic changes or osteolysis of the metatarsophalangeal and interphalangeal joints with the characteristic sucked candy appearance of the distal metatar­sals [52, 80]. Frequently, atrophic bone resorption of the dis-

Pattern IV involves the ankle joint, subtalar joint, and body of the talus. Disintegration of the talar body is equivalent to the central tarsal disintegration of Harris and Brand [88]. The destructive forces are created by joint incongruity and con­tinued mechanical stress which eventually erodes the talus and periarticular surfaces. Massive osteolysis is frequently observed in this pattern with attendant ankle or subtalar joint subluxation and angular deformity, often with concomitant ulceration. As noted, tibia or bular malleolar fractures are frequently seen in association with neuroarthropathy in this location and most likely precipitated by the development of joint dissolution. Pattern IV Charcot is found in approxi­mately 10% of reported cases [7, 49, 80].

Technetium (Tc99) three-phase bone scans are exquisitely sensitive for detecting Charcot arthropathy but are generally nonspecic in assisting in the differentiation between osteo­myelitis and acute neuroarthropathy [63, 91, 92]. Indium (In111) scanning has been shown to be more specic for infection; however, false-positive scans can be frequently observed in rapidly evolving acute osteoarthropathy without associated osteomyelitis [65, 92–94]. Additional studies helpful in differentiating Charcot arthropathy from osteomy­elitis include Tc-HMPAO labeled white blood cell scans and magnetic resonance imaging [64, 91, 95, 96].

signs” of osteomyelitis on MRI may help the clinician dis­cern between Charcot foot and osteomyelitis [97]. Table 26.3 lists the secondary signs of Charcot foot and osteomyelitis [97].

could not only detect early osteoarthropathy with 95% sensi­tivity but could also reliably distinguish between Charcot arthropathy and osteomyelitis even in the presence of implanted hardware [100]. However, no study is 100% accu­rate in distinguishing neuropathic bone lesions from infec­tious entities. Therefore, clinical acumen is necessary for detecting Charcot arthropathy at its onset, and clinical judg­ment remains paramount in properly assessing and manag­ing these patients. Rogers and Bevilacqua presented a simplied algorithm based on imaging studies to help dif­ferentiate Charcot foot from osteomyelitis (Fig.26.11) [68]. The management can therefore be extrapolated based on risk factors, level of injury, and level of instability [101].

When the patient enters the inactive stage, management is directed at a gradual resumption of weight-bearing with pro­longed or permanent bracing [17, 28, 59]. Care must be taken to gradually titrate the patient from non-weight- bearing (or TCC) to partial to full weight-bearing with the use of assistive devices (i.e., crutches, cane, or walker). Progression to protected weight-bearing is permitted, usually with the aid of some type of ambulatory, immobilizing device [112]. Charcot restraint orthotic walkers (CROW) or other similar total contact prosthetic walkers have gained acceptance as useful protective modalities for the initial period of weight­bearing after TCC or surgical reconstruction [114]. These custom-made braces usually incorporate some degree of patellar tendon bearing as well as a custom footbed with a rocker sole. A more readily available option is a pneumatic walking brace or similar removable cast walker that might incorporate a cushioned footbed or insole. These can be made less removable or nonremovable by simply applying adhesive tape or cast bandaging around the body of the brace to help encourage compliance (Fig.26.14) [115, 116].