Charcot neuroarthropathy, also known as Charcot foot, is a complication of diabetes mellitus where there is progressive degeneration of the joints, but it potentially is devastating in its consequences.1 It commonly affects the middle of the foot, hind-foot joints, the ankle, and forefoot joints, and it is believed to result from inflammation in the foot that becomes abnormally protracted due to the underlying neuropathy.2–8 The prevalence of Charcot neuroarthropathy is up to 13% in individuals with diabetes.9–11 Patients with Charcot neuroarthropathy encounter increased morbidity and decreased quality of life and mortality.2,4,5,12,13 If there is a delay in treatment, Charcot neuroarthropathy could result in ulceration and infection which can lead to amputation of the limb.12–16 These patients have a significant financial impact on the health care system through primary care, community care, outpatient costs, increased bed occupancy, and prolonged stays in hospital. Charcot neuroarthropathy poses many clinical challenges in its diagnosis and management. The often asymptomatic nature of the condition is very similar to ankle sprain, cellulitis, venous thrombosis, inflammatory arthritis, or gout in a healthy patient.5,16–22 Missed diagnosis is as high as 79% which ultimately leads to a delay in treatment for an average of 29 weeks.11,16,17,20,23–25 Charcot neuroarthropathy is caused by multiple factors, but essentially it is the result of peripheral neuropathy which is a complication associated with many diseases.2,4,5 The underlying peripheral neuropathy can skew the pain perception the patient experiences and can mislead the clinician on their differential diagnosis of an “inflamed foot”. A thorough neurological examination of the foot can uncover the underlying inflammatory and osteolytic disease process of Charcot neuroarthropathy.2,4,11,19,26–29 Early recognition and intervention is imperative to avoid the rapid progression toward permanent foot deformity, ulceration, and the possibility of limb loss.16,30,31 There are multiple review articles about Charcot neuroarthropathy2,11–13,16,23,25,28,32–34, but a lack of guidance on foot screen strategies for primary care and emergency room physicians. There is a need for a comprehensive guideline for initial diagnoses and management on foot care to advocate for increased awareness, thereby leading to earlier diagnosis and treatment by a multi-disciplinary team. In the current study, a thorough literature review of Charcot neuroarthropathy was conducted to evaluate efficacious methods of protocol design and potential barriers to implementation. The literature review also encompassed treatment goals for patients with Charcot neuroarthropathy. Based on the literature review, a foot screen strategies protocol for Charcot neuroarthropathy was devised by the authors and reported here. This protocol contains three parts: (1) pathophysiology of acute Charcot neuroarthropathy to highlight the relationship between the clinical findings and the development of the disease, (2) a comprehensive guideline on how to screen and evaluate Charcot neuroarthropathy, and (3) a brief overview on prevention of Charcot neuroarthropathy in patients with diabetes and other forms of peripheral neuropathy. Pathophysiology The underlying cause for Charcot neuroarthropathy is due to peripheral neuropathy, which is a loss of function of the nerves in the periphery of the body.2–4 The primary episode of inflammation can result from a number of factors, but ultimately leads to an increase in pro-inflammatory cytokines (interleukin-1β and tumor necrosis factor-α) which leads to receptor activator of the nuclear factor-κB ligand (RANKL-NFκB) pathway. Osteoclasts are activated leading to bone lysis followed by clearing of debris. In the presence of autonomic neuropathy, there is increased blood flow to the area, which acts to clear away bony material demineralizing the bone, cartilage, and soft tissue in the region.3 However, in the presence of diabetic neuropathy, the patient does not have the protective pain perception. Therefore, they continue to walk on the inflamed foot exacerbating the progressive pathway of osteolysis and osteopenia and weakening the pedal skeleton, leading to the high risk for dislocation and/or fracture.5–8,34,35
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