Charcot Foot: An Overview - Wounds Canada
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Charcot Foot: An Overview By Robyn Evans, BSc MD CCFP FCFP and Mariam Botros, DCh DE Case Presentation: Red, Hot Foot Mr. R.T. is a 63-year-old who presents to his local walk-in clinic with a warm, red, swollen right foot. He had noticed for the previous couple of days that it was becoming more difficult to get his work boots on. He says it is not painful. His past medical history is significant for type 2 diabetes for 14 years. He has hypertension. He is a non-smoker and drinks 12 beers per week. He does not test his blood sugars. His body mass index (BMI) is 28. Medications include: metformin 1g bid, ramipril 10 mg qd, rosuvastatin 10 mg qd. He takes these prescriptions as indicated. He works in a factory and wears steel-toed boots. His job requires a lot of walking. The attending physician examines the right foot and notes: • Pulses bounding at the right dorsalis pedis and posterior tibial • No skin breakdown; specifically, web spaces are clear • Right foot is swollen and warm to touch • Homan’s sign (the dorsiflexion sign) is negative • No palpable tenderness anywhere in the right foot or calf • Nail changes consistent with a fungal infection • Patient's temperature: 37° C; heart rate: 76 beats per minute; BP: 136/87 mmHg • Monofilament score 10 negatives/10 bilaterally • Left foot shows no swelling or redness Mr. R.T. is sent home with a prescription for cephalexin for 10 days and instructions to follow up with his own family doctor. Blood work is ordered to check complete blood count (CBC), C-reactive protein (CRP), uric acid, creatinine, blood sugar and HbA1c. Four weeks later Mr. R.T. presents to his own family doctor concerned that his foot has a different shape at the arch and that there is a small open area. 42 Wound Care Canada Volume 17, Number 1 · Spring 2019
Avoiding a Devastating Table 1: Common Misdiagnoses of Acute Charcot Foot2 Misdiagnosis Infection Inflammatory Other The scenario in this case study • Cellulitis • Acute arthritis • Deep vein thrombosis • Osteomyelitis • Gout • Sprain/Strain is not an unusual presenta- • Septic arthritis • Pseudogout • Fracture tion or management for a red, swollen foot. However, What is Charcot well as expense to the patient the diagnosis of infection was for ongoing accommodative incorrect, as the patient, in fact, neuroarthropathy? Charcot neuroarthropathy (CN), footwear. The risk of amputation had Charcot neuroarthropathy with CN is 15% but increases to also known as Charcot foot, is (CN). Charcot neuroarthropathy 35 to 67% in patients with an a rare inflammatory disease is often misdiagnosed.1 The associated ulcer.2 This condition involving the musculoskeletal most common misdiagnoses has been classified based on system of the foot and ankle.3–4 for an acute CN are listed in clinical and radiologic findings The disease process ultimately Table 1: Differentiating infec- (see Table 2). results in deformity of the foot tion/osteomyelitis from CN can or ankle due to collapse, fracture be a particular challenge. This and destruction of structures The Pathophysiology article outlines the basics of CN under significant pressure. of Charcot and highlights the need for a Unfortunately, this can lead Neuroarthropathy high index of suspicion when a to increased risk of ulceration, The pathophysiology of CN is patient with diabetes presents amputation, use of financial not entirely known. In 1868 Jean- with a hot, swollen foot. resources for patient care, as Martin Charcot was the first to Table 2: Classification of Charcot Neuroarthropathy2, 5–6 Eichenholtz Description Management Classification (plus Stage 0) Stage 0 This is the beginning of the acute stage, • Immobilize (e.g., using a total contact cast [ TCC], characterized by erythema, edema and instant total contact cast [ITCC] or removable heat. walking cast [RCW]). • Reduce weight-bearing activity. X-ray evidence may not be seen. • Manage blood glucose levels. Stage 1: The actue stage is characterized by • Immobilize (TCC/ITCC/RCW). Development erythema, edema and heat. • Reduce weight-bearing activity. • Manage blood glucose levels. Bone resorption, bone fragmentation and joint dislocation may all be seen on X-ray. Stage 2: The subacute stage is characterized by • Use patellar tendon-bearing brace (PTB). Coalescence decreasing warmth, edema and erythema, • Use Charcot restraint orthotic walker (CROW and by absorption of fine debris and walker). fusion of large fragments and new • Manage blood glucose levels. periosteal bone formation on X-ray. Stage 3: The chronic stage is characterized by • Use patellar tendon-bearing brace (PTB). Reconstruction resolution of swelling and erythema. • Use Charcot restraint orthotic walker (CROW Consolidation of fractured bone and walker). evidence of deformity may be seen on • Use custom-made shoes with or without a brace. X-ray. • Manage blood glucose levels. Volume 17, Number 1 · Spring 2019 Wound Care Canada 43
Figure 1: Most common areas for CN Table 3). Though only a third of patients will report an inciting Ankle joint 19% trauma, this cause should be considered.3 Patient co-morbid- Hindfoot 28% ities as well as gait and balance are important to consider when Midfoot 50% making management decisions. Forefoot 3% Unfortunately, 40% of patients will have an ulcer at the time of presentation with a Charcot foot.3 If an ulcer is present, superim- posed infection should be con- sidered. Some patients have been treated for recurrent episodes of cellulitis with little response and describe Charcot foot as a late no laboratory or systemic signs flow also increases osteoclastic sequela of tertiary syphilis,6 but activity. If the patient continues of infection. The most common it was not described in diabetic to walk and the process goes patients until almost 70 years unchecked, it results in destruc- later.7 The two basic theories of its tion of the susceptible joint of the Risk Factors etiology are neurotraumatic and ankle or foot. Although diabetes is Associated with CN neurovascular.3,8 In the neurotrau- the major cause, any patients with • Peripheral neuroarthrop- matic theory, some form of trauma peripheral neuroarthropathy can athy (acute, subacute or cumulative develop CN. Epidemiologic studies • Advanced age and repetitive) in the neuropathic have identified other risk factors • Male gender foot initiates a cascade of inflam- for CN (see sidebar, this page).9 • Caucasian mation. This then leads to intense • Lower education level osteoclastic activity and joint • Increased body-mass index destruction. In the neurovascular What are the physical, • Decreased bone mineral theory, autonomic neuroarthrop- historical and density athy results in vasodilation and laboratory findings? • Pancreas and/or kidney increased blood flow. This causes The diagnosis of CN should be transplant congestion in the venous system based on a careful history and • Elevated HbA1c and ischemia to the ligaments clinical examination of the skin • Osteomyelitis and tendons, leading to joint and the neurologic, vascular and • Recent surgery instability. This increased blood musculoskeletal systems (see Table 3: Physical and Historical Features of CN2–3 Skin Neurologic Vascular Musculoskeletal Other Varying amounts of swelling, Sensory, motor Pulses Varies depending on the Complaint erythema and warmth (3 – 5° C and autonomic bounding stage of CN. Early on, nothing of pain in warmer than the contra-lateral, changes of in the foot. will be seen. Later, joint the foot. unaffected foot). Use infrared diabetes. Test deformity or instability will cutaneous temperature monitor. using the 10 g be present; classic “rocker Ulceration may be present. Positive Semmes-Weinstein bottom” deformity. probe-to-bone test. monofilament. 44 Wound Care Canada Volume 17, Number 1 · Spring 2019
Indications of Possible Infection or Cellulitis • Proximal streaking of erythema, which is not a feature of CN • Presence of constitutional symptoms • Decrease of dependent rubor if the affected limb is elevated for several minutes. If there is infection, this erythema will remain. • Laboratory evaluation indicating significant elevation of erythrocyte sedimentation rate (ESR) and CRP, which may be consistent with infection. (Unfortunately, patients with diabetes often have a muted response to infection, so these values may not increase as expected.) • Presence of an ulcer, skin breakdown or other portal of entry. • Presence of an ulcer with a positive probe-to-bone test. areas involved are the midfoot For patients with diabetes and Eichenholtz classified Charcot (50%) followed by the hindfoot an ulcer, X-rays should look foot based on radiological find- (28%), the ankle joint (19%) and for bony abnormalities, soft ings in three stages,11,12 and the forefoot (3%)6 (see Figure 1 tissue gas or the possibility of later Shibata proposed an addi- on facing page). a foreign body.10 Table 3 lists tional Stage 0, which is charac- the musculoskeletal changes terized by erythema, edema and that can be expected at each heat without X-ray confirma- Imaging Considerations stage of CN. A venous duplex tion.11 Patients at this stage are Radiographs are the recom- ultrasound scan should be con- often misdiagnosed with cellu- mended initial imaging study sidered if deep vein thrombosis litis, gout or deep vein thrombo- to be done. The characteristic is suspected. Magnetic reson- sis due to lack of radiographic bony changes of CN can take ance imaging is able to detect evidence.5 weeks to see on plain X-rays and therefore are not useful bone marrow changes, soft for diagnosing CN in the early tissue edema and joint effusion Management stages—when clinical interven- early in the disease.8 Nuclear Management of Charcot foot tion is critical. It is helpful to imaging techniques may be is based on the acuteness of take bilateral X-rays to pick up used when MRI is not available symptoms, anatomic location subtle changes in the bone.4 or contraindicated. and degree of joint destruction.4 If a clinician is initially unsure about the diagnosis, it is rec- Figure 2: Factors Leading to Microfractures or Joint Collapse ommended that they treat the Autonomic neuroarthropathy condition as Charcot neuroarth- – vasomotor dysregulation ropathy by offloading until diag- and increased blood flow nosis is confirmed or disproven. Early detection and protection are key to preventing further Motor and sensory Other risk factors: neuroarthropathy destruction of the foot. Inflammatory lower bone – abnormal state with In the acute stage, immobil- density, changes to plantar pressure, increase in the ligaments due ization and reduction of loss of protective osteoclasts to hyperglycemia weight-bearing activities for sensation eight to 12 weeks is the mainstay of treatment. The gold standard for immobilization of Charcot Microfractures/joint collapse foot is a total contact cast (TCC), Volume 17, Number 1 · Spring 2019 Wound Care Canada 45
Important Facts about An Alternative Scenario CN/Diabetes The physician at the walk-in clinic was • Patients with peripheral aware of a rare condition called Charcot vascular disease are some- foot. He was still concerned, however, that what protected from CN as he would miss an infection in this patient vasodilation is part of the with diabetes. He prescribed cephalexin pathogenesis.3,8 but also advised the patient to remain • Joints are the weak link in non-weight bearing as if he had an the structure of the foot, acute fracture. He sent him home with and therefore more sus- an RCW, which was available in his phar- ceptible. macy, instructions to stop working, and • The midfoot is most often an urgent referral to a multidisciplinary affected as it is subjected clinic that deals with diabetic foot issues. to more force during the The following day the blood report was phases of walking. This is obtained and indicated a normal CBC, the classic “rocker bottom” creatinine, and CRP. His HbA1c was 9.6%. deformity. However, any joint of the foot can be affected.9 but devices like a removable cast imaging or laboratory. Early diag- • Hyperglycemia causes walker (RCW) are also commonly nosis is important for leading to increased risk of ligament used to offload the foot. Continue early, appropriate management and tendon weakening.3,10 immobilization until lower and prevention of further compli- • Patients with diabetes extremity edema and warmth cations. CN should be suspected often have lower bone min- resolve accompanied by evidence in any patient over 40 years old eral densities, a factor for of fracture consolidation.2,6 with peripheral neuropathy that development of CN. This is In the subacute and chronic presents with an acutely swol- more of an issue with type 1 stages, recommend devices len foot with little or no known than type 2 diabetes.2 include the Charcot restraint • Only a third of patients will orthotic walker (CROW) and the report trauma leading to Key Points patellar tendon-bearing brace their symptoms.3 (PTB). In the chronic stage, cus- ✔✔ A high index of suspicion tom-made shoes are indicated.2,6 is required to correctly Surgery may be considered if diagnosis CN in a timely conservative treatment fails to manner. establish a plantigrade foot. ✔✔ Develop an approach to the There is currently no evidence red, hot, swollen foot with for the use of bisphosphonates or without pain. Consider the possibility of infection, in managing CN.2,6 which can co-exist with Charcot changes. Conclusion ✔✔ I f Charcot neuroarthrop- Charcot neuroarthropathy is a athy is a concern, advise commonly missed diagnosis. the patient to remain It relies on an astute clinician, non-weight bearing while appropriate referrals are because early physical findings arranged. can be subtle with little help from 46 Wound Care Canada Volume 17, Number 1 · Spring 2019
trauma. It is unclear why not all References 8. Strotman P, Reif T, Pinzur M. Charcot arthropathy of the foot and ankle. patients with diabetic neuroarth- 1. Schmidt B, Holmes C. Updates on diabetic foot and Charcot osteopath- Foot Ankle Int. 2016;37(11):1255–63. ropathy develop Charcot foot. ic arthropathy. Curr Diabetes Rep. 9. Holmes C, Schmidt B, Munson M, Inflammation seems to be at the 2018;18(10):74. Wrobel J. Charcot stage 0: A review core of the process, and this may 2. Marmolejo V, Arnold J, Ponticello M, and considerations for making be related to risk factors and gen- Andersen C. Charcot foot: Clinical the correct diagnosis early. J Clin clues, diagnostic strategies, and treat- Endocrinol Diabetes. 2015;1(18). etic predisposition.13 ment principles. Am Fam Physician. 10. Lipsky B, Berendt A, Cornia P, Pile J, It can be difficult for health- 2018;97(9):594–99. Peters E, Armstrong D, et al. Infectious care providers on the front line 3. Rogers L, Frykberg R, Armstrong D, Diseases Society of America clinical to access the appropriate refer- Boulton A, Edmonds M, Ha Van G, et al. practice guideline for the diag- The Charcot foot in diabetes. Diabetes nosis and treatment of diabetic rals in a timely manner. Enlist Care. 2011;34:2123–29. foot infections. Clin Infect Dis. help from colleagues when 2012;54(12):e132–e173. 4. Dodd A, Daniels T. Charcot neuroar- referral to a multidisciplinary thropathy of the foot and ankle. J 11. Holmes C, Schmidt B, Munson M, team is not possible. An ortho- Bone Joint Surg Am. 2018;100:696– Wrobel JS. Charcot stage 0: A review pedist, podiatrist or chiropodist 711. and consideratons for making the cor- 5. Mautone M, Naidoo P. Charcot rect diagnosis early. Clinicial Diabetes should be able to help with and Endocrinology. 2015;1(18):12 pp. neuroarthropathy: An imaging these difficult cases. review. J Med Imaging Radiat Oncol. 12. Schmidt MB, Holmes CM. Updates on Consider CN in the differen- 2015;59:395–402. diabetic foot and Charcot osteopathic tial diagnosis of a red, swollen 6. La Fontaine J, Lavery L, Jude E. Current arthropathy. Current Diabetes Reports. concepts of Charcot foot in diabetic 2018;18(74):11 pp. foot to prevent the devastating patients. The Foot. 2016;26:7–14. 13. Gökhan K, Birsel O, Güven MF, Öǧüt consequence of a deformed foot 7. Jordan W. Neuritic manifestations in T. An overview of the Charcot foot and long-term effects on quality diabetes mellitus. Arch Intern Med. pathophysiology. Diabet Foot Ankle. of life, morbidity and mortality. 1936;57(2):307. 2013;4(10). YOU HAVE THE POWER TO 1 DISRUPT AND DESTROY BIOFILM 2,3 TO ADVANCE HEALING 78% CHANCE OF BIOFILM4 NON-HEALING WOUNDS NEED MORE THAN SILVER™ Specifically developed to win the battle against biofilm, MORE THAN SILVERTM technology harnesses the synergistic power of three key components; ionic silver, a surfactant and a metal chelating agent working together to deliver superior1 performance.* 1. Bowler PG, etVolume al. Parsons, 17, Number Wound 1 (2016) Medicine 14 · Spring6–11. 2019 2. Metcalf DG et al. J. Wound Care 2016; Vol25, No3. 3. Metcalf DG, et al. Int Wound J 2017; 14: 203-213. 4. Malone M et al. 2017. JWC; 20-25. +Wound Care=Canada 47 AQUACEL, Hydrofiber and MORE THAN SILVER are trademarks of ConvaTec Inc. ©2019 ConvaTec Inc. AP-019908-MM MORE THAN SILVER™ * When compared to AQUACEL™ Ag Extra™ dressing and other silver-only competitor dressings: ACTICOAT™ 7 and SILVERCEL™ Non-Adherent dressings.
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