Charcot Neuroarthropathy (CN)Charcot foot also called, as Charcot Neuroarthropathy (CN) is one of the rare, uncommon and often under diagnosed complication of chronic Diabetes mellitus although it can also occur in other medical conditions resulting from nerve injury.CN is potentially a mobility-limiting condition that affects the neuromusculoskeletal structures of the foot and ankle, resulting in fractures, destruction of weight-bearing bones and joints and progressive deformity marked by inflammation (body's response to injury or infection) with little or no documented trauma. Recognising Charcot, particularly in its early stage remains challenging.Although the actual cause of CN is unknown, it is presumed to be caused by neuropathy, inflammation, and trauma as stated by the two major theories, the 'French theory' and the 'German theory'. The former, also referred to as the neurovascular theory, contends that skeletal abnormalities are brought on by the damage to the nervous system, which leads to uncontrolled inflammation. It also implies that the destruction of the bones and joints is a result of autonomic neuropathy. Autonomic neuropathy has been observed to increase blood flow to the foot bones, which has been linked to increased bone resorption (osteopenia), decreased bone mineral density, and an increased risk of fracture.The latter, also known as 'neurotraumatic theory,' proposes that multiple subclinical traumas in a denervated foot are the first triggering factor. This minor trauma can activate the inflammatory response via complex pathways, resulting in micro- fracture, subluxation, and dislocation of bones. Continued, abnormal weight bearing is exacerbated by lack of pain perception due to neuropathy leading to further destruction of bones and joints.Peripheral neuropathy is likely to be an essential criterion for the onset of CN. There have been no reported cases of CN development in the absence of neuropathy. Repetitive microtrauma that outpaces the rate of healing may result in fractures and dislocations. Almost half of those who have CN describe a triggering, minor traumatic incident, such as an ankle sprain or a previous foot procedure. Diabetes duration, increased HbA1c, and the development of CN are all strongly linked.The initial manifestation of the Charcot foot is mild in nature. Some cases of Charcot may become unstable early and have destabilised even before they present to their doctor. Even if the foot and ankle are protected early, some case may destabilize later. In some patients, early protection may help reduce the likelihood of subsequent instability. This massive bony destruction of bone in CN may cause instability very differently than a fracture resulting from a trauma in a non-neuropathic patient. Charcot foot may recur or flare up or may occur in both sides.PresentationIn the acute stage, patients with CN may present with a red, hot, swollen foot with mild to modest pain or discomfort, there may or may not be deformity. Foot looks stable with no loose bones; there will be a marked temperature elevation noticed on the affected foot as compared to the other side on touch. In the advanced stage of CN, there can be bony projections, sometimes a flabby, enlarged appearance, resembling a “bag of bones”. Usually there is a unilateral involvement of the foot although rare simultaneous bilateral involvement is certainly possible. If the condition is not diagnosed and treated early or left untreated, it can cause extensive damage lending to deformities, ulceration and even amputation of a part of a foot or a limb.At times, charcot and osteomyelitis (infection of bone) can happen at the same time even though they are different and distinct processes. The osteomyelitis evolving into Charcot is further escalated if surgery was performed to remove the infected bone. This is because osteomyelitis and surgery are types of trauma that encourage an inflammatory response.Apart from the trauma induced by surgery, changes in the bone architecture of the foot following surgery can also contribute to inflammatory triggering events due to biomechanical changes that lead to high plantar pressures. For example, Amputation of a part of the foot can result in altered pressure points for which the foot is unable to compensate. Variations in plantar pressure even though it is mild, can produce microtrauma, triggering the inflammatory reactions that contribute to Charcot foot.In chronic CN, the foot is no longer inflamed. There may be palpable loosebones, which are the consequence of a substantial bone and joint destruction. There is a progressive deformity leading to rocker-bottom foot, the typical end stage appearance of Charcot foot. Due to continued weight- bearing there is a progression of deformity giving an appearance of “rocker bottom foot” (collapse of arch) that is prone to ulceration and amputation..DiagnosisEarly diagnosis and appropriate treatment lower the risk of CN causing permanent, debilitating foot deformity or amputation. Sometimes acute CN may be misdiagnosed due to its comparable appearance to other conditions such as cellulitis (bacterial skin infection that causes redness, swelling, and pain), deep vein thrombosis (when a thrombus or blood clot develops in veins), osteomyelitis etc. The chances of misdiagnosis are as high as 79 per cent, which, eventually, leads to a delay in treatment for an average of 29 weeks.A delay in diagnosis of up to 8 weeks may result in faster progression and greater problems such as foot and joint deformity, ulceration, infection, and, in the worst-case scenario, limb loss. The duration between the onset of symptoms and the diagnosis can range from weeks to months.Acute CN is primarily diagnosed clinically, but imaging modalities should be used to confirm the diagnosis. It should be suspected in any individual with Diabetes who presents with a unilateral, inflamed foot, profound neuropathy, bone and joint abnormalities. An individual with CN may recall a precipitating, mild traumatic event. If no traumatic episode is remembered, then the time frame during which the changes in foot form or gait was observed should be documented. One of the important physical examination findings that may be seen in CN is bounding (quick and prominent) pedal pulse on palpation. A temperature difference of 2°C or more on the infrared thermometer in comparison to the contralateral foot suggests the presence of CN. A simple physical examination to differentiate between an infectious process and CN is to have the patient lay supine and elevate the affected extremity for 5 to10 minutes. Localised oedema will decrease with elevation in CN while it is less likely in an infectious process.The components of diagnostic clinical findings and assessment include neurological, vascular, musculoskeletal, and imaging modalities. A neurological exam should be carried out to determine the degree of sensory loss. Early X-ray of the foot might indicate soft tissue oedema without any skeletal abnormalities (X-ray may be normal up to 4 weeks), but follow-up X-rays a few weeks or months later might reveal bone and joint alterations. The disease progression is then monitored using serial foot and ankle radiographs. Other superior tests such as a nuclear scan and a magnetic resonance imaging (MRI), can be used to rule out Charcot foot. A nuclear imaging has a high sensitivity and specificity in distinguishing charcot versus osteomyelitis. Surgically, a computerized tomography (CT) may be warranted to visualize the extent of the bone destruction for pre-operative planning..ManagementThe management objective in CN is to halt the progression, and preserve the architecture of the foot and ankle from further deformity. The goal is to achieve a stable foot that fits into a shoe and to prevent ulcers from occurring and recurring. CN management depends on a number of factors, including stage of the disease, location, deformity, presence or absence of infection, and other comorbidities.For the majority of patients, medical management of the charcot foot with immobilization in total contact cast (TCC) plaster continues to be the gold standard of care, with surgical intervention saved for the most challenging situations. In the acute or early stage, CN can be successfully treated with immobilisation using TCC along with frequent follow-up, temperature-monitoring using an infrared thermometer (helps track healing, associated with "foot cooling," and recurrence, associated with "foot warming"), radiographic assessment, and serial casting (TCC) until the inflammation is resolved. In the first few weeks, the cast or device should be inspected and changed frequently to avoid “pistoning” as oedema reduction is remarkable.Once the inflammation has subsided, it is critical to protect the foot for the rest of the life. After the inflammation is settled and radiographic stability is achieved the TCC is changed, and then treated with controlled weight bearing devices such as Charcot restraint orthotic walker (CROW) or a pneumatic walker or a patellar tendon bearing prosthesis, which helps to further offload the foot and eventually, with a customised insole footwear. Controlled weight bearing device is used for six months to two years, until a stable foot is obtained. Return to conventional footgear may not be possible.In case of a non-plantigrade, unstable, or if the foot cannot be braced or supported in any way or in case of recurrent history of ulcerations, surgical options are considered. The main rationale behind Charcot reconstruction is surgical offloading to prevent ulceration and progression of deformity. The surgical techniques include simple exostectomy, open reduction and internal fixation, external fixation with Ilizarov, arthrodesis, Achilles tendon lengthening and, eventually, amputation.Although CN recurrence appears to be rare, there is always a chance of ulceration because of the significant deformity. Proper footwear or bracing in cases of severe deformity may assist stop further progression and the development of an ulcer. If there is clinical evidence of non- compliance or bilateral involvement, a wheelchair should be recommended.Utilising offloading devices such as a walker or crutches may allow for complete non- weight bearing; nevertheless, a three-point gait may increase strain on the contralateral leg, resulting in repeated stress injury, ulceration, or neuropathic fracture.MedicineMedical treatments appear to play a limited impact in the treatment of CN. Certain medications, such as bisphosphonates, intranasal calcitonin, and RANKL antibody, are utilised in the acute stage to reduce inflammatory activity.Post-care and educationLimiting weight-bearing using appropriate orthosis is integral aspect of lifelong foot protection. After the cast is removed, the joint must be protected for the rest of the patient's life. This necessitates patient education as well as foot care from a foot care expert. The entire healing process in CN normally takes about 1-2 years, thus preventing further injuries, noticing temperature changes, inspecting feet daily, reporting trauma, and receiving competent foot care are all essential. The patient must be educated about the dangers of injuring a painless foot. Diabetes control is critical to prevent neuropathy progression. Getting regular foot checks is very critical.K.V. Kavitha is a Consulting Podiatrist.
Charcot Neuroarthropathy (CN)Charcot foot also called, as Charcot Neuroarthropathy (CN) is one of the rare, uncommon and often under diagnosed complication of chronic Diabetes mellitus although it can also occur in other medical conditions resulting from nerve injury.CN is potentially a mobility-limiting condition that affects the neuromusculoskeletal structures of the foot and ankle, resulting in fractures, destruction of weight-bearing bones and joints and progressive deformity marked by inflammation (body's response to injury or infection) with little or no documented trauma. Recognising Charcot, particularly in its early stage remains challenging.Although the actual cause of CN is unknown, it is presumed to be caused by neuropathy, inflammation, and trauma as stated by the two major theories, the 'French theory' and the 'German theory'. The former, also referred to as the neurovascular theory, contends that skeletal abnormalities are brought on by the damage to the nervous system, which leads to uncontrolled inflammation. It also implies that the destruction of the bones and joints is a result of autonomic neuropathy. Autonomic neuropathy has been observed to increase blood flow to the foot bones, which has been linked to increased bone resorption (osteopenia), decreased bone mineral density, and an increased risk of fracture.The latter, also known as 'neurotraumatic theory,' proposes that multiple subclinical traumas in a denervated foot are the first triggering factor. This minor trauma can activate the inflammatory response via complex pathways, resulting in micro- fracture, subluxation, and dislocation of bones. Continued, abnormal weight bearing is exacerbated by lack of pain perception due to neuropathy leading to further destruction of bones and joints.Peripheral neuropathy is likely to be an essential criterion for the onset of CN. There have been no reported cases of CN development in the absence of neuropathy. Repetitive microtrauma that outpaces the rate of healing may result in fractures and dislocations. Almost half of those who have CN describe a triggering, minor traumatic incident, such as an ankle sprain or a previous foot procedure. Diabetes duration, increased HbA1c, and the development of CN are all strongly linked.The initial manifestation of the Charcot foot is mild in nature. Some cases of Charcot may become unstable early and have destabilised even before they present to their doctor. Even if the foot and ankle are protected early, some case may destabilize later. In some patients, early protection may help reduce the likelihood of subsequent instability. This massive bony destruction of bone in CN may cause instability very differently than a fracture resulting from a trauma in a non-neuropathic patient. Charcot foot may recur or flare up or may occur in both sides.PresentationIn the acute stage, patients with CN may present with a red, hot, swollen foot with mild to modest pain or discomfort, there may or may not be deformity. Foot looks stable with no loose bones; there will be a marked temperature elevation noticed on the affected foot as compared to the other side on touch. In the advanced stage of CN, there can be bony projections, sometimes a flabby, enlarged appearance, resembling a “bag of bones”. Usually there is a unilateral involvement of the foot although rare simultaneous bilateral involvement is certainly possible. If the condition is not diagnosed and treated early or left untreated, it can cause extensive damage lending to deformities, ulceration and even amputation of a part of a foot or a limb.At times, charcot and osteomyelitis (infection of bone) can happen at the same time even though they are different and distinct processes. The osteomyelitis evolving into Charcot is further escalated if surgery was performed to remove the infected bone. This is because osteomyelitis and surgery are types of trauma that encourage an inflammatory response.Apart from the trauma induced by surgery, changes in the bone architecture of the foot following surgery can also contribute to inflammatory triggering events due to biomechanical changes that lead to high plantar pressures. For example, Amputation of a part of the foot can result in altered pressure points for which the foot is unable to compensate. Variations in plantar pressure even though it is mild, can produce microtrauma, triggering the inflammatory reactions that contribute to Charcot foot.In chronic CN, the foot is no longer inflamed. There may be palpable loosebones, which are the consequence of a substantial bone and joint destruction. There is a progressive deformity leading to rocker-bottom foot, the typical end stage appearance of Charcot foot. Due to continued weight- bearing there is a progression of deformity giving an appearance of “rocker bottom foot” (collapse of arch) that is prone to ulceration and amputation..DiagnosisEarly diagnosis and appropriate treatment lower the risk of CN causing permanent, debilitating foot deformity or amputation. Sometimes acute CN may be misdiagnosed due to its comparable appearance to other conditions such as cellulitis (bacterial skin infection that causes redness, swelling, and pain), deep vein thrombosis (when a thrombus or blood clot develops in veins), osteomyelitis etc. The chances of misdiagnosis are as high as 79 per cent, which, eventually, leads to a delay in treatment for an average of 29 weeks.A delay in diagnosis of up to 8 weeks may result in faster progression and greater problems such as foot and joint deformity, ulceration, infection, and, in the worst-case scenario, limb loss. The duration between the onset of symptoms and the diagnosis can range from weeks to months.Acute CN is primarily diagnosed clinically, but imaging modalities should be used to confirm the diagnosis. It should be suspected in any individual with Diabetes who presents with a unilateral, inflamed foot, profound neuropathy, bone and joint abnormalities. An individual with CN may recall a precipitating, mild traumatic event. If no traumatic episode is remembered, then the time frame during which the changes in foot form or gait was observed should be documented. One of the important physical examination findings that may be seen in CN is bounding (quick and prominent) pedal pulse on palpation. A temperature difference of 2°C or more on the infrared thermometer in comparison to the contralateral foot suggests the presence of CN. A simple physical examination to differentiate between an infectious process and CN is to have the patient lay supine and elevate the affected extremity for 5 to10 minutes. Localised oedema will decrease with elevation in CN while it is less likely in an infectious process.The components of diagnostic clinical findings and assessment include neurological, vascular, musculoskeletal, and imaging modalities. A neurological exam should be carried out to determine the degree of sensory loss. Early X-ray of the foot might indicate soft tissue oedema without any skeletal abnormalities (X-ray may be normal up to 4 weeks), but follow-up X-rays a few weeks or months later might reveal bone and joint alterations. The disease progression is then monitored using serial foot and ankle radiographs. Other superior tests such as a nuclear scan and a magnetic resonance imaging (MRI), can be used to rule out Charcot foot. A nuclear imaging has a high sensitivity and specificity in distinguishing charcot versus osteomyelitis. Surgically, a computerized tomography (CT) may be warranted to visualize the extent of the bone destruction for pre-operative planning..ManagementThe management objective in CN is to halt the progression, and preserve the architecture of the foot and ankle from further deformity. The goal is to achieve a stable foot that fits into a shoe and to prevent ulcers from occurring and recurring. CN management depends on a number of factors, including stage of the disease, location, deformity, presence or absence of infection, and other comorbidities.For the majority of patients, medical management of the charcot foot with immobilization in total contact cast (TCC) plaster continues to be the gold standard of care, with surgical intervention saved for the most challenging situations. In the acute or early stage, CN can be successfully treated with immobilisation using TCC along with frequent follow-up, temperature-monitoring using an infrared thermometer (helps track healing, associated with "foot cooling," and recurrence, associated with "foot warming"), radiographic assessment, and serial casting (TCC) until the inflammation is resolved. In the first few weeks, the cast or device should be inspected and changed frequently to avoid “pistoning” as oedema reduction is remarkable.Once the inflammation has subsided, it is critical to protect the foot for the rest of the life. After the inflammation is settled and radiographic stability is achieved the TCC is changed, and then treated with controlled weight bearing devices such as Charcot restraint orthotic walker (CROW) or a pneumatic walker or a patellar tendon bearing prosthesis, which helps to further offload the foot and eventually, with a customised insole footwear. Controlled weight bearing device is used for six months to two years, until a stable foot is obtained. Return to conventional footgear may not be possible.In case of a non-plantigrade, unstable, or if the foot cannot be braced or supported in any way or in case of recurrent history of ulcerations, surgical options are considered. The main rationale behind Charcot reconstruction is surgical offloading to prevent ulceration and progression of deformity. The surgical techniques include simple exostectomy, open reduction and internal fixation, external fixation with Ilizarov, arthrodesis, Achilles tendon lengthening and, eventually, amputation.Although CN recurrence appears to be rare, there is always a chance of ulceration because of the significant deformity. Proper footwear or bracing in cases of severe deformity may assist stop further progression and the development of an ulcer. If there is clinical evidence of non- compliance or bilateral involvement, a wheelchair should be recommended.Utilising offloading devices such as a walker or crutches may allow for complete non- weight bearing; nevertheless, a three-point gait may increase strain on the contralateral leg, resulting in repeated stress injury, ulceration, or neuropathic fracture.MedicineMedical treatments appear to play a limited impact in the treatment of CN. Certain medications, such as bisphosphonates, intranasal calcitonin, and RANKL antibody, are utilised in the acute stage to reduce inflammatory activity.Post-care and educationLimiting weight-bearing using appropriate orthosis is integral aspect of lifelong foot protection. After the cast is removed, the joint must be protected for the rest of the patient's life. This necessitates patient education as well as foot care from a foot care expert. The entire healing process in CN normally takes about 1-2 years, thus preventing further injuries, noticing temperature changes, inspecting feet daily, reporting trauma, and receiving competent foot care are all essential. The patient must be educated about the dangers of injuring a painless foot. Diabetes control is critical to prevent neuropathy progression. Getting regular foot checks is very critical.K.V. Kavitha is a Consulting Podiatrist.
