Management of Charcot Foot
Charcot neuroarthropathy is potentially a limb threatening condition that can affect the feet or legs of those persons with significant peripheral neuropathy of almost any etiology. While first described in patients with tertiary syphilis, diabetes mellitus has become the disease most commonly associated with this devastating condition.
The development of peripheral neuropathy in individuals with diabetes is attributed to a complex interaction of glycosylated hemoglobin with arterioles of both central and peripheral nerves. The resultant progressive loss of function is first appreciated in the smallest nerve fibers, leading to conduction defects in sensory, motor, and autonomic nerves. Precipitation of glycosylated hemoglobin at the arteriolar level is likely responsible for many of the co-morbidities associated with diabetes.
There is no singular cause for the development of the Charcot foot, but there are factors that predispose to its development, as well as a number of likely precipitating events. The current belief is that once the disease is triggered in a susceptible individual, it is mediated through a process of un-controlled inﬂammation in the foot. This inﬂammation leads to osteolysis and is indirectly responsible for the progressive fracture and dislocation that characterizes its presentation.
The evidence to support this hypothesis is largely circumstantial. A neurally mediated vascular reﬂex leading to increased peripheral blood ﬂow and active bone resorption has been proposed as an etiological factor in the development of bone and joint destruction in neuropathic patients. However, the relationship between increased blood ﬂow to bone and active bone resorption has not been conclusively deﬁned.
Acute or sub-acute repetitive trauma is likely a key initiating event of the pathologic process that leads to Charcot foot arthropathy. The suggests that the inciting event is trauma. Without the neurotraumatic theory presence of protective sensation, the patient continues to bear weight, eventually leading to a clinical scenerio that mimics a hypertrophic non-union. The is predicated on an neurovascular theory autonomic peripheral neuropathy that creates a high-flow vascular state in affected patients. This increased blood flow simplistically “washes out” structural calcium from the bone, leading to localized osteopenia and mechanically induced deformity associated with continued weight-bearing. The truth is likely a combination of both theories.
Patients typically present in the sixth or seventh decade. The vast majority were diagnosed with diabetes (both Types I and II) many years earlier. Most have clinical evidence of peripheral neuropathy, as measured by insensitivity to the Semmes-Weinstein (10 gm) monofilament. Occasionally, patients with neuropathy of other etiologies, such as alcohol, chemotherapy, and heavy metal, will present for treatment. Most patients are morbidly obese. Better than half of patients can cite a specific traumatic episode, often trivial, that initiated the process. Patients classically were thought to present with painless swelling of affected joints. In fact, many patients have pain associated with the swelling and deformity. While the involved foot is warm, swollen, and erythematous, the patient has an absence of clinical signs of sepsis, such as fever, leuccocytosis, elevated blood sugar, or increased insulin requirement. A further clinical differentiation from infection can be made by limb elevation. The erythema will decrease with elevation associated with arthropathy, as opposed to infection. Patients with infection generally have some element of purulent drainage. Patients with Charcot arthropathy have drainage only if there is secondary infection of a pressure ulcer.
Patients with type 1 diabetes have reduced bone density which renders them susceptible to fractures and then to Charcot’s osteoarthropathy. Patients with type 2 diabetes have normal bone density and Charcot’s osteoarthropathy is more frequently associated with subluxation and fracture-dislocation. Bone and joint destruction can occur in any part of the foot or ankle, but the common presentations can be divided into forefoot, mid-foot and hindfoot. The forefoot involves the metatarsophalangeal and interphalangeal joints. The mid-foot involves the tarsometatarsal joints and the hindfoot includes the ankle and subtalar joints.
Charcot’s osteoarthropathy can be divided into two phases:
- Acute active phase
- Chronic stable inactive phase.
Acute active Charcot’s osteoarthropathy The acute active phase is characterized by unilateral erythema and oedema . The foot is at least 2°C hotter than the contralateral foot and the difference may be as great as 10°C. This may be measured with an infrared skin thermometer. Patients may present early in the acute active phase when the X-ray is normal, or later when there may be already existing deformity and radiological changes of Charcot’s osteoarthropathy.
The well known Eichenholtz staging system is important in helping to determine appropriate treatment, since it emphasizes physiologic activity of the disorder as recognized by radiographic parameters
The developmental stage is characterized by significant soft tissue edema, joint effusions, osteochondral fragmentation, fractures and dislocation of varying degrees. The stage of coalescence is noted by a reduction in soft tissue swelling, bone callus proliferation and consolidation of fractures. Finally, the reconstructive stage is indicated by bone healing, joint ankylosis, and osseous hypertrophy without further clinical signs of inflammation. While this system is very descriptive from a radiological standpoint, its clinical usefulness is less so. Therefore, most clinicians will simply consider the initial stage as being active, while the coalescent and reconstructive stages combined are regarded the quiescent or reparative stages.
Presentation in the acute active phase with normal X-ray
If the X-ray is normal, we then proceed to two investigations. Initially a technetium methylene diphosphonate (MDP) bone scan, which will detect early evidence of
bone damage . If the result of the bone scan is positive, proceed to an MRI which will describe in more detail the nature of the bony damage. The other advantage of carrying out the bone scan is that it locates the site of the damage and therefore it allows the MRI to be focused in detail on that particular part of the foot. Patients awaiting bone scan should be treated as if the diagnosis has been conﬁrmed. Although patients with an early injury may appear to be developing Charcot’s osteoarthropathy, it is not possible yet to differentiate between those who have a soft tissue injury only and those who will develop extensive bony destruction. For this reason, all patients in stage 2 with a history of trauma, redness, warmth and oedema should be treated with a cast.
This presents with generalized swelling of the forefoot and osteonecrosis of the metatarsal heads. It is rare for a signiﬁcant structural deformity to develop in forefoot Charcot’s osteoarthropathy. The resorption of the distal metatarsal bones giving ‘sucked candy’ appearances usually associated with chronic ulceration and infection. Rarely, Charcot’s osteoarthropathy may present as a red, hot, swollen toe, usually the ﬁrst toe.
This is the commonest site of presentation of Charcot’s osteoarthropathy and it is recognized clinically by the rocker-bottom deformity and the medial convexity. The medial convexity is associated with the classical Lisfranc’s tarsometatarsal fracture-dislocation. The rocker-bottom deformity develops when there is disintegration and displacement of the cuneiforms or the proximal tarsal bones, resulting in collapse of the mid-foot. Rocker-bottom deformity is frequently associated with plantar ulceration.
The early presentation is of a swollen ankle. Later, there is severe structural deformity and instability of the ankle joint. This can lead to a ﬂail ankle on which it is impossible to walk. Ulceration can often develop over the malleoli.
Treatment of the acute active phase of Charcot’s osteoarthropathy with normal X-ray
Initially the foot is immobilized in a non-weightbearing plaster cast. The cast is checked after 1 week, and replaced if it has become loose due to reduction of oedema, then regularly checked and replaced as necessary. The patient should use crutches and be encouraged to avoid weightbearing on the affected side. However, we recognize that in many cases it is difﬁcult to be completely non-weightbearing because the patient has multiple comorbidities including loss of proprioception, postural hypotension, high body mass index and, in some cases, neuropathy of the upper limbs, all of which can make it difﬁcult for patients to use crutches. Furthermore, a wheelchair existence is impractical in many home environments. In addition, total immobility has disadvantages in itself with loss of muscle tone, reduction in bone density and loss of body ﬁtness. The casting is continued until the swelling has resolved and the temperature of the affected foot is within 2°C of the contralateral foot.
Patients at this stage may receive further treatment with bisphosphonates.
|90 mg intravenous
(IV) over 2-4 hours
Pregnancy (Cat. D)
|70 mg orally (PO)
pregnancy (Cat. C),
disorders, those at
risk for aspiration
|1 spray (200 IU) in
|Pregnancy (Cat. C)|
Treatment of speciﬁc fractures
The toe is strapped to its neighbour for a splinting effect.
The patient is put into a total-contact cast until X-rays conﬁrm healing, which may take up to 6 months. In some cases full union is not attained. However, at this stage the initial swelling has usually resolved and patients are mobilized slowly out of the cast.
The limb should be immobilized in a plaster cast until radiological healing has occurred.
Tibial and ﬁbular fractures
These fractures can be treated either by open reduction and internal ﬁxation or by cast immobilization.
Chronic stable inactive Charcot’s osteoarthropathy
The foot is no longer warm and red. There may still be oedema but the difference in skin temperature between the feet is usually less than 2°C. The X-ray shows fracture healing, sclerosis and bone remodelling. The average amount of time spent in a cast by diabetic patients before reaching the chronic stage is 6 months but some patients may need a cast for over a year. This is a crucial stage in the treatment. The patient must now be rehabilitated and gradually moved from cast treatment to suitable footwear. The patient needs close observation to detect any relapse which will be evident from further swelling and heat in the foot. Careful rehabilitation is always necessary after a long period in a cast.
This usually stabilizes without bony deformity but patients may need moulded insoles in bespoke shoes.
When the mid-foot has stabilized, the patient can progress from a total-contact cast to a bivalved cast or Aircast or other cast walker ﬁtted with a cradled moulded insole. When the patient comes out of the cast there will be wasting of the calf muscles and joint stiffness. The physiotherapist must be aware of the dangers of re-activating the bony destruction phase by excessively rapid mobilization or protracted weightbearing in the early stages of rehabilitation. Too rapid mobilization can be disastrous, resulting in further bone and joint damage. Extremely careful rehabilitation should be the rule, beginning with just a few short steps in the new footwear. The patient rests for the remainder of the day and monitors the foot. If there is no increase in warmth, swelling and redness then he can walk a few more steps the next day, and very carefully build up to a reasonable amount of walking.
Hindfoot Charcot’s osteoarthropathy may be difﬁcult to stabilize. An attempt may be made with total-contact casting. The cast may have been used during the acute phases, to reduce oedema and halt progressive bony changes and deformity. Continued use of the cast will help to achieve stability of the hindfoot. Alternatively, a Charcot restraint orthotic walker (CROW) may be used, followed by an ankle–foot orthosis (AFO) with bespoke footwear.
In the neuropathic foot there are three primary indications for surgery;
Elective reconstruction (arthrodesis)
The diagnosis of Charcotioints mayattimes be difficult for there are a number of conditions which may mimic this syndrome both radiographically and clinically. The picture is classically complicated by the presence of persistent ulcerations which may have led to the development of osteomyelitis. Both septic arthritis and osteomyelitis may occur simultaneously with neuroarthropathy. The definitive diagnosis of Charcot joints rests upon a synovial biopsy. The specimen will demonstrate the presence of multiple shards of bone and cartilage embedded with in the deeper layers of the synovium. lf osteomyelitis is of concern then a bone biopsy is essential for diagnosis.
A simple approach to ulcerative lesions within the lower extremity is to excise the offending osseous prominence. Preferably this is done through an incision site removed from the ulceration to minimize bacterial contamination of the bone. More recently complete elliptical excision of ulcer with exostoses and primary closure has been advocated.
- Elective Reconstruction (Arthrodesis)
In selected patients reconstruction of the Charcot foot may result in the creation of a functional part and prevent amputation. We have been traditionally led to believe that nothing definitive can be accomplished with the Charcot foot and consequently many such patients have succumbed to amputation. The key to successful reconstruction is proper patient and procedural selection. The following factors must be considered prior to surgery.
Arthroplasty is generally contraindicated in the neuropathic foot as the end result of this procedure is an unstable joint space; a situation which already exists in this foot type. U n Iike the average patient with osteoarthritis or joint contracture, Charcot patients have no Iimitation of motion. On the contrary, the motion is typically quite excessive in the neuropathic joint. lmplants are generally contraindicated and implant arthroplasty in general is associated with a very high rate of failure.
One needs to carefully examine the quality of bone prior to surgery. In order to ensure the highest rate of arthrodesis, good healthy osseous tissue must be present. Any bone which is suspect must be resected and grafts used if necessary to achieve suitable alignment. Provisions may need to be made prior to surgery to harvest good corticocancellous autogenous bone for grafting.
When performing arthrodesis in the neuropathic foot the most rigid form of fixation suitable to the procedure is necessary. Preferably this involves the use of screws and/or plates.