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.

 

PATHOGENESIS

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.

 

Clinical presentation

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.

 

Forefoot

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.

Mid-foot

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.

Hindfoot

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.

 

	Dosage	Side Effects	Contra-indications
Pamidronate	90 mg intravenous (IV) over 2-4 hours	Fever, fatigue, myalgias, nausea, vomiting (flu-like symptoms)	Renal failure, Pregnancy (Cat. D)
Alendronate	70 mg orally (PO) weekly	Acid reflux, abdominal pain, nausea, musculoskeletal pain	Renal insufficiency, pregnancy (Cat. C), esophageal disorders, those at risk for aspiration
Calcitonin	1 spray (200 IU) in nostril daily, alternate nostrils	Rhinitis, epistaxis, other nasal symptoms	Pregnancy (Cat. C)

 

Treatment of specific fractures

Toe fractures

The toe is strapped to its neighbour for a splinting effect.

Metatarsal fractures

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.

Calcaneal fractures

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.

Forefoot

This  usually  stabilizes  without  bony  deformity  but patients may need moulded insoles in bespoke shoes.

Mid-foot

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

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.

 

Surgical  lntervention

In the neuropathic  foot  there are three primary  indications  for surgery;

Biopsy

Exostectomy

Elective reconstruction  (arthrodesis)

1. Biopsy

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.

2. Exostectomy

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.

3. 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.

Procedural  selection:

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.

Bone quality:

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.

Fixation:

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.