CHARCOT FOOT. What Should we Know?? I Wayan Subawa. Orthopaedi & Traumatology Subdivision Udayana University Sanglah General Hospital, Denpasar-Bali
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1 CHARCOT FOOT What Should we Know?? I Wayan Subawa Orthopaedi & Traumatology Subdivision Udayana University Sanglah General Hospital, Denpasar-Bali
2 INTRODUCTION Peripheral Neuropathy The most insidious complications of diabetes can lead in the lower limb to foot ulcers, Charcot neuro-osteoarthropathy and amputation Denervation-induced joint destruction was described by the French neurologist Jean-Martin Charcot in 1868 as a complication of tertiary syphilis Degenerative neuropathic arthropathy was first associated with diabetes in 1936 Early identification the best way to limit morbidity
3 HISTORY 1703 William Musgrave described arthralgia in association with venereal disease 1831 John Mitchell described effects of peripheral neuropathy in lower limbs secondary to Tuberculous spinal disease 1868 Jean-Martin Charcot described neuropathic osteoarthropathy affecting long bones and joints in Tertiary Syphilis Charcot Disease 1936 William Jordan linked Charcot Disease to Diabetes Mellitus
4 EPIDEMIOLOGY Onset occurs after the patient has been diabetic for 15 to 20 years The age of 50 or older Men = women The prevalence ranges from 0.1% to 13% DIABETIC FOOT DISORDERS. THE JOURNAL OF FOOT & ANKLE SURGERY. VOLUME 45, NUMBER 5, SEPTEMBER/OCTOBER 2006
5 DEFINITION Progressive degeneration of a weight bearing joint, a process marked by bony destruction, bone resorption, and eventual deformity Neuropathic arthropathy Neuropathic osteoarthropathy "Charcot foot
6 ETIOLOGY Diabetes (major cause) Leprosy (Hansen s disease) Tabes dorsalis Spinal cord tumor Charcot Marie Tooth disease Pernicious anaemia Medications like steroids, phenylbutazone, indomethacin, vincristine Alcoholism Cerebral palsy Hereditary insensitivity to pain Myelodysplasia Poliomyelitis Syringomyelia Tertiary syphilis
7 PATHOPHYSIOLOGY French theory (Charcot ) German theory (Volkman and Virchow) Dysregulated autonomic nervous system loss of peripheral sensation and proprioception hyperemia - desensitized joints receive increased blood flow Repetitive micro trauma Increased osteoclastic resorption of bone Inflammatory resorption of traumatized bone
8 DEVELOPMENT OF CHARCOT FOOT
9
10 L. Molines et al. / Diabetes & Metabolism 36 (2010)
11 STAGES OF THE CHARCOT FOOT Stage I - The Stage of Development, Acute inflammation with hyperaemia, bone softening and fragmentation and joint subluxation, dislocation and destruction. Stage II -The Stage of Coalescence, Periosteal new bone formation is apparent along with reduction of swelling. Stage III - The stage of Reconstruction Bony consolidiation takes place and healing occurs
12 PROGRESSION OF CHARCOT
13 SANDERS-FRYKBERG ANATOMICAL CLASSIFICATION
14 EICHENHOLTZ CLASSIFICATION
15 Medical imaging has advanced very much computed tomography (CT) and magnetic resonance imaging (MRI) scans exceed plain X- ray by far in detecting foot fractures and other injuries. The earliest, non deforming, X-ray-negative inflammatory stage of the acute Charcot joint of the diabetic foot can be visualised only by use of MRI.
16 DIAGNOSIS HISTORY CLINICAL FINDING IMAGING Trauma History Fever Clinical Finding Imaging Past medical history 10+years with DM type 11 30% bilateral involvement Appearance of limb/foot Swelling Erythema Deformity ulcers Neurological exam Neuropathy Strength/ROM
17 HISTORY a patient with long-standing diabetes a history of poor glycemic a red, hot, swollen foot with no history of open ulceration peripheral neuropathy
18 CLINICAL FINDING Neurological abnormalities Musculoskeletal abnormalities Vascular abnormalities
19 IMAGING Radiographs Computed Tomography (CT) Magnetic Resonance Imaging (MRI) Scintigraphy Positron emission tomography (PET)
20 PLAIN X RAY The X ray of forefoot can show demineralization, bone destruction and periosteal reaction. Severe changes can develop in this form of Charcot foot with pencil and cup deformity at the metatarsophalangeal joints or fragmentation of the metatarsal heads. In the midfoot, dislocation or fracture develops after initial joint swelling and ligamentous laxity
21 COMPUTERIZED TOMOGRAPHY (CT) Computerized tomography scanning can detect the presence of sequestra, cortical destruction, periosteal reaction and intraosseous gas which might not be detected on MR imaging
22 MAGNETIC RESONANCE IMAGING MRI Magnetic resonance is superior for soft tissue imaging Gives exquisite anatomical detail Magnetic resonance scan of foot is extremely sensitive
23 RADIONUCLIDE (ISOTOPE) IMAGING Radionuclide imaging can be a useful investigative tool in some instances. The three phase bone scan using technetium (TC- MDP) will be positive in all three phases and merely reflects the increased turnover of bone in Charcot foot. It is very sensitive but not very specific
24 DIAGNOSIS ALGORYTHM
25 DIFFERENTIAL DIAGNOSIS Osteomyelitis Acute gout Cellulitis Abscess Neuropathic fracture Deep venous thrombosis
26 TREATMENT Goals of treatment Avoid osseous prominences (which can lead to ulceration) To restore foot stability 2 Phase acute phase post acute phase
27 ACUTE TREATMENT PHASE ONSET UNTIL CHARCOT IS INACTIVE, 3-6 MONTHS AFTER ONSET IMMOBILIZATION TO PREVENT FURTHER DESTRUCTION OFFLOADING the foot most important to prevent deformity progression treating bone disease preventing further foot fractures.
28 POSTACUTE TREATMENT PHASE END OF ACUTE PHASE THROUGH 1-2 YEARS AFTER ONSET Following acute treatment phase, it is necessary to protect the foot throughout the remainder of the healing process. Protection methods include: Accommodative footwear with rigid soles and shanks Accommodative foot orthoses to protect insensate feet Orthopedic equipment (such as braces, inserts, or orthopedic shoes) may make it easier to walk.
29 CHARCOT TIME LINE
30 TREATMENT OPTION Non Operative Operative Immobilization Bisphosphonates Calcitonin Remove bone deformities and reduce disability Techniques Arthrodesis Exostectomies Reconstruction Achilles tendon lengthening
31 NON OPERATIVE The role of conservative management is to prevent further injury to the joint instigate a non-weight bearing regime as soon as possible elimination of movement at the joint either via a brace, plaster or total contact cast A non-weight bearing period of 3 months has been recommended
32 IMMOBILIZATION Immobilization usually is accomplished by casting Total contact casts have been shown to allow patients to ambulate while preventing the progression of deformity Cast is worn until the redness, swelling, and heat subside (8 to 12 weeks) Use of removable braces or a Charcot restraint orthotic walker (4 to 6 months of treatment)
33 CROW CHARCOT RESTRAINT ORTHOTIC WALKER For patients who have foot ulcers or insensate feet (can t feel). This is an orthosis that is clamshell in design and covers the entire foot and calf of the leg, resembling a ski boot The crow gives tremendous support by preventing foot and ankle movement. it is fully padded on the inside. A shoe is not worn with this orthosis.
34 A reconstructed foot in a Charcot restraint orthotic walker (CROW)
35 J Bone Joint Surg Am. 2008;90:754-9 doi: /jbjs.f Results: No deleterious effect from weight-bearing, specifically with regard to skin ulceration or rapid deterioration of the osseous architecture, was observed in thirty-three of the thirty-four feet. Conclusions: Immobilization in a weight-bearing total contact cast appears to be a safe method of treatment of acute Eichenholtz Stage-I Charcot arthropathy of the foot and ankle
36 BISPHOSPHONATES Synthetic analogues of inorganic pyrophosphate that decrease bone resorption by inhibiting the recruitment and activity of osteoclasts, while stimulating osteoblastic activity Shorten the lifespan of osteoclasts Provide pain relief through effects on prostaglandin E2
37 BISPHOSPHONATES CONTROVERSY Have not been approved by the US Food and Drug Administration for use in Charcot arthropathy patients In 1994, Selby et al. studied the effect of pamidronate on 6 patients with Charcot joint significant improvement Increase 25% ALP level
38 CALCITONIN Secreted by the C-cells of the thyroid, calcitonin directly affects osteoclasts In a recent study, 32 patients were randomized receive a combination of intranasal calcitonin (200IU/day) and calcium supplementation (100mg/day) calcium supplementation alone Calcitonin treated patients had significantly faster healing compared to controls
39 OPERATIVE TREATMENT For severe ankle and midfoot deformities that are susceptible to skin ulcerations In the acute stage I of the Charcot foot, surgery is almost totally contraindicated Techniques Arthrodesis Exostectomies Reconstruction
40 EXOSTECTOMY Indication Removal of bony prominences is perhaps most common the Rocker Bottom Foot, where patients develops a plantar midfoot prominence which is liable to recurrent breakdown
41 EXOSTECTOMY A midfoot plantar exostosis can be excised through an incision along the medial or lateral border of the foot. The soft tissues are stripped off the underlying bone and then either an oscillating saw or osteotome is used to remove the prominence and flatten the bony surface. Postoperatively, the wound is allowed to settle and weight bearing can then be commenced with or without a cast depending on whether any ulceration is still present
42 ARTHRODESIS For midfoot and hindfoot deformities that are unbraceable and causing recurrent ulceration This is a considerably more complex surgery that carries the risk of amputation if it is unsuccessful Once the destructive phase has radiologically ceased and bone reconstruction has started, then surgical intervention can be considered. Commonly achieved using an intramedullary nail
43 CONCLUSION Antibiotic-impregnated cement beads and spacer blocks have been used successfully in the treatment of open fractures, infected nonunions, and infected joint arthroplasty Treatment with the antibiotic-coated nail leads to local antibiotic delivery as well as stable internal fixation
44 TREATMENT ALGORYTHM
45 CHARCOT FOOT DIABETIC FOOT DISORDERS. THE JOURNAL OF FOOT & ANKLE SURGERY. VOLUME 45, NUMBER 5, SEPTEMBER/OCTOBER 2006
46 COMPLICATIONS The Rocker Bottom Foot overloading of the medial aspect of plantar prominent bones Inversion Deformity Excessive weight and pressure at the base of the fifth metatarsal and cuboid bones Pressure and chronic ulceration Osteomyelitis
47 CONCLUSION Early diagnosis is a key factor in the management of the Charcot foot and plays a central role in the prevention of severe deformity. If diagnosed early, medical and conservative measures will usually suffice in this regard. Surgery is most often reserved for those patients with severe or unstable deformities that are not amenable to long-term bracing or footwear therapy alone. A team approach is recommended to prevent patients with these high risk foot deformities from succumbing to limb loss
48 DIAGNOSIS DIABETIC FOOT DISORDERS. THE JOURNAL OF FOOT & ANKLE SURGERY. VOLUME 45, NUMBER 5, SEPTEMBER/OCTOBER 2006
49 THANK YOU
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