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Dr. Saima Hashim Khan Dept. of Diabetes & Endocrinology HMC. PGMI

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1 Dr. Saima Hashim Khan Dept. of Diabetes & Endocrinology HMC. PGMI
Charcot Arthropathy. Dr. Saima Hashim Khan Dept. of Diabetes & Endocrinology HMC. PGMI

2 Case History : 1 55yrs old married female Type2 diabetic 25yrs
HTN 7yrs Swelling right foot >1month, treated as cellulitus with antibiotics


4 INVESTIGATION Hb 10.8g/dl, TLC 9900/cmm S.creatinine 0.7mg/dl
S.uric acid 4.0mg/dl X ray foot.


6 MRI Foot


8 Case History : 2 45yrs old married female
DM2 15yrs (Retinopathy: PRP, Nephropathy: crt clr 103 ) HTN 5yrs Post amputation RT big toe 3yrs Swelling LT foot 2 months, treated as cellulitis with antibiotics


10 Investigations Hb:9.5 gm/dl, TLC 9600/cmm URIC ACID 4.2mg/dl
CREATININE 1.02mg/dl DOPPLER U/S LT FOOT : no DVT normal arterial flow and subcutaneous edema. Xray Foot:

11 X Ray Foot



14 Tragic “Rule of 15” 15% of diabetes Foot ulcer in lifetime of patients
15% of foot ulcers Osteomyelitis 15% of foot ulcers Amputation Clinical Care of the Diabetic Foot, 2005 Foot ulcers precipitate about 85% of diabetic amputations. Key epidemiologic points about diabetic foot ulcer can be summarized by the “Rule of 15”: 15% of diabetes patients will experience a foot ulcer during their lifetime. 15% of these foot ulcers will progress to osteomyelitis. Even with optimal multidisciplinary care, 15% of diabetic foot ulcers will result in a lower extremity amputation at some level.

15 Tragic “Rule of 50” 50% of amputations 50% of patients
Transfemoral/ transtibial level 2nd amputation in  5 years Die in  5 years However, more important than expense, amputations have tragic consequences for the individual that can be summarized by the “Rule of 50”: 50% of diabetic amputations occur at the very disabling transfemoral or transtibial levels. 50% of these patients will require a second amputation within just 5 years. 50% of these patients will die within 5 years, most from concurrent coronary artery disease or cerebrovascular disease. Clinical Care of the Diabetic Foot, 2005

16 History of charcot foot
Mitchell,1831: The first association between joints and neurological diseases. Charcot 1868: Arthropathy and tabes dorsalis. Jordan 1936: Neuritic manifestation of DM

17 Charcot’s Foot A Neuropathic Arthropathy
Caused by repetitive trauma in the setting of: Diminished sensation & proprioception Motor neuropathy results in muscle imbalance & abnormal weight bearing. “Rocker Bottom Deformity” a convex deformity of the foot’s plantar aspect caused by the collapse of metatarsal bones WHEN YOUR FEET THEY START TO CRUMBLE TO YOUR DOCTOR YOU SHOULD FUMBLE



20 Etiology Peripheral sensory neuropathy is always present +/- motor.
Autonomic neuropathy leads to increased blood flow. Trauma may be an important precipitating factor, although 2/3rd of patients don’t remember any injury. Bone metabolism both osteoblastic and osteoclastic activities are increased.


22 Epidemiology Incidence : 0.1 – 0.5 % . General:
Increased in patients with neuropathy. Diabetics: 3-5% Common in the 4th or 5th decades of life. Bilateral in 30 % of patients. Sex difference : No Type 1 or type 2: Both are at risk. Majority: in the mid foot but any bone or joint in the foot or ankle can be affected.

23 Clinical Features and Diagnosis
Acute Charcot Warm, inflamed and swollen. Misdiagnosed as cellulitis, osteomyelitis or inflammatory arthropathy as gouty or septic. Although sensory neuropathy, pain is common feature followed by discomfort. Diagnosis by exclusion as investigations in early stages are negative.

24 Clinical Features and Diagnosis
High index of suspicion is necessary so that appropriate treatment is immediately instituted to prevent severe deformity!

25 Clinical Features and Diagnosis
Chronic Charcot, may be months, painless, without temperature difference and deformed. Reactivation by further trauma is frequent. Patients are at high risk of ulceration and amputation, so long term follow up is recommended.

26 Investigations X-ray : Early; absent or subtle finding.
Late; bone and joint destruction, fragmentation. bone scan: Increased bone uptake. In labeled leucocytes scan to differentiate from osteomyelitis. MRI: Bone marrow edema is the earliest sign.

27 Treatment Immobilization Pharmacological Treatment.
Surgical Treatment.

28 Treatment Immobilization:
Almost 16 weeks (3-6 months) but may be more. (temp gradient less than 1 on 2 occasions or serial radiology).

29 Treatment Immobilization: Bed rest Half-shoes
Crutches, Walkers and Wheelchairs Total contact cast (TCC) -gold standard Prefabricated pneumatic walking brace ( Air cast )

30 Total contact cast

31 Air cast

32 Half shoe

33 Modified/custom shoes/orthoses

34 Treatment 3. Pharmacological Treatment.
Pilot study first using pamidronate,1994. Other Bisphosphonates were used to decrease disease activity and bone turnover markers. Calcitonin were also used. Given for 12 weeks or till temp gradient is less than 2 on 2 consecutive visits.

35 Treatment Surgical treatment: No role in acute.
Later may be to remove bony deformities or constructive surgeries to achieve a stable shape. Techniques include; Arthrodesis, exostectomies, reconstruction and Achilles tendon lengthening.




39 Take Home Message High degree of suspicion to diagnose acute Charcot arthropathy. High risk categorization. Immobilization Bisphosphonate. Customized Foot Wear

40 Thank You

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