Shafqat Ullah Memon  ( Department of Medicine, Jinnah Postgraduate Medical Centre, Karachi. )
S.M. Rab  ( Department of Medicine, Jinnah Postgraduate Medical Centre, Karachi. )

Neuro-osteoarthropathy (Charcot’s Joint) in diabetic patients has been well described in literaturc^1-9. It has been defined as a chronic progressive degenerative process principally occurring in weight-bearing joints in the feet of diabetic patients who have underlying peripheral neuropathy and loss of sensation^6,9,10. Al­though considered as a clinical rarity^3,6, it has been reported more frequently in recent years^7-9,11,127-9,11,12. This observation can be attributed to the longevity of diabetic patients and dramatic decrease in mortality since the insulin era⁷.
The association between juvenile onset diabetes and skeletal lesions is relatively uncommon^12,13. We report a case of young woman who had juvenile onset diabetes and developed bilateral neuro-arthropathy in­volving feet.

A 23 year old female, known diabetic for 8 years and on insulin therapy was admitted in January, 1990 with uncontrolled diabetes and severe hypertension. She complained of swelling of both feet for the past 2 years but denied having sustained any trauma to them. Clinical examination revealed a blood pressure of 210/130 mm Hg and fundal changes consistent with diabetes and hypertension. Both feet appeared swollen with slight tenderness. Neurological examination revealed decrea­sed sensation to pinprick and bilaterally impaired sensa­tion of position and vibration. Her ankle and knee jerks were absent on both sides. Pulses were palpable in both femoral and popliteal arteries. Dorsalis pedis and post­tibial appeared normal. Investigations revealed an elevated blood urea (114 mg %) and creatininc (2.6 mg %). Radiographs of feet showed slight flattening of calcaneus and a crack in the bony bridge between calcaneus and navicular bone on the left side, while on
the right side there was beginning of disorganization of the subtalar joint with loss of depth of the body of talus. (Figures 1,2).



Her diabetes was controlled on insulin and blood pressure reduced and maintained on medication. For her feet she was instructed complete bed rest, non-weight bearing and special protective shoes. She was discharged after control of her blood pressure and was advised periodic follow-up but she did not report back and died 3 months later of renal failure.

Since Charcot’s initial report of neuropathic joints in association with tabes^{1,4,8,10,12,14}. a multitude of under­lying causes have been ascribed to the development of this lesion, the predominant being syringomvelia, leprosy, spina bifida, cord trauma, multiple sclerosis and spinal dysraphism^{1,2,4,7-9,15-16} Diabetes mellitus, however, remains the commonest causeS, 16 and its associated bone and joint abnormalities are nowwell recognized^{2,3,5,7,10,12,13}
The reported incidence varies between 0. 1 to 6.8%^5,8,18-20. Majority of the cases are of adult onset diabetes often non- insulin dependent^13,14,16 lesions occurring over the age of fifty^5,6,13,14,16 after the Patient has had diabetes for an average of 1 3to 15 years 6,13 The blood sugar levels are often poorly controlled 5,68 although osteopathy may even precede overt diabetes⁵. While the high risk group constitutes those with charac­teristic triopathy^6,12, the diabetics with renal transplants are at greatest risk^12,21. More recently an association between joint lesions and pulmonary changes in diabetics has been described^22-24. Therefore, patients with impaired respiratory funct ion can constitute another high risk group.
Typical neuropathic joints in diabetics can be seen in any pari^16,25-27 hut the foot remains the area most frequently involved¹⁴ The sites most often affected are the tarsometatarsal joints (60%) and to a lesser extent the joints of metatarso-phalangeal area (30%) and ankle (10%)^6,9,18. A clear distinction has been made between proximal foot destruction and distal foot erosion^7,10. On roentgenogram two forms exist - ATROPIIIC and HYPER­TROPHIC, the latter being described as osteophytic fragmentation,joint space narrowing, capsular disten­tion and lipping that predominantly affects the lower extremities. The atrophic form commonly affects the upper extremities and the only change is resorption of bone ends^1,2,6,9,16.. Transition from one form to the other does not occur^6,16. Extensive periartieular calcification is characteristic^28,29 occasionally bone shards may be seen far from the joint suggesting their denovo origin from the joint capsule²⁹.
The pathophysiology of Charcot’s joint remains controversial, In attempts to elucidate pathogenesis various mechanisms were described pertaining to trophic disturbances, trauma^1,5,6,8 autonomic impair­ment³⁰, infection³¹, isehaemia³², bone atroph³³, OS teoporosis^5,6, small vessel disease³⁴, and to an error of protein metabolism³. However no explanation was based on conclusive evidence that focussed on any single process. Current concepts suggest that osteolysis and bone resorption play a major role in the development of Charcot’s joints^33-36. and for this an adequate blood supply is a prerequisite^37,38. The clinical finding of bounding pulses^39-41 and the development of Charcot’s joint in ischaemic limbs following revascularization surgery⁹ strongly support this hypothesis. Edelman et al9 have suggested that while peripheral neuropathy is the initial primary defect, a neurally initiated vascular reflex leading to increased blood flow may play a pivotal role in the development of Chareot’s joint. Mechanical trauma in an insensitive foot is contrihutary but a secondary mechanism⁹,
Whatever the mechanism, a marked disproportion between the radiologic severity of the disease process and the relatively slight complaint of discomfort is thc most consistent clinical feature. Often there is no history of trauma and, when inflicted, may be trivial. This explains why the lesions remain unreeognised for long and the changcs are far advanced when first presented¹⁸.
Our patient clinically had a classical Charcot’s joint. She had severe clinical manifestations of diabetes and represented the high risk group The lesion developed without known or obvious trauma and at the time of presentation her blood sugar levels were poorly control­led. Nevertheless the case is unusual in several aspects. The patient was rather young and had juvenile onset insulin dependent diabetes which is relatively uncom­mon in patients developing neuropathic joints. Moreover, the lesion appeared rather early. Harris & Brand¹⁰, observed five patterns of disintegration in the anaesthetic foot and our case resembled type TI thcy described as central destruction which is infrequently encountered, as it is not common for talus to be the primary focus of disintegration. The pathogenctic factors in our ease remain speculative. Where- as the destruction of talus seems to he entirely due to mechanical stress¹⁰, the presence of unimpaired peripheral circulation favours the hypothesis of osteolysis and bone resorp­tion⁹. Probably both these factors in a neuropathie limb favour the development of Chareot’s joint.
Diabetic neuro- osteoarthropathy has a charac­teristic intermittent course of activity⁵. Trauma unques­uonably causes deterioration^5,6. Current treatment protocol,therefore, includes non- weight-bearing and immobilization of the involved extremity and prophylac­tic immobilization of contralateral extremity. Control of blood sugar levels is desirable and serial, roentgenograms are advised to monitor progress^6,8,9,11,12. In absence of marked bony deformities the long term prognosis is generally favourable⁶.

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