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Year : 1981 | Volume
: 27
| Issue : 3 | Page : 194-6 |
Charcot's elbow (a case report).
Bhaskaran RR, Suresh KK, Iyer GV
How to cite this article: Bhaskaran R R, Suresh K K, Iyer G V. Charcot's elbow (a case report). J Postgrad Med 1981;27:194 |
Neuropathic joint, although first described by Charcot in tabes dorsalis in 1868, has subsequently been observed in a variety of conditions including syringomyelia, diabetes mellitus and peripheral nerve disorders. There is a progressive disorganisation of architecture in the insensitive joint, leading to painless joint swellings with radiologic evidence of pronounced bone destruction as well as new bone formation in abnormal sites. This condition is apparently rare as evidenced by the paucity of reported cases in Indian literature. However, it must be pointed out that the diagnosis can be missed unless it is suspected.[1], [12] In this paper we are describing a patient who presented with neuropathic joint involving the right elbow.
A 30 year old female presented with diffuse swelling of the right upper limb and multiple painless ulcers of 8 years' duration. Painless swelling of the right elbow joint was noticed 3 years later which increased rapidly in size over 6 months. Specific enquiry revealed that she had weakness of grip on the right side, with loss of pain and temperature sensations of the right hand. She had no inolvement of the left upper limb, lower limbs or sphincters. She was not a diabetic, and gave no history of exposure to sexually transmited diseases. Examination disclosed diffuse swelling of the right upper limb with scars of old injuries. There were trophic ulcers behind the right shoulder joint, elbow, wrist and also over the right iliac crest. She had scoliosis with convexity to the right and winging of the right scapula. The right elbow joint was markedly swollen, 46 cm in circumference and painless on manipulation with abnormal mobility. All cranial nerves were normal. Her grip was weak and there was wasting of the small muscles of the right hand. The marked swelling of the right elbow precluded proper elicitation of reflexes in the right upper limb. Sensory system showed loss of pain and temperature from C2-L2 segmental level on the right, with preservation of touch. Vibration and position senses were impaired over the right upper limb. Other reflexes were normal. A clinical diagnosis of neuropathic joint involving the right elbow was made, the probable etiology being an intramedullary lesion most likely syringomyelia. Investigations revealed that routine urine examination and blood counts were normal. Fasting blood sugar was 98 mg%, blood VDRL was non reactive and the X-ray chest normal. X-ray cervical spine showed increase in interpedicular distance. Patient was unwilling for myelogram. X-ray of the right elbow joint showed marked destruction of articular surfaces with dislocation of the bone ends, periosteal thickening and new bone formation within the joint cavity. Aspiration of the elbow joint with wide-bore needle yielded a thick pultaceous material. [Fig. 1] Neuropathic joints are known to occur in a variety of conditions, which are summarised in [Table 1]. A study by Johnson[8] involving 118 cases of neuropathic joints revealed the following causes: 88 cases were tabetic, 10 were associated with diabetes, 10 with syringomyelia, 4 with a spinal lesion (congenital or traumatic), 3 with peripheral nerve injuries and 2 with undiagnosed neurological disease; one case was associated with congenital absence of pain. In patients with syringomyelia, such changes occur in about 25% of cases as compared to 4-10% in tabes dorsalis. The site of involvement varies depending upon the cause. The knee, ankle and foot are most often affected in tabes whereas the upper limbs in syringomyelia. Among the various joints the shoulder was maximally affected in Barnett's series,[2] the elbow being the next common. In our patient, the elbow was predominantly affected. The reason for the predilection of elbow in this patient is not clear. The pathogenesis of neuropathic joints has been the subject of discussion by several authors.[1], [3], [6], [9], [14] The basic factor seems to be lack of appropriate sensory input from the joint. Abolition of proprioceptive and/or sensory impulses from the joint leads to it being exposed to unusual trauma for a prolonged time. Repetitive trauma leads to fibrillation and fragmentation of the joint cartilage resulting in the so-called loose bodies. The joint capsule is often stretched beyond tolerance both by the hemarthrosis and by the stresses on the joint. In addition, there is hyperemic bone resorption and softening and the resultant atrophic bone is easily traumatized. The result is a vicious circle which may go on until the joint is totally destroyed. The principle in the management of neuropathic joint consists of minimising the trauma to which the unstable and insensitive joint is exposed, by efficient bracing, weight relieving calipers or leather corset. Attempts should be made to minimise the deformity and retain maximal functional utility of the joint. Large effusions may be aspirated and in rare cases arthrodesis may be necessary, although the results are often disappointing.
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2. | Barnett, H. J. M., Foster, J. B. and Hudgson, P.: "Syringomyelia". 1st Ed., W. B. Saunders Company, London, Philadelphia, and Toronto, 1973, pp. 11, 12, 29, 158, 167, 168. |
3. | Basu, S. P.: Bone changes in leprosy. Ind. J. Radiol., 26: 239-249, 1972. |
4. | Chandler, G. N., Jones, D. T., Wright, V. and Hartfall, S. J.: Charcot's arthropathy following intra-articular hydrocortisone. Brit. Med. J., 1: 952-953, 1959. |
5. | Daughady, W. H.: Extreme gigantism. Analysis of growth velocity and occurrence of severe peripheral neuropathy and neuropathic anthropathy (Charcot's joints). New Eng. J. Med., 297: 12671269, 1977. |
6. | Eloesser, L.: Fractures Calif. State J. Med., 15: 259, 1917. |
7. | Fitzgerald, J. A. W.: Neuropathic arthropathy secondary to atypical congenital indifference to pain. Proc. Roy. Soc. Med., 61: 663-664, 1968. |
8. | Johnson, J. T. H.: Neuropathic fractures and joint injuries. J. Bone & Joint. Surg., 49A: 1-30, 1967. |
9. | Key, J. A.: Clinical observations ;on tabetic arthropathies (Charcot's joints). Amer. J. Syph., 16: 429-446, 1932. |
10. | Peitzman, S. J., Miller, J. L., Ortega, L., Schemacher H. R. and Fernandez, P. C.: Charcot's arthropathy secondary to amyloid neuropathy. J. Amer. Med. Assoc., 235: 1345-1347, 1976. |
11. | Segovia, A. and Ward, L. E.: Charcot like arthropathy in rheumatoid arthritis. J. Amer. Med. Assoc., 193: 1052-1054,1965. |
12. | Singh, M. J. and Gupta, S.: An atypical case of Charcot's knee joint. had. J. Surg., 36, 81-82, 1974. |
13. | Steinberg, C. L., Duthie, R. B. and Piva, A. E.: Charcot's arthropathy following intra-articular hydrocortisone. J. Amer. Med. Assoc., 181: 851-854, 1962. |
14. | Stendler, A.: Tabetic arthropathies. J. Amer. Med. Assoc., 29: 250-256, 1931. |
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