NERVE INJURY FOLLOWING STEROID INJECTION FOR CARPAL TUNNEL SYNDROME A report of two cases S. P. TAVARES and G. E. B. GIDDINS
From the Nuffield Department of Orthopaedic Surgery, Oxford and the Royal National Orthopaedic Hospital, Stanmore, Middlesex, UK Two cases of nerve injury are reported following steroid injection as treatment for carpal tunnel syndrome. One caused an ulnar nerve lesion that recovered well. The other caused a more severe median nerve lesion which responded poorly to conservative treatment. Steroid injection for carpal tunnel syndrome is generally safe but nerve injury may occur and is difficult to treat.
Journal of Hand Surgery (British and European Volume, 1996) 2lB." 2:208-209 Steroid injection for carpal tunnel syndrome was first reported by Kopell (1958). it was popularized by Phalen (1966) and was considered almost harmless (Phalen, 1966; McGrath, 1984). There have recently been reports of median nerve injury caused by steroid injection for carpal tunnel syndrome (McConnell and Bush, 1990; Linskey and Segal, 1990). Injury to the ulnar nerve at the wrist has not previously been reported following attempted carpal tunnel injection. We report two cases of nerve injury following steroid injection for treatment of carpal tunnel syndrome.
Functionally, however, she had some continuing impairment of the intricate finger movements necessary for playing the 'cello. Case 2
A 62-year-old, right-handed, male manual worker presented to his general practitioner with nocturnal paraesthesiae in the median nerve distribution. He had an injection of Depo-Medrone (Methylprednisolone acetate) into the region of the carpal canal. After 3 days his hand started to swell and the symptoms of carpal tunnel syndrome increased; he presented to the hospital after 7 days. His hand was uncomfortable at rest and he had paraesthesiae in the distribution of the median nerve. It was so swollen that he was unable to flex his fingers more than 30% of normal. His sensation was normal to testing. He was apyrexial and his FBC showed a WBC of 11.4, and ESR of 29 and otherwise normal indices with negative blood cultures. The differential diagnosis was of infection or possibly a chemical reaction to the injection. His hand was elevated and he was given intravenous flucloxacillin and penicillin. His hand rapidly became less swollen and less painful, and the paraesthesiae settled. After 8 days his hand was sufficiently improved with 75% hand function to allow discharge from hospital. Neurophysiological testing at 6 months revealed sensory latencies of 2.9 ms at onset, and 3.5 ms at peak, in the median nerve recorded at the wrist from ring electrodes on the index finger. These were comparable with the ulnar nerve indices of 2.8 and 3.3 ms respectively, recorded from the little finger. The motor latency at the wrist was 4.4 ms. These results were interpreted as being within normal limits. Nine months later, he still had some stiffness in the hand and discomfort and occasional paraesthesiae in the distribution of the median nerve. Thereafter he was lost to follow-up.
CASE R E P O R T S Case 1
A 55-year-old, right-handed, semi-professional female cellist presented to her general practitioner with paraesthesiae in the ulnar nerve distribution of the left hand, after kneading dough. This was interpreted as carpal tunnel syndrome and hydrocortisone was injected into the region of the carpal tunnel. This caused marked pain for 3 days in the distribution of the ulnar and median nerves. Thereafter, she rapidly developed marked wasting of the first dorsal interosseous muscle and reduced abduction and adduction strength of the fingers, noticed particularly whilst playing the 'cello. On presentation 3 months later, she no longer had paraesthesiae, or sensory loss in the median or ulnar nerve distribution, but there was gross wasting of her interossei (especially the first dorsal interosseous) and mild wasting of the hypothenar eminence. Froment's sign was positive. There was no evidence of carpal tunnel syndrome. Neurophysiological studies were performed. These confirmed normal median nerve conduction and evidence of a left ulnar nerve lesion with no focal slowing or block. There was no evidence of a compressive lesion in Guyon's canal. Needle examination showed changes of reinnervation in the left first dorsal interosseous muscle. At follow-up 6 months later she had full return of muscle bulk and normal function on clinical testing.
DISCUSSION In the first case it would appear that the injection was too ulnarwards and caused a chemical injury, primarily 208
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to the motor branch of the ulnar nerve. This may in part have been due to the preexisting ulnar nerve injury which was probably a post-traumatic neurapraxia. This probably caused axonal degeneration but fortunately there was subsequent axonal resprouting and recovery. In the second case the patient appears to have suffered a chemical reaction to the steroid injection, as in the cases reported by McConnell and Bush (1990), and Linskey and Segal (1990). The patient might have benefited from an acute carpal tunnel release. Steroid injections for carpal tunnel syndrome have proponents (Richmond, 1 9 5 8 ) and opponents (McGrath, 1984). The injections seem to provide only temporary relief in the majority of cases, but they can provide some further diagnostic evidence. Nonetheless, they are not without hazard as shown by these cases. The frequency of complications is not known but is probably uncommon with very few cases reported in the world literature. Given the serious risks and limited therapeutic value, they should perhaps be reserved for patients in whom temporary relief may be all that is necessary, as in pregnancy and where temporary relief may be of value and the diagnostic help will also be useful. Physicians giving these injections should be fully conversant with the techniques and landmarks and patients should be warned of the possibility of an acute inflammatory reaction following a steroid in injection
for carpal tunnel syndrome. If this occurs and there are signs and symptoms of acute median nerve compression, then acute carpal tunnel release should be considered, as recommended by Linskey and Segal (1990), and McConnell and Bush (1990), because expectant treatment, as in case 2, may not lead to a complete recovery. Even early decompression, as in McConnell and Bush's case 3, may also not lead to complete recovery (McConnell and Bush, 1990).
Acknowledgements We thank Mr J. Angel and Mr R. Birch for allowing us to report their cases.
References KOPELL H P (1958). Carpal tunnel compression median neuropathy treated non surgically. New York State Journal of Medicine, 58: 744-745. LINSKEY M E and SEGAL R (1990). Median nerve injury from local steroid in carpal tunnel syndrome. Neurosurgery, 26: 512-515. M c C O N N E L L J R and BUSH D C (1990). Intraneural steroid injection as a complication in the management of carpal tunnel syndrome: a report of three cases. Clinical Orthopedics and Related Research, 250: 181-184. M c G R A T H M H (1984). Local steroid therapy in the hand. Journal of H a n d Surgery, 9A: 915-921. PHALEN G S (1966). The carpal-tunnel syndrome: 17 years' experience in diagnosis and treatment of 654 hands. Journal of Bone and Joint Surgery, 48A: 211-228. R I C H M O N D D A (1958). Carpal tunnel syndrome (letter). British Medical Journal, 1: 773-774.
Accepted: 15 June t995 O. E. B. Giddins, Orthopaedic Department, Royal United Hospital. Combe Park, Bath, BA1 3NG, UK. © 1996The British Society for Surgery of the Hand