971 MEDIAN-NERVE PALSY AND ACUTE INFECTIONS OF THE HAND
SIR,—May I add a similar case to those described by Bailey and Mr. Bolton Carter in your issue of March 12It is one of 42 cases of carpal-tunnel syndrome treated during the last four years, upon which a report is now being prepared. A butcher, aged 49, was seen on July 7, 1953, with a pulp Mr.
right thumb which had been drained two days previously. He had had systemic penicillin for one day before incision and for the next two days, and this was continued. He had much pain in the hand and wrist, aggravated by extension of the fingers, which were held in the position of rest. Movement of the middle and ring fingers was greatly restricted, the index and little fingers less so. infection of the
The thumb could be moved more freely but this caused some pain. Pain at rest was in the median-nerve distribution and was severe enough to keep him awake. There was tenderness on the palmar aspect of the hand over the carpus and wrist-joint, with diminution of sensation of light touch but not pin-prick over the median-nerve distribution in the hand. The dorsum of the hand was considerably swollen. For the previous eighteen months he had had pain in the right hand with acroparæsthesiæ in the distribution of the median nerve every Friday night, which had repeatedly woken him. On Saturday mornings the hand was stiff and numb with limited finger movement and some residual, though lessening, pain ; this subsided completely by midday on Saturday, not to recur until the following Friday night. These symptoms had become progressively worse until he had lately been having pain on occasional nights during the week, sufficient to awaken him. (Butchers are busy in South Australia on Fridays, because they have to prepare large orders for the weekend for a population that eats a lot of meat; and they do not open on Saturdays.) In spite of continued penicillin and rest in a plaster backslab with elevation, the hand grew steadily worse, the fingers more immobile, and their movement more painful, until finally he could have no finger moved passively into extension without great pain. Sensation loss by July 11 was complete over the medianto light touch and much impaired to Tenderness at the wrist was much nerve distribution. increased. Decompression of the median nerve was therefore done on July 12 by longitudinal incision through a convenient palmar crease. The flexor retinaculum was divided fully. The nerve was found to be swollen and reddened in the proximal half of the carpal tunnel and relatively narrowed and dark red in its distal half. A little serous fluid was present but there was no abnormality of the tendons... The skin was loosely sutured, and it healed well. Convalescence was slow but satisfactory. He was back at work in four weeks, although sensory loss and strength of the hand did not recover fully for four months. On April 18, 1955, he said that he has had no trouble since, the hand has remained normal, and his working capacity is unimpaired. The scar is supple, pain-free, and hardly visible.
pin-prick
I feel little doubt that the infection caused an inflammatory swelling in the carpal tunnel which converted a periodic occupational carpal-tunnel syndrome into a relative emergency. I think it probable that Mr. Bailey and Mr. Bolton Carter’s cases fall into the same category. "
In case 1 there was a history of rheumatism " in the hands which may well have been a carpal-tunnel syndrome, and they mention osteo-arthritis in the left hand, which in the carpus may be a factor in the production of the syndrome. In case 2 there is no mention of previous history, but it is just possible that inquiry might reveal that the patient had previous symptoms of median-nerve compression. Both of these patients fall into the age and sex group most commonly affected by carpal-tunnelsyndrome-i.e., women at or about the time of the menopause. Case 1 had been having symptoms for years, and these probably first arose at the time of the menopause. In both of these cases the early and marked loss of sensation
particularly interesting. As well as the butcher, I have it in one other patient-a man with a severe carpal injury and projection of part of a fractured lunate into the carpal tunnel. His flexor retinaculum was divided and the projecting bone removed three weeks after the original
was
seen
but by that time he had complete anaesthesia over the median-nerve distribution in the hand, which took six months There was acute tenderness over the median to recover. nerve at the wrist, but apart from some loss of finger movement by mechanical interference, there was little motor
injury,
impairment. The restriction of finger movement in all these cases must be due to mechanical interference in the carpal tunnel by compression of the tendons. The dominance of sensory loss seems to be a feature of the more acute lesions ; in the usual and much less acute carpal-tunnel syndrome, wasting of the thenar eminence and weakness usually come before definite Such patients, however, often complain of sensory loss. numbness at the finger-tips, especially in the early morning, which interferes with knitting and sewing.
I agree with Mr. Bailey and Mr. Bolton Carter that the compression in their cases was the result of inflammatory exudate and consequent ischæmia of the median nerve, but I think that there was a pre-existing lesion which narrowed the carpal tunnel, predisposing to the nerve compression. This may in some cases be a stenosis comparable to De Quervain’s disease or some other factor, possibly hormonal; but whatever the predisposing factor, the median nerve lies in the carpal tunnel in a particularly vulnerable -position. In none of my cases has any disability resulted from division of the flexor retinaculum. This is not surprising in view of the fact that all strong movements of the human hand occur The flexor retinaculum with the wrist in extension. in man seems to be a useless structure. I was interested to read that Mr. Bailey and Mr. Bolton Carter required a longitudinal palmar incision to be sure of adequate exposure and division of the flexor retinaculum. I have tried the transverse wrist incision, found it inadequate, and reverted to the longitudinal. There are objections to this incision, but in practice they all heal rapidly and well with no disability, especially if carefully made in a crease. As soon as the diagnosis of median neuritis from compression has been established I make it a rule to divide the flexor retinaculum as soon as possible, to avoid the chance of irreversible damage to the nerve. The only exception to this rule is in menopausal women with mild symptoms, which may sometimes be completely relieved by aestrogens. But should there be no improvement within a short time, the rule still applies. Royal Adelaide Hospital, Adelaide, South Australia.
J. D. SIDEY.
IRON-DEFICIENCY ANÆMIA IN PREGNANCY
SiR.,-The question of iron therapy in pregnancy is
a
and articles such as that by Dr. Gatenby topical and Dr. Lillie in your issue of April 9 are very helpful in dealing with the practical aspects of this subject. May I make one or two comments on points made by them ?It is true that there is a high incidence of intolerance to the ordinary ferrous-sulphate tablets, but I have hardly ever found intolerance to enteric-coated ferroussulphate tablets, so it is to this form of therapy I turn when the former fails. The enteric-coated tablet costs only about double the ordinary variety. Ferrous gluconate, however, I am told costs about ten times as much as the simple ferrous.sulphate tablet. This may be worth considering. It is true that some might argue that there is a danger of the enteric-coated tablet passing through the gut undissolved, especially as the ordinary tablet passes a long way (as demonstrated radiologically). However, the clinical response appears to be adequate, so I am not unduly disturbed by this. Another point is in connection with parenteral forms of iron therapy, so widely used now. Why should an anaemia discovered late in pregnancy be an indication? All the evidence I have seen shows that the response to oral iron should be as quick as to parenteral iron.1 A one
1.
Jennison, R. F., Ellis, H. Lancet, 1954, ii, 1245.