1125 been gathered from a vast area over some 13 years. Two distinct clinical syndromes were discernible, presumably reflecting different portals of entry. Secondary infection of superficial wounds or lacerations of the skin occurred in 15 instances; and so-called primary septicaemia in 24 persons, 13 of whom died. In the primary-septicxmia group, the illness began abruptly with chills, fever, and then collapse, without any apparent foci of initial infection. The L+ vibrio in question was isolated by blood-culture from 20 of the 24 patients. In many instances, ecchymoses, bullous eruptions, or necrotic ulcers of the skin subsequently developed, sometimes with other signs of blood-borne spread. Despite intensive treatment, including antibiotics such as penicillin, gentamicin, chloramphenicol, and tetracycline, 13 of these patients died. It is noteworthy that all but 1 of the 24 patients either had serious underlying disease, especially of the liver, or were alcoholics. In contrast, all but one of the wound infections were in healthy people. Most of the cases, whether septicxmic or septic, arose in summer, and the usual victim was an elderly or middle-aged man. A somewhat tenuous hypothesis is advanced for oysters, consumed raw, as a likely source of infection in the patients with primary septicaemia, though gastrointestinal upset was uncommon. The natural habitat of L+ vibrios, by analogy with V. parahæmolyticus and V. alginolyticus, is presumed to be the sea, but the actual incidence and distribution are unknown. Although the American workers were unable to calculate the risks to those eating seafoods raw, they state that "patients with hepatic disease appear to be more susceptible than healthy persons to infection with the L+ vibrio by the oral route". As to the wound infections, they usually developed a day or two after a crab bite or exposure to sea-water; of the 15 patients, 1 with leukaemia died. There seems no way of preventing these infections; but it does seem that some cases of "primary septicxmia" might be avoided if people with liver disease ate their seafood well-cooked or not at all.
ORAL IRON PREPARATIONS—DO WE NEED THEM ALL? are over forty oral iron preparations available prescription in the United Kingdom, varying from simple salts to complex formulations. Many owe their continuing success to the wide and erroneous belief that elaborate formulations are less apt to cause gastrointestinal troubles. The side-effects are, in fact, much more dependent on the dose than on the nature of the preparation, and can be greatly reduced by prescription of lower doses2 and by getting the patient to take the medi-
THERE
on
cine after food. Some iron intolerance also seems to have a psych6logical basis;3 so if the patient expects gastrointestinal symptoms from iron, a word of explanation and reassurance from the doctor and dispensing pharmacist can be of great preventive value. Iron-deficiency anaemia is common and there is a temptation to correct it with large doses over a short 1. Drug Therapeut. Bull 1979, 17, 33. 2. Crosby, W H. Archs intern. Med. 1978, 138, 616. 3. Kerr, D. N. S , Davidson, L. S. P. Lancet, 1958, ii, 489. 4. British National Formulary 1976-1978; p 157.
period. But, adverse effects apart, replacement of body stores in an iron-deficient patient takes at least three months’ oral treatment of at least 100 mg elemental iron a day after the haemoglobin deficit has been corrected,4 and in most patients this can be achieved with twice daily doses of ferrous sulphate 200 mg (60 mg Fe) or ferrous fumarate taken after food. No advantage is offered by preparations that contain trace amounts of other metals such as copper or manganese. Furthermore, most of the liquid and slow-release iron preparations are 2-10 times more expensive with little, if any, evidence of
superiority.1
SURGICAL TREATMENT OF CARPAL-TUNNEL SYNDROME Sir James Paget described the symptoms of carpaltunnel compression in 1854, but it was nearly a century before Sir James Learmonth did the first successful surgical operation to decompress the median nerve at the wrist. Nowadays this is one of the commonest operations on the hand, but the result is not always perfect: from 1.2% to 25%6,7 of patients have residual symptoms of mild persistent numbness and continuing weakness in the thumb. Precise diagnosis and careful operative technique are essential for surgical relief of the pain and paræsthesiæ, which can be very unpleasant. Harris and others8 survey the factors related to a successful outcome. In all their 124 cases the diagnosis was confirmed by nerve-conduction studies. Patients with motor-nerve delay had a more favourable result than those with only sensory abnormalities. The preoperative duration of symptoms did not influence the surgical result. Classic symptoms were sometimes present with normal nerve conduction times, and this is particularly true in the patient with rheumatoid arthritis. Age did not affect the outcome of operation. A common cause for surgical failure is incomplete division of the volar carpal ligament.9 This is most likely if the ligament is sectioned "blindly" through a small skin incision in the hope of producing a very small scar. The skin incision must be long enough to display the whole length of the ligament. Another factor predisposing to failure is tenosynovitis, either nonspecific or associated with joint disease in the carpus. Synovectomy should be done if adequate decompression cannot be obtained without removal of at least a portion of the synovium. The carpal tunnel should be inspected for possible occasional intrusions such as a ganglion, a lipoma, or a large bony spur from an adjacent osteoarthritic joint. Harris et al.8 recommended neurolysis of the median nerve when it is surrounded by thickened synovial tissue. The recurrent motor branch should be decompressed when it passes through instead of around the distal edge of the carpal ligament. Routine nerveconduction tests are useful not only for indicating the degree of nerve compression but also for providing a baseline for postoperative studies should recovery be slow. ’
5. Das, S. K., Brown, H. G. Hand, 1976, 8, 243. 6. Hybbinette, C. H., Mannerfelt, L. Acta orthop. scand. 1975, 7. Semple, J. C., Cargill, A. O. Lancet, 1969,i, 918. 8. Harris, C., Tanner, E., Goldstein, M. N., Pethee, D. S. 1979, 61A, 93. 9. Langloh, N. D., Linscheid, R. L. Clin. Orthop. 1972, 83, 41.
46, 610.
J.
Bone
Jt Surg.
ORAL IRON PREPARATIONS—DO WE NEED THEM ALL? are over forty oral iron preparations available prescription in the United Kingdom, varying from simple salts to complex formulations. Many owe their continuing success to the wide and erroneous belief that elaborate formulations are less apt to cause gastrointestinal troubles. The side-effects are, in fact, much more dependent on the dose than on the nature of the preparation, and can be greatly reduced by prescription of lower doses2 and by getting the patient to take the medi-
THERE
on
cine after food. Some iron intolerance also seems to have a psych6logical basis;3 so if the patient expects gastrointestinal symptoms from iron, a word of explanation and reassurance from the doctor and dispensing pharmacist can be of great preventive value. Iron-deficiency anaemia is common and there is a temptation to correct it with large doses over a short 1. Drug Therapeut. Bull 1979, 17, 33. 2. Crosby, W H. Archs intern. Med. 1978, 138, 616. 3. Kerr, D. N. S , Davidson, L. S. P. Lancet, 1958, ii, 489. 4. British National Formulary 1976-1978; p 157.
period. But, adverse effects apart, replacement of body stores in an iron-deficient patient takes at least three months’ oral treatment of at least 100 mg elemental iron a day after the haemoglobin deficit has been corrected,4 and in most patients this can be achieved with twice daily doses of ferrous sulphate 200 mg (60 mg Fe) or ferrous fumarate taken after food. No advantage is offered by preparations that contain trace amounts of other metals such as copper or manganese. Furthermore, most of the liquid and slow-release iron preparations are 2-10 times more expensive with little, if any, evidence of
superiority.1
SURGICAL TREATMENT OF CARPAL-TUNNEL SYNDROME Sir James Paget described the symptoms of carpaltunnel compression in 1854, but it was nearly a century before Sir James Learmonth did the first successful surgical operation to decompress the median nerve at the wrist. Nowadays this is one of the commonest operations on the hand, but the result is not always perfect: from 1.2% to 25%6,7 of patients have residual symptoms of mild persistent numbness and continuing weakness in the thumb. Precise diagnosis and careful operative technique are essential for surgical relief of the pain and paræsthesiæ, which can be very unpleasant. Harris and others8 survey the factors related to a successful outcome. In all their 124 cases the diagnosis was confirmed by nerve-conduction studies. Patients with motor-nerve delay had a more favourable result than those with only sensory abnormalities. The preoperative duration of symptoms did not influence the surgical result. Classic symptoms were sometimes present with normal nerve conduction times, and this is particularly true in the patient with rheumatoid arthritis. Age did not affect the outcome of operation. A common cause for surgical failure is incomplete division of the volar carpal ligament.9 This is most likely if the ligament is sectioned "blindly" through a small skin incision in the hope of producing a very small scar. The skin incision must be long enough to display the whole length of the ligament. Another factor predisposing to failure is tenosynovitis, either nonspecific or associated with joint disease in the carpus. Synovectomy should be done if adequate decompression cannot be obtained without removal of at least a portion of the synovium. The carpal tunnel should be inspected for possible occasional intrusions such as a ganglion, a lipoma, or a large bony spur from an adjacent osteoarthritic joint. Harris et al.8 recommended neurolysis of the median nerve when it is surrounded by thickened synovial tissue. The recurrent motor branch should be decompressed when it passes through instead of around the distal edge of the carpal ligament. Routine nerveconduction tests are useful not only for indicating the degree of nerve compression but also for providing a baseline for postoperative studies should recovery be slow. ’
5. Das, S. K., Brown, H. G. Hand, 1976, 8, 243. 6. Hybbinette, C. H., Mannerfelt, L. Acta orthop. scand. 1975, 7. Semple, J. C., Cargill, A. O. Lancet, 1969,i, 918. 8. Harris, C., Tanner, E., Goldstein, M. N., Pethee, D. S. 1979, 61A, 93. 9. Langloh, N. D., Linscheid, R. L. Clin. Orthop. 1972, 83, 41.
46, 610.
J.
Bone
Jt Surg.
