743

Fig. 2-Thyroid of twin dying at 38 days, showing poorly filledvesicles and flattened epithelium ( x 110).

fibrosis. The main differences from the second twin were thereduced colloid content, smaller vesicles, and the lowerepithelium.

Discussion

PathogenesisIt is generally held that high levels of plasma-iodides

prevent the organic binding of iodine in the thyroidgland. The ultimate effect is lack of thyroxine andclinical hypothyroidism, and the goitre is thought to becaused by excessive thyroid stimulating hormone releasedby the pituitary.When, as in the case of this mother, there is no primary

maternal thyroid disease but a known goitrogen hascaused a maternal and foetal goitre, the pathogenesis ofthe foetal goitre is more difficult to interpret. Normallythe foetal pituitary-thyroid axis appears to function

independently. Maternal thyroxine is known to cross

the placenta slowly (Hubble 1959) but in insufficient

quantities to interfere with the foetal thyroid. It is

generally held that T.s.H. does not, in the normal pregnantwoman, cross the placenta. Since iodides can cross the

placenta freely it seems most likely that they directlycaused the goitres in our cases. We suggest that in eachcase the organic binding power of the foetal thyroid wasblocked and that a goitre resulted from oversecretion ofthe T.S.H. from the foetal pituitary. The possibilityremains however that the maternal T.S.H., which mightwell be increased in this mother, could have crossed theplacenta and stimulated the foetal thyroids.

HistologyIodide goitres have been described by some as colloid

(Bell 1952, Morgans and Trotter 1953, Burrows et al.

1960) and by others as hyperplastic (Turner and Howard1956, Paley et al. 1958, Paris et al. 1960). Burrows et al.(1960) point out that the histological appearance of thethyroids in these cases probably depends on whether thepatients are taking iodides continuously up to the timeof operation.

Petty and DiBenedetto (1957) reported an infant witha congenital iodide goitre which weighed 42 g. Themother had taken iodides for longstanding asthmathroughout the pregnancy up to the delivery. The infantlived 30 minutes and the thyroid showed a colloid goitrewith large vesicles lined by flattened inactive epithelium.The appearances in the thyroid of our second twin,

dying at 11 hours after birth, are regarded as abnormal,having the features of a colloid goitre but also showing

some evidence of hyperplasia of the vesicular epithelium.It is possible that the withdrawal of the iodides for 9days before delivery was sufficient to account for the

epithelial hyperplasia in a goitre basically colloid in type.In the longer-lived twin iodides had been withdrawn for47 days. The goitre disappeared and the size of thevesicles and their colloid content were reduced. We

interpret our cases as supporting the contention ofBurrows et al. (1960) that an iodide goitre is colloid intype. When the iodides are withdrawn, however, theinitial histological response is one of epithelial hyper-plasia. The crucial factor therefore in the histology ofiodide goitre is the time interval since the last dose ofiodide, or felsol powder, taken by the patient beforeoperation.

SummaryTwo cases of goitre are described in the binovular

twins of a mother who for years had taken Felsol’

powders for chronic bronchitis and bronchospasm. Thepathogenesis and histology of these goitres are discussed.We are indebted to Prof. J. K. Russell, Prof. S. D. M. Court,

and Dr. C. E. Cooper for permission to publish these cases.

AddendumSince this paper was submitted Oppenheimer and

McPherson (Amer. Y. Med. 1961, 30, 281) have publisheda case of iodide goitre and myxcedema, and they concludethat both depend on the length and regularity of iodidetherapy or on a sensitivity to iodides possibly associatedwith some subtle thyroid defect.

REFERENCES

Bell, G. O. (1952) Trans. Amer. Goiter. Ass. p. 28.Burrows, B., Niden, A. H., Barclay, W. R. (1960) Ann. intern. Med. 52, 858.Falliers, C. J. (1960) Amer. J. Dis. Child, 99, 428.Hubble, D. (1959) J. Irish med. Ass. 155, 86.Morgans, M. E., Trotter, W. R. (1953) Lancet, ii, 1335.

— — (1959) ibid. ii, 374.Paris, J., McConahey, W. M., Owen, C. A., Woolner, L. B., Bahn, R. C.

(1960) J. clin. Endocrin. 20, 57.Paley, K. R., Sobel, E. S., Yalow, R. S. (1958) ibid. 18, 79.Petty, C. S., DiBenedetto, R. L. (1957) New Engl. J. Med. 256, 1103.Turner, H. H., Howard, R. B. (1956) J. clin. Endocrin. 16, 141.

SKELETAL INFECTION AS A COMPLICATION

OF GENERAL SURGERY

F. HOWARD BEDDOWM.Ch. Orth. Lpool, F.R.C.S.E.

ORTHOPÆDIC REGISTRAR *

HANU&Sbreve; WEISLM.D. Manch., M.Ch. Orth. Lpool, F.R.C.S.

ORTHOPÆDIC REGISTRAR †SEFTON GENERAL HOSPITAL, LIVERPOOL

* Present appointment : senior orthopædic registrar, Royal Infirmary,Liverpool.

† Present appointment: senior registrar, Prince of Wales OrthopædicHospital, Rhyd Lafar, near Cardiff.

THIS paper describes acute osteomyelitis and septicarthritis complicating relatively clean general surgicaloperations. The occurrence of 8 such cases in one generalhospital within three years suggests that the condition ismore common than a total of 56 published cases wouldindicate. A disturbing feature of this complication is thatit is often due to a penicillin-resistant Staphylococcusaureus.

Case-histories

Case l.-Female, aged 72. Partial gastrectomy. Eight daysafter the operation she developed suppurative arthritis of theleft knee due to a pneumococcus. Treatment with systemicand intra-articular penicillin resulted in complete recovery.Case 2.-Male, aged 63. Suprapubic prostatectomy. Ten

weeks after the initial operation a urethral dilatation was carried