1174

postnatally; and their presence in these cases representsonly some delay in the normal maturation ’process of theliver-which is scarcely surprising when that organ isgrossly abnormal in other respects. Dible and his col-leagues justifiably conclude that the pathological findingsin these infants were attributable to their stage ofdevelopment and were in no way incompatible with viralhepatitis.The relationship of this neonatal hepatitis, apparently

contracted in utero, to juvenile cirrhosis is next con-sidered by Dible and his associates. In 2 infants who

developed jaundice within a few days of birth and diedafter three and seven weeks, necropsy showed distinctdiffuse hepatic fibrosis such as occasionally follows infec-tive hepatitis in adults. In the absence of any other

aetiological factor Dible et al. conclude that these 2 casesmay represent the sequelae to the acute type of diseaseseen in the 4 previous cases.

It seems unlikely that the virus of ordinary infectivehepatitis is responsible for in-utero infection, for there isno evidence that infective hepatitis in the mother istransmitted to the fcetus. On the other hand, Stokeset a1.2 have reported the case of a woman, subsequentlyshown to be a carrier of an icterogenic virus, whoseinfant developed jaundice at four months and died withhepatic cirrhosis at eighteen months. In view of the

frequency of icterogenic virus in blood-plasma, the rarityof in-utero infection implies either a considerable resistanceto transplacental transmission of the virus or a simulta-neous transmission of antibodies. Possibly neither typeof infective-hepatitis virus is responsible, but some otheragent such as herpes virus.3 Virological studies in furthercases should answer this very important question.

2. Stokes, J. jun., Wolman, I. J., Blanchard, M. C., Farquhar,J. D. Amer. J. Dis. Child. 1951, 82, 213.

3. France, N. E., Wilmers, M. J. Lancet, 1953, i, 1181.4. Brown, J. J. M. Brit. J. Surg. war suppl. no. 2, 1948, p. 354.5. DeBakey, M. E., Simeone, F. A. Ann. Surg. 1946, 123, 534.6. Ziperman, H. H. Ibid, 1954, 139, 1.7. Maybury, B. C. Brit. med. Bull. 1944, 2, 142.8. Moore, H. G. jun., Nyhus, L. M., Kanar, E. A., Harkins, H. N.

Surg. Gynec. Obstet. 1954, 98, 129.

VASCULAR INJURIES IN WAR

IT has long been known that primary ligation of majoiperipheral arteries gives poor results. In the 1939-4fwar the results were possibly worse than those previousl3reported,4 and DeBakey and Simeone found that o:

2471 patients with arterial wounds only 135 had beertreated by primary repair and reconstitution of th{

damaged artery. Since division of " critical " arterie:

(axillary, brachial, femoral, and popliteal) so often lead,to loss of limb or life, it is understandable- that a mor(active policy of arterial repair was initiated by th(American medical services in the Korean conflict. Som{

encouraging preliminary reports are now appearing.The interval between wounding and arrival at th{

surgical centre is vitally important ; and in Koreaevacuation by helicopter reduced the average intervalbelow the critical level of ten hours. Ziperman notesa definite correlation between lack of vascular-surgicalexperience and amputation-rate ; this was so evidentthat a special centre for the teaching and practice ojvascular surgery was established in Korea. Zipermanreviews 218 peripheral vascular injuries, of which 162involved " critical " arteries. In 132 cases the arterialwounds were repaired by end-to-end anastomosis, arteri-orrhaphy, and vein grafting. The outstanding featureis the proportion of extremities lost-20% in the wholeKorean series, compared with 40% in a 1939-45 series.5Results were especially impressive in partial arterialtears which after debridement can be repaired by evertionsutures. Longitudinal closure of a defect may be followedby such narrowing of the lumen that thrombosis ensues. 7Moore et al.8 emphasise that damage of the intima alwaysmuch exceeds that of the adventitia, and conclude thatresection of the entire length of the injured vessel followed

by end-to-end anastomosis gives the most satisfactoryresults with the least disturbance of blood-flow. Wherethe severed ends of the artery cannot be safely approxi-mated a free vein graft seems to be the best method ;the place of preserved arterial grafts has not been fullydetermined. The use of ’Vitallium tubes and other

prostheses has apparently been abandoned. Zipermanstrongly advises against ligation of the concomitant

undamaged vein-a point which most surgeons wouldendorse.

1. Dowling, G. B., Wetherley-Mein, G. In Modern Trends inDermatology. Edited by R. M. B. MacKenna. London, 1954.

2. Griffith, A. S. Lancet, 1916, i, 721.3. Jensen, K. A. Cited by Marcussen (footnote 9).4. Lomholt, S. Acta tuberc scand. 1946, 20, 136.5. Ustvedt, H. J. In Modern Practice in Tuberculosis. Edited by

T. Holmes Sellors and J. L. Livingstone, London, 1952.6. Tolderlund, K. Cited by Marcussen (footnote 9).7. Kalkoff, K. W. Hautarzt, 1950, 1, 366.8. Gilje, O. Acta derm.-venereol., Stockh. 1952, 32, 51.9. Marcussen, P. V. Brit. J. Derm. 1954, 66, 121.

LUPUS FROM B.C.G.

Lupus vulgaris usually starts with the implantationof tubercle bacilli from an external source. In childrenit may develop from a primary tuberculous sore. Inadults, who have probably already done battle with thetubercle bacillus in the lungs or bowel, bacilli implantedin the skin more commonly give rise to a different kindof lesion-verrucous skin tuberculosis. This suggests toDowling and Wetherley-Mein 1 that the type of immunityderived from primary infection of the skin differs fromthat derived from extracutaneous foci. The bacillusrecovered from the lesion of lupus is of low virulence,and such strains are rarely found in tuberculosis in othersystems,2 so it seems probable that the organism isattenuated in the skin itself ; once lupus is initiated,the attenuated strain is of sufficient virulence to maintainthe characteristically chronic process.

Jensen 3 predicted the production of lupus vulgaris bythe intentional inoculation of artificially attenuatedtubercle bacilli-i.e., B.C.G. Lomholt 4 first reportedsuch a case. Ustvedt 5 thought that the lupus must havearisen through superinfection, but Tolderlund 6 con-sidered that the bacillus recovered from this case wasindistinguishable from B.C.G. 2 further cases of lupusfollowing B.C.G. vaccination were reported 7 8 but withoutbacteriological proof of the causal organism. Marcussen 9has now described 3 cases, in 2 of which there was goodclinical and bacteriological evidence that the lupus wasnot due to superinfection. In all 3 cases the lesion

spread from the site of B.C.G. vaccination, and in 1 ithad persisted for three years. All 3 patients weretuberculin-negative before vaccination. 2 had no knowntuberculous contact, and a tubercle bacillus recoveredfrom their lesions proved identical with B.C.G. in culturalbehaviour and pathogenicity.

In B.c.G.-vaccinated patients who subsequently developtuberculosis of organs other than the skin, it is usualto find tubercle bacilli of high virulence ; and such casesare attributed to fresh infection. The close similaritvof the bacillus of lupus to B.C.G. makes this attributionless convincing in cases of skin tubercle. If, however,the laboratory criteria for their separation are valid,B.C.G. vaccination can probably give rise to progressiveinfection of the skin for at least several years. It has

long been known that B.C.G. can survive in the tissuesfor up to eighteen months, and a case of tuberculouslymphadenitis attributed to B.C.G. was diagnosed threeyears after vaccination.

Marcussen raises the question of variation in the

potency of the vaccine. If this were a material factor,one might have expected many more cases of lupus.Also, the accidental injection of enormous doses of B.C.G.has not provoked long-standing local infection. Variationin the host’s response is a more probable explanationof these rare cases. It may be significant that one ofMarcussen’s cases was inoculated four times before