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aftXÌOUS persons should be associated with an increase infinger pulse-volume, whereas untroubled patients, or

normal people, would show no such change. The findingsshowed that the three groups studied differed significantlyboth in the size of the pulse-volume during the restingstate and in the increase in pulse-volume during sleep.The increase in finger pulse-volume in the anxious patientsclearly distinguished them from the other two groups.The findings therefore indicate that anxiety is associatedwith an increased level of peripheral vasomotor activity.Other somatic manifestations of anxiety-tachycardia,

increased blood-pressure and respiration-rate, and changesof skin electrical resistance-were found to be unreliableas measurable indications of anxiety. Further work mayindicate whether the degree of anxiety is related to theamount of pulse-volume change as sleep ensues ; if itdoes so, then we would have an objective method ofassessing the degree of anxiety at different times in anyone patient. It is very unlikely that the method couldbe used to assess by how much the degree of anxiety inone patient differs from that in another.After this good beginning, standards are not quite so

high in the other papers in this new journal. If the"narrow factual basis " of psychosomatic research is tobe widened, somatic manifestations and psychologicaldisorders must both be clearly defined and described inspecific terms. " Mixed neurosis," " social inadequacy,""neurodermatosis" or "-itis," and "social isolation"are not precise terms. Control groups must be impartiallyinvestigated, and the tests used must be such that, whenthey are repeated in the same subject, the difference isless than the differences between normal and abnormalsubjects. It seems likely that secure progress cannot bemade in psychosomatic medicine until a better knowledgeof psychosomatic physiology is available. Psychoso-matic research needs the work of investigators com-parable to Harvey, Claude Bernard, Starling, Dale, andLewis, and one of the new journal’s aims will be to

encourage this fundamental work.

1. Cairns, H. Lisboa méd. 1942, 19, 375.2. Sedzimir, C. B. J. Neurol. Psychiat. 1955, 18, 293.

CAROTID THROMBOSIS IN THE YOUNG

SEEMINGLY spontaneous carotid thrombosis in the

young adult has been known as a rarity for fifty years ormore. Carotid angiography has more recently uncovereda surprising number of such cases. The finding posesafresh the problem of aetiology, because the usual degen-erative factors held to contribute to thrombosis do not

apply at this age. A few thromboses can be clearlyclassified as traumatic. Blows to the neck, in boxing, forinstance, may occasionally be responsible : the natureof the local injury and the timing of symptoms leave littledoubt about the causal link. In one or two cases thecircumstances suggest that some upset in water or elec-trolyte balance is the cause. Thrombo-angiitis obliteransand giant-celled arteritis are uncommon in any form,and even rarer as a cause of carotid obstruction. 111-defined constitutional factors, such as operate in familiesmore than usually susceptible to thrombosis in general,presumably play a part ; but in most cases the causeand even the occasion remain obscure.In 1942 Cairns 1 first suggested the possibility that

damage to the carotid at some distance from the site ofblockage may start a local thrombosis which then extendsspontaneously. He described a closed head injury withthrombosis at the carotid syphon. Sedzimir 2 reconsideredthe matter recently and gave details of 6 cases in whichblunt injury to the head seemed to precipitate carotidthrombosis, starting intracranially and spreading downinto the neck. In the 4 cases where the diagnosis wasconfirmed by necropsy or angiography the injury wasfrontal. In 1 there was an associated atheroma whichprobably contributed to the thrombosis. In all 4 some

time elapsed between injury and the onset of signs ofthrombosis, and in 2 this amounted to several days.Some of these cases undoubtedly confirm the view thebthead injury may initiate a spreading carotid thrombosis.Such a cause must therefore be carefully considered inapparently spontaneous carotid thrombosis in the young.The relationship may the more easily be missed since notall the recorded cases had severe head injuries and therewas a variable interval between the trauma and its effects.At a time when thrombotic disease seems to be on theincrease, any information about the factors causing orfavouring its production has a general interest andapplication.

1. DeBakey, M. E., Cooley. D. A. Ann. Surg. 1954, 139, 763.2. Bahnson, H. T. Ibid, 1953, 138, 377.3. Holmes Sellors, T. Brit. J. Surg. 1956, 43, 365.4. Lancet, Jan. 14, 1956, p. 93.5. Brock, R. C. Guy’s Hosp. Rep. 1953, 102, 203.6. Hamblin, R. G., Lord, J. W. J. Amer. med. Ass. 1954, 155, 1406.7. Voorhees, A. B., Jaretski, A., Blakemore, A. H. Ann. Surg.

1952, 135, 332.8. Wesolowski, S. A., Sauvage, L. R. Ibid, 1956, 143, 65.9. Quoted by Edwards and Tapp (ref. 10).10. Edwards, W. S., Tapp, J. S. Surgery, 1955, 38, 61.

SYNTHETIC ARTERIES

THE replacement of diseased or blocked arteries byhuman homografts is undoubtedly one of ’the majorsurgical triumphs of recent years. Large series of success-ful transplants in the distal aorta have been recorded byDeBakey and Cooley and Bahnson 2 ; more recentlyHolmes Sellors 3 has described 3 patients with coarctationof the aorta associated with a proximal aneurysm inwhich both lesions were resected en bloc and continuityrestored by an arterial graft. We recently suggested 4that the by-pass operation for femoral-artery blocks holdsgreat promise. Admittedly, despite many experimentswith the preservation and sterilisation of homologousvessels, there remain many objections to their use. It isnot always easy to obtain a sufficient number and rangeof young homologous aortas or smaller arteries, and theirsterility may be difficult to ensure. Freeze-dried or

quick-frozen arteries are non-viable and depend essentiallyon their elastic fibres to prevent the dilatation and

disruption which is occasionally reported.5 6 Even so,the results of homologous arterial transplantation aregood, although sufficient complications and difficultieshave been described to make safer replacements desirable.

Blakemore et al. suggested that fabric tubes mightbe used as an alternative, and they later demonstratedthat’ Vinyon N ’ cloth, folded and stitched longitudinallyin a tube, was in fact capable of acting as a scaffoldingfor the ingrowth of fibroblasts. Many technical questionsimmediately presented themselves, some of which are-

gradually being answered. Impermeable tubes are lesssatisfactory than a mesh weave which allows fibroblasticingrowth for the surrounding host tissue to form a newintima ; but if the mesh is too big, with holes of largerthan 50-100 ., then there may be uncontrollable andfatal oozing through the wall.8 Hufnagel 9 used ’ ‘ Orlon ’’and’ Dacron cloth because their water-repellent qualitieslimit this type of bleeding : others have used ’ Ivalon ’sponge and polyvinyl sheets. A serious objection to allfabric grafts is the possibility of kinking with subsequentclotting if the insert material is too long or if the graftcrosses a flexion area such as the groin, axilla, or poplitealspace. To overcome this " wrinkle " thrombosis, Edwardsand Tapp 10 have experimented with crimped or " con- ,certinaed " nylon tubes, which are treated with siliconeto discourage bleeding through the open mesh. This

design has the advantage of allowing the graft to takeup slack and pass round sharp angles without wrinkling.The rough corrugated inner surface to the crimped tubescauses much turbulence in the blood-flow ; but,although one might suspect that this would encouragepostoperative clotting, this was not in fact so, even withtubes of a diameter of 0.5 cm.

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The various combinations of filament size, weave,

synthetic material, and its treatment which are now

obtainable from the manufacturers are enormous, andit is obvious that much further research is needed todefine the best type of tube. It seems likely, however,that improved fabrics will very soon be in use, and theymay largely replace arterial homografts.

1 Lancet, Jan. 21, 1956, p. 141.2. Chalmers, J. M., Fitzgerald, M. G., James, A. H., Scarborough,

H. Ibid, p. 127.3. Chart, J. J., Shipley, E. G., Gordon, E. S. Proc. Soc. exp. Biol.,

N.Y. 1951, 78, 244.4. Venning, E. H., Singer, B., Carballeira, A., Dyrenfurth, I.

Beck, J. C., Giroud, C. P. Colloq. Endocrinol. 1955, 8, 190.5. Venning, E. H., Dyrenfurth, I. J. clin. Endocrin. 1956, 16, 426.6. Simpson, S. A., Tait, J. F. Rec. Progr. Hormone Res. 1955, 11, 206.7. Neher, R., Wettstein, A. Acta endocrinol. 1955, 18, 386.

ALDOSTERONE

RECENT work has illustrated that our understandingof the syndromes associated with excessive secretion ofaldosterone is by no means completed The chief problemat present lies in reconciling the clinicians’ identificationof a syndrome which they believe to be due to increasedaldosterone secretion with the biochemists’ failure todetect increased amounts of aldosterone in the urine orblood. This difficulty has arisen on at least two occasions.The first patient was described in our columns by,Dr.Chalmers and his colleagues,2 and had the characteristicfeatures believed to be due to excessive aldosteroneformation : intermittent muscular pains, cramps, weak-ness, and paralysis ; hypertension ; polyuria, nocturia,and albuminuria ; hypokalemia and alkalosis. Thesecond case (an even more difficult diagnostic problem)was described by Dr. M. D. Milne to the section of endo-crinology at the Royal Society of Medicine on April 25.An otherwise healthy woman complained of occipitalheadaches, was found to have hypertension, and wasreferred to hospital. A routine electrocardiogram revealedthe changes of hypokalaemia which was confirmed byflame photometry. There was no muscle weakness or

tetany, and no adrenal tumour was seen on X-rayexamination, even after air insufflation and tomography.Nevertheless both patients were found at laparotomy tohave adrenocortical tumours, removal of which rightedthe biochemical abnormalities, and in neither was therepreoperative evidence of increased urinary excretion ofaldosterone. One possible explanation for this paradox isthat the tumours were secreting some hormone otherthan aldosterone but with similar physiological effects ;or it may be that the present methods for estimatingaldosterone are unsatisfactory. A similar difficulty hasalso arisen in the investigation of toxemia of pregnancy.In patients with this condition increased amounts of asodium-retaining substance are excreted in the urine, asjudged by bio-assay procedures.3 4 With justifiablespeculation it has been suggested that this substance is

aldosterone, but Dr. J. D. Martin and Dr. 1. H. Mills

reported, in a communication to the Society for Endo-crinology on May 4, that they had failed to find anydifference in the amounts of aldosterone excreted bynormal pregnant women and patients with toxaemia.

Venning and Dyrenfurth 5 have briefly reported similarnegative results.At the Royal Society of Medicine Dr. J. F. Tait reviewed

very clearly the methods, biological and physicochemical,for estimating aldosterone. Since the ratio of hydro-cortisone to aldosterone secreted is about 60 to 1, theamount of aldosterone in the blood (0-08 ug. per 100 ml.)and in the urine is extremely small, and this is largelyresponsible for the difficulties of estimation. Neverthelessthere remains a disturbing and unexplained difference inthe quantity of aldosterone found in normal urine byBritish and Swiss 7 workers. Little is known of the formor forms in which aldosterone is excreted. According to

Dr. Tait, the yield is increased threefold by hydrolysisat pHl ; Venning and Dyrenfurth 5 used both acid andglucuronidase hydrolysis. Failure to hydrolyse all the

conjugates, as well as lack of knowledge about the meta-bolites of aldosterone, may therefore be in part responsiblefor the low urinary excretion in some cases of allegedhyperaldosteronism. Dr. Tait suggested that the nephro-pathy caused by hypokalaemia 8 9 might result in dimin-ished excretion of aldosterone in patients with hyperaldo-steronism, but he emphasised that in the patient studiedby Chalmers et al. the blood-level was not raised. Dr.I. Bush put forward a point in favour of regarding somecases of " hyperaldosteronism " as due, not to aldosterone,but to some unidentified hormone. He contrasted thelarge amounts of aldosterone excreted in secondaryaldosteronism (cirrhosis, nephrosis, and congestivecardiac failure) and the much smaller or normal amountsin some cases of alleged primary aldosteronism. Untilthese questions have been resolved, diagnosis and manage.ment of primary aldosteronism must rest, as ably shownby Dr. Milne, on the clinical findings and metabolicdisturbances, without depending on the detection ofincreased amounts of aldosterone in the urine or blood.

8. Schwartz, W. B., Relman, A. S. J. clin. Invest. 1953, 32, 258.9. Relman, A. S., Schwartz, W. B. Ibid, 1955, 34, 959.10. Cayley, F. E. de W. Lancet, 1950, i, 417.11. Heard, K. H., Campbell, A. H., Hurley, J. J., Ferguson, E.

Med. J. Aust. 1950, ii, 606.12. McIntyre, P. A. Bull. Johns Hopk. Hosp. 1953, 92, 210.13. Werner, C. A., Tompsett, R., Muschenheim, C., McDermott, W,

Amer. Rev. Tuberc. 1951, 63, 49.14. Pitts, F. W., O’Dell, E. T., Howard, O. P., Schmidt, C. H.,

Chambers, J. S. Transactions of the 11th Conference onChemotherapy of Tuberculosis, Veterans Administration, 1952;p. 279.

15. Thorn, G. W., Howard, R. P., Dayman, H. Bull. Johns Hopk.Hosp. 1940, 67, 345.

16. Crofton, J., French, E. B., Sandler, A. Tubercle, Lond, 1956,37, 81.

17. Rapoport, S., West, C. D., Brodsky, W. A. J. Lab. clin. Med.1951, 37, 550.

ELECTROLYTES IN TUBERCULOSIS

ABNORMALITIES of the serum-electrolytes have beendescribed in tuberculous patients, both with and withoutantibacterial treatment. Hypokalaemia has been demon-strated during treatment with p-aminosalicylic acid 10-12and with viornycinP 14 Low serum-sodium or serum-chloride may be found in untreated patients who arevery ill with miliary, meningeal, or pulmonary tuber-culosis, but no important changes in serum-potassiumhave been found.l5 Crofton and his colleagues 16 havelately reported 4 instances of low serum-potassium inpatients with miliary tuberculosis having antibacterialtreatment that included neither isoniazid nor viomycin.The serum -chlorides were also low in 3 of their patients.In all 4 there were severe symptoms of hypokalsemiawith lethargy and profound muscular weakness ; but in

only 1 did the symptoms appear during the acute phaseof the illness. 2 patients had symptoms during con-valescence, and in another they were preceded by anattack of biliary colic and vomiting. Simple replace-ment therapy with sodium, potassium, and chlorideproduced considerable improvement, and in at least2 patients it may have been life-saving. Crofton et al.conclude that the electrolyte disturbances were due tothe cumulative effects, in severely ill patients, of decreasedpotassium intake (the result of poor appetite), and toincreased potassium loss caused by mild diarrhoea andoccasional vomiting, with, possibly, poor renal conserva-tion,17 It was not possible to examine the electrolytebalance in such gravely ill patients ; but Crofton et al.’s

paper is published at an incomplete stage of their

investigations in order to draw attention to the condition.Electrolyte upsets in tuberculosis may be more commonthan published reports suggest ; and it is possible thatsome who " just fade away " may in fact die from thisremediable cause.