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1948. Slight variations in technique may lead to mis-interpretation, especially when judging progress by com-parison with previous films, and the routine suggestedin the revised report will be examined with interest byall radiologists. It has been assumed that before longmost chest radiographs will be taken by X-ray tubescapable of carrying at least 400 milliamperes. When themaximum available output is less, it is better to reducethe tube-film distance rather than increase the exposuretime. The photo-electric timer, which automaticallyends the exposure after a time appropriate to the sizeof the patient, is mentioned as a means of achievingmore uniform radiographs. Those who have had theopportunity to examine a series of radiographs of thesame patient taken by different radiographers with theaid of the phototimer will appreciate its value. Detailsof processing are included to re-emphasise the importanceof great care in the darkroom.

1. Oliver, J., MacDowell, M., Tracy, A. J. clin. Invest. 1951, 30,1305.

2. Dunn. J. S., Gillespie, M., Niven, J. S. F. Lancet, 1941, ii, 549.3. Darmady, E. M. Brit. med. J. 1950, ii, 349.

ACUTE RENAL FAILURE

I ACUTE renal failure has been the subject of muchdebate in the past decade. There are several distinct

types, which can be identified by the clinical history andpathologically. Once anuria has developed, however,the clinical course and the treatment are similar in alltypes. This similarity has led many workers to postulatefor every type of acute renal failure a

"

unity of patho-genesis "-a unity either of the initiating disturbance inthe kidney or of the morphological lesions which developthere, or of the functional disturbance which results fromthese lesions. The number of these unifying hypothesesis increasing. Some of the clearly defined explanationsappear to apply to one type of renal failure but not toothers. By contrast, other explanations apply to all

types but are so vague that they have little significance.A refreshing paper on the pathogenesis of acute renal

failure comes from Oliver et al.1 who have made a carefulstudy of the kidney by microdissection-a very old

technique which has been perfected and used with greatsuccess by Oliver in the investigation of other renalconditions. These workers distinguish two kinds of lesioninvolving the renal tubules, and offer an setiologicalexplanation for each. The less common lesion is necrosisof tubular epithelium, confined to the proximal convolutedtubules and distributed evenly among all the nephrons.This necrosis is caused directly by tubular toxins whichaffect a specific part of the proximal tubule. The toxinis believed to act chemically on the epithelium ; but

experimentally Schlegel’s technique revealed that it alsogreatly disturbed the blood-supply to the renal cortex.The second lesion, described as tubulorrhexis, was

present in all clinical cases of acute renal failure. Thislesion was originally identified histologically in thecrush kidney by Dunn et a1.,2 and was recorded byDarmady 3 who used the microdissection technique.Oliver’s account is more detailed and more fully docu-mented than the earlier descriptions. The change consistsin localised necrosis of tubular epithelium associated withdisintegration of the basement membrane at the samepoint, so that the tubule is disrupted. The lesion occursprincipally in the distal convoluted tubules or the

collecting tubules, but is common also in the spiralsegment. It can sometimes be found in other parts of theproximal convoluted tubule or in the loops of Henle,but is difficult to identify at these sites. It is alwaysvery irregular in its distribution among different nephrons;and Oliver and his colleagues interpret this irregularityas indicating that the tubulorrhexis must be producedby patchy ischaemia. This interpretation is, however,open to doubt. In man the kidneys did not show any ofthe other lesions which are accepted as characteristicstigmata of severe ischsemia. Furthermore, in dogs pure

renal ischaemia produced necrosis of proximal convolutedtubules but not localised tubulorrhexis. Oliver thus

suggests that exactly the right degree of ischaemia mustbe applied to produce tubulorrhexis. It is difficult toaccept that so delicately balanced a mechanism canaccount for a lesion found so very commonly in thekidneys of patients with anuria.The common type of tubulorrhexis affects the " lower

nephron " and is invariably associated with casts in thesesegments. It can be reproduced experimentally in dogswith renal ischsemia followed by intravenous injectionof haemoglobin, which produces casts in the lower seg.ments of the nephron. The casts are often above or belowthe site of the tubulorrhexis, rather than at it ; and Oliverbelieves that they do not cause the lesion. It must,however, be pointed out that in most of the clinicalcases the patient had survived for nine to twelve daysafter the original damage to the kidney; and thus thecondition of the affected tubule at the time of this damagecan only be inferred. Secondly, those unversed in thetechnique will inevitably ask whether casts might notbe moved along the tubule in the course of the dissectionand disentangling of the individual nephrons with needlesafter the kidney has been macerated in concentratedhydrochloric acid for twelve to twenty-four hours. The

possibility therefore remains that -the tubulorrhexis inthe lower segments of the tubule may be a mechanicaleffect of casts in the lumen.

Other problems are raised by this work. Oliverinterprets the monocytic infiltration of the intermediatezone as a local reaction to tubulorrhexis of the spiralsegments rather than as an indication of tubular leakagein the medulla. He maintains that tubulorrhectic lesionscan heal only with great difficulty, either by the adhesionof connective-tissue fibres or by the irruption of granu-lation tissue. He believes that tubulorrhexis is importantbecause the urine from the affected tubule escapes intothe interstitial tissue or neighbouring vessels, instead ofbeing excreted. Furthermore, it is suggested that theleakage of albuminous urine into the interstitial tissueproduces aedema there, which impedes the flow of urinedown the tubules of the region and compresses thecapillaries, producing further ischsemia.These ideas are all debatable, and there is no doubt

that they will be widely discussed.

1. Cushny, A. R. Digitalis and its Allies. London, 1925.2. Dock, W., Tainter, M. L. J. clin. Invest. 1929, 8, 467.3. Tyrer, J. H. Med. J. Aust. April 12, 1952, p. 496.

DIGITALIS AND VENOUS PRESSUREEXACTLY how digitalis works is still uncertain-though

not for want of trying. It seems definitely to increase thecontractile power of the heart, and, as Cushny 1 showedover a quarter of a century ago, it causes arteriolarconstriction. There is also a good deal of evidence thatin normal animals its administration is followed bydiminished cardiac output ; - but the reason for this isstill disputed. Dock and Tainter 2 suggested thatthe explanation lay in a constricting action on the

hepatic veins which reduced the venous return to theheart ; but subsequent investigations have not consis.tently confirmed this observation.Tyrer 3 has approached the problem afresh in a study

of sheep in which the heart was replaced by a double.perfusion pump, thus excluding cardiac action on venouspressure. In four such sheep the addition of digoxin tothe systemic venous reservoir was followed by a rise ofpressure in the inferior vena cava. Since pulmonary andsystemic circulations were perfused at a constant rate,total blood-flow through the venae cavae into the systemicvenous reservoir was constant ; and the central venouspressure was fixed at zero. Tyrer suggests that the rise ofvenous pressure evoked by digoxin can be explained inthree ways : (1) " a slight general venoconstriction alongthe length of the inferior vena cava, increasing slightlythe gradient of pressure fall along this portion of the

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venous system from the periphery"; (2) a localised

sphincter-like venoconstriction of the upper part ofthe inferior vena cava ; or (3) a selective action bythe digoxin, causing a diminished blood-flow along thesuperior vena cava and an increased blood-flow along theinferior vena cava. Tyrer regards this third possibilityas unlikely ; and he concludes that the evidence of aperipheral action of digoxin on venous pressure is

unequivocal. On the other hand, this " is not to suggestthat the principal action of digoxin in intact sheep is onvenous pressure." Indeed Tyrer describes experimentsin four control sheep with intact circulations in whichthe intravenous injection of digoxin caused either noalteration or a slight fall of mean right atrial pressure.This fresh evidence from Australia strongly supports

the hypothesis that digitalis has a primary action onvenous pressure, and it will be interesting to see whetherother investigators can confirm these observations.

1. Burger, H. C., Casteleyn, G., Jordan, F. L. J. Acta med. scand.1952, 142, 108.

PERCUSSION

Leopold Auenbrugger (1722-1809), the son of an

Austrian innkeeper, and in his youth a picturesque tapperof wine-barrels, later gained eminence as a physician byhis ability to apply his powers of careful observationand percussion ; but his Inventum Novum (1761),like many good discoveries, lay unnoticed for fiftyyears until Napoleon’s physician, Courvoisart, trans-lated it into French. Though some now regard percussionlightly, others hold it so useful that they practise itnot only on the chest but also on the head, abdomen, andjoints ; and at least one eminent teacher draws attentionto the " dull sound of an absent knee-jerk." There isno doubt that, as a means of comparing the resilienceof one part of the body-surface with another, percussionis a valuable art.One of the difficulties with percussion is in trying to

remember the absolute quality of a sound; and themost successful exponents limit their observations toa comparison of sounds from adjacent points, or fromcorresponding points on the two sides of the body.Burger et al.l have gone some way towards defining howpercussion is done ; but what factors determine the

quality of a percussion-note, and why do the underlyingstructures of the body influence the character of a soundradiated when the surface is struck 1 The sound thatreaches the ear is radiated from the body-surface ;each minute area of surface disturbs the air in itsimmediate neighbourhood, and the disturbance is trans-mitted to the ear with the velocity’ of sound in air.The ear summates the multitude of small componentsinto a whole " sound," movements of air particles inone direction cancelling out those that arrive at theear simultaneously with an opposite movement. Thusthe two sides of a vibrating sheet produce oppositeeffects, and if the distance to the ear from oppositesides is the same no sound is heard however violentlythe sheet is shaken. One has only to percuss one’s

finger lightly in space, or shake a small fragment ofpaper, to demonstrate this. For this reason loud-speakers need a baffle. Every sound can be regardedas the sum of a number of pure tones. The note middle Chas a frequency of 256 cycles per second, and in thetime of one complete oscillation sound travels about50 inches. Thus for this frequency of vibration tocause a maximum sound, the vibrating surface mustbe of such a size that the sound-path difference fromthe two surfaces to the ear is about 25 inches. Somesound will be heard, however, if the path-difference isless-say, greater than 5 inches. High notes are readilyradiated from small surfaces, but low notes requirea large vibrating surface or baffle area.When a well-ventilated part of the chest is percussed

a large area of the surface is momentarily depressed

and vibrates as a whole ; a relatively low note is pro-duced and dies away at a speed depending on the

viscosity of the skin and adjacent structures, of whichthe pleximeter finger is a small part. When fluid ora structure such as the liver underlies the surface, thepart, although equally elastic, is less compressible.The surface is not depressed as a whole ; but the partunder the struck finger is depressed while the surround.ing tissue rises at the sides of the finger and a wavespreads over the surface with the velocity of soundin tissue, just as a pond surface is disturbed by a fallingstone. Such a surface gives a higher-pitched sound,and the more complex wave pattern gives rise to a higherrate of damping, with the characteristic dull sound.Echoes from internal surfaces or cavities are sometimessaid to contribute to the quality of the sound. Possiblya large air cavity near the surface may resonate and pro-duce surface ripples ; and this may account for the

high-pitched, undamped, resonant quality known as

tympanic which is elicited over an empty stomach ora pneumothorax.Sound echoes of frequencies beyond the range of

hearing-e.g., 2 megacycles per second-can be elicitedfrom internal body structures, in the same way as theocean bed is depth-sounded by sound pulses from piezo-electric or magneto-striction radiators. The echoesare amplified and presented on a radar-type cathode-ray screen. Flaws in machinery and other industrialproducts are commonly located in this way ; and worknow proceeding in this country shows that in the bodygross changes in internal density or elasticity can bedetected similarly, though the waves do not go beyondan air interface. Such a procedure will determine thethickness of tissue overlying bone, show some defectsin bones, and enable some structures, such as the liverand heart and pleural effusions, to be outlined.

THE BIRTHDAY HONOURS

THOSE who value tradition in such matters will be

happy to see that a baronetcy has been conferred on SirCecil Wakeley, as on so many of his forerunners in thepresidency of the Royal College of Surgeons. Since hisfirst election in July, 1949, Sir Cecil has both exemplifiedand reinforced the vitality of his college, and the honourhe has so well deserved will give all the more pleasurebecause Lady Wakeley and his son are also members ofour profession. Mr. Walter Elliot, who must have beendisclaiming other titles since the ’20s, becomes a Com-panion of Honour, a designation earned alike by hispublic work and personal distinction. As is similarlyappropriate, Lieut-General Sir Neil Cantlie is promotedK.C.B. in recognition of his notable work as director-

general of medical services. The knighthood for Prof.W. E. Hume sets the seal on a valuable and distinguishedcareer which included service in France as a consultingphysician to the Army in the first world war, the chair ofmedicine at Newcastle, and the offices of senior censorand Harveian orator in the Royal College of Physicians.Group-Captain H. R. G. Poate, who is also created a

knight, was president of the Royal Australasian Collegeof Surgeons from 1945 to 1947, and Dr. Edgar Laurentis a member of the Executive and Legislative Councils ofMauritius. The names of other doctors appearing inthe Birthday Honours are set out on p. 1205, and theyform an impressive group. Outside the confines ofmedicine we are glad to note that Mr. J. M. K. Hawton,secretary to the Ministry of Health, is created K.C.B.,in somewhat tardy recognition of his important con-

tribution to the planning of the health service. Prof. R.A. Fisher, F.R.S., the eminent geneticist and statistician,and Mr. B. H. C. Matthews, F.R.S., the new professorof physiology at Cambridge, are among the new knights,and Miss Mabel Liddiard, retiring president of the RoyalCollege of Midwives, is appointed c.B.E.