422

united, but there is no redness round the edges of woundor points of suture; the pedicle is sloughing. Wounddressed with dry lint; pads removed, but strapping andbinder still used. Pulse 98; temperature 99.1°.—4.15 P.M.:Has had more pain in abdomen since the removal of pads;pads replaced.-10 P.M. : Felt much more comfortable afterthe pads were replaced; is nearly free from pain.

15th.—9.30 A.M.: No pain. Pulse 90; temperature 992°.- 8.30 P.M.: Has a good deal of pain; flatus relieved byclyster-pipe. Feels better; urine contains a slight trace ofalbumen.

16th.—Wound dressed and one superficial suture re-moved ; wound looks healthy. Pulse 90; temperature98’50.

19th.-Several hard scybalous masses were removed fromrectum, with much relief to patient. A warm water enema

given, which was not returned. Pulse 80; temperature 96°.20th.-The clamp, being attached only by a few shreds,

was cut away ; the deep sutures removed. Patient had avery copious evacuation of the bowels, the motion beingpartly solid, and causing much pain in passing. Was muchrelieved after it. Pulse 78; temperature 97°.

21st.—Passed water naturally for the first time. Remain-ing superficial suture removed.26th.-Bowels not opened since the 20th. An enema of

gruel and castor oil administered, which was returned un-altered.27th.-Bowels not opened. Ordered ten grains of mercury,

rhubarb, and hyoscyamus pill.28th.-Bowels open freely. No pain.29th.-Catamenia have appeared. Bleeding somewhat

copious.- Feb. 1st.—Sat up for a short time, and felt no worseafter it.From this time the convalescence was rapid and uninter-

rupted. The wound did not heal by first intention, butgranulated from the bottom. On Feb. 19th she left theinstitution to go to a convalescent home. The wound hadnot quite healed, but it was merely superficial, dischargingvery little. The strapping and binder were continued up tothe time of her leaving.

Medical Societies.PATHOLOGICAL SOCIETY OF LONDON.

THE ordinary meeting of this Society was held on the20th inst.; the President, Dr. Murchison, occupying thechair. The meeting was fully attended, and a paper wasread by Dr. G. Johnson on arterial changes in Bright’s dis-ease, illustrated by a large number of microscopical prepara-tions. The meeting was prolonged beyond the usual timeto allow of the conclusion of the subject.The proceedings commenced by the exhibition by Dr.

GOODHART of specimens of Cerebral Aneurism from Embolism.The first case was that of a youth eighteen years of age, ad-mitted for mitral disease, and with a history of two previousattacks of acute rheumatism. Whilst in the hospital he hadsigns of plugging of the left brachial artery, and he diedwith cerebral symptoms. There was found haemorrhage intothe right cerebral hemisphere, and a small aneurism on abranch of the middle cerebral artery. The left brachial

artery was dilated into a fusiform pouch, which, when opened,was found to be filled by soft clot. The heart weighedtwenty-three ounces ; long vegetations depended from themitral cusps; and there were splenic infarctions. (2) Male,aged thirty-four, with rheumatic history. He was attackedwith right hemiplegia and aphasia, and died from con-vulsions. There was a small aneurism on the left middlecerebral artery, which had ruptured into the frontal lobe.The heart weighed sixteen ounces, the mitral valve was

ulcerated, and the spleen contained infarctions. (3) Male,aged nineteen. A year before his death he had an attack of

hemiplegia, and a second attack preceded the fatal issue.

At the post-mortem a, sacculated aneurism was found in theright posterior cerebral artery, the heart weighed twentyounces, and there were vegetations on the aortic valve.(4) Male, aged fifty, who, whilst suffering from subacuterheumatism, presented a swelling on the forearm, red andhot, which in a few days began to pulsate. Digital com-pression of the brachial was tried, and whilst in the hospitalthe man died from apoplexy. Some layers of laminated clotexisted on the inner surface of the dura mater, in the regionof one of the branches of the right middle cerebral artery;and there was also a clot in the ulnar artery, which wasitself dilated into a large cyst just below its origin. Themitral valve was inflamed, and there were embola in thespleen and kidneys. Dr. Goodhart said that embolism as acause of aneurism still required proof, although, since Dr.K’rkes drew attention to it, cases had been published byJoliffe Tufnell, Holmes, Church, and Gowers. It had alsobeen long known that aneurism was the cause of apoplexyin young people; and he thought he might go further andsay that cerebral aneurism was usually associated with endo-carditis. Mr. Holmes attributes the formation of aneurismsto dilatation behind the plug ; but such dilatation does notoccur in ligature, or only very rarely. Ponfick attributes itto injury of the artery from the plugs being calcareous andspiculated; but this was by no means a frequent case. Dr.Goodhart’s own view was that the embolic plug was pushedon by the blood-stream into a vessel of smaller calibre, andthat the softening of the clot led to softening of the arterialwall at the seat of obstruction. However, a large numberof cases of embolism occurred without leading to aneurism,so that perhaps the nature of the clot itself played somepart in the result. -

Mr. BRYANT showed specimens of Aneurism of theFemoral and Popliteal Arteries from Embolism, which lentsupport to Dr. Goodhart’s views. Case 1. A male, thirty-nine years of age, the subject of extensive heart disease, whohad suffered from rheumatism for some time. Three weeksbefore admission he suffered from pain in the groin after aslight strain, and in a few days a pulsating tumour formedin the inguinal region. The diagnosis was at first that ofa deep-seated abscess pushing forwards the internal iliacartery, but the progress of the case showed it clearly to beone of aneurism. Mr. Bryant accordingly tied the commoniliac, but the patient died from the effects of his heartdisease a few hours after the operation. A large falseaneurism was found behind the external iliac artery, thevessel itself being healthy, except at its posterior part,where a slit half an inch in length existed. There wasmuch old and recent disease of the mitral and aortic valves,and embolism of the spleen and kidneys. It appearedprobable that the aneurism had followed upon an embolicplug in the artery. Case 2. A male, thirty-three years ofage, who had had three attacks of acute rheumatism, andwas suffering from marked aortic and mitral disease. Twoweeks before admission, after exertion, he had pain in theright foot, followed by swelling of the leg, and pulsatingtumour in the ham. Failing to cure the aneurism by pres-sure, Mr. Bryant introduced a quantity of horsehair intothe sac with marked result. The patient died a few daysafter from heart disease, and the existence of the aneurismjust above the bifurcation of the popliteal artery was veri-fied. The arterial system was elsewhere healthy, but therewas much old and recent endocarditis with vegetations onthe mitral and aortic valves, with ulceration of the former,and embola in the spleen and kidneys.

Dr. WILKS said the cases were very important, as clearlyproving the causation of anemism by embolism. It wasdue to Dr. Ogle to state that he first propounded this viewtwenty years ago; and he himself (Dr. Wilks) also broughtforward specimens illustrating it. The discussion whichthen took place dealt also with the subject of a rheumaticarteritis, but the question could hardly be said to have beenproved, else it would have been found in the text-books.Dr. Goodhart’s and Mr. Bryant’s specimens, however,carried conviction with them.-The PRESIDENT said that he

, had himself seen two similar cases, one in which an aneurism,

foimed suddenly in the arm in a case of endocarditis.Dr. GEORGE JoHNsoN read a paper on

11 The Changes in’

the Bloodvessels in Bright’s Disease." He commenced by’ stating that in the 33rd vol. of the Med.-Chir. Trans. he

first described muscular hypertrophy of the renal arterioles. in chronic Bright’s disease, especially in the small red

423

granular kidney. That paper was published in 1850 before the at the conclusion that these changes were the resultresearches of Bernard and Brown-Sequard had made known of the renal degeneration, and not simply of impuritythe true functions of the muscular coat, and of the vaso- of the blood. Coming to the physiological explanationmotor nerves; and Dr. Johnson then erroneously concluded Dr. Dickinson attempts to cast ridicule on his view by say-that the hypertrophy of the arterial walls was the result of ing that the heart and arteries, on that view, resemble twotheir excessive contraction in propelling the blood through athletes, who, in striving each to get the better of the other,the obstructed capillaries. The vaso motorial function was each undergo considerable muscular hypertrophy. But thisto regulate the supply of blood in the various tissues and is not consistent with what we know of the action of theorgans. The contraction of the arterioles increases the arteries in health; and Dr. Dickinson has misapprehendedarterial tension, and leads to more forcible and frequent the precise point involved. The arterial contraction was acontraction of the left ventricle. In the 55 bh vol. of the reflex contraction excited by the impure blood, and the in-Med.-Chir. Trans., Sir W. Gnll and Dr. Sutton published creased cardiac contraction was simply the physiologicaltheir well-known paper, in which they deny or doubt the result of the increased arterial resistance. Dr Dickinson’sexistence of arterial hypertrophy, and describe the condi- own theory was that there was impediment to the circula-tion of arterio-capillary fibrosis, and express their belief tion in the capillaries, and that the arteries hypertrophiedthat the cardio-vascular changes and the renal degeneration in order to assist the heart in propelling the blood ; anare the result of this general morbid state. He was willing explanation put forward by himself in 1850, and abandoned,to leave their theory to the 11 verdict of the profession," as above stated, when the facts of vaso-motor action becameprovided his own criticisms on that theory, published in the known. Various forms of impurity of blood would lead to56th vol. of the Med.-Chir. Trans., were also considered. the same hypertrophy of the arterioles-e. g., imperfectThe specimens he showed side by side for comparison of oxygenation ; and Dr. Mahomed had shown the existencenormal and hypertrophied arteries from the same tissue- of increased arterial tension in acute Bright’s disease priorkidney, skin, intestine, muscle, and pia mater—sufficiently to the appearance of albuminuria Dr. Johnson then passeddisproved, he thought, the objection that the " hyper- on to repeat his conviction that the small red granulartrophy" was due to the contraction of the vessel. kidney is not the result of a fibrosis; and he was happy toSuch comparison was easy between the afferent vessels find that Drs. Wilks and Moxon were in accord with him,of the Malpighian tuft, which are remarkably uniform for they state that although some writers describe anin the size of their canals and the thickness of their increase of fibrous tissue, they think there is only slightmuscular walls. No amount of post-mortem contrac- increase around the vessels, but not much. The de-tion of an artery can simulate the appearance of hyper- scription he published in 1850 (Med. Chir. Trans.,trophy, which consists in an increase of the muscular vol. xxx.) was, he maintained, strictly correct. No ma-

layers from one to three or four in vessels of equal terial additions had been made to the pathology of thissize. He asserted that a drawing of a transverse section of disease in the interval to lead him to alter the conclu-a renal artery, figured in the paper of Sir W. Gull and Dr. sions he then- arrived at. These conclusions werp, briefly,Sutton, was inaccurate, in that the outer circular layer of that the primary change was one of disintegration of themuscular fibres had been styled by them as hyaline-fibroid epithelium of the tubules, leading to the denudation andthickening of the adventitia, and the inner layer only atrophy of some of them, with perhaps slight thickening ofreferred to as composing the muscular coat. This the basement membrane. Some of the tubes were dilatederroneous description proved that these authors are so into cysts; others retained their natural epithelial lining.possessed by their hyaline-fibroid change as to mistake The change, then, being essentially intratubular, was pro-for it a most unquestionable example of arterial by- bably determined by a morbid quality of the blood, as inpertrophy. In reply to their statement that the mus- gout, lead-poisoning, or alcoholism, which produced alsocular layer sometimes varies in thickness in different changes in the skin and liver. There might be a slight in-parts of the same vessel, and that it is often manifestly crease in the thickening of the basement membrane and in thediminished in thickness. Dr. Johnson said this was quite Malpighian capsules ; but it was very slight, for pencilledconsistent with the doctrine of hypertrophy ; for it was sections of normal kidney showed a network of consider-quite conceivable that an hypertrophied artery might able thickness due to capillaries and basement membranedegenerate just as an hypertrophied heart did, and that the alone. At the same time that he published bis paper Mr.increased arterial tension of advanced Bright’s disease would Simon studied the subject also, and arrived independentlycause dilatation of the calibre and atrophy of the walls of at the same conclusion, as could be seen in the similaritythe degenerated vessel. The morbid quality of the blood between the drawings of the microscopical charactersin advanced stages of renal disease probably excited inflam- illustrating both papers. These striking appearances ofmatoryand degenerative changes in some arterioles, as intratubular change were ignored by the advocates of arterio-in the larger arteries and various other tissues; but dege- capillary fibrosis, and others, who directed attention solelyneration of the walls of the arterioles and loss of their to inter-tubular appearances. To the argument raised bycontractile power will not explain the hypertrophy of the Dr. Dickinson that many of the tubules retained healthyleft ventricle. It was well known that alcoholism-a epithelium, Dr. Johnson replied that this surely told againstcommon cause of renal degeneration-also often excites the view of fibrosis, for were the interstitial change so pro-inflammatory and degenerative changes in the bloodvessels, found as to cause the contraction of the kidney, it was in-and it may sometimes happen that a certain amount of conceivable that it should not affect the delicate struc-

vascular degeneration precedes the renal disease; but such ture of the renal tubules themselves. Dr. Johnson con-vascular changes would not be correctly designated as eluded by summing up his objections to the accepted"arterio-capillary fibrosis" of unknown origin. Since the doctrine of renal fibrosis, and pointed out that the very vas-discussion at the Royal Medical and Chirurgical Society cularity of the granular kidney told against there beingevidence in favour of the muscular hypertrophy had been inter-tubular growth, which would destroy capillaries, andabundantly adduced by Atkins, Galabin, Grainger Stewart, lead rather to ansemia of the organ, such as was producedand others. The most complete review of the question is in the large white kidney by the swollen contents of thecontained in Dr. Dickinson’s work on Albuminuria recently tubules compressing the capillaries, or as in limited patchespublished, and Dr. Johnson begged to express his admiration in renal embolism. The hypothesis of interstitial fibrosisof the ahility, industry, and candour of that author in was completely upset by the fact that, in sections of granu-treating this subject, with whom he himself agreed as to lar kidney, the characteristic inter-tubular changes maythe facts, but from some of whose conclusions he dissented. often be seen in various stages of progress, while theDr. Dickinson admits that the muscular coat is hypertro- surrounding capillaries are injected and normal. He scarcelyphied, and says that other coats are thickened also, and this felt called upon to express any opinion with regard to thehe (Dr. Johnson) had never denied. The same writer also beautiful series of specimens exhibited by Sir W. Gull anstates that degenerative changes occur in the arteries, and Dr. Sutton at the last meeting. He thought that t"that he bad met with the arterial change in the advanced attached undue importance to interstitial fibroid char ges’

stage of the large white kidney and in granular kidney in and too little to more essential pathological conditio-1. Thethe young subject—one patient being under six years of age etiology and clinical history of these changes we still to—a. very early period for "senile" changes to occur. be desired, particularly as regards the share tal-’n by alco-Finding also the same changes in cases of obstructed holism and other forms of blood contamiation in theiroutflow of urine in renal calculus, Dr. Dickinson arrived causation. It would require a large number a well-observed

424

facts, and a very careful induction from them, to justify the also. Some such explanation might be given for theconclusion that the appearance of an excess of fibroid tissue specimens shown by Sir W. Gull and Dr. Sutton.in the spinal cord is more than a secondary result of ante- The conditions of oedema, nucleated growth, and fibroidcedent and more essential changes. Knowing that the change, traced by them in the spinal cord, might heauthors of " arterio-capillary fibrosis " attach undue and due, not to a fibrosis parallel to that in the kidney,exaggerated importance to the appearance of fibrosis in but to a change common to the spinal cord and other

the kidney, he suspected that they over-estimated its im- organs, produced by the general arterial tension, andportance in other organs. that in some cases the spinal cord shouid be solely affectedThe PRESIDENT said that whatever might be the indi- might be considered a mere chance.-Dr. MAHOMED pointed

vidual opinions of members upon the question, the Society out the frequent occurrence of high arterial tension in in-must be unanimous in thanking Dr. Johnson for bringing dividuals who were not albuminuric, but who probably hadthe subject before them, and bestowing so much labour on its a gouty history, were given to excesses in eating andpreparation.-Dr. DICKINSON said that, while holding a drinking, or showed some cause of blood-contamination;different opinion from Dr. Johnson, he had not the slightest and he showed sphygmographic tracings token from suchintention of casting ridicule upon his views; on the con- subjects. Prolonged high tension must, as Dr. Dickinsontrary, hehad the highest respect for Dr. Johnson’s researches, said, produce thickening of vessels. This symptom of highseeing that he was an authority upon the subject when he arterial tension is one of great importance in arterio-

was "studying the bones." It was with some diffidence, capillary fibrosis; and many of the cu,ses of Sir W. Gallandindeed, that he differed from him in any respect. He would Dr. Sutton showed no evidence of renal disease. Fibrosisconfine himself to but one part of Dr. Johnson’s criticism, from congestion had long been known ; Sir W. Jenner andthat which related to the nature of the granular kidney. Dr. Handneld Jones had written about it. The occurrenceHe thought that hardly anybody at present held that this of arterial changes in kidneys atrophied from calculus mightform of renal disease was produced solely by changes in the be due to the underlying general condition, gouty or other-tubes. The more such kidneys were studied, and the higher wise, producing the calculus. He showed a tracing from athe microscopic power brought to bear on them, the more case in which the kidney weighed only three ounces; thereevident it was that there was a large quantity of rapidly was no increase of arterial tension, no hypertrophy 01 heart.growing fibro-nucleated tissue, an abundant nuclear forma- or thickening of arteries. Such a case was unexplained attion which could not be produced simply by the relics of present. Dr. Mahomed also pointed out that in acutedegenerate tubules. He was quite sure that when such Bright’s disease the passing off of the heightened arterialobservers as Sir W. Gull and Dr. Sutton and Dr. Johnson tension was an indication of improvement in the blood-came to different opinions upon a subject, their ob- condition, although dropsy and albuminuria might still beservations could not be erroneous, but that. they were present.probably viewing different sides of a real truth, and he The usual hour for adjournment having arrived, the Hon.himself believed the observations on both sides to be Secretary, Dr. Powell, proposed, and Sir W. Gull seconded,very nearly correct. He had examined arteries and tissues that the meeting be prolonged for half an hour in order toin various conditions of renal disease, and was sure of the complete the discussion that night.existence of a real genuine hypertrophy. By examining Dr. GowERS had brought a female patient the subjectalarge number of specimens much error may be eliminated; of chronic Bright’s disease, in whom the retinal arteriesand he held that Dr. Johnson had done good service in were distinctly smaller than normal, as could be well seenpointing out and insisting upon the fact of this hyper- in comparison with the veins. There was no other retinaltrophy. He bad also found the condition described by Sir change beyond a few small haemorrhages. The pulse wasW. Gull and Dr. Sutton, and was persuaded that the fibroid hard and incompressible, the heart evidently hypertrophied,coat of the arteries was thickened too, and that the change and the urine of low specific gravity. Dr. Gowers showedwas not due to reagents. He had examined specimens pre- also a drawing of the fundus oculi from another case, wherepared in various ways, and was fully convinced of the fact of the arteries did not appear to be contracted, but ratherfibroid thickening and of muscular hypertrophy. The changes thickened by fibrous tissue, appearing as white threads on thewere not limited to kidneys that were fibrotic. In almost sides of the arteries when examined by the ophthalmoscope.any condition of renal disease-in chronic nephritis, in It seemed to be a condition of periarterial fibrosis, and mustlardaceous disease sometimes, in degeneration following on be regarded as a local change consequent upon the renal dis-calculus, or in tubercular disease. He had thought that ease, and similar to the change described by Sir W. Gull andsome light could be thrown on the pathology of the subject Dr. Sutton.-Sir WM. GULL somewhat regretted that Dr.by examining the lesion in children, and to that end he had Johnson had extended his remarks over so wide an area. Hespecially studied the condition of the arteries in children had taken in points which Dr. Sutton and himself were stilldying from renal disease. He had found the heart hyper- going to inquire into, and Sir William protested against thetrophied and the arteries thickened (especially in their assumption that the pathological history of the fibroid kidneymuscular coats) in children dying from the results of acute was concluded. No communication in natural science cannephritis, whether due to cold or to scarlet fever, and that be said to be concluded ; certain parts may be, but freshin the short space of four or six weeks from the onset of discovery always opened up fresh paths of investigation.symptoms. The cardiac and arterial changes appeared to We were too prone to write the clinical history of Bright’sbegin almost simultaneously, and the muscular change was disease backwards from the lesions found in the dead-house;followed by a thickening of the outer coat of the affected but Sir William was certain that Bright’s disease neverarteries. He thought it might fairly be conceded that in began in the kidney, but that the renal changes were purelysuch cases the changes in question come on in consequence secondary to the general morbid condition. - He disclaimedof the renal disease, and are not due to a general morbid being styled an opponent of anyone holding different views;condition. Passing to consider the reason why the arteries he and they alike laboured simply to inquire into the condi-become thickened from the renal disease, Dr. Dickinson tions of disease, and if they turn out to be wrong theypointed out that increased arterial tension appeared and deserve as much, if not more, praise than if they were right,proceeded consentaneously with the cardiac and arterial for the exposition of their views leads to a fuller survey ofhypertrophy. There was clear evidence that the arterial the whole subject. It was so with the great discussionsystem was aboormally full of blood, as indicated by the about the origin of life from inorganic matter, andstate of the pulse and the action of the heart. It did not although he differed from Dr. Bastian in the positionmatter whether the obstruction was in the capillaries or in he had taken up, and thought that he would be shownthe arterioles. When the increased arterial tension did not to be in the wrong, yet science was very greatlyoccur, the arterial and cardiac lesions were wanting. Thus indebted to him for having caused a full ventilation

lardaceous disease there was no evidence of increased of the subject. Sir William was, therefore, much indebtedart’ial tension, and no marked changes in the heart and to Dr. Johnson for still maintaining his views, although he

the absence of tension being explained by Dr. Sib- could pot agree with him. When the paper by himself andcontinued discharge of fluid and consequent Dr. Sutton was written five years ago, they said that thediminutic in the quantity of blood from diarrhoea, sup- arteries seemed to be hypertrophied. Since then, after

puration, &c. Venous congestion may cause an organ to repeated observation, one of them still thinks there may bebecome fibrotr. and it might be supposed that increased slight hypertrophy of the muscular coat, but the other holdsarterial tension would cause thickening of the vessels it to be impossible. Sir W. Gull then read a passage from

425

the work of MM. Cornil and Ranvier, who cannot agreewith either view. They say that the vessels constantlyundergo very marked anatomical changes in interstitial

nephritis, the thick and rigid state of the arteries beingvisible to the naked eye, They say that although theexistence of the lesions has been known and described fora lon time, of late years the subject has been much dis-cussed by English authors. 11 M. Johnson rapporte l’indu-ration des parois arterielles a une hypertrophie de la tuniquemusculeuse." But now Dr. Johnson says the muscularcoat may undergo atrophy. The French pathologista, how-ever, do not agree with the opposite view, for they go on tosay, "Tandis que MM. Gull et Sutton la regardent commedue an dep6t d’une maS3e hyaline firooide ou hyalinegranuleuse infilrrant lps parois des artérioles et des capil-laires. Nous ne pouvons nous ranger A l’opinion de l’un ni desautres ......... And then attribute the change to a chronicarteritis. He would repeat that the clinical history ofchronic Bright’s disease was not a renal affection, but thatthe latter was part and parcel of a general change. Hewas indebted to Dr. Mahomed for his demonstration of thefact of increased arterial tension apart from renal affection,for he felt that it was in this direction that the conditionmust be studied. He was going, however, to take up thismatter in its clinical aspect before the Clinical Society. Thequestion of the etiology of these arterial changes, he main-tained, was a larger one than that of simply consequents ofrenal disorder. No doubt there is right in b:th theirviews, but the larger included the less, and the viewpropounded by himself and Dr. Sutton was the larger.-Dr. SUTTON, referring to the drawing criticised by Dr.Johnson, said that it showed projection of the elastic tissueof the interior, probably from contraction of the muscularcoat. He admitted the difficulty in distinguishing betweenthe circular fibres of the muscular coat and those of theadventitia when transverse sections of vessels were aloneviewed. He had seen many vessels which at first sightlooked as it’ the muscle were hypertrophied, but there wasalways the question as to how far such thickening might besimulated by contraction. Admitting that the muscle layerdid frequently seem to be thickened (and he had never seenit as much as four times the normal), how was one to knowwhat is the true size of the vessel examined ? a It was onlyby tracing vessels over a large area, and that could only beby examining them in glycerine, that an approximate ideaof their thickening could be formed. Another difficulty wasthe want of a sufficient test that this new material was notmorbid material and not healthy muscle. It looked far morelike fibroid tissue than muscular fibre. What criterion wasthere of the muscular hypertrophy-i. e., that the musclehas a strength greater than normal ? He had hoped thatDr. Johnson would have thrown some light upon these diffi-culties. He would simply add that the wavy folds of theintima might be taken as evidence of a contracted artery.With regard to the minute anatomy of granular kidney, Dr.Sutton said that there could be no doubt at all as tothe quantity of new material, spindle corpuscles andthe like, which could not be attributed to wasted tubules.-Dr. JOHNSON, in reply, said that Dr. Sutton bad not alludedto the intra-tubular changes, and that when the completehistory of the morbid condition was written these changesmust be included. That the heart was not hypertrophiedin lardaceous disease was probably because the diseased ves-sels offered less resistance than hypertrophied vessels did.The increased blood-pressure in acute Bright’s disease wasdue to the poisoned blood. He did not say that the ques-tion was completed ; but he said that he doubted if muchhad been materially added to the knowledge of the renalchanges since the paper in 1850.-Sir W. GULL said berefer:ei to the clinical history of the disease.-Dr. JOHN-soN did not in the least doubt that chronic dyspepsia andcontinued excretion of ill-digested matters very frequentlyresulted in disease of the kidney, and he agreed certainlythat granular kidney does not begin in the kidney. Ran-vier was probably referring to the changes in the largerarteries and not in the arterioles....... - Sir WM. GuLL:The words of Ba.nvier are "Artérioles et capillaires." -Dr. JOHNSON submitted to the correction. He could notaccept Dr. Sutton’s defence of the drawing he had referredto.The PRESIDENT announced that the Council had resolved

to appoint a Committee to investigate and report indepen-

dently upon the changes undergone by the arteries inBright’s disease.The Society then adjourned.

Reviews and Notices of Books.The Practitioner’s Handbook of Treatment; or the Principles

of Therapeutics. By J. MiLrrz;R FOTHERGILL, M.D.,M.R.C.P., &,^,. London: Macmillian and Co. 1876.THIS is a very readable bo,)k, and is well adapted for a.

young practitioner, or such as have a scientific educationwithout a corresponding acquaintance with actual practice.The author tells us that he has been labouring for nine

years with the definite design of producing the present work,which consists of twenty-four chapters.In the first chapter the necessity of a careful diagnosis

and a definite plan of treatment, rational if possible, or atall events selected from a well-chosen empiricism, eitherpersonal or acquired, is inculcated.The second chapter gives a clear account of the process of

assimilation, and of the function of the liver in connexionwith digestion. The different agents which modify or promote ’digestion are next considered.The third chapter treats of the waste matters, and the

albuminoid nature of the secretions, and gives a generalisedview of the excretory organs, in their community of originand function in relation to nutrition. In reference tothe ailments arising from imperfect elimination of nitro-genised matter the principal points to be attended to areindicated. A section is devoted to fsesal ansemia, due to

absorption of the secretions of the intestinal canal duringpersistent constipation among poorly-fed sedentary women,and to the necessity of getting rid of the noxious materialin the blood previous to the specific remedy being ad-ministered.In the fourth chapter, on Body Heat and Fever, the

source of heat is said to consist chiefly of the oxidation oflactic acid, in union with soda, in the minute capillaries ofthe body, by the liberation of the hydrocarbons (as glycogen)in the liver becoming sugar, and then splitting up into lacticacid, the permanent storage being fat. Then follows themanner in which heat is lost by the skin, designated a heat-losing external area, and in hot countries especially by thedilatation of the vessels of the skin, diminishing the quan-tity of blood circulating in the internal area, and conse-quently heat-producton.There is little of novelty in the fif;h and sixth chapters,

devoted to Inflammation and Anæmia.The chapter on Acute and Chronic Diseases discusses the

subject of acute disease becoming chronic, but it is chieflyremarkable for the theory of stimulants and of their action,first upon the heart, and secondly, upon nerve-cells.The chapter devoted to Diabetes, Rheumatism, and Gout,

is fairly written, but contains nothing of novelty; whilethat on Action and Inaction relates more than anythingelse to the physiological and therapeutical effect of differentagents on the nervous system, and is well worthy of perusal.And with this chapter the first half of the work terminates.We look upon the chapter on the Circulatory System as

one of the best, whether as regards the physiology of thesystem or as regards its appropriate therapeutics in disease,and more particularly as regards the chief agent by whichthe heart is acted upon. Nearly equally good is the chapteron the Respiratory System.In the chapter devoted to the Digestive System the author

reviews the various affections of the digestive tract, andpoints out the means, rational and empirical, by which they,and chiefly indigestion, may be treated. His own expe-