531

lower part of the trunk, and a short experience of cases ofthis disease will show a remarkable uniformity in the extentto which the lower half of the body is involved. You -willfind almost always that the paralytic affection in commonparaplegia ceases to give evidence of its presence about thelower dorsal or upper lumbar region. Numbness and

paralysis are not traceable above the lower margins of thethorax, ceasing often along a rather well-defined line. Theanatomical state of the substance of the cord found post-mortem to account for this is a condition of " softening "-i.e., a pathological state which is the same as that foundin the brain as a consequence of impairment of nutrition

by deficiency of the supply of blood. The causes ofthis condition are often obscure, but are in many casesevidently debilitating causes, such as in this verytypical case which I met with. An Irish dock-labourerhad been standing about the entrance of the docks forsome days without employment, and getting little food,when he felt pins and needles run up and downhis legs; and after he got home that evening he felt veryweak, and went to bed. In the night, being taken withdiarrhcea, he went from his bed, feeling very cold and feeble,and he could not return, being totally unable to move hislegs. This man lived about a year, his disease showing allthe characters of common paraplegia, and post-mortem ex-amination showed the lumbar cord in a state of " whitesoftening." This was one of my cases when I was clinicalclerk, and it puzzled me much to know why the poor manshould thus suddenly suffer from so chronic a change aswhite softening, and why he should only have symptomsjust up to the top of the lumbar cord, and never higher inthe whole course of his ailment; but I seem to know wellnow why it was. He was paralysed through starvation ofhis cord on account of the difficulties of supply to it, and theparaplegia did not extend above the lumbar cord, becausethe cauda equina does not extend above it, and the upperdorsal part of the cord obtained enough blood along shortarteries through which the blood pressure had been able toforce a sufficient supply. Indeed, the very different kindsof cause which agree in producing paralysis of the lower ex-tremities would show that there must be some such simpleand general explanation of its ready occurrence. An instancecame under my observation so like that of my poor docklabourer that the similarity of effect was as remarkableas the unlikeness of causation. It was in the personof a very well-fed and healthy female cat which suffered, Iam sorry to say, at my hands. A nest of thrushes was eatenby cats in my garden, and I thought it fair to retaliateby putting down a bowl of milk also containingprussic acid, and I warned a relative to keep her cat inbut, to my grief, next morning the only cat in trouble wasmy relative’s fine cat, which lay beside the bowl of poison ina curious state, quite paralysed as to the hind legs, butotherwise unaffected. The front paws were active andvigorous, so that she could pull herself about on the levelground by means of them, but the hind legs did not makeany movements for three weeks. I did what I could for her,but it was four weeks before the cat could leave the basketshe was placed in, and six months elapsed before she couldspring upon a wall ; after this she quite recovered, and hadseveral large families. Now, prussic acid acts by loweringthe tension of the blood after a slight temporary rise, andwhereas it is very difficult to suppose that the prussic acidhad any preferential power over the nervous centres of onepair of legs as compared with those of the other pair,it is, I think, quite readily to be accepted that as thehinder pair draw blood through longer and very slen-der pipes of vessel, the cat, lying with depressed cir-culation nearly dead all night, suffered so much in thenutrition of the end of her spinal cord that it became almostirrecoverable. Indeed, it is interesting to observe how thevery temporary action of the poison should have so damagedthe cord that it was six months in recovering, whilst thedamage was so adjusted that recovery was finally possible.Such an occurrence throws some light upon the curiouslyprotracted tenacity of injury on the part of the cord, whichthe history of paraplegia brings so painfully forward. Butit is not only prussic acid that affects the hind legs ofcreatures more than their fore legs. Although toxicologistshave paid no attention to the difficulties of circulation inthe lower end of the cord, so that no experiments have beenmade with the intention of developing this point, yet inreading through a book on Materia Medica one finds re-peated examples of drugs which are depressants of the cir-

culation, and which paralyse the hind legs of animalswithout affecting their fore legs. Among these I mentionaconitia, conia, and, doubtfully, veratria and chloral. Withreference to prussic acid, it is said to benumb the hind legsfirst.Again, for other instances, take the very complete para-

plegia of the lower extremities which so much impressedDr. Bristowe in the highly interesting cases of Rupture ofAbdominal Aneurism, which he recently published. Surely,if we consider the mode in which the arterial supply of thespinal cord would be reduced by the bursting of the aneu-risms, the paraplegia in these cases is immediately compre-hensible. Again, if we take the so-called urinary paraplegia,or functional paraplegia of any kind, including what iscalled hysterical paraplegia, we find these affections nevertroubling the upper limbs, but always the lower. And Ithink the point I have raised will suggest lines of investiga-tion that may throw great light on this obscure class ofnervous diseases. I believe that it is by impediment to theexceedingly and peculiarly difficult blood-supply of thecaudal end of the spinal cord that all these variousconditions lead to paralytic weakness of the lowerlimbs, and they are to be met by conditions improving thecirculation if possible. Why the lumbar cord should bethus straitly supplied is an interesting question. Perhapsit may be connected with a necessity that the economyshould be so organised as to feel fatigue early enough in theparts which directly put forth exhausting exertion, leststrain of effort should first overtake more vital parts thatsecondarily share in all such exertion. In short, the cordis supplied scantily, so that we should sit down when wehave walked enough, and lie down when we are tired, andespecially that we should, if necessary, fall down whenfaintness overtakes us, to the end that in the horizontalposition the circulation may be able to restore itself.

Gulstonian LecturesON

A N Æ M I A.Delivered before the Royal College of Physicians,

BY SIDNEY COUPLAND, M.D., F.R.C.P.,PHYSICIAN TO THE MIDDLESEX HOSPITAL.

LECTURE 11. -part I.

Idiopathic Ancemia: Earliest Recognition of it by Addison-Records of Cases (1851-1871) by Barclay, Lebert, Wilks,Habershon, King-Gusserow-Biermer-’s New Departure(1871)-Growth of its Literature in the last Decade-TVide Extension given to the Term" Pernicious " -Clinical Features of "Pernicious" Ancemia - Onset -Progress-Digestive, CÙculatory, and Nervolls Symptoms- Hcemorrhage-Irregular Pyrexia-Duration - Termi-nation in Recovery-In Recovery followed by Relapse-In Death-Post-mortem Appearances.MR. PRESIDENT AND GENTLEMEN,-It is impossible to

speak of idiopathic anaemia, without reference to Addison,for he it was who seems to have distinctly called attentionto a class of cases in which ansemia is the prevailing sym-ptom from first to last-an anaemia not depending uponrecognised causes, not associated with wasting of the tissues,but insidious in its onset and slowly downward in its pro-gress, revealing after death no changes but those of fattydegeneration, especially of the heart. The passage in whichhe summed up his experience of this condition occurs earlyin his essay on Disease of the Suprarenal Capsules. This

passage has been so often quoted that it is hardly necessaryfor me to repeat it now, much as I am tempted to do so, forit is a model of a succinct summary of clinical observation.It was written in 1855, but Addison’s observations dated farbefore that period, and indeed he described the condition in

1 See Addison’s Collected Works (New Sydenham Society), p. 212.The passage is quoted by Dr. Pye-Smith in Virchow’s Archiv, vol. lxv.,p. 507 ; by Dr. S. Mackenzie, THE LANCET, 1878, vol. ii., p. 799; byDr. Finny, Brit. Med. Jour., 1880, vol. i., p. 5; and many others.

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his lectures as early as 1843.2 There is no doubt also thatsimilar cases had been observed, and a few recorded aboutthe same period. In 1851 Dr. Barclay published the notesof two fatal cases of anaemia8 occurring in St. George’s Hos-pital. One was the case of a man aged thirty-four, admittedunder Dr. Page on Jan. 21st, 1852. He had been ailing fortwelve months, and had suffered from inconstant achingpain in the loins, accompanied by scanty, loaded urine. Hehad lately lost flesh and had a slight cough, was remarkablypallid, complained of shortness of breath and palpitation;pulse 120, and very weak; and he suffered from constipa-tion. There was deficient breath-sound at both apices,especially the right, where it was distant and tubular; therewas then no cardiac murmur. A fortnight later he wasattacked by vomiting. A bellows-murmur with the systoledeveloped, best heard in the mid-praeeordia and towards theapex. He rather rapidly passed into a state of exhaustion,ending in coma, on Feb. llth. Mr. P. Hewett, who madethe autopsy, found the body well nourished, the brain veryanaemic, a few extravasations in the pia mater, cretifieddeposits at the apex of the right lung, emphysema else-where, the posterior parts being engorged with frothy serum.The heart was healthy and pale, but contained largefibrinous clots in all its cavities. The abdominal viscerawere bloodless, and a few cysts were observed in the leftkidney. The dark and healthy colour of the muscles wasobserved in contrast with the pallor of the integument, andthe extremely yellow colour of the subcutaneous fat wasalso noted. The other case was that of a married womanwith several children, admitted under Dr. Wilson, Jan. 29th,1851. She had not been well since her last confinement,four months before; had been weak, but had not sufferedfrom haemorrhage; she had, however, been troubled withdiarrhoea for two months previously. She was extremelvansemic; pulse quick, feeble, and empty; appetite bad;urine scanty and loaded; her only complaint was of generalweakness. The diarrhoea was checked by remedies, but shedid not gain strength. She suffered from insomnia, and hadsome attacks of dyspnoea, after one of which she died, aboutthree weeks after admission. The post-mortem examinationby Dr. Ogle revealed the pallor and slightly yellowish tintof skin, slight oedema of the lower extremities, great pallorof abdominal walls, fatty kidneys, frothy serum in thelungs, some ecchymoses in the larynx, a healthy heart con-taining little or no coagulum, but a small quantity ofsemi-fluid blood.

Lebert, too, in 1853 had recorded cases of fatal " puerperalchlorosis " at Zurich-the seat of the subsequent observa-tions of Gusserow and Biermer-and had spoken of theseas examples of what he regarded as an " essential anaemia."Then, however, a long silence on the subject occurs inmedical literature, broken only by the publication in Guy’sHospital Reports for 1857 of a series of cases by Dr. Wilks,under the head of " Idiopathic Fatty Degeneration," and ofa case in THE LANCET for 1863,4 by Dr. Habershon in apaper on this subject. The patient in this case was a sparewoman aged forty, who had for many years been subject toattacks of vomiting, which for eight months before heradmission had been almost of daily occurrence. She hadmuch gastralgia, pain in the back and limbs, and was verypallid. The attacks of pain were renewed with muchseverity. She, however, improved, and left the hospital,to return a year later, " blanched, emaciated, and extremelyfeeble." No gastric disturbance was present now, only anextreme degree of asthenia and anaemia, under which shesank in two months. The necropsy by Dr. Wilks disclosedonly intense anaemia of organs, marked fatty degenerationof the heart, and slight, passive effusions in the serous sacs.Thus, these observations showed that in the hospital of Addi-son, at any rate, the existence of the disease was recognised ;and Dr. F. Taylor did good service in collecting all the casesobserved there up to the year 1878-namely, as many astwenty-three.

Curious to learn whether the like experience had befallenthe physicians of the Middlesex Hospital, I have searchedthe post-mortem records for any fatal cases which could bethought to have belonged to this class, and from 1844 to 1871(excluding 1852 and part of 1851) I can find only one un-equivocal case, which, it will be seen, was associated with acertain amount of gastric disease. This case occurred in1865, its subject being a woman aged fifty-one, who was

2 See Dr. S. Mackenzie’s Lecture, loc. cit.3 Medical Times, 1851, vol. i., p. 480. 4 Vol. i., p. 518.

admitted for extreme anaemia three days before her death.No satisfactory history could be obtained, save that she hadbecome rather rapidly anaemic. The skin was of a peculiaryellow hue, and she suffered from constant vomiting duringher brief stay in hospital. After death the sallowness of thesurface was noted, also a considerable layer of subcutaneousfat. There was effusion in the serous sacs, and oedema of thelungs. The heart was of normal size, contained a little fluidblood-no coagula, but the condition of its walls is notrecorded. There was slight atheroma of the aorta. Thespleen was small and normal ; the kidneys small, and theseat of a few minute cysts. The gastric mucous membranewas thickened in the pyloric region and the seat of a smallpolypus. Recent haemorrhages had occurred under the duramater, and the brain was bloodless. Of other cases whichcome less clearly under this category I find one in 1844, of a.woman, complicated by old pulmonary tubercle and recentpneumonic hepatisation ; one of a boy aged eight, in 1857,thin and sallow, with slight serous effusions, ecchymoses inthe heart, which is described as "yellowish, mottled, andvery fatty," the liver of a deep yellow-brown colour, withbleeding points and white specks on the surface ; and one inthe same year of a man aged thirty-five, who died suddenlyof fatty heart. These practically comprise all the cases

within the period mentioned, with evidences after death ofextreme ansemia and cardiac degeneration ; other cases

being chiefly those of cancer, renal disease, and purpura, oneor two of which latter might possibly belong to the class inquestion. In 1871, however, an undoubted case occurredunder Dr. Greenhow’s care, and was published by my friendand former colleague, Dr. R. King, then medical registrar.I shall give the details of this case subsequently, but men>

tion it now because its publication, antedated by a few weeksthe appearance of an essay by Biermer, which did more thananything else to draw general attention to the subject.

Biermer’s work must be taken in connexion with that ofGusserow (for both laboured in the same field), who in 1871published six cases of a fatal form of ansemia in pregnantwomen. Biermer, who had previously related a case beforea society at Dresden in 1868, described and summarised inthe essay referred to fifteen cases of a "peculiar form ofprogressive pernicious anoemia, usually accompanied byfatty degeneration of the circulatory passages, and, secon-darily, by haemorrhages of the skin, retina, brain, and itsserous membranes." This publication marked a distinctdeparture in the knowledge of this disease, and its takingand rather startling title assisted to draw attention to it.From that time to this, just ten years, a whole literature hassprung up around the subject.5 For a time it was eventhought that in this " progressive pernicious anaemia" ofBiermer a new disease had been discovered, but Drs. Wilks,Taylor, and Pye-Smith reasserted the claims of Addison, andproved conclusively that no new discovery had been launchedupon the world. Nor has the new nomenclature been with-out its drawbacks. It designates more than is implied bythe term "idiopathic," much as we may wish to banish thatterm from nosology, and it has rather obscured than em-phasised that leading fact of the condition described byAddison. For by the use of this terminology authors havebeen led to class together cases of ansemia depending onknown causes with those truly " idiopathic," and some evenspeak of the supervention of pernicious ansemia in cases ofcancer, for example. I shall show that this extension isperhaps justifiable provided that at the same time a distinc-tion be made between the cases which arise spontaneouslyand those where the anaemia is obviously secondary. At

present I will merely state my belief that pernicious ansemiaincludes, but does not comprise, idiopathic anaemia.

I have collected 110 cases, including most of thosementioned by M. Lepine in a review published in 1877. Thenumber might, I believe, well be doubled, before embracingall those cases which have been recorded. Seldom has sucha mass of evidence bearing on any one disease been accumu-lated in so short a time ; and yet it is not possible to arriveat a satisfactory solution of the question of its origin. Itpresents m, however, with the symptomatology of anaemiain its most severe form, and throws light upon the mostmarked lesion produced by ansemia,. Of these 110 cases, 56were males and 54 females. The ages at which the patientscame under notice-often, that is, only a short time before

5 An analysis and review by M. Lepine in 1877 (Rev. blensuelle) hasfacilitated reference to this literature, but much has appeared and continues to appear since that time.

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death-varied with the sexes, for among the male cases themajority-viz , 33 or 59 per cent., occurred between the agesof forty and sixty ; and among the female series-34 or 63per cent.-between twenty and forty.

Somewhat different statistics are given by Hermann Miillerof Zurich,6 who describes 44 cases from Prof. Biermer’s clinic,9 only being males, and 28 of the 35 females being betweenthe ages of twenty and forty.

U_’- --u.’-

The preponderance of females corresponding to the period ofchild-bearing.The onset of this severe affection is sometimes quite

sudden-in such cases following severe mental shock or

some violent emotion ; or a profuse haemorrhage, which atthe time may threaten life, leaves behind it an anaemiawhich never disappears, and may become pernicious-i.e.,may deepen in intensity in spite of treatment. More com-

monly this exciting cause is added to a pre-existing andlong-standing anaemia, which then takes on a fatal form, orthe determining event may occur in some other exhaustingdischarge. Leaving for the present the consideration ofthese prodromal influences, I may simply state now that inmany cases the onset is gradual and insidious, having per-haps in some cases a foundation in conditions of blood im-poverishment, but in others arising quite apart from suchconditions. Or the patient may have been always below thestandard of health as regards blood; may have suffered morethan once from extreme anaemia, and have regained the pre-vious level, to be finally again lowered beyond restoration.However this may be, the symptoms which usher in the con-dition can all be attributed to it. There is a growing pallorof the skin and visible mucous membranes: a pallor fre-quently mingled with a yellowish tint, and even with aslight degree of actual jaundice ; and the face becomes wax-like in appearance. At the same time there is an increasingdisinclination for physical exertion, partly from mere list-lessness, partly from the breathlessness and palpitationwhich any physical effort evokes. The nutrition of the bodyis often well preserved; there may be, as Addison remarked,even an excessive amount of cutaneous fat. Then, as theblood becomes more impoverished, dropsical effusions mayappear in the eyelids and lower limbs; but such oedema isnot a constant symptom, and is generally late in its appear-ance. With the muscular asthenia there is often complaintof pain in the limbs or back; and headaches, vertigo,and tinnitus are frequent. Sleep is sometimes, but not

usually, heavy, a lethargic, drowsy state supervening to-wards the end, which may pass into semi-coma. But in-somnia is a more constant symptom. Delirium may occurat the close, and sometimes convulsions. On the side of thedigestive system there is generally loss of appetite, it maybe with actual intolerance of food, and dyspepsia with

6 Die Progressive Perniciòse Ansemie. Zurich, 1877; kindly lent meby Dr. Pye-Smith.

nausea and vomiting are common. Indeed, vomÜing standsout prominently among the symptoms of the disease, so

common, so frequent, and so early in its occurrence as tolend support to the view of Drs. Flint and Fenwick as tothe essential dependence of obscure and fatal anaemia uponprimary gastric derangement. Although in some cases suchvomiting and other symptoms of gastro-intestinal distur.bance do precede the appearance of the weakness and pallor,yet it is not always so. Thirst, too, is marked in manycases. Gastralgia and epigastric tenderness are generallyassociated with the dyspeptic symptoms. Then, as to theintestines, diarrhoea is almost as often met with as vomiting,occurring sometimes early in the disease, sometimes justtowards the close, which it determines ; and although it isamenable to treatment it may recur again and again withmuch severity. Constipation is not so common as diarrhoea.As a rule, in the earlier stages, the breathing is quiet,

except on exertion, which induces marked breathlessness ;but sometimes, at an advanced stage, attacks of dyspnaea arefrequent and painful, and may lead to a fatal result. In thecases I have had the opportunity of reading I have not foundthis dyspnoea recorded as being of the peculiar ascendingand descending rnyt’1m, with a period of apnoea, known asCheyne-Stokes respiration. The association of that type ofrespiration with fatty degeneration of the heart was noticedby its discoverers, and though it occurs under other condi.tions also-e. g., uroemia, cerebral haemúrrhage, embolism,&c.-yet its association with fatty heart is still accepted.As such degeneration is the most constant morbid lesion ofanaemia, it is at least singular (if it be a fact) that this typeof dyspno-a does not occur. As a rule, unless there be olddisease in the lungs, there are no abnormal physical signs,except towards the end of life, when these organs becomeengorged, and serous effusions may take place in the pleura.Attacks of syncope are liable to occur, but do not seem to

be so frequent as might be imagined. The action of theheart is generally regular and quick, often very feeble. The

impulse is often widely visible, undulating, and thrilling;the area of prascordial dulness laterally increased, signsattributed by some to retraction of the lung, by others todilatation of the heart itself. The so-called 11 boemic " bruitsare commonly, but not invariably, met with; a systolicblowing murmur at the apex and xiphoid cartilage, a bruitof coarser character simulating pericarditic friction at thebase. The large arteries of the neck often visibly pulsate,and are the seat of loud murmurs. The jugular hum isseldom absent, and pulsation of the jugular vein is oftenobserved. The pulse is soft and compressible, quick,jerking, and empty.

In all these symptoms there is nothing peculiar or special.They simply denote the presence of an anaemia of pronounceddegree, but there is one group of symptoms which occurs withsuch frequency in those severe forms as to be almost re-garded as distinctive of them. I refer to the supervention ofhaemorrhages, and here it seems to me important to makesome reservations. In several cases haemorrhages of onekind or another-e.g., epistaxis, menorrhagia, take place inthe prodromal period, and antedate the development ofthe anaemia, which they have much share in producing.Such haemorrhages must be distinguished from others, oftenquite as profuse, which follow upon the appearance of theanaemia, and when appearing they add greatly to the in-tensity of the disease. In a case the particulars of whichI shall presently narrate the patient had been anaemic, andprogressively so, for years ; then supervened profuse men-struation, and finally a severe uterine haemorrhages whichnothing would check till it carried her off. Epistaxis, too,is common as a secondary result. Sometimes cerebralhaemorrhage may ensue and carry off the patient, but this isnot common. More frequently towards the close of lifepetechial and purpuric eruptions occur, and beneath serousmembranes, and the dura mater ecchymoses are common,as well as in the substance of mucous membranes. In one

very curious case, both in its rapid development, intensecharacter, and as rapid recovery, recently recorded byLachmann from Riegel’s Clinic at Giessen there developedduring the progress of the anaemia a considerable tumour inthe iliac region, with oedema of the lower limb on that side ;from its physical characters and manner of disappearance itwas conjectured (and with probable truth) that this swellingwas due to a haemorrbagic effusion beneath the peritoneum.The patient was a young man of nineteen, and the anaemiahad developed rapidly withno other exciting cause than heavywalking through snow. That patient, like the great

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majority of those in whom the anaemia is protound,presented retinal haemorrhages. These haemorrhages andthe other retinal changes, oedema of the disc, andneuro-retinitis have been described and figured by Drs. S.Mackenzie and Gowers, the latter of whom says :-" Theextravasations are often numerous, and more or less striatedor flame-shaped from their situation in the layer of nerve-fibres. They are usually most abundant around the opticnerve-entrance. They are frequently associated with whitespots and areas, due in part to leucocyte-like cells, in partto degeneration in the disturbed retinal tissues. Occa-sionally a pale spot may occupy the centre of a smallhaemorrhage. "7 7 Quincke in his 31 recorded cases met withretinal haemorrhages in all but 7-and notes the rapiditywith which they disappear. We cannot, I think, regardthem as invariably present; although their existence is a Ivery valuable indication of the advanced stage of the disease.Moreover, as they are not commonly met with in other formsof anaemia, their presence has a certain diagnostic as wellas prognostic value ; but on the latter point Quincke givescases which have recovered. Of the 110 cases (which includeQuincke’s) there are only 39 in which the ophthalmoscopicexamination is recorded, and in 30 the haemorrhages werefound, but only 17 were fatal cases, 1 left unrelieved, and nofewer than 11 were regarded as recovered. Of the 9 casesin which these haemorrhages were absent, 6 were known toend fatally. I should not like to lay much stress upon suchmeagre statistics ; especially as it is possible that the traces- of previous haemorrhage might have escaped the observers;but so far as they go, they point to this-that retinal haemor- Irhages do not imply a fatal termination, and that their z,absence does not necessitate a favourable prognosis.

’

There is usually no enlargement, or to only a slightdegree, of either liver or spleen or lymphatic glands, and inonly a very few cases has any special tenderness been notedover the bones.Albuminuria, slight and transient, has been noted ; but

as a rule the urine is free from this abnormal constituent,of low specific gravity, mostly pale, sometimes high coloured,,and deficient in urea and uric acid ; but the latter consti-tuent is not diminished in proportion. Chlorides are re-

- duced (Hugenin), but the excretion of phosphoric acid issaid to be increased relatively to the nitrogenous matters(Edelfesen). A marked indican reaction was always observedby Hugenin. Inonecase recorded by Dr. Finny of Dublin8 theinteresting observation was made by Dr. Emerson Reynoldsof an appreciable quantity (viz., 0-308 grain in 72 ounces-of urine) of iron in the urine sixteen days after treatment byiron had been discontinued.There remains another symptom of peculiar significance-

viz., pyrexia. The charts before you, both from marked 11cases of the disease-one by Immermann, the other by IQuincke-illustrate the irregular course taken by the tem-perature, and this often without any concomitant changes ;appreciable in the patient’s condition. The former (Chart 1)9 Iis that of a single woman aged thirty-one, who was under Itreatment at Basle from August 23rd, 1872, to September i19th. The case is of some interest, for she had chloroticsymptoms develop when the catamenia began, at the ageof seventeen; but apparently recovered completely. Thesymptoms dated from three weeks before admission, whenshe became feverish and lost appetite, and ansemic. Theanaemia rather rapidly increased, and with it its cardio-vascular signs developed, but no retinal haemorrhages. An

appreciable hemiparesis of the facial muscles and of the

tongue made the diagnosis difficult, so that the possibility ofulcerative endocarditis was entertained. Some diarrhceaoccurred towards the close of the case. Slight splenicenlargement (no increase of white corpuscles) was also

present. The post-mortem examination revealed, in addi-tion to an enlarged firm spleen, only the ansemic con-

dition of organs and fatty changes met with in perniciousansemia. No brain lesion was found to account for thefacial and lingual paresis. The other case (Chart 2,Case 11 in Quincke’s series), is that of a woman thirty-three years of age, who had been married nine years andhad two children, the younger of whom, aged four, shehad suckled for six months. She came into hospital onMay llth, 1876, having for five months suffered fromdebility, palpitation, and vertigo. She lived in very poor I

7 Manual of Medical Ophthalmology, p. 190.8 Brit. Med. Journal, vol. i., p. 44. 1880.9 Deutsches Archiv fiir Klin. Med., xiii., p. 233.10 Deutsches Archiv filir Klin. Med., xx., p. 1.

circumstances, and was auuiHjHid. 111 au eXLleUl<5iY vveukand anaemic state. Cardio-v ascnlar signs of anaemia weremarked; there were retinal haemorrhages and oedema, andthe blood showed marked variations in the red corpuscles,their numbers being only 143,000 per cubic millimetre(l-38th). Transfusion was performed on May 24th, and thechart shows the course of the temperature f<’r the followingdays, so that its irregularities must, I suppose, hnrdly beconsidered as due to the anaemia alone. This patient re-covered, left the hospital on Aug. 25th, and was "een againin November, looking well-nourished and healthy. The

CHART 1. (IMMERMANN.)

third chart (No. F) n one wbme profuse menorrhagia wasadded to the ansen ia, the details of which I propose to givepresently. As a rule, the temperature is liable to suddenexacerbations, sometimes reach]Dg remarkable heights (in oneof Dr. Finny’s cases lOGo) from a normal or nearly normallevel; or it may have a more or less continuous course, variedby such exacerbations. Exceptionally there is no abnormalrise of temperature throughout. The apparently pprarloxicalevent of fever occurring undH conditions of diminishedoxygenation&mdash;as in anania&mdash;is discussed by Inmnermann,who points out that the same ob’ains in levikbamia and

CHART 2. (QUINCKE.)

9 Transtusioii. Collapse during operation, followeti bysnsatlOn of c"Jd, but 110 1l1!"r. ’llJgor. t 1’10Ulthis date the couise vaa ttp)n.x:a.).

Hodgkin’s disease-between which affections and ai)8em!athere is the common link of poverty in red corpuscles. Heshows also that the temperature rises after copious yenesec-tion ; and the instability of temperature in aJ ceiiiie conva-lescents is well known. He is inclined, then, to relate thepyrexia to the reduction in red corpuscles helow certain

point ; not that it is produced by increased metabolism, butby the decay of the tissue elements-their conversion fromcomplex unstable compounds ihto more stable substances-a conversion which must be accompanied by the setti1,g freeof heat, although not requiring increased oxidation. And to

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this increased heit-production, combined probably withhe.tt-!etention, h’) attributes the " anmmic fever" of thesednea-ies. The blood has, when examined, been found to bealtered; but I will speak of that when I come to discuss thepathoeny of the disease.

It is not easy to fix the duration of many cases. The

patients themselves cannot tell when their anaemia, began,and some have been, they say, pale all their life. Of theseries of cases I have collected (viz., 110) I find that in32 the total duration of symptoms was from one to sixmonths ; in 24 from six to twelve months; in 25 from oneto two years ; and the remaining 12 for periods exceedingtwo years. As many writers only speak of many weeks ormonths, such estimation does not include all the cases ; andin those cases where the symptoms date back only a fewweeks there is often found a history of some antecedentanaemia or a period of variable length of slight languor andill health.There can be no doubt that pernicious anaemia is not in-

variably fatal. Cases of recovery have been recorded byQuincke and others, where all the symptoms have beenmarked. Dr. Finny gives a striking case, and of the seriesto which I have so frequently referred no fewer than twentyare regarded by their observers to have recovered. Some ofthese did recover perhaps permanently, but of this it is notpossible to speak with certainty, the last-recorded note oftenreferring to them as being in perfect health ; and these werecases which clinically were indistinguishable from those thatran a lethal course ; some of them undoubtedly were rescuedby prompt transfusion, and others got well under medicinaltreatment; but their occurrence is encouraging, the naturaltendency of the disease being undoubtedly towards death. ’,Four ca,es passed away unrelieved; and 4, after an appa-rent recovery lasting a few weeks or months would relapseinto the previous state, to again be temporarily restored tocomparative health-once more to relapse without possibilityof recovering. The greater number, however, die (86 out of110) sooner or later (4 of these after temporary recovery andrelapse). the mode of death being a simple asthenia andexhaustion, or passage into a comatose condition, or insyncope, or bv dyspnoea, or convulsions. To briefly para-phrase MiiHer’s vivid description of the manner in whichdeath approaches : the distress attains a painful intensity,sleep i3 hindered by the constant beating in the head, thehum and roar in the ears, whilst the faculties became dimand unspeakably dulled. Vertigo and headache grow sosevere that even sunlight causes pain. The prostration andweakness are so great that spontaneous effort is annulled, andthe slightest movement, even the weight of the bedclothes,is irksome, and the patient groans and sighs in his distress.Now and then, towards the close, the hunger for air growsexcessive, complaints are made of the painfulness withwhich every breath is taken, and relief is begged from thistonnentmg need. Some become so feeble, and sink into sodeep a lethargy, as to cease to take interest in anything,or they lie impassive, breathing deeply and heavily, pale asa waxen figure, motionless as a corpse. Others toss rest-lessly from sice to side, and in their delirium make vainefforts to escape, and then die suddenly from exhaustion.What is this but the picture of death from loss of blood-aloss, not from haemorrhage, but from impoverishment of theblood in its chief elements ?The post-mortem appearances show extreme pallor of the

surface and viscera. There is often a considerable amountof subcutaneous fat, and frequently slight cederna of thelower limbs. Dropsical effusions, never to large amount,occur in the serous sacs. The blood is fluid, thin, andwatery, and scanty, pale clots are mingled with the fluidblood in the chambers of the heart. H&aelig;morrhages are metwith in the form of subcutaneous eccbyoioses, and similarextravasations benea’h the pleura, pericaidium, intestinalmucous membrane, and in the pia mater. Sometimes bloodeffusions of large amount occur in the latter situation. Butthe brain is pale, bloodless, and " wet" from oedema. Thelungs are generally cedematous, and, owing to the fluidity ofthe blood, appear engorged in their dependent parts, con-trasting with the marked ansemia, of their other portions.Almost without exception the heart is in a state of fattydegeneration ; its walls are pale, flaccid, and friable ; theinterior of the ventricles, particularly of the left ventricle,,how irregular whitish striae running transversely across themuscular bundles, and especially the papillary muscles, anappearance to which Dr. Quain gave the name of "tabbycat"striation. Microscopically the muscular fibres are pale,

and destitute of striation, granular, or’ loaded withfatty molecules and cell globules of various sizes. Opaquepatches of fatty degeneration occur on the mitral valve andstud the lining membrane of the aorta. Fatty degenerationof the intima of the smaller arteries, and even of capil-lary walls (especially in the retina) are observed, andserve to explain the liability to their rupture and hoemor-rhage. Sometimes, but not invariably, there is fatty de-

generation of the liver and kidneys. The spleen, lymphaticglands, and supra-renal capsules do not show any changesfrom the normal (except sometimes slight enlargement of thespleen), but in some cases the bone-marrow is found to be ofa red colour and to show microscopical evidence of markedhyperplasia.Such in brief are the essential features of progressive

ansemia.

ON A CASE OF

CAROTID ANEURISM TREATED BY DIGITALCOMPRESSION AND SUBCUTANEOUS

INJECTION OF ERGOTIN.

BY EDWARD BELLAMY, F.R.C.S.,SURGEON TO CHARING-CROSS HOSPITAL, HON. FELLOW OF

KING’S COLLEGE, LONDON.

I MAY mention at starting that, although I cannot recordan absolute cure in this case, there was such marked anddecided improvement that I feel convinced had my patientallowed an extension of the treatment adopted I should havebeen enabled to add another to the list of successful cases of

digital compression. As to the action of the ergotin I amsomewhat sceptical.

Mrs. C-, aged sixty-five, stout and florid, was broughtto me in March, 1880, by the late Dr. Campbell, of West-bourne-place, with an aneurism at the root of the neck onthe right side. After most careful examination, institutedon several occasions, before I began treatment, I madeout that the aneurism was situated at the commencement ofthe right common carotid, and that, as far as my diagnosiswent, the innominata was free. The tumour was freelyexpansile in all directions, was increasing, and the " whirr-ing " noise well heard even without the stethoscope. Theinternal jugular vein was not compressed, and there wasconsequently no venous congestion of that side of thehead and face. No difficulty in swallowing was com-

plained of, neither had the tumour caused any displace-ment of the clavicle. There was no dyspncea. The sacwas very thin, and, in one point in particular, felt asthough it might give way at any moment, more especiallyas my patient was an active woman, with a strong will of herown, and accustomed to take a great deal of pnysical exer-tion. The skin over the aneurism was movable and notreddened. The pupils on both sides were equal, and re-sponded in the same degree to light. No difference could bedetected in the temperature of the two sides of head andface.

Mrs. C- decidedly objected to any "operation,"andwould not hear of it; yet, as far as I could judge, both from itsposition and the ease with which the trunk of the vessel abovethe tumour could be got at, it would have been a suitable casefor distal ligature. Moreover, she would not hear of ananaesthetic for the rapid method of pressure. I noticed,however, that Chassaignac’s tubercle (transverse process ofsixth cervical vertebra) was very distinct, and that the vesselseemed of normal lumen as it passed over it. I thereforedetermined to try digital pressure on this tubercle, not withsuch force as to occlude the artery entirely, but to slow anddiminish the current through the aneurism.As Langenbeck, Dutoit, and others had apparently had

such good results with the assistance of the injection of thewatery extract of ergot, I determined to give it a trial, andbefore the first day of pressure (March 9th) I injected sub-cutaneously in the neighbourhood of the tumour two grains,dissolved in one part glycerine to five of alcohol. On March10th, with the help of my late colleague, Mr. Amphlett, andMessrs. Whitehead, Clarke, and Tuiton, I commenceddigital pressure on the vessel over the tubercle.The pressures were maintained on the succeeding days as