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In six the only foci that could possibly be primary werefound in the lymphatic glands of the mediastinumalone or along with those of the mesentery. In threethe lungs were the only organs affected, and in one

the lungs and mediastinal glands contained the oldertubercle nodules. He had also pointed out at the same timethat, in children, mesenteric or abdominal tubercle was theform far most frequently met with, and had tried to show theconnexion between abdominal tuberculosis and tubercularmeningitis, especially in cases where there was tuber.cular peritonitis or extensive affection of the mediastinaland retro-peritoneal glands. It appeared that therewere two channels by which tubercle made its wayto the base of the brain, in addition to the more com-mon form of generalisation by an embolic process.The first of these is best seen where there is anytubercular menicgitis, in which the retro-peritoneal glandsare affected, and where the chain of posterior medias.tinal glands becomes the channel of infection. In thesecond form there is usually tubercular peritonitis. Wehave the tubercle usually spreading by the lymphatics ofthe diaphragm behind the sternum, the small glands behindthe xiphisternum being invariably affected, and then passingalong the posterior meoiaatinal glands, but also affecting thepost-sternal chains of glands on either side ; for it was foundthat wherever there was tubercular meningitis, one or otheror both of these sets of glands were invariably affectedwhere there was any probability of abdominal tuberculosisbeing the primary source of the disease.

Dr. Woodheadgavesomecorrespondingcases in guinea-pigs,as he thought they would prove ot some interest. On Aug. 1st1 cc. of sterilised milk from a cow with a tuberculous udderwas injected intra-peritoneally into a strong buck guinea-pig. On the 19th, from the appearances presented, we at oncesuspected that there must be some meningitis. On openingthe abdominal cavity, there was well-marked tubercle at theseat of inoculation in the lumbar glands, in the peritonealcavity, in the omentum, in the glands in the lesser peritonealsac, and in the mesenteric1 and retro-peritoneal glands ; inthe liver, small grey points and large bile-stained nodules ;whilst on the under surface of the diaphragm there was aplentiful crop of typical miliary tubercle. The spleen, theglands immediately behind the sternum and in the falsiformligament, immediately behind the xiphoid cartilage andabove the diaphragm, were tuberculous; whilst behind thesternum the glands between the clavicle and the first rib andbetween the third and fourth ribs on either side were alsotuberculous. In the diaphragm the tubercle nodules wereconverging from the margins towards the central tendonson both the pleural and peritoneal surfaces. The lungswere somewhat collapsed at points; there were some earlycatarrhal pneumonic patches, probably tubercular,but therewas no miliary tubercle. At the base of the brain therewas a considerable accumulation of fluid and some slightthickening of the pia mater, with one or two suspiciousgrey points in the interpeduncular space. In order todetermine whether this was a case of tubercular meningitistwo guinea-pigs were inoculated, and from these two otherswith an emulsion of the brain in sterilised broth. In alltubercle was developed, so that there could be no doubt thatthe accumulation of fluid in the first case was due to aslight tubercular inflammation at the base of the brain.In order to test the virulence of the milk from tubercular

cows, for quite a different purpose, a considerable numberof guinea-pigs had been inoculated intra-peritoneally intothe abdominal cavity, killing them with chloroform-although they were usually outwardly in splendid condition-as soon as the tubercle was thought to have had time to de-velop, at least six weeks being allowed in most cases. In allof them very much the same condition as regards the spreadby the diaphragm and by the two chains of glands abovementioned was found. A number of feeding experimentshave also been made, the animals being killed in the samefashion. Here, especially where there has been tubercularulceration and enlargement of the mesenteric glands, theretro-peritoneal and the posterior mediastinal glands havebeen found to be in an advanced stage of tuberculosis.

Dr. Woodhead, at the close of the lecture, gave a demon-stration by means of a very powerful lantern of a series ofspecimens made in the course of his attempt to trace theconnexion between abdominal and meningeal tuberculosis.This series proved that in the cases which he hadexamined in which there was any old tubercular peritonitisor tubercular affection of the mesenteric glands the posteriormediastinal glands were also markedly affected.

The Bradshaw LectureON

DUODENAL INDIGESTION.Delivered at the Royal College of Physicians, London, onNov. 26th, 1891,

BY W. H. ALLCHIN, M B., F.R.C.P.,PHYSICIAN TO WESTMINSTER HOSPITAL.

(Concluded from page 1268.)

I HAVE so far spoken of dietetic errors in the main group31of alimentary principles as they may occur singly, but it is,.of course, often the case that two or more of these impro-prieties coexist, with, it may be presumed, a correspondingcomplexity in dyspeptic results. The interactions, if any,,which take place among-or, at least, the influences exertedon each other by-the different food stuffs in the progress.of their digestion are but little known in health, and stillless in the course of disease.The chief imperfections in the chyme, then, that we can

fairly assume to exist, exclusive of noxious substancesoccurring in the food, are a large excess of proteids verypartially and deficiently treated by the gastric juice, and a,very considerable excess of lactic, butyric, and other acids,the results of carbo-hydrate decomposition. Both impro-prieties may coexist, and the former certainly in the wayshown, and possibly also the latter may be the cause of-mal-digestion in the intestines.

Supposing, however, the diet be all that is satisfactory,so far as it conforms to what is required in digestibility andcomposition-and how often are the most careful and?regular in their feeding, severe sufferers from indigestion,--there yet may be a very imperfect gastric digestion due to.improper quantity or quality of the gastric secretion, or to*some deficiency in the movements of the stomach wherebythe contents are not properly mixed or are not ejected into,the duodenum as they should be, the whole process being,thereby delayed, and giving rise to organic fermentations of’the contents, as may be seen in an aggravated form in theordinary state of gastroectasis. It is apart from my sub-ject to discuss the causes of gastric indigestion suffice itto say that, whatever they may be, the resulting chyme.which is submitted to duodenal digestion is impaired as.regards the changes in its proteid elements, and may containlarge amounts of lactic and butyric acids and other productsof carbo-hydrate fermentation-similar results, that is, tú.those which may attend an excessive ingestion of either ofthese alimentary principles. Should both the diet be im-proper and the gastric juice be deficient, it is reasonable to-suppose a still further defect of the chyme in the absenceof any compensations or adjustments which are at present,quite unknown to exist. In these various directions,.then, may we conceive of the chyme being abnormaland as such the cause of duodenal indigestion. Anothercause for the same is to be found in the deteriorated*quality of the duodenal secretions, or a deficiency in theirquantity, which may happen with either a perfectly normal opa seriously vitiated chyme. Practically, as we have seen,the pancreatic juice is alone to be taken account of as &

digestive agent, the bile being only accessory thereto. Asregards the composition of the juice, we have only an un-certain knowledge, though occasionally opportunities haveoffered to obtain it from the main duct, and we certainlyhave no definite indications as to any modifications it mavundergo in disease, such as we possess in respect to the-amounts of the acid and pepsine of the gastric juice; butits efficiency may be suspected to be impaired in generalstates of mal-nutrition, such as fever, anaemia, and the like.But if we know nothing of alterations in the compositioD>,we are not infrequently able to detect deficiencies, or, indeed,.entire absence, of one or both of these secretions from theintestine. Occlusion of the main ducts by calculi or pres-sure of tumours will lead to this condition and afford oppor-tunity for the study of intestinal digestion in their absence.Deficiency or absence of these fluids signifies, of course, in-complete digestion of the chyme, and, apart from the direct;dyspepsia which such may cause, indirect effects maybe in-duced by failure in arrest of the peptic digestion. which should

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rnormally be brought about, but which, however, may be a’beneficial compensation, thereby permitting a continu-ance of the proteid changes and peptone formation bythe gastric juice, which otherwise the pancreatic tiuid.shoud have accomplished. In exclusion of these secre-

tions from the duodenum the precipitation of the albu-moses above described can hardly be supposed to take,place, perhaps again advantageous in the absence ofthe trypsin ferment. Sir William Roberts has shown, in,contradiction of views that had been maintained, that theactivity of the pancreatic juice is arrested by the acids ofthe stomach, and it is not improbable that in those condi-tions already described, where the chyme contains a largeexcess of the gastric acids, the power of the pancreatic.juice is diminished or even temporarily destroyed.A third group of conditions which are undoubted causes

of intestinal indigestion are those abnormal or excessiveorganic fermentations which have already been referred toas liable to follow a defect in the quality of the chyme. Thebile is usually regarded as specially concerned in the pre-vention of these fermentations, or, at least, those of a putre-factive character, and entire absence of bile ought to befollowed by considerable changes of this nature in the in-,testinal contents. Yet my own experience would lead meto very much question the great power of the bile in thisrespect; at all events, it is no uncommon thing to find thestools absolutely free from bile, and yet with no speciallyputrid characteristics; whilst, on the other hand, thosewhich may contain fully the normal quantity, so far as can’be estimated by colour, may be remarkably offensive. Irelieve myself the putrefactive changes are mainly effectedlow down in the canal, and are nob much influenced by thebile, and I am quite unaware of any control being exercisedby this fluid over those toxic substances which may beformed in the intestine from the decomposition of the.proteids.

Lastly, as causes of intestinal indigestion may be men-tione.d deficient or exaggerated peristalsis and insufficientabsorption into the vessels of the villi, with consequentretention of the digesta in the canal. Perversions ofIperistalsis may be induced by the irritating character ofthe chyme, causing diarrhoea, with mal-digestion and im-perfect absorption ; or the movements may be hindered bydema of the muscular coat from congestion, by degenera-tion, by excessive distension or disturbed innervation. Thedelay in the onward progress of the chyme favours the;activity of the micro-organisms present with the resultsalready indicated, whilst deficient peristalsis means insufii-,dent mixing of the food with the secretion, and alsolessens the secretion itself as well as hindering absorption,both of which the movements of the canal very considerablystimulate. But there is a special disorder of the movements,of the stomach to which I am of opinion not a littleindigestion is due-viz., an exaggeration of the normal pro-pulsive movements with undue relaxation of the pylorus,thereby facilitating exit of the gastric contents, especiallythe larger solid portions, before the peptic action is suin-<eiently advanced, and so, in the ways already referred to,interfering with pancreatic digestion. The opposite condition-namely, deficient gastric movements, with consequentretention of food in the stomach-has also to be mentioned-as causing an abnormal chyme and subsequent liability to- duodenal dyspepsia. There is good reason to believe that,if the diffusible products of digestion be not absorbed asthey are formed, the continuance of digestion is un-

favourably interfered with, whether in stomach or intestine,owing to putrefaction taking place in the substances re-’tained; and it would further seem that the due secretion of’the various juices-certainly the gastric-is very directlydependent, among other things, upon the regular absorption’of material from the canal. ’

To recapitulate the conditions which are immediately pro-vocative of an indigestion in the upper part of the intestine,they are : (1) Initial errors in diet; (2) defects in thepreparatory buccal and gastric changes; (3) perversion of’biliary or pancreatic digestion ; (4) excessive and abnormalmicro-organism activity; (5) exaggerated or deficient peri-stalsis ; and (6) imperfect absorption of the already digestedmaterials. It is probably rare that one of these conditionsoccurs alone, more commonly several contribute to theexistent dyspepsia. It is to be understood that I speak hereof immediate causes only; the circumstances which lead tothem time does not allow me to touch upon; but it is ofcourse implied that these conditions, in their turn, are the

expressions of structural changes in the organs involved,whether these be as obvious as a gastritis, or as impossible ofdetection as a disturbed innervation. But it should not beforgotten that among the antecedent circumstances of theseimmediate causes is often to be reckoned dyspepsia itself,since the imperfect tissue changes thereby determined leadto an impaired structural condition of the digestive organswith deteriorated functions and vitiated secretion of juices,thus maintaining a vicious circle which intensifies itself.The dependence of indigestion also upon disorders of meta-bolism or of the excretion of tissue waste is too obvious torequire more than mention.Looking at the subject in the way I have done, the

following alternatives suggest themselves, and, though nobcapable of solution at present, are, I think, worth statingas helping to define the limits of our knowledge and to indi-cate the direction of future inquiry. Given a case of gastricdyspepsia, from whatever cause, with its special symptoms,must the resulting abnormal chyme determine a furtherduodenal dyspepsia with fresh symptoms, though other con-ditions in the bowel may be taken as satisfactory ? Or maythe duodenal process correct and compensate the stomachfailure, with the result that the indigestion is restricted tothe latter region? Or, again, in a case in which there is noevidence of gastric indigestion, can a true duodenal dys-pepsia arise from any local causes-deficiency of secretions,micro-organisms, &c.-producing symptoms, if not of a dis-tinctive character, at least primarily attributable to it ?Admitting that gastric indigestion may cause pancreaticindigestion, the two coexisting, may each occur inde-pendently and alone ?Passing now to the symptoms, are we able to discriminate

any which especially betoken mal-digestion in the intestineas there are those which may be regarded as diagnostic ofgastric dyspepsia? To answer this it will be requisite verybriefly to consider the various symptoms referable to dis-ordered digestion in general before proceeding to groupthem in respect to their immediate causation. For con-venience of description of such numerous and varied pheno-mena, it is almost necessary to attempt some sort of classi-fication, and the first and most obvious division is intothose which are clearly connected with the alimentaryviscera-i.e., local symptoms-and those which are remoteand manifested through other than the digestive organs :an artificial distinction, I admit, and not capable of beingrigidly drawn. Among the former or local symptoms will Ibe included-1. Pain and all other sensory perversions,varying from a mere sense of weight at the epigastrium toacute, griping colic, or sensations of a peculiar character, suchas heartburn. 2. Evidences of perverted peristalsis, such asdiarrhoea, constipation, vomiting, with all varieties of ejectafrom unaltered food to blood, bile, clear acid fluid, or yeastyfermenting material. 3. Signs of undue distension of partsof the canal, flatulence and meteorism, causing generalabdominal fulness. 4. State of the tongue and mouth;salivation. 5. Character of the evacuations.The remote symptoms of dyspepsia almost defy arrange-

ment, and complete enumeration would occupy too long.Again pain heads the list in shoulders, back, or limbs;and, above all, headache, frontal, occipital, or vertex; aswell as various neuralgias. The muscular system manifestsa general weakness, lassitude, and distaste for exercise,which is badly borne ; or there may be cramps, specially inthe muscles of the calf. Affections of the circulation are ofextreme frequency-such as flushings after food, cold ex-tremities, palpitation, cardiac irregularity, fainting, andangina. The respiratory function exhibits such perversionsas cough, dyspnoea, and hiccough; whilst vertigo, muscsevolitantes, subjective sensations of hearing or smell, alldegrees of mental perversion, from a passing irritability to alasting hypochondriasis, or apathy, drowsiness, or insomnia,as well as impaired appetite, may be conveniently set downas nervous manifestations, as well as pain already men-tioned. Characteristic among the remote symptoms areskin eruptions, mainly of the erythematous type. Andfinally may be mentioned abnormalities of the urine. It isnot, of course, claimed that this list is complete or

precise in arrangement, any more than it is sug-gested that those symptoms mentioned are all of equalfrequency of occurrence. The extreme variety of com-bination among a number of various cases is scarcelyless remarkable than the multiplicity of the phenomena.Is it possible to select from among them any which mayserve to localise the primary or, may be, sole seat of the

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digestive failure ? I fear only very partially, at least, sofar as the duodenal digestion is concerned. The complexityof causation of most of these phenomena renders the un-ravelling of the problem wellnigh hopeless ; but it is nonethe less desirable to set forth what may be affirmed withapproximate certainty, remembering that at this pointoccurs the risk of confounding symptoms which are clearlydue to defective tissue metabolism, such as obesity, withthose which are purely dyspeptic.Attempts have been made to refer dyspeptic phenomena

to stomach or intestine, based on an observance of the timeof their occurrence in respect to the taking of food. But acircumstance which goes far to vitiate the results is thatboth gastric and duodenal digestion progress to a great ex-tent simultaneously; for very soon after the food enters thestomach the propulsive movements of the viscus beginwith the object of propelling the fluid portions into theduodenum, there to be submitted to the action of the bileand pancreatic juice; and hence symptoms which may arisewithin three or four hours after taking an ordinary mealcannot with certainty, on the ground of time of their occur-rence, be attributed to stomach or intestine. Nor could anygreater probability be well asserted for symptoms occurringlater, since mauy such are dependent upon long-delayedgastric digestion with deferred propulsion into the duo-denum.

Certainly, I do not think we can find among the localsymptoms many that may be termed diagnostic of situation,however, suggestive some may be; and the fact that not afew are equally associated with structural diseases of thecanal itself, as well as with assumed imperfections of thedigestive process taking place therein, adds much to thedifficulty, more especially if both abnormalities coexist.The sense of weight and sinking at the epigastrium so oftencomplained of, so far as we know its explanation, willequally be referable to the stomach or upper part of theintestine; but the time of its occurrence in relation tomeals would usually suggest its greater frequency whilemost of the food is still in the stomach, and that it reallydoes depend upon mere bulk of substance, with impairedmovements of the organ. Mr. Golding-Bird’s case of

jejanostomy already referred to bears this out; for on

introducing from fifteen to twenty ounces of food into thejejunum the patient immediately experienced a feeling ofsinking, or, as he said, "faintness," with flushing of face,rapid pulse, and extreme discomfort. These symptomswere invariably repeated so long as the bulk of the mealremained as stated, but did not appear when the quantityof food given was much reduced; and from this circumstanceMr. Golding Bird suggested that these symptoms may besometimes due in patients to a too rapid passage of the con-tents of the stomach through an unduly relaxed pylorus. ButI think it would be difficult to discriminate between such, ifsuch cases there be, and those where the same symptoms areapparently caused by too great a bulk of food in the stomach,and disappear on vomiting-too greab, that is, for that par-ticular stomach at that particular time, though not neces-sarilygreater than maybe taken at other times with impunity.Actual pain that may occur in the course of digestion isextremely obscure in cause, if we exclude irritating ingestaof all kinds and pain due to lesions of the canal, which thenbecomes a symptom of definite disease of the organ, such asulcer, and is not an evidence of disordered digestion proper.It is of course possible that during a faulty digestion acridsubstances may be developed and produce pain as surely assimilar materials do when swallowed in the food, and it isalso probable that, if such do occur, they are formedduring pancreatic digestion. But it is also probable thatmany cases of intestinal colic are of a spasmodic origin,expressions of some want of harmonious action between thenerves and muscles of the bowel, perhaps induced by thecharacter of the contents ; or, on the contrary, may becentric in origin. Nor can such irregularities as constipa-tion or diarrhoci be made a ground upon which to determinethe existence of a gastric rather than a duodenal indiges-tion, since it would be easy to show that failures in eithersituation might determine either of these conditions, justas in a large number of cases both depend on states of thelower part of the intestine beyond where the in flaence ofthe pancreatic juice may be supposed to extend, and there-fore on conditions beyond the limits of my subject.Some of the local symptoms I have enumerated are more

or less significant of gastric disturbance, and gastric disturb.ance only, finding no explanation in intestinal states. Such

are especially acidity, heartburn, and pyrosis, all due to thepresence, whether in excess or not is doubtful, of gastricacids, hydrochloric, lactic, or butyric, with possibly some’hyperacathesia of the mucous membrane. The occurrence ofthese symptoms, whilst undoubtedly pointing to stomachindigestion, does not of necessity exclude a coexistent duo-denal failure. Somewhat less positive gastric symptoms arenausea and vomiting. Both may be due to causes quite-remote from the digestive organs, and I have had reasonsometimes to think that the former, if not both, have been,the result of absorption of toxic intestinal digesta. Butnevertheless, in the great majority of cases, these two sym-ptoms are referable to stomach rather than bowel.My experience so far has not led me to recognise any ap.

pearance of the tongue which can in any way be considereddiagnostic of intestinal indigestion, even if there be anypositively indicativeof true gastric dyspepsia. Generalstates,such as pyrexia or local conditions of the mouth and salivaryflow, are, as Dr. Dickinson has shown, far more potent)causes of morbid states of the tongue than disturbances ill’the functional performance of digestion lower down.

Setting aside, then, those phenomena which are eitherdistinctly or mainly gastlic in nature, or are indifferentlyevidence of stomach or intestinal disorder, there onlyremain to us for diagnostic purposes, among the local sym-ptoms, flatulence and the character of the stools. Withoutrdoubt the former is, with certain reservations, to be regardedas a valuable diagnostic sign. But it is needful to diminate-those cases in which the excessive formation of gas is strictly.limited to the stomach. Such cases are usually easy todetect; physical examination suffices to demonstrate them ;,but apart from the fact that the gastric distension may notalways exceed normal limits, the excess of gas beingeructated or passed on into the bowel, there still remain a.

number of cases in which there is reason to supposethat there is a regurgitation of carbonic acid from theduodenum into the stomach, as Sir William Robertssupposed, and it is probable that most gas of an ill-smelling character which is eructated originally comes’

from the intestine. Speaking generally, however, over-dis-tension of the bowels with flatus, especially if accompanied’with much voidance per anum, is to be accounted as

evidence of mal-digestion in the intestine, though even thenit cannot be always set down to mal-performance within thescope of the duodenal processes, since fermentation changes,accompanied by formation of much gas, does also occur imthe colon without any reason to suspect failure higher up.Sulphuretted hydrogen and marsh gas may be looked upodas exclusively developed in the intestine, but the latter may-certainly originate in the large bowel as a decompositionproduct of its contents. But it is not all cases of true-flatulence of the small intestine that are the results of aoindigestion. There undoubtedly take place throughout thecanal extensive gaseous interchanges between the bloodin its vessels and the air it contains, and interference with.this interchange may readily determine accumulations ofgases in the bowel independently of any defect in digestion.Utherwise, making due allowance in the directions I have’indicated, intestinal flatulence is probably the most reliablelocal sign of duodenal dyspepsia, owing its origin to exces-sive ferment action of micro-organisms.Neither the appearances presented by the stools nor their-

chemical investigation are as reliable as evidences of in-digestion as they might reasonably be supposed to be, or a9we may hope, with more extended knowledge, they will be.An excessively hurried passage of the ingesta along thecanal may lead to much of it appearing in the evacuationsunchanged, or almost so; but though such a condition wouldde facto indicate both gastric and intestinal indigeetionthere would be nothing to show that the secretions were inany way at fault, and that it was anything beyond a much-increased peristalsis. Excepting such cases and the par..ticles of food which have accidentally escaped digestion andare always found in the faeces, the only aliment which passesunchanged and unabsorbed in any quantity is fat-that is,the one which receives no treatment until it has escapedfrom the stomach. When the bile and pancreatic juice areexcluded from the duodenum, this substance appears bothunaltered and as crystals of fatty acids with soda, lime, andmagnesia. Such motions as these often contain also a largequantity of peptones which are wanting in health. But thislatter condition may be as much a sign of defective absorp.tion as it is of imperfect digestion, though, so far as it goes, it,like the presence of fats, suggests the probability of duodenal

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failure. Of such bodies as ptomaines and other products o:abnormal micro-organism activity, we know too little t(allow of their occasional presence in the evacuations beinuseful for diagnostic purposes.Before any attempt can be made to select from among the

numerous and varied distal symptoms of indigestion thosewhich may serve to indicate duodenal failure, it is almosinecessary to seek what explanation there may be for theiroccurrence. Their diversity, their interchangeability, thei]frequent rapid appearance and disappearance, no less tharthe intrinsic character of many of them, irresistibly suggestthat in some way or other the nervous system is concerned.Some such, as pain, paraesthesia and subjective disorders ojthe senses, are clearly to be so explained; whilst others areobviously vaso-motor disturbances, as others are expressionsof perverted trophic influence. Such phrases, I admit, dcnot carry us very far, but they represent our prese n BB-ay ojthinking. There is also the question, How are these dis.ordered nerve influences themselves originated ? Are theyreflex, determined by gastro-intestinal peripheral stimula-tion ; or are they centric, induced by toxic agents absorbedfrom the canal and conveyed by the blood to the cortical"nervous arrangements," from which, in consequence, theyemanate and come to be expressed by the symptoms wespeak of as dyspeptic? These are questions easier askedthan answered, but they are framed entirely in accordancewith our present conceptions.Many of these symptoms may be caused by drugs taken

into the stomach or injected subcutaneously, so that we havewarrant for the suggestion of their poisonous origin, andcertainly most of the vascular phenomena, if not others aswell, are capable of being artificially produced reflexly byperipheral stimulation. It is not easy to suppose any othermethod of action from the gastro-intestinal tract than bythe blood to the nerve centres, or by nervous irritation, butthe supposition does not help very much to distinguish be-tween gastric and upper intestinal situation ; the bloodchannels are the same, and the nerve paths take the samecourse. If it could be shown that these remote symptomsare wholly reflex in origin, I do not see how we could suggestany grounds for referring any given symptom to stomachrather than to duodenum, or vice vers&acirc;; but if the pheno-mena be toxic in cause, then probability would lead us torefer them to the intestine rather than higher up, since inthat situation poisons are more likely to be developed. But,as I have more than once said, the responsibility for manyof these symptoms must not be thrown on the digestive pro-cess. The assimilative power of the tissues themselves maybe at fault, or between the actual results of the digestionand their final presentation to the tissue elements abnormalchanges may take place in the pabulum in connexion withthe many protoplasmic influences which intervene.Certain products of digestion, peptones and albumoses, as

well as further results of proteid decomposition, such asindican, are of frequent occurrence in the urine. But thepresence of the first-named is by no means associated withdyspepsia; and, indeed, since the object of digestion is theformation of these bodies, their existence rather proves theexcellence of the digestive powers, and their occurrence inthe urine when derived from the alimentary canal would bedue to some errors in their destination after digestion andabsorption, much as glycosuria is. As regards indican andits allies of the ether-sulphuric acid series, it is probablethat they may ultimately become valuable aids to the de-tection of abnormal splitting up of proteids in the alimen-tary canal under the influence of micro-organisms.From this survey of the symptoms of indigestion the

conclusion, I think, would be warranted that those whichare capable of being specially referred for their causation toimperfect digestion in the upper part of the intestine, andthat may be considered in any way diagnostic of such im-perfection, are attributable to excessive, if not perverted,micro-organism activity-a condition which we have goodreason to believe is quite a superfluous accessory to thenormal biliary and pancreatic changes, and one liableto be attended with much risk. A clinical point whichto my mind has much significance in this connexionis that in those not infrequent cases where the bileand pancreatic secretions are entirely excluded from theintestine, and when therefore a normal duodenal digestionis impossible, symptoms ordinarily described as dyspepticare noticeably absent. Symptoms dependent on thestructural disease causing the obstruction to the entranceof these fluids may of course exist, but few if any directly

: due to improper treatment of the ingesta. The patient willprobably emaciate, and fat will occur in the stools, the

; digestive agents for that special alimentary principle beingabsent. Hut we look in vain, as a rule, for headache,

I palpitation, flushing, or even flatulence-that is, for thoseI phenomena which perverted germ activity would produce. I! am inclined to explain this by the chyme from the stomach, meeting with no neutralising fluids ; the acids of the gastric, juice pass on into the intestine and destroy the organisms

which might otherwise have given rise to noxious fermenta-I tions. But be that as it may, the point I would urge i8

that complete absence of proper duodenal digestion may beunattended with dyspeptic symptoms, which goes far tosupport my contention that such symptoms are in the maindue to imperfections of gastric action giving rise to primaryphenomena of stomach indigestion; and, secondarily, byproviding a chyme that is vitiated, determining additionalsymptoms originating in the intestine, and mainly due tothe action ot micro-organisms which in normal circum-stances would not have taken placf.Let me conclude w, th a few words by way of summary.

In view of the object of my remarks-viz., the nature,causation, and diagnosis of duodenal dyspepsia,-I have in-sisted on the necessity, for the proper study of the subject,that a strict understanding should be come to on what isexactly the scope of digestion, since many symptoms re-ferred to mal-performance of it are in reality due to perver-sions of functions-absorption and tissue metabolism,-which do not commence until digestion has finished, andthat are wholly different in nature and conditions of exerciseto the physico-chemical processes which take place in thealimentary canal. Also that the character of the successivedigestive changes is such that interference with one is liable toseriously modify those which follow, and that this especiallyholds good in respect to the gastric digestion, which is anecessary preliminary to the duodenal, the normal per-formance of which is intimately dependent on a healthychyme-far more, in fact, than upon the action of its ownproper secretion?. Further, that the most important factor ofduodenal dyspepsia is its dependence on abnormal fermen-tations, caused by micro-organisms introduced ab extra,which in healthy conditions do not assert themselves, andare wholly superfluous adjuncts to digestion. And, lasily,that any symptoms which may at all serve to localise theimperfect performance in the intestine are the results ofthese organic activities.

I do not pretend to have treated my subject exhaustively;it were impossible in the time at my command. The entirequestion of treatment I have not been able to touch upon,but I have attempted to map out the outlines and broadfeatures and to lay down a course for the further study ofan obscure and important subject in accordance with presentphysiological knowledge and the prevailing conceptions ofpathology. It may be objected that in so doing I haveunnecessarily, if not unwarrantably, restricted the scope ofthe question, and have regarded digestion and its faults toomuch apart from the influences of other functions, and thatno such limitation as I have drawn can occur. But I feelsure that to obtain correct notions of the problems presentedno limitation can be too definite at first ; when they areacquired we may more profitably enter on the subject ofother influences.

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ALBUMINURIA IN RELATION TO LIFEASSURANCE.1

BY R. HINGSTON FOX, M.D., M R C. P.,PHYSICIAN (FOR LONDON) TO THE FRIENDS’ PROVIDENT INSTITUTION.

Tms paper is based upon the records of 282 cases,examined by me for several insurance companies duringthe last seven years, exclu8ive of all in which no detailednotes of the condition of the urine were kept, and of allre-examinations of the same person. Two only of the caseswere women ; the urine of other female cases was notobtained. The ages varied between fourteen and sixty-fiveyears; average 32-8 years. Most of the men were engagedin commercial or professional life in or near London,

1 A paper introducing a discussion (reported in another column) atthe Hunterian Society, on Nov. 25th.