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COMMENTARIES ON DISEASES OF THE KIDNEYS. PART I. By ARTHUR WYN~E FOOT, M.D., Univ. Dubl. ; Senior Physician, Meath Hospital and County of Dublin Infirmary; Fellow and Ex-censor, King and Queen's College of Physicians in Ireland; Diplomate in State Medicine, Trinity College, Dublin; Lecturer on Practice of Medicine in the Ledwich School of Medicine and Surgery; Fellow, Royal Geological Society of Ireland, &c. [Gontinued from page 88, Vol. LXVII.]. THE DOCTRINEOF Ua~MIA.--UrtelnJc symptoms : (a) acute ; (b) chronic--(a) Acute characterised by epfleptiform convulsions succeeded by coma or maniacal excite- ment; (b) Chronic, by apathy, somnolence, coma. Defects of sight included among the group of ur~emic symptoms--amblyopia ur~emiea--amaurosis ur~emica. Retinitis apoplectica not necessarily associated with nr~emia. Ur~emic coma; sometimes a difficulty in diagnosis. Asthma ur~emica, description of according to Hertz due to interstitial cedema. The theories of Ur~emia. First, or English theory (Wilson, 1833)--Frerich's theory (1851)--elaborated by Treitz--Criticism of all the theories of urmmia by Rommelaere. Investigations of Traube on the cause of nrmmia--the physical hypothesis as opposed to the chemical. Cases in which ursemia most commonly occurs. Urmmic coma. Temperature in urmmia-- itching in, exudation of urea on the skin. Proclivity to inflammatory affections in ureemia---their tendency to purulent infiltration--frequency of phlegmons and gangrene. Effects of renal disease on the general nutrition of the body--anmmia~ emaciation, weakness. Dyspepsia, vomiting, diarrhcea, frequent symptoms. Causes of the dyspepsia. Causes of the vomiting of renal disease. JDiarrhoea more rare than vomiting, due to a variety of causes. The hcemorrhagic cachexia in renal disease--petechi~e--epistaxis; heemorrhagic symptoms most common in con- tracked kidney. UNDER the name of Urcemia a series of symptoms have been ranked together which have been regarded as the direct result of blood poisoning with urinary matters, the consequence of the retention in the blood of the dross of the capillary interchanges--the nitrogenous substances and specific urinary constituents. The very various functional diseases of the nervous system which~ in accordance with general custom~ are regarded as symptoms of urzemia~ sometimes pursue an acute, sometimes a chronic, course. Acute urcemia manifests itself in the form of epileptic convulsions, which are often terribly violent, and are succeeded by coma, or~ in some instances, by a condition of maniacal excitement. In most cases the convulsions succeed each other at short intervals, often before the patient can recover from the coma of the preceding seizure. I~ot infrequently N

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C O M M E N T A R I E S O N D I S E A S E S O F T H E K I D N E Y S .

PART I.

By ARTHUR WYN~E FOOT, M.D., Univ . Dubl. ; Senior Physician, Meath Hospi ta l and County of Dubl in Inf i rmary; Fel low and Ex-censor , K i n g and Queen's College of Physicians in I r e l and ; Diplomate in State Medicine, Tr in i ty College, Dub l in ; Lec turer on Pract ice of Medicine in the Ledwich School of Medicine and Su rge ry ; Fel low, Royal Geological Society of Ireland, &c.

[Gontinued from page 88, Vol. LXVII.].

THE DOCTRINE OF Ua~MIA.--UrtelnJc symptoms : (a) acute ; (b) chronic--(a) Acute characterised by epfleptiform convulsions succeeded by coma or maniacal excite- ment; (b) Chronic, by apathy, somnolence, coma. Defects of sight included among the group of ur~emic symptoms--amblyopia ur~emiea--amaurosis ur~emica. Retinitis apoplectica not necessarily associated with nr~emia. Ur~emic coma; sometimes a difficulty in diagnosis. Asthma ur~emica, description of according to Hertz due to interstitial cedema. The theories of Ur~emia. First, or English theory (Wilson, 1833)--Frerich's theory (1851)--elaborated by Treitz--Criticism of all the theories of urmmia by Rommelaere. Investigations of Traube on the cause of nrmmia--the physical hypothesis as opposed to the chemical. Cases in which ursemia most commonly occurs. Urmmic coma. Temperature in urmmia-- itching in, exudation of urea on the skin. Proclivity to inflammatory affections in ureemia---their tendency to purulent infiltration--frequency of phlegmons and gangrene. Effects of renal disease on the general nutrition of the body--anmmia~ emaciation, weakness. Dyspepsia, vomiting, diarrhcea, frequent symptoms. Causes of the dyspepsia. Causes of the vomiting of renal disease. JDiarrhoea more rare than vomiting, due to a variety of causes. The hcemorrhagic cachexia in renal disease--petechi~e--epistaxis; heemorrhagic symptoms most common in con- tracked kidney.

UNDER the name of Urcemia a series of symptoms have been ranked together which have been regarded as the direct result of blood poisoning wi th ur inary matters, the consequence of the retention in the blood of the dross of the capil lary in te rchanges - - the nitrogenous substances and specific urinary constituents. The very various functional diseases of the nervous system which~ in accordance with general custom~ are regarded as symptoms of urzemia~ sometimes pursue an acute, sometimes a chronic, course.

Acute urcemia manifests itself in the form of epileptic convulsions, which are often terr ibly violent, and are succeeded by coma, or~ in some instances, by a condition of maniacal excitement. I n most cases the convulsions succeed each other at short intervals, often before the patient can recover f rom the coma of the preceding seizure. I~ot infrequent ly

N

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a series of such epileptic attacks terminate at last with death. Cases, however, occur in which patients afflicted with a chronic renal affection, who have had one or a few such attacks following acute urmmic poison- ing, recover again completely, and live on for a long time, pursuing their usual avocations. Occasionally, epileptiform convulsions are the first symptoms to suggest an insidiously progressing renal disease, attacking an individual in apparently perfect health. But, in other cases, these acute urmmic fits are preceded by other striking symptoms of the com- plaint--such as dropsy, dyspepsia, or obstinate vomiting. In rarer instances the characteristic convulsions are ushered in by cramp-like twitchings of particular groups of muscles, lasting for some days, or by tetanic spasms, which at first do not disturb the intellectual faculties. But far more commonly the first epileptic seizure assails the patient quite on a sudden and without any of these premonitions.

In the Chronic forms of Urcemla convulsive phenomena may be entirely absent, or they may appear in the shape only of twitchings of certain groups of muscles. The urmmia may show itself only by increasing somnolence, apathy, or stupefaction, advancing at last to complete coma. But this mental obfuscation is very often preceded by dyspeptic difficul- ties, by stubborn and incessant vomiting; and the vomited matters in such cases quite often contain large quantities of carbonate of ammonia, which gives them an alkaline reaction, can be perceived by the smell, and admits of chemical recognition withou~ any great difficulty. There is often in this form of ur~emia a most tormenting itching of the skin, which drives the patient, though in a stupefied state, to continually scratch himself. Lastly, it may happen that a patient who has been lying some days in a state of complete coma, is seized by one or by repeated epileptic attacks before death closes the scene.

In urmmia, either of the acute or chronic form, delirium is rare~ while coma is frequent; paralysis of the limbs is scarcely known~ unless there be some anatomical lesion of the brain superadded, while convulsions are frequent. The ureemic symptoms in the chronic form generally begin insidiously with headache or vomiting~ followed by heaviness, indifference, and somnolence. The most common of these symptoms is headache; a sense of heavy weight or compression over the forehead or vertex is com- plained of; sometimes the pain is obstinately fixed at the back of the neck or behind the orbits. Ur~emie convulsions are of the epileptic type. They arc accompanied with complete insensibility, rolling of the eyes~ biting of the tongue, and foaming at the mouth. The paroxysms com- monly leave the patient deeply comatose. Ureemic coma may either creep on very gradually, passing on, in the course of two or three days~ into complete stupor~ or may culminate quickly--the patient falling down as if in apoplexy, perhaps while walking in the street or occupied with his usual avocations. Cases of this class, where there is no anasarca and

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the previous state of the urine is unknown, are very liable to be confounded with apoplexy (and, in fact, have been described as serous apoplexy) or narcotic poisoning.

Among the group of ur~emic symptoms are reckoned certain defects of s~ght which possess great clinical importance. One of these is a dimness of vision--amblyopia urcemica--which comes and goes, objects appearing as if veiled in mist. There is also the amaurosls ur~mlca--a sudden and complete blindness, which is usually temporary, and, as a rule, disappears as suddenly as i t comes. This is to be distinguished from the disturbances of vision which so often occur in the course of chronic renal disease, and which are due to grave structural alterations of the retina, and are permanent in character. This latter affection--the hmmorrhagic blind- ness, retinitis apoplectica--is in no sense urmmic, though not uncommon in Bright 's disease. I t has been shown by yon Graefe to be due to rupture of the retinal vessels, and its production is probably due to the hyper- trophy of the left ventricle which so commonly accompanies a contracting kidney and the increased tension in the arterial system consequent thereon. I t is believed that the pathological alteration in the eyes of those who, while suffering from renal disease, become suddenly amam'otic, consists in simple (edema of the retina.

Amongst urmmic symptoms are also to be reckoned those asthmatic attacks which sometimes assail the subjects of chronic renal affections a long while before their death. These attacks of asthma come on in paroxysms, with intervals of complete freedom, and are more frequent at night-time. This hmmic or urmmic asthma impresses a bystander like the breathlessness following over-exertion in health ; the respiration is not seriously out of proportion with the pulse, and usually the subjective sensation of want of breath is, comparatively speaking, little felt; the patient breathes like a man out of breath from rrmning (noisily), says he feels short-breathed, but does not look as i f suffering therefrom. Pathologists are not agreed in ascribing this form of renal dyspnoea to irritation of the respiratory centre from poisoned blood. According to Hertz ~ this condition is nothing more nor less than an interstitial (edema of the' lungs with infiltration and swelling of the mucous membrane of the terminal bronchi. He fully agrees with Rosenstein iu believing the so-called urcemic asthma to be due to an (edematous swelling of the bronchial mucous membrane, and not to the effect of the blood- poisoning upon the nerves governing respiration. He (Hertz) has hitherto only observed this (edema in persons in whom, during their illness, he was able to diagnose a primary cirrhosis of the kidneys, and subsequently verify it by post mortem examination ; and he remarks that it is certainly surprising that (edema of the lungs is met with just in those patients who, while having the contracted kidneys, do not suffer from extensive

a Cyclop. Med. Edited by Voa Ziemssen. Vol. V. 1 ). 279.

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(edema of the surface or from fluid accumulations in the large internal cavities of the body, until death is near at hand.

The most strenuous efforts, made by quite a host of able inquirer% to discover the essential nature of urc~mia, have only led to very conflicting views upon the subject, and the doctrine of urcemia has been subject to many fluctuations of opinion even in very recent times. In order to get possession of the more important of these opinions, it will be necessary to review very briefly some of the principal theories which have been entertained on this matter. The relation of the neuroses which are comprehended in the term urmmia to renal disease was clearly recog- nised by Bright, and the general opinion of that time was that the blood was contaminated with urinary elements, and so exercised a poisonous effect upon the nervous system. This idea was chiefly fostered by the proofs--first furnished by English observers--of an accumulation of urea in the blood of many patients affected with kidney disease. Babbington found, during life, 1"5 per cent. of urea in the blood-serum of a woman s twenty-four years of age~ who was dropsical s had albuminous urine~ and finally died with epileptic convulsions--the autopsy showing her to have had granular kidneys ; and he remarked on it that this woman's blood- serum was as rich in urea as her urine. The promulgation of this, the firsts or English, theory of ur~emia, was made by Dr. Wilson, of St. George's Hospital, in a communication " O n Fits and Sudden Death in connexion with Diseased Kidney. ''~ Dr. Wilson attributed the symptoms to diminished albmnen and excess of urea in the blood--the discovery of Bostock and Christison. This theory soon came to be objected to on the ground that large quantities of urea might be present in the blood without any special nerve symptoms resulting therefrom. Owen Rees observed a case in which, while one kidney was altogether absent, the ureter of the other~ enlarged by compensative hypertrophy, had been blocked up by a calculus. The consequence was a total suppression of urine. Although the patient had remained in complete possession of all his faculties up to the last moment, still O. Rees found more urea in the blood drawn from him during life than had ever been shown to be present in the urine of any case of Bright's disease with which he was acquainted. Furthermore s experiments made upon animals with injections of filtered urine and with solutions of urea have failed to induce fits, or conditions at all like ureemia. I t may be taken as established, from many clinical observations, that the overloading of the blood with urea is certainly not, in every instance s the cause of the urmmic symptoms.

In 1851 s Frerichs adopted the urea theory in a modified form. His proposition was that the urea in the blood s under the influence of some special ferment, is decomposed into ammonium carbonate, and that this was the pernicious principle which produced the functional disorders.

a ]~edical Gazett% 1833. Vol. XI. P. 177.

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Henceforth the term ammoni~emia came to be used by many instead of ur~emia. Treitz perfected this theory of Frerichs by submitting that the urea retained in the blood and passing into all its secretions appears most generally and in the largest quantity on the mucous surface of the intestines. This urea, however, is regularly decomposed into ammonium carbonate by the intestinal fluids, especially the gastro-intestinal mucus, and the salt is then reabsorbed and carried back into the blood. In the course of time, however, objections from various quarters were raised against the doctrine of ur~emia as propounded by Frerichs and elaborated by Treitz. The instances became constantly more numerous in which, notwithstanding the most careful analyses, no ammonia could be dis- covered either in the expired breath or in the blood of ureemic persons, even where ur~emic coma and repeated epileptic convulsions were present, and where the face was covered with crystals of urea left behind by by the evaporation of the sweat. A severe blow to the tottering theory was also given by Schottin, who called attention to the fact that ammo- nium carbonate can be found in the breath of any person in whose mouth the natural secretions collect and pass into decomposition--as, for example, in typhoid states, pymmia, and other cases. From the observations which have been made up to the present, the only conclusion which we can accept is, that there are cases of ursemia in which ammonia is con- tained in the blood, and others of apparently the same nature in which chemical analysis has hitherto entirely failed to detect a trace of that substance, so that the theory of Frerichs can only be the correct one in, at most, a few cases.

Recent experiments of Oppler, ttoppe-Seyler, and others, indicate that ur~emic manifestations depend mainly and essentially on the accumulation in the blood and tissues of those primary products of tissue metamorphosis (creatin, creatinin, leucin, and other extractives) which, in a later stage of histolysis, are converted into urea and uric acid, and excreted as such by normal kidneys. Zaleski concludes, from observations made in Hoppe- Seyler's laboratory on animals--such as snakes and birds, which do not in health produce urea, but stop short at the formation of ammonium ura te- - tha t Frerichs' theory of ammonia poisoning must be given up, and that the urea theory cannot be maintained, since ur~emia occurs in animals that never form urea. Schottin found in urtemia the proportion of extractive matter to albumen in the blood to be increased from 5 : 100 to 40 : 100, and I-Ioppe found the creatin to be five times more than in healthy blood.

Dr. W. Rommelaere, Fellow of the Royal Society of Medicine and Natural Philosophy in Brussels, has subjected to a critical examination all the theories which from time to time have been proposed regarding the essential causes of the urmmic symptoms, and concludes that we can no longer accuse any one substance that may occur in the blood after

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suppression of the urinary excretion, of being Mone and by itself the cause of the nervous symptoms. The suppression of the urinary excretion prevents the further elaboration of Mbuminoid substances throughout the entire organism, if nature does not provide some other vicarious mode of supplementing this excretion. Urea is the last step or stage of the metamorphosis of these albumiaoid substances, and when urea aceumu- lates in the blood it changes the character of this fluid, and consequently the vital (nutritive) processes in various parts of the body. The entire work of transforming the albuminoid substances is arrested, so that we have to deal with the retention in the system, not merely of urea, but also of nitrogenous substances in all the different stages of oxidation through which they pass within the organism. I t may be accepted as invariable that the maladies which entail urmmic disturbances are eharac. terised at the time when the urmmic complications break out by the presence, in the tissues of the body, of an excessive amount of nitrogenous excretory materials. In suppression of the ur inary excretion it is not one single element like urea or uric acid, creatin or creatinin, the ex- tractives, or uroehrom (pigmentary matter)~ which does the harm. I t is the mass together.

I t was the absence of anatomical lesions in the brains of persons who die of urmmic coma and convulsions which had constrained pathologists to invoke the aid of chemistry to explain the phenomena, and we have seen how ineffectual their efforts to do so have been up to the present. Traube, however~ has insti tuted investigations in quite a different direc- tion, and seeks to find out the essential cause of urmmia in local lesions of the central organs of the nervous system. He connects the symptoms with e d e m a and anemia of the brain, the result of two factors : one is the thinning of the blood serum, which is so customary in renal disease ; the other is hypertrophy of the left ventricle of the heart, by means of which an abnormal excess of pressure throughout the arterial system is effected at the same time that the blood serum is impoverished. Traube's hypothesis then is a physical one as opposed to the chemical hypotheses which have been just alluded to, and is as follows : - - I f from any cause the liquefac- tion of the serum or the tension of the arteries suddenly increases, o~dema and anemia of the brain follow, and, in consequence thereof, the syrup- toms of urmmia are produced. I f only the cerebrum becomes oBdematous and anemic, simple coma arises; but if at the same time the middle brain (thalami and corpora striata) also becomes anmmi% convulsions occur; if only the latter becomes anemic, convulsions merely are pro- dueed. Traube's theory has had in its turn to bear a trying examination, for which i t does not seem to be in all eases equal; for example, in the post-cholera urmmia both the conditions laid down by him as requisite for the production of u remia - -namely , a watery blood and an elevated arterial blood pressure--are absent as a matter of certainty. Yet it is

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equally certain that these attacks fairly merit the title of ur~emic. They come on after long-continued complete suppression of urine~ and are not infrequently accompanied by secretion of urea upon the surface of the skin. Fur ther doubts as to the correctness of Traube's theory of (edema of the brain~ or as to its applicability to every case of ur~emia~ are aroused by the fact that ur~emic attacks do not by any means occur chiefly in those cases of renal disease which are characterised by dropsy. Indced~ so long as the dropsical swellings are still increasing~ ur~emic symptoms ar% comparatively speaking~ rarely observed. I t is~ indeed~ a striking fact that ur~emic symptoms often occur in persons suffering from renal disease who never~ either at the time of the attack or pre- viously~ have been affected with anasarca or dropsical accumulations in the serous cavities. I t seems that ur~emia is both absolutely and rela- tively more common among the very cases of renal disease which are not dropsical~ and in persons~ therefore~ who are but little hindered from following their ordinary avocations.

I t has been gathered from clinical observations that the outbreak of ur~emic convulsions is generally preceded by a diminution in the excre- tion of nrin% and especially of the urea~ "to a figure far below the ordinary mean average~ but i t has not been explained why it is that ur~emlc symptoms are not forthcoming in cases which~ with the daily excretion of urine and urea reduced to quite as low an ebb~ advance to a fatal issue without the occurrence of convulsions or protracted coma. I t is also a remarkable fact that ur~emic convulsions come on in paroxysms~ with intervals of perfect remission between them~ the exciting cause remaining in undiminished force. The coma following a ur~emic con- vulsion is ordinarily more protracted than that which succeeds the uncomplicated epileptic convulsion~ because the former are usually more violent than the latter~ and follow each other with so much greater rapidity that the patients sometimes do not recover their senses at all between the fits. ]~artels has observed in every case of ur~emie convul- sion which he has seen~ with the exception of one single instance~ that the temperature of the body~ taken directly after the first attack~ has been considerably elevated above the normal. During ur~emic coma the temperature may fall far below the norma|~ even quite a long time before death. Ur~emia is often associated with an itching of the skin~ which compels the patient to scratch himself incessantly~ even while lying in a state of unconsciousness. Baxtels has noticed this symptom oftener in cases of chronic ur~emia where there have been no convulsions, and in such especially as exhaled a urinous odour from their persons. In ur~emia crystals of urea are sometimes left on the skin upon evaporation of the perspiration in which i t was held in solution. This occurs especially on the face, and may even give to the beard an appearance as if it were frosted over.

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Among the results of the contamination of the blood by urinary matters retained in it is to be included a marked proclivity to inflam- matory affections. So common are they in renal disease that, according to some, these inflammations are the immediate cause of death in the larger proportion of cases of Bright's disease, so-called; and they pro- bably do lead to death, in the various forms of diffuse nephritis, more frequently than do dropsy, ursemia, and apoplexy reckoned together. The peculiarity of these processes of inflammation in renal disease is the tendency which they manifest towards purulent infiltration--the purulent infiltrations showing themselves most commonly as phlegmons of the subcutaneous connective tissue. Then~ again, erysipelatous inflammations of the skin are often seen occuring in renal cases, and, next to these, per- haps, soft infiltrations of the lungs are the most common complications. Death by gangrene is the ordinary issue of the phlegmonous inflammations.

The general nutrition of the body is seriously influenced by renal disease in a variety of ways. The loss of albumen entails serious con- sequences upon the organism, and it is a matter of clinical experience that renal diseases produce their injurious effects upon the general nutrition--namely, anaemia, emaciation, and weakness--all the more quickly in proportion to the abundance of the loss of albumen which the organism experiences in consequence of the albuminuria which accompanies such affections. The waste of muscle and of subcutaneous fat which is commensurate with the waste of albumen that drains away in the urin% is apt to escape observation owing to the presence of dropsical swelling of the subcutaneous tissue. The wasting, however, becomes apparent at onc% when, from profuse sweating, eolliquative diarrhcea~ or other similar evacuation, a sudden absorption of the dropsy takes place.

Dyspepsia, vomiting, and diarrhoea, are such frequent and ordinary symptoms of renal disease, that the mere fact of the repeated concur- rence of these functional disorders of the digestive apparatus proves some causal relation between it and them. In some cases the dyspepsia appears to be the result of the extreme anaemia, provoked by renal disease, and, like that produced by all other anaemic states~ is to be referred to an insufficiency of the secretion from the peptic glands of the stomach; and, at an autopsy, the mucous membrane of the stomach~ beyond exhibiting extreme emptiness of its blood vessels, shows no appreciable pathological alteration. In other cases considerable cedem~ of the mucous membrane is discovered at the post mortera examination, which must have prevented the glands from furnishing a normal secre- tion. Finally, the contents of the stomach are sometimes found to be highly ammoniacal, showing that urea has made its way out of the blood into the secretions of the stomach, and has been transformed by the influence of the gastric mucus into ammonium carbonate, which, neutral;s- ing the acid reaction of the gastric juices, has deprived these of their

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digestive virtue. The dyspepsia due to this last cause is generally brought about only a very short time before death.

The vomiting of renal disease, like the dyspepsia, owes its origin to a variety of causes which have been ably summarised by Barrels. In the first place, in cases of acute swelling of the kidney, or of violent inflam- mation of the pelvis, or of the ureter of one of these organs, the attendant vomiting may be looked upon as a strictly reflex act ; it is excited by an irri tant impression made upon the nerves--ei ther those connected with the capsules of the kidneys, and therefore implicated in the tension to which these organs when swollen would be subjected, or those which run to the pelvis of the gland, and which may either be involved themselves in the process of inflammation, or have suffered directly from the same cause (a calculus for example) tha t produced this. In much the same way vomiting may succeed an inflammatory irritation of the peritoneal coat of the kidney, as in nephritic abscess, or in the course of the development of new growths, or after abnormal distension of the pelvis of the organ by pyelitis or hydronephrosis. In all these instances the vomiting is attended by pain of more or less acute kind, and usually paroxysmal in its na ture - -pa in which subsides in one class of cases with subsidence of the swelling, and in the other with the abatement of the sharp irritation provoked by the presence of the calculus in the pelvis of the kidney. The vomiting of renal disease may be also due to (edema of the mucous membrane of the stomach. In such cases the vomiting, as a rule~ takes place in the morning before breakfast~ when a quantity of watery fluid of very low specific gravity (1,002) of a faintly acid reaction is rejected. The co-existence of anasarca~ the absence of urinary constituents in the vomit, and the results of post mortem examination, justify the assumption that such cases are due to (edema of the gastric mucous membrane. I t is likely that the fluids effused in the submucous membrane of the stomach transude into its cavity and by their mere volume excite the vomiting. Furthermore, in many cases of renal disease obstinate and irrepressible vomiting follows upon the retention of urinary materials in the blood, and is then symptomatic of urmmia. In many cases this troublesome and invincible symptom is the first warning of chronic urmmia, and the precursor of severe nervous manifestations, convulsions, and coma. This ur~emic vomiting produces serious effects upon the general state of nutrition by interfering with the assimilation of food already ingested, and usually causing it to be rejected as soon as it is swallowed. I t is frequently associated with the greatest possible dislike to all solid articles of food, and especially to meat, and hence the rapid deterioration of strength observed from the moment this urgent symptom appears. I t is probable that this form of vomiting is to be referred to direct irritation from the impure state of the blood, of those nervous centres which co-ordinate the act of vomiting.

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Diarrlwea may also arise as a complication of renal disease. I t occurs more rarely than vomiting~ but is quite as obstinate and exhausting. The loss of strength is due to the rapidity with which the intestines are emptied, whereby the absorption of the food taken is prevented. The diarrhoea in renal cases may arise from a variety of causes, quite apart from that process of ulceration in the intestines which occurs so very frequently as a complication of the amyloid degeneration of the kidney. The diarrhoea may b% in the first place, due to oedema of the mucous membrane of the intestines~ and then occurs only in the dropsical forms of renal disease. In such cases the stools are abundant~ very watery, and but slightly coloured, and in this way the dropsy is either greatly reduced or completely removed. The diarrhoea may also be produced by the passage of urinary constituents into the intestinal canal and their conversion into ammonium carbonate. In such cases, which may be contemporaneous with vomiting of ammoniacal matters, the strong ammoniacal odour of the fmces may be sometimes recognised. Such a diarrhoea is practically one of the final symptoms.

There is yet another disturbance of the general nutrition which is of the utmost gravity in cases of renal d isease--a hcemorrha.qic diathesi~. Petechial spots appear on the skin, and besides these the predisposition to bleed is evinced by spontaneous epistaxis~ and by h~emorrhages from other tracts of mucous membrane-- f rom that of the stomach and of the intestines, from the mucous membrane of the mouth, and by hsmoptysis. The most common source of all is the nasal mucous membrane. I t is singular that there seems to be little tendency to bleed exhibited by the genito-urinary apparatus of women. After death there is not found the slightest anatomical lesion to explain these often profuse bleedings which must take place per diapedesln. I t is only when this heemorrhage takes the form of epistaxis that it may occur repeatedly during a prolonged period, and ought not therefore to be accepted as an immediate harbinger of death; when derived from other sources, and accompanied by pete- chi~e, i t invariably indicates the near ~pproach of dissolution. In every example of well-established h~emorrhagic cachexia which Bartels has observed, the patients whom it has befallen have not survived two weeks from the commencement of the bleedings--which may occur simultaneously from different mucous tracts. These hmmorrhages gene- rally occur in cases of genuine contracting kidney (granular atrophy)~ and very rarely in dropsical persons. As to the exact cause of these hmmorrhages there is a division of opinion--some connect them with the increase of tension in the arterial system from the hypertrophied left ventricle, so frequently associated with contracted kidney, acting on an excessively thinned blood; others regard them as a sign of ammonimmia. I t is true that epistaxis occurs in guinea-pigs when solution of ammonium carbonate has been injected into their veins ; and bearing on this matter

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is a case in Huxham's Essay on Fevers, in which "vas t h~emorrhages from the intestines~ nose, and gums," were observed in a young gentle- man of fortune and family who had acquired a pernicious habit of eating smelling-salts (ammonium sesquicarbonate). However, a case most carefully observed by Bartels does not find its explanation on either of these hypotheses--for in this case the h~emorrhages continued up to the very last, whereas the heart's power had sunk to a low ebb several days before death, the pulse being soft and empty ; and in the same case the blood drawn from a vein before death, and tested in the most exact manner by the method of Kiihne and Strauch, showed that there was not a trace of ammonia present.

[To be continued.]

l~oTE.--The text of the essays of Professor Carl Barrels, of Kiel, and P r o f e s s o r

Wilhelm Ebstein, of Goettingen, in Vohune XV. of the "CyclopEdia of the Practice of Medicine," edited by I)r. H. Von Ziemssen, has been followed as closely a s

possible, with additional notes from all the best authorities on the subject. .A.W. Foo~.

TRACHEOTOMY IN LARYNGEAL TUBERCULOSIS.

SERKOWSKI has performed tracheotomy twice for tuberculosis of the larynx. One of the patients died three years after from advanced pul- monary phthisis; the other is still alive, seven years after the operation, and is apparently in good health except that there is dulness at the right apex, and thickening of the vocal cords. She wore the cannula for two years. He believes in this case that the opening in the trachea was not only of temporary benefit, but prevented the further development of tuberculosis. The opening should be large enough to allow the free passage of purulent secretion from the lungs and the admission of air. The operation is absolutely required when the larynx is more affected with tubercle than the lungs. The passage of the current of air through the inflamed and often narrowed larynx is no doubt a frequent source of irritation. Tracheotomy obviates this and prevents vocalisation, thus enabling the larynx to be in a state of comparative rest, which is most important, especially if there be extensive ulceration.--Allg. Med. CMr. Zeit. and St. Louis Med. orour,

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