Chapter VI: Front Matter (6)

The symptoms which can be ascribed directly to the presence of the kidney disease are--(1) The changes in the composition of the blood. We have still very little exact knowledge of what these changes are, but we may say generally that there is an increase in the relative quantity of the watery constituents of the blood and of the excrementitious products which should be eliminated by the kidneys. (2) The changes in the quantity of urine probably depend partly on the changes in the circulation, partly on the composition of the blood, and partly upon the structural changes in the kidneys. The albumen and casts seem to be directly due to the kidney lesion. (3) The changes in the nutrition of the patient, the disturbances of digestion, and some of the headaches, all seem to belong directly to the kidney disease.

Now let us try to apply these principles to the practical treatment of the different symptoms.

The Urine.--As regards the presence of albumen and casts, it is doubtful whether we are able to do anything, although it is customary to give the tr. ferri chloridi and the bichloride of mercury in order to diminish the excretion of albumen. As regards the quantity of urine, we must distinguish whether the patient is in the ordinary course of the disease, whether he is having an uræmic attack, or whether he is having an acute exacerbation of the nephritis with congestion of the kidney and blood in the urine. Under the circumstances last mentioned the indications are to apply wet or dry cups over the lumbar region, to use hot fomentations to the back or hot-air baths, to open the bowels freely, to put the patient on a milk diet, and, if the heart's action is too strong, to give aconite in small doses.

If during the ordinary course of the disease the urine is constantly diminished, diuretics are often of good service, although the cases differ as to the particular drugs which answer best. The preparations of digitalis, the diuretic pill of digitalis, squills, and bichloride of mercury, the iodide and acetate of potash, and jaborandi in small doses, are the most reliable agents of this class. Sometimes the frequent use of milk or of water in small quantities (half an ounce or an ounce every half hour) will {97} answer the purpose. There can never be any use in continuing the employment of diuretics in these cases if after a fair trial they do not increase the flow of urine.

During the progress of uræmic attacks diuretics do not act, and the same is often the case with cathartics and diaphoretics. The urine is only to be increased by the same means which are indicated for the relief of the whole uræmic condition, and of these we will speak later.

The dropsy in many cases will vary in amount, and even disappear at times without any treatment. It is regularly most marked with the large white kidneys and with those kidneys which are neither large white nor atrophied, especially when there is complicating heart disease and the patient is anæmic. Generally speaking, it is best to keep dropsical patients in bed most of the day. We attempt to get rid of the oedema by the skin, the bowels, and the kidneys, to regulate the heart's action, and to improve the condition of the blood. Hot-air baths or hot-water baths repeated every day, the milder hydragogue cathartics, and the different diuretics may all be used with advantage. If the dropsy is excessive, it may be necessary to tap the peritoneal or pleural cavities or to puncture the skin of the legs and scrotum. Sometimes bandaging the legs so as to exert moderate pressure seems to assist in getting rid of dropsy. To regulate the heart's action we find that digitalis, convallaria, and the iodide of potash are often of service. To improve the condition of the blood the systematic use of iron and oxygen is indicated. The most hopeless cases are those in which there is complicating heart disease and those in which the dropsy steadily increases, although the patient is passing from 60 to 100 ounces of urine daily.

Disturbances of the stomach are of different kinds and dependent upon different conditions. There may be simply loss of appetite or discomfort after eating, or nausea, flatulence, and vomiting; and these symptoms will be associated with chronic catarrhal gastritis or with a stomach that is anatomically normal. Sometimes, although there is occasional nausea and vomiting, the appetite continues good, or as part of an uræmic attack there will be constant vomiting.

The habitual dyspeptic disturbances are to be treated like other cases of gastric dyspepsia. A regulated diet, the vegetable bitters, the mineral acids, or the alkalies are sometimes of service. The repeated and persistent vomiting of uræmic attacks is a most distressing symptom and one often very difficult to control. The patients must be fed with small quantities of fluid food or of prepared meat. The most efficient remedies are those addressed to the condition of the circulation. Hypodermic injections of morphia, enemata of chloral hydrate, inhalations of nitrite of amyl, convallaria in small doses by the mouth, are all of service.

The anæmia from which the patients suffer is to be combated by the systematic use of iron and oxygen. Any efficient preparation of iron will answer, but it must often be given in considerable doses. Sometimes the bichloride of mercury in small doses answers better than iron. The oxygen should be inhaled for from five to thirty minutes twice a day.

The so-called uræmic attacks, although they have a general similarity, yet vary in their manifestations in different cases. In some cases the {98} patient develops an unnatural restlessness and anxiety, an inability to sleep, now and then a sudden twitch of one of the facial muscles, and headache. Or a patient whose color is still good will only complain of pain in the epigastrium and moderate dyspnoea, and yet will be in bed and evidently seriously ill. Or a patient who has been troubled with dyspeptic symptoms and gradual loss of strength suddenly develops vomiting, intense headache, sleeplessness, a single convulsion followed by facial paralysis. A man with a previous history of chronic Bright's disease becomes persistently anæmic and dropsical; he has constant dyspnoea, cannot lie down, cannot sleep, and yet looks drowsy and stupid; is mildly delirious and has very little intelligence; then gradually becomes unconscious, then comatose, and so dies. Or there are first attacks of dyspnoea, either spasmodic or from exertion, but which are temporary and can be relieved. Then the dyspnoea becomes more constant and severe; the patient cannot lie down at all, all remedies become less and less efficacious, and the dyspnoea only ends with the life of the sufferer. In other cases a patient will suddenly become unconscious, although not comatose; he will lie flat in bed, the skin livid and bathed in perspiration, the respiration labored and rapid, with coarse râles all over the lungs, the heart's action rapid and feeble, the temperature perhaps a little elevated; or sudden and profound coma or noisy delirium or repeated convulsions may be the prominent features.

There is hardly a limit to the variety of the precise manner in which all these symptoms--restlessness, sleeplessness, headache, vomiting, delirium, convulsions, and coma--may present themselves. It is to be remembered that although all these symptoms are always dangerous, and often fatal, yet patients may pass through a number of such attacks before the fatal one arrives.

To relieve these attacks the most effectual remedies are opium, chloral hydrate, nitrite of amyl, convallaria, digitalis, caffeine, bloodletting, purging, sweating, and cathartics.

Opium is a very valuable remedy, but great judgment is required in selecting the preparation and the dose for each case. The old doctrine that opium is a dangerous drug for patients suffering from Bright's disease is perfectly true, but it is equally true that it is also a valuable remedy. Generally speaking, the more marked the uræmic attack the larger the dose of opium that will be borne. It is always well to try to obtain a free movement from the bowels, although this is not always possible.

In the milder cases the fluid extract of convallaria in ten-minim doses will often diminish the frequency of the heart's action, increase the production of urine, and improve the general condition of the patient.

In the earlier stages of dyspnoea five-grain doses of the iodide of potash with a little opium will sometimes keep the patient comfortable for months. For the severe attacks of dyspnoea dry cups over the chest and inhalations of oxygen are of service. In the worst and most uncontrollable dyspnoea it seems justifiable to keep the patient under the influence of ether or chloroform.

{99} SUPPURATIVE NEPHRITIS AND PYELO-NEPHRITIS.

Suppurative inflammation of the tissue of the kidney and of its pelvis and calices occurs under several different conditions: It is the result of injuries; it is due to emboli; it occurs without discoverable causes; it is secondary to cystitis, the cystitis being due to strictures of the urethra, to stone in the bladder, to paraplegia, to operations on the urethra, bladder, and uterus, to gonorrhoea, to enlarged prostate.

Chronic suppurative pyelo-nephritis is often caused by the presence of calculi in the pelvis of the kidney.

1. Suppurative Nephritis from Injury.--Gunshot wounds, incised or punctured wounds, falls, blows, and kicks are the ordinary traumatic causes. If the injury is a very severe one, it causes the death of the patient in a short time; if it is less severe, suppurative inflammation may be developed.

The inflammatory process may be diffuse, so that the whole of one or both kidneys is converted into a soft mass composed of pus, blood, and broken-down tissue, or it is circumscribed, and one or more abscesses are found in the kidney which may communicate with the pelvis.

SYMPTOMS.--Rigors mark the beginning of the suppuration, and are often repeated through its course. A febrile movement is developed which is apt to assume the hectic character with sweatings. There is often vomiting. There may be very severe pain, referred to the region of the inflamed kidneys. The urine is diminished or suppressed; it contains blood alone or blood and pus.

In the bad cases the patients pass into the typhoid condition, become delirious, and die comatose or with a very rapid or febrile pulse. Or the disease is protracted, the patients become more and more emaciated, and finally die exhausted.

In other cases the symptoms abate, the urine returns to its natural condition, and the patients recover.

TREATMENT.--The management of these cases is rather surgical than medical. The external wound is to be treated antiseptically, and the general condition of the patient to be looked after in the ordinary way.

Such traumatic abscesses are of infrequent occurrence. I have no personal knowledge of them.

2. Abscesses produced by Emboli.--In ordinary endocarditis with vegetations on the valves it often happens that fragments of the vegetations become fixed in the branches of the renal arteries. When this is the case infarctions are produced, usually of the white variety.

With malignant endocarditis, with surgical pyæmia, and with the curious cases called idiopathic pyæmia, small emboli seem to find their way into the smallest branches of the renal artery. They do not produce infarctions, but small abscesses. In these cases the kidneys are increased in size and dotted with little white points surrounded by a red zone. These little white points are formed by an infiltration of pus-cells between the tubes, and in the larger foci by a breaking down of the kidney-tissue. Colonies of micrococci are sometimes, but not always, found in the Malpighian tufts, the veins, and the abscesses.

{100} SYMPTOMS.--These embolic abscesses can hardly be said to have any clinical history. Whatever symptoms may belong to them are lost in those of the general disease from which the patient is suffering.

3. Idiopathic Abscesses.--Occasionally cases of abscesses of one of the kidneys are met with. They last a long time, and when the patient dies both the kidney tissue and the pelvis are involved to such an extent as to render the anatomical diagnosis difficult. The greater part of the kidney-tissue is destroyed and replaced by sacs full of pus; the pelvis is dilated and its walls thickened. The surrounding connective tissue is thickened; perforations and sinuses may extend into the surrounding connective tissue, into the large intestine, and through the diaphragm into the lung.

SYMPTOMS.--At first these cases are apt to be very obscure. An irregular febrile movement accompanied with rigors comes and goes, lasting for shorter or longer periods. The patients lose appetite, vomit occasionally, and become emaciated and anæmic. With this there may be pain over the region of one of the kidneys.

After a time a tumor may make its appearance in the position of one kidney--a tumor which can be felt through the anterior abdominal wall. If the abscess communicates with the pelvis of the kidney and the ureter remains pervious, pus and fragments of kidney-tissue are discharged with the urine. The pus is usually discharged at intervals, and at such times the size of the tumor diminishes. In other cases the pus burrows in other directions--into the retro-peritoneal connective tissue, the peritoneal cavity, the colon, or through the diaphragm into the lung. These cases are apt to run a protracted course and terminate fatally.

TREATMENT.--The only plan of treatment likely to cure the patient is a surgical one--either to extirpate the diseased kidney, or to cut down on the abscess and treat it on the antiseptic plan like any deep abscess.

4. Suppurative Pyelo-Nephritis with Cystitis.--LESIONS.--Usually both kidneys are affected. They are increased in size, and both the kidneys and their pelvis are congested. The mucous membrane of the pelvis is thickened and coated with pus or patches of fibrin. Scattered through the kidneys are abscesses and purulent foci of different sizes. The smallest foci are not visible to the naked eye, but with the microscope we find collections of pus-globules between the tubes, with swelling and degeneration of the epithelium within the tubes. The larger purulent foci look like white streaks or wedges running parallel to the tubes and surrounded by zones of congestion. The larger abscesses replace considerable portions of the kidney.

The ureters in some cases are inflamed, their walls thickened, their inner surface coated with pus or fibrin. The bladder presents regularly the lesions of acute or chronic cystitis.

ETIOLOGY.--For the production of this form of nephritis inflammation of the bladder seems to be necessary. How the inflammatory process is transmitted from the bladder to the kidneys is still uncertain, but it seems probable that it is effected by bacteria. The cases of cystitis in which a suppurative nephritis is likely to be developed are those due to strictures of the urethra, stone in the bladder, operations on the urethra, bladder, and uterus, paraplegia, gonorrhoea, and enlarged prostate.

SYMPTOMS.--When the nephritis occurs with cystitis due to stone in the bladder, strictures, or operations on the genito-urinary tract, the {101} symptoms are much the same. The patient has first the symptoms belonging to the cystitis, then he is attacked with rigors, followed by a febrile movement. The rigors are often repeated; the febrile movement is very irregular and often accompanied by profuse sweating. There is a rapid change in the general condition of the patient. He becomes much prostrated and emaciated from day to day. The face is drawn and anxious, the tongue dry and brown, the pulse rapid and feeble, and delirium is developed, and the patient finally dies in a condition resembling that of typhoid fever or of pyæmia. The urine is diminished in amount; it may be suppressed. It contains blood, pus, and mucus. The pus and mucus belong to the cystitis; the blood seems to be derived both from the kidneys and the bladder.

Cases of suppurative nephritis complicating gonorrhoea are fortunately not common, but several of them have been observed. Murchison[2] describes two cases, in both of which the cerebral symptoms were very marked--delirium, convulsions, and coma. I have seen one such case. The patient was a prostitute who came into the hospital with a specific vaginitis. After a few days she developed symptoms of an acute cystitis; then after a few more days she was attacked with rigors and a febrile movement, passed rapidly into the typhoid condition, and died. At the autopsy there were found acute cystitis, pyelitis, and numerous small abscesses in both kidneys.

[Footnote 2: _Lancet_, 1875, p. 80.]

When suppurative nephritis complicates the cystitis due to enlarged prostate, the clinical symptoms are somewhat different. The patients are usually men over fifty. They have generally suffered from the symptoms of enlarged prostate--retention of urine, either constant or intermittent, and more or less cystitis, with pus and mucus in the urine in varying amount. Sometimes, however, no such history is obtained; the patients assert that they have had no previous bladder trouble. The first symptom is diminution in the amount of urine passed and the appearance of blood. The quantity of urine is only a few ounces or it is completely suppressed. The blood is present in considerable amount; often the patients seem to pass pure blood instead of urine. The patients rapidly become prostrated and very anxious. There are usually no rigors, and there may be no febrile movement. After this the prostration becomes more marked, the pulse is rapid and feeble, the skin cold and bathed in perspiration, and the patients die in collapse at the end of a few days.

PROGNOSIS.--Suppurative nephritis secondary to cystitis is a very fatal disease; so far as I know, all the cases die.

TREATMENT.--The treatment for these cases is altogether a preventive one directed to the cystitis. In the cases of paraplegia, stone in the bladder, stricture, and enlarged prostate constant care must be used to prevent the accumulation of urine in the bladder and the development of cystitis.

In all cases of operation on the genito-urinary tract the supervention of cystitis is to be guarded against.

{102} PERINEPHRITIS.

The loose connective tissue which is situated around and beneath the kidney may become the seat of suppurative inflammation, and in this way abscesses of considerable size are formed.

LESIONS.--The connective tissue behind the kidney seems to be the usual point of origin of the inflammatory process, and it is here that the pus first collects. After the abscess has reached a certain size the suppuration seems to have a natural tendency to spread and the pus burrows in different directions--backward through the muscles; downward along the iliac fossa, even as far as the perineum and scrotum or vagina; forward into the peritoneal cavity, the colon, or the bladder; upward through the diaphragm. The kidney is either compressed by the abscess or its tissue also becomes involved in the suppurative process. The soft parts around the abscess become thickened.

ETIOLOGY.--Perinephritis is either secondary or primary. The secondary cases are due to extension of the inflammation from abscesses in the vicinity, such as are formed with caries of the spine, pelvic cellulitis, puerperal parametritis, perityphlitis, suppuration of the kidneys, and pyelo-nephritis. The primary cases occur after exposure to cold, after contusions over the lumbar region, great muscular exertion, and without discoverable cause. The lesion is said to complicate typhus and typhoid fever and smallpox. The disease occurs both in children and adults, most of the cases reported having been between the ages of twenty and forty years.

SYMPTOMS.--The disease begins regularly with pain and tenderness referred to the lumbar region on one side between the lower border of the ribs and the crest of the ilium, sometimes to a point above or below this. At about the same time are developed repeated rigors, a febrile movement with evening exacerbations, sweating, loss of appetite, vomiting, and prostration. These are all the symptoms for from one to two weeks. Then the skin over the lumbar region on one side becomes red and oedematous; the corresponding thigh is kept flexed and rigid, for any movement of it gives pain. Then the lumbar region becomes more and more swollen until fluctuation can be made out, and finally the abscess breaks through the skin. If such cases are left to run their course the abscess may reach a very large size. If the pus does not extend backward, but in some other direction, the symptoms are more obscure, for the local symptoms of an abscess in the back are absent.

If the abscess ruptures into the peritoneal cavity, the symptoms of acute general peritonitis are suddenly developed. If it perforates into the colon or bladder, the pus is discharged with the feces or the urine. If the perforation is through the diaphragm, there will be empyema, or the lung becomes adherent and pus is coughed up from the bronchi. As soon as the abscess is opened and the pus escapes the acute constitutional symptoms subside.

Trousseau believes that the inflammatory process sometimes stops short of the production of pus. In such cases of course there are no evidences of the formation of an abscess.

The disease may terminate in different ways: {103}

1. The inflammation may terminate in resolution (Trousseau).

2. The abscess is opened by operation or spontaneously and the patient recovers.

3. Although the abscess is opened either by the surgeon or spontaneously, the suppurative process continues and the patient dies exhausted, usually with waxy viscera.

4. Perforation into the peritoneum, the pleura, or the lung causes death.

TREATMENT.--The main point in treatment is to discover the abscess and to open it. The longer the suppurative process goes on and the larger the abscess, so much the worse is the prognosis. It is proper to explore with the aspirator after the disease has lasted for a few days, even if no fluctuation can be made out. The abscess is to be opened and treated on antiseptic principles.

{104}

HÆMATURIA AND HÆMOGLOBINURIA OR HÆMATINURIA.

BY JAMES TYSON, A.M., M.D.

The above terms are applied, the first to a condition of urine in which, of the constituents of blood, red discs at least are present; the second to that in which, while no corpuscles are found, blood coloring matter is abundant. Each of these conditions has been repeatedly observed as a distinct state at the moment when urine is passed; but it is also to be remembered that a true hæmaturia may, in the course of a few hours, become a hæmatinuria or hæmoglobinuria, by solution or disintegration of the red blood-discs. So far as I know, this subsequent solution and conversion can take place only in an alkaline urine; but as any urine through decomposition may become alkaline, it is evident that any hæmaturia may, in the course of time, become a hæmoglobinuria--a fact sometimes overlooked. I have, for example, known urine to be sent from Southern parts of the United States which, when shipped, contained blood-corpuscles, but which, when received in Philadelphia, contained no blood-discs, only large amounts of blood coloring matter. Especially does this occur in warm weather, when urine decomposes quickly. Such a hæmoglobinuria might be characterized as secondary. Doubtless, too, a more rapid solution is contributed to in some instances by the state of the blood-discs themselves, which are at times disintegrated before or at the moment they leave the blood-vessels, at others are intact, and at others, still, may be just ready to fall to pieces. In the hæmoglobinuria, where the blood-corpuscles have been secondarily dissolved and disintegrated, their remnants may be found in the shape of dark-brown or red granules, which form a sediment of varying bulk.

The immediate cause of this dissolved state of the blood-discs, where not due to the solvent action of an alkaline urine, appears to be the difference in degree of the cachexia which is at the bottom of the renal hemorrhagic tendency.

The term hæmaturia is applied to blood in the urine from whatever part of the urinary passages it may come, whether the bladder, ureters, kidney, or even urethra; whereas the blood in primary hæmoglobinuria always comes directly from the kidney.

In this paper I shall confine myself to the consideration of renal hæmaturia and hæmoglobinuria in the strict sense of the term; nor will I include such renal hæmaturia as constantly occurs in the first stage of acute Bright's disease.

Emphasizing again that all primary hæmoglobinurias are renal, it is {105} important to be able to say of a given hæmaturia whether it is renal or not. Even coarse methods are often sufficient to settle the question. Blood from the kidney, so far as my experience goes, is never discharged in the shape of clots, at least large enough to be recognized as such by the naked eye. More frequently coagula of blood are passed when hemorrhage takes place into the pelvis of the kidney. These coagula generally cause severe pain in their descent, and by this symptom are distinguished from coagula from the lower part of the ureter and bladder.

The smoky hue, which is characteristic of the presence of small quantities of blood in an acid urine, affords presumptive evidence that the blood is renal in its origin, because the conditions which are associated with blood from other parts of the genito-urinary tract are very apt to be associated with an alkaline urine, to which blood imparts a bright-red hue. This is, however, not invariable, as smoke-hued urine may be due to admixture of blood from the bladder and parts of the genito-urinary tract other than the kidney.

The microscope affords valuable assistance in determining the source of blood in the urine. In addition to blood-discs or their molecular débris, tube-casts made up of cemented blood-discs or their débris are very constantly, although not invariably, found in such urine. This evidence is conclusive, and, although sometimes wanting, the invariable absence of clots from blood descended from the kidney, together with the absence of irritation of the bladder, makes it usually quite easy to recognize a renal hæmaturia.

It is scarcely necessary to say that all urine containing blood or hæmoglobin contains albumen, the quantity varying with that of these substances present. Any further deviations from the normal composition of the urine are, in the main, due to admixture of other constituents of blood.

Causes which give rise to Hæmaturia and Hæmoglobinuria.

Hæmaturia is due to a variety of causes, which may be local or general. Local hæmaturia is caused by wounds, blows upon the kidney, or falls in which the kidney receives the force of the blow, as in striking the edge of a fence in falling; from cancer of the kidney, impacted calculus, parasites, embolism, acute Bright's disease; also poisoning from carbolic acid, cantharides, and mustard. General causes of hæmaturia are malaria, purpura, scurvy, blood-dyscrasias due to continued and eruptive fevers, especially typhus fever and smallpox, septicæmia and pyæmia, and cholera. Finally, it must be admitted that there is a hemorrhagic diathesis manifested by hæmaturia and hæmoglobinuria. Primary hæmoglobinuria may be produced by any of the general causes just named, or by the prolonged inhalation of arseniuretted hydrogen and carbonic acid, and the introduction of numerous substances into the blood, as iodine, arsenic, etc.

While a rupture of the blood-vessels of the kidney may be supposed to be at the bottom of a certain proportion of cases of hæmaturia, it is by no means a necessary condition of their occurrence, as it is well known that in inflammations there may be extravasations of blood without rupture of {106} the blood-vessels. There is implied, however, in all these conditions an alteration of the vessel-walls which permits such transudation. Indeed, Ponfick[1] goes so far as to say that even transudations of hæmoglobin through the blood-vessels of the kidney are impossible without the presence of serious diffuse nephritis. There is every reason to believe, however, that simple alterations of the blood are of themselves sufficient to cause such transudations. Take, for instance, the extravasations in purpura, which are not confined to the vessels of the kidney. It is impossible to conceive inflammatory conditions so general as would have to be presupposed in this disease.

[Footnote 1: "Ueber die Gemeingefährlichkeit der essbaren Morchel," _Virchow's Archiv_, Bd. lxxxviii. S. 47.]

Hæmaturia from Local Causes.

It is unnecessary to consider in detail the local causes of hæmaturia. It is evident how injuries and blows upon the kidney, and impacted calculus may produce hemorrhage. The history of nephritic colic or of gravel in urine, along with blood, would suggest the latter cause. Nor is it necessary to detail the phenomena of hemorrhagic infarction which succeeds embolism and is the direct cause of hemorrhage into the tubules of the kidney. Hæmaturia is by no means a constant symptom in sarcoma and cancer of the kidney. A small amount of blood in the urine is a constant symptom in acute nephritis, where it is due to a rupture of the blood-vessels of the Malpighian tuft. It is accompanied by blood-casts and other symptoms of acute Bright's disease. Carbolic acid, cantharides, oil of mustard, and similar substances produce hæmaturia by causing congestion and inflammation of the kidney.

The parasites which may cause hemorrhage in the substance of the kidney are the Bilharzia hæmatobia, the Filaria sanguinis hominis, the Strongylus gigas, and possibly common intestinal worms which may reach the kidney through fistulous openings. The first is a thread-like worm three or four lines in length, which was discovered by Bilharz, and infests the small vessels of the mucous and submucous tissue of the veins of the intestinal tract, the pelvis of the kidney, ureter, bladder, and more rarely of the kidney itself. It is very frequent in Egypt, where Griesinger found it 117 times in 363 autopsies; also in South Africa (Cape of Good Hope), where it gives rise to an endemic hæmaturia. It has been studied by Bilharz, John Harley, and William Roberts.

The Filaria sanguinis hominis is a long, narrow microscopic worm, not wider than a red blood-disc, and one seventy-fifth of an inch long, which infests the blood. Hemorrhages result from its accumulation in the vessels, causing rupture. The cases which have been studied occurred mostly in India, China, and Australia.

The Strongylus gigas is a large worm, resembling the ordinary lumbricoid, but larger, the male being from ten to twelve inches long and one-fourth of an inch wide, while the female is sometimes more than a yard in length. It infests the kidneys and urinary passages of certain lower animals (the dog, wolf, horse, ox, etc.), but rarely those of man.

{107} Malarial Hæmaturia and Hæmoglobinuria.

SYNONYMS.--Intermittent hæmaturia; Paroxysmal hæmaturia; Malarial yellow fever; Swamp yellow fever; Paroxysmal congestive hepatic hæmaturia (Harley).

Perhaps the most important form of hæmaturia and hæmoglobinuria resulting from general causes is that due to malarial poisoning. I prefer the term malarial to intermittent or paroxysmal, not only because it more precisely indicates the cause of the condition, but also because the condition itself is by no means always intermittent, sometimes continuing without interruption until checked by appropriate treatment; and I have known it to continue uninterruptedly for a year, in spite of all treatment.

The first complete report of an undoubted instance of this affection appears to have been published by Dressler in 1854,[2] although incomplete and uncertain cases were reported prior to this date--one as early as 1832 by Elliotson.[3] G. Troup Maxwell of Ocala, Florida, writes me, in 1883, that he first observed cases in Florida thirty years ago, and published an article on the disease in the _Oglethorpe Medical Journal_, Savannah, Ga., July, 1860. George Harley[4] early contributed to our accurate knowledge of the subject in 1865, and since then numerous papers and reports of cases have appeared in English and American journals, the southern part of the United States being a fertile scene of the affection, while it is by no means rare in the Middle States.

[Footnote 2: "Ein Fall von intermittirender Albuminurie und Chromaturie," _Virchow's Archiv_, Bd. vi. S. 264, 1854.]

[Footnote 3: "Clinical Lecture on Diseases of the Heart, with Ague (and Hæmaturia)," _London Lancet_, 1832, p. 500.]

[Footnote 4: "Intermittent Hæmaturia," _Medico-Chirurg. Trans. London_, 1865.]

Two degrees of the disease are met with--a milder form, in which other symptoms as well as the hæmaturia are less pronounced, and of which instances occur in the Middle States as well as the South and West of the United States. Of this kind seem to be the cases studied by Harley and other English physicians. In addition to this, there is a second, more malignant, form, attended by great prostration, vomiting, and yellowness of the skin, along with copious discharges of bloody urine. Instances of the latter are numerous in the Southern States of this country, where they have recently been studied with much care; also in the East and West Indies and in tropical countries generally. In neither degree of the disease is it necessary that the red corpuscles of the blood should be present. They may be represented by their coloring matters alone, when the condition is called a hæmoglobinuria or a hæmaturia.

The Milder Form.--The subjects, in my experience of eight cases, have been, with one exception, men, and I believe the experience of others included more men than women. They are generally able to recall a history of exposure to malaria, and often of distinct attacks of malarial fever, intermittent or remittent. The hæmaturia appears suddenly, and when paroxysmal may occur daily or on alternate days or a couple of times a week, or even at longer intervals. When the attacks occur at longer intervals, say of ten days or two weeks, if the disease is left alone the interval is apt to gradually diminish until the passage of bloody urine becomes daily. The urine in the {108} morning may be perfectly clear, and at two o'clock is evidently bloody. It continues so through one or two acts of micturition, and then becomes clear again; or it may be bloody on rising and clear up by noon. Sometimes the bloody urine is preceded or accompanied by a sense of weariness and chilly feeling, or sometimes simply by cold hands and feet or by cold knees, or by pallor and blueness of the face, or by accelerated pulse, or by no other symptoms whatever. There is sometimes a sense of fulness in the region of the kidney and sacrum. The attacks are often induced by exposure to cold.

Harley states that in one of the two cases which he reported there was a slight jaundice, and in the second a "sallowness which appeared to be due to a disturbance of the hepatic functions," but in none of the cases which I have met was this symptom present. In the more malignant form occurring in the tropics and the Southern States of America, jaundice is a constant symptom.

While a majority of cases of malarial hæmaturia are intermittent, many are continuous, and of my eight cases only three were distinctly intermittent. One of these cases I published in a clinical lecture in the _Philadelphia Medical Times_ as far back as September 1, 1871.

Negroes are not exempt from this milder form of the disease, as they seem to be from the more malignant form of the South. While writing this paper I was consulted by a negro thirty-one years old who had a true malarial hæmoglobinuria, which yielded promptly to the treatment by quinine. But this was the only negro out of seven cases.

The duration of the disease is very various, and if neglected may be indefinite. Stephen Mackenzie[5] reports a case which lasted twenty-three years.

[Footnote 5: "On Paroxysmal Hæmoglobinuria," _London Lancet_, vol. i., 1884, p. 156.]

PHYSICAL AND CHEMICAL CHARACTERS OF THE URINE.--The urine is usually acid in reaction when passed, sometimes neutral, rarely alkaline, and ranges in specific gravity from 1010 to 1028. It is always albuminous, and always tinged by blood coloring matters, the depth of color varying from the trifling degree known as smoke-hued to a dark-red or claret color. Sometimes it is even darker, and is often compared to porter, though this degree of coloration is more characteristic of the malignant form. The urine deposits a dark, reddish-brown sediment, generally copious, but varies in quantity with the degree of coloration of the urine. This sediment is made up chiefly of red blood-discs or the granular débris resulting from their disintegration.

Casts of the uriniferous tubules are also often present. They are usually made up of aggregated red blood-discs or the granular matter referred to; but they may also be hyaline or hyaline with a moderate amount of granular matter attached. Granular urates also at times contribute to the sediment and also adhere to the casts. Renal and vesical epithelium may occur. Crystals of oxalate of lime and of uric acid are sometimes present, while blood-crystals have been found by Gull[6] and Grainger Stewart, and a hæmatin crystal once by Strong.[7]

[Footnote 6: _Guy's Hosp. Reports_, 1866, p. 381.]

[Footnote 7: _British Med. Journ._, 1878, vol. ii. p. 103.]

That red blood-discs are at times exceedingly scarce, and even totally absent at the very moment when urine is passed, is a well-recognized fact; while that the coloring matter present is still that of the blood, {109} even though no corpuscles are present, is easy of demonstration by the production of Teichmann's hæmin crystals,[8] by spectrum analysis, or by the guaiacum test.

[Footnote 8: Place a drop of the sediment upon a glass slide and allow it to dry. Mix thoroughly with a few particles of common salt and cover with a thin glass cover, under which allow two or three drops of glacial acetic acid to pass. Carefully warm the slide for a few seconds over a spirit-lamp, and when most of the acetic acid is evaporated, examine by the microscope. Hæmin crystals will be seen to crystallize out as the mixture cools.]

In the matter of the presence or absence of blood-discs, it is to be remembered that these may be present at the moment the urine is passed, but disappear by subsequent solution if the urine happens to be alkaline or becomes so secondarily. It is an interesting fact, too, that colorless blood-corpuscles are often present intact, even when red discs are absent. While I have frequently examined urine sent me from the South in which the coloring matter of the blood and no corpuscles were present, only one of the cases coming under my own observations furnished urine of this character. The proportion of urea varies, and bears no evident relation to the condition itself.

PATHOLOGY AND MORBID ANATOMY.--The pathology of malarial hæmaturia consists, as yet, chiefly of theoretical deductions. We can only conclude that the malarial poison acts upon the blood and blood-vessels, impairing the integrity of both. This goes so far occasionally as to produce an actual destruction of blood-discs, and always so alters the capillaries that they permit the transudation of blood-elements ordinarily retained.

The morbid anatomy is scarcely more precisely defined. Ponfick[9] goes so far as to say that the exudation of hæmoglobulin is not possible without the concurrence of marked diffuse nephritis. Recently Lebedeff[10] has sought to investigate the more minute alterations of the kidney in hæmoglobin exudation, but without very definite results. These, however, on the whole, seem to confirm Ponfick's view as to the presence of an inflammatory process, as also do those of Litten[11] and Lassar.[12]

[Footnote 9: "Ueber die Gemeingefährlichkeit der essbaren Morchel," _Virchow's Archiv_, Bd. lxxxviii. S. 476, 1882.]

[Footnote 10: "Zur Kenntniss der feineren Veränderungen der Nieren bei der Hämoglobinausscheidung," _Virchow's Archiv_, Bd. xci. S. 267, Feb., 1883.]

[Footnote 11: "Verhandl. des Vereins für innere Medicin," _Deut. Med. Wochenschr._, No. 52, Dec. 29, 1883.]

[Footnote 12: _Ibid._, No. 1, Jan. 3, 1884.]

DIAGNOSIS.--The diagnosis of this condition is not usually difficult. We have first to determine whether the hemorrhagic discharge is from the kidney rather than the bladder or ureters. The former is the case when tube-casts are found. But tube-casts are not always present even when the hemorrhage is from the kidneys. The absence of clots and of vesical irritation, and of pain in the course of the ureters, is characteristic of blood from the kidneys. Finally, all hæmoglobinurias are renal.

It being certain that the blood comes from the kidney, we have to distinguish it from that due to cancer, to calculus-irritation, and to cachexias, as purpura and scurvy; or to grave forms of infectious disease, septicæmia, pyæmia, etc.; or, finally, to poisonous substances introduced into the blood, such as arsenic, iodine, arseniuretted hydrogen, carbonic acid and carbonic oxide gas, and even certain species of edible fungi.

The diagnosis is greatly aided if it is found we have to do with a {110} hæmoglobinuria rather than a hæmaturia. For although the former condition is produced by toxic and septic agencies of another kind, the attending symptoms, when it is thus produced, are so characteristic that it is not likely that error can be made.

To aid in distinguishing it from cancer we have the history of malarial exposure, and often that of other forms of malarial disease; and, notwithstanding the seeming drain upon the system, none of the cases I have ever seen present the profound anæmia of cancer. The bloody discharge in cancer of the kidney is always a true hæmaturia; there are always blood-discs in the urine. There is often pain in the region of the kidney in cancer, but never in malarial hæmaturia.

In calculous disease there is almost always pain before or during the hæmaturic attack, and characteristic crystalline sediments often appear in the urine.

The disease, being comparatively rare in this latitude, is sometimes overlooked on this account. Of the 8 cases which I have noted during sixteen years, 5 originated in Pennsylvania, 1 in New Jersey, 1 in Delaware, and 1 in North Carolina.

TREATMENT.--The treatment is distinctly that of malarial disease, and I have seldom seen more brilliant and satisfactory results than have followed the use of quinine in a case accurately determined, although such success is not invariable; and I have known the disease to resist for a long time the most thorough and judicious use of anti-malarial remedies. Usually, however, I take hold of a case of this kind with considerable confidence. When there are distinct remissions my practice has been to administer 16 to 20 grains of sulphate of quinia in the usual manner of anticipation of the paroxysm in intermittent fever--from 3 to 5 grains every hour until the required amount is taken; the whole amount may be taken in two doses, or even in one dose. Where there is no distinct remission I more usually direct 3 to 5 grains every three hours, until the hemorrhage ceases or decided cinchonism is produced.

The advantage well known to accrue in malarial disease from the combination of mercurials with quinine applies to hemorrhagic malaria as well, although I usually reserve the mercurial until I have ascertained whether the simple quinine treatment answers the purpose. If the usual method fails, I give 8 or 10 grains of calomel in the evening, followed by a saline in the morning, before reinstituting the quinine treatment. In the case of the colored man alluded to who had malarial hæmoglobinuria 36 grains of quinine failed to break the attack; but the same quantity, given after 10 grains of calomel had acted, succeeded.

Where these means failed I have not found the other methods of treatment commonly resorted to in obstinate malarial disease to be any more efficient. I allude to the treatment by arsenic or by iron and arsenic. Indeed, in the only two cases in which, after failure with the quinine treatment, iron and arsenic were used at my suggestion, they failed absolutely. In the one case, under the care of James L. Tyson, this treatment was carried out most faithfully. After four weeks' treatment with quinine without effect, Fowler's solution was given, at first in 5-drop doses three times daily, subsequently increased to 10 and 15, along with 20- and 30-drop doses of tincture of the chloride of iron, until oedema of the eyelids occurred, when the arsenic was discontinued, but {111} the iron continued. In two or three days the arsenic was recommenced in 3- and 4-drop doses for three or four weeks longer without effect. Fluid extract of ergot in 20-drop doses was then substituted for the iron, alternating with the arsenic for two weeks longer, when some slight favorable change was apparent, but it was temporary. Repeatedly throughout the treatment the patient complained of weariness and backache, cold feet and knees, headache and acceleration of pulse, and a feeling of utter wretchedness; and then again he would feel quite comfortable for a day or two, but with little or no change in the urine, except occasionally in the morning, when it would sometimes be quite light-hued, but after breakfast would again assume its bloody character. A sojourn at the seaside for two weeks was without effect.

It will appear from the above that ergot, which has been found useful in some forms of hæmaturia, is of little service here, as is attested by two other cases in which I tried it faithfully. At the same time, it is a remedy which should be tried in case of failure with others.

The usual astringents, mineral and vegetable, of known efficacy in the treatment of hemorrhagic conditions, should be used alone or in conjunction with the specific anti-malarial treatment after the latter has been found of itself insufficient. To this class of remedies belong the mineral acids, persulphate of iron, acetate of lead, alum, gallic acid, catechu, kino, the astringent natural mineral waters, etc.

Rest is certainly an important adjuvant in the treatment of this form of malarial disease. I have known a recurrence to take place after a long drive.

It is claimed for many natural mineral waters that hemorrhage from the kidneys is one of the affections cured by their use. Chalybeate and alum springs might be expected to be of advantage by the local action of these astringents in their transit through the kidneys, and they frequently are. The following case illustrates their efficiency: The patient was a lawyer who consulted me in June, 1881, at the suggestion of W. W. Covington of North Carolina. He had frequently had chills, and a congestive chill in 1873. Three months before I saw him he began to pass bloody urine. He had no other symptoms, except a soreness and weakness in the neighborhood of the sacrum, extending into the outer part of the left thigh. The urine passed for me at the time of his visit was dark reddish-brown in color, acid in reaction, had a specific gravity of 1028, highly albuminous, and deposited a sediment of almost tarry consistence, which was made up almost entirely of blood-corpuscles. There were no tube-casts. He had been a dyspeptic since seventeen years of age, and medicines disagreed with him; but he was treated faithfully with quinine, iron, arsenic, ergot, benzoate of lime, all without the slightest effect. At the end of about a year from the time he consulted me he heard of the Jackson Spring, located in Moore county, North Carolina, fifteen miles distant from Manly Station on the Raleigh and Augusta Railroad. He went there, and remained one week. He stated that for the first two or three days the water acted decidedly on his kidneys, and he voided a number of clots of blood. On the third day all traces of blood disappeared, and it recurred but once since, on a very cold day in November last, but again disappeared after a day or two in the house. Unfortunately, no precise analysis of this water seems to have been made, but {112} from what my friend writes it evidently contains iron and sulphur, and magnesia is also said to be present. It is promptly diuretic. Since this occurred I have used the water of alum springs in other instances with advantage.[13]

[Footnote 13: See the report of a case treated successfully by Rockbridge alum-water by Radcliffe, _Med. News_, Jan. 12, 1884.]

The following are some of the chalybeate and alum springs the waters of which may be expected to be of service in hæmaturia: Orchard Acid Springs, New York; Rockbridge Alum Springs, Pulaski Alum Springs, Bath Alum Springs, Stribling Springs, and Bedford Alum Springs, all in Virginia. In all of these waters iron and alum are both present, accompanied, in many instances, by free sulphuric acid, by which their efficiency is increased. In one of my cases the hemorrhage disappeared temporarily under the use of the water from the Bedford Springs, Penna., but again returned. These waters contain a little iron, but no alum. Subsequently, the same patient was promptly relieved by quinine, which had not been previously tried.

But the cases most promptly relieved by the alum waters are the non-malarial cases depending, upon hemorrhagic diathesis without other local disease. A remarkable instance of this kind was related to me by letter by J. Macpherson Scott of Hagerstown, Md. After enormous doses of quinine had been used under the supposition that it was malarial, it was promptly and totally cured.

Malignant Malarial Hæmaturia.

The second more serious form of this disease, as it occurs in the tropics and the southern part of the United States, is characterized by such increased intensity of all the symptoms that it may be well called malignant. Singularly, however, the disease has seemed to be much more prevalent during the last fifteen years. My attention was first called to it in September, 1868, when I received specimens of urine and the history of some cases from R. D. Webb of Livingston, Ala., who wrote also that it was not known in that part of his State prior to 1863 or 1864.

In this, as in the milder form, there is a distinct but more invariable history of malarial exposure, and the attack often begins as an ordinary case of chills and fever, there being often one or two paroxysms before the hæmaturia appears. At other times the hemorrhage ushers in the disease suddenly. The urine is often black and almost tarry in consistence, and passed in unusually large quantities--it is said as much as a pint every fifteen or twenty minutes until a couple of quarts have been passed, or one or two gallons in the course of twelve hours. But after twenty-four hours the quantity diminishes. Epistaxis sometimes occurs, but is not often profuse. Distressing nausea, and vomiting of bilious and even black matter, like that of black vomit, also occur. Intense jaundice rapidly supervenes--said to come on sometimes in the course of an hour, often in from two to six hours. The tongue is brown and dry. The bowels are at times constipated, and at others loose. Although the patient may be feverish at first, with a temperature of 104° to 106°, and the skin dry, the pulse rapidly becomes small and feeble until it is {113} scarcely perceptible. Drowsiness and coma sometimes intervene, and at others the mind is clear until the moment of death, which frequently supervenes within twenty-four or sixty hours; or the symptoms may subside, to be repeated again the next day if not prevented by treatment. If recovery takes place, which it sometimes does, and lately more frequently, convalescence is slow and tedious, the patient remaining for weeks in an enfeebled and anæmic state.

In this form, especially, of the disease it often happens that the coloring matter and the débris of blood-discs only are found in the urine, very few and often no entire ones being discernible: in other words, we have a true hæmoglobinuria or hæmatinuria. The urine is of course albuminous. A specimen recently received from North Carolina and analyzed by Wormley contained no corpuscles, but revealed the spectroscopic band characteristic of hæmoglobin. It contained 2½ per cent. of urea. The specific gravity of the urine ranges between 1010 and 1020, being lower when it is copious.

As to the jaundice, it is evidently a hæmatogenetic, and not a hepatogenetic, form with which we have to deal. It is due, not to the retention of bile, but to the disintegration of blood-corpuscles and the solution of their coloring matter, which diffuses through the tissues and stains them yellow or yellowish-green. This form too, apparently, is more frequent in males, and negroes appear to be exempt. This is not the case with the milder form, for it will be remembered that one of my patients was a negro.

Autopsies reveal the same intense yellow coloration of internal organs--lungs, liver, spleen, stomach, kidneys--anæmia rather than congestion, while the blood is dark-hued and is indisposed to coagulate. The spleen is often enlarged.

The TREATMENT for the breaking of the paroxysm is pre-eminently quinine or quinine with mercurials, and although this does not always succeed, there seems to be no other remedy. The quinine may be given hypodermically. The nausea has been controlled by morphia and lime-water, by carbolic acid, and by creasote. In addition, restorative measures are necessary, including the free use of stimulants. Turpentine has been used in large doses (fluidrachm j), it is said with advantage, in Alabama.

{114}

CHYLURIA.

BY JAMES TYSON, A.M., M.D.