But usually it is not till the third or fourth day of scarlet fever that this complication begins. The patient has been progressing favorably with the scarlet fever, till on a certain day a marked aggravation of symptoms occurs. A higher temperature, more pungent heat, and the physiognomy of a more serious malady are present. On inspecting the fauces to discover the cause we observe a pellicle forming over the tonsils and perhaps other portions of the faucial surface. Often the entire aspect of the case changes by the occurrence of this complication, a mild case of scarlet fever becoming grave and fatal in consequence. Thus in a case which I saw with Dr. Hardy of New York the membranous inflammation of diphtheria, commencing upon the fauces on the third day of scarlet fever, extended to the Schneiderian membrane, and thence along the left lachrymal sac to the eyelids, producing redness and swelling along the side of the nose and upon the cheek like that of erysipelas. A thick diphtheritic pellicle occurred upon the under surface of each eyelid on the left side, with great tumefaction of both lids, gangrene of the cornea, and destruction of the eye. The case soon ended fatally.
The diphtheritic inflammation sometimes extends to the larynx and trachea, producing hoarseness and more or less obstruction to {517} respiration. A thin film or flakes of fibrinous exudation, rendering the respiration noisy, developed on the laryngeal or tracheal surface, is, I think, not infrequent in diphtheria complicating scarlet fever, but the rapid development of a thick and firm pseudo-membrane, so as to imperil the life of the patient from the stenosis in the air-passages, has been much less frequent in my practice than it is in primary diphtheria and in diphtheria complicating measles or pertussis. The following were cases of this severe complication occurring in a recent epidemic in the New York Foundling Asylum. In these cases the respiration was noisy, but the obstruction to breathing seemed to be due to infiltration and swelling around the aperture of the glottis, rather than to diphtheritic croup, which the autopsies showed to be present.
Case 2.--A child aged three and a half years, who previously had symptoms of mild catarrhal croup, with moderate redness of the fauces, sickened with scarlet fever on Oct. 1, 1882, the rash being profuse and soon covering nearly the entire body. The axillary temperature was 103°, pulse 140; slight stridor in breathing and some cough; fauces very red, but free from membrane. Oct. 2d, restless, sleeping but little; has vomited four times. Oct. 3d, temp. 103.5°, pulse 120; fauces much swollen; still vomiting; rash abundant. 4 P.M., temp. 104.3°, pulse 128; tongue clean; some discharge from nares; urine not albuminous, but its quantity diminished. Oct. 4th, aspect that of very severe sickness; profuse discharge from nostrils; fauces of a deep red color, and a diphtheritic pellicle over tonsils and uvula; tumefaction along the sides of the neck; temp. 104°, pulse 140; breathing moderately stridulous; urine is passed more freely than yesterday; evening temp. 105°. Oct. 6th, croupy symptoms more marked; tonsils and uvula greatly swollen, so that the fauces are almost occluded; temp. 103.5°; breathing difficult, but apparently sufficient oxygen is received; profuse nasal discharge, and other symptoms as before. About 1.30 P.M. he was raised to take some milk, and suddenly became asphyxiated. His face was dusky, his eyes protruded, and he voided urine and feces. Dr. Swift, who attended the child, and to whom I am indebted for this history, immediately performed tracheotomy, which gave temporary relief by the expulsion of a considerable quantity of pseudo-membrane through the opening. On the following day the respiration again became obstructed at some point below the canula, so that it could not be removed; the features grew livid, and death occurred in convulsions twenty-six hours after the tracheotomy.
The autopsy was made by Dr. W. P. Northrup, curator of the asylum, who found the pharynx covered by a membrane which was traced to the posterior nares; larynx, trachea, and bronchial tubes as far as the third divisions also covered with membrane; portions of the tracheal surface denuded, and the mucous membrane underneath of a bright red color and smooth; tonsils sloughy and fetid; mucous membrane of smaller bronchial tubes very red and covered with viscid mucus and pus; a portion of the left lung, extending from the root posteriorly to the surface, gangrenous, discolored, and honeycombed; two or three intensely hyperæmic spots, as large as a bean, in left lung; right lung congested, but not consolidated; slight catarrh of stomach; circumscribed areas of congestion in intestines; solitary glands of intestines swollen, and some {518} of them ulcerated; spleen of normal size, rather pale; liver congested and somewhat enlarged.
Case 3.--Katie, aged six and a third years, was returned to the asylum on Nov. 18th. Three days later (Nov. 21st) she had sore throat, reddened fauces, coated tongue, and a faint rash upon the neck, chest, and arms; eyes injected; temperature 102°. In the afternoon temperature 103°; eruption still faint. Nov. 22d, temperature 103.5°; an eruption on chest, abdomen, arms, and legs in patches. Evening, temperature 104°; voice clear. Nov. 23d, temperature 103.5°; tongue red; fauces deeply reddened, but without any visible pseudo-membrane; eruption of a scarlatinous appearance over the back and abdomen; on the extremities dusky, livid patches. P.M., temperature 104°; is slightly delirious; eruption abundant. Nov. 24th, temperature 103.5°; eruption well out on abdomen; it is the same as yesterday upon the extremities, except perhaps a little more dusky; still no pseudo-membrane to be seen upon the fauces; is restless and delirious. P.M., during the day has been very restless, suffering from dyspnoea; no croupy voice nor croupy cough, though the dyspnoea continues, and a pseudo-membrane is now visible over the tonsils and adjacent faucial surface; eruption dusky; skin cool; pulse very frequent and feeble. From this time she sank steadily, and died at 11.30 P.M. During her sickness her urine seemed to be diminished, but it was not properly examined.
Autopsy Nov. 25th by Dr. W. P. Northrup, curator: Points of redness, apparently a hemorrhagic eruption, over the face, shoulders, and parts of the trunk; a few of the same on the extremities; no pseudo-membrane visible in nostrils or in buccal cavity; brain not examined. Naso-pharynx covered by a thick fibro-purulent membrane. Larynx contains a well-marked pseudo-membrane, but not continuous. Trachea covered by a pseudo-membrane, continuous over most of its surface, but in places broken and flaky. Where it is detached the mucous membrane is seen underneath, dusky and deeply injected. At the root of the lungs the pseudo-membrane can be traced along the tubes about an inch in all directions. Lungs oedematous, with deep congestion in places, but apparently no pneumonia; about two drachms of clear, straw-colored fluid in pericardium; a few stringy decolorized clots in the cavities of the heart; left ventricle contracted. The heart-fibres, carefully examined, microscopically, in the laboratory, are found to be normal, not having undergone granular or fatty degeneration. Liver normal in size; pale-yellow areas upon the superior surface, either from anæmia or fatty deposition. Kidneys of usual size, capsule not adherent; pyramids congested; cortex pale; markings distinct. Spleen enlarged about one-third; consistence normal. Stomach and intestines not examined.
Case 4.--Scarlet fever complicated by diphtheria, nephritis, and broncho-pneumonia. (History by house physician, Dr. Swift.) Phoebe, aged three and a quarter years, was delicate, but in her usual health till Oct. 29, 1882, when she became languid and vomited several times, and her tongue was coated. Oct. 30th, occasional vomiting; fauces reddened; tongue coated. Oct. 31st, remains languid; fauces deeply reddened; a faint scarlatinous eruption over back, wrists, and feet; temperature 100.5°. P.M., eruption of scarlet fever well out over the surface; tongue cleaner. Nov. 1st, {519} rash over entire body; temperature 100.2°. Nov. 2d, fauces deep-red; tonsils and uvula swollen; diarrhoea and vomiting. Nov. 3d, temperature 102.5°; the eruption, which has been bright red, is now more dusky. Nov. 5th, temperature 104.5°; dusky-red color of the eruption; skin beginning to desquamate in places; urine normal; a discharge from nostrils. Nov. 6th, temperature 103.5°; eruption still present, but skin of abdomen and back desquamating; has otorrhoea on both sides; fauces deeply hyperæmic, but no pseudo-membrane visible upon them. Nov. 7th, temperature 103°; respiration and cough have a slight croupy character; other symptoms as yesterday. Nov. 8th, temperature 101°. A careful inspection of the fauces shows that it contains no pseudo-membrane; nostrils discharging a dark-brownish liquid; examination of urine negative. Nov. 11th, eruption, which appears to have been hemorrhagic in points, is fading and the desquamation is less. Nov. 14th, nostrils still discharging; glands of neck swollen. Nov. 16th, temperature 103°; sp. gr. of urine 1010, no casts, nor albumen; the chest seems clear; less discharge from nostrils; fauces clean and but slightly inflamed. Nov. 17th, 18th, temperature 103.5°; vomits; lungs healthy, but breathes with considerable effort, though without stridor; urine diminished; its sp. gr. 1020, albuminous, contains blood-corpuscles and granular casts. Nov. 19th, is very pallid; temperature 104°; very restless; vomits; urine diminished; bowels freely open. Nov. 20th, respiration still embarrassed; subcrepitant râles over the entire chest and percussion resonance not clear; temperature 102.5°. Nov. 21st, physical signs the same; temperature 103.5°; respiration 80. Nov. 22d, urgent dyspnoea; dulness on percussion over top of right lung and over lower part of left lung; is delirious; no perspiration; urine scanty; bowels freely open. From this date the dyspnoea became more urgent, and death occurred at 4 P.M. on the 23d.
Autopsy by Dr. W. P. Northrup, curator: Body well nourished; slight oedema of both legs; swelling at angles of jaws, most marked on left side. Vessels of brain moderately injected; otherwise appearance normal. Cicatrizing ulcers on both sides of fauces; a diphtheritic pseudo-membrane on septum of nose, larynx normal. Trachea, upper half apparently normal; a thin film of pseudo-membrane extends from just above the bifurcation upward to nearly the middle of trachea. About an ounce of fluid in each pleural cavity; on the right side a few loose flakes of fibrin floating in the serum, and consolidation of lung at apex; collapse in one or two places. Left side, recent adhesions over whole of posterior surface and base; surface of lower lobe dark, and when it is detached strings of fibrin adhere to it, and it is consolidated. The cut surface shows marked oedema, injection, increase of mucus in bronchi, and disseminated miliary tubercles in every part; no tubercles in the pleura, and none elsewhere in the body except in the left lung; tubercles in the lower lobe larger and more thickly grouped than in the upper lobe. Decolorized clots in heart, extending from ventricles into auricles of both sides. The capacity of the ventricles seems normal. Liver and spleen, normal. Kidneys rather large; capsules not adherent; superficial veins injected. The cut surface shows congested pyramids and pale cortex; markings indistinct and irregular; about four ounces of clear straw-colored fluid in abdominal cavity, and the solitary follicles of {520} large intestines show pigmentation; two simple intussusceptions, each three-fourths inch in length, in small intestines.
Coryza frequently commences at or about the time of the pharyngitis. The inflammation of the Schneiderian membrane is continuous posteriorly with that of the fauces, and is announced by redness and swelling, inability to breathe freely through the nostrils, and an irritating ichorous discharge. Simple coryza in itself involves little danger, though it is an unpleasant complication, and in the nursing infant it may interfere with sucking. Diphtheritic coryza, on the other hand, which is frequently present when diphtheria complicates scarlet fever, involves danger, since it is apt to cause ulcerations, hemorrhages, and septic poisoning. When the local symptoms are unusually severe and the discharge abundant, it is probable that inflammation has in some cases extended to the antrum of Highmore.
Inflammation of the middle ear is another unpleasant and not infrequent complication. It is attributed to extension of the catarrh from the pharynx along the Eustachian tube to the tympanum. In a considerable proportion of cases of otitis media this tube is occluded by the infiltration and swelling of its mucous membrane, so that the muco-pus escapes with difficulty or is retained. Hence severe earache, an increase of the febrile movement, and outward bulging of the membrana tympani occur. Sometimes headache or other cerebral symptoms arise, probably from the fact that the meningeal artery, which supplies the meninges, is connected by anastomosing branches with the tympanum. In one of the cases related above it will be recollected that the ulceration and abscess extended from the fauces to the middle ear, the entire Eustachian tube having disappeared in the ulcerative process.
Frequently, the otitis escapes detection, its symptoms being masked or obscured by the general disease, until the membrana tympani is perforated and otorrhoea begins; but by careful examination the nature of the complication can usually be ascertained before the ear is injured to this extent, for a patient too young to speak will often press with the fingers against the painful ear or lie with the ear pressed upon the pillow, evidently having an increase of suffering if placed in any other position. One old enough to speak and in proper mental condition makes known the earache as soon as it occurs.
The mucous membrane of the tympanum, red and swollen from inflammation, secretes muco-pus abundantly; and this, pent up in the cavity, must obtain an exit before relief occurs. It is well if this secretion escape, though with difficulty, down the Eustachian tube. The destructive action of the pus upon the delicate structure of the ear is often such that, within a few days, irreparable harm is done and more or less deafness results. Relief can occur, if the Eustachian tube remain closed, only by perforation of the membrane and the discharge of the secretions into the external meatus. When this occurs the inflammation in the most favorable cases gradually abates, the aperture in the drum closes, and the integrity of the auditory apparatus is preserved. In severe cases the mastoid cells participating in the inflammation become filled with muco-pus and tender to the touch, and often the collateral oedema causes tumefaction and narrowing of the external ear, which subside with the discharge of pus from the tympanum.
{521} Unfortunately, there is for many a more melancholy history--a more destructive inflammation, involving permanent impairment or total loss of hearing. This is especially apt to occur in strumous and feeble children. All grades of inflammation and destructive action occur in different cases. The perforation in the drum-membrane may be large or the membrane may be completely destroyed, and the detached ossicles escape one by one into the external meatus, and in a few instances, fortunately rare, this occurs in both ears, producing complete and permanent deafness. In my own practice this has never occurred, but I have met one or two adults who were totally deaf from this cause.
The mucous membrane which lines the bony wall of the middle ear has the function of the periosteum, and therefore, when inflamed and subjected to pressure, is liable to ulcerate. As in other parts of the skeleton under similar conditions, superficial caries or necrosis of the underlying bone is apt to occur. The carious or necrotic process may extend to the mastoid cells. An offensive otorrhoea, continuing for months or years, indicates the persistence of this pathological state of the tympanum, which is rendered so obstinate by the presence of dead bone. A moment's survey of the anatomical relations of the middle ear shows the danger to which these patients are liable. A thin bony septum, perforated with blood-vessels and sometimes containing congenital apertures, separates the tympanum from the cranial cavity above. Posteriorly lie the mastoid cells, connected with the tympanum by one large and several small apertures. Anteriorly is the commencement of the Eustachian tube and in close proximity to the tympanum lies the carotid canal, and at one point also the superior petrosal sinus. Virchow has shown how inflammation extending from the ear in otitis media sometimes produces such compression of the veins or sinuses by the swelling from the infiltration and exudation that the circulation is arrested, and the fibrin contained in the blood of these vessels is precipitated, forming thrombi, with the most disastrous effect upon the individual. Pus may also burrow in the interstices of the bone, causing great pain, or the pent-up secretions, having no outlet for escape, may in time undergo caseous degeneration, producing the conditions in which tuberculosis so often originates.
Death not infrequently occurs in chronic otitis media in another way. The otorrhoea, after months or years, suddenly ceases, the child complains of constant severe headache and is feverish, and the case ends in coma, preceded perhaps by convulsions. Meningitis has occurred, produced by extension of the inflammation through the thin bony septum which divides the tympanum from the cranial cavity, and at the autopsy hyperæmia of the meninges, fibrin, pus, perhaps softening of the brain and an abscess, are formed in the portion of the encephalon adjacent to the tympanum. Therefore, otitis media, though it often ends favorably, is in many patients an obstinate, dangerous, and even fatal sequel of scarlet fever.
The complication known as scarlatinous rheumatism is regarded by some as a synovitis, but its symptoms, especially its shifting from joint to joint, seem to ally it to the rheumatic affections. In some epidemics it is common. It usually begins toward the close of the first week or in the second week, and its common seat is in the ankle, phalangeal, and wrist joints. It is attended by very little swelling in {522} most patients, though the joints are tender and painful on pressure. It does not seem to retard convalescence materially, though it produces suffering and involves danger as regards the heart. It subsides in a few days with the ordinary treatment of acute rheumatism, and even without special treatment, the chief danger being that, as in idiopathic rheumatism, endocarditis may arise, with permanent crippling of the valves. The following was a case of valvular disease having this origin. It occurred in my practice.
Case 5.--Freddy M., aged four years, sickened with scarlet fever March 6, 1879. The usual vomiting occurred on the first day, and the temperature was 104°. The case progressed favorably till March 14th, when he complained of pain in both wrists, both ankles, and both knees. On March 17th the general condition was good, the urine contained no albumen, and apparently few urates, but he still had pain in the joints of the upper and lower extremities and in the back; pulse 140, temp. 103°; breathes with a slight moan; urates in the urine, but no albumen. A distinct mitral regurgitant murmur is now heard for the first time. Under the use of salicylate of sodium the pain in the joints soon ceased, but the mitral murmur is permanent.
The following prescription is for a child of five years:
Rx. Ol. Gaultheriæ fl. drachm iss; Sodii Salicylat. drachm iii; Syrupi fl. oz. ii; Aquæ fl. oz. iv. M.
S. Give one teaspoonful every four hours.
Of the serous inflammations occurring in scarlet fever, pericarditis has been, according to Rilliet and Barthez, most frequently observed. In this country it is probably more frequent than is usually supposed, but it is less frequently detected than pleuritis, the symptoms of which are more conspicuous. It is apt to occur in connection with endocarditis.
The following case, showing the liability to pericarditis and other serous inflammation which exists in scarlet fever, occurred in my practice:
Case 6.--C----, girl aged five years and ten months, sickened with severe scarlet fever on April 4th. Was delirious; pulse 158; had vomiting and constipation. April 10th, pulse varies from 124 to 153, no delirium; a considerable quantity of urates in the urine. April 11th, has to-day, for the first time, severe pain in the epigastrium, with tenderness and moderate distension. Otherwise symptoms favorable, but severe; pulse 140; respiration moderately accelerated, and vesicular in every part of the chest. From this date the symptoms continued about the same till April 14th, when the dyspnoea became more marked and the action of the heart rapid and tumultuous. The epigastric pain, distension, and tenderness continued; the percussion sound was dull over the lower part of the chest; the dyspnoea became rapidly worse, although the pulse had considerable volume; and at 5 P.M. death occurred. At the autopsy about one ounce of turbid serum, with a soft deposit of fibrin, was found in the pericardium. Each pleural cavity contained from six to eight ounces of transparent serum, and both lungs were readily inflated, except a little of the posterior portion of each lower lobe, which could not be; no fibrinous exudation over the lungs. The liver extended four inches below the margin of the ribs, and upon its convex {523} surface in the epigastrium, corresponding with the seat of the pain, was a rough patch of fibrin about one and a half inches in diameter. The bronchial mucous membrane was moderately injected, as was also that of the colon, and the kidneys appeared hyperæmic.
Among the serous inflammations which complicate or follow scarlet fever, pleuritis is one of the most important. It usually begins in the desquamative stage, and is apt to be suppurative on account of the feeble state of the patient when it commences. It has always, in my practice, been tedious, as all empyemas are, and it does not differ in its clinical history from the idiopathic disease. I have met cases of scarlatinous empyema in which, from opposition of the family or for other reasons, thoracentesis was not performed, and death occurred; others in which this operation effected a cure, and one at least in which the patient recovered by escape of pus through a bronchial tube. The pleuritis is seldom latent, or so masked by the symptoms of the general disease that it is apt to be overlooked. On the other hand, the cough, embarrassment of respiration, and pain referred to the affected side render diagnosis easy.
Dilatation of the heart is common in grave cases of scarlet fever, such cases as are properly termed malignant. It is indicated by a feeble and quick pulse. Acute infectious maladies, especially those of a malignant type and accompanied by high febrile movement, are very apt to cause parenchymatous degenerations in organs, prominent among which is granulo-fatty degeneration of the muscular fibres of the heart. This weakens very much the contractile power of these fibres. But early in malignant cases, probably before the muscular fibres are damaged, the contractile power of the heart is feeble from impaired innervation, the result of the general weakness. Hence this organ, when weakened by structural change and insufficiently stimulated through diminished innervation, may not fully empty itself during the systole, and consequently it becomes dilated. Dilatation of the heart and imperfect contraction of the auricular and ventricular walls are apt to result in the formation of clots in the cavities of the heart; and this appears to be the immediate cause of death in not a few instances. An ante-mortem clot occurring in any of the cavities of the heart necessarily seriously obstructs the circulation, unless it be of small size. Hence the dyspnoea, which may occur perhaps suddenly, and the change of pulse to one of marked feebleness and frequency. Large, firm white clots are most frequently found in the right cavities. They interlace with the chordæ tendineæ, lie even within the auriculo-ventricular opening, and send prolongations into the pulmonary artery and the cavæ. Associated with the white clots are dark, soft clots and fluid blood. The left cavities may be contracted and empty, or they may contain dark, soft clots or white ante-mortem clots. Clots in the left ventricle are sometimes prolonged into the aorta as far as the brachio-cephalic branches, while those in the left auricle may extend to the pulmonary veins. If dilatation of the heart be so great that clots form in its cavities, speedy death is probable. Sometimes a patient passes through scarlet fever and appears in a fair way to recover, when he succumbs to some exhausting sequel distinct from the heart, and at the autopsy the heart is found dilated and containing whitish clots, which are probably ante-mortem, and which hastened {524} death by obstructing the circulation. Under such circumstances this state of the heart is attributable in great measure to the complication which has weakened its contractile power.
The following was a case in point. It occurred in the New York Foundling Asylum:
Case 7.--R. A., aged three years, had scarlet fever, beginning March 23, 1882. The symptoms were favorable at first, but serious complications and sequelæ occurred, which were fatal. The record of April 18th reads: "Appears well nourished, but is anæmic; has otorrhoea; no oedema; skin desquamating; dulness on percussion over upper third of right side of chest, anteriorly and posteriorly; mucous râles and rude breathing over same area; fine râles posteriorly over lower part of left side of chest; pulse 160, respiration 68, temperature 101-2/5°." April 20th, is feeble and takes nutriment with difficulty; tongue thickly coated; pulse 160, respiration 68, temperature 101-2/5°. April 26th, condition about the same as at last record, but he is evidently weaker; the lips are ulcerated and fauces still swollen. May 2d, cannot speak distinctly; a brownish, foul-smelling secretion lodges on the spoon used in depressing the tongue; left side of face swollen. On the following night eight convulsions occurred, attended by orthopnoea, and mucous râles in the chest from pulmonary oedema. Diarrhoea supervened and the patient died about midnight. Autopsy: Body moderately wasted and very white, several dark-blue spots on scalp and face from hemorrhages underneath; lips covered with dry crusts; brain of normal appearance; aperture of the larynx narrowed at the chink by infiltration and swelling of the tissues; surface of the vocal cords covered by a thin white film, apparently a fibrinous exudation; tracheal surface hyperæmic; about a drachm of straw-colored fluid in each pleural cavity; right lung wholly adherent by recent exudation of fibrin; left lung also largely adherent. A careful examination showed the presence of broncho-pneumonia in each lung, with considerable infiltration of the walls of the bronchi, and cylindrical dilatation of many of them; cavities of the heart dilated, so that this organ appears much enlarged, and its shape approaches the globular; its apex is rounded or obtuse; transverse diameter of the right ventricle, when its walls were open and drawn apart, was three and one-quarter inches; that of the left ventricle three and a half inches. Similar measurements of the heart of another child of about the same age, believed to be normal, were about one inch less in each direction. All the cavities contain white firm clots along with soft dark clots. Liver of normal size, pale; the outer surface and all cut surfaces are studded with nodules of the size of a pin's head, of a dull, opaque white color. These white spots, examined microscopically by Professor Delafield, are found to be neither tubercles nor gummy tumors, but to consist of polygonal cells, lying in the meshes of the capillary plexus of veins, which are perfectly preserved. He has not observed a similar case. The walls of the gall-bladder are one line or more in thickness, and the gall-duct is pervious. The microscope shows general hypertrophy of the gall-bladder and hypertrophy of its papillæ. The urine removed from the bladder was found to contain albumen and hyaline casts, and a microscopic examination showed a small amount of parenchymatous inflammation. The spleen was somewhat enlarged. Punctate congestion of small areas of {525} gastric surface, no increase of mucus; mesenteric glands uniformly enlarged; jejunum, ileum, and colon exhibited a slightly increased vascularity. The immediate cause of death appeared to be imperfect contraction of the heart and the formation of clots in its cavities, due, apparently to the pleuro-pneumonia as much as, or more than, to the primary disease, scarlatina.
There can be little doubt that nephritis in its milder form is much more common than was formerly supposed. A few years since little attention was given by a large proportion of physicians to the state of the kidneys, and the urine was not examined till dropsy made its appearance, which only occurs in the more severe forms of nephritis and is a late symptom. It is now known that catarrh of the renal tubes frequently occurs in a mild form early in scarlet fever, without causing albuminuria, dropsy, or any notable symptom. It may produce a smoky color of the urine, and the appearance in it of granular epithelial cells, with an increase of mucus, but no albumen. With careful treatment and no exposure to cold, the renal catarrh abates with the decline of the scarlet fever. It is scarcely severe enough to merit the name desquamative, tubal, or parenchymatous nephritis, though it is a mild form of the same pathological state. Steiner states, as the result of many careful examinations of cases, that hyperæmia of the kidneys was always present in those who died early in scarlet fever, and that in a certain proportion of these cases catarrh of the renal tubules was present in addition to the congestion. Even in some who died on the second or third day he found cloudiness of the epithelium in the renal tubes, although the urine had not indicated such a change. The opinion has even been expressed that catarrh of the renal tubes is as common in scarlet fever as that of the bronchial tubes in measles; that is, that it is a uniform element in the disease; but this appears to be an exaggerated statement, for others have failed to find any evidence of renal catarrh in certain cases.
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