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.[3]

[Footnote 3: Dr. Goodhart (_Guy's Hospital Reports_, 1879) reports

several interesting cases to confirm his opinion that acute dilatation

of the heart is a not infrequent sequel of scarlatinous nephritis, and

is the cause of death in some apparently inexplicable cases.]

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.

The nephritis which gives rise to symptoms, and therefore interests

the practitioner, commonly begins in the declining period of scarlet

fever or during the desquamative stage, and is in many instances

plainly attributable to exposure to cold or to currents of air. It

originates either during this period, or, if it have previously

existed as a mild renal catarrh, it now becomes aggravated. Dropsy,

which always attracts attention, does not occur till the nephritis has

continued for some time.

Why nephritis, with the subsequent dropsy, so frequently occurs after

scarlet fever is not fully understood. Rilliet and Barthez attribute

it to disturbance of the function of the skin. The fact has long been

observed that the kidneys become affected nearly if not quite as

frequently after mild as after severe cases. Indeed, the chief danger

in mild cases, when the patients are but a short time in bed and are

soon allowed to go about, is from the nephritis. Chilling the surface

and checking cutaneous transpiration appear to be the immediate cause

of this inflammation in a considerable proportion of cases. Therefore,

severe attacks of scarlet fever with abundant rash and desquamation,

which require the patient to be kept in bed the proper time and in a

warm room two or three {526} weeks, appear to be less frequently

followed by this renal disease than are milder cases which are more

carelessly treated.

The most thorough and minute microscopic examination of the state of

the kidneys in scarlet fever which have come to my notice were those

by E. Klein, published in the _Lond. Path. Soc. Trans._, and

illustrated by microscopic drawings. It appears from these

examinations that the changes in the kidneys are complex, among which

we recognize both those of parenchymatous or desquamative nephritis

and interstitial nephritis; but we would infer that the interstitial

nephritis is mild in degree and quite subordinate, or else confined to

portions of the organ, from the fact that so many permanently and

fully recover. The following is a resumé of Klein's examinations in

twenty-three cases: We conclude from these microscopic researches that

the anatomical changes of both parenchymatous and interstitial

nephritis are commonly present in greater or less degree in cases of

scarlet fever. If they are mild or confined to portions of the

kidneys, no symptoms occur; but if they are sufficient in extent or

degree to impair the function of these organs, then symptoms, as

albuminuria, diminution of urine, etc., appear.

1. Parenchymatous Nephritis, Proliferation of Nuclei, Hyaline

Degeneration of Arterioles, the Glomerulo-Nephritis of Klebs.--Klein

found increase of nuclei (probably epithelial) upon the glomeruli and

hyaline degeneration of the intima of minute arteries, especially

marked in the afferent arterioles of the Malpighian bodies. The intima

of these vessels was in places so swollen as to resemble cylindrical

or spindle-shaped hyaline masses, and cause narrowing of the lumina of

the vessels in which this degeneration occurred. Klein observed in

some specimens so great hyaline degeneration of the capillaries of the

Malpighian bodies that circulation through them was obstructed. In the

more advanced or protracted cases this hyaline substance in the

glomeruli began to assume a fibrous appearance. Bowman's capsule was

considerably thickened. This hyaline degeneration of the Malpighian

bodies Klein discovered in the earliest cases which fell under his

observation.

Also in the earliest cases the multiplication or germination of the

nuclei of the muscular coat of the arterioles was observed, with a

corresponding increase in the thickness of the walls of these vessels.

This change in the muscular element was observed in the arterioles in

different parts of the kidney, but it was most conspicuous in

arterioles at their point of entrance into the Malpighian bodies; and

it was distinctly observed in other arterioles, both in the cortex and

in the base of the pyramids.

In the glandular portion of the kidneys other anatomical alterations

were observed, indicating parenchymatous nephritis. There were

swelling of the epithelial lining of the convoluted tubes;

multiplication of nuclei of epithelial cells, especially in ascending

tubules, which lay close to the afferent arterioles of Malpighian

corpuscles; granular matter, and even blood, in the cavity of Bowman's

capsule and in the convoluted tubes; cloudy swelling and granular

disintegration of epithelium in some parts of the convoluted tubes;

detachment of epithelium from the membrane of larger ducts of the

pyramids in some cases. These parenchymatous changes are already known

to the profession through the observations and writings of Dickinson,

Fenwick, Johnson, John Simon, and others.

{527} Klein, in commenting on the hyaline degeneration which he

observed, states that Neelsen found the walls of the capillaries of

the pia mater thickened, highly refractive, and of a lardaceous

appearance in certain acute infectious maladies, as variola, typhoid

fever, measles, and in one case of scarlet fever.[4] Usually, only a

small portion of the capillaries were thus affected, most frequently

at the point of division into branchlets. In a few instances Neelsen

observed degeneration of arterioles extending a considerable distance,

with fusion of the intima, media and adventitia, and chemical

examination showed that the substance produced by this degeneration

had similar properties to elastic tissue. Although the examinations by

Neelsen relate to the pia mater, two of his observations are

especially interesting--first, that the hyaline change affects chiefly

vessels near their point of branching; and, secondly, that the hyaline

substance is of the nature of elastic tissue, for in the kidney in

scarlatinous nephritis the arterioles undergo the change in question

chiefly near their point of branching into the capillaries of the

glomerulus; and the intima being the part which undergoes the hyaline

change, it is probable, in the opinion of Klein, that the same

substance is produced by the degeneration in walls of the vessels of

the kidney which Neelsen observed in the pia mater, and therefore that

it is of the nature of elastic tissue.

[Footnote 4: _Archiv der Heilkunde_, 1876.]

This hyaline degeneration of the arterioles is also very marked in the

spleen in scarlet fever; and in studying the minute anatomy of the

intestines and spleen in typhoid fever Klein has found the same

degeneration of the intima of the minute vessels. He believes that

this hyaline change and the proliferation of muscle-nuclei which thus

occur at an early period in scarlet fever in the renal vessels when

the kidneys become affected are due to an irritating cause acting

similarly to that in typhoid fever.

Klein calls attention to the interesting examinations of the

scarlatinous kidney made by Klebs, who attributed the diminished

urination and the uræmic poisoning in certain cases in which the

kidneys do not exhibit any marked change to the naked eye, to what he

designates glomerulo-nephritis. Klebs says: "In the post-mortem

examination the kidneys are found slightly or not at all enlarged,

firm, ... the parenchyma very hyperæmic. Only the glomeruli appear, on

close inspection, pale like small white dots. The urinary tubes are

often not changed at all. Occasionally the convoluted tubes are

slightly cloudy. The microscopic examination shows that there are

neither interstitial changes nor proliferation of epithelium, the

so-called renal catarrh generally supposed to be present in these

conditions on account of the absence of other perceptible

derangements; and there seems, therefore, leaving out the glomeruli,

the congestion of the kidneys alone to remain to account for the

symptoms during life." But that mere congestion is insufficient to

produce the symptoms appears from the fact that it does not produce

them under other circumstances. Klebs finds, "on microscopic

examination of the glomerulus, the whole space of the capsule filled

with small somewhat angular nuclei, imbedded in a finely granular

mass. The vessels of the glomerulus are almost completely covered by

nuclear masses."

Klein, commenting on these examinations by Klebs, states that in all

{528} early cases which he examined he observed great abundance of

nuclei of the glomeruli, but a condition like that described and

figured by Klebs[5] he has seen in only a few glomeruli; for a general

state of these bodies, as described by this observer, and such an

excessive proliferation of the nuclei that the blood-vessels are

completely compressed, was not seen in one of the twenty-three cases.

Klein therefore questions whether the diminished urination and

retention of urea in scarlet fever, when the kidneys do not exhibit

any conspicuous catarrhal or other change, is due, unless in

exceptional instances, to compression of the vessels of the glomeruli

by nuclear germination, but believes, rather, that the obstructed

circulation, and consequent diminished urinary excretion, is largely

due to the changed state of the arterioles. Klein adds that perhaps

undue contraction of the arterioles, through stimulation by the

blood-irritant, may also be a factor in causing arrest of circulation

in the Malpighian corpuscles. As regards cases that perished early, he

found the parenchymatous change slight, so that a careful examination

was required in order to detect cloudy swelling and granular

degeneration.

[Footnote 5: _Handbuch der Pathol._, p. 646, fig. 72.]

2. Interstitial Nephritis.--A second set of changes Klein observed in

cases that died on about the ninth or tenth day. In such cases he

found changes due to interstitial, in addition to those produced by

parenchymatous, nephritis. Round cells, lymphoid cells, or whatever

else they should be called, were seen in the connective tissue of the

kidneys. In the kidneys of those that died at the end of the first

week after the commencement of nephritis, infiltration with round

cells was observed in the connective tissue around the large vascular

trunks. At a later stage this infiltration had extended into the bases

of the pyramids and into the cortex. The gradual increase in extent

and intensity of this infiltration was so decided in the cases which

Klein observed that he has no hesitation in concluding that when

interstitial nephritis occurs it begins about the end of the first

week, in the manner already stated--to wit, as a slight infiltration

of the tissue around the large vascular trunks, and gradually extends,

so that portions of the cortex, and rarely portions of the base of the

pyramids, are changed into firm, pale, round-cell tissue, in which the

original tubes of the cortex become lost.

The infiltration of the cortex with round cells, beginning at the

roots of the interlobular vessels, spreads rapidly toward the capsule

of the kidney, and laterally among the convoluted tubes around the

Malpighian bodies.... In the course of this process considerable parts

of the peripheral cortex, occasionally of a more or less distinctly

cuneiform shape, with the base nearest the capsule of the kidney,

become changed into whitish, firm, bloodless, cellular masses, in

which Malpighian corpuscles and urinary tubes are only imperfectly

recognized, being more or less degenerated. In some cases attended by

this infiltration of the cortex Klein observed a more or less dense

reticulation of fibres, especially around the interlobular arteries,

containing in its meshes lymph-cells, chiefly uninuclear.

A system of practical medicine. By American authors. Vol. 1 · 第 69 / 149 段