uniform, but far from constantly so. Its quantity in the majority of
cases is reduced, frequently not exceeding twenty-four ounces per diem,
and occasionally not exceeding fourteen. This is owing in some degree
to profuse sweating, but also, as in other febrile affections, to
retention of water. Its density is usually high--1020 to 1030, or even
1035--which is due chiefly to its concentration, and not, as has been
generally supposed, mainly to an increase in the total solids
excreted.[34] Its color is a very dark red or deep reddish-yellow,
partly from concentration; but it is yet not known whether the deep hue
is partly from increase of the normal pigments or of one of them
(urobilin),[35] or from the presence of some abnormal coloring matter.
Its reaction is generally highly acid, and continues so for many hours
after its discharge, unless in subacute cases, when it is occasionally
neutral or sometimes alkaline at the time of its escape, or becomes so
in a very short time afterward. It is commonly toward the decline of
the attack that the urine becomes neutral or alkaline. As a very
general rule, the amount of urea and of uric acid excreted during the
febrile stage exceeds what is physiological, and begins to decline when
convalescence commences; but this may be reversed (Parkes,[36]
Lede,[37] Marrot[38]). The sulphuric acid is notably increased
(Parkes), the chlorides often diminished and sometimes absent, and the
phosphoric acid very variable (Beneke, Brattler[39]), but usually
lessened (Marrot).
[Footnote 34: See _Guy's Hospital Reports_, 3d Series, vol. xii. 441.]
[Footnote 35: Jaffe, _Virchow's Archiv_, xlvii. 405, quoted in
_Ziemssen's Cyclopæd. Prac. Med._, xvi. 41.]
[Footnote 36: _On Urine_, p. 286.]
[Footnote 37: _Recherches sur l'Urine dans le Rheumatisme Artic.
Aigue_, Paris, 1879.]
[Footnote 38: _Contribution à l'Étude du Rheumatisme Artic., etc._,
Paris, 1879, 41.]
[Footnote 39: Quoted by Parkes, _op. cit._, 290.]
During convalescence the urine increases in quantity, while, as a
general rule, the urea and uric acid lessen relatively and absolutely,
and the chlorides resume their normal proportions to the other
ingredients. The reaction frequently becomes alkaline, and the specific
gravity falls considerably, although not always as soon as the
articular inflammation subsides. Temporary albuminuria occurs very
frequently in the febrile and occasionally in the declining stage, but
generally disappears when convalescence is completed. It obtained on
admission in 8 out of 43 cases lately reported by Dr. Greenhow.[40] A
more abiding albuminuria, due very rarely to acute parenchymatous
nephritis, may be met with (Johnson, Bartels, Hartmann, Corm). Blood,
even in considerable amounts, has also rarely appeared in the
urine,[41] sometimes in connection with embolic nephritis and
endocarditis, for such appear to have been the nature of Rayer's
nephrite rheumatismale.[42]
[Footnote 40: _Lancet_, 1882, i. 913.]
[Footnote 41: _Clinical Lectures_, R. B. Todd, edited by Beale, 1861,
p. 346.]
[Footnote 42: _Traité des Maladies Reins_. See also Dr. Weber, _Path.
Trans. of London_, xvi. p. 166.]
The saliva, which is normally alkaline, has usually a decidedly acid
reaction in acute articular rheumatism, and Dr. Bedford Fenwick states
that it always in this disease contains a great excess of the
sulpho-cyanides, and that these slowly and steadily diminish, till at
the end of the third week or so they become normal in amount.
A profuse, very acid, sour-smelling perspiration is one of the striking
symptoms occurring in the course of acute articular rheumatism, and
{31} until very lately it has been generally held to indicate an
excessive formation in, and elimination of acid from, the system,
either lactic acid or some of the acids normal to the perspiration, as
acetic, butyric, and formic. However, not only have chemists failed to
detect lactic acid in the perspiration of acute rheumatism, but late
research tends to show that the excessive acidity of the perspiration
in this disease is but very partially due to the perspiration itself,
and is chiefly owing to chemical changes taking place in the overheated
and macerated surface of the skin and its epidermis, and to the
retention of solid products accumulated on that surface. Besnier says
that if in acute articular rheumatism or other disease attended with
much perspiration the surface be kept well washed, the sweat will be
found in the greater number of cases at the moment of its secretion to
be nearly neutral as soon as actual diaphoresis occurs, more decidedly
acid when the perspiration is less abundant or begins to flow, and
exceptionally alkaline. Most physicians are aware that the profuse
perspiration of acute rheumatism is non-alleviating; it is not a real
critical discharge of noxious materials from the system, nor is it
followed by prompt reduction of the temperature and other symptoms. It
is but a symptom of the disease, and occurs especially in severe cases,
and when it continues long after the reduction of the temperature it is
a source of exhaustion, and may be checked with advantage.
The blood is deficient in red globules, Malassez finding in men from
2,850,000 to 3,700,000 per cubic millimeter instead of 4,500,000 to
5,000,000, and in women 2,300,000 to 2,570,000 instead of 3,500,000 to
4,000,000. The hæmoglobin and the oxidizing power of the blood are also
considerably reduced; the fibrin is largely increased (6 to 10 parts in
1000 instead of 3); the albumen and albuminates are lessened, the
extractives increased; the proportion of urea is normal, and no excess
of uric acid is found in the blood. Instead of that fluid being less
alkaline than normal, Lepine and Conard have recently stated that its
alkalinity is increased in acute rheumatism, but constantly diminished
in chronic rheumatism,[43] and no excess of lactic acid has been proved
to exist in the blood in either acute or chronic rheumatism. A
condition of excessive coagulability of the fibrin, independently of
its excessive amount (inopexia), is an habitual character of acute
rheumatism; however, in very bad cases, especially those attended with
hyperpyrexia and grave cerebral symptoms, the blood after death has
been black and coagulated and the fluid in the serous cavities has
given an acid reaction. The above alterations in the blood usually are
proportionate to the intensity of the fever and the number of the
joints and viscera involved.
[Footnote 43: Lepine, "Note sur la determination de l'Alcalinité du
Sang," _Gaz. Méd. de Paris_, 1878, 149; Conard, _Essai sur l'Alcalinité
du Sang dans l'État de Sante, etc._, Thèse, Paris, 1878.]
The manifestations of acute articular rheumatism other than the
articular are various, and some of them, more especially those observed
in the heart, may be regarded as integral elements of the disease, for
they occur in a large proportion of the cases, often coincidentally
with the articular affection, and may even precede it, and probably may
be the sole local manifestation of acute rheumatism, although under the
last-mentioned circumstances it is difficult to prove the rheumatic
nature of the ailment.
The cardiac affections may be divided into inflammatory and {32}
non-inflammatory. The former consist of pericarditis, endocarditis, and
myocarditis; the latter embrace deposition of fibrin on the valves,
temporary incompetence of the mitral or tricuspid valves, and the
formation of thrombi in the cavities of the heart. For practical
purposes hæmic murmurs may be included in the latter group.
No reliable conclusions can be drawn respecting the gross frequency of
recent cardiac affections in rheumatic fever, for not only do authors
differ widely on this point, but they do not all distinguish recent
from old disease, nor inflammatory from non-inflammatory affections,
nor hæmic from organic murmurs. Nor does it appear probable, from the
published statistics, that these differences are owing to peculiarities
of country or race. The gross proportion of heart disease of recent
origin in acute and subacute articular rheumatism was in Fuller's[44]
cases 34.3 per cent.; in Peacock's,[45] 32.7 per cent.; in Sibson's[46]
(omitting his threatened or probable cases), 52.3 per cent.;[47] in
3552 St. Bartholomew's Hospital cases analyzed by Southey,[48] 29.8 per
cent.; in Bouilland's cases, quoted by Fuller,[49] 5.7 per cent.; in
Lebert's,[50] 23.6 per cent.; in Vogel's,[50] 50 per cent.; in
Wunderlich's,[50] 26.3 per cent. I am not aware of any analysis,
published in this country, of a large number of cases of rheumatism
with reference to cardiac complications, but Dr. Austin Flint,[51]
after quoting Sibson's percentage of cases of pericarditis, which was
(63 in 326 or) 19 to the 100, remarks, "I am sure that this proportion
is considerably higher than in my experience."
[Footnote 44: _On Rheumatism, Rheumatic Gout, etc._, 3d ed., p. 280.]
[Footnote 45: _St. Thomas's Hospital Reports_, vol. x. p. 19.]
[Footnote 46: Reynolds's _Syst. of Med._, Eng. ed., vol. iv. 186.]
[Footnote 47: Those familiar with the accuracy and diagnostic skill of
the lamented Sibson will not hesitate to add his 13 cases of very
probable endocarditis to his 170 positive cases of cardiac inflammation
in 325 examples of acute rheumatism, which will raise his percentage to
56.3.]
[Footnote 48: _Lib. cit._, vol. xiv. 6.]
[Footnote 49: _Lib. cit._, 264.]
[Footnote 50: See Senator in _Ziemssen's Cyclopæd. Pract. of Med._,
xvi. 49.]
[Footnote 51: _Pract. Med._, 5th ed., 314.]
The frequency of cardiac complications in rheumatism is influenced by
several circumstances. Some unexplained influence, such as is implied
in the terms epidemic and endemic constitution, appears to obtain.
Peacock found the proportion of cardiac complications in rheumatism to
range from 16 to 40 per cent. during the five years from 1872 to 1876,
and a similar variability is shown in Southey's statistical table[52]
covering the eleven years from 1867 to 1877. Be it observed that these
variations occurred in the same hospitals and under, it may be
presumed, very similar conditions of hygiene and therapeusis. Youth
predisposes to rheumatic inflammation of the heart, so that it may
still be said that the younger the patient the greater the proclivity.
Of Fuller's cases, 58 per cent. were under twenty-one, and the
liability diminished very markedly after thirty. Of Sibson's cases, 62
per cent. were under twenty-one. In infancy and early childhood the
liability is very great, and at those periods of life the heart, and
more especially the endocardium, rarely escapes; and the cardiac
inflammation often precedes by one or two days the articular. The
careful observations of Sibson confirm the spirit, but not the letter,
of Bouilland's original statement, and proves that the danger of heart
disease is greater in severe than in mild cases of acute rheumatism,
and that this is especially true of pericarditis. (It may be remarked
here, en parenthese, that the number of joints affected is {33} very
generally in proportion to the severity of the attacks.) However, the
mildest case of subacute rheumatism is not immune from cardiac
inflammation, and it has occasionally been observed even in primary
chronic rheumatism.[53] Occupations involving hard bodily labor or
fatigue, whether in indoor or outdoor service, render the heart very
obnoxious to rheumatic inflammation. Existing valvular disease, the
result of a previous attack of rheumatism, favors the occurrence of
endocarditis in that disease. Some authorities maintain that treatment
modifies the liability to rheumatic affection of the heart, and this
will be spoken of hereafter. The period of the rheumatic fever at which
cardiac inflammation sets in varies very much, but it may be
confidently stated that it occurs most frequently in the first and
second weeks, not infrequently in the third week, seldom in the fourth,
and very exceptionally after that, although it has happened in the
seventh. An analysis of Fuller's experience[54] in 22 cases of
rheumatic fever and 56 of endocarditis--a total of 78--shows that the
disease declared itself under the sixth day in 8; from the sixth to the
tenth in 29; from the tenth to the fifteenth in 17; from the fifteenth
to the twenty-fifth in 18; and after the twenty-fifth in 6. The
friction sound was audible in Sibson's 63 cases of rheumatic
pericarditis--from the third to the sixth day in 10, and before the
eleventh day in 30, or nearly one-half of the whole. That observer
concludes "that in a certain small proportion of the cases, amounting
to one-eighth of the whole," the cardiac inflammation took place at the
very commencement of the disease, and simultaneously with the invasion
of the joints.[55]
[Footnote 52: _Lib. cit._]
[Footnote 53: Raynaud, _Nouveau Dict. de Méd. et de Chir._, t. viii.
367.]
[Footnote 54: _Lib. cit._, pp. 77-278.]
[Footnote 55: _Lib. cit._, p. 209. See also Dickinson in _Lancet_, i.,
1869, 254; Bauer in _Ziemssen's Cyclopæd._, vi. 557.]
Of the several forms of rheumatic cardiac inflammation, endocarditis is
the most frequent, and in a large proportion of cases it may exist
alone; pericarditis is also very often observed, but it seldom is found
per se, being in the vast majority of cases combined with endo- and
occasionally with myocarditis. It is generally the ordinary verrucose
endocarditis that obtains. The ulcerative form occurs sometimes, and
should be suspected if in a mild or protracted case of acute rheumatism
endocarditis sets in with, or is accompanied by, rigors, and the
general symptoms are of pyæmic or typhoid character or both, even
although an endocardial murmur is not present, for extensive vegetating
ulcerative endocarditis frequently exists without audible murmur. It is
remarkable, as Osler has shown,[56] how few instances of ulcerative
endocarditis developing during the course of acute rheumatism are
reported; and I would add that by no means all of these were examples
of first attacks, chronic valvular lesions, the consequence of former
illness, existing in many of them at the time of the final acute
attack. Southey's[57] patient, and both of Bristowe's,[58] had had
previous rheumatic seizures. However, Peabody's case,[59] one of Ross's
three cases,[60] and Pollock's[61] case appear to have been examples of
ulcerative {34} endocarditis occurring during a first attack of acute
articular rheumatism. The united and thickened condition of two
segments of the aortic valve in one of Ross's cases indicates
old-standing disease, although no history of former rheumatism is
given. Goodhardt[62] has lately insisted upon the tendency of
ulcerative endocarditis to appear in groups or epidemics, but the
evidence is not conclusive.
[Footnote 56: _Archives Médecine_, vol. v., 1881; _Trans. International
Med. Cong._, vol. i. 341.]
[Footnote 57: _Clin. Soc. Trans._, xiii. 227.]
[Footnote 58: _Brit. Med. Jour._, i., 1880, 798.]
[Footnote 59: _Medical Record N.Y._, 24th Sept., 1881, 361.]
[Footnote 60: _Canada Med. and Surg. Journ._, vol. xi., 1882, 1, and
_ib._, vol. ix., 1881, 673.]
[Footnote 61: _Lancet_, ii., 1882, 976.]
[Footnote 62: _Trans. Path. Soc. London_, xxxiii. 52.]
Space will not permit any detailed description of the symptoms and
signs of endo- or pericarditis: these will be found in their proper
places in this work, but a few observations are needed upon
myocarditis, which occasionally occurs in combination with rheumatic
pericarditis, and is a source of much more danger than the latter is,
per se. Dr. Maclagan[63] is almost the only authority who recognizes
the occurrence of rheumatic myocarditis independently of inflammation
of the membranes of the heart. He maintains that the rheumatic poison
probably and not infrequently acts directly on the cardiac muscle; in
which case the resulting inflammation is apt to be diffused over the
left ventricle and to produce grave symptoms, while in other instances
the inflammatory process begins in the fibrous rings which surround the
orifices of the heart (especially the mitral), extends to the substance
at the base of the heart, and is there localized. As in this latter
form the inflammation usually extends also to the valves, "any symptoms
to which the myocarditis gives rise are lost in the more obvious
indications of the valvulitis." However, this limited inflammation of
the myocardium is not dangerous. Dr. Maclagan asserts that the more
diffused and dangerous inflammation of the walls of the left ventricle,
while always difficult, and sometimes impossible, of diagnosis, can be
determined with tolerable certainty in some cases. In this view,
however, he has been preceded by Dr. Hayden,[64] who states that the
diagnosis of myocarditis is quite practicable irrespective of the
accompanying inflammation of the membranes of the heart.
[Footnote 63: _Rheumatism: its Nature, Pathology, and Successful
Treatment_, 1881.]
[Footnote 64: _Diseases of the Heart and Aorta_, 1875, 746.]
From the observations of the author just named, as well as of many
others, it may be inferred that acute diffused myocarditis of the left
ventricle exists in rheumatic fever when either with or without
coexisting pericarditis there are marked smallness, weakness, and
frequency of pulse, anguish or pain or great oppression at the
præcordia, severe dyspnoea, the respiration being gasping and
suspirious, feeble, rapid, and irregular action of the heart, great
weakness of the cardiac sounds, and almost extinction of the impulse,
evidence of deficient aëration of the blood combined with coldness of
surface, tendency to deliquium, and when these symptoms and signs
cannot be fairly attributed to extensive pericardial effusion or to
pulmonary disease, or to obstructed circulation in the heart consequent
upon endocarditis with intra-cardiac thrombosis or upon rupture of a
valve. It might, however, be impossible to exclude endocarditis
complicated with thrombosis, conditions which do occur in rheumatic
endocarditis, or a ruptured valve, which, although rarely, has been
occasionally observed. Grave cerebral symptoms, delirium, convulsions,
coma, though frequently present, are not peculiar to acute
myocarditis.[65] {35} Hence, even with the above group of clinical
facts, the diagnosis at best can be but probable. The disease, too, may
be latent, or, like Stanley's[66] celebrated case, produce disturbances
of the cerebral system rather than of the circulatory.
[Footnote 65: In illustration see case by Southey in which the symptoms
and signs agree very well with the above description, and yet, although
the heart's substance was of dirty-brown color and the striation of its
fibre lost, Southey did not believe these appearances due to carditis.
(_Clin. Trans._, xiii. p. 29.)]
[Footnote 66: _Med.-Chir. Trans._, vol. vii.]
Dr. Maclagan has advanced the opinion that a subacute myocarditis is
not of uncommon occurrence in acute articular rheumatism, and may be
unattended by endo- or pericarditis. Such a condition, he says, may be
diagnosed when early in the course of the case the heart's sounds
quickly become muffled rather than feeble. As he quotes but one
case[67] in which an autopsy revealed alterations in the walls of the
heart, and as endocarditis and a little effusion in the pericardium
coexisted, it is premature to accept the evidence as final, and the
great importance of the subject demands further investigation.
[Footnote 67: _Lib. cit._, p. 175.]
Admitting with Fuller the occasional deposition of fibrin upon the
valves and endocardium in rheumatic fever independently of
endocarditis, the murmur resulting therefrom could not be reliably
distinguished from that of inflammatory origin. It remains to speak
briefly of temporary incompetence of the mitral and tricuspid valves
and their dynamic murmurs, and of hæmic murmurs. Occasionally, in
severe cases of rheumatic fever, more especially in the advanced stage,
there may be heard a systolic murmur of maximum intensity either in the
mitral area or over the body of the left ventricle, unaccompanied by
accentuation of the second sound, or, as a general rule, by evidence of
pulmonary obstruction. Such murmurs are apt to be intermittent, and as
they disappear on the return of health, they have been satisfactorily
referred to temporary weakness of the walls of the heart, so that the
auriculo-ventricular orifices are not sufficiently contracted during
the ventricular systole for their valves to close them, and
regurgitation follows. Yet, inasmuch as Stokes distinctly mentions the
absence of murmur in many cases of softening of the heart in typhus, it
is probable that an excessive weakness of the ventricular wall is
incompatible with the production of murmur, and that the presence of
murmur in such circumstances is evidence of some remaining power in the
heart.
Dr. D. West[68] has published some cases of acute dilatation of the
heart in rheumatic fever which strongly corroborate these views. The
murmur in one of them became appreciable only as the heart's sounds
increased in loudness and the dilatation lessened. One ended fatally,
and acute fatty degeneration of the heart's fibres was found in
patches.[69] I believe that some of these temporary mitral murmurs in
acute rheumatism depend upon a moderate degree of valvulitis quite
capable of complete resolution. Sibson[70] has lately stated that he
has met with the murmur of tricuspid regurgitation without a mitral
murmur in 13 out of 107 cases of rheumatic endocarditis, and with a
recent mitral murmur in 27 out of 50 {36} cases. "The tricuspid murmur
generally comes into play about the tenth or twelfth day of the primary
attack, along with symptoms of great general illness;" it appears
earlier, as a rule, in those cases in which it is associated with
mitral regurgitation than when it exists alone; it is of variable
duration, but usually short--from one to nineteen days or more. He
regards it as of non-inflammatory origin, and dependent upon
regurgitation due to the so-called safety-valve function of the
tricuspid valve; and when limited to the region of the right ventricle
he infers that it is usually the effect and the evidence of
endocarditis affecting the left side of the heart. These novel
statements are confirmed by the observations of Parrot, Balfour, and
William Russell,[71] which go to prove that tricuspid regurgitation
occurs frequently in the more advanced stages of debility. No other
authority than Sibson, however, insists upon its frequent occurrence in
acute rheumatism.
[Footnote 68: _Barth. Hosp. Repts._, xiv. 228.]
[Footnote 69: On this subject see Stokes, _Dis. Heart and Aorta_, pp.
423, 435, 502; Stark, _Archives générales de Méd._, 1866; DaCosta,
_American Journal Med. Sci._, July, 1869; Hayden, _Dis. Heart and
Aorta_, 1875; Balfour, _Clin. Lects. on Heart and Aorta_, 1876; Cuming,
_Dublin Quart. Jour. Med. Sci._, May, 1869; Nixon, _ib._, June, 1873.
I. A. Fothergill has seen several cases in which such mitral murmurs
have followed sustained effort in boys, and have disappeared after a
time: _The Heart and its Diseases_, 2d ed., 1879, p. 177.]
[Footnote 70: Reynolds's _System. Med._, Eng. ed., vol. iv. 463.]
[Footnote 71: See _Brit. Med. Jour._, i. 1883, 1053.]
The anæmia which is so striking a symptom of rheumatic fever,
especially when several joints are severely inflamed, coexists very
frequently with a systolic basic murmur, which is most often louder
over the pulmonary artery (in second left intercostal space and more or
less to left of sternum) than over the aorta. The murmur may appear
early in the disease, but sets in most frequently when the disease is
subsiding. When thus appearing late in a case accompanied by
endocarditis and pulmonary congestion, it is of favorable omen and
indicates improvement in the thoracic affection. The growing opinion,
however, respecting so-called anæmic murmurs is, that they depend
chiefly upon regurgitation through the tricuspid orifice, although Dr.
W. Russell refers them to pressure of a distended left auricle upon the
pulmonary artery.[72]
[Footnote 72: _Ib._, 1065.]