Alfred Martinet.

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(Fig. 586). ^

Sometimes the fibrillary twitchings of the auricle may even
be discerned rather clearly on a good polygraphic tracing (Figs.
587 and 588).

Electrocardiography alone yields an objective observation
and reliable record of auricular fibrillation.

For clinical and practical purposes the diagnosis may, how-
ever, be made either with or without the help of graphic pro-

Fig. 586. — Electrocardiograms illustrating the 3 leads in a case of
mitral stenosis with auricular fibrillation. The R wave is very small
with Lead /, whereas 5 is pronounced; with Lead ///, R appears the
highest. There are evidences of hypertrophy of the right ventricle. The
ventricle is beating very irregularly. There is no P wave, but on the
other hand there are found a number of rapid oscillations, /, /, resulting
from the fibrillation of the auricles {Cambridge Association),

The following 3 practical rules may be given in this connec-
tion :

1. Any case of tacJty-arhythmia unth a heart-rate exceeding 130
is nearly always associated with auricular fibrillation and per-
petual arhythmia (the factor of irregularity comprised in the
arhythmia excludes instances of increased heart-rate due to fever
or emotion, as well as tachycardia of the nervous or paroxysmal
types, etc.).

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2. Any persistent arhythmia coupled with signs of advanced
cardiac impairment is almost always dependent upon auricular
fibrillation. The probability becomes practically a certainty if
the arhythmia is associated with tachycardia.

3. Any case of arhythmia, even if unaccompanied by manifest
signs of existing cardiac impairment, any arhythmia which is in-
creased by acceleration of the pulse, such as might be induced
by moderate exercise, is likely to be a perpetual arhythmia. The

Fig. 587. — Auricular fibrillation {Daniel Routier).

other types of arhythmia, on the other hand, and in particular
extrasystolic arhythmia, are reduced or even disappear under
the influjMice of pulse acceleration.

The polygraphic method records an extreme and permanent
arhythmia in these cases. The radial tracing consists of unequal
and irregular systoles, constantly varying in duration and power ;
the jugular tracing generally assumes the so-called "ventricular
type," showing a series of oscillations synchronous with the


Fig. 588.— Case 248. H., 56 years; 169 cm.; 64.8 kilograms. Auricu-
lar fibrillation (perpetual arhythmia).

6. 23. 1913; pulse, 72 (?) ; pressures, i3%oo (?) ; viscosity =
4.3. H = 1200. Albumin absent.

ventricular contractions, but with absence of the a wave charac-
teristic of auricular systole. Sometimes, on the most successful
tracings, there is noted a series of minute and rapid presystolic
undulations, an aictual expression of auricular fibrillation (Figs.
587 and 588).

Electrocardiography records auricular fibrillation more or
less clearly (Fig. 586).

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Is tricuspid insufficiency always present in perpetual arhyth-
mia, and does recognition of the presence of perpetual arhythmia
necessarily mean recognition of the presence of tricuspid insuffi-
ciency? Some observers have thought themselves justified in
giving a positive answer to this question. The author, however,
has met with many cases of perpetual arhythmia in which there
were no apparent signs permitting of recognition of the presence
of tricuspid insufficiency. This latter condition has seemed to
him relatively frequent in these cases, but not constant.

Auricular fibrillation and perpetual arhythmia are always as-
sociated with and probably dependent upon a deep-seated degen^
eration of the myocardium and advanced cardiac insufficiency.
Their signs are therefore likely to be observed in association
with those of myocardial degeneration and heart weakness,
znc, dyspnea on exertion, cyanosis, venous stasis, passive con-
gestions, hepatic engorgement, edema, reduced output of urine,
etc. ; and it is very hard to say whether any one of these symp-
toms is dependent upon them or even whether they are exagger-
ated through the presence of fibrillation and arhythmia — which,
however, is very probably the case.

Attacks of paroxysmal fibrillation with manifest recrudes-
cence of both the arhythmia and the associated symptoms —
dyspnea, cyanosis, edema, etc. — may be witnessed. Other pa-
tients, however, seem hardly influenced by the condition. The
same is true, indeed, of paroxysmal tachycardia ; probably these
reactions, seemingly so diflFerent, are both actually dependent
upon the state of the myocardium ; if it is but slightly impaired,
the general circulation is comparatively little influenced by recru-
descence of the arhythmia; if, on the other hand, it is profoundly
degenerated, the usual signs of cardiac insufficiency will rapidly

Mitral stenosis, myocardial degeneration, and arterio-renal
sclerosis are the conditions nearly* always associated with per-
petual arhythmia.

The prognosis of perpetual arhythmia must therefore always
be guarded, since auricular fibrillation in itself constitutes a
positive sign of more or less advanced degeneration of the myo-
cardium and a probable sign of widespread degeneration.

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Nevertheless — and in this condition the therapeutic test is often
conclusive — certain instances of perpetual arhythmia are mark-
edly reduced by well-directed drug treatment, while others are
completely refractory. The prognosis is obviously profoundly
influenced by these factors. On the whole, the same conclusion
always follows, vis,, that the prognosis is governed much more
by a study of the contractility of the heart muscle than by a
study of its conductivity.

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[dax^Sy a water-bag; an abdomen havingX
the shape of a water-bag. J

Ascites^ derived from the word d(T;^6$, a water-bag, on ac-
count of the resemblance of the abdomen distended with serous
fluid to such a vessel, consists of an intraperitoneal serous effu-
sion (hydroperitony, dropsy of the peritoneum, dropsy, etc.).

Becognition of Ascites.— Accumulation of fluid in the peri-
toneal cavity is generally a slow, gradual process ; in the excep-
tional cases of ascites spoken of as a frigore, due to sudden ob-
struction of the portal vein, effusion may take place rapidly.

Though sometimes obvious^ especially when it has attained
a certain size, when the abdominal parietes are relatively thin,
and when the fluid is freely movable, its recognition may in
other instances be attended with considerable difficulty when,
as is frequently the case, the parietes are thick and infiltrated,
when the effusion is of slight or moderate extent, when its
mobility is limited owing to adhesions, etc.

Clinically, its recognition is to be based on a systematic ex-
amination of the case:


(a) Shape of the Abdomen. — 1. Vertical position: Abnormal
prominence of the hypogastrium and the iliac fossa.

2. Recumbent position: The flanks broaden and flatten out,
like the abdomen of an amphibian; the fluid moves about, on
the whole, according to gravity, therefore passing to the de-
pendent side when the patient is in lateral decubitus.

3. Occasionally the umbilicus, turned out like a glove finger,
forms a small, soft, fluctuating, depressible, translucent tumor.

(6) Condition of the Skin. — The skin is frequently smooth,
white, even, polished, and shining; sometimes thickened, infil-
trated, and edematous; at times erythematous. Striae compar-
able to tttose of pregnancy may be noticed upon it.

47 {7i7)

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(f) Superficial Venous Circulation. — ^The accessory portal
veins, normally only slightly developed, enlarge, sometimes to
a considerable size, in the event of obstruction to the blood-
current through the portal vein. The circulation is in part re-
established through these vessels, whence there occurs dilata-
tion of the subcutaneous veins of the abdomen, with the pro-
duction of a prominent network of veins between the pubis and
the xiphoid appendix, especially on the right side, in the form
of a peri-umbilical venous plexus.

(d) Sometimes there is concomitant hydrocele, owing to per-
sistence of the vagino-peritoneal duct

Palpation. — ^The abdomen exhibits an even, tense, sometimes
elastic^ and firm enlargement

The fluid present masks the intestinal mass and forms an
obstacle to detailed examination of the abdominal viscera,
whence the necessity of puncture in cases where such examina-
tion is imperative.

Percussion. — Flatness manifestly varies in extent according
to the amoimt of effused fluid.

1. Its primary localization is over the iliac fossae and the hy-
pogastrium (fluid) ; the umbilical and epigastric regions are gen-
erally the seat of tympanitic resonance (intestines), the transi-
tion from flatness to tympany being, however, gradual.

2. A small effusion may be unrecognizable on percussion ;
but if the patient is turned on the side, the fluid will collect on
that side and flatness be detectable.

3. The flatness exhibits movable margins, which vary accord-
ing to the patient's position if the ascites is movable and free;
it is fixed, however, if the effusion is encysted or walled off (Fig.

Combined Palpation and Percussion. — ^This procedure yields
one of the most important indications of ascites, viz., fluctuation.

With one hand applied flat over one side of the abdomen,
the physician taps lightly with the other on the opposite side,
either by light percussion or by flipping a finger; the former
hand notes a sensation as of a blow or wave. It is often useful
to have some one else apply the ulnar border of one hand along
the linea alba, in order to prevent transmission of* wave-like

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movements of the abdominal parietes, which would constitute
a source of error.

At all events, fluctuation is almost pathognomonic of ascites,
as it occurs in the absence of ascites only in a few exceptional
cases of ovarian cyst with thin walls.

Vaginal Palpation. — ^With this procedure, a doughy, firm con-
dition in the culs-de-sac is occasionally found.

Sometimes vaginal palpation may prove of service in aflford-
ing an early diagnosis of ascites (descent and reduced weight
of the uterus, and extreme mobility of the cervix).

Functional Evidences.

(a) Chiefly manifestations due to distention and pressure.

1. Increased size of the abdomen: The patient can no longer
button up his trousers.

2. Digestive disturbances: Constipation due to pressure on the
intestines, resulting in paralysis (Chopart's law: Any muscle
underlying an inflamed serous membrane is paralyzed). Indi-
gestion and tympanites.

3. Urinary disturbances: Dysuria, diminished secretion of urine,
oliguria, and opsiuria, chiefly on account of the loss of fluid
resulting from the ascitic accumulation.

4. Cardiopulmonary dyspnea due to pressure on the diaphragm,
causing reduced lung expansion and displacement of the heart.

5. Edema of the lower extremities, due either to the same cause
as the ascites or to pressure exerted on the inferior venae cavae.

{b) Functional disturbances attending the primary disorder
(cirrhosis, peritonitis, etc.).

With What Oonditions Might Ascites be Oonfounded?— (a)
Abdominal Meteorism. — Here, resonance and tympany are in-
creased ; yet, in truth, ascites is frequently accompanied by mete-
orism; in fact, meteorism may conceal an ascites. The best
differential sign in these cases, in the author's estimation, is the
displacement of the dullness upon assumption of lateral decu-
bitus, the dullness appearing in the most dependent area, at a
point previously resonant.

(&) Edema of the Abdominal Wall. — ^The finger leaves a
depression in the parietal tissues; dullness is uniformly distrib-

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uttd, knd fluctuation is absent. Abdominal edema and ascites,
however, frequently coexist

(f) Retention of Urine. — The bulging and dullness are dis-
tinctly located in the hypogastrium, with their convex aspect
directed upward — the opposite of the condition in ascites. Urine
is passed by overflow; palpation of the hypogastrium is more
or less painful.

In the event of doubt, which is seldom excusable, catheteriza-
tion of the bladder will dispel both the doubt and the abdominal

(d) Pregnancy. — ^The enlargement is hard, in the median
line, rounded, pyriform, and hypogastric in situation. Palpation
reveals that the uterus is the cause of the bulging. The convex
aspect is directed upward — the opposite of the condition in as-
cites. On the whole, the mere thought of the possibility of
pregnancy is enough to eliminate this source of error. If doubt
should nevertheless exist, the other signs of pregnancy should
be examined for, vis., cessation of menstruation, secretion of
colostrum and other mammary changes, progressive enlarge-
ment, and after four and a half months, the diagnostic fetal

{e) Ovarian Cysts. — ^The following distinguishing features
may with advantage be recalled:

1. Shape of the abdomen. — Globular, and with umbilicus nor-
mal, in ovarian cyst.

Flattened out and with prominent umbilicus in ascites.

2. Flatness. — In ascites : Flatness in the lumbar regions ; umbili-
cal region resonant; flanks flat; the .flat area is, in a general
way, convex below ; the areas of flatness are movable and vary
with the position of the patient.

In ovarian cyst: Resonance in the lumbar, iliac, and epigas-
tric regions ; flatness rather median and hypogastric in location,
and sometimes umbilical, with convexity directed upward; flat-
ness is not changed by altered position of the patient.

3. Fluctuation. — Practically constant in ascites; exceptional in
ovarian cyst.

4. History of case. — Often negative in ovarian cyst.

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Dorsal decubitus.

Lateral decubitus.

Fig. 596. — Abdominal areas of flatness in ascites and various
other abdominal disorders.

1. Frank ascites of hepatic origin. 2. Encysted ascites of the peritoneal
type. 3. Ovarian cyst. 4. Pregnancy; retention of urine.

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Always positive in ascites, comprising such features as he-
patic disorder (cirrhosis), cardiac affections, general impairment
of health (tuberculous peritonitis), some serious organic affec-
tion (cachexia), etc.

Notwithstanding all these distinguishing features, many mis-
takes are made; the possibility of coexisting ascites and cyst
further complicates matters.

Oaases of Ascites. — In the presence of ascites, attention
should be particularly directed to the liver, peritonetim, and heart.

The diagnosis is based largely on the history of the case,
the existing physical signs, the course of the ascites, and the
nature of the fluid withdrawn by puncture.

(a) Ascites of Hepatic Origin (General Type: Atrophic Cir-
rhosis; Typical Ascites). — ^The. onset is slow, gradual, more
rarely abrupt, rapid after exposure to cold; the fluid is free in
the abdomen, movable, and fluctuation is readily elicited.

The history includes a more or less well-defined precirrhotic
stage, characterized by manifestations of increased portal pres-
sure (hemorrhoids, collateral circulation), indigestion and gas-
tro-intestinal disturbances, catarrhal disorders, meteorism, diar-
rhea, hepatic congestion and incipient jaundice, reduced output
of urine, etc.

1. The course of the disease is progressive.

2. The liver is always found diseased, generally reduced in
size (Laennec's atrophic cirrhosis), sometimes enlarged (hyper-
trophic or alcoholic cirrhosis of Hanot and Gilbert) ; the spleen
shows enlargement; there are manifest evidences of portal hy-
pertension, together with distinct impairment of nutrition. As-
cites may be encountered in syphilis of the liver or in primary
or secondary nodular cancer.

3. The fluid obtained by puncture is serous and poor in fibrin,
cellular elements, and protein material.

4. Nevertheless, it is well to bear in mind that peritonitis
may and frequently does accompany many forms of cirrhosis,
and that cases of fibrous, alcoholic, tuberculous, and syphilitic
hepatitis are quite often associated with localized peritonitis
(perihepatitis) or generalized peritonitis of a similar. or hybrid

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type (e.g., alcoholism with tuberculosis, alcoholism with syphilis,
syphilis with tuberculosis, or even alcoholism with tuberculosis
and syphilis).

(b) Ascites of Peritoneal Origin (General Type : Tuberculous
Peritonitis). — 1. The ascites is of moderate extent, often but
slightly fluctuating, and advancing by alternate exacerbations
and recessions.

The fluid is but slightly movable, and frequently encysted.

Cardiac obstrui Dyscrasias

hezia, Bright's

Hepatic obstruct


of the peritoneuzE

Fig. 597. — ^The causes of ascites.
Cardiac. — Hepatic. — Peritoneal. — Pylephlebitic. — Dyscrasic.

Sometimes there are coexisting dull and hard infiltrations, best
palpated after puncture.

2. The concomitant signs should be looked for, vis., peritoneal
and pleural friction rubs, pleural effusion, ganglia, signs of pleu-
ropulmonary, genital, or articular tuberculous disease or typho-
bacillosis, fever, vomiting, etc.

3. The ascitic fluid is serofibrinous, containing a much larger
amount of fibrin, protein, or cells than that of mechanically
produced ascites. In short, it presents the typical features of
inflammatory exudates. Guinea-pig inoculation will give posi-
tive results in the presence of tuberculosis. Certain laboratory

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procedures are available for examining ascitic fluid for the tu-
bercle bacillus (Jousset's inoscopy).

4. It is well to note that tuberculosis of the peritoneum com-
prises by far the greatest number of the cases of peritonitic ascites,
but that one should also think of the possibility of cancer of the

Low blood-pressure







Fig. 596. — The syndrome of increased portal pressure.

peritoneum in an old, cachectic individual. The reactions involving
the lymph-glands; examination of the fluid, which generally
contains red blood cells; the history of the case, and the sub-
.sequent course of the disease, will soon confirm the latter diag-
nosis if the possibility of the condition is merely recollected.
Nor should it be forgotten that tuberculous peritonitis with
ascitic effusion may occur in any grade of severity, from the mild-

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est forms, such as the long standing idiopathic ascites of young
girls, running a slow course, without fever or constitutional
disturbances, and nearly always ending in spontaneous recovery
(dropsy of the peritoneum), to the most serious varieties, such
as the ulcero-caseous forms which lead so quickly and inevitably
to the hectic state.

Finally, reference should be made to the frequent, not to
say constant, participation of the pleura in the process of peri-
toneal tuberculous involvement, almost always constituting
more properly a pleuro-peritoneal tuberculosis. At all events and
for practical purposes, in the presence of a suspicious peritoneal
disorder the physician should systematically examine the pleurae
and always perform an exploratory puncture of the pleura; this
procedure will supply a solution of the problem in the majority
of cases.

(c) Ascites of Cardiac Origin (General T3rpe: Heart Failure).

1. One of the most specific features of these cases is that here
the ascites clearly follows other manifestations of edema, as in
the lower extremities, scrotum, and lumbar regions — in contrast
with what occurs in cirrhotic and peritonitic ascites, — and that
it is frequently combined with hydrothorax.

2. The diagnosis is clear from observation of the attending
circumstances, the coexisting heart failure, and the physical
sig^s of cardiac disease. At the most, doubt might occur in the
very advanced cases in which — ^the primary hepatic cirrhosis
having led to secondary cardiac insufficiency, or, on the other
hand, primary heart disease having resulted in cirrhosis of car-
diac origin — a combined cardio-hepatic inadequacy, manifested
in both heart failure and hepatic cirrhosis, has been produced.
A careful inquiry into the past medical history as regards the
heart and liver, along with observation of the course of the
edema and the heart sounds, will nearly always settle the ques-
tion of priority, even though such an aim is of academic rather
than practical interest, since the therapeutic indications, like the
disturbances of function, are in close combination in these cases.

Other Oauses. — Apart from the above three cardinal sources
of ascites, mention should be made of :

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1. The Ascites of Nephritis. — This is, on the whole, rather
uncommon and is associated with the usual signs of Bright's
disease (see Albuminuria and Edema). The high urea content
in the ascitic fluid of azotemic cases should be borne in mind.

This diagnosis should not be accepted unless one has become
convinced from careful examination of the absence of hepatic
cirrhosis, peritoneal inflammation, or heart weakness.

The differential features include, more particularly: Albu-
minuria and, in the absence of all cardiac inadequacy, precession
of the edematous manifestations (lids, extremities, and scrotum).

2. The Ascites of Cachexia. — ^This is likewise an exceptional

^2 4 8 " U

Meal Meal

Fig. 599. — Normal rhythm of urinary elimination (above).
Opsiuria (below).

form, and one which, upon thorough investigation, can nearly
always be relegated to one of the three above-mentioned groups,
7n2., hepatic, peritoneal (tuberculous or neoplastic), or cardiac

3. Chylous Ascites. — Also a rare form, at least in our own
countries, and doubtless of varied and complex causation.

The fluid withdrawn is whitish, opalescent, milky in appear-
ance, containing little protein but much fat, which is dissolved
by ether, thereby clearing up the fluid. Its composition is some-
what similar to that of pus (hyperleucocytosis).

In the presence of this form of ascites there have been de-
tected filariasis (Lancereaux), tuberculosis (Courtois-Sufiit),
chronic inflammation of the peritoneum (Letulle), and pressure
on the thoracic duct by enlarged mediastinal glands (Strauss).

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Fig. 600. — ^Tributaries of the portal vein (after Birard and Vignard).
X. Internal mammary vein. 2. Superior vena cava. S- Inferior vena cava.
4, Suprahepatic vein. 5. Liver. 6. Trunk of the portal vein. 7. Gastro-
duodenal veins. 8. Pancreas. 9. Duodenum. 10. Mesentery. ;/. Ileo-

Online LibraryAlfred MartinetClinical diagnosis, case examination and the analysis of symptoms → online text (page 7 of 50)