contents of the stomach are brought up, then some glairy mucus only,
with repeated and exhausting straining efforts; and with the sudden
cessation of the pain there may appear in the vomit a quantity of
bilious matter, the contents of the gall-bladder liberated by the
passage of the stone into the intestine. If bile is present in the
vomit from the beginning, it may be concluded that the obstruction is
not complete.
Constipation is the rule. The abdomen may be distended with gas--is
usually, indeed, when constipation exists. Free purgation gives great
relief. The stools are composed of scybalæ chiefly at first, afterward
of a brownish offensive liquid, and when jaundice supervenes they
become whitish in color, pasty, and semi-solid. Now and then it happens
that a copious movement of the bowels takes place as the attack is
impending, but during the paroxysm no action occurs.
Jaundice is an important, but not an invariable, symptom. It comes on
within the first twenty-four hours succeeding the paroxysm, and appears
{1073} first in the conjunctiva, thence spreading over the body
generally. The intensity of the jaundice depends on the amount of the
obstruction: if complete, the body is intensely yellow; and if partial,
the tint may be very light. The very slight degree of obstruction which
suffices to determine the flow of bile backward has been already
stated. There may be no jaundice, although all the other symptoms of
the passage of gall-stones may be present. Such is the state of the
case when a calculus enters and is arrested in the cystic duct. Under
these circumstances the natural history differs from that which obtains
when the obstruction is in the common duct and ends abruptly by the
discharge of the calculus into the intestine. After the persistence of
the symptoms of hepatic colic for a variable period without jaundice,
this sign of obstruction may appear, indicating the removal of the
stone from the cystic into the common duct. The symptoms accompanying
the jaundice--the hebetude of mind, the slow pulse, the itching of the
skin, the dark-colored urine--have been sufficiently detailed in the
section on that topic in another part of this article.
The duration of the jaundice is different in different cases, and is
influenced by the degree and persistence of the obstruction. When the
obstruction is partial and the stone is soon removed, the jaundice will
be slight and will disappear in a day or two; on the other hand, when
the stone completely blocks the passage and is slowly dislodged, the
jaundice will be intense and will persist for ten days to two weeks.
After the paroxysm has passed, if severe, the liver will be swollen,
more or less tenderness will be developed by pressure, and in some
instances, a local peritonitis coming on, there will occur the usual
symptoms of that condition.
Although all the symptoms produced by the passage of biliary calculi
may be present, some uncertainty will always be felt unless the body
causing the disturbance is recovered from the feces. A
properly-conducted search is therefore necessary. As this is so often
done inefficiently and the calculus not found, an error of diagnosis
may seem to have occurred. Every stool should be examined in the mode
hereinafter described for a number of days after the attack until the
calculus is found. It should be remembered that only air-dried calculi
float on water. The stool, as soon as passed, should be slowly stirred
up in water sufficient to make a thin mixture, and all solid particles
removed for further examination, the thinner portion poured off, and
more water added from time to time until only solids remain at last. It
should not be forgotten that masses of inspissated bile, biliary sand,
may produce symptoms not unlike those due to gall-stones proper, and
hence all particles having the appearance of this material should be
examined chemically. Place some of the supposed bile on a white plate
and pour over it some drops of strong sulphuric acid, when the
biliverdin will take on a brilliant scarlet color.
The discharge of particles of inspissated bile causes symptoms not
unlike those due to the migration of biliary calculi, but there are
points of difference. A strongly-marked case diagnosticated biliary
calculi, and in which masses of inspissated bile were discharged in
great quantity, will furnish the symptomatology to be now described.
The onset of the paroxysms of pain is less abrupt than is the case with
gall-stones, and the attacks may occur at any time; the pain also
subsides more gradually, and hardly {1074} ceases at any time, but
revives every now and then, so that several days, even weeks, may be
occupied with one seizure. Jaundice is less apt to follow, and indeed
well-defined jaundice rarely occurs in this affection. There is much
swelling of the liver, also considerable tenderness, and relief is most
certainly afforded by free purgation, anodynes seeming rather to keep
up the disturbance, probably by checking the hepatic secretions.
Attacks of hepatic colic may be expected to recur when a calculus with
multiple facets migrates, but the time when its associates may be
expected to move cannot be predicated on any data now available. Single
attacks may happen at intervals of weeks, months, or years. The
migration of one large stone may so dilate the ducts as to facilitate
the passage of those that remain behind, thus ensuring a recurrence of
the seizures at an early period.
IMPACTION OF CALCULI AND MIGRATION BY ARTIFICIAL ROUTES.--The point at
which impaction takes place is an element of great importance. The size
of the calculus is far from being decisive as to the certainty of
impaction or as to the untoward results. A not unfrequent accident is
the blocking of the cystic duct at its opening, thus preventing the
influx or outgo of bile from the gall-bladder. If the stone does not
ulcerate through, in this position it does no damage, for the
gall-bladder, as has been stated, may be closed without any apparent
detriment. Just at the bend of the cystic duct, near its origin, is the
point where arrest of a calculus is most likely to take place. The next
most likely point is the duodenal end of the common duct. When
impaction occurs a local inflammation comes on, an exudation is poured
out, ulceration begins, and presently the peritoneum is reached.
Adhesions usually form with the neighboring organs, but now and then
perforation takes place, and bile, pus, and the calculus are
precipitated into the peritoneal cavity. A fatal peritonitis follows,
as a rule; but rarely the inflammation is localized, and an abscess
forms which pursues the usual course of such accumulations; or
adhesions may take place about the site of the perforation and prevent
a general inflammation of the peritoneum. In this way a very large sac
may be produced, with the ultimate result of rupture into the general
cavity, although a fistulous communication may be established with some
neighboring organ, permitting safe discharge in this direction.
A gall-stone impacted in one of the hepatic ducts or in the main duct,
ulcerating through, may form an abscess not distinguishable from other
solitary hepatic abscesses except by the presence of the concretion
causing the mischief and the absence of the usual conditions giving
rise to these accumulations of pus. It is probable that fatal abscesses
of the liver not infrequently are caused in this way in extra-tropical
countries. Adhesions forming to neighboring hollow organs or to the
external integument, such abscesses discharge, carrying out the
calculus with them. In this way may be explained the discharge by the
intestine of calculi much too large to have passed by the natural route
and unattended by the usual symptoms of hepatic colic. These
gastro-intestinal biliary fistulæ extend from the gall-bladder and the
larger ducts to the stomach, to the duodenum, and to the transverse
colon; but of these the communication with the stomach is the least
common. The adhesion of the gall-bladder or common duct to the duodenum
or colon may be direct, exudations uniting {1075} the two parts without
the intervention of an abscess cavity, or such a sac or cavity may be
interposed. In some cases the discharge of biliary calculi is effected
through these routes with so little disturbance as to escape notice, or
the symptoms may be only vague indications of a local inflammation in
the neighborhood of the liver.
Biliary fistulæ communicating externally, caused by the migration of
calculi, are comparatively common. They have the clinical history, and
are usually treated as cases, of hepatic abscess. Sometimes hundreds of
calculi are thus discharged. In such instances it may be assumed that
communication has been established with the gall-bladder. Hepatic
abscess thus due to the migration of calculi may discharge into the
pelvis of the kidney, into the ascending vena cava, or through the
lung, but these places of outlet are comparatively uncommon.
COURSES AND COMPLICATIONS.--Although symptoms cease for the time being
when the calculus passes into the duodenum, and although in most
instances no after unpleasant effects are experienced, there are cases
in which the presence of the concretion in the intestine proves to be
fruitful of mischief. Calculi of very large size--from a pigeon's to a
hen's egg--are also found in the intestine, without the occurrence of
symptoms indicative of their migration. It has been shown that this
silent migration of calculi from the liver-passages to the intestinal
is not uncommon. Hepatic concretions are distinguishable from the
intestinal by their crystalline form and by their composition. The
former are usually polyangular, and are composed of cholesterin
crystallized about a nucleus of bile-pigment, inspissated bile, or
mucus. After entrance into the intestine, lime salts and mucus are
deposited in successive layers, so that the form of the calculus is
modified and its size increased. The solitary ovoid concretion is most
frequently found in the intestine, without previous symptoms of hepatic
source, and, although increased in size in the intestine, it retains
its original shape. A specimen of this kind now in my possession
illustrates these points. It is composed of cholesterin crystallized in
radiating lines and concentric rings about a central nucleus of
inspissated bile. Around the hepatic concretion there have formed
layers of lime and mucus since it has reached the intestine, and after
drying this rind became brittle and was readily detached. The
polyangular calculus is apt to form the nucleus of a scybala-like mass
of feces; hence in the search for these bodies every such mass should
be broken up. An example of this has recently come under my own
observation. Concretions of all sizes, having reached the intestines,
as a rule pass down without creating any commotion, and are silently
discharged. But various disturbances occur in some instances.
Obstruction of the bowels is one of the results. A great may cases have
been collected by Murchison,[172] as many more by Leichtenstern,[173]
of impaction of the intestine produced by an accumulation of feces
about a biliary concretion. A calculus may be retained in a fold or
diverticulum of the small intestine, and may indeed cause a loop to be
formed which in turn readily twists, becoming an immovable obstruction.
This mode of obstructing the bowels is less common than the simple
impaction. It is affirmed by some authorities, especially by Von
Schüppel, that obstruction of the bowels--impaction--is more often
caused by stones that have ulcerated through into the {1076} intestines
than by those that have descended by the common duct; and this
conclusion must be reached if jaundice has not been present. It is not
only the size of the calculus which determines impaction, as has been
stated: several may be agglutinated in one mass, and reflex spasm of
the muscular layer may be induced by their presence in the bowel.
Nevertheless, some enormous concretions have been found in the canal,
and others have been discharged without special trouble. Hilton Fagge
exhibited to the Pathological Society[174] of London two gall-stones
passed with the stools, measuring 2½ by 1-1/5 inches in long and short
diameter, and Fauconneau-Dufresne[175] refers to concretions of the
size of a hen's egg. Mention has been made of one in the writer's
possession of the size of a pullet's egg, which, until its discharge,
caused a train of characteristic symptoms. These immense bodies may
have ulcerated through from the gall-bladder or may have grown by
successive deposits of carbonate and phosphate of lime after reaching
the intestine.
[Footnote 172: _Lectures on Diseases of the Liver_, p. 573.]
[Footnote 173: _Ziemssen's Cyclopædia_, vol. vii.]
[Footnote 174: _Transactions of the London Pathological Society_, vol.
xix. p. 254.]
[Footnote 175: _Op. cit._]
The symptoms caused by the presence of concretions in the intestines
are, when pronounced, sufficiently characteristic. At a variable period
after an attack or attacks of hepatic colic the disturbance begins. The
condition of impaction above referred to does not differ from ordinary
fecal accumulation. It is true that occasionally the intestinal
irritation due to the presence of these bodies in some instances
preceded the symptoms of impaction, but usually there is no evidence to
indicate that the stoppage of the bowel is due to anything else than
feces. The irritability manifested by the intestinal mucous membrane
when gall-stones are present varies remarkably. There may be only some
ill-defined pain which, as a rule, indicates the position of the
calculus, or it may be pain with a feeling of soreness, or it may take
the form of violent colic, with nausea, vomiting, and depression. In my
own cases pain was experienced at or near the ileo-cæcal valve, where
one was lodged, and along the descending colon, where the others were;
the pain and soreness ceased when these bodies were discharged.
In a few instances gall-stones are brought up by vomiting. The most
remarkable example of this is a case to be found in the _Transactions
of the Pathological Society_ (vol. xii. p. 129): A woman ninety-four
years of age vomited a stone the size of a nutmeg. In the reported
examples violent pain, nausea, and much vomiting preceded the discharge
of the calculus.
Like other foreign bodies, a gall-stone may ulcerate through the
intestine, producing fatal peritonitis.
Many conditions due to the presence of biliary concretions, and which
arise during their migrations, may be viewed as complications. Many of
those produced directly have been described as a part of the proper
course of the malady; others are local and reflex, and these may with
propriety be considered as complications. First in importance are those
due to obstruction and the local inflammation.
The passage of a calculus along the duct excites an inflammation of the
mucous membrane, which by contiguity of tissue invades the peritoneal
layer if the stone is retained for a sufficient time, and especially if
it is immovably lodged. The stoppage in the flow of bile leads to
dilatation of the ducts, and a change takes place in the character of
that fluid, {1077} owing to the admixture of mucus with the bile and to
the pouring out of a pathological secretion: it loses the bilious
appearance and becomes a merely sero-purulent fluid. Serious changes
ensue in the structure of the liver, as was first suggested by O. Wyss
and Leyden, and afterward more especially by Wickham Legg[176] and
Charcot.[177] A ligature to the common duct in animals is followed in
so short a time as two weeks by hyperplasia of the connective tissue
and atrophy of the gland-elements. It has been ascertained that similar
changes ensue in man from the impaction of a calculus in the common
duct. Under these circumstances the size of the liver, as indicated by
the area of hepatic dulness, at first enlarges, and subsequently more
or less contraction, coincident with the atrophy, ensues. When the
cystic duct is obstructed the contents of the gall-bladder increase,
and become ultimately sero-purulent (dropsy). In some instances, the
walls of the abdomen being thin, a globular elastic tumor may be felt
projecting from beneath the liver.
[Footnote 176: _St. Bartholomew's Hospital Reports for 1873_. See also
_Treatise on Diseases of the Liver_, by the same author, _loc. cit._]
[Footnote 177: _Leçons_.]
Angiocholitis, or inflammation of the duct, is caused by the passage,
especially by the impaction, of a calculus. The inflammation may extend
by contiguity of tissue and involve the surrounding parts. Several
cases have been examined by the writer in which the gall-bladder and
the cystic and common duct were imbedded in a mass of organized
exudation. An extension of inflammation may take place, and be confined
to the hepatic peritoneum. Heavy organized exudations will form,
adhesions be contracted to the diaphragm, to the parietal peritoneum,
and to the neighboring organs, and the capsule, thickened and
contracting, will ultimately induce changes in the structure of the
adjacent part of the liver. When the inflammation extends to the
peritoneum there are the usual systemic symptoms, and locally acute
pain, increased by the respiratory movements and by pressure, and
assuming a constrictive character; nausea and frequent vomiting, and
often a very troublesome hiccough, caused, doubtless, by implication of
some branches of the phrenic nerve; constipation, etc.
The relation of biliary colic to cancer of the biliary passages was
first noted by Frerichs, who ascertained the occurrence of gall-stones
in 9 out of 11 cases of cancer of these parts. Hilton Fagge[178]
reports a case of the kind, and the writer can add another from his own
observations.
[Footnote 178: _Guy's Hosp. Rep._, 1875.]
The most important of the reflex symptoms are those pertaining to the
circulatory system. The action of the heart becomes irregular in rhythm
and diminishes in force. The circulation of the bile acids in the blood
causes slowing of the heart's action, as has been set forth in the
section on jaundice; but that is a direct consequence, and is not a
reflex impression. Potain was the first to show that the structure of
the heart is affected. A mitral murmur is a recognized symptom in the
icterus of gall-stones, but Potain[179] has shown that the real seat of
this murmur is the tricuspid, and that the affection of the heart is a
dilatation of the right cavities. The physiological reason for this
condition of the heart is the rise of tension in the pulmonary artery,
which is secondary to irritation of the splanchnic nerves; and to this
factor is also due the reduplication of the first sound and the
accentuation of the second sound--characteristic signs of the cardiac
change in these cases.
[Footnote 179: Cyr, _Traité de l'Affec. calc. de Foie_, _loc. cit._]
{1078} There are certain reflex nervous troubles in cases of hepatic
colic, some of them of great importance. One of the lesser troubles is
herpes zoster. A very violent attack in the course of the distribution
of the first, second, and third cervical nerves has happened in a case
under the writer's observation. There have been reported from time to
time cases of sudden death during the paroxysms of hepatic colic, in
which a calculus lodged in Vater's diverticulum, at the intestinal
extremity of the common duct, was the cause of the accident. An
explanation of this result is to be found in the intimate nervous
communications between the liver and the heart through the solar plexus
and the large number of ganglia contained in Vater's diverticulum. The
most severe pain is felt as the calculus is passing through the orifice
of the common duct into the intestine, and here also the spasm of the
muscular fibre is most tense. The so-called crushing-blow experiment of
Goltz illustrates how intense suffering, such as the passage of a
gall-stone, can paralyze the heart through the solar plexus. The
depression of the heart's action does not always occur on the instant,
but it may be gradual--several hours, even a day or two, being occupied
in the suspension of activity. Leigh of Liverpool[180] has reported an
example of death in six hours in a female of thirty, previously in good
health; Cornillon,[181] another in a female of fifty-three, who died in
twelve hours from the beginning of the paroxysm; Williamson,[182] a
female of fifty-one years, who expired on the fourth day;
Habershon,[183] two, who died during the paroxysms at a period not
stated; and Brouardel, one which was the subject of a medico-legal
investigation. In the first case the calculus was yet in the
gall-bladder, the appearances indicating that persistent spasms had
occurred to force the calculus into the cystic duct; in the others in
which the position of the stone is mentioned, it was engaged in the
orifice of the common duct or had reached the intestine.
[Footnote 180: _Medical Times and Gazette_, 1867, vol. i. p. 248.]
[Footnote 181: Cyr, _op. cit._, p. 185.]
[Footnote 182: _The Lancet_ (London), vol. ii. p. 780.]
[Footnote 183: _Lectures on the Pneumogastric_, 3d Lecture.]
In several instances sudden death has resulted from uncontrollable
vomiting induced by the paroxysms of hepatic colic. Trousseau[184]
mentions a case in which strangulated hernia and death ensued in
consequence of the violent vomiting brought on by the passage of a
calculus.
[Footnote 184: _Clinique médicale_.]
DIAGNOSIS.--Unless the distension of the gall-bladder is sufficient to
cause a recognizable tumor, gall-stones in that organ do not produce
symptoms by which they can be diagnosticated. If sudden attacks of
violent pain in the right hypochondrium, accompanied by nausea and
vomiting and followed by jaundice, have occurred from time to time,
then the presence of biliary concretions may be suspected if the
symptoms belonging to them are present in the intervals between the
seizures. The migrations of calculi produce symptoms so characteristic
that error is hardly possible. The only disorders with which an attack
of hepatic colic may be confounded are gastralgia and hepatalgia. As
regards the first, the distinction is made by the seat of pain, by the
absence of after jaundice, and by the lack of a concretion passed by
stool. As the diagnosis may depend on the finding a concretion, the
writer must again affirm the importance of a properly-conducted search
of all the stools passed for several days after the paroxysm.
{1079} Hepatalgia is diagnosticated with great difficulty, for the pain
has the same seat, the same character, but as a rule it does not
terminate so abruptly, is not accompanied by such severe vomiting and
depression, jaundice is absent, and no stone can be found in the
evacuations. Both gastralgia and hepatalgia occur in the subjects of
neurotic disturbances--in the pale, delicate, and hysterical--whereas,
as a rule, hepatic colic happens to the obese, to the persons of active
digestion addicted to the pleasures of the table.
The passage of calculi may be confounded with flatulent colic, with the
pain caused by lead and other mineral poisons, with impaction, internal
strangulation, local peritonitis, and similar causes of sudden and
violent pain. The differentiation is made by attention to the seat and
character of the pain, by the previous history, and especially by the
absence of jaundice and of a concretion. From renal colic the hepatic
is separated by the position of the pain, by the direction taken by it,
and by the retraction of the testicle, the irritability of the bladder,
and the appearance of blood in the urine--all characteristic symptoms
of the renal affection.
TREATMENT.--The treatment of biliary concretions includes the remedial
management for the calculi in position, for the paroxysms of hepatic
colic caused by the migration of these bodies, and for the results and
complications.