cases of supposed obstruction of the cystic duct enable the physician
to decide with confidence points which before could only be matters of
mere {1093} conjecture. The writer of these lines was the first to
puncture the gall-bladder and to explore, by means of a flexible probe
passed through the canula, the course of the duct.[204] It is possible
in this way to ascertain the existence of gall-stones in the
gall-bladder, to find an obstruction at the entrance of the cystic
duct, to demonstrate the presence of echinococci cysts, and to remove
for microscopical examination pathological fluids of various kinds.
More recently, Whittaker and Ransohoff[205] of Cincinnati have
attempted the detection of a gall-stone impacted at any point by the
introduction of an exploring-needle; and this practice has been
imitated by Harley[206] of London, but without any reference to the
pioneer and prior investigation of his American colleagues. The case of
Whittaker and Ransohoff survived the exploratory puncture, but Harley's
case proved fatal from traumatic peritonitis. Notwithstanding this
untoward result, Harley persists in the advocacy of this method. It
must appear to any one familiar with the intricate arrangement of the
parts composing the anatomy of this region a most hazardous proceeding,
and hardly to be justified in view of the superior safety and certainty
of my method. To explore the interior of the gall-bladder an
aspirator-trocar is introduced; any fluid intended for microscopical
examination is then withdrawn, and through the canula a flexible
whalebone bougie is passed.
[Footnote 204: _The Cincinnati Lancet and Clinic_ for 1878-79; also, W.
W. Keen, M.D., "On Cholecystotomy," _The Medical News_, Sept., 1884.]
[Footnote 205: _Lancet and Clinic_, 1884.]
[Footnote 206: _Lancet_ (London), July, 1884.]
When icterus comes on in a few days after birth and persists until
death ensues by convulsions and coma, there can be no doubt regarding
congenital absence or impermeability of the common duct. Permanent
retention-jaundice, accompanied by the characteristic symptoms of that
condition immediately succeeding an attack of hepatic colic, is
probably due to impaction by a calculus. When, at or after middle life,
in a patient with a history of former attacks due to gall-stones, there
begins a fixed pain in the right hypochondrium, and subsequently
retention-jaundice, the existence of a malignant growth in connection
with the cicatricial tissue and ancient organized exudation should be
suspected; and this suspicion will be confirmed if subsequently a tumor
can be felt. If with a localized pain slowly-developing jaundice,
intestinal indigestion, fats and oils appearing unchanged in the
stools, and a condition of prostration more than is properly referable
to the derangement of the hepatic functions, come on in a man or woman
after thirty-five, cancer of the head of the pancreas should be
suspected; and this suspicion will be confirmed if a tumor can be
detected in that situation. It should not be forgotten, however, that
in emaciated subjects the head of the pancreas may be so prominent as
to be mistaken for a scirrhous growth.
A pulsating tumor of the right hypochondrium, accompanied by jaundice,
may be an aneurism of the hepatic artery. Pulsation may be communicated
to a bunch of enlarged portal lymphatic glands, which will compress the
common duct, but in this case, as the increase in the size of the
glands is due to caseous, amyloid, or cancerous deposits, there will be
found a source whence these morbid products are derived, and will
explain the nature of a tumor thus constituted.
The differentiation of hypertrophic cirrhosis from occlusion of a
slowly-forming character is by no means easy. In both jaundice {1094}
gradually appears; in both the liver is enlarged, but in hypertrophic
cirrhosis much more than in occlusion; and in the latter the
gall-bladder is full--may indeed be distended--whilst in the former it
is empty or contains but little bile. The history of the case may
indicate the nature of the symptoms. Previous attacks of hepatic colic,
and the symptoms of occlusion supervening on the last, are highly
significant of calculous occlusion.
TREATMENT.--To ascertain the nature of the occlusion is a necessary
preliminary to any exact treatment. In many cases this must remain a
mere conjecture, when, of course, the treatment is only symptomatic.
When it is probable or certain that the duct is obstructed by a
calculus, two methods may be resorted to for its removal: one method is
to break up the calculus by mechanical means; the other is to effect
its solution by chemical agents.
Fracture of an impacted calculus is not a merely fanciful expedient. If
the site of the obstruction is ascertained, an attempt may be made to
penetrate the calculus by an aspirator-needle passed through the
abdominal walls, according to the method of Whittaker and Ransohoff.
The dangers attendant on this mere puncture are great, and a fatal
result has occurred in one of the very few cases in which it has been
done. Less severe and dangerous methods for attempting the
disintegration of a calculus should be first tried, as follows: Make
firm friction with the fingers along the inferior margin of the ribs
and toward the epigastrium and umbilicus, whilst the opposite side
posteriorly is supported by the hand spread out and applied firmly. A
strong faradic current sent through the region of the gall-bladder and
ducts has in several instances seemed to do good--indeed, to remove
obstructions. A calculus impacted may be dislodged either by the
fracture of its surfaces or by the strong muscular contractions of the
abdominal walls and of the muscular layer of the duct. Most calculi are
easily broken, and when the smallest breach is made in the external
crust disintegration follows; and some calculi are so friable as to
yield to slight pressure. Furthermore, the slightest solution in the
continuity of the rind disposes the whole mass to dissolve in suitable
menstrua. Mechanical rupture is so important a step in the process of
disintegration of an impacted calculus that so serious an operation as
section of the abdomen as a preliminary to it should be considered. The
cavity exposed, the obstructed duct is found, and its retained calculus
is mashed without section of the duct. I find one instance[207] in
which this was done as a subordinate part of a cholecystotomy, and the
breaking up of the stone proved to be easy of accomplishment. It is
also the method of Tait, who proposes to mash the calculus by means of
suitable forceps fitted with padded blades.
[Footnote 207: Harley's case, _op. cit._]
I have suggested a means of effecting solution of an impacted calculus
which seems, on further reflection, well worthy of consideration. The
proposal is to inject, through a canula introduced into the
gall-bladder, one of the solvents of the cholesterin calculus before
mentioned. I have already used the canula as a duct for the passage of
an exploring-sound, and have by means of it explored the interior of
the gall-bladder. It is quite as feasible to inject through the canula
a solvent, successive charges of which can be thrown in and withdrawn
by the aspirator.
{1095} That the usual solvents introduced by the stomach can effect the
solution of impacted calculi has been declared impossible by
Trousseau;[208] and with this conclusion I unhesitatingly agree. I have
already discussed this part of the subject, and need now only refer the
reader to that section.
[Footnote 208: _Clinique médicale_, _loc. cit._]
The various causes of obstruction besides calculi do not offer an
inviting field for the exercise of therapeutical skill. Each case must
be treated according to the nature of the obstructing cause; hence to
make an accurate diagnosis is an essential preliminary to suitable
treatment.
IV. DISEASES OF THE PORTAL VEIN.
Thrombosis and Embolism of the Portal Vein; Stenosis; Pylephlebitis.
DEFINITION.--By the terms at the head of this section are meant the
various pathological processes which induce coagulation of the blood in
some part of the portal system. As the portal vein is made up of many
branches coming from the various organs of the abdominal cavity except
the kidneys, and as it empties, so to speak, into the liver, it is
obvious that various and complex derangements will ensue on the
formation of thrombi.
CAUSES.--Thrombosis of the portal vein occurs under three general
conditions: the blood is in a readily coagulable state; the action of
the heart is weak and the blood-current sluggish; the circulation
through the vein is impeded by external pressure. The coagulability of
the blood is increased in diseases characterized by an excess of its
fibrin-producing constituents, of which cirrhosis of the liver may be
mentioned as one having this peculiarity. In chronic maladies of a
depressing kind there may be simply a weak action of the heart, or the
muscular tissue of the organ may be affected by a fatty and atrophic
degeneration. The external pressure by which the blood-current through
the vein is impeded may be caused by the newly-formed connective tissue
of Glisson's capsule, by enlarged lymphatics in the hilus of the liver,
or by tumors of various kinds. The first named of these causes of
compression--atrophic cirrhosis--is most frequently acting. Very
rarely, organized exudations of the peritoneum may be so situated as to
compress the portal vein. This result can only happen when the hepatic
portion of the peritoneum is involved.
Pylephlebitis exists in two forms: the adhesive and suppurative. The
former results in changes not unlike those of simple thrombosis. The
blood coagulates in the affected part of the vessel, the clot is
organized, and the vessel ultimately forms a solid rounded cord which
is permanently occluded. The suppurative variety is so different in its
origin and in its results that it requires separate treatment, and I
therefore postpone the consideration of it to the next section.
{1096} SYMPTOMS OF THROMBOSIS AND ADHESIVE PYLEPHLEBITIS.--It is a
remarkable fact that the biliary function of the liver is not
necessarily affected in cases of occlusion of the portal vein. It is
true, in advanced cases of cirrhosis, when the interlobular veins are
obliterated by the pressure of the contracting newly-formed connective
tissue, the functions of the liver are arrested in so far as the damage
thus caused extends. Notwithstanding the blocking of the portal,
sufficient blood reaches the hepatic cells by the anastomosis between
the hepatic artery and the interlobular veins--an anatomical connection
demonstrated by Cohnheim and Litten.[209] So long as this anastomosis
continues bile will be formed, although the portal vein is occluded.
[Footnote 209: _Virchow's Archiv_, Band lxvii. p. 153, "Ueber
Circulationsstörungen in der Leber."]
The most significant symptoms of thrombosis of the portal vein are the
sudden formation of ascites, which quickly assumes a very high grade,
and equally sudden passive congestion of the gastro-intestinal mucous
membrane, enlargement of the spleen, and distension of the superficial
veins of the abdominal parietes. When these symptoms succeed to
cirrhosis of the liver, or appear after the formation of a tumor in the
hepatic region, or come on in the course of phthisis or chronic
inflammation of the hepatic peritoneum, the existence of thrombus of
the portal vein may be reasonably suspected.
Coincidently with the occlusion of the portal vein the
gastro-intestinal mucous membrane becomes the seat of a catarrhal
process, and to the fluid thus produced is added a much more abundant
transudation from the distended capillaries. Nausea, vomiting, and
diarrhoea result, the rejected matters being serous, watery, and in
many cases tinged with blood. Now and then quite a severe hemorrhage
takes place, and the blood is brought up by vomiting (hæmatemesis) or
is discharged by stool. Hemorrhoids form, and, in large masses
protruding, much pain is experienced, and free bleeding may result from
rupture of a distended vein.
The veins of the abdominal parietes, which in the normal state are
invisible or at least not prominent, and which form anastomoses with
the portal, when the obstruction occurs dilate, sometimes to a
remarkable extent. The most important anastomosis is that between the
femoral and saphena and internal mammary and epigastric veins. When the
hepatic branches of the portal are closed, but the trunk remains
pervious, the parumbilical vein enlarges greatly, and, communicating
with the superficial veins of the anterior part of the abdominal walls,
forms a radiating network of tortuous veins to which is given the
striking title of caput Medusæ.
The most significant symptom of portal thrombosis is a quickly-forming
ascites. It is true, ascites is a common symptom in advanced cirrhosis,
but the rapid accumulation of fluid and the prompt filling of the
cavity after tapping distinguish that which arises from portal
thrombosis from all others. Besides its excessive extent, the ascites
presents the usual symptoms.
Due to the same cause as the enlargement of the superficial veins, the
hemorrhages, the ascites, etc., there occurs considerable hypertrophy
of the spleen in many of the cases. It sometimes happens that the new
compensatory circulation and the hemorrhages from some part in the
{1097} usual route of the portal so dispose of the blood that the
spleen does not enlarge sufficiently to be readily made out.
COURSE AND TERMINATION.--It is obvious that a condition such as that
induced by thrombosis of the portal must be comparatively quickly
fatal; but the cases vary in duration as the compensatory circulation
is more or less complete. Whilst the majority of cases terminate within
two weeks, instances of several months' duration are not unknown, but a
fatal termination, sooner or later, is inevitable in all cases.
Coming on in the course of some chronic affection of the liver or some
obstructing cause exterior to the organ, there soon follow ascites,
nausea and vomiting, hæmatemesis, bloody stools of a liquid character,
enlargement of the spleen, distension of the abdominal veins, and the
distressing symptoms produced by an excessive accumulation of fluid in
the peritoneal cavity.
DIAGNOSIS.--As there is no symptom of thrombosis of the portal which
may not be caused by advanced cirrhosis, the diagnosis rests on the
rapid production of the attendant phenomena and their conjoint
appearance.
TREATMENT.--A symptomatic treatment is alone possible. The highly
irritable and congested intestinal mucous membrane precludes the
employment of hydragogue cathartics. Salines which cause outward
diffusion from the vessels are the only cathartics which can be used
with propriety. Action of the kidneys and of the skin must be
maintained. To this end the resin of copaiba in pilular form and
pilocarpine subcutaneously may be used. If the strength of the patient
will permit, leeches around the anus can be applied, and much relief
may be expected from free bleeding. It is probable that opening a
swollen hemorrhoid would give the same kind of relief as that caused by
a free hemorrhage. In any case the benefit derived from treatment must
be merely palliative and temporary.
Suppurative Pylephlebitis.
PATHOGENY.--Primary pylephlebitis rarely if ever occurs. On the other
hand, the secondary form is by no means uncommon; it succeeds to
ulcerative or purulent inflammation at some point in the circuit of
origin of the portal radicles. The most frequently-occurring cause is
ulceration and suppuration of some part of the intestinal tube, and
hence the most common result is multiple abscess of the liver.
Pylephlebitis has often resulted from typhlitis; from ulcers of the
large intestine, as in dysentery; from such traumatic injuries as tying
hemorrhoids; from proctitis; from ulcers of the stomach and similar
morbid processes elsewhere within the range of origin of the portal
system. The pathogeny is clear. The inflammatory or ulcerative action
extends to and involves the walls of the veins, or some morbid material
diffuses through the vein walls. In either case coagulation of the
blood in the vessel ensues, and the clot undergoes a series of changes
resulting in the formation of emboli, which, carried into the main
current, are subsequently lodged in the hepatic capillaries.
There are three steps in the morbid process: the changes in the vein
wall; the production and transformation of the thrombus; and the
formation of secondary suppurating foci in the liver.
{1098} The appearance of the tunics of the inflamed vessels varies with
the stage at which they are examined. At first the walls of the vessels
are reddish from congestion, succulent, and swollen, infiltrated by
leucocytes and inflammatory exudation and the cellular elements
undergoing proliferation. The intima especially is much altered in its
appearance and structure, becoming thick, opaque, grayish or yellowish
in color, and having adherent to it a thrombus passing through its
characteristic changes. Ulceration of the intima then occurs, and the
purulent elements, with shreds of tissue, mingle with the degenerating
blood-clot, and ultimately there remains a purulent dépôt lined with
sloughing, even gangrenous, contents. Emboli detached from such
decomposing thrombus are arrested in the vessels of the liver, and
there set up a suppurating phlebitis, ending in an abscess formation,
or a quantity of pus from the original point of ulcerative phlebitis
passes into the portal vein, and is generally distributed through the
hepatic branches, here and there foci of suppuration being established
by the deposit of decomposing emboli. There may be numerous small
abscesses irregularly distributed through the liver, or there may be
one or two larger collections of pus. Very often the vessel whose
occlusion by a suppurating embolus has caused the mischief is
destroyed, and hence no communication with the abscess-cavity can then
be traced. These abscesses are not limited by a line of inflammatory
demarcation or by a limiting membrane, but the hepatic tissue adjacent
is congested and infiltrated with pus.
Ulceration, abscesses, or purulent inflammation occurring at any point
within the area of origin of the radicles of the portal vein may induce
pylephlebitis and consequent hepatic abscess. There are two points at
which, suppuration established, secondary pylephlebitis is most apt to
occur: the cæcum; the rectum. As respects the former, the symptoms of
typhlitis precede the hepatic disturbance; and as respects the latter,
usually dysentery, or rather proctitis, is the initial disease. In both
sources of the hepatic trouble the inferior hemorrhoidal veins are
chiefly concerned--a fact explicable by reference to the sluggishness
of the circulation and the distended condition of these veins, whence
it is that thrombus is very readily induced. Numerous instances of
pylephlebitis following suppurative lesions of the cæcum have been
reported. One of the most recent, and at the same time typical,
examples of such conditions is that published by Bradbury[210] of
Cambridge, England. The initial lesion was "an ulcer the size of a
split pea" situated near "the junction of the vermiform appendix and
cæcum." "The hemorrhoidal veins and the inferior mesenteric above were
filled with breaking-down clot and pus," and "the liver contained many
abscesses of various sizes, the largest about the size of a lemon,
which had burst through the diaphragm." As is so often the case, the
ulcer of the cæcum produced no recognizable disturbance, and important
symptoms were manifest only when the emboli lodged in the liver set up
suppuration, when there occurred the usual signs of hepatic abscess. In
the West and South hepatic abscess due to pylephlebitis, induced by
proctitis, with ulceration of the rectum, is a common incident. Various
examples of this kind have fallen under my own observation. The
relatively greater frequency of this form of pylephlebitis is due to
the fact above {1099} stated, that the inferior hemorrhoidal veins are
voluminous, have a sluggish current, and are liable to over-distension
by pressure of feces and by external abdominal bands and clothing.
Cases of a corresponding character arise from suppuration and
ulceration elsewhere within the portal circuit. Thus, Bristowe[211]
reports a case in which pylephlebitis resulted from an ulcer of the
stomach, the neighboring veins becoming implicated and the usual
results following.
[Footnote 210: _The Medical Times and Gazette_, Sept. 27, 1884, p. 450,
"Proceedings of the Cambridge Medical Society."]
[Footnote 211: _Transactions of the Pathological Society of London_,
vol. ix. p. 278.]
When inflammation has begun in a radicle of the portal vein, it may
proceed to the liver by contiguity of tissue, the whole intervening
portion of the vessel being affected. Probably more frequently the
intra-hepatic portion of the portal is inflamed by emboli, and the
adjacent hepatic tissue then undergoes suppuration, as has been already
set forth.
SYMPTOMS.--There being two points of disease--the primary lesion of the
peripheral vessel and the secondary results in the hepatic portion of
the portal--the symptomatology must have a corresponding expression.
The stomach, the cæcum, or the rectum, or some other organ or tissue,
being occupied by a morbid process, there will be a characteristic
complex of symptoms. Taking up the most usual primary disturbance, a
typhlitis or an ulcer of the cæcum, there will be pain, tenderness, and
possibly fever, occupying in point of time the period proper to such a
malady and an amount of disturbance of function determined by the
extent of the lesion. The symptoms caused by a single small ulcer of
the cæcum, as in the example narrated by Bradbury, may present no
characteristic features and may have little apparent importance, and
yet the lesion is productive of very grave consequences.
When from any of the causes mentioned above a thrombus forms in a vein
of the portal system in consequence of the extension of the
inflammation about it, the case, what importance soever it previously
had, now takes on new characters. The onset of the inflammation of the
vein walls and the puriform degeneration of the thrombus is announced
by a chill--a severe rigor, or chilly sensations at least. At the time
of the chill, and sometimes before it, pain is felt, significant of the
lesion in the vein. When proctitis or typhlitis precedes the
pylephlebitis, pain appropriate to the malady is a significant symptom;
but the pain which comes on with the beginning of the inflammation in
the liver is a new sign. The most frequent sites of the pain are the
right hypochondrium and the epigastrium, but it may also be felt in the
left hypochondrium or in either iliac fossa. Unless there be diffuse
peritonitis the pain is accompanied by a strictly-localized tenderness
to pressure. The situation of the pain may afford an indication of the
vein attacked, and when there are two points at which pain is
experienced, one may originate at the first situation of the morbid
action; the other will be due to pylephlebitis.