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it is also true that these forms are all different in many particulars.

Their pathology, to begin with, is not the same. In one form — the
hypertrophic — the fibrous tissue is finer, less formed, accompanied by
a cellular growth, and runs along the smaller branches interstitially.
In the atrophic form this fibrous tissue is coarser, better formed, shows
greater tendency to contract upon and disorganize liver cells, extends
along larger branches of the interstitial tree, and is not accompanied
-by cellular growth to the same degree at all.

In connection with the increase of connective tissue it has been
proven experimentally that the action of alcohol on the liver of
animals is also to cause granular and fatty degeneration of the liver
cells. According to Vaughan, the increase of the connective tissue
is small in amount, and only reported by some observers. Vaughan
concludes that " the connective tissue changes are subsequent to and
dependent upon alteration in the hepatic cells." 1 Later on he writes
that with the clinical and experimental evidence hitherto obtained we
are justified in believing " that in alcoholic cirrhosis the pathological
changes begin in the hepatic cells."

From what has been said concerning the pathology and etiology of
atrophic and hypertrophic cirrhosis it has been shown that the two
forms may exist as types. They may also be present combined, as it
were, in the same individual and exist as one disease. The atrophic
form is clearly due, as a rule, to alcohol ; the hypertrophic to infection
(Vaughan) ; but the infection may precede or follow the toxic poison-
ing, and the result is a mixed form of cirrhosis. These forms, both
clinically and at the autopsy, are very difficult of precise diagnosis, so
intimately and curiously combined are their symptoms or lesions. 2

1 Journal of American Medical Association, October 5, 1901, pp. 878, 879.

2 In a patient I saw last summer, who subsequently died, the liver was stated during life to
be much enlarged by several very competent observers— both surgeons and physicians. I was
able to satisfy myself after death, by intra-abdominal digital exploration, that the liver was
not notably enlarged. I was also convinced that an intra-abdominal mass, in close juxtaposi-
tion with the lower margin of the liver, gave rise to an error of diagnosis in this regard,
although the case was proven not to be one of cirrhosis of the liver.


la the syphilitic cirrhosis we have those broad bands of fibrous tissue
which penetrate between the lobules and draw the liver down near the
surface in such manner as to leave the puckered, scarred appearance,
with bossy, prominent, irregular masses between which are so charac-

As to the course and clinical symptoms : These, we shall see, differ
widely and obviously in many ways. In atrophic cirrhosis, for exam-
ple, the main distinguishing clinical feature, as we could almost
premise from its pathology, is the evidence of marked portal obstruc-
tion — at least this is true almost as soon as the disease is clearly deter-
mined. Hence arises the abdominal effusion, and with this most
significant and almost portentous sign we have hemorrhages from the
stomach and bowels. Sometimes these are small and infrequent, and
give no great and immediate alarm if their quantity alone is consid-
ered ; but considered from the point of view of their evident causation,
great apprehension is invariably excited, and justly so. Shortly we
may have, and do often, those abundant and depressing blood losses
so difficult to arrest, and which point to the urgent necessity, and none
too soon, of employing all rationally known measures to ease up an
obviously crippled organ and to restore falling strength. How unfor-
tunate it is in such cases if the somewhat too enthusiastic surgeon finds
indications for abdominal exploration or an operation for internal
hemorrhoids ! Jaundice is a rare sign in these cases 1 — at least real
jaundice, with urine loaded with bile pigment and acholic stools. Of
course, the dull, earthy hue of the skin and the subicteric tint of
the sclerotics are frequent phenomena which serve in a measure to fix
our diagnosis. Sometimes " adhesive pyelophlebitis closely resembles
the atrophic form of interstitial hepatitis. The rapidity with which
the peritoneal effusion reforms after tapping is an important diagnostic
sign." 2

These cases of atrophic cirrhosis in reality are long as to duration.
They appear short merely because they are unrecognized prior to the
advent of the ascites, and then the inevitably fatal termination seems
to stand out imminently, since a few months or a briefer period may
bring about a fatal ending of the case.

The first and imperative thing to do 'with these patients is to lay
down the law which forbids alcoholic stimulation in any form, because,
as we know, in the chronic irritation thus produced we find the imme-
diate and efficient cause of the majority of such cases. Of course,
there are degrees of injurious action. The man who has drunk heavy

1 Where fatty degeneration and cirrhosis coexist profound, persistent jaundice is less infre-
quent. A patient thus affected, as shown by the autopsy, died in one of my wards at St. Luke's
Hospital May 8, 1902.

3 James H. Wilson, Medical Record, December 7, 1901, p. 909.



beers for a long while and in large quantities, combined, it may be
at times, with daily potations of spirits undiluted and containing fusel
oil, is the worst type with which we have to do. Such an one is the
longshoreman, hodcarrier, and other laboring man, or the chronic
loafer who comes to our out-door clinics or to our hospital ward, when,
on investigation, we find the contracted, small hobnailed liver, which
shows the condition of multilobular cirrhosis and also many accom-
panying pathological changes. The spleen and pancreas are often
hard and functionally decrepit, the kidneys show marked interstitial
changes, the stomach is thickened, atrophied, and congested ; but,
above all, the heart is weak, flabby, degenerated. Fibrous myocarditis
is sometimes made out at the autopsy ; more frequently we have more or
less fatty change, apparent to the eye and corroborated with the micro-
scope. The general vascular system does not escape, and capillary
arteriofibrosis has run its course, so that there is scarcely a sound
arterial coat to be found, no matter what organ we turn to. This is, in-
deed, a gloomy and, alas ! too true a picture. Alongside, fortunately,
we have another far more hopeful. The man-about-town, the broker, the
business man — even the lawyer and the not too wise physician — whose
drinking consists in two or three or more " Manhattan " or " Mar-
tigny " cocktails every day, taken upon an empty stomach and as " a
pick-me-up," as the saying goes ; the genial, pleasant fellow who gives
himself a rest of an evening, and who frequents the club and the
billiard-room, and who before the evening is gone has consumed several
drinks of "rye" or "Scotch" or "unsweetened," is also an apt
candidate for admission among the cirrhoses of the atrophic order.
Fortunately, such an one drinks "good spirits, as a rule, in the sense
that it is relatively pure and unadulterated. Moreover, his food is well
cooked and assimilable. He bathes, and is therefore cleanly and has an
active skin ; and with a healthier body, perhaps, to start with he does not
suffer so soon or so hopelessly as the poor chap I have previously con-
sidered. Moreover, when the first premonitory signs of disease occur,
if he be even moderately wise, he consults his family physician, when
I would fain believe he secures a mental and moral shaking up, with
which a little useful medicine added thereto allows him to guard more
carefully his still useful liver cells, and gives declared fibrosis an
opportunity to cease development and extension for a time.

Without going further in this description I trust I have been able
to show and bring home to my readers what they all know, what they
all feel and see around them every day. Turn, now, to our hyper-
trophic form of cirrhosis, and what may we note ? Here, instead of
atrophy and contracture and loss of size, we have enlargement and
increase of weight. In addition, there is to be found a singular devel-
opment of new biliary canaliculi on the periphery of the lobules,


which is so distinctly shown in sections for microscopic insight. This
latter division is the one so ably described by Hanot, Charcot, and
other French writers, and about which there is such wide divergence of
opinion elsewhere. Suffice it to add that in typical forms these must
be very rare, infrequent cases. For my own part, I do not recall to
have seen and observed a typical one — at all events, not one where
the post-mortem researches justified altogether a previous clinical diag
nosis. In the hypertrophic cirrhosis of the sort we do see from time
to time the fibrosis as it extends into the liver seems to mark for its
own a few cells here and there throughout the structure, or certain
individual lobules. In this hypertrophic form ascites does not often
occur, nor should we expect it if we pay due regard to the special char-
acters of the fibrosis formation. Jaundice, on the contrary, is a marked
and almost omnipresent symptom ; and it is the real jaundice — not the
aborted state, so to speak — to which I have referred in the atrophic
form of cirrhosis, i. e., icteroid hue.

Like to atrophic cirrhosis, haemateniesis is not infrequent, and, when
it occurs, abundant and very threatening. Many of these hemorrhages
in cirrhosis originate at the lower end of the oesophagus. They are
often confounded with hemorrhages which come from ulcer of the
stomach. 1 In either case, but especially the former, Ave should be
very chary about the introduction of a stomach-tube, as a dangerous
or even fatal loss of blood might take place immediately. With the
hemorrhage from the oesophagus or stomach we see developed many
acute symptoms. There is fever, and often the temperature ranges
high. There is delirium of an active kind, pointing to a toxaemia and
blood infection. "Chills and sweating are not common" in the
hypertrophic form of interstitial hepatitis, ' ' thus serving to differen-
tiate it from impacted gallstones." (Wilson.)

Later the patient may relapse into coma from which there is no
awakening. Before these symptoms of delirium and coma become
manifest we usually have several repeated intermittent attacks of pain,
with fever. The pain is localized over the hypochondrium, and the
liver is tender.

In these particulars we have an approach to the syphilitic form, and
except for the history, the different physical signs, and other symptoms,
we might have a difficult diagnosis ; but this is not true for the careful

1 According to Knapp (Medical Record, March 1, 1902, p. 334) these hemorrhages are some-
times erroneously "diagnosed as pulmonary tuberculosis," when they should be considered
" cases of ulcer of the oesophagus."

According to Bouchard (Revue de M6decine, October, 1902) hemorrhages in cirrhosis,
which occur outside the territory of the portal vein, are in relation with pre-existing arterial
lesions, affecting various organs, and do not depend upon abdominal plethora. The arterial
lesions are chronic degenerative changes probably due to arterio-sclerosis. — Boston Medical
and Surgical Journal, September 11, 1902.


diagnostician, who also considers the ordinarily chronic course of the

As to causation, it is obscure. Frequently the spleen also being
enlarged a malarial origin is suspected. There are too few observa-
tions accurately made in which the plasmodium has been discovered
to altogether justify this opinion. I rather believe that alcohol
is here again a more probable and efficient factor in bringing on this
change in liver structure. One statement would seem to be borne out
by facts that we do know, and it is that the obstruction of the bile
ducts by fibrous tissue seems to account for the genesis of the acute
symptoms which mark the course of the disease and point to inflam-
matory conditions, more or less lasting. According to some authors,
such inflammatory conditions are wholly ignored, and they affirm that
an infective process is the sole, undeniable cause of hypertrophic cir-
rhosis. In this conection Vaughan 1 writes : " With our present knowl-
edge it must be attributed in all cases to infection." If this be ad-
mitted, pathologically, it may be stated that " the epithelium of the
gall ducts is the site of the primary involvement." (Vaughan.)

In the syphilitic liver we find marked induration, at times fairly
recognizable by our tactile sensations. The liver itself is, as a rule,
larger than uormal. This is not an invariable rule, and just the con-
trary may be found, no doubt, in those instances where the fibrous
contracting bands are broad and numerous. The gummata on the
surface of the liver when they exist are often easily recognizable. Of
course, we may confound them with malignant nodules on the one hand
or perhaps the hobnailed condition of atrophic cirrhosis on the other;
but the bossy, lobular forms of the tumors, together with the previous
history and other signs of syphilis, or, in the absence of both, the
notable cachexia of cancer, if present, enable us to be pretty confi-
dent as to our differential diagnosis. In reasonable doubt an accurate
blood count with differentiation of white cells will help us much. A
decided and relative increase of lymphocytes and of eosinophile cells,
according to Neusser or Cabot, would make this point very valuable.
Of course, " a disappearance of the tumor after a tentative antisyph-
ilitic treatment argues most positively in favor of gumma." 2

So far as clinical symptoms go, syphilitic cirrhosis resembles one of
the other forms. There may be jaundice and no ascites ; there may
be both ascites and jaundice. 3 On the other hand, there are instances
in which neither sign is present. At an advanced stage, however,
ascites can usually be determined ; and what is of particular value is

1 Ibid. cit. 2 Einhorn, Medical Record, August 17, 1901.

* Stockton states when jaundice occurs, even with apparent alcoholic cirrhosis, especially
if accompanied by cachexia, it is well to suspect syphilis. — Medical News, June 28, 1902,
p. 1244.


the localized pain in the right hypochondrium which is usually present.
These pains are not constant, as a rule, but come on intermittently, or
at all events are greatly intensified if previously they have been present
in a mild, dull form. The pains during the exacerbations may become
so intense as almost to resemble those of gallstones. If the disease
has existed for a long while there is decided loss of weight, but scarcely
ever to the degree which characterizes malignant disease. Constipa-
tion and various functional disturbances of the stomach and intestines
are frequently present.

The congenital form of syphilis of the liver I do not remember to
have met with ; if I have my memory is too uncertain to be a faithful
reporter. 1 By those who have seen or described it it is said to be a
diffuse fibrosis, where the abnormal tissue formation penetrates into the
lobules or between the cells. The fibrous tissue is an immature devel-
opment. The liver itself is large and it is accompanied by jaundice,
ascites, and emaciation. 2 While as regards the pure pathology of
cirrhosis, as Cheadle says, there is more or less unanimity among
writers, this is not true of the causation of symptoms as connected with
morbid anatomy, nor of the course and clinical manifestations of the
disease in its various forms. One of the questions for settlement is to
know whether the atrophic form is anything more than a later stage of
the hypertrophic. Further, more definite judgment as to Hanot's
biliary cirrhosis is desired, and as to whether hypertrophic cirrhosis is
a real entity. These and many others are of singular interest. It is
ordinarily accepted that atrophic cirrhosis is mainly caused by alcohol ;
indeed, that it is the essential cause in the vast number of cases. Still,
malaria has seemed to be a sinning factor at times. Unfortunately, a
typical case of malarial origin is rarely found, at least with us in New
York. This may be accounted for, and doubtless is, by the relatively
mild form of malaria from which we suffer. The sestivo-autumnal
sort, with the characteristic crescents in the blood, does not occur
often. They are relatively exceptional. Now, it is in just these cases or
those of long-continued malarial cachexia, where we find great enlarge-
ment with fibroid induration of the spleen and also of other abdominal
organs, notably the kidneys. Why, then, should we anticipate finding

1 According to Osier it " is rare and nearly always overlooked."

2 Vide Cheadle. Lumleian Lectures for 1900. It affords me great pleasure in this connec-
tion to speak with admiration of these lectures, and to state that I have freely used them in
writing this paper. Indeed, I have followed his outlines (Cheadle's) because I could find
none better.

Since the above was written, Dr. George G. Sears and Dr. F. T. Lord have published in the
Boston Medical and Surgical Journal of September 11, 1902, a very important paper on cir-
rhosis of the liver, based on all the fatal cases in the Boston City Hospital and the Massa-
chusetts Hospital since 1896 in which the diagnosis was proved by histological examination.
Many of their conclusions, according to the London Lancet of October 15, 1902, are only con-
firmatory of those published in England by Dr. Cheadle and by Dr. Hale White.


well-marked morbid effects of this sort in the liver if, as I do believe,
the liver as an organ is not nearly so apt to be much affected by
malarial poison as is the spleen ? Also, I would state that it is most
unusual for us to discover cases of profound malarial poisoning where
we could absolutely eliminate the disastrous influence of alcohol from
the equation ; and yet it is stated, even by those who claim never to
have seen a case of malarial cirrhosis, that there is nothing absolutely
improbable in the assumption, inasmuch as malarial indurated spleen
is fully determined. To my mind, this reasoning by analogy is very
lame and inapplicable to the liver, in view of the fact of. its very dif-
ferent structure and functions. When we consider how prone the liver
is to become engorged and somewhat cirrhotic in all cardiac affections
as well as in all obstructive lung diseases, it would seemingly be doubly
reasonable to eliminate the malarial factor in causation, unless pretty
clearly evident. I direct particular attention to this statement, because
I know that in most text-books malaria is insisted upon as a cause of
atrophic cirrhosis of the liver. Osier, 1 in this connection, writes : " In
our large experience with malaria during the past nine years not a
single case of advanced cirrhosis due to this cause has been seen in
the wards or autopsy-room of the Johns Hopkins Hospital." Now, it
is well known that the malarial manifestations found in the city of
Baltimore — a few indigenous, many coming from regions farther South
— are more virulent than those we meet with in New York or other
cities of the North in the United States.

Osier also writes, 2 in speaking of the liver : " Only those cases in
which the history of chronic malaria is definite, and in which the
melanosis of both liver and spleen coexist, should be regarded as of
paludal origin."

There seems to be little doubt, also, that hypertrophic and atrophic
alcoholic cirrhosis are distinct forms of disease and not different stages
of the same form. This affirmation seems reasonable when we consider
the very marked difference in the distribution of the fibrosis as well as
of its nature in the two cases. In the one the affection is markedly
multilobular ; in the other it is monolobular in quite as pronounced
degree. According to Cheadle, the error in confounding the two dis-
eases arose originally from the hypothesis that Hanot's so-called biliary
cirrhosis was simply the hypertrophic form. In many instances of cir-
rhosis of the latter form there is unquestionably a period when the liver is
simply congested and enlarged, and yet no formation of abnormal fibrous
tissue is yet begun, not to speak of any degree of contracture which
later on may prevail. In these cases the liver is said to be much softer
than it is where hypertrophic cirrhosis has become developed. This

1 Practice, fourth edition, p. 570. " Ibid, cit., p. 209.


statement is no doubt true, and can be shown obviously in the autopsy-
room on rare occasions. When it comes to actual clinical work and
interpretation I am obliged to confess that this stated hardness as
compared with softness, where the large liver is merely congested, is
very difficult to differentiate. I have seen many cases of enlarged,
smooth liver where there were few or no symptoms of ill health, unless,
perhaps, slight evidences of dyspepsia should pass for such. In these
cases the tactile sensations, so far as relative hardness is concerned,
revealed little or nothing from this standpoint. This judgment is spe-
cially correct, I am confident, where the patient is corpulent, with thick
abdominal walls, due to the deposit of adipose tissue. In spare, meagre
individuals, with lack of muscular tone and relaxed abdominal walls,
the problem to be settled is much easier, and we may indeed say, truth-
fully, " Liver is hard or liver is soft." Of course, we should never
expect to find in hypertrophic cirrhosis the extreme hardness to tactile
sensations which is characteristic of the atrophic form ; nor is it
rational to expect it when we consider the very great difference which
exists in the variety of the fibrosis — fine in one case, coarse in the other.
The same cause — alcohol — which produces fibrosis of the liver also
effects interstitial changes in other abdominal organs, and particularly
the kidneys, which are thus affected in a large proportion of cases.

Despite the fact that it is affirmed that jaundice does not occur in
atrophic cirrhosis, this statement cannot on inquiry and research be
confirmed. On the contrary, it would seem as though we may and do
have jaundice in all forms of cirrhosis. What is true is that jaundice
occurs earlier in the hypertrophic form than it does in the atrophic,
and hence, of course, when it does show itself in the latter form it is
a sign of very bad augury. Many of the particular symptoms given
by Hanot to designate specially his form of biliary cirrhosis are to be
met with in the ordinary hypertrophic form, many of which are doubt-
less alcoholic ; but when we come to consider the whole description of
this writer we fail to find him in accord with other observers — mainly
outside of France. Even the hyperplasia of bile ducts which Hanot
considers so characteristic may be found in other forms. The jaundice
does not always occur in the usual hypertrophic form, nor, again, is
ascites always absent, and the spleen may not be visibly enlarged.
Pain and pyrexia simply show advent of perihepatitis, and, although
frequent in the hypertrophic form, it may also occur in other
forms. Nervous phenomena and the typhoid state are more frequent
in this form, but they are not absolutely distinctive. Chronicity is
not coastant, and, as we see, already, cases do not conform in all
respects to a purely classical type. Where alcohol is a prominent
factor in causation the symptoms approximate those of the atrophic
form. No doubt in just such instances the hypertrophic liver is spe-


cially hard. The syphilitic liver, like the hypertrophic form, is often
enlarged, extending in the right mammary line far beyond the right free
margin of the ribs. If gummata are present they may be recognized, as
already stated, by the distinct irregularities or bossing of the surface.
If instead of gummata there is a cirrhotic process due to syphilis, the
liver may also present a swollen appearance, and this is also true if
amyloid degeneration has become manifest, which may be. shown in
advanced syphilitic conditions of the liver. In both syphilitic cirrhosis
and amyloid liver the organ is hard and relatively smooth (Einhorn),
and in the former case the fibrosis is said to be diffuse and monolobular.

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