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Staining Ulcers 76

Standardization of Drugs 275

State Care of Consumptives 359

St. Joseph's Infirmary 35

Stomach-tube, The. By H. H. Roberts, M. D .... 61

Sudden Changing of Color of Hair 315

Suprarenal Extract in the Treatment of Addison's Disease (Clinic). By R.

Alexander Bate, A. B., M. D 90

Supreme Court Decision as to Medical Consultants 355

Surgical Hints 106

Tallest Children Bom in Summer 316

Taylor, Basil M., M. D .* 176

The Doctor's Pay. By John G. Cecil, B. S., M. D 401

Therapeutic Uses of Nitro- Glycerine 433

Third International Congress of Obstetrics and Gynecology 37

Three-Year Medical Schools 36, 153

Thyroid Treatment in Obesity 119

To Spit or Not To Spit 235

Traumatic Tetanus. By John A.Lewis, M. D 169

Treatment of Anthrax by Means of Lye , 471

Treatment of Fissure of the Nipple 159

Treatment of Harelip and Cleft Palate 32

Treatment of Indolent Ulcers 118

Treatment of Lobar Pneumonia. By John G. Cecil, B. S., M. D 121

Treatment of Scarlet Fever. By R. B. Gilbert, M. D 323

Tri- State Medical Society of Alabama, Georgia, and Tennessee 155, 238

Tuberculous Dairy Cattle 152, 198

Two Cases in which the Ordinary Clinical Evidences and Microscopical Exam-
ination were Misleading. By M. F. Coomes, A. M., M. D 248

Two Cases of Tetanus 315

Two Centenarians 38, 313



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xvi Contents of Volume XXVIII.

Typhoid Fever as a Systemic Disease of Manifold Manifestations 270

Typhoid Fever in the Massachusetts General Hospital During the Past Fifty

Years 389

Ulcerative Membranous Tonsillitis 272

Unusual Complications of Typhoid Fever 310

Upon the Use of Ethyl Chlorides as Anesthetic 308

Use of Chloroform in Labor. By Walker Bourne Gossett, ^. D 84

Utility of the Blood-clot in the Treatment of Wounds. By R. C. McChord,

M. D I

Vaginal Hysterectomy 112

Vance, Ap Morgan, M. D 41

Vegetarian King 317

Vegetarian Sanatorium in Great Britain 317

Venereal Diseases in Various Armies 308

Visible Outlines of the Stomach and Intestines 118

Vital and Mortuary Statistics of Kentucky for 1898, Prorated from the National

Census of 1890. By T. B. Greenley, M. D , 244

Vulvitis in Children 115

Western Surgical and Gynecological Association 359

Whalen, Charles J., M. D., LL.D 450

What Our State is Doing for the Training of Her Unfortunate Children 396

What To Do With Our Consumptive Patients '. 274

William F. Jenks Memorial Prize 113



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THE



American Practitioner and News.



NEC TENUI PENS A.'



Vol. XXVII. Louisville, Ky., January i, 1899. No. i

Certainly it is excellent discipline for an author to feet that he must say all he has to say in the
liewest possible words, or his reader is sure to skip them ; and in the plainest possible words, or hi^
leader will certainly misunderstand them. Generally, also, a downrisrht fact may be told in a plain
way ; and we want downright facts at present more than any thing else.— Ruskin .



©rtginal CtvtxcUs.



CIRRHOSBS OF THE LIVER.')'

BY JOSEPH B. MARVIN, M. D., LL. D.

The subject of cirrhosis of the liver has been extremely interesting
to me for a good many years. I suppose it has been to every physician
who looks for explanations of disease along definite mechanical lines.
The etiology, morbid anatomy, and clinical symptoms of this disease,
at first sight, appear more simple, clear, and comprehensible than the
phenomena of almost any other disease. If there was one disease
more than another about which the pathologist could say that knowl-
edge is complete, it is portal cirrhosis of the liver.

. I have never been thoroughly satisfied with the explanations given
by standard authors in regard to the etiology of all cases of cirrhosis
of the liver. I happen to have had some few cases under observation
extending over a series of years where I could rule out of consideration
the history of alcoholism, which is put down as the sole cause of
ordinary portal cirrhosis. I have had opportunity a few times in years
gone by of making autopsies in some of these cases confirming the
diagnosis of general portal cirrhosis without any history of alcoholism,
and in searching for a cause it seemed to me that a very plausible one
was that it was a toxemia ; that troubles in the intestinal or gastro-
intestinal tract cut a deeper figure in the etiology of the various cir-
rhoses of the liver than the books, as a rule, usually attribute to it.

Some year or more ago I incidentally came across a monograph by a
French author taking the same view, so I have searched the literature,

* Abstract of a psper read before the I«ouisviIle Medico-Chimrgical Society^ November iS, 1898.
For discussion see p. 19.



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2 The American Practitioner and News.

particularly the French, for further evidence on the subject during the
last two years. The French more than any other pathologists, as far as
my reading extends, have inclined to the view that certain forms of
cirrhosis of the liver are non-alcoholic in character. Beginning with
the so-called Hanot liver, as it is known in France, we may call it
the biliary or hypertrophic form ; it is put down as being non-alcoholic in
character, the process being infectious in origin. Lanceraux also in
the last few years published a series of experiments on this subject,
taking the view that the ordinary common wine which is consumed by
the French laborer and peasant was a more frequent cause of the
atrophic form of cirrhosis of the liver than whisky, and in attempting
to ascertain the cause he suggested that it was the adulteration of this
common wine with plaster of Paris, stating that it was a well-known
fact that the plaster of Paris itself was largely adulterated with
sulphate of potassium.. And he formulated the theory, which has not
been confirmed by others, that sulphate of potassium constantly
ingested through the medium of common wine cut a very important
figure- in the etiology of the atrophic form of cirrhosis of the liver. So
the French seem to be in the advance guard on this subject, claiming
that the two most common forms of cirrhosis of the liver, viz., the
small atrophic form, which we have generally regarded as synonymous
with chronic alcoholism, and next that the so-called hypertrophic or
biliary cirrhoses, as being non-alcoholic in character, perhaps infectious
or toxemic.

So recent a writer as Hawkins, in CliflFord AUbut's System of Medi-
cine, still holds to the old view and classifies cirrhoses of the liver under
very simple heads : First, the wasting or atrophic form, alcoholic in
character. Next, the so-called hypertrophic, large, or biliary cirrhosis,
sometimes alcoholic, sometimes not. Third, syphilitic cirrhosis, this
form being most frequently congenital. (My experience has been that
syphilitic cirrhosis is not always congenital; that some of the cases
that have been dignosticated as cirrhosis of the liver and reported
cured were not alcoholic in character, but were syphilitic in character
and yielded to the iodides.) Fourth, malarial.

This is a very simple classification: Alcoholic, by far the larger
number ; two forms more frequently noticed is the small or hob-nail
liver, next the hypertrophic. Syphilitic, a much smaller class. Lastly,
malarial, representing a smaller class than either of the others. Then
under the head of pathological curiosities or. freaks he groups cer-



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The American Practitioner and News. 3

tain others as due probably to cardiac trouble, tubercular trouble,
injuries, etc.

I do not believe the last word has been said about cirrhoses of the
liver, and my object in selecting this trite subject was to provoke dis-
cussion and lay before you some recent studies on this subject. In the
irst place, I do not believe we can correctly make the classification
bove outlined. The chances are that we are on the eve of very
important discoveries in regard to this disease, and when these dis-
coveries shall have been completed, radical changes will be necessary
in otuc it05ol<^;y. It would seem in the light of a recent paper, to
which further reference will be made presently, that the idea that
alcoholism is the prime factor in the causation of cirrhosis of the liver
would have to give place to other causes, and instead of being the primary
cause it is perhaps only a secondary cause. I do not believe we can
rule out alcoholism altogether, and it seems to me that alcohol might
act in one of two ways, either by being taken in sufficient quantity,
especially on an empty stomach, and kept up for a sufficient length of
time ; being taken directly into the portal circulation, it might act
injuriously upon the liver cells and upon the liver connective-tissue.
Next, I believe that it may act secondarily by interfering with diges-
tion, upsetting the stomach and intestine, allowing certain toxines to
be absorbed, the latter acting directly on the liver cells and liver con-
nective-tissue.

Now, if alcohol was the principal factor in the production of this
disease, and if alcohol had any such specific property as that, why do
we not have more cases of cirrhosis of the liver? The number of
cases of cirrhosis of the liver to the number of persons who drink
alcoholic beverages in this country or any other civilized country is
certainly out of all proportion to claim that there exists a direct cau?*?
and eflFect. Another thing I make bold to say, that I believe that a
small minority only of cases of very small livers or very large livers
are cirrhotic. I make bold to say another thing, that the detection of
a small liver, one of the most common forms of genuine cirrhosis of
the liver, is by no means an easy matter, and our so-called methods
of physical examination are very likely to mislead us.

I have reached the conclusion that alcohol is simply an irritant or
one of a class of irritants acting either primarily or secondarily in the
production of cirrhosis of the liver, and that we may have a host of
other causes grouped under the same heading — irritants.



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I Another point : Wq can not explain all the phenomena of cirrhosis
of the liver by the ordinary mechanical explanations as laid down in
text-books. If we could, we ought to have a picture that is always the
same. I thjnk all pathologists present will bear me out in this state-
ment, that in the majority of instances where there is a history of
alcoholism, a large, smooth, fatty liver, or one not diminished in size,
will be found. It is a rare thing to find the hob-nail liver. In the
majority of cases of so-called alcoholic cirrhosis, due to the degenera-
tive eflFect of alcohol, the liver cells are first destroyed ; next there is a
stimulation of the connective tissue, making it overgrow, and as it
overgrows, then contracts, following the usual characteristics of fibrous
tissue, and by contracting making the liver harder, firiner, thicker,
squeezing out the hepatic lobules. Under these conditions, why do we
not have jaundice?

If you cling to the idea of the pathology as laid down in the text-
books, even up to the last one issued, you have to believe that the
same cause can narrow the portal circulation and dilate the biliary
canals at the same time. I do not believe you can explain it upon this
ground. I think the classification as laid down by even the latest and
best authors is purely arbitrary and fictitious, and that under the
heading of cirrhosis you may have all shapes, from a large liver to a
small liver, from one with a large amount of fibrous connective-tissue
throughout it to others with a small amount, and so on.

There is a very interesting explanation as to why irritation should
act on the cells and destroy them and at the same time stimulate the
fibrous tissue. The cell of any organ is the highest possible develop-
ment, the highest point of evolution ; it has more functional activity,
more work to do ; it is the life of the organ. The connective-tissue is
phlebian, it is of less importance, it does not have much to do. If
there is sufficient irritation to destroy the life of the cell, then you will
have acute yellow atrophy. It might destroy a man in a few days. It
does it so quickly that I am sure all of you have seen cases in which
you have thought, here is a case of toxemia; there is some powerful
poison at work in the system which strikes at the life of the patient,
which destroys the secreting portion of the liver and overwhelms the
patient in a few days. I believe that cirrhoses of the liver are on the
same line, the poisons in smaller doses acting more slowly and chron-
ically. You have a gradual destruction of the parenchyma of the liver.
The toxine destroys the liver cells and constantly stimulates the fibrous



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The American Practitioner and News. 5

tissue, which makes it overgrow. It seems to me that the solution is
not so difficult as we are led to believe by the authorities.

Acute yellow atrophy, which is the most formidable and destructive
of all the hepatic troubles that we see, may be explained in the manner
stated. There are a number of authorities on cirrhosis of the liver
who state that all forms are characterized first by destruction of the
cells, which is accompanied by more or less evolution or development
of the connective-tissue stroma of the liver. I incline to the view that
the change is primarily in the cells, and only secondarily in the stroma.
The fibrous tissue overgrowth may be conservative.

(The recent studies of Adami were discussed at length.) In the
light of these investigations, we shall have to abolish the distinction
between the so-called acute and chronic cirrhosis; it seems as if the
bacteriologist would recast our entire pathology. His sphere of "infec-
tivity" has spread to embrace chronic as well as acute conditions.
Verily, the " trail *' of the microbe is over them all.

(A number of cases were detailed with results of the autopsies,
illustrating the views of the speaker.) Just as long as you can have
an anastomosis through the superficial veins, there may be no ascites;
congestion of various organs may occur, and bleeding from the nose,
stomach or bowels may be profuse and give temporary relief. Now,
as the disease progresses there may be either a narrowing of the
portal system, or by pressure stop the free anastomosis and cause
ascites. How did the blood get through without any ulceration?
How can you account for the sudden supervention of these cerebral
symptoms? I believe it is due to the absorption into the blood of
toxines, setting up an arteritis; I believe that in many cases you will
find an arteritis and peri-arteritis, and frequently associated with them
you will find valvular troubles of the heart. I believe it is the toxine
that gives rise to the arteritis and allows oozing to take place through
the vessel walls in such large quantities without ulceration or any visible
solution of continuity in the course of the vessels.

There are many interesting points that you might discuss, and that
are still being discussed in regard to these cases : Why in some you
have no jaundice, why some will start with gastric symptoms and in a
few weeks there will be some sallowness, dinginess, muddiness of the
complexion, slight jaundiced appearance of the face and sclerotics,
then after a little while an improvement in all these symptoms, to be
followed a little later by marked ascites.



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6 The American Practzttoner and News.

Another thin^ : I do not believe any of you can tell just what is
goin^ to be the result, as far as the prognosis is concerned, of puncture
of the abdomen. I believe tapping ought to be done early and repeated
if necessary.

I have seen a case where there was no ascites, but there was an
enormous edema of the abdominal walls.

Treatment. Strict regulation of the diet and an entire withdrawal of
alcoholics are of prime importance. I have seen a few cases that were
materially benefited by iodide of potassium in small doses, well diluted,
taken on an empty stomach, combined with or taken simultaneously
with salines, the sulphate of soda in hot water. Were these cases of
syphilis? Syphilis and whisky frequently go hand in hand. If syphi-
litic, then, of course, I believe that iodide of potassium and bichloride
of mercury might do some good.

Next, the duration of life is greater than many of us have been
taught to believe. I have generally had an idea that when a man came
to me with gastric symptoms, with a histor>' of alcoholism, with as I
thought a small liver, the patient later developing hematemesis or
piles, that he had cirrhosis of the liver and would soon succumb. Some
of these patients live a long time. Have we been mistaken in our
diagnosis ; was it simply gastric catarrh from alcohol and not cirrhosis
of the liver?

Then comes the so-called malarial cases: You see a man with symp-
toms simulating malarial fever ; you can only make a diagnosis by the
presence or absence of the Plasmodium malarise in the blood. Without
this blood examination, how can we say that it is or is not a case of
malarial cirrhosis ?

Another point is the use of saline injections. I believe that saline
injections ought to be practiced far more frequently than they have
been. That takes us back to the case mentioned previously : She had a
profuse hemorrhage one day. When I arrived she was pulseless, eyes
fixed and glazed, and her face had a death-like pallor. She had practic-
ally stopped breathing. I did not wait to find a vein, I simply injected
a pint in the axilla and a pint in the groin. I do not know of any
thing that acts as a hemostatic as quickly as injection of saline solu-
tion. This woman was virtually brought back to life on several occa-
sions by this plan of treatment. You can easily introduce a pint in
the axilla or under the breast. I believe in the hemorrhage of typhoid
fever it is a most admirable remedy. Instead of giving ergot, tannic



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The American Practitioner and News. 7

add, tannin, etc., give a saline injection. Of course it would be bet-
ter to inject it into a vein, but anywhere will do. I do not believe you
will find a particle of trouble from getting air in with it ; this has been
proven a fallacy. How it acts you can explain in any way you desire,
but it is very simple to me. I believe shock is best treated not by
strychnine, digitalis, whisky, etc., but by saline injections. In
making the saline solution I use forty or fifty grains of salt to a pint of
boiled water.
Louisvn.LK.



THE 5BRUM TREATMENT OF DIPHTHERIA.^

BY WILLIAM CHEATHAM, M. D.

I propose in this paper to endeavor to answer the objections which
have been urged to the use of the serum treatment of diphtheria, as,
strange to say, there are still some disbelievers.

First: Some refuse to use it, saying there have been some fatal

cases as the result. Prof. Langerhan had a son to die immediately

after an injection of antitoxin. Prof. Strassman, who at the request of

the State held an autopsy, came to the conclusion that it was the

result of the inspiration of food. Prof. Langerhan opposes this view.

The antitoxin was proven to be normal. Chas. T. McClintock says

such deaths are the result of shock. Adamkiewiaz attributes such

deaths as that of Miss Valentine and the son of Prof. L. to the forcible

injection of the serum and its specificity causing a disturbance of the

self-regulating apparatus. Tossett reports a fatal case in which a

cerebral embolism was found. Johannersen says it is the result of the

introduction of foreign serum into the blood, and for that reason the

antitoxin should be as concentrated as possible. Seibert and Schwyzer

think air must have entered the venous circulation. Moizard and

Bouchard report a case of angina in which the Loeffler bacillus could

not be found ; antitoxin was given, and the throat was clear in three

days. In three more days vomiting, diarrhea, and fever set in, and the

fourth day the patient had convulsions, strabismus, dilated pupils, and

coma, which they attributed to the antitoxin. Roux does not think so,

as the same serum had been used in one hundred thousand injections

in France with no accident.

« Read before the Mitchell District Medical Society. December 29. 1898.



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That sudden deaths do sometimes follow the injection of antitoxin
no one doubts, but it has not been proven that the antitoxin was the
cause. Death follows hypodermatics of other substances; it follows
the inhalation of anesthetics, yet who will give up their use? Deaths
following the use of antitoxin, even could it be proven that the anti-
toxin was the cause, considering the millions of times it has been
used, are exceedingly rare, and should keep no one from using a remedy
which has saved so many lives and has reduced the death-rate of diph-
theria at least one-half, and has rendered the management of a majority
of cases of this dreadful disease so simple and so painless.

Second: The claim has been made that paralysis with or without
death is more common after the use of antitoxin. Jacobi admits we
see more cases of paralysis because more cases of diphtheria recover.
If the death-rate has been reduced fifty per cent by the use of antitoxin
( which statistics prove), and in making this statement that old quota-
tion, "the lie, the damn lie, and statistics,'* is not forgotten, there are
just twice as many cases left to be paralyzed. Washbourn (British
Med. Jour., Aug. 17, 1895) agrees with Cohen as to the cause of the
increase in the number of cases of post-diphtheritic paralysis, and gives
as another reason that the antitoxin does not neutralize the eflFect of the
invasion of other bacteria and streptococci. Dana (Med. Record,
April II, 1896) says antitoxin does not decrease the number of the
palsies, and as a reason he says not enough is given to prevent the
specific action of the toxin upon the nervous system.

I admit there are more palsies since antitoxin came into use, but
not so many in proportion to the number of recoveries. To objection
second, then, I say it is not so.

Third : Nephritis is more common*after the use of antitoxin. The
International Medical Annual of 1896, page 237, says Thomas and Mapes
immunized one hundred and thirty-six children, aged from three weeks
to four years, introducing from 50 to 200 units, and found but four with
a trace of albumen in the urine, but this in no case persisted more than
four days. Reiche {CentralbLf. Innere Med,y No. 50, 1895) investigated
the kidneys of eighty-five fatal cases before the antitoxin period, and
found serious trouble with the kidneys of all ; there is positive evidence
that antitoxin does not damage the kidneys. The damage, if any, is
done by the toxin before the use of the antitoxin.

Fourth : That antitoxin has an unfavorable eflFect upon the blood,
decreasing the number of red corpuscles, etc. Billings (Med. Rec,



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The American Practitioner and News. 9

April 26, i8g6) investigated this subject thoroughly, and says the anti-
toxin treatment of diphtheria has no deleterious eflFects upon the blood
corpuscles ; on the contrary, it seems to prevent degenerative changes
which would otherwise be brought about. Schlesinger {Arch. f.
Kinderh.^ 1896, Bd. xix, S. 378) and Ewing (New York Med. Jour., Aug.
10, 1895,) arrive at the same conclusion.

Fifth: Antitoxin increases the temperature and disturbs the circu-
lation. It is true that within twelve hours after antitoxin is injected
the temperature may rise from one to three degrees, but in the next
twelve or twenty-four hours it becomes normal. The circulation
sympathizes with the rise and fall of the temperature.

Sixth : The use of antitoxin has not decreased the death-rate of
diphtheria. Statistics on this subject are becoming so large that they
are difficult to manage. Any one with an unbiased mind, and who has
treated many cases of diphtheria in pre-antitoxin days and since anti-
toxin has come into use, must say nay to objection six. The favorable
statistics on this subject are attacked in many ways. The objector
tells us continually that the disease is not so severe in type ; that many
cases called diphtheria now are not diphtheria ; that Loeffler's bacillus
is not the true bacillus ; that it is found in the mouths of many healthy
people ; that for these and other reasons our statistics are false ; that
the gross mortality is not decreased; that immunizing is a failure; that



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