or of the lining of the bile duct. 2. Pressure upon the bile ducts exerted
from without such as may occur in instances of tumors of the gall-bladder,
liver, pancreas or stomach, particiflarly cancer of the pylorus. Omental
tumors, displaced kidneys, enlarged glands in the fissvire of the liver, faecal
masses, the pregnant uterus and aneurysms of the abdominal vessels are less
common external causes of obstruction. 3. Obstruction of the biliary
passages from internal causes such as calculi, parasites, inflammatory stric-
tures or tumors of the duct itself or of the duodenum at its orifice. 4.
Reduced pressure in the hepatic blood-vessels, while a higher pressure obtains
in the bile passages, favors the resorption of bile from the latter.
Acute Catarrhal Jaundice.
Synonyms. Duodeno-cholangitis; Icterus Catarrhalis; Inflammation of the
Common Bile Duct.
Definition. An affection characterized by icterus of the tissues occurring
as a result of an obstruction to the flow of bile due to a catarrhal inflammation
of the mucous membrane of the bile ducts and of the duodenum.
.Etiology. Cholangitis is usually a sequence of the extension of an inflam-
454 DISEASES OF THE DIGESTIVE SYSTEM AND PERITONEUM.
mation of the gastric and duodenal lining into the common bile duct. These
latter conditions may be caused by exposure, errors in diet, over-indulgence
in alcohol, tea or coffee, over-work, mental emotion, or they may complicate
the acute infectious diseases such as pneumonia and enteric fever. The
passive congestion which occurs in chronic endocarditis and nephritis may
also result in jaundice of this type. An epidemic catarrhal jaundice has been
Pathology. The distinctive lesion is a swelling and congestion of the mucous
linfng of the common bile duct; the process may extend to the cystic duct or
even to the hepatic duct and its ramifications. The lumen of the duct is usu-
ally filled with mucus, a plug of which often occludes its orifice. This plug
may be expelled by pressure, following which free passage is afforded to the
bile. The liver itself may be slightly swollen, its color is lighter than normal
and its tinge icteroid. If the affection is protracted the retained secretion
may cause sufficient irritation to bring about an increase of the connective
stroma of the organ and a consequent cirrhosis with atrophy of the hepatic
cells may result.
Symptoms. Usually manifestations pointing to gastric disturbance, such
as anorexia, a coated tongue, nausea, vomiting and constipation, are first
noticed. Pain is not common but there may be slight epigastric tenderness;
a shght febrile movement is not infrequent. Following these symptoms the
jaundice appears. The sclerotics may be first discolored, the face and neck
are also early involved; thence the yellow color spreads over the whole body
including the mucous membranes. Even the perspiration may be tinged.
In instances of long standing the color deepens to a brownish or greenish-
yellow. The urine is dark reddish-brown or dark green and when shaken
its foam is of a yellow color. In protracted instances albumin and casts may
be found, the latter often being bile stained.
Constipation is usually present, the stools are foul of odor and light grayish
or clay-colored. Rarely there may be diarrhoea.
Infrequently the tears, saliva and milk are tinged with yellow.
The pulse rate is slowed, at times being even as low as 30 beats per minute.
The respiration is unaffected.
There is often an annoying itching of the skin and such cutaneous lesions
as urticaria, furunculosis, lichen and xanthelasma, a manifestation consisting
of slightly elevated yellow macules occurring upon the eyelids and rarely upon
other parts, may be observed. In grave instances of the affection ecchymoses
and even large haemorrhages may appear in the skin and mucous membranes.
Symptoms referable to the nervous system are common. The spirits are
depressed and the patient may be melancholic. The temper is irritable
and headache and dizziness are common. Visual disorders may occur,
objects may appear to be of a yeUow color, the patient may see better by a
ACUTE CATARRHAL JAUNDICE. 455
dim light or vision in the dusk may be indistinct. Marked and severe nervous
symptoms occur in grave instances of jaundice but more particularly in asso-
ciation with acute yellow atrophy, carcinoma and fatty degeneration of the
liver than in catarrhal inflammation of the bile passages. These symptoms
are acute delirium, convulsions or suddenly appearing coma. Usually there
are accompanying fever, rapid pulse and prostration, which with the nervous
manifestations, comprise the symptom complex to which the term cholmmia
has been applied; this condition is probably due to the presence in the blood
of some poisonous constituent of the bile.
Physical examination may reveal the presence of a more or less enlarged
and tender liver; sometimes the gall-bladder is distended and palpable.
The diagnosis. Jaundice occurring acutely with symptoms of gastro-
duodenitis, a history of dietary indiscretions and in the absence of manifesta-
tions suggestive of acute yellow atrophy, carcinoma or hepatic cirrhosis is
distinctive of catarrhal obstruction of the bile passages. The pigmentation
of the skin of Addison's disease may be mistaken for jaundice but in the former
condition the eyes are not colored and the faeces are not clay-colored. The
same is true of the cutaneous discoloration observed in uterine affections,
malaria and cancer.
The prognosis of uncomplicated catarrhal jaundice is uniformly favorable.
The duration of the disease is usually from 10 days to 8 weeks; if the course
is protracted beyond this limit the possibility of mistaken diagnosis must be
considered. A febrile movement and the incidence of haemorrhages are
Treatment. The patient should be kept in bed while there remains any
elevation of temperature and while there are active symptoms of gastric irrita-
tion. While there is interference with the flow of bile the food should be such as
does not need this secretion to promote its digestion and assimilation, conse-
quently fats are to be avoided. Milk, however, while containing a certain
amount of fat, seems to be well borne, and while it may seem advisable to
remove the cream, this need not be done. Other substances which are
allowable are egg-albumin and meat broths. As the digestive irritation
diminishes and the flow of bile increases the diet may be more liberal and
we may add eggs, fish and other non-irritating foods. When the bile stasis
persists for some weeks and a generous diet is needed to maintain the patient's
nutrition the fats should be replaced by carbohydrate foods. In convalescence
small meals taken frequently are to be preferred to those of large amount
at more infrequent intervals. The diet in any individual instance should be
governed by the condition of the stomach and intestine, consequently it may be
said that the feeding in catarrhal jaundice after the acute stage is passed is
that of gastro-intestinal catarrh.
At the beginning the bowels should be freely opened by small repeated
456 DISEASES OF THE DIGESTIVE SYSTEM AND PERITONAEUM.
doses of calomel â€” J grain (0.016) every ^ hoiir until 6 doses have been taken â€”
followed by a saline; here we may give the natural Carlsbad salt in doses of
2 or 3 drachms (8.0 to 12.0), Hunyadi, Apenta or any of the similar laxative
waters. During the progress of the affection free daily evacuations should
be induced by the administration of sahnes such as magnesium or sodium
sulphate, sodium phosphate, Carlsbad salts or Vichy, Hunyadi, Friedrichshall,
Rubinat or Saratoga Hathorn waters. By this means the catarrhal process in
the duodenum is lessened and the mucus is dissolved from the lining of this
visciis. The drastic vegetable purgatives should be avoided on account of
their irritant properties.
The patient's thirst may be relieved by any of the palatable alkaline waters
such as Vichy, and frequent draughts will aid in freeing the duodenum from
its accumulated mucus, thus acting in connection with the laxatives suggested
In relieving the stasis of bile and hastening the flow of this secretion no drug
is more active than salicylic acid in doses of from 10 to 20 grains (0.66 to 1.33).
Calomel, also, has been suggested in this connection but its cholagogue
action is disputed in the light of oiir present knowledge. Its effect is evidenced
by a retiu-n of the stools and urine to normal color rather than by a disap-
pearance of the jaundice. High rectal enemata of ice water may assist in
removing the plug of mucus from the opening of the bile duct; their action is
probably due to a stimulating effect upon peristalsis. Massage over the
region of the gall-bladder may be employed in the hope of stimulating the flow
of bile and the same may be stated concerning the faradic current, which
should be used in considerable strength. While not much is to be expected
of these latter measures their employment is, to say the least, harmless.
The gastric irritability may be relieved by regulation of the diet and by the
administration of sodium bicarbonate in watery solution or in connection with
cerium oxalate â€” 20 grains (1.33) of the former and 10 grains (0.66) of the
latter being added to each glass of milk that the patient takes. Plain water,
taken in considerable amount and as hot as possible, is often effective. If
there is uncontrollable vomiting all food should be stopped, the patient being
allowed to suck bits of cracked ice; small doses of dilute hydrocyanic acid
may be effective in combating this symptom.
Diarrhoea is uncommon but if present may be controlled by means of bis-
muth subsalicylate or subnitrate in the usual doses or still better by such intes-
tinal antiseptics as bismuth naphtholate â€” gr. 5 (0.33) three or four times a
day â€” combined with an equal amount of phenyl salicylate (salol) or 2 or 3
grains (0.13 to 0.2) of resorcinol.
When the symptoms of gastro-intestinal irritation have ceased we may
substitute for the remedies previously given for their relief a bitter tonic such
as the following: ^ acidi nitrohydrochlorici diluti, 5vi (24.0); fluidextracti
TOXIC JAUNDICE. 457
nucis vomica, fluidextracti gentiainae, aa 5i (4.0); aquae cinnamomi q.s. ad
Â§iv (120.0). One teaspoonful to be taken in a little water before each meal.
Instead of this 10 minims (0.66) of dilute hydrochloric acid may be added
to a tumblerful of water and drunk with the meals.
The pruritus may be relieved by warm baths to which a pound (1500.0) of
sodium bicarbonate has been added, by lotions of i to 60 phenol, 10 percent,
menthol in albolene, by powdering the skin with talc, bismuth subgallate or
zinc stearate and by the administration of calcium chloride in doses of from
15 to 20 grains (i.o to 1.33) 2 or 3 times daily or of a powder containing 10
grains (0.66) of sodium bromide and five (0.33) of antipyrine at similar
In persistent instances of the disease the patient will usually derive much
benefit from a stay at one of the spas such as Saratoga or Bedford in the
United States, Harrogate in England or Vichy or Carlsbad upon the continent.
Here the good effect of the internal use of the waters, of the bathing and of
the systematic life will soon be felt.
This type of jaundice, formerly considered haematogenous in origin, is now
held to be the result of biliary obstruction caused by increased viscidity of the
bile accompanied by angio-cholitis.
Toxaemic jaundice is produced by the following causes:
1. The action of such poisonous substances as arsenic and phosphorus.
2. Specific infectious diseases such as yellow fever, malaria, enteric and
typhus fevers, pyaemia, scarlatina, etc.
3. Obscure conditions, probably of infectious origin such as Weil's disease
or acute febrile jaundice, and acute yellow atrophy of the liver.
The poisons are believed to cause obstruction in the following way:
there is destruction of the blood by haemolysis which results in the liberation
of haemoglobin and an increased production and excretion of bile pigment ; the
bile becomes more viscid and produces a transient obstruction with reabsorp-
tion of bile and consequent jaundice. As the toxaemia disappears the viscidity
of the bile becomes diminished, the secretion flows more freely and the jaundice
The symptoms of toxic icterus are less marked than those of the more truly
obstructive type of the affection; while the skin may be yellowish the stools
are seldom clay-colored and, although the lurine may be darkened, there is a
conspicuous absence of bile pigment. In some instances there are extremely
severe constitutional symptoms such as high fever, great prostration, marked
mental disturbances, coma, aniiria and haemorrhages into the skin and from
the mucous membranes.
458 DISEASES OP THE DIGESTIVE SYSTEM AND PERITONEUM.
Jaundice is a common manifestation in newly-born infants. It occvirs in
both a mild and a severe t}'pe. The former is quite common and often
makes its appearance within 2 or 3 days of birth. Its causation is not definitely
known but it is probably due to biliary stasis in the smaller bile ducts. Certain
authorities have attributed it to the destruction of red blood cells by haemolysis^
the jaundice resulting in the same fashion as in toxic icterus. The condition
is characterized by yellowish discoloration of the skin, darkened urine and
light colored stools. There is seldom any digestive disturbance and the
symptoms usually disappear within a week or two.
The grave type of jaundice of the newly-born may be the result of con-
genital absence of the common or hepatic ducts, congenital syphilitic inflam-
mation of the liver or of septic phlebitis of the umbilical vein. The outcome
is usually fatal.
Treatment. The mild form of infantile jaundice needs no treatment.
Treatment of the severe form is fruitless unless the condition is due to syphil-
itic hepatitis, when antiluetic measures are indicated.
Synonyms. Acute Infectious Cholecystitis; Acute Inflammation of the
Definition. An acute inflammation of the gall-bladder resulting from
the invasion of pathogenic micro-organisms.
Etiology. Although the presence of biliary calculi in the bladder itself
or in the ducts leading to this structure, is an important predisposing cause
of infectious cholecystitis, the inflammation may occur in their absence.
The direct cause of the affection is infection with some one of the pathogenic
bacteria, especially the streptococcus, the staphylococcus, the pneumococcus
and particularly the colon bacillus and the bacillus of enteric fever. As pre-
disposing factors other than biliary calculi all obstructive influences, such as
inflammatory adhesions or catarrhal inflammation of the lining of the cystic
duct, must be considered since they diminish the local resistance to bacterial
Pathology. This depends upon the activity of the infective process. Usu-
ally the gall-bladder is distended and tense, its lining is congested and its
cavity contains dark muco-pus, sanious pus or pus. Gangrene with perfora-
tion may take place in which case the contents of the gall-bladder is of foul
odor. The perforation may be shut off by adhesions and form a localized
abscess cavity or it may result in a generalized infection of the peritonaeum.
Inflammatory adhesions to adjacent structures, particularly the colon and
ACUTE CHOLECYSTITIS. 459
omentum, are common. The cystic duct may be occluded by an impacted
calculus or by inflammatory swelling of its wall.
Symptoms. The affection may first indicate its presence by perforation
but usually the earliest symptom to be noted is pain, often sudden and parox-
ysmal, referred to the region of the liver. In some instances the pain is farther
to the left than this situation and it may even be as low as the right iliac region.
There are early symptoms of gastric irritation such as nausea and vomiting,
there is prostration with a rise of temperature often accompanied by rigors
and sweats. The pulse is usually accelerated but at times may be extremely
slow. Jaundice is rare unless the hepatic or common duct is involved.
Palpation of the abdomen elicits tenderness, often extreme and generally
localized, but at times in an unexpected situation. There is rigidity of the
abdominal muscles and the distended gall-bladder may be felt. Adhesions
between the intestine and the gall-bladder may result in the partial or
entire occlusion of the bowel with attendant symptoms.
The diagnosis. Here the history is of great value, symptoms suggestive
of cholecystitis and yet resembling those of appendicitis or those of intestinal
obstruction when occurring after pneumonia, enteric fever or previous affec-
tions of the biliar}^ tract, being much less puzzling than when they appear inde-
pendently. In the absence of history it is often very difficult to differentiate
acute cholecystitis from appendicitis, pancreatitis and localized peritonitis.
Jaundice is more likely to appear in pancreatic disease but the true nature
of the condition is often not determined until laparotomy has been performed.
The prognosis naturally depends upon the type of infection and its severity;
the acute suppurative form is a grave condition on account of the probability
of perforation peritonitis, local or general; in the latter instance death is certain
unless operation is undertaken.
Treatment. The mild types of the affection in which there is no distinct
evidence of suppuration should be treated by rest in bed and light diet. Sali-
cylic acid or sodium salicylate, preferably the former, should be given 3
times daily in doses of about 10 grains (0.66) in order to increase the bile
flow and to prevent extension of the inflammatory process into the ducts.
The bowels should be kept open by means of mild laxatives and the pain may
be relieved by the application of hot or cold compresses; morphine should
not be given unless absolutely necessary for it is apt to obscure the symptoms.
Nausea and gastric irritation may be controlled by the usual means. Meth-
ylthionine hydrochloride (methylene blue) in capsules containing i grain
(0.065) 3-nd sodium succinate in doses of 5 grains (0.33) have been recom-
Upon the incidence of the slightest signs of suppuration immediate surgical
interference, consisting of free incision and drainage of the gaU-bladder, is
460 DISEASES OF THE DIGESTIVE SYSTEM AND PERITONEUM.
Synonyms. Gall-stone Disease; Biliary Calculus; Hepatic Calculus.
.Etiology. Biliary calculi are either (i) hepatic in source, originating in
the bile ducts because of a slow catarrhal process which results in the secretion
of an albumin substance, which in combination with the bile precipitates
a bilirubin-calcium calculus, or (2) are formed in the gall-bladder because of a
low grade catarrhal process which induces a secretion of cholesterin from the
muious glands and cells of its waUs. Of these the former origin is by far
the more frequent. This explanation of the source of gaU-stones also accounts
for the fact that oftentimes after the performance of a cholecystotomy gall-
stones continue to be discharged from the fistula for weeks and even months.
It also points out why removal of the gall-bladder itself is not followed by a
cessation of attacks of gall-stone colic.
The recognition of the microbic origin of biliary calculi dates only to 1886.
In 1897 it was clearly shown that the colon baciUus could be responsible,
gaining access by either (i) the intestinal canal by way of the common duct,
or (2) through the portal vein. Although jaundice as a sequel to enteric
fever had been observed as early as 1826, it was not until 1889 that the typhoid
bacillus was recognized as a causative factor entering by way of (i) the portal
vein, (2) the hepatic artery, or (3) the common duct. That other infections
are also directly responsible has been shown, for low grade cholecystitides
have been observed after acute infectious pneumonia, acute rheumatic poly-
arthritis and chronic tuberculosis. That gaU-stones do not oftener result,
the explanation may be that acute suppurative inflammations of the bile
ducts or gaU-bladder do not result in calculi but rather these are due to atten-
The mechanical causes of gaU-stones: (i) Foreign bodies if sterile are
harmless. If they produce stagnation they favor catarrhal processes and so
give opportunity for infection. (2) Stagnation of bile in itself does not
favor calculus formation but since stagnation favors infection it may lead
directly to the formation of stone. (3) Chronic venous congestion of the
portal system is a more potent cause of the production of gall-stones since it is
the great underlying cause of cholelithiasis. The congestion of the portal
circulation may occur as a result of (a) chronic heart disease â€” especially
mitral obstruction â€” (b) chronic pulmonary disease â€” particularly chronic
emphysema and chronic interstitial pneumonia â€” (c) intestinal catarrhs due
to the abuse of alcohol, gluttony and rarely to the excessive employment of
vigorous purgatives; a more common cause of intestinal catarrh than either
of the preceding is constipation which not only predisposes to infection but
offers opportunity for auto-intoxication. (4) Of mechanical causes not
hitherto enumerated worthy of mention are (a) pregnancy, (b) visceroptosis â€”
CHOLELITHIASIS. 46 1
Glenard's disease â€” (c) over-fitted hepatic flexure of the colon, (d) displace-
ments of the duodenum, all of which may cause biliary stasis and, as above
mentioned, predispose to the production of gall-stones. (5) Of extraneous
causes anything vi^hich reduces the vitality of the individual such as (a) anxiety,
(b) bodily exhaustion from excessive physical or manual labor, or (c) wasting
diseases may be mentioned.
Gall-stones may be single or multiple; they are usually brownish in color,
rounded, oval or polyhedral in shape. In size they vary from that of a millet
seed to even 5 inches (12 cm.) in length. The small calculi are often very
numerous, thousands having been found in a single gall-bladder. A number
of stones impacted together become faceted as a result of their pressure upon
one another. Irregular (mulberry) calculi are sometimes found. Section of
a gall-stone reveals a nucleus usually consisting of bile pigment or more
rarely a foreign body. Collections of micro-organisms are said to have been
found at the nucleus of certain kinds of gall-stones. Chemically the calculi
consist chiefly (70 to 80 percent.) of cholesterin arranged concentricaUy. In
some instances the stone is composed wholly of this substance, usually,
however, other constituents such as bile pigment, calcium carbonate, magne-
sium salts, fatty acids, organic matter and traces of copper and iron, are found.
Rarely calculi may be composed almost wholly of bilirubin-calcium. The
most common type of gaU-stone is the mixed cholesterin calculus; these are
yeUow, brown or white and are generally faceted. Mixed bilirubin and
cholesterin stones consist of a nucleus of the latter substance covered by dark
Calculi are formed in the gall-bladder where they may exist, as stated, in
enormous number; they may also be formed in any part of the biliary tract
either without or within the substance of the liver. Lodgment of calculi
often takes place in the cystic and common ducts. In the latter the point
of lodgment is usuaUy in the ampulla of Vater; dilatation of the duct behind
the obstruction may take place. Obstruction of the cystic duct, if permanent,
results in dilatation of the gall-bladder, which may be so distended as to be
mistaken for an ovarian cyst. The contents of the bladder is a colotless,
sometimes viscid, fluid of neutral or alkaline reaction and contains albumin.
The gaU-bladder which contains calculi is not enlarged except in so far as the
contained stones increase its size (Courvoisier's law). Ulceration or suppu-
ration may restilt from the presence of a calculus and rupture may take place
into any adjoining structure.
Symptoms. In many instances the presence of biliary calculi causes no
symptoms as is shown by the facts that post mortem records prove that from
6 to 10 percent, of aU cadavers evidence the existence of gaU-stones, while not
more than i person in 20 of those who carry calculi becomes aware of their
presence through any symptoms which may result from them.