its acidity above normal, and floating in it, usually visible to the
naked eye, are reddish masses composed of uric acid. More or less pain
in the back, referable to the situation of the kidneys, and sometimes
extending along the course of the ureters, is common. The bladder is
rather irritable, and the passage of the urine produces heat and
scalding. The testicles are apt to feel sore and are somewhat
retracted. On standing, the urine may deposit uric acid and the urates
copiously, or the acid may be seen to form a cloud which slowly
subsides.
COURSE, DURATION, AND TERMINATION.--The course and duration of lithæmia
are much influenced by the habits of life of the person affected. When
unopposed by treatment and no change is made in the conditions
producing it, a gradual increase in the various disturbances takes
place. After a time structural changes occur in the liver; the organs
of circulation early undergo atheromatous degeneration; various
cerebral disorders due to degenerative changes arise; and acute
intercurrent affections may terminate life. Amongst the secondary
maladies due to lithæmia are gout, diabetes, renal calculi, and
nephritic colic. If the cases are subjected to appropriate treatment,
curative results may be certainly obtained. The prognosis, then, will
be influenced materially by the moral strength of the patient. If he is
one who can surrender his appetites and live abstemiously, a cure may
be promised. The case is far different with those who will continue the
use of malt, vinous, or alcoholic drinks, and will persist in indulging
in the pleasures of the table.
DIAGNOSIS.--The differentiation of lithæmia from other affections
offers no special difficulties. From gastro-duodenal catarrh it is
separated by the {971} excess of uric acid in the urine only, the other
symptoms being for the most part the same. The cerebral symptoms--the
vertigo, headache, etc.--are to be distinguished from the same due to
actual disease of the brain by the previous history, by the absence of
changes seen on ophthalmoscopic examination and of other signs of brain
disease, and by the subsequent behavior. Cases of cerebral mischief
producing such effects would rapidly develop into serious states,
whereas in lithæmia there are great fluctuations, but no apparent
progress in many months. In lithæmia also there are no changes in the
fundus oculi, whereas in brain diseases choked disk, hemorrhage into
the retina, white atrophy, etc. are often discovered. Further, in
lithæmia there are no disorders of sensibility, of motility, or of
intellection, whilst these are ordinary evidences of cerebral mischief.
TREATMENT.--Attention to diet is of the first importance. As uric acid
is an intermediate product in the metamorphosis of albumen, it might be
supposed that to diminish the quantity of this constituent of the food
would be sufficient. In some cases this suffices, but usually attention
must be given to the peculiarities of digestion characteristic of each
patient. More frequently trouble arises from indulgence in the starchy
and saccharine constituents of the diet; in some a very considerable
gastro-duodenal catarrh exists, and the mucus, acting as a ferment,
sets up an acetic fermentation in the starchy and saccharine
substances, with the necessary production of much carbonic acid gas. If
the fats disagree, the butyric fermentation also takes place, and very
irritating fat acids result. In these cases there is usually much gas
formed in the stomach and intestine, and an immediate ratio appears to
exist between the degree of mental despondency and the quantity of gas
in the intestinal canal. It follows, then, that in cases of lithæmia
the saccharine, starchy, and fatty constituents of an ordinary diet
should be omitted from the food of such subjects. Bread should be
partaken of very sparingly, and the foods containing starch, sugar, and
oil ought not to be partaken of at all. The succulent vegetables, as
lettuce, spinach, celery, cole-slaw, tomatoes, etc., ought to be
substituted. Lean fresh meats, poultry, game (plainly cooked), fresh
fish, oysters, eggs, etc. should constitute the basis of the diet. On
the other hand, there may be those who do better on a diet of
vegetables and fruit, excluding meat. In such we may suppose the fault
lies in the stomach digestion, where the albuminoids are converted into
peptones, the intestinal digestion being active and normal. All kinds
of wine and malt liquors should be prohibited. Coffee and tea must also
be relinquished. Without the carefully-regulated diet medicines can
accomplish but little; hence he who would obtain curative results must
give careful attention to every dietetic detail.
As deficient oxidation is an important factor in developing lithæmia,
active exercise must be enjoined. The amount of exercise must be
determined by the condition of the individual and the time, regulated
as far as may be by the period after meals. As when the food prepared
for assimilation is entering the circulation oxygen is needed to
perfect the final changes, it seems clear that exercise should be taken
three or four hours after the process of digestion has begun. Walking
exercise is better than any other for this purpose, but it should not
be carried to the point of exhaustion from fatigue. Sea-air and
sea-bathing are oxidizing agents of considerable value, and are
especially useful to the {972} subjects of lithæmia suffering at the
same time from malarial infection.
Medicines are administered with the view to accomplish two purposes: to
correct the disorders of digestion, to promote oxidation. One of the
most useful remedies is nitric acid, five to ten minims of the official
diluted acid being given before meals. It is more especially effective
when there is an excessive production of acid. The fermentation which
produces acid and the diffusion of acid-forming materials from the
blood are alike prevented by it. The injunction to administer it before
meals must be borne in mind when these purposes are to be subserved.
Nitric acid, as well as the other mineral acids, but in a greater
degree, promotes the flow of bile. This well-known clinical fact has
been confirmed by experiments. Under the use of nitric acid, as above
advised, uric acid and the urates disappear from the urine, being
excreted as urea, and hence this remedy accomplishes both of the
objects for which medicines are administered in this disorder. No other
mineral acid can fill its place in this connection.
Alkalies possess very decidedly the power to promote oxidation. The
soda salts are objectionable, for, combining with uric acid, they form
the insoluble urate of soda. The salts of potash and lithium, on the
other hand, form soluble combinations, and they also increase
elimination. Much depends on the time at which they are administered,
as Bence Jones,[9] and since Ralfe[10] especially, has shown. To
increase the alkalinity of the blood and urine, they must be taken
after meals, for then the acid materials of digestion are pouring into
the blood. For the same reason, if alkalies are administered to
neutralize the acidity of the intestinal canal, they must be given
after meals. The most useful alkaline remedies are liquor potassæ,
bicarbonate of potash, Rochelle salts, citrate of lithium, etc. The
effervescing preparations of potash and of lithium are elegant and
palatable forms in which to administer these remedies. They may also be
taken dissolved in Vichy water, in our Saratoga Vichy, or in Carlsbad
or Bethesda. When the use of mineral waters is not contraindicated in
the state of the digestive organs, great good is accomplished by the
persistent use of Vichy, foreign or domestic, of Carlsbad, and the
alkaline waters of Wisconsin.
[Footnote 9: _Lectures on Pathology and Therapeutics_, by H. Bence
Jones, London, pp. 90, 280.]
[Footnote 10: _Physiological Chemistry_, by Charles Henry Ralfe,
London, 1883.]
The so-called cholagogues are unquestionably useful, but they become
less and less necessary according to the success achieved in the
dietetic course. Phosphate of soda is one of the most effective of this
group of medicines. As it acts as a compound, and not as a salt of soda
merely, it does not come within the prohibition against the use of soda
salts. It promotes the flow of bile and appears to remove the catarrhal
state of the mucous membrane. A teaspoonful three times a day is the
quantity usually required. Under some circumstances it may be
advantageously combined with arseniate of soda. Mercurials were
formerly almost universally used, but they have been largely supplanted
by podophyllin, euonymin, baptisin, etc., and by the phosphate of soda
above mentioned. Podophyllin is indicated when constipation is a
symptom. An efficient mode of giving it is in the form of granules, but
it must be continued without intermission for some time or during the
existence of {973} the lithæmia. The quantity given should be
sufficient to maintain the evacuations in a soluble state. Good results
are obtained from a combination of podophyllin with extracts of
physostigma, nux vomica, and belladonna. When distinct torpor of the
liver without constipation exists, euonymin, combined with physostigma,
may be advantageously used. For the vertigo and hypochondriasis no
remedy is more beneficial than arsenic (Fowler's solution) in small
doses kept up for some time, and it is also distinctly curative of the
catarrhal state of the mucous membrane. When malarial infection is the
cause of lithæmia, quinine becomes indispensable.
Topical agents in some cases render important aid to the other curative
measures. A daily sponge-bath, the water made more stimulating by the
addition of sea-salt, is very useful in the absence of sea-bathing.
Friction of the hepatic region with the official ointment of the red
iodide of mercury unquestionably stimulates the hepatic functions.
General faradization and faradic and galvanic excitation of the
chylopoietic system promotes activity of the digestive apparatus and of
the organic functions in general.
Hepatic Glycosuria (Temporary).
DEFINITION.--By the term hepatic glycosuria in this connection is meant
a temporary glycosuria due to excessive formation of glycogen. The
liver, unduly stimulated, produces more glycogen than can be disposed
of, and hence it is excreted by the kidneys as grape-sugar.
PATHOGENY.--In the normal condition it is supposed that the glycogen
produced by the liver is converted into grape-sugar, and soon oxidized
and thus consumed. One theory of diabetes maintained that in some way
the conversion of glycogen into grape-sugar was excessive and beyond
the oxidizing power of the blood, and hence this substance was
discharged in the urine. The recent discovery by Pavy[11] of glycogen
in considerable amount in the blood of all parts of the body renders it
certain that there are peculiar conditions necessary to the formation
of grape-sugar in sufficient quantity to constitute diabetes. It is
tolerably certain that an excess of acid in the intestinal canal,
diminishing thus the alkalinity of the blood, will have as a symptom
sugar in the urine. Persons disposed to the accumulation of fat, and
eating freely of sugar and starchy food, are apt to have intestinal
indigestion, and the acid produced by the fermentation of these
substances will, after its absorption, hinder the conversion of any
food-sugar. In such subjects also there may be an increased conversion
of the glycogen of the blood into sugar under the same conditions. Such
a glycosuria must necessarily be temporary and a purely functional
disorder.
[Footnote 11: _The Lancet_, vol. ii., 1883.]
SYMPTOMS.--The subjects of the malady under consideration are of full
habit, even obese. They habitually consume considerable quantities of
malt liquors and a diet composed largely of the starchy and saccharine
foods. If not in malt liquors, they at least indulge freely in bread,
potatoes, pastry, cakes--in all forms of farinaceous food, fats, and
sweets. They have a keen appetite, eat largely, and drink freely of
fluids. As {974} a rule, these subjects are but little disposed to
physical exercise and lead rather sedentary lives. Indulgence in such a
mode of life tends to increase the accumulation of fat, weakens the
muscles, and with them the heart-muscle, and slowly induces a
gastro-intestinal catarrh accompanied by stomachal and intestinal
indigestion. At first, heaviness, oppression, and drowsiness after
meals are experienced; then acidity, pyrosis, and eructations follow;
and ultimately the evidences of intestinal indigestion--flatulence,
pain, irregular and unhealthy evacuations, etc.--come on. Meanwhile,
the appetite is not usually impaired, and the disposition to drink
fluids increases; the amount of urine voided is greater, and to rise
during the night for the purpose of emptying the bladder comes to be a
fixed habit. The urine under these circumstances is copious,
high-colored, acid, and deposits on cooling abundantly of uric acid and
urates. The amount passed in twenty-four hours will reach sixty,
eighty, or more ounces, and the specific gravity will range from 1025
to 1035. On testing in the usual way, traces of sugar, more or less
distinct, will appear,[12] but not constantly, and hence repeated
examinations are necessary to determine the quantity. As a rule, the
evidence of the presence of sugar in small amount is satisfactory.
[Footnote 12: In testing for sugar, when the urine contains the urates
in such abundance there is danger of error. In using Trommer's,
Fehling's, or Moore's test, on heating, the urates will effect a
reduction of the copper or bismuth. It is necessary, therefore, to
separate them before applying the test. This is accomplished as
follows: The urine is evaporated to dryness on a water-bath; the sugar
in the evaporated residue is dissolved out by absolute alcohol, and
then an aqueous solution is prepared, to which the test is applied. An
experienced operator will not need to take such precautions, for,
familiar with the reactions, he can readily judge of the results.]
Various affections of the skin appear in the subjects of this malady,
and urticaria, prurigo, eczema, and boils are the forms most usual.
COURSE, DURATION, AND TERMINATION.--Slow in developing, this temporary
glycosuria is also slow in its course. It remains nearly stationary for
months, even years. Meanwhile the degenerative changes associated with
it slowly develop on all sides. The quantity of sugar does not greatly
increase, for its amount, being apparently dependent on the quantity of
acid entering the blood from the intestinal canal, must continue nearly
at the same standard. It is comparatively rare for true diabetes to
develop out of this state, although such a termination must be regarded
as a natural outcome. One reason, it may be, why such a conclusion is
not often reached is because of intercurrent maladies. It is an
important fact that acute serous--less often
parenchymatous--inflammations are very apt to occur during the
existence of even temporary glycosuria. Under appropriate management
this disorder is readily amenable to treatment. Hence the prognosis
will be favorable or not according to the skill exhibited in its
treatment.
DIAGNOSIS.--This malady offers no special difficulty in diagnosis. From
gastro-duodenal catarrh and from lithæmia it is distinguished by the
saccharine condition of the urine. From diabetes it is separated by the
rate of progress, by the protracted duration of the case without any
distinct advance, and by the temporary and fugitive character of the
glycosuria.
TREATMENT.--To carefully regulate the diet is the first consideration.
The traces of sugar and the excess of urates rapidly disappear when the
{975} starches, sugar, and fats are withdrawn from the diet. Indeed,
the rule as to alimentation must be as rigidly enforced as in true
diabetes, but after the gastro-intestinal catarrh has subsided the
ordinary mixed diet--that before the disturbance began--may be returned
to gradually. Active exercise must be enjoined under the same
conditions and for the same purpose as in the treatment of lithæmia. In
these obese subjects, unaccustomed to movement, exercise must be
cautiously undertaken; beginning with short excursions, it must be
gradually increased. Horseback riding is an excellent expedient, but
should not take the place of walking.
The merely medical measures have a twofold direction: to remove the
gastro-duodenal catarrh; to promote oxidation of the sugar in the blood
or prevent the conversion of glycogen into grape-sugar. Vichy water,
the potash salts, and alkalies generally serve to accomplish the
latter, and phosphate and arseniate of soda, tinctures of nux vomica,
and of physostigma, bismuth, and carbolic acid, relieve the former.
Small doses of Fowler's solution (two drops ter in die), and a minim
three times a day of a mixture in equal parts of tincture of iodine and
carbolic acid, are effective remedies in gastro-duodenal catarrh.
Jaundice (Icterus).
DEFINITION.--The term jaundice has its origin in the French word jaune,
yellow. Icterus, which has come to be a more technical word, is of
uncertain Greek origin, and is much employed by French writers as
ictère. The common German name is Gelbsucht, a highly expressive
designation. Jaundice signifies a yellow discoloration of the skin
caused by the presence of bile. It is a symptom rather than a disease.
As a symptom it will receive much consideration in the pages to follow,
but there is also a functional disorder--a jaundice due to a
disturbance in the biliary functions, without evidences of structural
change--which must be discussed here. This preliminary statement of our
present knowledge of jaundice will facilitate the comprehension of it
as a symptom, and will render unnecessary explanations that will be
merely a repetition of previous ones.
CAUSES.--The theories of the causation of jaundice may be reduced to
three: 1, that it is due to a disorganization of the blood in which the
coloring matter is set free, and hence is known as hæmatogenous; 2,
that the materials of the bile, which it is the office of the liver to
remove from the blood, are not so disposed of; 3, that the bile, after
being formed by the liver, is absorbed into the blood because of an
obstacle to its escape, and hence this is called hepatogenous jaundice.
The modern view of hæmatogenous jaundice had its origin in the supposed
discovery of the identity of hæmatoidin with bilirubin. If the pigment
of the blood has the same composition as the pigment of the bile,
hæmatogenous jaundice will be produced whenever hæmatoidin is set free
in the blood. Virchow[13] was the first investigator to show the close
resemblance between these two pigments. Since his observation was made
an identity of hæmatoidin and bilirubin has been maintained by Zenker,
Valentiner, Kühne, and others, and as strenuously denied by {976}
Städeler, Preyer, Young, and others. At the present time it appears to
be established that although the blood- and bile-pigments are closely
related, they are not identical.[14] Nevertheless, a hæmatogenous
jaundice is still admitted to exist by Leyden,[15] Immermann,[16]
Gubler,[17] Ponfick,[18] and some others. The existence or
non-existence of this form of jaundice is, however, of little
importance in this connection, since, if it ever occur, the malady of
which it is a symptom is not an affection of the liver, but of the
blood, as phosphorus-poisoning, pyæmia, etc.
[Footnote 13: _Archiv für path. Anat., etc._, Band i. p. 370, 1847.]
[Footnote 14: Legg, J. Wickham, _On the Bile, Jaundice, and Bilious
Diseases_, p. 243.]
[Footnote 15: _Beiträge zur Pathologie des Icterus_, Berlin, 1866, p.
6.]
[Footnote 16: _Deutsch. Archiv für klin. Med._, Band xii. p. 502.]
[Footnote 17: _Union médicale_, 1857, p. 503.]
[Footnote 18: _Ziemssen's Cyclopædia_, vol. ix. p. 24.]
The second theory, that the bile is preformed in the blood and
separated by the liver, and that jaundice results because of the
failure of the liver to perform this office, is no longer entertained,
although largely held down to within a very recent period. As the bile
acids and bile-pigments are not to be found in the blood, chemistry
lends no support to the theory of jaundice by suppression of the
hepatic function. As they do not exist in the blood and are found in
the secretion of the liver, there can be no other view held than that
they are formed by this organ.[19]
[Footnote 19: The old doctrine of jaundice by suppression, which has
always been maintained by Harley (_On Jaundice_, London, 1863, p. 20
_et seq._), has been again restated and strongly advocated by him in
his treatise on _The Diseases of the Liver_, p. 83, which was issued in
1883. In the two following postulates he formulates his view:
"1. The biliary secretion can be actually retarded, and even totally
arrested, without alteration of hepatic tissue.
"2. When the liver strikes work and secretes no bile, the animal body
becomes jaundiced as a direct consequence thereof."
This view, he affirms, "can be made comparatively easy of absolute
proof."
The evidence on which he chiefly relies is exceedingly fallacious. It
rests on two facts: the existence of a case of jaundice in which the
ducts and gall-bladder contain no bile, but only ordinary mucus; the
appearances presented by a liver in a case of jaundice due to
obstruction of the common duct. The evidence afforded by the former is
entirely fallacious, because in an old case of jaundice with catarrh of
the bile-ducts such changes take place in the bile that it loses all of
its distinctive characteristics. This may be seen in an ancient example
of obstruction of the cystic duct, where the bile which the
gall-bladder contained is ultimately transformed into a whitish or
colorless mucus. The changes which occur in the so-called cysts of the
arachnoid are comparable, and exhibit the entire transformation of
blood-pigment, which is closely allied to bile-pigment.]
The third theory of jaundice--that which refers the disease to an
absorption of the bile into the blood after it has been formed by the
liver--is the one now most generally held, and, indeed, as one of the
causes is universally held. The bile is absorbed into the blood because
an obstacle to its passage by the bile-ducts exists at some point in
their course. This is the principal, but not the only, cause of
absorption. When the pressure in the vessels falls below that in the
ducts, bile will pass toward and into the vessels. Again, it sometimes
happens that a considerable part of the bile discharged into the
intestines is reabsorbed unchanged, and enters the portal vein and the
general circulation, thus causing jaundice.