exudations into the pelvic and adjacent cellular tissue, after the
acute symptoms have subsided the attention should be directed to the
afternoon fever and to promoting the assimilation of food. So soon as
the sweating and fever are checked the absorption of the plastic
materials begins. The most important agents for accomplishing this
object are quinia, in moderate doses, combined with some form of
alcohol and with tepid sponging. Deep-seated pain in the iliac region
is best relieved by a large blister upon the side over the point where
the tenderness is felt. Prolonged rest in bed should be enjoined. Even
after convalescence is well advanced, so long as the exudation remains
unabsorbed the resumption of household duties is pretty certain to be
followed by a relapse or by the development of a chronic condition of
a most intractable description. The sooner the patient's stomach can
be got to digest and absorb beefsteak and iron the more speedy will be
her recovery.
In pelvic exudations the hot vaginal douche, warm baths, and the
application of flannels wrung out in water to the abdomen aid in
diminishing the local pain, and, perhaps, in causing a disappearance
of the tumor. The action of mercurials or of iodide of potassium in
melting away plastic inflammatory materials is sometimes very
striking, but more frequently they either do no good or else do harm
by disturbing the digestion.
If fever, chills, and sweating announce the presence of pus, the most
careful exploration should be made to determine, if possible, the seat
of suppuration. It is of great advantage to treat pelvic abscesses as
abscesses are treated elsewhere in the body. If the redness of the
skin above Poupart's ligament indicates a tendency to point in that
direction, an aspirator-needle should be introduced to make sure of
the diagnosis. If the sac is near the surface, a free incision should
be made and the pus should be allowed to escape. In many cases I make
these incisions three to four inches in length. The redness of the
external skin makes it certain that the abscess has become adherent to
the abdominal wall, and that the incision consequently will not
communicate with the peritoneum. After the abscess has been opened it
should be cleansed twice daily, and the cavity should be filled with
oakum. If, after a time, the granulations become flabby, Peruvian
balsam or iodoform should be introduced into the sac at each change of
the dressing. I can recommend this plan as essentially a mild
procedure. With a large opening for the discharge of {1037} pus the
fever and sweating disappear, the appetite returns, and the abscess
fills rapidly by granulation. With a small incision hectic is apt to
persist, and the abscess to end in the formation of interminable
fistulæ.
If softening and bagginess or distinct fluctuation indicate that the
pus can be reached through the vaginal cul-de-sac, the
aspirator-needle should be inserted deeply at the suspected point, and
if a large amount of pus is detected, an incision should be made with
a long-handled bistoury, using the needle as a director, and making
the opening large enough to permit the introduction of a
drainage-tube. I prefer for this purpose a self-retaining Nélaton
catheter, which is easily passed by means of a uterine sound inserted
into the eye at the extremity. Through the tube--without disturbing
the patient--the pus-cavity can be washed as frequently as required,
and with drainage and cleanliness cases of the longest standing may be
expected to recover.
P. F. Mundé[78] has reported a number of cases of chronic character
where the aspiration of pus has been followed by rapid absorption of
the intra-pelvic exudation. The presence of pus was suspected because
of a boggy, doughy feeling in the exudation tumor.
[Footnote 78: "Diagnosis and Treatment of Obscure Pelvic Abscess,"
etc., _Arch. of Med._, December, 1880.]
{1038}
BERIBERI.
BY DUANE B. SIMMONS, M.D.
DEFINITION.--Beriberi is a disease of inanition, most common in
tropical countries, though found in high latitudes (41° N.),
especially in low-lying seaboard towns, during the summer months, and
is both endemic and epidemic. It is usually chronic in form, but is
subject to exacerbations of varying degrees, and has for its
characteristic symptoms anæsthesia of the skin, hyperæsthesia and
paralysis of the muscles, anasarca, palpitation, cardiac and arterial
murmurs (in the wet form), præcordial oppression, and abdominal
pulsation.
HISTORY AND GEOGRAPHICAL DISTRIBUTION.--It was for a long time
confounded with a great variety of other diseases. The Anglo-Indian
physicians of Ceylon and the Malabar coast were no doubt the first to
recognize the specific nature of the disease, though it is claimed
that Chinese medical works of the thirteenth century contain a fairly
accurate description of it.
The literature of beriberi, at the first glance, appears to be very
meagre, as some of the most popular medical works make no mention of
the disease at all, while others only give it a passing notice. Its
bibliography, however, is very considerable, as may be seen in the
exhaustive list in Billings' _Index Catalogue_, but for want of space
we refer only to the most recent contributions to the subject. These
are--an article by A. LeRoy de Mericourt;[1] an essay by Tarissan,
entitled _Beriberi in Brazil_; an article by Anderson,[2] and an essay
by myself.[3]
[Footnote 1: _Dictionnaire Encyclopédique des Sciences Médicales_,
Paris, 1876.]
[Footnote 2: _Guy's Hospital Reports_.]
[Footnote 3: _Chinese Maritime Customs Medical Report_ (1880).]
For a long time beriberi was supposed to have a peculiar territorial
limitation. It is now known to be more or less prevalent on all the
islands and shores of Eastern Asia and Africa from Japan to the Cape
of Good Hope, and in Brazil.
ETIOLOGY.--I know of no disease in regard to which a greater diversity
of opinion exists as to its cause. Indeed, as one has observed,
"autant d'auteurs, autant d'opinions diverses." Ten years' study and
observation of the malady under a great variety of circumstances and
conditions have led me to the definite conclusion that its exciting
cause is a specific poison or germ, having many striking resemblances
in its mode of production to paludal or marsh miasm, though entirely
distinct and separate from it. A great variety of predisposing causes,
however, exert a powerful influence in rendering individuals or
classes susceptible to the {1039} disease, such as age, sex,[4]
occupation, race, mode of life, diet, and climate.
[Footnote 4: Women suffer from the disease much less frequently than
men.]
CLINICAL HISTORY AND SYMPTOMS.--There are three forms of the disease:
1st. Beriberi hydrops (wet beriberi), in which there is a hydræmic
condition of the blood, distension of the general areolar tissue, with
serum, and effusion into the serous cavities. 2d. Beriberi atrophia
(dry or atrophic beriberi), in which there is a notable deficiency of
fluids in the vessels and areolar tissue, and atrophy of the muscles.
3d. Mixed beriberi, in which the above forms lose the sharp lines of
distinction and merge into each other. Cases complicated with
dysentery, diarrhoea, and especially with continued fevers of the
typhoid type, are not uncommon.[5] These last, besides being of grave
prognosis, are frequently very embarrassing and difficult of
diagnosis.
[Footnote 5: Some authors have designated fatty or convulsive forms of
the disease, which I think unnecessary.]
In general terms, wet beriberi may be divided into two stages--the
prodromic stage and the stage of attack; and into several types--the
acute or pernicious, and the chronic. From the very insidious nature
of the approach of the disease, sometimes extending over a period of
several weeks, it is often very difficult, or even impossible, to
determine the exact time of its invasion. It is generally admitted
that a residence of some weeks in an infected locality is necessary
before any decided symptoms make their appearance. As in many other
diseases of slow development, the symptoms of the prodromic stage are
certain not easily defined feelings of indisposition, such as an
occasional sense of chilliness, inaptitude for mental exertion, and
especially a tired feeling in the lower extremities. A period of
uncertain length now intervenes, during which the characteristic
symptoms appear and constitute the stage of attack. The first of these
symptoms is, generally, anæsthesia of the skin over the anterior
tibial muscles, in the tips of the fingers, and around the mouth, in
the order given. Paralysis in varying degrees next declares itself in
certain groups of muscles, usually those immediately underlying the
regions of anæsthesia. One of the consequences of this is a drooping
of the toes, causing the patient while walking to lift the feet high
so as to clear the ground, thus occasioning the peculiar gait noticed
by many observers as characteristic of the disease. A sense of
constriction in the muscles of the calves is experienced at the same
time, arising from a veritable contraction, which causes their
apparent enlargement and hardening, with tension of the tendo
achillis. A feeling of tightness in the chest usually accompanies this
condition, due, no doubt, to partial paralysis of the muscles of
respiration. If firm pressure be now made upon the muscles in various
parts of the body, a greater or less degree of tenderness will be
found to exist in many of them, and especially those occupying the
posterior part of the leg, back of the forearm, inside of the arm, and
upper part of the chest. Tenderness of the periosteum of the long
bones and a peculiar roughness of their surfaces often exist also.
Palpitation of the heart, especially on making any considerable
exertion, is a frequent and often troublesome symptom, even at this
stage of the disease.
Up to this point the above symptoms are common to both the wet and
{1040} dry forms of the malady, and to them the characteristic
features either of beriberi hydrops or atrophia are now added. The
first manifestation of anasarca, the pathognomonic symptom of wet
beriberi, is in an oedematous condition of the areolar tissue of the
anterior part of the legs. This, in reality, is more or less general
even at an early stage of the disease, as is evident from the plump
appearance of the patient and a certain sallow-white color of the
skin, especially of that of the face. In uncomplicated cases the
temperature is normal, or it may be at times a little below the normal
point. There is also little or no increase in the frequency of the
pulse. Its quality, however, is changed, and somewhat characteristic
for both forms of the disease. Thus in the wet form it is full, large,
and easily compressible, indicating a great diminution of arterial
tone, while in the dry form there is nearly an opposite condition. If
the heart be now examined, a decided systolic murmur will be heard,
most distinctly over the pulmonary valves; and in most cases of wet
beriberi it exists in all the large arterial trunks. The heart
furnishes the usual signs of dilatation and want of tone. In the dry
form the cardiac murmurs are either slight or wanting altogether, and
the area of cardiac dulness is variable, and frequently diminishes as
the disease advances.
In both wet and dry beriberi the appetite is little impaired in the
earlier stages, but if in the former the stomach is over-distended,
there is increased præcordial oppression, and sometimes sudden death.
The bowels in the wet form are sluggish, and urine scanty; in the
other there is but little deviation from the normal in these respects.
The cases of the subacute type are by far the most numerous. From this
it is evident that the acute or pernicious type of the malady is, in
most cases, only an exaggeration of the subacute, as observed in some
other diseases, notably rheumatism and those of marsh malarial origin.
The term pernicious is, strictly speaking, applicable to the wet form
of the disease only, as the dry form is rarely, if ever, rapidly
fatal. A marked case of wet beriberi is always to be regarded as
dangerous, from the suddenness with which pernicious symptoms often
declare themselves. In these the anasarca (which, as has been stated,
constitutes the leading clinical difference between the two forms of
the malady) plays an important rôle. It often happens that in the
course of a few hours the local oedema in the extremities and the
slight puffiness of the face become general and extreme, and the neck
is enormously swollen by the distension of the veins, both deep and
superficial. The pleural and pericardial sacs are more or less
distended with serum, thus mechanically embarrassing the action of the
organs they contain. The action of the heart now becomes laborious,
the lungs oedematous and filled with coarse râles, and a terrible
sense of suffocation comes over the patient, causing him to seek
relief by constant change of position. The stomach is irritable, a
greenish-yellow fluid is vomited, and death closes the scene. The
acute stage of dry beriberi, on the contrary, is characterized by a
rapid diminution of the fluids of the body and muscular atrophy.
The annual appearance in the same individual of either wet or dry
beriberi, and its long continuance, constitute the chronic type of the
disease.
MORBID ANATOMY.--The morbid anatomical changes in beriberi vary
considerably with its form. Few, if any, observers claim seriously to
{1041} have found in either the wet or dry form of the disease
evidences of acute inflammatory action in any of the tissues or
organs. The blood undoubtedly undergoes important morbid changes,
whereby its nutritive and oxygenating power is impaired, indicating
that this is a disease of inanition. This shows itself most markedly
in necrobiotic and degenerative changes, especially in the muscular
tissues, which are the seat of the leading morbid phenomena in all
stages of both forms of this disease. The respiratory, digestive, and
glandular systems rarely undergo morbid changes other than those of a
secondary or passive kind, such as engorgement with serum and venous
blood.
The condition of the organs contained in the cranial and spinal
cavities is variable and inconstant. According to some observers, the
substance of the brain and spinal cord is hardened. The greater number
by far, however, have found it more or less softened.[6] The heart in
wet beriberi is habitually large and flabby, its muscular tissue
softened and of a pale-yellow and macerated appearance. Its cavities
are engorged with dark blood, sometimes fluid, but more often clotted.
These clots are often voluminous in the right heart, semi-fibrinous,
and extend into the pulmonary artery and great venous trunks, which
are enormously enlarged. The cardiac muscular tissue I always found to
have undergone metamorphic changes, varying from granular clouding to
advanced fatty degeneration.[7] The tissue of the paralyzed voluntary
muscles undergoes degenerative changes in both forms of the disease.
In the extreme atrophy of dry beriberi I have not unfrequently found
many of the sarcolemma sheaths completely emptied of their contents.
The power of regeneration in these cases is often wonderfully
displayed by an almost complete restoration of the lost elements, and,
in a corresponding degree, of the function of the part.
[Footnote 6: The former condition was undoubtedly observed in
autopsies made of the dry or atrophic form of the disease, though this
fact is not mentioned. The latter, or softened, condition of the
cerebro-spinal contents belongs to the wet form of the disease (my own
cases being of this kind). I regard this softening as not ante-mortem,
but as consecutive to serous imbibition (as observed by Eismann and
Sanders in chlorosis), and as taking place during the last moments of
life or after death, when the vital forces no longer oppose themselves
to the mechanical disintegrating power of the fluid with which the
nervous as well as all the other tissues of the body are engorged.]
[Footnote 7: I believe this to be the condition of the heart-muscle in
all cases of death from the wet form of beriberi. In this opinion I am
supported by Oudenhoven and many of the Dutch observers.]
It would appear that in wet beriberi the heart is first weakened by
paresis of the cardiac ganglia, with consequent incomplete emptying of
its cavities. This, in connection with rapid degenerative changes in
its muscular tissue, causes the walls to yield to the blood-pressure,
producing dilatation and tricuspid insufficiency, with regurgitation
and consequent capillary stasis and dropsy. Vaso-motor
nerve-paralysis, acting at the same time on the pulmonary artery and
arterioles, and on other large arterial trunks, probably gives rise to
the murmurs heard in them. In the dry form of the disease the
vaso-motor nerve-paralysis is less pronounced, and the degenerative
changes in the muscular tissue of the heart slower, while the marked
decrease in the fluids of the system and the great failure of
nutrition tend toward atrophic changes. From this it follows that we
usually have, instead of a large dilated heart, a small weak one, with
a narrow tricuspid orifice instead of a dilated one; little or no
{1042} intercostal pulsation, and hence less cardiac dulness; no
venous distension or capillary stasis, and hence no dropsy.
PROGNOSIS.--In temperate climates the prognosis of uncomplicated
beriberi is favorable in a majority of cases. In seasons of its
epidemic prevalence, however, all cases of the wet form of the disease
must be carefully watched, as it not unfrequently happens that grave
symptoms suddenly appear at a time when no danger has been
anticipated. An unfavorable prognosis may be ventured when, in a case
of wet beriberi, relief is not obtained by free purging or when
vomiting sets in. In dry beriberi the termination in death is
exceedingly rare as a direct result of the action of the poison
producing the disease, so that when death does occur it is chiefly
from exhaustion. The time of recovery depends on the amount of
muscular degeneration, and also upon the season of the year when the
attack occurred, as all cases of both forms of beriberi usually get
well without treatment during the winter months.
TREATMENT.--The well-established fact of the influence of certain
localities in the production of beriberi makes the removal of the
patient from them a hygienic measure of great importance, and this is
frequently the only treatment necessary if it can be done early. The
effect of the change is often almost magical, especially if it be made
to an elevated locality and among the mountains.
Diet is an important element in the treatment of beriberi. At the head
of the list of foods to be avoided is rice. Coarsely prepared grains,
such as wheat, barley, certain kinds of beans,[8] apparently because
of more or less laxative properties, are preferable as articles of
food.
[Footnote 8: A small red bean called adzuke, possessing both laxative
and diuretic properties, is a favorite remedy with the Japanese for
beriberi. It is used alone or mixed with rice, and is not unfrequently
the only means resorted to for the successful cure of mild cases.]
No drug has been discovered possessing specific properties in this
disease. In the wet form, medication consists in the administration of
drugs calculated to draw off the excess of serum in the areolar
tissues and in the serous sacs. First in point of efficacy for this
purpose are the hydragogue cathartics. In my own practice the sulphate
of magnesia, in large and repeated doses, has given the best results;
elaterium, a powder of jalap, squill, and digitalis, and, in fact, any
medicine which will give frequent and copious stools, are sure to
afford marked relief to the more urgent symptoms, and in many cases
will alone effect a cure. Care must be taken, however, not to exhaust
the patient, though I have never seen the judicious use of this method
of treatment do harm.
Copious bleeding is recommended by Anderson, especially in the stage
of greatest danger, but I have never been able to convince myself of
its safety.
The almost specific virtue claimed by the old Indian physicians for
treeak farook is no doubt due to its cathartic properties.
Diuretics are indicated for the same reason as cathartics, and any of
the more active are productive of good results. They are too slow in
their action, however, to be relied on otherwise than as adjuvants to
cathartics. I have found juniper gin to answer an excellent purpose,
both as a stimulant and diuretic, where there was danger of exhaustion
from the free use of cathartics.
The medical treatment of dry beriberi differs materially from that of
{1043} the wet disease. Cathartics and diuretics are alike useless,
and the former injurious. The ordinary means, such as electricity,
strychnia, frictions, etc., employed in cases of muscular atrophy and
paralysis from other causes, are indicated when the active stage has
passed, but they are useless, and even injurious, before this time.
The muscular hyperæsthesia common to both forms of the disease may be
generally greatly relieved by anodyne liniments containing aconite.
The internal use of the latter is highly recommended by some.
Hypodermic injections of morphia afford relief to the painful sense of
constriction in the calves of the legs so often complained of.
{1045}
INDEX TO VOLUME I.
A.
Abdomen, state of, in cholera, 741
in general peritonitis of puerperal fever, 1010
in relapsing fever, 390
in septicæmia, 977
in septicæmia lymphatica, 1011
in septicæmia venosa, 1012
Abdominal cavity, lesions of, in general peritonitis of puerperal
fever, 989
glands, lesions of, in typhoid fever, 264
organs, alterations of, in scarlet fever, 531
Abortion from septicæmia, 972
Abortive form of the plague, 777
of relapsing fever, 395
of typhoid fever, 298
of typhus fever, 354
Abortive treatment of erysipelas, value, 638
Abscess in symptomatic parotitis, date of pointing, 627
metastatic, of lungs, complicating relapsing fever, 404
Abscesses complicating cholera, 735
variola, 445
following the plague, 781
frequency of, in pyæmia, 976
in erysipelas, treatment, 638
in para- and perimetritis, 1008
in puerperal fever, 989
metastatic, of pyæmia, modes of production, 963
of pyæmia, treatment, 981
pelvic, of puerperal fever, treatment, 1036
pulmonary, in puerperal fever, 989
Acids, mineral, use of, in cholera, 768
Aconite, use of, in rubeola, 580
in scarlet fever, 543
in yellow fever, 651
Acute diseases, relation of, to rubeola, 561
form of glanders in man, 920
in horse, 914
Adenitis complicating scarlet fever, 511
vaccination, 468
Adenopathy complicating erysipelas, 634
Adhesions from infiltration, 55
Adulteration of food, 197
Adynamic form of typhus fever, 354
Age, influence of, on causation of anthrax in man, 940
of cerebro-spinal meningitis, 802
of diphtheria, 680
of erysipelas, 630
of influenza, 860
of idiopathic parotitis, 620
of the plague, 775
of pertussis, 839
of relapsing fever, 371
of rötheln, 583
of rubeola, 561
of typhoid fever, 242
of typhus fever, 342
proper for vaccination, 477
Aged, typhoid fever in the, 301
Agminated glands, lesions of, in cholera, 745
Air, amount supplied in ventilation, 179
carbonic acid as a cause of impurity, 177
-currents, direction of, test, 178
distribution of, in ventilation, 180
estimation of carbonic acid, 178
fresh, value of, in convalescence, 206
humidity of, as a cause of disease, 133
impure, as a cause of disease, 177
influence of, on causation of glanders, 912
impurities of, due to offensive effluvia, 181
sources of impurity, 177
standards of impurity, 178
transmission of the plague by, 776
velocity of, in ventilation, 180
vitiated, as a cause of pyæmia, 959
supply, method of calculating amount of, in ventilation, 179
Albuminoid infiltration, 72
Albuminuria complicating diphtheria, 674
relapsing fever, 407
scarlet fever, 525
typhus fever, 355
following rubeola, 574
in typhoid fever, treatment, 334