hæmoptysis. There remain those other forms of pulmonary hæmoptysis
connected with cardiac disease and hemorrhagic infarction. Practically,
these are reduced to the first variety, as cardiac disease is the
question we have most frequently to consider in this connection. We are
justified in assuming the parenchymatous origin of cardiac hæmoptysis,
because it rarely appears until chronic valvular disease has prepared
the way for its occurrence by its well-known degenerative effects on
the pulmonary circulation whereby thrombosis appears, and because at
those advanced periods emboli are often injected into the pulmonary
artery capable of producing hemorrhagic infarction and consequent
hæmoptysis. This latter is accompanied by aggravation of symptoms
already serious--increase of dyspnoea, cardiac perturbation, and
probably cough. If the hemorrhage be copious, shock may appear, and
varies {286} according to the size of the obstructed vessel and the
amount of hemorrhage. The patient may have some premonitions, but not
of the kind noted in the initial hæmoptysis of phthisis, such as the
superficial soreness, burning, or pain localized in the substernal
regions. The hæmoptysis, after it has begun, continues more regularly,
at shorter intervals, and for a longer time, with the coarse appearance
of the blood already mentioned, such as dark, non-aërated, coagulated
sputum. The quantity may equal that from the most typical bronchial or
broncho-pulmonary hæmoptysis in phthisis; usually it is not copious.
Fever is not an ordinary accompaniment, but may develop in consequence
of increased structural lesion, as from pneumonic infiltration around a
large infarction. It has not then the typical range of ordinary
pneumonia, seldom going beyond 100 or 101. The physical signs exclusive
of the primary cardiac lesion are those pointing to limited
infiltration of lung-tissue about the middle or lower region of the
lung. We have limited areas where percussion is dull, almost as much so
as over pleuritic effusion, and where the respiration is very feeble or
suppressed, and later a bronchial breathing adjoining as a consequence
of pneumonic complication. There may be several of these areas, varying
in size. Sometimes the localization by physical signs is impossible
because of the hemorrhage or infarction being small and deep-seated.
Pain becomes a localizing symptom when the infarction is superficial
and the pleura becomes involved. The form of valvular disease most
likely to produce hæmoptysis is mitral disease, especially mitral
obstruction disease.
Beside infarctions originating in cardiac disease there are others of
peripheral origin, as in the puerperal condition from phlegmasia
dolens. Hæmoptysis is a rare symptom in such cases, but when it does
appear it has the same basis. It is seldom severe, and soon merges into
an expectoration of pneumonic character, with the clinical forms of
embolic pneumonia, or possibly of abscess or gangrene of the lung.
PATHOLOGY.--Incidentally, the pathological relations of hæmoptysis have
been already indicated as being connected with phthisis and cardiac
disease--principally with the former. If phthisis be an infectious or
specific disease, as a large and growing professional opinion claims,
hæmoptysis has its specific relations with it. Few symptoms have
greater differentiating force than it has. Its occurrence, outside of
well-known cardiac or dyscrasic disease, removes any case of primary
pulmonary disease from the category of simple inflammation. There may
be much more congestion in bronchitis, more catarrhal products in
simple catarrhal pneumonia, and more fibrinous or croupous exudation in
pneumonia, than in the primary stages of phthisis, and yet no
hæmoptysis appear. The mechanical conditions are present in greater
degree, but the infective element is wanting. Its closest affinity is
with apex pneumonia or alveolar catarrh, yet probably most of such
cases occur without it. A blood-dyscrasia contributes an important
element in the pathogenesis of hæmoptysis.
In cardiac hæmoptysis the pathology is more simple. Extreme mechanical
conditions of obstruction and reversal of the circulation are
reinforced by nutritive changes of the vessels and heart, until the
so-called cardiac cachexia is established. There is no infective
element, and such cases are seldom if ever followed by phthisical
destruction.
MORBID ANATOMY.--Reference has already been made to anatomical changes
having direct or indirect relation to hæmoptysis, such as those in the
blood-vessels. The anatomical basis of the slight hemorrhages of the
early stage of phthisis is seldom if ever discoverable. The belief in
vascular fragility and congestion with special origin rests much more
upon clinical reasoning than demonstration. The large hemorrhages are
now and then fatal within short periods of time or instantly, and we
then have the opportunity of noting the general appearance of the
lungs.
{287} It is notable that cases are not very frequent where the source
of the bleeding has not been found by the most careful search. The
general appearance varies according to the length of time that has
elapsed since the bleeding which preceded death.
In the cases immediately fatal the tubes are filled with fresh blood,
which has stained the mucous membrane and has changed the general
surface of the sections of lung into a dark, mottled, or patchy color.
The greater amount of blood is to be found in the lung from which it
has primarily come, but in the more profuse hemorrhages, and
particularly where there has been time for the struggles of the
threatening suffocation, much blood may either overflow or be inhaled
into the other lung and carried into the extreme portions of the
air-sacs. If the flow be not overwhelming, the patient may survive long
enough to allow other effects from the blood, which has by gravitation
or insufflation been carried into certain parts of the lung. We are
indebted to Reginald E. Thompson[62] for the most important study of
the secondary effects of the blood thus remaining. He says that the
relics of blood are to be found in the presence of hard nodules, often
deeply, though not always, pigmented. They are mostly found at the
summit and middle part of the upper lobe, the middle axillary region,
between the third and fifth ribs, close to the pleura, the anterior
inferior border, and the middle part of the base corresponding to the
summit of the arch of the diaphragm. "Absorption, decoloration, and
fibrination go on; the outlying portions of the blood disappear; the
central nodules become hard and white, and alone remain to show what
has taken place." They are in some cases of varying color, slight red
or of an ivory white, mottled with old blood-pigment, around the
bronchioles especially, and in the shape of small black granules.
Microscopically, they consist of "a group of alveola firmly packed with
a semi-opaque, homogeneous fibrinous material, and there is some
thickening of the alveolar tissue and also of the interlobular tissue,
which thickened tissue forms the limiting capsule."
[Footnote 62: _Op. cit._, p. 46, etc. These researches are an important
epoch in the history of hæmoptysis.]
The ultimate fate of these nodules is variable. Sometimes they go on to
formation of cavities, or softening occurs around the periphery or in
the centre, and leads to general liquefaction of the nodule, or they
may separate from the surrounding tissue by traction. Sometimes the
effect of retention of the blood in the air-passages is a catarrhal
pneumonia, with the ordinary anatomical proofs of it referred to in the
paragraph on modes of termination of hæmoptysis.
Accepting the observations, we have the demonstration of a phthisis ab
hæmoptoe.
The morbid anatomy of cases fatal from rupture of aneurisms of the
branches of the pulmonary artery has been made prominent by the
researches of Rokitansky and Rasmussen.[63] He describes small sac-like
aneurisms and ectasias situated in the vessels running along the wall
of the cavity. The aneurisms have the shape of a bag and an even
surface. The walls of the unbroken aneurisms are of great thickness,
and those of the broken ones thin. The opening is always found on the
most protruding part of the sac; the edges are thin; their size varies
from a pea to a small orange. Powell[64] says a microscopic section
taken from a specimen in an early stage shows new connective-tissue
elements, causing induration affecting the whole thickness of the wall
and obscuring the distinction between the coats. The wall is brittle,
becomes thinner from want of support, and yields to an inciting cause,
with rupture and death as the result.
[Footnote 63: _Edinburgh Med. Journal_, 1868-69.]
[Footnote 64: _Trans. London Pathological Society_, vol. xxii. pp. 54,
55.]
{288} The morbid anatomy of cardiac hæmoptysis is found mostly in two
conditions--that of degenerated, atheromatous, varicose blood-vessels,
brought about by the condition of chronic obstruction and increased
venous tension in valvular disease; and in that of pulmonary
infarction.
The first prepares the way for diapedesis or rupture, and consequent
hæmoptysis. The rupture takes place in the parenchyma, or, as the
anatomical details formerly given make probable, from the blood-vessels
of the bronchial mucous membrane also.
Pulmonary infarction is recognized by a dark, dense, pyramidal or
wedge-shaped area of varying size situated at the surface of the lung,
with the base of the pyramid coming to the pleura. It is found oftener
in the lower lobes and in multiple form. It is caused by an embolic
obstruction of a terminal branch of the pulmonary artery; sometimes by
a thrombosis or by both. A venous reflux from the neighboring districts
is supposed to fill the empty vessel, and after a certain time has
elapsed changes are supposed to have occurred in their walls by which
the blood escapes into the air-cells and interstitial tissue.
Litten's[65] explanation, sustained by his experiments, is that the
venous reflux, after a closure of the pulmonary artery, is by no means
necessary to the formation of an infarction. The infarction fails if
the pulmonary artery and the bronchial artery, and those arteries lying
outside the lungs, but in circulatory connection with them--the
pleural--are simultaneously shut off. If the whole arterial supply be
thus taken away, but a living connection be maintained by means of the
veins, an infarction does not follow, while it immediately follows if,
at the same time with the open veins and closed pulmonary arteries, the
collateral or supplementary circulation be kept free. A venous reflux
cannot occur so long as a circulation in the capillaries of the lung is
sustained by collateral arterial branches. The explanation is that in
an unobstructed circulation the entire resistance which is offered to
the blood-stream in the capillaries of the lung is overcome by the
pressure existing in the pulmonary artery, which, corresponding to the
greater width of the capillaries, is much less than the pressure in the
corporeal arteries. If the pulmonary artery becomes suddenly
impermeable, the pressure in the collateral arteries, which originates
partly from the bronchial artery, and partly from those outside of, but
in connection with, the lungs, as the pleural, etc., is sufficient to
prevent a venous reflux, but not sufficient to overcome the entire
resistance in the lungs and to drive the blood beyond the capillaries
into the left auricle. Then follows an accumulation and stasis of the
blood in the capillaries and smaller veins, and hence results at first
a hyperæmia and later a diapedesis. Litten makes another important
change in Cohnheim's doctrine: he maintains that the hemorrhage appears
before the integrity of the vessel-walls is impaired.
[Footnote 65: _Zeitschrift für klin. Med._, vol. i. p. 148, Berlin,
1880.]
Other fatal cases find their anatomical basis in the softening and
ulcerating processes, which while forming cavities are liable to open
vessels of greater or less size in their walls or trabeculæ.
The condition of the heart in phthisis is one which has an effect in
influencing the occurrence of hæmoptysis. The general statement by
Peacock, that the weight of the heart in phthisis, though less than in
acute diseases, is greater than that in other chronic diseases, needs
to be modified somewhat, as he did not make a distinction between
different forms of phthisis. The more the case approaches the fibroid
variety the more likelihood of some increase of size, particularly in
the right ventricle. Spatz,[66] a later authority, gives as the result
of his examination that phthisis diminishes the size of the left
ventricle--that an absolutely compensatory hypertrophy of the right
ventricle, which is apparent in special cases, does not as a rule
exist, although {289} the resultant decrease does not throughout stand
in relation to the decreased weight and volume of the whole body in
phthisis. The ratio between the depth of the left ventricle and
circumference of the aorta is diminished; and, as this is not
compensated for by hypertrophy of the walls of the ventricle, arterial
tension diminishes and the pulse becomes soft and small. The chance of
rupture of weak vessels by relatively excessive tension is thus much
weakened in the later stages of phthisis.
[Footnote 66: _Deutsches Archiv für klinisch Med._, vol. xxx. p. 154.]
Another element capable of modifying the hæmoptysical features of
phthisis is claimed by Jaccoud[67] as existing in the insufficiency of
the tricuspid valve, which compensates the increased tension in the
field of the pulmonary artery arising from obstruction of a
considerable part of it. The amount of blood passing from the right
ventricle is thus, by a reflux, proportioned to the area of obstruction
in the artery, and the tension is reduced so as to prevent rupture of
the weak vessels. His conclusions are based on 18 cases of measurements
of the tricuspid orifice. They varied from 111 to 130 millimeters. The
evidence obtainable during life was a systolic murmur heard at the
ensiform cartilage and cervical venous reflux.
[Footnote 67: _Clinique médicale_, vol. ii. p. 346, etc.]
DIAGNOSIS is mostly called for with regard to the chances of
hæmatemesis. Inspection of the blood is naturally an early point for
attention. Its bright-red color, frothy look, freedom from extraneous
matter, and its coming up by coughing are strong evidences easily
acquired of its pulmonary origin. Corroborative circumstances are the
family history of phthisis or hæmoptysis, the presence of pulmonary, or
in fewer instances of cardiac, physical signs, the immediately
premonitory symptoms spoken of before. Fever, the age of the patient,
and the continuance of the discharge of blood in its later gradations
of color and mixture of catarrhal elements, inspection of the mouth,
fauces, and larynx, would exclude those possible sources. Each has its
limitations, but together they are conclusive as against hæmatemesis.
Recent and accumulating experience attributes some diagnostic value to
the presence of bacilli tuberculosis in the expectorated blood.
Hiller[68] reports 6 cases of hæmoptysis in which the blood showed in
bacilli: 3 were completely initial. The bacilli were easily
demonstrated by preparations and also by inoculation on guinea-pigs.
They have also been found in the blood of cases of acute tuberculosis
by Weichselbaum.[69] Resort may be had to the well-known tests for the
presence of the elastic tissue of the lung in sputum.
[Footnote 68: _Centralblatt für die med. Wissenschaft_, March 24,
1883.]
[Footnote 69: _Wiener med. Wochenschrift_, No. 13, 1884.]
As positive data for hæmatemesis we have the dark color of the blood,
its firmer clotting, greater density and want of aëration, acid
reaction, the presence of extraneous matters of food and drink, their
ejection by vomiting, and pain or uneasiness at the epigastrium. As
corroborative we have the less frequent occurrence of hæmatemesis, the
individual history of gastric disease, such as ulcer of the stomach or
presence of hepatic cirrhosis from intemperate habits, and the history
of a blow on the abdominal surface: discharges of blood from the bowels
are more likely to occur in hæmatemesis.
Hæmoptysis may be simulated, as by scratches or cuts on some part of
the internal surface of the throat or mouth. The blood is then likely
to be thinned by secretion from the mouth. Inspection would detect the
imposture. The chance of blood from an epistaxis being swallowed and
afterward ejected by vomiting is to be remembered. Cardiac hæmoptysis
is distinguished in most cases by the presence of symptoms and physical
signs of valvular, usually mitral, disease in a considerable degree of
advancement. These are so pronounced as to exclude phthisical disease.
Other and fewer cases occur where the hæmoptysis is the first evidence
of the cardiac disease, and they require a careful exclusion of all the
features of tubercular disease, so as to be able to {290} arrive at a
correct conclusion. There are no conclusive considerations pertaining
to the amount and character of the blood. In the severe and copious
hemorrhages there is likely to be present a marked shock.
PROGNOSIS.--Hæmoptysis usually implies phthisis existing or imminent,
and yet it has in general a favorable effect on its course. This
applies more to its first stage than subsequently, and more to the
small than to the large hemorrhages. The gravity of the small ones
increases in proportion to their frequency. The family and personal
equation is of more importance than the mere quantity. We may have a
slight hæmoptysis and a large increase of the morbid condition
following it, and the reverse, the result depending on the individual
tolerance of and susceptibility to reaction. As in the second stage the
reactive elements are more potent, the small hemorrhages then are less
beneficial. They are the index of activity in the destructive lesions,
and yet may relieve the accompanying congestion. The easiest
appreciable symptom of the progress of the disease is the fever. We may
fail to properly interpret physical signs because of want of
familiarity with the individual case before us. If besides more fever
there be more cough, dyspnoea, and debility, the prognosis increases in
gravity. These remarks will apply with more force to the large
hemorrhages than the smaller ones, and are guides for prognosis in all
the clinical forms of hæmoptysis. In the special clinical form, the
hemorrhagic variety of phthisis, bleedings recur often and in large
quantities during years, and some of the cases end with final recovery.
The fever and constitutional irritation give way under seemingly very
unfavorable conditions. The fact that a great part of them have no
history of heredity, and that they come on at a late period of life,
may account for this, because they thus escape the influences which
heredity and age are known to impose upon the other classes of
phthisical subjects. Some interesting conclusions have been drawn from
the history of cases of profuse hemorrhages. Pollock[70] thinks that
they shorten the duration of the first stage and lengthen the duration
of the second and third. Out of his 351 cases, 204 occurred in the
first three months of illness: 45 had remained in the first stage when
examined, 142 having undergone softening, while 164 had cavities. Of
286 cases of profuse hæmoptysis classified by Williams,[71] the number
of cases in the first stage was 187, and the percentage of deaths was
13.95; 65 cases were in the second stage, and the percentage of deaths
was 24.61; 31 were in the third stage, and the percentage of deaths was
67.74, showing increased effect of hemorrhages upon pulmonary
structures advancing in destructive processes and upon constitutions
being progressively undermined by them. In other clinical varieties the
symptom is so clearly subordinated to the general process that it loses
its prognostic importance in the established disease. There is an
imminence of fatal hemorrhage in many of them, as in fibroid phthisis,
cancer, abscess, gangrene, and hemorrhagic infarction of the lungs. In
extra-pulmonary hæmoptysis or in that from rupture of pulmonary
aneurism there is seldom opportunity for prognosis.
[Footnote 70: _Elements of Prognosis in Consumption_, p. 139.]
[Footnote 71: _Pulmonary Consumption_, p. 150.]
If the condition be recognized, we can but say that the fatal attack is
liable to come at any moment. In cardiac hæmoptysis the hemorrhage is
an event coming toward the close of organic and obstructive changes
which are not much within our control. There are minor degrees, as
shown by expectoration of single small masses of dark coagulated blood
and by the absence of marked aggravation of the symptoms, which do not
prognosticate unfavorably for the immediate, but do show impending
dangers of a future, attack. Morbid anatomy shows traces of a recovery
from a number of premonitory threatenings. The elements of a serious
prognosis are the appearance of a shock, increased dyspnoea, a large
amount of hæmoptysis, increased perturbations in the heart-action, and
increased areas of dulness or râles at certain parts of {291} the lung
other than the usual sites of consumptive disease. These and other
evidences of constitutional initiation are not as available as in the
other varieties mentioned.
TREATMENT.--In the cases of the mildest form very little more need be
done than to keep the patient quiet. His apprehensions may require
attention. They may be allayed by assuring him that the hemorrhage will
be more of a security than a danger, because it is the expression of a
local congestion that will be relieved by the discharge. We have found
that a large dose of quinine (ten or fifteen grains) will answer the
double purpose of a nervous sedative and of controlling the congestion
and hemorrhage if the latter object be necessary. This suggestion
becomes still more applicable in the severe forms of hæmoptysis. The
dose may be repeated within twenty-four hours if needed. If congestion
be manifested by its symptoms of substernal heat, soreness, oppression,
dyspnoea, and cough to a greater degree, and if the hemorrhage is
becoming copious and the hemorrhagic pulse developed, and the
temperature elevated, the necessity of a more active interference is
evident. Absolute quiet in bed, fresh air, a calm and equable behavior
on the part of the family or friends in attendance so that no
excitement may be reflected to the patient, are essential. The
medicines selected should be such as may control the vascular
excitement, and hæmostatics. Ergot will fulfil such indications. It has
its limitations in its unpleasant taste, but it should be pushed to the
points of tolerance. Of the fluid extract one teaspoonful should be
given every hour or two until some effect is observed in slowing the
pulse or checking the hemorrhage. If the stomach rebel, ergotin pills
may be substituted in doses of three to five grains at the same
interval. Should all the resources of ergot medication be required or
the above mode of use fail or disagree, hypodermic injections may be
added. Two to three grains of the extract of ergotin would form a
proper dose, to be repeated every one or two hours. It has been quite
the exception in our experience to have serious irritation follow the
use of it in this way. Failure in this and other uses of ergot will
follow because we do not administer it with sufficient freedom.[72]
Another most valuable hæmostatic is turpentine. It should also be given
freely. From ten to thirty drops in an emulsion or in sugar may be
given every two to four hours, according to tolerance and to the
threatening character of the case. The ergot and turpentine are best
alternated at intervals of one to three hours, according to the
requirements of the attack. Some preparation of opium is often required
to quiet cough--morphine or codeine, one-fourth grain of the former and
one-half grain of the latter, repeated at intervals until their effects
are obvious. By adding the use of broken ice and the external
application of cold compresses frequently repeated, and, if time and
strength permit, the inhalation of persulphate of iron spray twenty or
thirty minims in half an ounce of water, we get a plan of treatment
adapted to the urgent cases. Some recent reports have confirmed the
confidence of the ancients in the use of ligatures. They may be applied
to both lower limbs. A dozen dry cups may be applied to the chest.
There is no occasion or time for the use of many medicines, but if a
general plan, such as the above, must be changed, acetate of lead in
doses of two grains every two hours would be an excellent substitute,
due regard being had to the possible toxic effects from too long
continuance of it in such doses; it is usual to add a little opium to
it. Gallic acid is an effectual remedy for the control of different
kinds of hemorrhages. Like ergot, it is usually given in too small
quantities. Twenty to thirty grains must be given every two to four
hours. {292} It is better borne by the stomach, and can often be
continued longer, than the medicines above mentioned.
[Footnote 72: A medical friend, T. C. Minor of Cincinnati, has in his
own case used three or four drachms of the fluid at a dose, with the
effect of reducing his pulse twenty beats in a few hours.]