not account for all the cases with which we meet. We are surprised
occasionally by the appearance of pulmonary hemorrhage where heredity
of phthisis cannot be traced. Such persons present the aspect of a
vulnerable state; they yield readily to a phthisical invasion. Some of
the so-called cases of phthisis ab hæmoptoe are found in this class,
yet they may have inherited a phthisical predisposition, brought about
by various degenerating influences acting on their ancestors, such as
antihygienic surroundings, bad air, insufficient food, frequent
childbearing, and excessive nursing. The heredity is not in special
symptoms, but in a predisposition which needs only some exciting cause
for a specific symptomatology that may be carried forward to the next
generation.
One individual may himself yield to the same degenerating influences,
and live with more or less of an acquired predisposition until similar
exciting causes reveal his specific weakness. Another may find that he
has a phthisis directly acquired from a single attack of severe illness
without the aid of any element of heredity or of the acquired
predisposition. The gradation would then be inherited predisposition,
acquired predisposition, and acquired phthisis. Hæmoptysis may find its
origin in these several relations of heredity. Combined, they represent
the law of uniformity and the law of variation in hereditary
transmissions. If these general observations be correct, they show that
the ordinarily stated percentage of transmission of hæmoptysis in
inherited phthisis does not express the totality of influence operating
in the production of hæmoptysis. Something must be subtracted from the
so-called non-inherited phthisis and added to the inherited form.
When we attempt to express the relation of acquired or non-inherited
phthisis to hæmoptysis, we find no sufficient data. Thompson's table
above given is assumed by him as showing that the influences
superinducing hæmoptysis in the non-hereditary class are equivalent to
the heredity operating through the father, which is quite subordinate.
R. Thompson[26] states that out of 1064 of his cases of well-marked
inherited phthisis, 426 had hæmoptysis; of 1016 when phthisis was not
known to be inherited, 558 had hæmoptysis.
[Footnote 26: _Loc. cit._, p. 110. In a later work Thompson (_Family
Phthisis_, London, 1884) states that the general effect of the paternal
inheritance is to reduce the number of cases of copious bleeding for
the total period of life, but an excess is observed for the special
period between twenty and twenty-five; that in the inheritance of the
females from the father the number of cases of bleeding is large, the
number of the copious cases being twice as many as the moderate. The
effect of double heredity upon males was to make the cases of copious
bleeding numerous, and that nearly half the total number of cases were
disposed to bleed. In females there was an increase in the number of
cases of moderate amount. As regards acquired phthisis among males,
that hæmoptysis is a well-marked feature, and nearly three-fourths are
cases of copious bleeding; as to acquired phthisis among females, that
the number of cases is considerably smaller, the reduction being marked
in the cases of copious bleeding.]
{275} In a collection of cases of phthisis taken from the Cincinnati
Hospital records, amounting to 1266, there were of
Cases of hæmoptysis 475, or 37.51 per cent.
" phthisis,
with family history of same 332
" hæmoptysis in same 127, or 38.25 "
" acquired or non-inherited phthisis 934
" hæmoptysis in same 348, or 37.25 "
In 10 cases there was a family history of hæmoptysis; that is, of a
general family peculiarity in that direction. These percentages show no
great difference between the relations of inherited and non-inherited
phthisis to hæmoptysis, the inherited exceeding by 1 per cent. that of
the non-inherited form.
Without here attempting a comprehensive statement of what the
predisposition, transmitted or acquired, is, we may mention two
influences of important force--a tendency to fragility of vessels and
to the catarrhal disposition. It is sufficient to speak of the fact
that in no other disease of the lungs than phthisis have we as a common
feature this vascular fragility. It differentiates the disease and the
symptoms. If it appear in any of them, it should at once excite a
suspicion of the phthisical constitution. That it does appear in some
such cases without ulterior effects does not invalidate the general
statement. It may be put down as a part of the phthisical habit
directly concerned in the liability to hæmoptysis. The proof of this
proposition is more clinical than anatomical.
The attempt to prove that it is hæmophilic rests upon the application
of a few histological examinations of hæmophilic vessels to the
phenomena of phthisical hæmoptysis. The assumption of identity has only
the doubtful force of analogy. Histological examinations of the vessels
in the earliest stages of phthisis and hæmoptysis are too rare to
afford sufficient data. In the latter stages the condition is too
complex, because of positive inflammatory and ulcerative processes.
Although alterations in the vessels in the early stage of simple
inflammation cannot be histologically demonstrated, yet they must exist
in order to allow diapedesis. So with early phthisis: in the
pre-hæmoptoic stage the alterations are not demonstrated, yet that such
disorder of function must have accompanying structural change
underlying the phenomena of the initial hæmoptysis is in accordance
with physiological and pathological doctrines, and has much consistent
clinical force. When we presuppose a delicacy of, or injury to, the
blood-vessels of a part, there is the imminence of not only a rupture,
and consequent hemorrhage, but of those changes which, leading through
stasis and congestion, come to be inflammatory, and which affect still
further the vascular structures and adjoining parenchyma.
Besides these changes initiated in the blood-vessels, there are others
of close relation to the phthisical constitution, which begin in the
vulnerable epithelial elements of the bronchial mucous membrane and of
the air-cells. They are the evidences of the dispositio catarrhalis,
which received its name from the old observers, and the validity of
which has been confirmed by modern pathological and clinical
researches.
It is responsible for the great susceptibility to catarrhal affections
of the bronchi and air-cells which lays the foundation for chronic
catarrhal pneumonia.
These two elements, of fragility of vessels and of the catarrhal
tendency, are the tangible instruments of heredity. They are also the
factors of the acquired predisposition.
The Vienna Hospital reports, running through more than fifteen years,
and embracing more than 20,000 cases, give as the ages most liable to
hæmoptysis those between eighteen and twenty-nine years. No statistics
as to sex are given.
{276} Of 1266 cases of phthisis[27] taken without selection from the
records of the Cincinnati Hospital, there were
Between 10 and 20 years, 81; in this class, hæmoptysis 20
" 20 " 30 " 459; " " " 208
" 30 " 40 " 363; " " " 143
" 40 " 50 " 191; " " " 62
" 50 " 60 " 110; " " " 28
" 60 " 70 " 45; " " " 9
Over 70 " 7; " " " 1
Age not stated 10; " " " 4
---- ---
1266 475
[Footnote 27: We desire to acknowledge the services of Walter A. Dun,
then a resident physician at the Cincinnati Hospital, in collecting
these cases from the hospital books.]
Ware in _Mass. Med. Soc. Proc._ gives ages in 317 cases:
43 up to 20
139 between 20 and 30
77 " 30 " 40
Of Pollock's[28] 351 cases of profuse hæmoptysis,
43 were under 20 years of age.
168 between 20 and 30 " "
100 " 30 " 40 " "
40 over 40 " "
These figures from widely-different sources testify to the fact that
the greatest number of cases of hæmoptysis occurs between twenty and
thirty years of age, or at least with a variation of only about a year
from those extremes. The possibility of hæmoptysis, if we may judge by
cases reported, lies anywhere between sixteen days of age and the limit
of life. A case of hæmoptysis in a child sixteen days old is alluded to
in _Nouv. Dict. de Méd. et de Chirurg_.[29] The oldest on the list of
the Vienna Hospital reports is seventy-two. In our Cincinnati Hospital
list we have 7 over seventy years. Others have reported cases beyond
these figures.
[Footnote 28: _Prognosis in Consumption_, p. 311.]
[Footnote 29: Vol. xxix. p. 391.]
A case of death from pulmonary aneurism and hæmoptysis in a child aged
two and a half years is reported in _London Path. Soc. Trans._;[30]
also one by Powell[31] of a child seven months old from a similar
rupture--illustrations of the remark that children are subject not so
much to initial as to terminal hæmoptysis.
[Footnote 30: Vol. ii. p. 35.]
[Footnote 31: _Med. Times and Gaz._, June, 1874.]
As to the relations of sex to the amount of hæmoptysis, we have the
Table XI. from the second medical report of the Brompton Hospital:
+------------------+-------------------+--------+----------+--------+
| | Males. | Females. | Males. | Females. | Total. |
+------------------+--------+----------+--------+----------+--------+
| Below drachm j | | | | | |
| in quantity | 843 | 700 | 55 | 83 | 1681 |
| From drachm j | | | | | |
| to drachm iv | 616 | 482 | 34 | 69 | 1201 |
| From ½ oz. | | | | | |
| to 4 oz. | 429 | 268 | 13 | 21 | 731 |
| Above 4 oz. | 343 | 153 | 9 | 7 | 512 |
| Entirely absent | 588 | 193 | 74 | 65 | 920 |
| | ---- | --- | --- | --- | ---- |
| | 2819 | 1796 | 185 | 245 | 5045 |
+------------------+--------+----------+--------+----------+--------+
These results correspond with the general one stated by Williams,[32]
that large hemorrhages occurred in 34.76 per cent. of males, and in
only 17.67 per {277} cent. of females. In the above table, where
quantities of blood above four ounces were noted, the male figure is
more than double that of the female. As regards exemption, it is stated
that of the cases of decided phthisis which had been free from
hæmoptysis, about five-sevenths were males, and under two-sevenths
females. In general it may be said that females are more liable to
small and males to the larger hemorrhages.
[Footnote 32: _Treatise on Consumption_, p. 156.]
Of 268 females in our Cincinnati Hospital list, 44 had
hæmoptysis--about 13 per cent. Of 998 males, 431 had hæmoptysis, or
about 43 per cent.
In the second Brompton Hospital report[33] it is stated that "many of
the most violent attacks of this nature (sudden fatal terminations)
have depended on a sudden rise in the temperature." The peculiar
prevalence of hæmoptysis on the coasts of some warm countries has long
since been noted. Archibald Smith,[34] in giving his practical
observations on the diseases of Peru, says: "There appears to be a
general predisposition to this disease, hæmoptysis." An intelligent
individual, himself a sufferer while then a resident on the lower
portion of the North American south-western coast, has given me the
same statement. Pasley[35] says at least 10 per cent. of the cases of
phthisis in Trinidad which die in the hospital terminate in a profuse
hæmoptysis; the quantity of blood varies from 15 to 70 or 80 ounces,
and the duration of life from the beginning of the hæmoptysis till the
end five to fifteen minutes. Of Ware's cases,[36] 83 were in winter,
101 in spring, 69 in summer, 102 in autumn, or 185 in autumn and
winter, 170 in spring and summer. In four months of warm weather, June,
July, August, and September, 97 cases; in October, November, December,
and January, 134; in February, March, April, and May, 124--an average
of 129 for the eight cold months, an excess of 32 cases, or about 33
per cent.; in the transition seasons, spring and autumn, 101 and 102.
The highest numbers were in March and November, 38 and 39; lowest
number in June, 18. These are the only figures obtainable as to our
climate, and they do not agree with those given by R. E. Thompson's
table,[37] showing the prevalence of hæmoptysis as to months in 1000
well-marked cases:
Jan., Feb., Mar., Apr., May, June, July, Aug., Sept., Oct., Nov., Dec.
67 61 90 95 112 130 128 64 64 55 81 63
The summer months of June and July show the largest numbers, and the
months of December, January, and February lesser numbers. The decrease
in August is explained in great measure by the diminution in
attendance. It is possible that other elements of climate besides
temperature may account for this difference between American and
English figures.
[Footnote 33: Page 17.]
[Footnote 34: _Edinburgh Med. and Surg. Journ._, vol. liv., 1840.]
[Footnote 35: _Brit. Med. Journ._, Jan. 10, 1880, p. 53.]
[Footnote 36: _Mass. Med. Soc._, 1860.]
[Footnote 37: _On Pulmonary Hemorrhages_, p. 114.]
A more correct opinion as to the effect of altitude is developing.
Archibald Smith[38] more than forty years ago testified to the good
effects of removal from the coast to the high sierras of Peru in cases
of phthisis with hæmoptysis. His own instances of great improvement
following removal to high levels, 5000 to 8000 feet, are conclusive. He
also gives instances where renewals of hemorrhagic attacks followed the
return to the coast. It was the custom for physicians to send their
consumptive patients to the sierras without reference to their
hemorrhagic attacks.
[Footnote 38: _Loc. cit._]
Similar testimony is accumulating in this country. The Colorado regions
are supplying, through their physicians, much material bearing upon the
effect of altitudes on hæmoptysis. H. K. Steele of Denver, Col.,
writes, June, 1883, that "it is the opinion in the profession
generally, and I endorse it, that this country acts beneficially in the
hæmoptysis of phthisical patients." Jacob {278} Reed, Jr., says[39]
that not only does the ascent to this altitude (6000 feet) not
predispose to pneumorrhagia in consumptives, but that "hemorrhagic
cases do well here; in most cases the bleedings becoming less frequent,
in many cases ceasing altogether." By letter May, 1883, he says these
cases number between 500 and 600, and he feels justified in the
positive statement that not only does altitude not precipitate
hæmoptysis, but that "those suffering from this symptom are benefited
here, their bleeding becoming less frequent and less in quantity." He
makes an exception of florid cases in active progress or old cavities
waking up to new action.
[Footnote 39: "Altitude in Reference to Pneumorrhagia," an analysis of
70 cases, read at the eighth annual convention of the Colorado Med.
Soc., 1878, p. 66.]
Denison,[40] after an analysis of 90 cases of hæmoptysis out of 202 of
phthisis, says: "The advantages of high altitudes are pre-eminently for
hemorrhagic cases in the first stage, while hemorrhagic cases with
excavations, especially if the bleeding has been recent and softening
is in progress, should be interdicted from going to great elevations."
[Footnote 40: _Rocky Mountain Health Reports_, p. 140.]
He also quotes Herman Weber[41] as recommending "alpine climates, not
only as a prophylactic measure against hæmoptysis, but also as a means
to promote the cure of the effects of the inflammatory processes
resulting from pulmonary hemorrhage."
[Footnote 41: _Hæmoptysis as a Cure of Inflammatory Processes and
Phthisis, with Remarks on Treatment_.]
These statements are sufficient to show that the view formerly
prevalent, and still more or less so, that high altitudes have the
effect of prolonging or favoring hæmoptysis, is not altogether correct.
It should be understood as applying to the extreme heights of 10,000 or
15,000 feet, and that rapidity of transfer and unusual exertion are
necessary and qualifying considerations. Jourdanet[42] places the
region of safety in phthisis about the mid-point between the level of
the sea and the snow-line. The preservative level is lower in Alpine
than in American regions. The line of perpetual snow in Mexico being
about 4500 meters, the preservative zone would be 2250 meters. In
Switzerland, where the line of snow marks 2700 meters, the same zone
would be 1350 meters. No such definite limitations are attainable as
regards hæmoptysis, but a correspondence of zones might be conjectured.
[Footnote 42: _Influence de la Pression de l'Air_, vol. ii. pp. 183,
184, 213.]
The belief that pregnancy in some way favors hæmoptysis is a very old
one. It has been more or less accepted by modern writers. Trousseau[43]
gives his observations to the effect that there are women who during
pregnancy, and others who during nursing, spit blood. His belief was
that such hæmoptyses were not symptomatic of pulmonary tubercle nor of
cardiac disease, but he classifies them as cases of hemorrhagic
deviation. Peter[44] speaks of a gravid pulmonary hyperæmia, proven in
part by his determination of increased local temperatures in the lower
intercostal spaces. Some of his cases do not sustain his theories, and
can properly be referred to puerperal accidents, such as emboli in
phlegmasia alba dolens. Such cases as we have met with in connection
with pregnancy or lactation have had hereditary or acquired tendencies
to phthisis. We have under view a case where hæmoptysis always recurs
during pregnancy and where there is a family history of phthisis. A
brother has pulmonary hemorrhages preceded by inflammatory attacks,
which stand in a relation to him corresponding to the pregnant
hyperæmia of the sister. The well-known effects of pregnancy or
prolonged lactation in developing phthisis are a sufficient explanation
of this class of cases.
[Footnote 43: _Clinique Medic. Trans._, vol. i. p. 531.]
[Footnote 44: _Leçons de Clinique médicale_, vol. ii. p. 664, 2d ed.]
Many exciting causes are assigned by patients in explanation of a
dreaded {279} event, and some are otherwise misinterpreted. Their mode
of action is not intelligible unless we keep in view the anatomical,
physiological, and pathological data heretofore given. Numerous cases
occur where no exciting causes can be found, such as those coming on in
the quietude of sleep. The insidious agencies of the predisposing
causes must be responsible. A study of many cases will show that the
alleged causes have become operative only after a considerable time has
elapsed, during which a congestive or inflammatory condition has
appeared, the expression of a latent tendency. Dancing in a warm room
or speaking long in the open air, followed in twenty-four hours by
bleeding, are such instances. The physical effort was only so far
instrumental as it gave a chance for the development of a potential
diathetic condition. It was not the direct cause. Falls, frights, blows
on the chest, heavy lifting, playing on wind instruments, and emotional
excitement are sufficient to bring on a hemorrhage by direct influence,
and by so increasing arterial tension as to overcome the resistance of
vessels already weak. It is not intended to maintain the impossibility
of rupture of healthy vessels under some circumstances, but the large
provision made in the great distensibility of the pulmonary vessels and
in the supplementary functions already alluded to make it necessary to
be cautious in such admissions. The fact that hemorrhages from the
direct causes are sometimes not followed by phthisical effects does not
necessarily disprove their diathetic origin.
The effect of blows on the chest in producing hæmoptysis and phthisis
has been the subject of medico-legal examinations in suits for damages.
In all of such cases within our knowledge there has been the element of
fright or great emotional excitement, and hence a complexity of
causation. An hereditary tendency to phthisis was also present--a fact
which diminished the force of the plea that the blow was alone
responsible for the injuries to the health of the parties concerned.
Diseases or injuries of the brain may be mentioned as causes of
pulmonary hemorrhage, which may occasionally be shown by hæmoptysis.
Experimental pathology has recently thrown much light on these cases.
(See PULMONARY APOPLEXY, _infra_.)
It may be worth while, in view of recent researches, to refer to a form
of hæmoptysis closely associated with a newly-discovered parasite,
named Distoma Ringeri,[45] after Ringer of Tamsui, Formosa, who
discovered the parasite, but did not at once recognize its etiological
relation to the endemic hæmoptysis. In a post-mortem of a man dead from
rupture of an aortic aneurism he found the parasite lying on the
lung-tissue, probably escaped from a bronchus. There were some small
deposits of tubercle, no cavities, and slight congestion of the lungs.
Manson found that these parasites were associated with a
frequently-recurring hæmoptysis. Baely of Tokio[46] discovered the
parasite, probably before any others. It is quite common in North
Formosa and through Japan. Manson says:[47] "Endemic hæmoptysis can be
readily diagnosed. There is a history of irregular, intermitting
hæmoptysis, associated with a slight cough, and in the intervals of
more active bleeding the expectoration once or several times a day of
small pellets of viscid, brownish mucus. Examination of a small portion
of the sputum with the microscope at once settles the diagnosis,
sometimes as many as twenty parasites being found in a single field."
Further examination is necessary to determine the manner in which this
parasite produces the hæmoptysis.
[Footnote 45: _The Filaria sanguinis hominis and certain New Forms of
Parasitic Disease in India, China, and Warm Countries_, p. 134, by
Patrick Manson, Amoy, China.]
[Footnote 46: _London Lancet_, Oct. 2, 1880.]
[Footnote 47: _Ibid._, p. 143.]
The association of bacilli tuberculosis with hæmoptysis is proven by a
number of examinations. These will be referred to in their diagnostic
relations at another page. It is not intended here to imply an
etiological relation, {280} because as yet our knowledge does not point
to the blood-vessels as being the special or usual habitat of bacilli
or the place of their most destructive efforts.
Hydatids of the lung are a cause of hæmoptysis which may come from
congestion accompanying their growth, or from their rupture and
consequent opening of blood-vessels.
Before proceeding farther we shall refer more fully than before to the
conditions prepared by heredity, age and sex, etc. for the action of
the exciting causes. The agencies were stated to be the peculiar
vulnerability of the vascular and epithelial structures of the lungs.
When the morbid imminence is reinforced by an infective element, as in
phthisis, certain results follow which make easy the action of the
incidental causes. Because of the enormous vascularity and great
delicacy of structure of the lungs, and their liability to external
influences, slight external irritants in such constitutions produce
more than what follows in other cases. Instead of a transient hyperæmia
or mild catarrhal inflammation, we may have that fluxionary hyperæmia
of which an early outcome is hæmoptysis. Experimental pathology
explains such occurrences by demonstrating that while a normal vessel,
as in the mesentery, will require a pressure of seventy millimeters of
mercury to produce extravasation of its contents, an inflamed one will
not stand more than twenty-five millimeters. If catarrhal pneumonia
proceed in its phthisical form, it adds its elements of danger.
After its early stage of congestion we have the initiative processes
extending from the epithelial structures of the bronchi and alveoli to
the alveolar wall, which becomes thickened. By means of the double
pressure of abundant epithelial and fibrinous products retained within
the alveolar cells, and of the increased growth in the alveolar walls,
obliterative endarteritis and obstruction of blood-supply follow, the
final result of which may be destructive changes opening the way for
softening and ulceration, and consequent hemorrhage.