Chapter XVIII: Part 18

SYNONYMS.--If we go back far in the history of medicine, we find many synonyms, such as Hæmoptoe, Emptoe, Emptoica passio, Pneumorrhagia, Hæmorrhagia pulmonis, Crachement de sang, etc., etc.

DEFINITION.--Bronchial hæmoptysis is the spitting or expectoration of blood which has been effused into the bronchi or bronchioles from the bronchial vessels. Pulmonary hæmoptysis is the spitting or expectoration of blood which has been effused into the air-cells, the inter-alveolar and interlobular tissues. This distinction is not always practicable in diagnosis or practice. It may, however, serve for a grouping of some well-known clinical forms of hæmoptysis.

It is not possible to give indications by which the origin of blood in the lungs may be positively determined except by a reference to other symptoms than the hæmoptysis. In general, bronchial hemorrhage is characterized by a bright-red, fresh color, is aërated, unmixed, and uncoagulated. In pulmonary or parenchymatous hæmoptysis the blood is dark, non-aërated, and coagulated to some degree, and often alternates with a mixed blood and mucus sputum. These distinctions are not reliable, and must be supplemented by all of our clinical resources in the case before us. The author maintains that in the hæmoptysis of phthisis the hemorrhage in the large majority of cases is both bronchial and pulmonary. The typical parenchymatous hemorrhage is found in hemorrhagic infarction and pulmonary apoplexy, which, compared with phthisis, are rare occasions for hæmoptysis. This general statement will form the basis of what follows in this exposition.

HISTORY.--Historically, there are not many phases in the doctrine of hæmoptysis. Controversy has been chiefly confined to its relations to phthisis as cause or effect.

The simplicity and directness of observation of the ancients give a special interest to their views of hæmoptysis. They believed that it was oftener cause than effect. They found a warranty of that opinion in what they thought was a direct conversion of blood into pus, and in the irritating qualities of the latter. Hippocrates'[1] fundamental statements are, "Ex sanguinis sputo, puris sputum malum;" "Ex sanguinis vomitione tabes et puris purgatio per superiora purgatio;" "Ex sanguinis sputo puris sputum et fluor, ubi autem sputum retinetur moriuntur." Another statement of his is given in translation by Peter:[2] "When some of the veins of the lung are ruptured the hemorrhage is in proportion to the size of the vessel; a part, on the contrary, unless the vein be very small, diffuses itself in the lung, putrefies {267} there, and after having putrefied forms pus. As a result, it is at one time true pus, at another pus mixed with blood, and another time it is pure blood, which is rejected; and if the vein was very full it is from it that the mass of the blood comes, and thick pus, mixed with putrefied pituitous secretion, is expectorated."

[Footnote 1: Edition 1696, book 7, p. 1141, Aphorisms 15 and 16, 80 and 81.]

[Footnote 2: _Clinique médicale_, tome 112, p. 243. The precise locality of this quotation is not given by Peter, but it is from Hippocrates' _Opera_, ed. Kuhn, Leipsic, 1825, vol. ii. p. 178.]

Thomas Young[3] gives the following sentences from Hippocrates' _Predictions and Aphorisms_: "The most dangerous consumptives are cured by a rupture of the great vessel which corrodes the lungs;" "Purulent expectoration after hæmoptysis is dangerous;" "In some cases consumption originates from an effusion of blood into the lungs without hæmoptysis, especially after a strain or accidental injury; a collection of phlegmatic humors form around it by causing pain and cough, with purulent and bloody expectoration." All of these quotations show the Hippocratic doctrine distinctly, that the hæmoptysis where it appeared in a case was mostly the cause of the subsequent phthisis, and that phthisis ab hæmoptoe was not only one of the most common, but one of the most dangerous forms.

[Footnote 3: _A Practical Historical Treatise on Consumption Diseases_, London, 1815, p. 111.]

The doctrine that blood effused into the lungs became pus, and produced corroding and ulcerating effects, appears in many other prominent authors between the Hippocratic writings and the nineteenth century. Celsus[4] (30-40 A.C.) says: "Hæmoptysis is one of the causes of purulent expectoration." Galen[5] (131-201 A.C.) says: "Phthisis is lung ulceration;" and he thinks "that in the greatest number of cases it originates in a mechanical way, through tearing of the tissue by means of an outpouring of blood in consequence of a catarrh or strain." This extract would imply that he thought the hæmoptysis in many cases secondary, but that when it did occur it had the effect which Hippocrates attributed to it, that of producing "purulence of the lungs." Sylvius[6] (1614-1672) says: "Hæmoptysis is one of the causes of purulent expectoration."

[Footnote 4: Young, _op. cit._, p. 128.]

[Footnote 5: Waldenburg, _Die Tuberculose_, p. 19.]

[Footnote 6: Waldenburg, _op. cit._, p. 28.]

Morton's[7] (1689) language partly is: "Decantatum istud medicorum adagium, quod pus sequitur sanguinem;" and then, translated, he says: "It (the adage) appears to have originated in the fact that 'purulence' of the lungs, or phthisis pulmonalis, usually follows hæmoptysis more quickly and oftener than any other disease." In the sentence immediately following he suggests this result may be due to a putrefaction of clots that the hæmoptysis has left behind in the lungs, or to a copious effusion of humors from the whole body to the tender lungs, or to an erosion of some vessel.

[Footnote 7: _Phthisiological Ed._, 1727, lib. 111, chap. v. p. 95.]

Another theory appears in Hoffmann's language,[8] and was probably suggested, directly or indirectly, by Sylvius's description of tubercles: "The blood is easily extravasated into the pulmonary vesicles, stagnates there and putrefies, corrodes the neighboring parts, and finally destroys the air-passages or they are converted into nodes or tubercles." The blood becomes tubercularized, and the phthisis ab hæmoptoe is established. This idea is found at different periods, and we find a recent French author arguing against this hypothesis.

[Footnote 8: Peter, _loc. cit._, p. 244; Young, p. 211, _Opera_; Hoffmann, _Physico-medica_, Geneva, 1740.]

The reversal of these ideas is generally acknowledged as the results of Laennec's energy and genius, yet similar opinions to his had been expressed by French and English physicians. Bayle does not place phthisis ab hæmoptoe in his classification. Desault,[9] one of Laennec's countrymen, near a hundred years before him, "insists that tubercles constitute the essence of consumption, being generally anterior to hæmoptysis." Mudge[10] says that hæmoptysis is often the consequence of the obstruction produced by tubercles. A {268} preparation for the positive opinions of Laennec is discernible in these and other authors. His views on this particular topic were opposed by Andral. The latter modified his earliest expressions to some extent.

[Footnote 9: Young, p. 220, _Desault sur les Maladies venériennes, la Rage et la Phthisic_, Bordeaux, 1733.]

[Footnote 10: Young, _loc. cit._, _Radical Cure for a Recent Catarrhic Cough_, London, 1779, 2d ed.]

The next important historical epoch in the causative relations of hæmoptysis and phthisis is in the energetic protests of Niemeyer. They were in some respects a return to the Hippocratic doctrine, in that he asserted the predominance of hæmoptysis as cause; but he gave the doctrine a basis better adjusted to a better pathology, in that he made the important element of inflammatory lesions the medium between the effusion of blood and the final purulence or ulceration (ulcus pulmonum) of the ancients. He energetically advocated the doctrine of the positive effect of effusion of blood in the bronchi or pulmonary substance in producing disorganization of the lungs, without reference to any hereditary or predisposing element or existence of tubercles.

Jaccoud[11] calls attention to the fact that Graves had anticipated Niemeyer in the partial revival of the Hippocratic doctrine and the teachings of Morton and Hoffmann on phthisis ab hæmoptoe.

[Footnote 11: _Clinique médicale_, vol. ii. p. 302, Graves.]

In a recent work[12] there is a general adhesion to the modern modifications of the Hippocratic doctrine in regard to the pathogenetic relations of hæmoptysis and phthisis. There is a decided rejection of the causative influence of tubercle in producing hæmoptysis.[13] "The connection between pulmonary hemorrhage and tubercle stands on no pathological proof;" "From all the evidence I have been able to obtain on this point, tubercle seems to have been very unjustly credited with hemorrhage."[14] He differs from others in attributing much more to the hæmophilic constitution in the production of hæmoptysis. Other phases of the history of hæmoptysis might be given. We shall allude to two only: one is the classification of the varieties. Alexander of Tralles treats of hæmoptysis under three heads: 1, Hæmoptysis by rupture; 2, by erosion; 3, by dilatation. Bricheteau[15] makes four divisions: 1, constitutional; 2, accidental; 3, succedaneous; 4, critical and symptomatic. These two classifications show in themselves their origin, in that the one is representative of a local, and the other of a constitutional, pathogenesis.

[Footnote 12: _On Pulmonary Hemorrhage_, Reginald E. Thompson, London, 1879.]

[Footnote 13: Page 32, _op. cit._]

[Footnote 14: Page 33, _op. cit._]

[Footnote 15: _Maladies chroniques de l'Appareil respiratoire_, Paris, 1851, p. 523.]

The last historical phase is the therapeutic one. We find in the practice of the present day survivals from the ancient authors. Morton recommended ligatures around the limbs to arrest hemorrhage, and bark to prevent hæmoptysis from becoming phthisis.[16] Venesection, which to some extent is a modern remedy, was frequently practised by the older physicians. Erasistratus[17] recommended ligatures, applied to the limbs in several places, to prevent the return of the blood to the lungs; Asclepiades thought this practice founded on an erroneous theory, but experience is in its favor. The head should be kept high, the face wetted with water, the room cool, and the patient perfectly at rest. Lietaud (1765) is cautious of employing astringents or purgatives, but recommended ligatures to the limbs and cold to the scrotum. A drachm of rhubarb was given by Fernelius in hæmoptysis. Bryan Robinson[18] (1752) relates a case in which an emetic of ipecacuanha, taken three times a week, kept off hæmoptysis for eight years, while tar-water constantly brought it on. Marryat (1758, London) "advises two grains of tartarized antimony, and as much of the sulphate of copper, in half a spoonful of water." Ipecacuanha was frequently employed in hæmoptysis by the practitioners of the centuries preceding the nineteenth.

[Footnote 16: Young, pp. 201, 202.]

[Footnote 17: _Op. cit._, p. 128.]

[Footnote 18: _Op. cit._, p. 156, ed. 1660.]

As an important preface to the subjects considered in this article we introduce an account of the vascular supply of the lungs.

{269} Before entering into a statement of the distribution of the minute vessels to the lungs it is desirable, in view of the possible diseased connections between the larger bronchial and vascular trunks, to recall some points of the topographical anatomy of the latter. "The root of the left lung passes below the arch of the aorta and in front of the descending aorta. The bronchus, together with the bronchial arteries and veins, the lymphatics and lymphatic glands, is placed on a plane posterior to the great blood-vessels. The pulmonary artery lies more forward than the bronchus, and to a great extent conceals it, while the pulmonary veins are placed still farther in advance." The left bronchus "in passing obliquely beneath the arch of the aorta is depressed below the level of the pulmonary artery, which is the highest vessel."[19] Practically, the chances of abnormal communications lie in the relations of the aorta, more especially the different parts of the arch, to the left bronchus and pulmonary artery, and to the trachea, of the innominate artery to the trachea, and of the glandular structures at the root of lung to the pulmonary artery.

[Footnote 19: Quain's _Anatomy_, vol. ii. pp. 897, 898.]

The encroachment of aneurism of the subclavian artery on the lung, and consequent communication between it and the bronchus, is another form of accidental or extraneous hæmoptysis.

A recognized classification of the vascular systems of the lungs is into--1st, functional; 2d, nutritive. To the first belong the pulmonary arteries and veins, and to the second the bronchial arteries and veins. Both physiological and pathological experience justifies this division.

Notwithstanding the great attention and labor bestowed upon the circulation of the lungs, there are still unsettled some important points. We adopt from Küttner[20] some of the anatomical data applicable to our subject. The branches of the pulmonary artery follow uninterruptedly the bronchial ramifications. The mutual relations of the artery and bronchus are such that the larger vessel lying in any preparation of the lung directly next to the bronchus, and running in the same direction, can be pronounced to be a branch of the pulmonary artery. In the lungs of the embryo both lie in the same connective-tissue sheath that originates at the root of the lung, enters with them into the root of each lobule, and there spreads out. In the lobules both run not only closely alongside of each other; there appear also branches of the pulmonary artery on the bronchus itself, and press on to the mucosa of the same.

[Footnote 20: "Beiträge zur Kentniss der Kreislaups-verhältnisse der Saugethierlunge," _Virchow's Archiv_, vol. lxxiii. p. 476, etc.]

With the appearance of the terminal bronchiole this relation is changed. The bronchial artery, as such, ceases; the pulmonary artery--or rather its lateral branches--exclusively surround the alveolar diverticulæ on their external surfaces. At the point where the terminal bronchiole is developed into the infundibula the corresponding trunk of the pulmonary artery divides into a number of branches--"pinselförmig;" each infundibulum receives its stem, which spreads itself after the manner of a feather on its external surface. The terminal branches of the pulmonary artery cover the terminal alveoli. On every lung in which the infundibula and lobules are well distributed the terminal branches of the pulmonary artery extend beyond the borders of the infundibula and lobules into the interlobular and subpleural connective tissue, and here either lose themselves in a capillary distribution or extend to the periphery of an adjoining acinus, being lost in its capillaries.

One peculiarity of the pulmonary artery is that from a large trunk relatively fine lateral branches come. From a vessel of 0.136 mm. come branches of 0.033, 0.016, 0.011, 0.010 mm. The finest disappear immediately as vasa vasorum; the larger pass to the perivascular or peribronchial connective tissue {270} and become capillary, or they appear on the surface of the immediately adjoining lobules and disappear in the capillary paths of the alveoli.

The terminal branches of one and the same principal artery behave differently according as they are distributed to the connective tissue or to the alveoli. In the first case they form wide meshes and narrow tubes, and are not different from the capillary terminations of the body in general. In the other case the meshes are narrow; the vessels in all of the pulmonary capillaries are wide. If these vessels are followed from their origin to their final termination, it will be seen that a considerable part of the pulmonary artery is spread in the interlobular connective tissue; that it is not exclusively a secretory vessel; that the capillary network of all the lobuli are in anastomotic connection.

An anatomical investigation shows that between the branches of the pulmonary artery no anastomoses exist. It is, however, proved that under certain conditions connections between the larger branches of the artery may occur. This artificial connection is favored through peculiarities of terminal branching: wherever two parallel branches of the pulmonary artery are followed, it will be seen that the terminal branches lie alongside of each other without anastomosis. One can be convinced of that, and, further, that the capillaries of only one or two alveoli separate them. These unusually short capillaries between two arteries are those in which differences of pressure in one or the other artery produce wide connections. Küttner agrees so far with those observers who think that between the larger branches of the pulmonary artery no wide anastomoses exist already formed. In this sense the pulmonary artery can be designated a terminal artery; on the other side, however, it must not be forgotten that such connections can arise at any time, and the artery there loses the type of a so-called terminal artery.

He further remarks that the vascular-district supply of the pulmonary artery is not so limited as Cohnheim and Litten believe; that, more than that, some branches of it pass from one lobule to the adjoining one; that others are distributed in the subpleural and interlobular connective tissue and in the bronchial wall.

If the lung of an animal be injected from the pulmonary artery, there is produced a complete filling of the vessels of the bronchial wall and into the subepithelial layer--a fact the more interesting that a similar event can scarcely be produced by a filling of the bronchial artery.

Pulmonary Vein.--Only at the root of the lung do the bronchus, pulmonary artery, and pulmonary vein lie close to each other. In the continuance of the same the artery and the bronchus remain close by each other, but the vein pursues its own course. The branches of the same are, from the hilus to their capillary termination, situated in the interlobular connective-tissue paths. They form on the external margins of the lobules wide blutbuchten, in which the veins of the infundibula enter with short stems. The artery lies intralobular--the vein interlobular. The bronchial veins connect not only with branches of the azygos and superior cava, but also with those of the pulmonary vein.

Bronchial Vessels.--The variety of origin of the bronchial arteries is notable. Whatever their origin, they follow with their chief trunk the bronchus into the parenchyma of the lung, and give off insignificant lateral branches to the connective-tissue layers. There is still another kind of artery, which divides independently in the connective tissue of the lungs, without resting on the bronchial walls; they come from the oesophageal, mediastinal, and pericardial arteries, branch in the mediastinal pleura, appear with these at the hilus of the lung, and form partly an independent mesh of pleural arteries, and partly spread themselves in the interlobular connective tissue.

All the vessels of the serous membranes of the diaphragm can contribute {271} in many ways blood to the hilus of the lung: the unusually fine-branched arteries appear in this way to be in condition to compensate for obstructions (or lesser). The bronchial arteries in comparison with the other vessels of the lungs give off sparingly lateral branches; among the most interesting are the branches which spring directly from the trunks of the bronchial artery, pass through the peribronchial connective tissue, appear at the adjoining infundibula, and lose themselves in capillary terminations.

The capillary districts of the bronchial arteries pass immediately into those of the pulmonary. It is a fact that besides the pulmonary artery the bronchial artery provides the infundibula and alveoli with blood. If the bronchial artery springing from the intercostal and internal mammary arteries be ligated or cut, leaving open the vessels of the mediastinal pleura, and the lung be injected from the abdominal aorta, a mere inspection will show a filling of the parenchyma of the lung; anastomoses between the pleural arteries and the intra-acinous trunks of the pulmonary arteries can be recognized. There is an anastomotic connection between the pleural branches of the pulmonary and bronchial arteries.

The bronchial, as also the pulmonary, artery can be filled by means of the fine arterial branches from the mediastinal pleura.

The principal branches of the bronchial arteries go to the bronchi; at the alveolar passage they here stop as such; their capillaries become continuous with those of the pulmonary artery. The greater part of the few collateral branches nourish the submucous peribronchial and perivascular connective tissue, the nerves, the lymphatic vessels; the smaller part enter the alveoli of other bronchial systems and become capillary.

The branches going to the lung with the mediastinal pleura spread themselves in the pleura and interlobular connective tissue, nourish the large subpleural and interlobular lymphatic vessels, but lose themselves in capillary distribution on the alveoli and infundibula.

The pleural and bronchial arteries anastomose partly with each other and partly with branches of the pulmonary artery.

With reference to the branches of the pulmonary artery going to the bronchi, it may be said that they, without giving special branches to the external layer of the bronchi, press on to the basal membrane and form a compact capillary network in common with the proportionately few branches of the bronchial artery.

Amidst differences of opinion, as between Küttner, Lalesque, and Cohnheim and Litten, there is a concurrence as to the chances of supplementary function by anastomoses between channels that are ordinarily separate. Küttner admits a modified form of terminal arrangement in the pulmonary artery, but at the same time claims an amount of potential connection that is liable to come into actual operation and suspend, if not destroy, the terminal type.

The correlation of both functional and nutrient vessels is so intimate that we believe there is no conclusive argument against the actual transfer of office from one to the other in certain strained conditions of disease; Virchow's experiment proves it.

The wonderful delicacy and distensibility of the enormous network of pulmonary vessels (relation of uncovered space in the alveoli to that covered by the vessels being 50 out of 200, Kuss); their capacity of response to great variations of supply and tension; the prompt supplementary function proven by Litten[21] to belong to the tracheo-oesophageal, pericardial, phrenic, and pleuro-mediastinal arteries, and their equilibrium under the sensitive changes of the aortic system; the slower submission of the lesser circulation to the peripheral impressions, which markedly affect the aortic system; the facts {272} verified by Lichtheim[22] that on closure of any portion of the pulmonary artery the same quantity of blood will pass through the portion remaining open as before; that this is brought about through increase of pressure in the sections still open, and through the simultaneous increased rapidity of circulation and distension of the vessel walls; and that this mechanism is able to compensate for obstruction of three-fourths of the pulmonary artery,--are important factors in the anatomical and physiological relations of hæmoptysis.

[Footnote 21: "Ueber den Hämorrhagischen Infarct," _Zeitschrift für klinische Medicin_.]

[Footnote 22: _Die Störungen des Lungenkreislaufs_, by L. Lichtheim, Berlin, 1876, p. 65.]

ETIOLOGY.--The natural history of hæmoptysis is practically that of phthisis: exceptions to this will be noted hereafter. As heredity is largely a determining influence in the latter, it may be assumed that it qualifies its principal symptoms. More or less uniformity prevails in the transmission of normal or abnormal conditions, and we seem to find an illustration of the latter in the correspondence between the percentages of hereditary phthisis and those of hæmoptysis in such cases. Reginald Thompson[23] says that "out of 1064 cases of well-marked inherited phthisis, 426 suffered from hæmoptysis." In his calculation he omitted all those in which the disease began with hæmoptysis. Had these then been included, they would have raised the percentage over that shown by the figures, which is slightly above 40. The rate would not then be much below that given as an average of cases of hereditary phthisis. This percentage of cases of hæmoptysis in hereditary phthisis is a sufficiently uniform transmission to prove the influence of heredity. Its influence is shown not only in the number of transmissions, but in the transmission of types; so that, as we have a family type of phthisis, we may have a family type of hæmoptysis, such as the cases where all the phthisical members of a family are subject to hæmoptysis of uniform characteristics, instances where the same uniformity in type is transmitted, and instances where the phthisical heredity appears to have its survival in moderate and transient attacks of hemorrhage.

[Footnote 23: _The Causes and Results of Pulmonary Hemorrhage_, p. 110.]

Atavism is also seen in some family histories. We have in view such an instance, where the marked hæmoptysical tendencies of one generation skipped the next to reappear in the third.

A special study of the relation of cases of copious hæmoptysis to different forms of heredity has been made by Reginald Thompson. His table is as follows:

COPIOUS HÆMOPTYSIS.
+-------------------+----------------------------------+
| | Cases. |
+-------------------+--------+--------+----------------+
| Age at which | Mother | Father | Non-hereditary |
| attack commenced. | 123 | 102 | 105 |
+-------------------+--------+--------+----------------+
| 5 | ... | 1 | ... |
+-------------------+--------+--------+----------------+
| 10 | ... | 4 | 2 |
+-------------------+--------+--------+----------------+
| 15 | 27 | 16 | 14 |
+-------------------+--------+--------+----------------+
| 20 | 30 | 22 | 20 |
+-------------------+--------+--------+----------------+
| 25 | 34 | 24 | 24 |
+-------------------+--------+--------+----------------+
| 30 | 18 | 19 | 16 |
+-------------------+--------+--------+----------------+
| 35 | 8 | 9 | 12 |
+-------------------+--------+--------+----------------+
| 40 | 2 | 4 | 8 |
+-------------------+--------+--------+----------------+
| 45 | 3 | 1 | 5 |
+-------------------+--------+--------+----------------+
| 50 | 1 | ... | 2 |
+-------------------+--------+--------+----------------+
| 55 | | 1 | |
+-------------------+--------+--------+----------------+
| 60 | | 1 | |
+-------------------+--------+--------+----------------+
| 65 | | | |
+-------------------+--------+--------+----------------+

He claims that this table shows that of the cases of direct heredity, cross-heredity, and non-heredity, those who were the subjects of cross-heredity--that is, those from the mother--were more liable to copious hæmoptysis than either the cases of direct heredity or of non-heredity; and the numbers of the two latter so closely correspond as to show that heredity from the father has little influence as regards hemorrhage. The conclusion he draws from the table is that "an heredity is drawn from the mother which differs from that derived from the father, and to this must be attributed the excess of cases of copious hæmoptysis."

{273} This difference will be seen in the following table, which shows the number of cases occurring before and after thirty:

+-----------------+-----+-------------------+------------------+
| Cases. | | Before age of 30. | After age of 30. |
+-----------------+-----+-------------------+------------------+
| Mother | 123 | 91 | 32 |
+-----------------+-----+-------------------+------------------+
| Father | 102 | 65 | 37 |
+-----------------+-----+-------------------+------------------+
| Non-hereditary | 105 | 60 | 45 |
+-----------------+-----+-------------------+------------------+

He thinks the explanation is to be obtained from the statistics of hæmophilia, which show a large proportion of transmissions from mothers to sons, and that we have here a strong argument connecting copious hæmoptysis, not with tubercle, but with hæmophilia.

His next table is one of 125 cases of double heredity, calculated upon the same basis as the others, that of 400:

+----------+-------------------------+
| | Cases. |
+----------+------------+------------+
| | Double | Calculated |
| | heredity | to |
+----------+------------+------------+
| | 125 | 400 |
+----------+------------+------------+
| 5 | ... | ... |
+----------+------------+------------+
| 10 | 3 | 10 |
+----------+------------+------------+
| 15 | 20 | 74 |
+----------+------------+------------+
| 20 | 40 | 128 |
+----------+------------+------------+
| 25 | 23 | 75 |
+----------+------------+------------+
| 30 | 15 | 48 |
+----------+------------+------------+
| 35 | 12 | 37 |
+----------+------------+------------+
| 40 | 9 | 29 |
+----------+------------+------------+
| 45 | 1 | 3 |
+----------+------------+------------+
| 55 | 1 | 3 |
+----------+------------+------------+
| 60 | 1 | 3 |
+----------+------------+------------+
| 65 | | |
+----------+------------+------------+

which shows a close approximation to the table of cases of cross-heredity from the mother, and that the calculated number for 400 cases of double heredity are almost identical with that of the actual number of 400 cases of cross-heredity between the ages of fifteen and twenty-five--in the first case being 202, in the second 203--and the calculated number of cases before thirty amount to 287, not quite equal to actual number for cases of cross-heredity, which is 294. He concludes that these cases do not show a greater tendency to hemorrhage than is shown in cases of direct and non-heredity. We may accept these figures and calculations as important without endorsing the conclusion which they are intended to sustain--viz. that such hæmoptyses are essentially of hæmophilic origin. It may be stated as a general opinion that hæmophilia does not especially manifest itself in pulmonary hemorrhages, and that hæmophilic families are not specially liable to phthisis.

The hemorrhagic diathesis, as distinguished from the specific bleeders' heredity, does not often manifest its activity through the lungs, and, as correlative, phthisis does not often show hemorrhages in other organs than the lungs.[24] Leudet has met in 244 cases of phthisis 9 times hemorrhages in other organs than the lungs; oftenest by the intestine, the skin, the nasal mucous membrane; more rarely by the brain and urinary organs; 10 times between the muscles of the abdominal walls. These considerations suggest that the phthisical hæmoptysis is distinct from that of hæmophilia or the hemorrhagic diathesis, and has an independent origin.

[Footnote 24: "Rémarques sur la Diathese hémorrhagique," _Mém. Soc. de la Biologie_, 1859, p. 179.]

Some facts in regard to the previous diseases of patients admitted into the Brompton Hospital with phthisis are given in the second medical report of that institution, which may have a bearing on the special features, such as hæmoptysis. Among 1973 patients admitted, 275 were found to have suffered with well-marked attacks of rheumatism, and 16 had acute symptoms of it while in the hospital, making a larger number than of any other disease, fevers coming next with 238. The connection of forms of hemorrhage with {274} so-called rheumatism suggests a possible influence of that kind in favoring hæmoptyses during the evolution of phthisis. We know of no facts collected with the view of studying this relation. If such a conclusion were sustained, it would tend to confirm the view connecting hæmoptysis with hæmophilia or the hemorrhagic diathesis.

Williams[25] gives a statement qualifying the assumption that the hemorrhagic variety of consumption specially originates in family predisposition, for in 72 cases out of 1000 tabulated cases of phthisis family predisposition was present in only 25 instances. This percentage is scarcely small enough to exclude a predisposition.

[Footnote 25: _Pulmonary Consumption_, p. 157.]

Considering hæmoptysis in this aspect, as a result of heredity, does 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.