The same early hyperæmia accompanies the development and growth of tubercle, whether it come from the bronchioles, the blood-vessels, or alveolar walls. Trasbot48 says: "A tubercle is found to be developed along a small artery, most frequently at the angle formed by a terminal division of the vessel—some around a capillary, around which it forms a kind of bead, or in the network of an anastomosis, which envelops it on every side. Vessels are more numerous in the tissues round the nodules and in the septa or interstices of the large masses than in the healthy connective tissue: there the vascularity is often so great as to be mistaken for inflammation."
48 Quoted by Creighton Bevine, Tuberculosis in Man, p. 133.
Hamilton,49 speaking of the formation of tubercle in the alveolar wall and cavity, says: "Capillary blood-vessels, filled with blood-corpuscles, are drawn into it, and in this stage are distinctly visible. They are all much engorged, and occasionally minute extravasations are visible, the blood-corpuscles being thrown into the alveolar cavity." The chance of an earlier obliteration of vessels is greater under these circumstances than where the process begins in any other structure. The final result is that combination of catarrhal and tubercular products characteristic of mixed phthisis.
49 The Pathology of Bronchitis, Catarrhal Pneumonia, Tubercle, etc., 1883.
As increased vascularity accompanies and surrounds the nascent tubercle, so vascular neo-formations accompany or are intermixed with the obliterated zone of vessels, as long since described by Guillot and recently substantially confirmed by Ewart. The former says:50 "There result numerous and inextricable anastomoses, which extend incessantly, and of which the whole forms a mass of vessels proportional in extent to the age of the tubercles and cavities that they entirely surround."
50 L'Expérience, vol. i. p. 553.
There ensues a connection between this system and that forming on the false pleural membranes, and a supplementary function of supply for regions outside of the area of obliterated vessels and for walls of cavities is established. Considering the want of vitality of new formations generally, it is quite probable that these become sources of hemorrhage occasionally. Successive extensions of the diseased regions reduce the amount of this supply, so that the converse follows—comparative anæmia of the lung involved and diminished tendency to hæmoptysis in some of its forms.
These observations, involving considerations of predisposition and its tangible forms, do not apply to the important class of cardiac hæmoptysis. The factors here are increased venous tension, pulmonary hyperæmia of mechanical rather than vital origin, sclerosed or atheromatous vessels, capillary ectasis, and embolic obstruction of the pulmonary artery with resultant infarction, etc.
SYMPTOMS.—The definition requires that the blood be pure or unmixed, yet the coarse physical appearances may vary a good deal. The color is usually a bright red, but may be dark or venous in hue. There is sufficient inconstancy in color to prevent its being reliable in distinguishing the special source of the bleeding, though usually the bright color is of bronchial and the dark of pulmonary origin. If bright red at the onset, it loses some if not the whole of its brightness as the attack progresses or is subsiding, sometimes because of retention in the air-passages. The mass is more or less frothy, and varies in density and specific gravity, in diffluence or adhesiveness, the latter quality increasing in proportion to congestive or inflammatory conditions, whether in the early or later stages. This is dependent on the increase of the plastic, fibrinous, or reactive elements in the blood and adjoining tissues. The mass may lie in a circumscribed or in a splashy form in the bottom of the vessel, circumstances of distance and force of ejection, as well as of physical quality, producing the variations. The quantity varies greatly, both as to the amount at each act of expectoration and as to the amount during all of them. The whole amount throughout an average attack of initial hæmoptysis might be placed at about one and a half to two ounces. Such would be called moderate but decided hemorrhage. The extremes would range between a teaspoonful and several pounds, and the time consumed in the attack may vary between the time taken up by one or two ejections and several months. The intervals between the successive ejections will vary from a few minutes to twenty-four hours or more in a case lasting a week. The manner of ejection is sometimes by a single effort of hawking or throat-scraping or clearing, sometimes by a slight hacking cough or by a vigorous effort of expulsion; at other times the outflow is so rapid through the mouth and nostrils that it resembles vomiting and may suggest a hemorrhage of the stomach.
The effect which a severe attack may have on the patient is often notable. He becomes pale out of proportion to the amount of blood that he has lost; the pulse is full, bounding, and corresponds to what is called the hemorrhagic pulse. This is sometimes due to the mental shock, but again it is independent of any excitement on the part of the patient, or of even any sort of constitutional disturbance, as fever. We have seen it in full development in connection with a profuse hæmoptysis and a temperature of 105°. It has been noted also as part of the phenomena of hemorrhage produced by septic influences upon the vaso-motor system. Walshe's dictum is no doubt true, that there is a calm and excited variety quoad cardiac action.51 In the former there is little vascular or mental excitement or debility, and the patient does not willingly yield to the necessary restraint.