49 Étude critique de l'Embolie, Paris, 1869.
50 Bucquoy, Des Concrétions sanguines, Paris, 1863, p. 147.
2d. Grave Form.—In this form neither the pulmonary trunk nor one or both of its primary divisions had become obstructed. The embolic clot or clots have been carried farther into the pulmonary structure and filled up one or more of the secondary bronchial divisions. Nevertheless, the accidents declare themselves with the same remarkable suddenness, and are accompanied by chilly feelings and pallor of the face, just as we have for a brief period after all great shocks to the system (Levrat). In spite of the rapid occurrence of the accidents, they last a considerable time, and hence we are able to study more carefully the respiratory and circulatory symptoms proceeding from the pulmonary obstruction. The pallor of the face soon passes away, and we have in its place cyanosis of the features and a livid hue of the extremities, and in fact of the entire surface. Sometimes, owing to tricuspid regurgitation, we have a venous pulse rapidly produced in the veins of the neck. The patient constantly suffers from oppression and anxiety, and sighs and utters complaints, whilst he makes powerful and ineffectual efforts to diminish his uneasy sensations by deep and rapid inspirations. Occasionally partial convulsions are noted. At times, also, the patient complains of cephalalgia and vertigo, but rarely shows signs of delirium. After a time the accidents narrated become less, and there is relative ease. Soon, however, there is a recrudescence of the attack, and the anxiety and oppression are even greater than before. A succession of such occurrences may take place, and are attributable to a change of location of the clots. If we examine the chest by our physical means of exploration, the result is little better than negative. Percussion shows no abnormal dulness. There are no abnormal râles, and at most there is only a certain rough timbre of the respiratory murmur. After a short time the heart-beats become irregular and feeble, the temperature falls one or two degrees (Cohn), the body is covered with abundant clammy perspiration, and the patient succumbs. Sometimes death is due, where the accidents are prolonged, as much to the secondary effects in the lungs of the embolus as to the embolic plug itself. The accidents commence, indeed, by intense dyspnoea and oppression, but are soon followed by sanguinolent sputa. Luzzato has mentioned one case where the hæmoptysis was an initial symptom of pulmonary embolism, but it is very probably explained by concomitant chronic cardiac disorder. Whenever we find the local signs of an infarctus, the general condition is apt to become more and more serious, new clots reach the lungs, and death occurs in a few days from asphyxia. Frequently albuminuria and oedema of the extremities are observed. In those instances where the patient recovers the mucous râles and localized dulness caused by the infarctus remain for a while, but the sanguinolent sputa diminish, and little by little respiration becomes more vesicular. The patient is now only exposed to dangers due to ulterior transformations of the infarctus. Occasionally new infarctions may form several times and produce accidents similar to those referred to. If there is no hæmoptysis, an infarctus can only be suspected, and often after death this condition is discovered when during life it was wholly overlooked. Sometimes the pulmonary embolisms, although quite numerous, affect vessels of very small calibre, and remain latent during life or occasion no characteristic symptoms. In those examples in which some of the secondary divisions of the pulmonary artery are filled with embolic plugs there is of course a diminished supply of oxygenated blood sent by the left heart to the brain, and there is likewise an accumulation of carbonic acid in the nerve-centres. The lack of oxygen is not enough to cause rapid death, and the accumulation of carbonic acid produces, no doubt, the symptoms of temporary excitability and the local convulsions which are so often present under these and analogous conditions. Whenever after this period of excitement symptoms of slow asphyxia become apparent, they are due either to an excessive afflux of blood into the free arteries of the lung and the passage of the plasma through their walls into the pulmonary vesicles, or they are caused by a succession of emboli blocking up the remaining vascular twigs. Upon the mechanism of death resulting from pulmonary embolism Jacquemet51 has made a careful study, showing the cases of death attributable to syncope and those solely explained by asphyxia. The only physical sign observed in the region of the chest in fatal cases which would appear without question to be caused by a pulmonary clot is a prolonged basic murmur extending itself to the right and left of the sternum in the direction of the primary divisions of the pulmonary artery. "This sign," says Walshe,52 "I most certainly heard in an old gentleman whose life was brought to a sudden close in the course of an acute affection by coagulation in the pulmonary artery."
51 Congrès médicale de France, 2ème session, Lyon, 1864, quoted by Levrat.
52 Diseases of the Heart, 4th ed., 1873.
Whilst authors have usually insisted with much emphasis upon the habitual fatal termination of pulmonary embolism, especially where the plug fills one or both of the large divisions of the pulmonary artery, they have not referred as a rule to the possibility of the patient's recovery. Now, if the arteries be only partially filled by the plugs, and a current of blood can pass around them, the lungs may be sufficiently supplied with oxygenated blood to sustain life for a while and until the clot can be reabsorbed. That this clot can be reabsorbed in the pulmonary artery is shown by what has been frequently observed in regard to clots which have been contained in other vessels of the body.53 Not infrequently, simultaneous with or following upon54 obstructed pulmonary circulation, the phenomena due to peripheral thrombosis have been observed (phlegmasia dolens). In a somewhat analogous manner, after anxious respiration had occurred, obviously due to pulmonary embolism, a peripheral thrombus previously present has been known to have disappeared.
53 Humphrey, Med.-Chir. Trans., vol. xxvii. p. 14.
54 Case reported by Playfair in Treatise on Midwifery, Part V., amongst those illustrative of recovery after symptoms of pulmonary obstruction.
3d. Benign Form.—This form occurs frequently after the traumatisms as described by Besson.55 Habitually we have few or no symptoms which are at all characteristic. The embolisms are capillary and remain latent. Now and then there may be a sudden attack of difficulty of breathing, accompanied by constriction of the thorax which shall probably be explained in this manner. Sometimes the sputa are slightly covered with blood, and this fact lends additional authority to the diagnosis. According to Ball, the physical evidences of the embolisms in the chest are wholly disappointing. Besson, however, finds distinct evidences of their presence in crepitant and subcrepitant râles and dulness on percussion. Levrat56 believes we may have probable signs of the existence of capillary emboli, and cites as an example a case of traumatism in which there might be present a thrombus, and where there would be sudden hæmoptysis followed by sanguinolent sputa, and yet the examination of the chest remained negative. There are cases reported by Paget, Colin, and Feltz in which fatal terminations, caused by a succession of asphyxic paroxysms, took place just as they do after sudden plugging of the large pulmonary divisions. This is true only when the capillary embolisms are very numerous.
55 Paris, 1878.