PULMONARY EMBOLISM.
BY BEVERLEY ROBINSON, M.D.
DEFINITION.—Pulmonary embolism signifies the transport during life of clots, or of other solid substances appearing within the right heart or systemic veins, from these parts to the trunk or divisions of the pulmonary artery.
SYNONYMS.—Fr. Embolie pulmonaire; Ger. Embolie der Lungenarterie; It. Embolia pulmonare.
CLASSIFICATION.—A rigorous classification of the different kinds of pulmonary emboli or a clear separation of them into distinct orders is very difficult on account of the rôle in producing them, partly mechanical, partly dyscrasic, of some of the affections in which they are likely to occur. This is particularly true of the puerperal state, uterine affections, and fractures.1 Bertin, however, has made of them four divisions, according as the cause is mechanical, dyscrasic, mixed, or undetermined; but these are objected to by Luzzato on the ground of their inadequacy, and he deems it preferable to regard them from the point of view of their medical, surgical, or obstetrical origin. From this latter point of view we also consider it best to consider them until a more satisfactory separation shall be established.
HISTORY.—Latterly, the subject of pulmonary embolism, or the obstruction of this artery by means of a clot which has had its origin in the right heart or one of the systemic veins, has been very carefully studied. Many cases of sudden death are properly and readily explained in this manner, where formerly they would have been doubtful or inexplicable. Sometimes the previous existence of a fibrinous coagulum in the right heart or in the crural vein has been recognized previous to the symptoms indicating plugging of the pulmonary artery; occasionally these coagula have been wholly overlooked, and the sudden cry with intense dyspnoea, pointing to obstruction of the blood-supply to the lungs, is a matter of dread surprise to the beholder. According to Trousseau,2 our knowledge of embolism is due mainly to Legroux. This is not, however, the view of Ball3 nor of Walshe, who attribute the clearest insight into this process to the clinical and experimental observations of Van Swieten, who, half a century before Legroux's time, had injected different coagulating materials into the veins of animals and produced the characteristic symptoms of pulmonary embolism. To Virchow's4 exhaustive researches, however, we are principally indebted for a great deal of what is actually known upon this subject to-day. True it is that contemporaneous writers have added many new facts to those he so well elaborated, but the greater part of credit in this line of study should be awarded to him. After Van Swieten's time the doctrine of pulmonary embolism fell somewhat into disrepute, owing to the lukewarmness of Hunter and Morgagni. Cruveilhier (1842) recognized their existence, but was so much impressed by his doctrine of phlebitis that he believed the majority of pulmonary coagula were autochthonous (formed on the spot), and not the consequence of transport or migration in the venous current. This opinion was strongly combated by Virchow, who held that pulmonary coagula formed some time before death were not the result of an inflammation of this arterial vein (Galien), but always had for origin a migratory clot which came from some part of the venous system.5 This doctrine of Virchow's is certainly too exclusive, and although primary or secondary inflammation of the pulmonary artery is certainly rare, it is certainly not unknown, and when it exists will sufficiently explain the formation of a fibrinous clot. Facts of this kind have been reported by Bumann, Bouillaud, Andral, and more recently still by Lancereaux, who has shown to the Anatomical Society of Paris6 distinct new formations in the pulmonary artery. Until further investigations are made on this point it seems wise to abstain from having an opinion too categoric on one side or the other. Virchow's first studies on pulmonary embolism were published in 1846, and were based upon 11 cases of this disease. All these cases were caused by migratory clots from the heart or one of the systemic veins. In this first publication, and later on (1854–56), Virchow gave the results of numerous experiments in which he had injected bits of fibrin of diverse origin, particles of flesh, and fragments of rubber into the jugular veins, and showed in an admirable description the immediate effects of embolic plugs upon the blood, the arterial coats, and the surrounding pulmonary tissues.7
1 Étude critique de l'Embolie, Paris, 1869.
2 Clinical Lectures, Sydenham Society's ed., vol. iii. p. 414.
3 Des Embolies pulmonaire, Thèse de Paris, 1862.
4 Froniep's Neue Notizen, 1846, p. 910.
5 Bucquoy, Des Concrétions sanguines, Paris, 1863, p. 138.
6 Bullétin, 1861, p. 377.
7 Dict. de Médecine et de Chirurgie, vol. xxix. p. 334.
In 1852, Senhouse Kirkes8 also studied very carefully different cases of embolism, and showed how they were connected with organic disease. Most of these cases, however, showed rather the effects on the brain and the production of right or left hemiplegia than the asphyxic sequelæ of obstruction of the trunk or divisions of the pulmonary artery. In France the doctrine of embolism was at first received doubtingly, and was the subject of animated discussions at the Medical Society of the Hospitals in 1857. In this year Charcot and Ball published the first case of pulmonary embolism which had been observed in that country. Five years later (1862) pulmonary embolisms formed the subject of a remarkable inaugural thesis by Ball, and articles of considerable value were also written in regard to it by Velpeau, Lancereaux, Lemarchand, Trousseau, etc. Spontaneous coagulation of the blood in the right heart and pulmonary artery was considered by Meigs in 1855 to be a frequent cause of death in the puerperal state. Analogous cases, although none of them occurred after childbirth, had five years previously been carefully studied by Paget.9 The cases of sudden death subsequent to confinement are now generally considered to be due to pulmonary embolism.10 Amongst the later sources of information on the subject of pulmonary embolism or its consequences we would direct special attention to the work of Luzzato11 and the theses of Duguet12 and Levrat.13 These and numerous other writers have made researches as to the different varieties of pulmonary embolism, such as the fatty (Flournoy), atmospheric, specific, those following confinement, or traumatism.
8 Med.-Chir. Trans., vol. xxxv.
9 Ibid., vol. xxvii. p. 162, and vol. xxviii. p. 352.
10 Playfair, A Treatise on the Science and Practice of Midwifery, Philada., 1882.
11 "Embolia dell' Arteria pulmonale," Annali Univers. di Med. e Chir., Milano, 1877–79.
12 De l'Apoplexie pulmonaire, Paris, 1872.
13 Des Embolies veineuses d'Origine traumatique, Paris, 1880.
ETIOLOGY.—The great majority of emboli which are found in the pulmonary artery after death come from the systemic veins. They may also be transferred from the right heart. According to Hayden,14 in fact, the migratory clot is usually derived from cardiac thrombosis of the right heart. This opinion, however, is not generally accepted as correct. Of all the veins of the economy, those of the lower extremities give the largest number of emboli. This statement is notably true of the femoral and internal saphena veins. According to Lancereaux,15 the reason why coagula form in the veins of the lower limbs high up and in the cerebral sinuses is the fact that in these locations the action of the vis-a-tergo and thoracic aspiration is scarcely or at all felt. Besides, we know that coagula of these veins are very frequently found in cachectic conditions (tubercle, cancer) and in the puerperal state (phlegmasia alba dolens). As we shall have reason to remark further on, embolism of the pulmonary artery is often due to fragments of cancer, of pus, of a valve, etc., which have made their way into the return blood-current, or indeed have formed there in the first place. The direct cause of the separation of a portion of thrombus is either some mechanical cause or the influence of regressive changes affecting the clot. We are called upon, however, to consider briefly—1, the causes in a general way which predispose to the formation of thrombi; 2, the diseases, dyscrasic and local, in which emboli occur most frequently. Virchow, Richardson, and others have shown conclusively that the blood is prone to coagulate in the vessels—1, whenever it stagnates or is arrested in its course; 2, if there be, by reason of morbid alteration of vascular wall or presence of an embolus, a mechanical obstacle present; 3, if the blood be modified by septic conditions or increase of fibrin. Now, then, in the veins of the lower extremities we have a considerable tendency to stasis—greater indeed than exists elsewhere in the economy—because these veins have to contend against the weight of the blood in the iliac veins, the venæ cavæ, and the right heart. Further, they are often obliged to resist the effects of accidental pressure in the abdominal cavity, or that which takes place in lungs altered by some chronic diseases16 (emphysema, pneumonia, bronchitis). Usually in these veins, as elsewhere, when a thrombus exists there is local inflammation at its level of the walls of the vein. This inflammatory condition itself is dependent upon mechanical injury, change of the blood (gout),17 or the introduction of septic material. At times septic material is introduced into the blood and absorbs from disintegration of a clot. Hence arise typhoid or pyæmic symptoms.
14 Dis. of the Heart and Aorta, Part ii. p. 1029.
15 Gaz. hébdom., 1862, quoted by Bucquoy.
16 Hayden, Diseases of the Heart and Aorta, Part ii. p. 1023.
17 Tuckwell, St. Bartholomew's Hosp. Reports, vol. x., 1874.
I. Amongst the medical causes which frequently occasion pulmonary embolism we should mention diseases of the heart,18 of the lungs, the stomach, the kidneys, and the uterus. Mitral affections which have reached their ultimate period are a fruitful source of pulmonary embolism on account of the effect produced on the right heart. The slowing of the circulation in this condition by digitalis has been wrongly accused by some writers of favoring the production of emboli. Evidently, digitalis does not promote this formation when given with circumspection, as it increases the force of the heart-beats. Sometimes constitutional disease precedes the formation of emboli. This is particularly true of leucocythæmia, which is an efficient cause of it, at times, when sudden death has followed plugging of the trunk and both branches of the pulmonary artery.19 In the convalescence of typhoid fever pulmonary embolism is quite frequent, and follows upon the formation of thrombi in the veins. Such a specimen was presented by Fagge at the meeting of the London Pathological Society on Nov. 16, 1876. The patient died suddenly in the fourth week of an attack of typhoid fever following an attempt to get out of bed. The marked symptom of the case was intense dyspnoea.20 It would appear that emboli are more apt to take place in acute than chronic disorders, because in the former they grow more rapidly, are less intimately attached to the vascular walls, and in consequence are prone to become detached and carried in the current of the circulation.21 Chlorosis has been invoked as a cause of venous thrombosis of the lower extremities,22 but rarely under these circumstances has pulmonary embolism been due to its existence. Hayden23 reports a case of similar formation in advanced pulmonary phthisis. In this instance death occurred, but no symptoms of pulmonary embolism were at any time present. At the autopsy a firm, decolorized clot was discovered in either femoral vein. Although phthisis is a frequent cause of phlegmasia alba dolens, owing to the compression of enlarged lymphatic ganglia or the blood-dyscrasia, it is not often the source of pulmonary embolism (9 cases out of 160 of all kinds, according to Luzzato). A probable explanation of this fact is that the fibrinous coagulum does not form in the veins until a late period of the disease, and death results before it has had time to soften and disintegrate.24
18 Am. Journ. Med. Sci., Oct., 1876.
19 Hayden, Case 124, p. 1030.
20 Lancet, Nov. 24, 1876.
21 At times septic material is introduced into the blood and absorbed from disintegration of a clot. Hence arise typhoid or pyæmic symptoms.
22 Reports of Pathol. Soc. of London, vol. xvi.
23 Op. cit., p. 1024.
24 Dict. de Méd. et de Chirurgie, vol. xxix. pp. 336, 337.
II. Surgical affections are frequently the efficient cause of pulmonary embolism. Thus, out of 160 cases of the latter disease collated by Luzzato, 66 owed their origin to conditions embraced in this division. Wounds, contusions, compressions, diseases of, and all surgical operations upon, the veins are specially liable to be followed by pulmonary embolism. Sometimes the thrombus formed originally in the implicated vein takes place there spontaneously; sometimes it is the direct consequence of a localized phlebitis. Several times the injection of tincture of iron into varicose veins of the inferior extremity25 or into a nævus26 has been the occasion of symptoms indicating sudden obstruction of the pulmonary artery; again, it is an accident, more frequent than is generally admitted, of the operation of transfusion (Vulpian). According to Le Dentu,27 the varicose veins tend to cause stasis of the blood, and thus to favor coagulation. They are, therefore, a predisposing cause of the formation of thrombi, and hence of pulmonary embolism. Extensive burns and frostbite are also efficient causes of venous thrombus, and after this manner predispose to pulmonary embolism. The separation of the placenta after delivery leaves an open condition of the uterine sinuses which is a real traumatism, and which occasions the formation of sanguineous coagula. The irritation of the sinuses may extend to the large extra-uterine veins (iliacs), and lead to further deposits of fibrin which may give rise to pulmonary embolism. In these latter cases the inflammation of the veins, if it occurs, is apt to follow the formation of the coagulum. Cases of pulmonary embolism have sometimes been occasioned by the compression of the lower extremities with Esmarch's elastic bandage.28 Massari indeed cautions his readers against the use of elastic bandages for varicose subjects. Even if their use be deemed advisable, never should the limbs be permitted to remain bandaged during several consecutive hours, for fear lest fibrinous clots be formed. Azam cites a case of cyst into which an injection of iodine was made, and quickly followed by obliteration of the pulmonary artery. Hélie (1837), Gütterbock, and Marjolin (1837) have each related a case of pulmonary embolism following a sprain. The most frequent cause, in this division, of pulmonary embolism is without question fractures. The first case reported is probably one by Virchow in 1846 of an extra-capsular fracture of the thigh which led to a fatal termination by a pulmonary embolism.29 Sixteen years later (1862) a second fact of pulmonary embolism following upon a fracture was communicated to the Institute by Velpeau.30 In 1864, Azam31 read two memoirs—the first before the French Academy of Medicine, the second before the Congress of Bordeaux—in which not only the relation of fractures, but all kinds of traumatisms, to pulmonary embolism was fully considered. In these two articles several illustrative cases were recorded as being seen by Gosselin, Richet, and Labat. In the following years several articles of value appeared on the subject of emboli and of their relations with contusions and fractures. Among authors we should cite the names of Bertin (1868), Durodié (1874), and Besson (1878) as workers in this direction. It has been noted not only that the fractures amongst traumatisms cause a large proportion of cases of pulmonary embolism (16 times in 30 cases), but also that the number of instances of fracture of the leg largely predominate (11 cases).32 The explanation given to the latter circumstance is in part the near proximity of the bones with large veins (Verneuil), and second the dilatation of the veins themselves (Le Dentu). Occasionally the embolism of the pulmonary artery has consisted mainly of fat: in one instance there was fracture of the thigh consequent upon a fall;33 in the other the patient was suffering from a gunshot wound of the left knee.34 In both specimens examined after death under the microscope fatty matter was found in the capillaries and pulmonary arteries. It was probable that the fat had been transported by the veins—in part from the lacerated marrow, in part from the subcutaneous adipose tissue.
25 Soc. Méd. Bordeaux, 15 Nov., 1867.
26 Annales d'Oculistique, 1864.
27 Discussion à la Soc. de Chirurgie, 14 Avril, 1875.
28 Annali Universali di Medicina, Milano, May, 1877; Wiener Med. Woch., 1875, No. 48, quoted from Dr. Dobell's report on Diseases of the Chest, vols. ii. and iii.
29 Traube's Beiträge sur experimentalen Path. und Phys., 1846, Heft 551, quoted by Levrat.
30 Comptes rend. de l'Académie des Sci., 7 et 14 Avril, 1862.
31 Gaz. hébd. de Méd. et Chirurg., 1864.
32 Levrat, Des Embolies veineuses d'Origine traumatique, p. 54, Paris, 1880.
33 Hesch, Anzeiger d. K. K. Gesellschaft der Aerzte in Wien, 1876, No. 3, quoted in Dobell's Reports, vol. cxi., 1877.
34 Dorpater Medicin. Zeitschrift, Bd. vi., Heft iii. and iv., 1877, pp. 326–338, cited by Dobell.
III. The puerperal state has been considered by Behier, Dubreuilh, and others with some degree of reason as one closely resembling a condition of traumatism. In fact, the raw surface with widely-open uterine veins and sinuses which exists so soon as the placenta is fairly separated is analogous to that of a limb which has just been amputated. The differences which present themselves are those which arise from the special state of the patient herself. During gestation, and particularly toward its terminal period, the relative quantity of fibrin to the mass of the blood is greatly augmented. According to Andral and Gavarret, this excess of fibrin may become so great as to reach a third more than the normal quantity. After delivery of the foetus and placenta involution of the uterus begins. This process lasts several weeks, and during this period the blood is filled with effete material. Besides these favoring causes of thrombosis which are special to the puerperal state and mark its blood-dyscrasia, we have the fact of loss of blood, both during and after confinement, as an efficient and well-known cause of this accident. According to Leishman,35 who cites Merriam, this is doubtless the reason why after placenta prævia cases of phlegmasia alba dolens are so frequently observed. Not only does Richardson consider the loss of blood as predisposing toward pulmonary thrombosis, but also syncope or exhaustion in other depressed states of the system. In some such instances, however, we must not ignore possible disease of the myocardium or compression from an abscess of the broad ligament (Charcot and Ball). The coagula formed in the femoral or saphena veins may sometimes extend into the iliacs, venæ cavæ, and become a frequent source of pulmonary embolism. Owing to the rapid softening of clots formed in the uterine veins during septic endometritis, we have a special cause of pulmonary embolism accompanied by toxic phenomena (Virchow). Several of the operations necessary in certain complications of this condition, such as application of the forceps, detachment of the placenta, etc., have been followed by pulmonary embolism (Massari). It is not remarkable that with so many predisposing causes of thrombosis blood-clot should be of frequent formation in the puerperal state.
35 System of Obstetrics, p. 710.
Phlegmasia and pulmonary embolism have been well studied on account of their gravity; the other situations of fibrinous deposit are very imperfectly known. Playfair36 believes that clots may form in the right heart and pulmonary artery, just as they may be produced in other portions of the venous system and under the influence of the same causes. This conviction is opposed to that of Virchow and Bertin,37 who hold that an embolus must be the starting-point of a blood-clot, and that without its presence it cannot form. Virchow, indeed, considers stagnation of the blood as the most essential condition of the formation of a coagulum. It would seem, however, that the action of the heart is so feeble in certain debilitated persons, or in diseases in which there is strong tendency to adynamia, that this objection is at least partially met. Certainly, as Humphrey38 has shown, the pulmonary artery, owing to its numerous divisions and the prominent angles it offers, is favorable to coagulation by its anatomical formation. Moreover, if coagulation may form around an embolus, why cannot similar causes which bring this about also occasion a spontaneous deposit of fibrin? The greater number of cases of pulmonary embolism in the puerperal state occur in young women not many days after confinement (Hennig, Luzzato). Occasionally a case is seen as late as the fifth week. Cases also occur, though exceptionally, during pregnancy. Playfair39 has endeavored to show, partly by post-mortem appearances, partly by the date of the accidents, the distinctions to be drawn between pulmonary embolism and pulmonary thrombosis. After the nineteenth day from the date of delivery the accidents are usually due to embolism, before this date to thrombosis. This would appear to be rationally explained when we consider that the degenerative changes which alter the vascular clot sufficiently to permit its transport from the place of its formation to a distant organ take a certain time to become effected. The causes of the pulmonary thrombosis are those which produce coagulation elsewhere in the vascular circuit during the puerperal state. Pulmonary embolisms are more frequent with women than men on account of affections of the uterus and the puerperal condition (80 to 66, Luzzato). In children pulmonary embolisms generally come from clots first formed in some one of the peripheral veins (renal, umbilical, diploe, etc.). Autochthonous clots in the pulmonary artery may be due to direct pressure from enlarged ganglia of the neck. The great number of pulmonary embolisms form in the vessels of the lower extremities. Thus far, thrombi have not been shown in the larger lymphatic trunks of the body.
36 "The Puerperal State," being Part V. from a Treatise on Midwifery, p. 50, Philada., 1882.
37 Des Embolies.
38 On the Coagulation of the Blood in the Venous System during Life, quoted by Playfair.
39 Lancet, 1867.
SYMPTOMATOLOGY.—The symptoms thus far observed of pulmonary embolism are not usually very full or accurate. Many of the cases occur so suddenly and fill the beholders with such dismay that clinical observations are imperfect. Opposed to this statement we note the fact that what pertains to pathology and morbid anatomy of pulmonary embolism is particularly complete. Nevertheless, for the sake of clearness and in view of accidents really observed, we may divide the cases into—1st, sudden, fatal form; 2d, grave form; 3d, benign form.
1st. Sudden, Fatal Form.—In this category should be placed those instances in which the main trunk or both primary divisions of the pulmonary artery have become wholly obstructed in a sudden, almost instantaneous, manner. Immediately the patient is a prey to the most intense dyspnoea and anxiety; the chest-walls rise and fall in an exaggerated degree and with great rapidity; the heart-pulsations are tumultuous and irregular; there is intense pallor of the face; a groan or cry is heard; there is a vain and brief struggle for breath; and death may occur before aid can be offered, with symptoms resembling those of asphyxia. These rapidly fatal accidents are always deeply impressive, but never so appalling as when they take place in convalescence, when everything appears to be going on well, and there is no reason to apprehend such an occurrence had not numerous recorded facts affirmed their verity. Such cases have been observed40 particularly after fractures of the lower extremities and during recovery after confinement.41 The accidents are not always asphyxic in character, even though they be equally sudden and destructive. According to Trousseau,42 this is true where the embolus is arrested in the right ventricle and is of sufficient size to cause stoppage of cardiac contractions and an attack of fatal syncope. In instances which are not mortal in a few moments, and where the gasping and struggling for breath continue during half an hour, an hour, or more, the excessive pallor gives way to a deeply cyanosed tint of the face. When the face assumes a livid purple hue it has been considered as proof of a condition of spontaneous thrombosis rather than embolism.43
40 Azam, 1re Mémoire, Gaz. hébd. de Méd. et Chirurgie, 1864; Observ. II., reported by Levrat.
41 British Medical Journal, March 27, 1869.
42 Clinique méd., t. iii. p. 715.
43 Such a case is reported by Playfair in Part V. of his Treatise on Midwifery, and is also recorded in Obst. Trans., vol. xii. p. 194.
Although the heart-beats are vigorous at first, they soon become weak, intermittent, and irregular. Similar characters may be noted in the pulse, which is very soon compressible, thready, and at times almost imperceptible. These latter conditions of the cardiac movements may exist from the beginning of the accidents, and may be accompanied by coldness of the extremities and chilly sensations (Cohn). Frequently we observe convulsive movements and foam at the mouth just before death. When these symptoms have been remarked, the question has been raised as to whether the patient was suffering from an epileptic seizure.44 The first impressive effects of pulmonary embolism undoubtedly attach themselves to the respiration and circulation. The nervous system is not always so visibly affected. Frequently the patients preserve complete mastery of their intelligence to the end, and cry out in no doubtful accents, "I am stifling! I am dying!" Occasionally they even point with their fingers to the exact seat of the sudden obstruction in the chest. In a case of Vidal45 the peculiar and painful sensations indicated by the patient in the precise location of the embolus had considerable diagnostic importance. This indication, however, is not always valuable, and may be misleading, as in the case reported by Ormerod, when the patient, a young girl, paraplegic, was attacked suddenly with intense feelings of suffocation and pointed to the throat as being the seat of the obstruction.46 Frequently these suddenly fatal cases occur in the course of an acute or chronic disorder, and usually the terrible phenomena manifest themselves after some movement or effort, as one makes in sitting up in bed or reaching for a desired object. Under these latter circumstances sudden pallor may overspread the features, the heart cease to beat, and the patient expire in a true syncopal attack, without any of the asphyxic appearance previously referred to. Usually, however, the need of air is most acutely felt, the muscles of the neck and thorax are violently contracted, whilst the patient suffers from intense anxiety and oppression. Meanwhile, air enters the lungs freely with each successive inspiration. Percussion and auscultation of the chest do not reveal any notable change in the pulmonary structure, and the peculiar asphyxia which is present results rather from the want of blood to be oxygenated than from the lack of air or sanguineous stagnation. Indeed, Lancereaux affirms that death in all cases of fatal pulmonary embolism follows upon these progressive asphyxic features. Never, according to him, does it occur from a real attack of syncope.47
44 Picot, Les grands Processus morbides, 1876.
45 Ball, Des Embolies pulmonaires, Observ. xxvii., Thèse, Paris, 1862.
46 London Med. Gazette, vol. ix. p. 788, quoted by Hayden, p. 1029.
47 "Comptes rendus de la Société de Biologie," 1861, Dict. de Méd. et de Chirurgie, vol. xxix. p. 365.
The immediate cause of death in these cases is differently regarded by eminent authorities. Virchow48 holds that the heart-beats suddenly stop and death is caused by syncope. Picot and Panum claim that inasmuch as the left heart does not receive any blood from the lungs, the brain cannot be supplied, and thus anæmia of the brain becomes the immediate source of a fatal termination. True it is that owing to the complete obstruction of the pulmonary trunk or its bifurcation no blood can reach the brain, but for a similar reason the coronary arteries cannot be supplied, and indeed the whole arterial system remains empty, whilst the surface of the body becomes livid, owing to marked venous distension. Paget holds to a conservative view, believing that death results at times from anæmia and on other occasions from syncope. It is the belief of the writer that most of the phenomena preceding death are in the majority of cases those of asphyxia, and he recognizes with Bertin49 and Lancereaux that deficient oxygenation of blood is, after all, the essential cause of death. In all cases of very rapid death, Lancereaux believes that the embolic clot must have originated in, and been transported from, one of the large veins of the lower extremities or the pelvis, and that the prolongation of clots formed elsewhere in the venous system, when broken off and carried in the blood-current, are insufficient by reason of their small size to block up completely the pulmonary artery.50
48 Gesamm., Abhandl., 1862, p. 316, quoted by Playfair.
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.
56 Thèse, Paris, 1880.
It has been noted that secondary changes of capillary embolisms are not apt to occur in the anæmic and cachectic; in the plethoric and those affected with chronic cardiac disorders the contrary is true. According to the condition of the nervous system, to its greater or less tendency to react, there will be more or fewer chances of the capillary embolisms making their existence known by an attack of suffocation (Luzzato).
PATHOLOGY AND MORBID ANATOMY.—Pulmonary embolism gives rise to different morbid lesions. The nature of these and their extent depend in great measure upon the size, situation, and character of the plug which fills the main trunk of the pulmonary artery or one or more of its divisions. The changes of tissue which take place are of course in close relationship with the length of time which has elapsed since the embolus first migrated. They are also influenced greatly by accidents or complications which have arisen. It shall be our effort first to narrate the important considerations which pertain to simple embolus, and whether it affect a large artery or only a small vessel. After speaking of the simple variety we will refer briefly to septic and fatty emboli and also to those of other nature.
The pulmonary artery may be blocked up by a clot formed in situ. This fact has been shown to be true by many writers—i.e. Lancereaux, Duguet, etc. When a thrombus is present it may be occasioned by an inflammatory condition of the artery (rare), or by a dyscrasic blood-condition, or again by localized compression in the vicinity of the coagulum, as from a tumor. We may find arterial thrombosis during pulmonary phthisis, in pneumonia, in pleurisy, and in cases of cardiac dilatation or degeneration.57 Endocarditis of the pulmonary valve and compression of the neck by enlarged ganglia have been mentioned as causes of these thrombi.
57 Here it is due to relative stasis of the blood.
Ordinarily, a pulmonary embolus is fixed at the point of division of the main vascular trunk. It more or less completely blocks up the calibre of the artery, and is usually situated in the midst of a soft new clot, which also covers it in front and behind. The embolus often manifests its origin from a clot contained in one of the large veins of the lower extremities. One end is rough and excavated, and fits into the coagulum we find lodged there. It is often twisted like a corkscrew, or has on its surface the mark of the valves of the vein from which it has migrated. It is white or yellow in color. If we examine the interior of an ordinary autochthonous clot, we find it softer relatively than the clot of an embolus, and, moreover, no prolongations proceed from it which fail to correspond with any vascular division. The suddenness of the accidents and the disappearance of a previous peripheric clot are strong reasons in favor of the existence of the embolus.
More emboli are carried into the right lung than into the left, on account of the larger size of the artery. The median and lower lobes are also the ones most usually affected. When the right lung is diseased the emboli are then more frequently transported on the left side. After a time an embolus goes through certain transformations. It softens at its centre, owing to degeneration of the white blood-corpuscles. The hematies disappear soon, and the fibrin also changes in structure, becoming soft and granular. This softening at the centre of the embolus must not be confounded with a purulent change which affects certain thrombi which come from or are carried to a focus of suppuration. Whenever an embolus has been a long while in the artery, a neo-membrane forms between it and the arterial wall. This neo-membrane is mainly constituted by fibrillous tissue and here and there some developed vascular twigs. As a whole, it forms a sort of cap or covering for the embolus, and finally it takes up by absorption the granular detritus which forms in the interior of the clot. We perceive from the foregoing statement that a pulmonary embolism may heal, and that the process of its cure differs in no respect from what occurs in the case of a coagulum which disappears by absorption from some other portion of the vascular system, or indeed from the surface of the serous membrane. When the embolic plug comes from a focus of suppuration or gangrene the vascular walls will probably be affected with similar alterations.
In consequence of the obstruction of the main trunk, or of the important branches of the pulmonary artery by embolic plugs, certain effects are directly produced. These are—1st, mechanical; 2d, nutritive; 3d, irritative.
Perhaps, however, before describing these effects in detail it would be well to mention certain anatomical facts with respect of the circulation of the lung which have considerable importance in view of certain morbid lesions to which we shall refer presently. It has now been proven experimentally, by the researches of Cohnheim, Litten, and Küttner, that there are no vascular communications between the pulmonary and bronchial arteries, and, further, that there are no branches coming off from the small divisions of the pulmonary artery by which a collateral circulation can be carried on when the arteries of the third order are obstructed by embolic plugs. It is also further corroborated by the investigations of the authors named that the pulmonary artery is mainly instrumental in keeping up the function of the lungs, whilst the bronchial artery is the artery of nutrition. If the latter were obstructed in any manner, gangrene of the pulmonary structure must surely follow; if the latter be ever so thoroughly closed, no death of tissue will ever result.
The mechanical effects caused by the obstruction of the main artery or of a primary division of it are much less considerable than when a smaller artery is plugged. In the first case the only observable condition is that of anæmia of pulmonary tissue. Occasionally Lancereaux has noticed atelectasis of certain lobules. The pathogeny of this condition is difficult to explain, as air enters the bronchi freely, and it should not be produced without effusion taking place. If life lasts a few hours hyperæmia and oedema of lung-tissue may be caused. The latter conditions are aided if there be existing organic disease of the heart. If, now, the smaller arteries be obstructed by embolic plugs, there is a strong tendency to the formation of hemorrhagic effusions, to which the name infarctus has been very properly given by Virchow. These infarctions vary in size from that of a small nut to that of a pullet's egg, just as they implicate one or more pulmonary lobules. They are situated at the periphery of the lung underneath the pleura. They are conoid in shape, with the apex turned toward the root of the lung. They seem like hard nuts under the surface of the lung when felt with the fingers. Their color is dark-brown or black; their cut surface is granular, even more so than the surface of a lobule solidified by broncho-pneumonia. The capillaries in and around these masses are filled with red blood-corpuscles. The same is true also of the alveoli, in which we find degenerated epithelial cells in large numbers containing granules of pigment. The connective tissue about the alveoli becomes thickened, the alveolar cavities contract, and finally the infarctions are changed into a real fibrous cicatrix, in the same way as they are transformed in other viscera of the body. Prior to this stage, however, we notice that the color of the infarction has gradually changed, and that it has become pale and yellow. This is due to the fatty degeneration of the fibrin contained in the alveoli, and the same affection of the enclosed cells. May any infarctions be restored to a condition of perfect integrity? It is more than doubtful, even if the obstructing plug of the pulmonary artery disappeared very soon, because the pulmonary parenchyma beyond the clot has suffered so much from fatty changes and hemorrhage that the vessels are unequal to their function. At times, owing to the stoppage of the nutritive action of the bronchial artery, the infarction may become a cheesy mass, which soon softens and is expectorated. This leaves a cavernous opening in the lungs. Sometimes the infarction becomes infiltrated with calcareous salts. It cannot be confounded readily with other lesions, especially pulmonary apoplexy, on account of its distinct limitations. Sometimes a lobule affected with broncho-pneumonia and hemorrhage may simulate it closely. The pathogeny or mode of production of the hemorrhage in a more or less limited area of the lung which is concomitant with an embolic plug in one of the branches of the pulmonary artery is difficult to present. This fact may be explained by the different solutions afforded by various authors as to the manner in which the apoplectic condition and the embolus are correlated. Certain writers have affirmed that the embolus itself is but a secondary phenomenon, and the surrounding hyperæmic state is the real cause of its production (Laennec). Later authorities have established that this statement is rarely true, and that the embolus always occurs first and the localized congestion follows closely afterward.
Precisely the way in which the congestion or hemorrhage was occasioned has not been elucidated in a similar manner by all. Virchow years ago (1856) recognized that one or other was due to vascular stasis and reflux of venous blood from neighboring vessels; in other words, the explanation here given was the same as for infarctus of the kidney or spleen. Jürgensen regards infarctus as being similar in structure to lobular pneumonia. It has been also affirmed that owing to incomplete obstruction tissue supplied by the artery was at first anæmiated, and later, by reason of excess of backward pressure from venous trunks, it became congested or hemorrhage was effected. Duguet states that the arterial walls beyond the embolic plug become inflamed, and thus act as a cause of hemorrhage. The first effect, then, of an embolic clot being arrested in the lung is that of anæmia. Soon this state is followed by hemorrhage occasioned in the way I have mentioned. In the lung the hemorrhage means of necessity rupture of a vessel; in the spleen and brain this is not so invariable. Whilst the smaller bronchi are sometimes congested, they are rarely infiltrated with blood. For this reason gangrene is not a frequent sequela of pulmonary infarctus. It is not admissible that hemorrhage should occur without rupture of the vessel in many instances, for the reason that the sanguineous effusion is not always limited to the area supplied by a given vascular division obstructed, nor is it in the centre of the lung conoid in shape. The catarrhal changes in the lungs are very constant, although usually superficial in character and only affecting the epithelium. As Cohnheim58 has pointed out, there is a proneness to degeneration rather than to inflammatory action.
58 Untersuchungen über die Embolischen Processe, Berlin, 1872.
Due consideration being given to the changes of tissue effected by an arrested embolus, we can more fully understand the clinical phenomena connected with them. True it is, however, that the troubles of innervation and respiration thus brought on may pass unperceived, and for the simple reason that the pathological lesion follows, as a rule, only the transport of an embolus into a small arterial division. In a similar way the intensity of the venous reflux is in direct relationship with the functions of the heart and lungs, and if either the diseased hemorrhagic effusion is rendered more certain.
It is probable that a simple embolus cannot be followed by a gangrenous focus in the lung. This result is recognized frequently when the embolus originates in a purulent deposit, whether it be the consequence of an abscess, of puerperal fever,59 of a compound fracture, etc. The gangrenous cavity finally softens, its contents are expectorated, and the pulmonary tissue becomes indurated and cicatrizes around the excavation.
59 Dublin Journ. of Med. Science, May, 1875.
Pulmonary embolism may at times be the occasion of a pneumonic consolidation limited to the area of distribution of an obstructed pulmonary division. Sometimes the consolidation extends beyond this limit, and is seemingly the immediate effect of neighboring irritation. When the consolidation exists near the surface of the lung, it may extend to the pleura, producing considerable effusion and pseudo-membranous deposit upon the visceral layer. Both sides of the chest may occasionally be thus affected.
Capillary emboli of simple nature have long been described. Unless they obstruct a great many vessels simultaneously, they rarely cause death (Feltz). They do not, moreover, produce hemorrhages or infarctus, inasmuch as a collateral circulation is so easily established. The principal sources of these emboli exist outside of the vascular system, and in this variety we find emboli of air, fat, of the débris of new growths, etc.
Since 1866, the period at which Zenker first directed attention to fatty emboli in the pulmonary capillaries as a complication of an accident in which a patient was crushed between two wagons, many observers have noted accidents due to these obstructing bodies. Fatty emboli may follow numerous causes (contusions, suppurations, osteomyelitis, etc.), but are more frequent and fatal after comminuted fractures of the limbs than from any other single cause (Flournoy).
Occasionally the patient will have recovered from the shock following the fracture, when he is suddenly attacked with intense dyspnoea and expires within a few hours. The only effectual remedy would seem to be immediate amputation of the limb above the seat of the fracture. When the vessels of the lungs have been examined in these instances, they have been found to contain elongated masses, several millimeters in length, possessing a particular brilliancy, "disappearing under the action of ether, and becoming a deep, black color with osmic acid."60
60 Déjerine, Le Progrès médical; Med. Record, Jan. 15, 1879.
Specific emboli may be followed by the mechanical effects of simple emboli, but they are also accompanied by specific phenomena which are in relation with the particular focus in which they took origin—i.e. purulent or septic focus, gangrenous cavity, cancerous tumor, etc.
In the region where the embolus is arrested, local alterations of tissue become developed which correspond with the nature of the changes which exist in the spot from which the embolus was derived. Very often these morbid effects are produced without any mechanical results of emboli being occasioned.
Septic emboli are observed in infectious diseases, such as pyæmia and puerperal fever, and are prone to occasion not merely mechanical effects, but equally the suppuration, liquefaction, and finally the absolute destruction of tissue. Cruveilhier has seen pulmonary embolism followed by metastatic abscesses. The formation of these was attributed by him to suppurative phlebitis affecting the capillaries.61
61 Dict. de Méd. et de Chirurgie pratique, vol. xxix. p. 360.
It is admitted to-day that infectious germs causing metastatic abscesses may be transported in the pulmonary vessels without being accompanied by pulmonary emboli. It is equally true, however, that the usual means of transport for these infectious bacteria or micrococci is an embolic plug (Jeannel).
The effects produced by the septic emboli are pneumonic consolidations involving the lobules and going on rapidly to suppuration, and sometimes to gangrene. The coloration of the lobules is red, gray, tending toward yellow as the tissue shows signs of softening. The contents of the abscess are yellow or brown and contain particles of the pulmonary structure. The tissue in the vicinity is gray and infiltrated with pus.
The number of metastatic abscesses is often very considerable. Their size is usually smaller than the infarctus due to simple emboli. The smaller abscesses are found usually near the surface of the lung. When several abscesses unite into one they may attain the size of the fist.
Whenever there exists a gangrenous lesion in some portion of the body, sphacelated débris may be carried from this focus into the venous system, and finally into the lungs. Arrested in some spot of the pulmonary tissue, the embolus will give rise to gangrenous changes similar to those of the region from which it started.62 The infarctus thus produced will assume a dark color, then become gray toward the centre, where it shows signs of softening. Later, under the form of a thick semi-fluid mixture of extreme fetid odor and dark-brownish color, it is expectorated by degrees, and leaves behind a gangrenous cavity. The process of change in this case is due to the proliferation of infectious germs. It may be, however, that the gangrenous particles transported into the lungs have the power in themselves to decompose the tissues by chemical action into more simple elements.63 According to the later researches of Doleris, septic bacteria have been found by him in these putrid infarctions.64
62 This process was first pointed out by Cruveilhier in his work on Phlebitis. It remained, however, for Virchow in his Cellular Pathology (p. 235, ed. Strauss), and later for Billroth in his Surgical Pathology, 1868, p. 395, to give greater development to this belief.
63 Lancereaux, Traité d'Anatomie pathologique, vol. i., 1875–77, p. 14 et seq.
64 Quoted by Levrat, p. 78.
The infecting power of cancer is certainly not equal to that of gangrene. Nevertheless, Lancereaux has shown that cancerous nodules may be produced by metastasis. This belief in the possibility of a simple embolus taking on a cancerous change, and carrying this disease to far-removed parts, has been strongly combated by Cohn. Neither experimental nor human pathology has thus far decided the subject in an absolute manner. Certain it is, however, that the power of emboli from cancerous foci to carry similar disease elsewhere depends partly upon the vitality of the cancerous particles, partly upon the power of receptivity as shown by certain constitutions for developing special diseases, and which relates, after all, to the general question of dyscrasia. Langenbeck has shown that certain animals will die within a few hours after the injection of cancerous juice. On the other hand, it is known that the infective power of the juice only lasts a very brief period. Weber, Luzzato, and others have reported numerous examples of secondary tumors of similar nature developed in the lungs when epithelioma, enchondroma, sarcoma, or carcinoma existed somewhere in the body. Finally, it would appear that emboli containing hydatids in embryo have been the means of transporting these parasites into the pulmonary structure.
DIAGNOSIS.—The sudden commencement of the accidents, especially when a peripheral thrombus has existed previously in one of the large veins of the extremities, renders the diagnosis almost certain. If the patient has been suffering from the effects of a traumatism (contusion, fractures, operation on the veins of the limbs or rectum, etc.), and is almost instantaneously attacked with intense dyspnoea and a feeling of anguish which he refers to the thoracic region, we shall be able usually to eliminate other intercurrent affections and to diagnosticate the existence of pulmonary embolism.
This accident is often confounded with cardiac thrombosis. It may usually be separated from it by the following differential symptoms: Cardiac obstruction from a clot usually comes on insidiously, by degrees; the heart-beats are irregular, tumultuous, muffled, and distant; there may be a murmur from one or other of the cardiac orifices; there is no initial chill; peripheral thrombosis is not present as a rule; there is no sensation of localized obstruction in the chest.
In pulmonary embolism the début may be instantaneous and death follow in a few seconds; or, again, the beginning may be rapid, ushered in by stifling in the chest, a chill, cyanosed face, followed soon by excessive pallor, a distinct sensation of obstacle to breathing in a particular region. Percussion and auscultation may remain negative. The patient may have a succession of similar accidents, and yet finally recover. According to Ball, pulmonary embolism and pulmonary thrombosis cannot be distinguished during life. In one case which he reports where pulmonary embolism should have been present without question the autopsy showed the presence of a thrombus in the pulmonary artery. A succession of chills, general malaise, febrile excitement, the localized phenomena of pneumonia or gangrene of the lung, point indubitably to the existence of septic emboli.
The differential diagnosis between pulmonary embolism and other affections, such as angina pectoris, a foreign body in the air-passages, pneumothorax, etc., may usually be reached without much difficulty. Sometimes the paroxysmal dyspnoea with sensations of great oppression which accompanies mitral stenosis may be mistaken for pulmonary embolism. In these instances the absence of a discoverable cause of the attack in pre-existing emboli, and the presystolic murmur with marked general anæmia, may surely lead to an accurate diagnosis. It must, however, always be remembered that in mitral stenosis it is not infrequent to have cardiac coagula formed in the right auricle, which may become detached and give rise to pulmonary emboli. Under these circumstances a severe localized pain in the side of the chest has considerable diagnostic importance as pointing to the presence of a pulmonary embolus (Cohn).
When there is pre-existing cardiac disease of organic nature a syncopal attack may sometimes occasion doubt with respect of a correct diagnosis. The sudden loss of consciousness, excessive pallor, and absence of pulse will ordinarily, however, confirm the diagnosis of syncope. Rupture of the heart is accompanied with symptoms of syncope rather than those of suffocation (Balzer). Emboli of the bronchial arteries are not accompanied by any characteristic symptoms which will enable us to make a differential diagnosis. There is the same sudden dyspnoea, the initial chill and hæmoptysis, as in pulmonary embolism (Penzold).
PROGNOSIS.—As will be readily understood, the prognosis is sometimes difficult to estimate and varies with many circumstances. Certain emboli, even among those which have occasioned severe symptoms, have never been recognized. Other pulmonary emboli always remain comparatively latent. In this connection we should mention those which take place in the lungs of tuberculous patients. Again, the size and seat of the embolus will always have great importance in regard to the prognosis. If the trunk or primary divisions of the pulmonary artery be suddenly and completely obstructed by emboli, sudden death will surely follow. If secondary divisions of the pulmonary artery are filled up, more or less grave symptoms will usually follow. When emboli are carried into the tertiary or still smaller branches of the artery, they may not occasion any appreciable phenomena other than a moderate and passing dyspnoea. If, however, there be a large number of small emboli carried into both lungs at the same time, it is possible that rapid death may follow their presence. It is true, however, according to certain authors, that even a large embolus blocking up the main trunk of the pulmonary artery may be followed by recovery. Such a case is that of Jacquemier, reported by Ball. Even in this case, whilst the presence of the embolus cannot perhaps be doubted, still the exact size and location may be called in question. And here we may add that in all cases of reported cure of this nature there will naturally and inevitably exist an atmosphere of legitimate doubt about the correct observations and diagnosis of the narrated facts.
What precedes relates exclusively to the existence of simple emboli. Of course if the embolus be of septic origin, it will be followed by the appearance in the lungs of foci of purulent pneumonia or of gangrenous changes of tissue which will finally produce such structural destruction as almost certainly to terminate in death.
TREATMENT.—The majority of those who have studied this subject have recognized how vain are our efforts of treatment in many instances. Pulmonary embolism is one of those accidents which we should always be prepared to admit, however, when its characteristic symptoms show themselves, and should endeavor rationally to combat by the therapeutic means in our power. Even before we have any signs present which indicate obstruction of the pulmonary circulation, we may have those which point in a very certain manner to the existence of a peripheral thrombus. This thrombus may block up completely one of the large veins of the lower extremities, and may, owing to its possible detachment and transport, be a constant menace to life. At times these peripheral thrombi are accompanied by local inflammatory symptoms which belong to phlebitis. This condition of things is not uncommon after fractures or other traumatisms. Frequently there is no evidence of any inflammatory state, and we recognize the thrombus solely by the signs which result directly from obstructed venous circulation and by the existence of a hard, indurated cord which fills the vein at a given level. Now, what are the means we have at our command to prevent the transport of this coagulum, or indeed to dissolve it, or absorb it in its place?
First, if inflammatory signs are present we should endeavor to subdue these by local applications of an emollient character, for the reason that excessive inflammation is apt to produce such changes as cause the disaggregation of the clot, and hence its detachment. In either case, whether there be or be not any local inflammatory condition, we should insist upon absolute repose and quiet. We should not permit the limb to be moved: we should be extremely careful in all our manipulations of it, and only employ those which are absolutely essential. The patient should not be permitted to raise himself in bed, nor even eat or drink without assistance. These counsels are very important, since we know how frequently a very slight movement or exertion has been followed immediately by the transport of the clot, pulmonary embolism, and sudden death. In cases of fractures or severe wounds where such a peripheral clot is discovered the surgeon should be particularly careful in applying bandages and retentive apparatus. The risk of displacement of the clot is greater after several days from the time of the fracture or wound than it is at first, and it is at this period that the most careful attention should be exercised. Instances are on record in which so late as the fifty-seventh day after a fracture of the lower extremity a peripheral thrombus was transported from its original site and caused a fatal termination (Bouchard).
Some eminent writers have thought by employing a suitable medication we might hasten the solution of the peripheral thrombi and thus prevent their migration. With this view Legroux has given the acetate of lead internally and applied it in solution over the seat of the thrombus. Richardson has vaunted the use of the carbonate of ammonium in large and frequently-repeated doses as a solvent of the fibrin. By its means he believes he prevents the fibrin from precipitating from the blood, and further helps it to resorb when it has already become solid. Prevost, Dumas, and Schutzenberger recommend specially the bicarbonate of sodium, taken internally, with a view of rendering the blood more fluid and also hastening the retrogressive changes in the clot by its oxidizing power. According to Boyer, the very object which is thus sought if it were accomplished would result injuriously to the patient, since it would favor the detachment of the clot. Further, the continued use of large and frequent doses of ammonia or soda is prone to lower the general system very much, and in this manner to act to the prejudice of the patient. According to Azam, it would appear that what we most desire to effect is the organization and adhesion of the thrombus to the walls of the vessel. This can best be accomplished by fortifying the patient in every possible way and raising his nutrition to the highest attainable point. Iron, cinchona, the most nutritious food, should be freely given. Further, the greatest attention should be paid to the hygienic surroundings. The air should be purified, and if by chance the patient is suffering from a wound close attention should be given to the renewal of the dressings and the employment of a disinfectant locally applied. One of the reasons for this last counsel is because if the thrombus were detached it is important that it should be free of any septic taint and not lead to specific accidents (purulent pneumonia, gangrenous abscess). In the above enumeration we include the means usually to be employed as preventive measures against the migration of clots.
Is there any other method which can be adopted with any chance of success? Of the surgical attempts we should mention favorably in certain cases, and especially in those where the affected vein is superficial, the adoption of persistent compression between the clot and the heart. This means has been alluded to by J. Hunter65 as far back as 1773. Ligature and section of the vein have also been supported by some writers as suitable operations to bring into use with a like intent. Unfortunately, we are obliged to make a second traumatism in order to carry out this object, and, further, we make by the ligature at least a second coagulation, which may be the origin of the very accident we seek to avoid. Nevertheless, J. Teissier66 of Lyons reports a case observed by himself in the service of Noël Guéneau de Mussey, in which a ligature was instrumental in arresting the onward progress of the clot, which otherwise would have given rise to the accidents of pulmonary embolism.
65 Observations of the Inflammation of the Internal Coats of the Veins, quoted in thesis of Levrat, p. 108.
66 Nouveaux Éléments de Pathologie et de Clinique médicale, t. ii. p. 931, quoted by Balzer.
In the event of pulmonary embolism taking place in spite of all preventive means employed, what shall we do in order to combat this terrible accident? According to Ball,67 there are three indications to be observed: 1. To establish collateral circulation in the lungs; 2. To diminish local congestions; 3. To favor the resorption of the obstacle.
67 Thèse quoted, Paris, 1862.
The first indication cannot be effectually responded to, by reason of the fact that there is no way in which a collateral circulation can be promoted in the lung, owing to its anatomical structure.
The second indication is best observed by the application to the chest-walls of dry cups in large number, mustard poultices, turpentine, blisters. In this place we must consider the propriety of bleeding. As a result of the embolism there is arterial anæmia and venous plethora. This latter condition can be temporarily relieved by venesection. In this method, indeed, we have an immediate help for the distended and burdened heart, and we give time to the system to recuperate somewhat. We should, however, remember that bloodletting establishes a greater tendency in the system to the formation of emboli, and is therefore to be avoided. Moreover, sometimes it is decidedly objectionable on account of cardiac degeneration, anæmia, or great weakness.
When this method is contraindicated we should not hesitate to recur to the use of drastic purgatives (Jaccoud). Digitalis has been recommended, so as to regulate the cardiac action and to increase its power. Bertin has gone so far as to praise emetics and the use of the faradic current over the thoracic parietes. It seems as if these were dangerous methods to employ, since if a portion of the clot is still undetached the efforts caused by these agents would be apt to separate whatever portion remained in its original site. In order that a quantity of oxygen should be inhaled in a given time sufficient to supply the needs of the economy until a greater power of oxygenating the blood is established, the inhalation of compressed air has been vaunted. The objection to this means is merely the one which arises as we reflect how improbable it is that this agent would be at hand in a serviceable form when the sudden accidents of pulmonary embolism take place.
The third indication, to favor the resorption of the obstacle, must be virtually attended to by giving the alkalies in large doses internally. The advantages and objections to this sort of treatment we have already referred to.
After this exposition of the different means to be employed, both as preventive and curative agents of pulmonary embolism, we are obliged to recognize that very frequently they remain ineffectual. Usually the accident takes place in a very sudden manner and when we are least suspecting its advent. When the phenomena do occur which are caused by its presence, they take place so suddenly, and terminate fatally in such a brief period, that we scarcely have the time to employ the remedial agents referred to. Finally, we must admit that in presence of this complication, especially when there is complete obstruction of the trunk or primary divisions of the pulmonary artery, all our therapeutic means are without avail, and we are indeed almost powerless.