Chapter XXV: Part 25

So soon, however, as the coexistence of catarrhal pneumonia is established the gravity of the disease should be promptly recognized, and the closest attention should be paid to every detail of treatment. The condition of the sick-room as to temperature, ventilation, the absence of drafts, and the suitable moisture of the air must be even more carefully watched. The clothing of the child and the bed-covers must be adapted to the season, the weather, and the patient's habit and strength. It is certainly true that aggravations of the disease are often induced by apparently slight indiscretions in the above respects. It is rarely desirable to employ poultices. Unless skilfully made and dexterously applied, they fatigue by their weight; dangerous exposure is incurred in the frequent changing necessary; and, especially in the case of children, they do not keep their position well. A layer of cotton batting stitched inside of a merino shirt of suitable weight, upon the outside of which oiled silk may be stitched, forms an equally efficient and vastly more comfortable and convenient protection. This should be directed when the bronchitis assumes a severe type, or certainly as soon as pneumonia is suspected. It will not be necessary to change this for a week or ten days, unless copious sweating calls for its more frequent renewal. Among the advantages of this application must be reckoned the fact that it allows us to employ at any part of the chest, and as often as desired, local stimulants or counter-irritants, such as turpentine liniment, mustard plasters, or, what is one of the most valuable, the repeated application of tincture of iodine of suitable strength so as not to cause too severe irritation.

The next most important part of the treatment relates to the restoration and maintenance of the digestive function, which is so commonly disturbed in this disease. No one factor contributes more powerfully to produce vital {370} debility, which in turn rapidly increases the gravity of the lung disease by the failure of respiration and the development of collapse, than does gastro-intestinal disorder. Not only the diet, but the entire medication, must therefore be rendered subordinate to the conditions of the digestive tract. It has been seen that, at the onset of the attack, vomiting and diarrhoea are not rare symptoms, and that throughout the course of the disease the condition of the tongue, of the appetite, and of digestion often shows that a catarrhal process exists in the gastro-intestinal as well as in the bronchial mucous membrane. It is therefore frequently advisable for a day or two to avoid all remedies directed to the condition of the lung, and to address the treatment, dietetic and medicinal, solely to the state of the alimentary canal. Thus it will often be of service to employ minute doses of calomel and bicarbonate of soda or of Dover's powder, as in the following formulas, adapted for children of five years of age:

Rx. Hydrargyri chloridi mitis, gr. j;
Sodii bicarb. gr. xxiv;
M. et div. in Chart No. xij or No. xvj.

S. One every two or three hours until the bowels are moved once or twice.

Or, Rx. Hydrargyri chloridi mitis, gr. j;
Pulv. ipecac. composit. gr. x;
M. et div. in Chart No. xij or No. xvj.

S. One every three or four hours.

During this early stage of cases attended with marked gastro-intestinal irritation it may be desirable to use remedies to allay high fever, for which purpose fractional doses of tincture of aconite by the mouth and quinia by enema or suppository are efficient, while avoiding all risk of injuring the stomach. The diet at first should be carefully restricted: it is not at this time that prostration is to be feared, while by a thorough allaying of gastric irritation and by the establishment of fair digestion an ally of immense value for the later and more dangerous stages is secured. But at all periods of this disease the occurrence of vomiting or of diarrhoea should be the signal for instant revision of the diet and for the omission of any remedy, no matter how strongly indicated on other grounds, which could be regarded as the cause of the disturbance.

Milk, skimmed or whole; gruel, light broths, or beef-tea; junket, arrowroot, or similar light yet nourishing articles, are most suitable. Stimulants are frequently indicated on account of the tendency to failure of the respiration and heart, and owing to the typhoid nervous symptoms. They are required at all ages, especially by young children and by the aged. Children in particular bear relatively large amounts, and respond to their use well and promptly. The form and strength of the stimulant must be adapted to the state of the stomach. Wine-whey and weak milk-punch are often serviceable. Many children will take brandy or whiskey in water, but will refuse the former preparations. Dry champagne has proved highly valuable in many serious cases, especially in older persons, for young children will rarely take it.

Other important indications are to favor expectoration and to stimulate the respiratory forces. These are closely associated, and are of prime importance, since in catarrhal pneumonia the principal danger to life undoubtedly comes from the progressive diminution of the pulmonary area open to respiration, and from the increasing failure of the respiratory muscles to overcome the obstruction to full inflation. It is through this agency that pulmonary collapse extends, that heart failure subsequently occurs, and that carbonic acid poisoning, with its attendant nervous symptoms, is finally developed.

The preparations of ammonia seem to be the most valuable remedies to meet these indications. In adults, where the disease is attended with high fever, the following may be ordered: {371}

Rx. Ammonii chloridi, gr. lxxx;
Syr. scillæ vel syr. senegæ, fluidrachm iij;
Liq. ammoniæ acetatis, q. s. ad fluidounce iv.

Ft. sol. S. A dessertspoonful in water every three hours. To this may be added one or two drops of tincture of aconite in each dose, watching carefully for the appearance of its effects; or small doses of morphia or of deodorized tincture of opium may be added, according to the severity of cough or of nervous restlessness. But to children in nearly all cases, and frequently to adults, it is best to give carbonate of ammonia at once, as follows:

Rx. Ammoniæ carbonatis, gr. xlviij;
Pulv. acaciæ et sacchari, _aa_ q. s.
Sp. lavandulæ comp. fluidrachm ij;
Aquæ, q. s. ad fluidounce iv.

Ft. mist. S. One teaspoonful in water every two or three hours for a child five years old.

It may occasionally be necessary, owing to the abundance and the viscidity of the bronchial secretions, to administer an emetic, but this should be avoided if possible. If required, choice should be made of one which will act promptly and decisively without subsequent nausea or relaxation. Such is a combination of alum and ipecacuanha, or of sulphate of zinc and ipecacuanha, which have proved very satisfactory in my hands. Jürgensen recommends apomorphine, administered hypodermically, as the agent which he has found most efficient. The dose of this substance is about gr. 1/12 for an adult, whilst for a child of five years it should not be more than gr. 1/30 or gr. 1/25. The dose may be repeated in 15 or 30 minutes if no emetic action is secured.

I attach great importance to the use of strychnia in catarrhal pneumonia after symptoms of respiratory failure appear. Its value as a stimulus to the muscles of respiration, and possibly directly to the respiratory nervous centre, is established. It may be given alternating with the ammonia mixture, thus:

Rx. Quiniæ sulph. gr. xxiv;
Strychniæ, gr. ¼;
Acid. muriatici diluti, gtt. xvj;
Glycerinæ, fluidrachm iij;
Liq. pepsinæ, q. s. ad fluidounce iv.

Ft. sol. S. Teaspoonful in water every three or four hours, for a child of five years of age.

But when urgent symptoms arise it may be given in much larger doses and hypodermically, so as to ensure its full absorption and effect. I have thus given in many severe cases, and at times with unquestionably good results, as much to an adult as gr. 1/24 every four hours, day and night, for seventy-two or ninety-six hours.

The fever in catarrhal pneumonia does not demand special treatment nearly so often as in the croupous form. Though the evening maxima may be quite high, yet the occurrence of the morning remissions brings some relief and obviates the necessity for vigorous antipyretic treatment. The nervous system and the heart do not therefore suffer severely and constantly from this cause in this disease. Still, there are not a few cases when hyperpyrexia occurs and demands prompt treatment. If the nervous symptoms are not threatening, and if the respirations are still fairly well performed, it will be proper to try the effect of a few full doses of quinia, or, if that fails, of antipyrine. But if, despite these remedies, or in the event of the stomach rejecting them, or, finally, if more urgent symptoms of nervous and respiratory failure are impending, recourse should be had to cold effusion, particularly if the highly laudatory statements of Bartels, Ziemssen, and Jürgensen be confirmed by further observation. I have not found it necessary, or may have failed to {372} appreciate the necessity, to resort to the external use of cold in catarrhal pneumonia; but the remarks of Jürgensen as to the remarkable influence of cold water dashed upon the surface of the chest or directed against the cervical spine in stimulating deep respirations accord with general observation, and suggest this mode of treatment, especially in cases of sustained high temperature with rapid, shallow, imperfect respirations and defective aëration of the blood.

The nervous symptoms frequently are so severe as to require the administration of sedatives. Remedies of this class must, however, be used cautiously and sparingly. It were unwise to give those which depress the heart and respiration, or, on the other hand, to administer opium in such doses as would blunt perception and lessen cough to an injurious degree. By the use of small doses of opium from the beginning of the attack, however, combined with strict attention to the other details of treatment, it is often possible to prevent the development of severe nervous symptoms which would require powerful sedatives. In cases of extreme restlessness and sleeplessness benefit may be found from the use of such a suppository as the following:

Rx. Pulv. assafoetidæ, drachm j;
Quiniæ sulph. gr. xxx;
Ol. theobromæ, q. s.

To be made into twelve suppositories of small size, suitable for a child of five years of age, one of which may be used and repeated in three or four hours.

Enemas of chloral hydrate, from five grains for a child of five years to twenty grains for an adult, may be used without fear of depressing the heart or checking the secretions, and with great relief to the nervous symptoms, especially if tending toward convulsions. In cases of extremely active and restless delirium, where prompt sedative action is demanded, and yet where the use of opiates is forbidden, the hypodermic use of hyoscyamia in doses of gr. 1/80 to 1/100 for an adult may give gratifying results.

In cases which pass into a subacute form a continuance is demanded of every precaution as to the diet, the hygiene of the sick-room, and the use of general tonic remedies. Advantage may then be found from the use of oil of turpentine, which has seemed to me the most valuable alterative and stimulating expectorant under such circumstances.

As the case progresses into the chronic form it becomes necessary to gradually substitute for the more strict and special method of treatment previously employed one in which the maintenance of the general health shall be the prime object. The regulation of the diet, care in dress, the cautious resumption of gentle exercise, and the use of carefully-regulated pulmonary gymnastics so as to favor the full inflation of the lungs and the invigoration of the respiratory muscles, are to be closely attended to.

The condition of the skin demands careful attention also, and dry friction, inunction, and suitable stimulating sponge-baths followed by friction, according to the constitutional condition of each patient, may be cautiously directed with great advantage.

The remedies suitable for the more acute stages may now be replaced by cod-liver oil, arsenic, or iodide of iron. Occasionally alterative expectorants, such as copaiba or yerba santa, with or without an alkali, as muriate of ammonia, will still be found desirable.

Most signal benefit will also be obtained from suitable change of climate, associated with a continuance of careful regimen and treatment; and, indeed, we may be gratified by witnessing a complete restoration to health, with the exception of unimportant residual lung lesions, of cases in which the general symptoms and the physical signs strongly indicated hopelessly incurable organic disease. Not only in the acute, but in the most tedious chronic, cases of catarrhal pneumonia must our efforts be continued to the very close.

{373}

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 Ball[3] 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's[4] 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 {374} 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 Paris[6] 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]

[Footnote 1: _Étude critique de l'Embolie_, Paris, 1869.]

[Footnote 2: _Clinical Lectures_, Sydenham Society's ed., vol. iii. p. 414.]

[Footnote 3: _Des Embolies pulmonaire_, Thèse de Paris, 1862.]

[Footnote 4: _Froniep's Neue Notizen_, 1846, p. 910.]

[Footnote 5: Bucquoy, _Des Concrétions sanguines_, Paris, 1863, p. 138.]

[Footnote 6: _Bullétin_, 1861, p. 377.]

[Footnote 7: _Dict. de Médecine et de Chirurgie_, vol. xxix. p. 334.]

In 1852, Senhouse Kirkes[8] 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 Luzzato[11] and the theses of Duguet[12] 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.

[Footnote 8: _Med.-Chir. Trans._, vol. xxxv.]

[Footnote 9: _Ibid._, vol. xxvii. p. 162, and vol. xxviii. p. 352.]

[Footnote 10: Playfair, _A Treatise on the Science and Practice of Midwifery_, Philada., 1882.]

[Footnote 11: "Embolia dell' Arteria pulmonale," _Annali Univers. di Med. e Chir._, Milano, 1877-79.]

[Footnote 12: _De l'Apoplexie pulmonaire_, Paris, 1872.]

[Footnote 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 {375} 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 diseases[16] (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.

[Footnote 14: _Dis. of the Heart and Aorta_, Part ii. p. 1029.]

[Footnote 15: _Gaz. hébdom._, 1862, quoted by Bucquoy.]

[Footnote 16: Hayden, _Diseases of the Heart and Aorta_, Part ii. p. 1023.]

[Footnote 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 {376} 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. Hayden[23] 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]

[Footnote 18: _Am. Journ. Med. Sci._, Oct., 1876.]

[Footnote 19: Hayden, Case 124, p. 1030.]

[Footnote 20: _Lancet_, Nov. 24, 1876.]

[Footnote 21: At times septic material is introduced into the blood and absorbed from disintegration of a clot. Hence arise typhoid or pyæmic symptoms.]

[Footnote 22: _Reports of Pathol. Soc. of London_, vol. xvi.]

[Footnote 23: _Op. cit._, p. 1024.]

[Footnote 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 extremity[25] or into a nævus[26] 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 {377} 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, Azam[31] 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.

[Footnote 25: _Soc. Méd. Bordeaux_, 15 Nov., 1867.]

[Footnote 26: _Annales d'Oculistique_, 1864.]

[Footnote 27: _Discussion à la Soc. de Chirurgie_, 14 Avril, 1875.]

[Footnote 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.]

[Footnote 29: _Traube's Beiträge sur experimentalen Path. und Phys._, 1846, Heft 551, quoted by Levrat.]

[Footnote 30: _Comptes rend. de l'Académie des Sci._, 7 et 14 Avril, 1862.]

[Footnote 31: _Gaz. hébd. de Méd. et Chirurg._, 1864.]

[Footnote 32: Levrat, _Des Embolies veineuses d'Origine traumatique_, p. 54, Paris, 1880.]

[Footnote 33: Hesch, _Anzeiger d. K. K. Gesellschaft der Aerzte in Wien_, 1876, No. 3, quoted in _Dobell's Reports_, vol. cxi., 1877.]

[Footnote 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 {378} 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.

[Footnote 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. Playfair[36] 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 Humphrey[38] 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. Playfair[39] 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.

[Footnote 36: "The Puerperal State," being Part V. from a _Treatise on Midwifery_, p. 50, Philada., 1882.]

[Footnote 37: _Des Embolies_.]

[Footnote 38: _On the Coagulation of the Blood in the Venous System during Life_, quoted by Playfair.]

[Footnote 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 {379} 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 observed[40] 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]

[Footnote 40: Azam, 1re Mémoire, _Gaz. hébd. de Méd. et Chirurgie_, 1864; Observ. II., reported by Levrat.]

[Footnote 41: _British Medical Journal_, March 27, 1869.]

[Footnote 42: _Clinique méd._, t. iii. p. 715.]

[Footnote 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 Vidal[45] 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 {380} 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]

[Footnote 44: Picot, _Les grands Processus morbides_, 1876.]

[Footnote 45: Ball, _Des Embolies pulmonaires_, Observ. xxvii., Thèse, Paris, 1862.]

[Footnote 46: _London Med. Gazette_, vol. ix. p. 788, quoted by Hayden, p. 1029.]

[Footnote 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. Virchow[48] 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 Bertin[49] 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]

[Footnote 48: _Gesamm., Abhandl._, 1862, p. 316, quoted by Playfair.]

[Footnote 49: _Étude critique de l'Embolie_, Paris, 1869.]

[Footnote 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 {381} 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 Jacquemet[51] 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."

[Footnote 51: _Congrès médicale de France_, 2ème session, Lyon, 1864, quoted by Levrat.]

[Footnote 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 {382} 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 upon[54] 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.

[Footnote 53: Humphrey, _Med.-Chir. Trans._, vol. xxvii. p. 14.]

[Footnote 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. Levrat[56] 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.

[Footnote 55: Paris, 1878.]

[Footnote 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.

[Footnote 57: Here it is due to relative stasis of the blood.]

{383} 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.