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.]