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.
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 {384} 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
{385} 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
Cohnheim[58] has pointed out, there is a proneness to degeneration
rather than to inflammatory action.
[Footnote 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.
[Footnote 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]
[Footnote 60: Déjerine, _Le Progrès médical; Med. Record_, Jan. 15,
1879.]
{386} 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]
[Footnote 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]
[Footnote 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.]
[Footnote 63: Lancereaux, _Traité d'Anatomie pathologique_, vol. i.,
1875-77, p. 14 _et seq._]
[Footnote 64: Quoted by Levrat, p. 78.]