in the etiology of this disease as predisposing causes of arterial
degeneration. Many persons affected have been immoderate
spirit-drinkers, which of itself does not directly tend to the disease,
but does so indirectly, in that it encourages an early senescence of
the tissues. In the same way any debilitating conditions may act as
predisposing causes. Chronic endarteritis is most frequently found at
the seat of the aneurism. Secondary or exciting causes are
peculiarities of occupation, as those which are laborious and require
much physical exertion and entail exposure to inclemencies of the
weather.
SYMPTOMS.--Pulsation is usually the first symptom observed. It is felt
in the epigastrium about two and a half inches below the ensiform
cartilage, or even higher, and a little to the left of the median line;
or it may be midway between the ensiform cartilage and the umbilicus,
on the left. It is not unfrequently of a distensile character, and is
unaffected by changes in the position of the patient. It is not
synchronous with the cardiac systole, but follows in rapid succession
to, and terminates with, the ventricular {842} diastole. A tumor,
usually globular, is felt in the region of the pulsation. It is of
variable size, from that of a hen's egg to a cricket-ball, or in case
of false aneurism even much larger. The tumor is slightly tender; it
moves with the diaphragm, and sometimes when it presses upon the
pancreas ptyalism has been observed, which in one instance was
increased by external pressure on the aneurism with the hands.
Another constant symptom is pain in the left side, extending from well
up in the chest to the region of the hip, or located in the lower part
of the chest alone, or perhaps in the epigastrium. This pain is either
constant or excited by exertion, and paroxysmal in character.
Flatness on percussion over the tumor of varying extent is observed in
many cases, and a systolic bruit, perhaps of a whistling character, is
heard.
The usual termination of aneurism of the coeliac axis is rupture with
internal hemorrhage. The symptoms of this accident do not differ from
those of the same occurrence in abdominal and thoracic aneurism, and
are likewise usually fatal.
PATHOLOGY.--Strain doubtless forms an important factor in the
production of this aneurism in an artery previously weakened by disease
of its coats. The tumor is frequently a false aneurism, and has for
walls connective tissue and the neighboring organs. When it is of large
size, on account of its position it sometimes presses upon the pancreas
or vertebræ, and produces absorption with consecutive symptoms. In the
former case ptyalism has been observed, which perhaps may have been due
to reflex action through the coeliac plexus and pneumogastric nerve,
the reflex centre being the medulla oblongata with the facial origin.
The wall of the aneurism is usually thin, and in some cases it has
given way, leading to the formation of so-called false aneurism. Not
infrequently the wall is atheromatous. The size of the aneurism varies
greatly, though it is never larger than the two fists.
DIAGNOSIS.--This aneurism is apt to be confounded with aortic aneurism,
and can only at times be distinguished from it by its locality and
small size.
PROGNOSIS.--This must be grave if a diagnosis is made, for the ultimate
result is usually rupture and hemorrhage.
TREATMENT.--The general principles recommended in treating abdominal
aneurism should be followed out. It is but rarely the case that
compression is admissible, and then the distal pressure is to be used.
Rest and diet form the most reliable means of treatment at our command.
{843}
DISEASES OF THE VEINS.
BY ANDREW H. SMITH, M.D.
The principal affections to which the veins are liable are the
following: Inflammation (phlebitis), acute and chronic; Dilatation;
Narrowing or obliteration; Degeneration; Concretions.
Inflammation.
Idiopathic phlebitis occurs for the most part under one of three
conditions: First, as a simple primary inflammation of the tissues
composing the walls of the vessel; second, as a participation in an
inflamed or diseased condition of surrounding structures; third, as the
result of the absorption of poisonous material into the blood.
Like any other structure of the body, the veins are liable to
inflammation as a purely local affection. It is nevertheless true that,
in the acute form, this inflammation is most likely to occur in
connection with certain conditions of the system which seem to act as
predisposing causes, although the connection between them and the local
phlebitis is not apparent. Thus it occurs (perhaps associated with more
or less of lymphangitis) in the puerperal state, in phthisis, in heart
disease, and in other conditions of general depression. I have met with
it, for example, during recovery from pneumonia after typhoid fever and
after suffocative laryngitis. Under these circumstances it constitutes
the chief element in the affection known as phlegmasia dolens. Now,
none of the above conditions implies, so far as is known, any source of
irritation to the venous structures, much less to a limited portion of
the venous system; and the only explanation of their association with
phlebitis seems to be in the assumption that these conditions favor
coagulation of the blood, and that, in these cases, the formation of a
clot precedes the local inflammatory process. The location of this clot
is probably determined by anatomical conditions.
In other cases, however, the process evidently begins in the wall of
the vessel, and the formation of the thrombus is secondary. Any change
which interferes with the smoothness of the inner coat, whether by loss
of endothelium or by producing inequalities of the surface, will very
certainly determine the deposition of fibrin and the formation of a
coagulum. The glossy smoothness of the intima seems to require the most
perfect nutrition of the subjacent tissues for its maintenance, and its
loss produces an immediate slowing and ultimate stoppage of the
blood-current. This is admirably shown by the experiments of
Nicasse,[1] which demonstrate that simply denuding a portion of a vein,
and thus cutting off its vascular and nervous supply, induces almost
immediately the formation of a thrombus coextensive with the denuded
portion.
[Footnote 1: _Des Plaies et de la Ligature des Veinse_, Thèse, Paris,
1872.]
{844} Inflammation affecting the inner coat of a vein and extending
along its surface, as in the case of a serous membrane, probably never
occurs. The picture of phlebitis formerly drawn, and which embraced the
exudation of false membrane or the formation of pus upon the inner
surface of a vein, the pus in the latter case floating off with the
blood and constituting pyæmia, the formation of a clot being a later
and unimportant event, has little or no resemblance to what actually
occurs.
The observations upon which these assumptions were based were
erroneous, as shown by Virchow, in that the staining of the intima by
absorption of coloring matter from the blood was mistaken for
inflammatory redness, and changes in the clot itself were confounded
with exudation and suppuration. Indeed, when we reflect that the intima
is not vascular, we should scarcely expect from it anything analogous
to serous inflammation. The only acute process to which it appears
liable is an erosion or crumbling away under the same conditions which
determine, in the middle or outer coats, increased vascularity,
exudation, and the formation of pus.
Thus, from some general condition favoring the coagulation of the blood
we may have a thrombus formed, followed by secondary inflammation of
the wall of the vessel, or, without such general condition, we may have
inflammatory changes, commencing in the outer or middle coat and
causing the secondary formation of a thrombus. In either case the clot
shuts off the affected portion of the vein from the general
circulation. Changes take place in the clot which are more properly
considered under the head of thrombosis, and by which it is ultimately
removed. Exudation takes place into and between the tunics which form
the venous wall, the latter becoming thickened and comparatively rigid,
so that when the vein is cut across its lumen remains open like that of
an artery.
Sometimes pus is formed between the different coats, constituting small
mural abscesses; sometimes the intima crumbles away and exposes the
middle coat, which suppurates on its inner surface, and the pus mingles
with the débris of the clot. In this way a larger abscess is formed,
bounded by the wall of the vein and by a partly-organized coagulum on
either side. These coagula sometimes break down, and fragments from
them, infected by the pus and its contained micrococci, are swept on in
the current of the blood until they find a lodgment, where the process
begins anew, and whence it may be propagated in like manner to other
and more distant parts.[2] It is only to the condition above described
that the term suppurative phlebitis can properly be applied.
[Footnote 2: Ziegler, _Path. Anatomie_, Jena, 1881, p. 429.]
But, instead of a suppurative process taking place, the endothelium may
be thrown off and replaced by minute vegetations of the character of
granulation-tissue, which, penetrating into and blending with the clot,
may temporarily or permanently occlude the vein, and the contraction
which follows may ultimately leave only a fibrous cord to represent the
vessel.[3]
[Footnote 3: Leroux, _Gaz. méd. de Paris_, 28 Juin, 1879.]
This process is designated adhesive phlebitis, and is one of frequent
occurrence and very important in its results. It takes place in
connection with suppurative phlebitis, and by closing the vessel on
either side of the suppurating portion serves to prevent the pus from
mingling with the general circulation.[4] By its action the largest
veins, including the venæ cavæ, are occluded, and extensive and
important changes in the circulation are brought about.
[Footnote 4: While this is true of a pus-cavity forming within a vein,
an abscess originating outside of a vein or between the layers of the
venous wall may open into the vessel at a point not protected by a
clot, and the pus mingling with the blood will constitute veritable
pyæmia.]
The second condition under which phlebitis occurs is that in which a
vein, {845} coursing through an inflamed or diseased structure, becomes
itself inflamed. This takes place most frequently in phlegmonous
erysipelas and in diffused inflammation of the cellular tissue, but it
may be the result of any inflammation in the neighborhood of a vein.
Under these circumstances the external layer of the venous wall is
first affected, and the others subsequently. Only a portion of the
circumference of the vessel may be involved, and the wall may bulge
inward considerably without necessitating the formation of a thrombus
(Virchow). But if the nutrition of the walls is seriously impaired, the
intima becomes roughened by the loss of its endothelium, the
blood-current is slowed by the increased friction thus caused, and, the
uneven surface favoring at the same time the adhesion of fibrin, a clot
is formed, and the course thereafter is the same as when the vessel is
primarily affected.
Suppuration may also take place between the vein and its sheath, and
extend for a considerable distance along the vessel. The walls
participate secondarily, and the vein becomes occluded as before
described.
In the third class of cases, those depending upon toxic infection, the
inflammation is caused by the irritation of some poisonous material
circulating in the blood. The phlebitis is therefore secondary, and is
to a great degree overshadowed by the general condition which
accompanies it. Aside from instances in which there is a direct
inoculation of a poisonous material--as, for example, the venom of a
serpent--the conditions merge into those which come under the
designations pyæmia and septicæmia--diseases which were formerly
confounded with phlebitis, but which are now recognized as distinct
from, though often coexisting with, it.
If in acute phlebitis the inflammation does not result in the formation
of pus, the vein may recover its normal condition, or the walls may
remain thickened and the lumen contracted, but still pervious, or it
may be entirely occluded. Suppuration, however, always results in
complete and permanent closure of the vein.
The symptoms of acute phlebitis are chiefly such as indicate
obstruction of the vein. When a large vein, situated in one of the
extremities, is the seat of the affection, there are usually severe
pain of a tensive character and decided tenderness on pressure. The
limb swells, sometimes to a very considerable extent, and becomes stiff
and unwieldy. If a superficial vein, such as the long saphena, is
affected, there will be subcutaneous oedema and pitting; but when the
vessel lies beneath a firm, tense fascia, this will limit the swelling,
and the limb will be hard and brawny, while the tension will greatly
aggravate the pain.
When the vein is sufficiently near the surface it may be felt at the
affected part as a hard cord, usually more or less knotted. The skin
over it may be discolored, presenting a red or somewhat coppery hue and
a streaked or mottled appearance, or the pressure from the effused
serum may empty the capillaries of blood and render the skin pale and
shining.
The temperature of the limb may be elevated, normal, or subnormal. In
the outset, under the influence of the inflammation, there is usually
increased heat, but as the tension from the oedema interferes more and
more with the circulation, the temperature falls, and the limb may
become colder than its fellow.
Inflammation of a limited portion of a vein may not be attended by any
notable symptoms, the collateral circulation being quickly established,
and the effects of the obstruction thus obviated, while, at the same
time, the local symptoms are masked by the morbid conditions in the
surrounding tissues which give rise to the phlebitis.
The constitutional symptoms accompanying phlebitis are those of
inflammatory fever, the grade of which will depend upon the extent and
severity of the inflammation. When a considerable length of vein is
involved, as {846} may be the case in the form of phlebitis already
referred to, which progresses along the sheath of the vessel, the
irritation of the general system may be great, especially if pus is
formed, when hectic or even typhoid symptoms are not uncommon.
The differential diagnosis of phlebitis in its local appearances
requires only its distinction from lymphangitis. The latter disease is
more abrupt in its invasion, depends almost always upon some wound or
injury with which the local symptoms are directly connected, is more
diffuse, affecting a network of vessels rather than a single one, and
is invariably accompanied by engorgement of the lymphatic glands to
which the affected vessels lead, as, in the case of the extremities,
the axillary or inguinal glands.
In complicated cases the occurrence of phlebitis may not be marked by
any distinctive symptoms. It may be suspected if, in the course of
erysipelas, diffuse cellulitis, etc. in the neighborhood of an
important vein there is a somewhat sudden increase of pain and
swelling, and if an enlargement of the tributary cutaneous veins is
soon observed.
The treatment of phlebitis consists in complete rest, in the use of
such constitutional means as may be necessary to allay the irritation
of the system, and locally in the application of leeches and warm
fomentations. If, on the other hand, the local temperature is very
high, the use of ice may be indicated.
Nonat, in cases of commencing phlebitis from venesection, tried the use
of flying blisters over the part affected. Obtaining good results, he
extended the treatment to phlebitis following typhoid fever, etc., and
the morbid phenomena were at once arrested.[5]
[Footnote 5: _Gaz. des Hôp._, No. 86 (_Med. Times and Gaz._, Aug. 7,
1858).]
Much disturbance of the parts, either in examining them or in the use
of frictions, etc., is to be avoided, as there are not a few instances
on record in which portions of thrombi have been detached in this way,
and, floating off in the current of the blood, have resulted in
pulmonary and even cardiac embolism, the latter causing immediate
death.[6] The tendency to oedema will be lessened by placing the
affected part in a position that will favor the return of the blood by
the collateral circulation.
[Footnote 6: _Lyon Médicale_, June 18, 1876 (_N.Y. Med. Rec._, Sept. 2,
1876).]
As an internal remedy the calcium sulphide is worthy of trial.[7] The
administration of ammonia is thought to lessen the tendency to the
formation of coagula and to promote their absorption if already formed.
Abscesses occurring in superficial localities should be promptly
opened, antiseptic precautions being observed. The strength of the
patient should be maintained by every possible means, the danger of an
extension of the mischief being proportioned to the lowering of the
vital forces.
[Footnote 7: "Report of N.Y. Therapeutical Society," _N.Y. Med.
Journ._, June, 1882.]
As already stated, acute phlebitis plays a very important part in the
affection known as phlegmasia alba dolens or white leg. Indeed, many
writers consider that it is the only essential factor in the affection.
This view is strongly insisted upon by Hervieux, but the researches of
Mackenzie,[8] Simpson,[9] Barker,[10] and others have shown that
something more than phlebitis is embraced in the disease. Tilbury Fox
claims that there is an association of lymphangitis with the phlebitis.
At all events, whatever may be the exact pathology of the affection, it
appears to be certain that an abnormal condition of the blood, favoring
the formation of coagula in the veins, is an essential prerequisite.
[Footnote 8: _Pathol. and Treat. of Phleg. Dolens_, London, 1862; _Med.
Times and Gazette_, Aug. 22, 1866.]
[Footnote 9: _Med. Times and Gazette_, Jan. 14 and 18, 1859.]
[Footnote 10: _The Puerperal Diseases_, New York, 1876.]
Phlegmasia dolens occurs chiefly in the puerperal state, and affects
chiefly {847} the lower extremities; but it may affect males and
non-puerperal females, and may be seated in the arms as well as the
legs. Outside of the puerperal state it is met with in conditions of
depressed vitality, as during convalescence from acute disease, and in
those suffering from phthisis, cancer, and other cachexiæ. When one of
these conditions is present a degree of venous obstruction--from
pressure, for example--which would ordinarily cause merely a slight
amount of oedema may result in an adhesive or even suppurative
phlebitis, and the associated phenomena which form the disease in
question.[11]
[Footnote 11: Murchison, _Med. Times and Gaz._, May 23, 1863, reports
the case of a man recovering from typhus in whom phlegmasia dolens
resulted from the pressure of a diverticulum from the bladder upon the
right iliac vein.]
The preponderance of cases, however, occurring from the second to the
fourth week after delivery indicates a special condition present at
that time tending to produce the disease. Some cases, doubtless, are
due to the cause suggested by Lee--viz. the formation of clots in the
uterine veins, and the growing out of these thrombi through the
hypogastric and into the iliac and femoral veins. But that this is not
the only or the usual cause is proved by numerous autopsies in which no
evidence of thrombosis has been found in the uterine veins. Still, the
puerperal period is very generally one of vital depression, in which
hyperinosis and inopexia are presumably present. To this is added
another source of irritation, in the loading of the blood with the
material absorbed from the uterus in the rapid reduction of its bulk
which is taking place.
It is not improbable also that small amounts of decomposing blood, and
even clots, may be retained in the uterine sinuses, and ultimately be
forced suddenly on into the venous circulation by the pressure
resulting from the shrinking of the tissues by which they are
surrounded. This would explain the suddenness with which symptoms of
toxæmia or embolism often occur.
The principal difference between phlegmasia dolens and simple
obstructive crural phlebitis is in the degree rather than the character
of the symptoms.
When, in a healthy animal, phlebitis of the crural vein is set up
artificially, causing complete obstruction, there is but little pain,
and only a comparatively slight effusion into the cellular tissue, and
the limb pits readily. In phlegmasia dolens, on the other hand, the
pain may be very severe and the oedema very great, and the limb is
stiff, hard, tense, and shining, and pits only with firm and continued
pressure (Barker). Moreover, crural phlebitis may occur and prove fatal
without causing phlegmasia dolens.
These facts have perhaps been allowed undue weight in the argument for
non-identity. It would seem that we have only to admit a depraved
condition of the blood favoring thrombosis and secondary phlebitis, and
disposing to more abundant effusion of a more plastic character as the
result of the obstruction, and all the distinctive phenomena of
phlegmasia dolens are covered. The experiment has never been tried of
producing phlebitis artificially in a subject, with the blood-condition
predisposing to white leg, in order to determine whether this condition
would follow; but clinically it has more than once been demonstrated
that in such a subject phlegmasia dolens may result from simple
pressure upon the iliac vein.
The fact, too, that the disease occurs three times in four on the left
side, where the iliac vein is pressed upon by the rectum and by the
iliac artery, is not to be forgotten in this connection. If
lymphangitis were a necessary factor in the disease, pressure upon the
vein would not have such a marked causative influence.
The symptoms of phlegmasia dolens may be gathered from the preceding
remarks, together with the description of the symptoms of acute
phlebitis. {848} It is to be noted, however, in addition, that the
majority of cases are ushered in by one or more chills, and that the
progress of the case is usually marked by a tendency to profuse
perspirations. In the puerperal woman lactation is generally very much
interfered with or entirely suspended. "The lochial discharges seem, in
very many cases, to be very little influenced by the onset and progress
of this disease, but in others they have been observed to become very
fetid and offensive" (Barker).
The tendency of this affection is to terminate by resolution. The
hardness diminishes before the size of the leg becomes less, and with
this diminution of tension the muscles regain their power. Gradually
the oedema subsides, and the knotted cords which indicated the course
of the affected veins disappear. If all goes well, the limb is restored
in the course of three or four weeks apparently to its normal
condition. Yet even in these cases the affected vein probably remains
entirely obliterated, the circulation being carried on by the
subsidiary vessels.
But in many cases the recovery is only partial, and for months or years
the limb remains larger than its fellow, the superficial veins are
enlarged, and the skin congested and of a dusky hue. Long standing or
walking causes increased oedema, and there is a disposition to eczema
and ulceration above the ankle.
What was said in regard to the treatment of phlebitis is applicable to
that of phlegmasia dolens. As the tension subsides the application of a
roller bandage will hasten the return of the limb to its normal size.
But care must be taken that it is not tight enough to still further
impede the already obstructed circulation. At a later period the
support of an elastic stocking may be required. Constipation is to be
avoided, especially in those cases in which the left lower extremity is
affected, as the pressure of the loaded rectum interferes with the
return circulation.