SYMPTOMS AND PHYSICAL SIGNS
=Special=
Our conception of arteriosclerosis as a degenerative process affecting
the vascular tree rather than a disease, removes the possibility of
discussing special symptoms. As a matter of fact, we know of very few
organs where even profound pathologic changes in the vascular system
produced during life any symptoms which could be laid to these arterial
changes. Kind nature has given to us such an excess of organs of every
kind that the destruction of large portions of any organ seems to affect
the function but little. So only particular groups of organs, which show
symptomatic changes as the result of arteriosclerotic processes, will be
discussed. It is realized that this may not give Teutonic completeness
to the discussion, but it certainly saves paper and has a distinct
practical value to the long suffering reader.
Although arteriosclerosis is a disease which affects the whole arterial
system, it nevertheless never reaches the same grade all over the body.
The difference in the structure and functions of the various organs
determines to great extent the eventual symptomatology. Endarteritis
obliterans of a small sized artery in the liver or leg would lead to no
marked symptoms, as the circulation is so rich that the anastomoses of
the blood vessels would soon establish a collateral circulation that
would be perfectly competent to sustain the function of the part. Quite
different would it be should one of the small arteries of the brain, the
lenticulo-striate, for example, which supplies the corpus striatum,
become the seat of a thrombosis or embolism caused by arteriosclerosis.
The arteries of the brain are terminal arteries and the blood supply
would be cut off entirely with a resulting anemic necrosis of the part
supplied by the artery and a loss of function of the part. What would be
of no moment in the leg or arm might prove even fatal in the brain.
The further symptomatology, therefore, of arteriosclerosis depends
entirely on the organ or organs most affected by the interference with
the blood supply. The following groups may be recognized:
1. Cardiac.
2. Renal.
3. Abdominal.
4. Cerebral.
5. Spinal.
6. Local vasomotor effects.
7. Pulmonary.
=Cardiac=
Most cases of arteriosclerosis sooner or later present symptoms
referable to the heart. When the organ is hypertrophied and is already
working against an enormous peripheral resistance, a slight excess of
work put upon it may cause a dilatation of the chambers with the
resulting broken compensation. There is dyspnea on slight exertion,
possibly some precordial distress, slight edema of the ankles and lower
legs and possibly scanty urine. With proper care, a patient with such
symptoms may recover, but the danger of another break in compensation is
enhanced. The next attack is more severe. The edema is greater, there
may be signs of edema of the lungs, effusions into the serous cavities
may occur. The heart shows marked dilatation. There is gallop or canter
rhythm and there are loud murmurs at the apex. When a patient is first
seen in this stage, it may be quite impossible to state whether or not
there is true valvular disease of the heart. The muscle is usually
diseased in that there is fibroid degeneration of more or less
extensive character. This factor causes the heart to lose much of its
elasticity and increases the tendency to permanent dilatation. Such
cases must be watched before one can say that true valvular
insufficiency is not present. The fatal termination of such a case is
quite like that of true valvular disease. There is increasing dyspnea,
increasing anasarca, and the patient usually succumbs to edema of the
lungs, drowned in his own secretions.
[Illustration: Fig. 59.--Aneurysm of the heart wall. (Milwaukee County
Hospital.)]
A very rare complication of the fibroid degeneration of the heart muscle
is aneurysm of the heart wall. (Fig. 59.) The apex of the left
ventricle is most commonly the site of the aneurysm and rupture
occasionally occurs. Such an accident is rapidly fatal. In the
arteriosclerotic process which occurs at the root of the aorta, the
coronary arteries become involved both at the openings and along the
courses of the vessels. A branch or branches or even one artery may
become blocked as a result of obliterating endarteritis. The arteries of
the heart are not terminal vessels but as a rule blocking of a large
branch leads to anemic infarct. These areas become replaced by fibrous
tissue which in the gross specimen appears as streaks of whitish or
yellowish color in the musculature. Anemic infarcts may not occur. In
such cases the anastomosis between branches of the coronary arteries is
unusually free. Through arteriosclerosis of the coronary vessels
extensive fibrous changes may occur that lead to a myocardial
insufficiency with its attending symptoms--dyspnea, irregular and
intermittent heart, gallop rhythm, edema, etc. One of the most
distressing and dangerous results of sclerosis of the coronary arteries
and of the root of the aorta is angina pectoris. While in almost every
case of angina pectoris there is disease of the coronary arteries, the
contrary does not hold true, for most extensive disease, even embolism,
of the arteries is frequently found in persons who never suffered any
attacks of pain. This symptom group is more common in males than in
females and as a rule occurs only in adult life. "In men under
thirty-five syphilitic aortitis is an important factor." (Osler.)
Since the valuable experiments of Erlanger on heart block, considerable
attention has been paid to lesions of the Y-shaped bundle of fibers, a
bundle arising at the auriculoventricular node and extending to the two
ventricles, known also as the auriculoventricular bundle of His.
Interference with the transmission of impulses through this bundle gives
rise to the symptom group known as the Stokes-Adams syndrome, which is
characterized by: (a) slow pulse, (b) cerebral attacks--vertigo,
syncope, transient apoplectiform and epileptiform seizures, (c) visible
auricular impulses in the veins of the neck. Many of the cases which
occur are in elderly people the subjects of arteriosclerosis.
[Illustration: Fig. 60.--Large aneurysm of the aorta eroding the
sternum. Death from rupture through the skin preceded by frequent small
hemorrhages. (Milwaukee County Hospital.)]
So far as we now know all cases of the Stokes-Adams syndrome are caused
by heart block which is only another name for disease in the
auriculoventricular bundle. Of interest here is the fact that besides
gummata, ulcers, and other lesions of the bundle, definite
arteriosclerotic changes have been found.
"The investigation of a typical case of Stokes-Adams disease has shown
that the symptoms of this case are caused by some lesion in the heart
which gives rise to the condition now generally termed heart block.
Practically all degrees of heart block have been observed, namely,
complete heart block and partial block with 4:1, 3:1, and 2:1 rhythm,
and occasionally ventricular silences. These stages occurred during
recovery.
"Experiments testing the reaction of the heart to various extrinsic
influences demonstrate that when the block is complete the ventricles do
not respond to influences presumably of vagus origin, although the
auricles still respond normally to such influences, that effects exerted
upon the heart presumably through the accelerators still influence the
rate of the ventricles as well as that of the auricles.
"When the block is partial the rate of the ventricular contraction
varies proportionally with the rate of the auricular contractions but
only within certain limits. When these limits are exceeded the block
becomes more complete, i. e., a 2:1 rhythm may be changed into a 3:1
rhythm, this into a 4:1 rhythm, and this into complete block, and vice
versa.
"The syncopal attacks are, in all probability, directly dependent upon a
marked reduction of the ventricular rate. Such reductions of the
ventricular rate are always associated with an increase of the auricular
rate, and it is believed that the latter is the cause of the former."
(Erlanger.)
The epileptiform seizures of the syndrome may be caused by the anemia of
the brain resulting from failure of the heart to supply a sufficient
quantity of blood.
The apoplectiform attacks are most probably caused by venous congestion
when the slowing of the ventricular contractions is not sufficient to
cause convulsions, but will just cause complete unconsciousness.
=Renal=
Chronic nephritis, hypertension, arteriosclerosis form a most important
trinity. Some stoutly affirm that in all cases of high tension there is
chronic renal disease. Certainly the very highest blood pressures which
we see occur in the chronic interstitial forms of kidney disease. The
cause is most probably to be sought in some poison which is elaborated
in the kidney, is absorbed into the circulation and acts powerfully
either on the vasoconstrictor center as a stimulus, or directly on the
musculature of the small arteries all over the body. Usually
hypertension is progressive but it may be temporary.
A man, 43 years old, entered the Milwaukee County Hospital in uremic
coma. The systolic blood pressure was 280-290 mm. Hg, the diastolic
pressure 220 mm. (Janeway instrument). Under treatment his blood
pressure gradually became lower, at the same period the albumin and
casts gradually disappeared from the urine. In two weeks from admission
he seemed perfectly well, there were no albumin or casts found in the
urine, and the systolic blood pressure was 136 mm., not a high figure
for a muscular man of the laboring class. It must be admitted, however,
that such cases are the exception, not the rule.
Patients suffering from the association of chronic nephritis with
hypertension die slowly, usually. There is gradual development of
anasarca. Headache is frequent and severe. Pains all over the body may
occur. The sight may suddenly become dim or may even be lost. Dizziness
may be complained of and dyspnea is usually marked. Cyanosis comes on,
the pulse becomes weak, irregular or intermittent, heart failure sets
in, and the patient dies with edema of the lungs.
Another class of renal arteriosclerosis is characterized by a small
granular kidney in which fibrous changes of a patchy character have
taken place. These scattered areas are the result of obliterating
endarteritis of renal arteries here and there with consequent anemia,
death of cells, and replacement by fibrous tissue. It occurs as part of
a generalized arteriosclerosis in which the whole arterial system is the
seat of diffuse (senile) sclerosis. The palpable arteries are usually
beaded or even encircled with calcareous deposits and the aorta is the
seat of an extensive nodular and ulcerating sclerosis. The heart is
usually small, shows extensive fibrous and fatty changes and possibly
the condition known as "brown atrophy;" the blood pressure is low. Such
cases do not show any special symptoms. They are anemic, short of breath
on exertion, have the appearance and show the signs of senility.
In the first group it is, at times, difficult to say whether the kidney
disease or the arterial disease is the most important. From a clinical
standpoint the decision is not essential as the end results are much the
same in both. However, when actual uremic symptoms dominate the picture,
it becomes evident that the disease of the kidney is the chief feature
in the causation of the symptoms.
=Abdominal or Visceral=
There is an important group of cases to which but little attention has
been paid until quite recently. This is the abdominal or visceral type
of arteriosclerosis. It has been stated that arteriosclerosis of the
splanchnic vessels almost invariably causes high tension. Among others,
Janeway has shown that general arteriosclerosis without marked disease
of the splanchnic vessels does not cause as a rule increase of blood
pressure.
There are cases in which the brunt of the lesion falls upon the
abdominal vessels. Such cases have been called "angina abdominalis." It
has been suggested (Harlow Brooks) that this type of arteriosclerosis
may be determined by constant overloading of the stomach with food,
especially rich and spiced food. This causes overwork of the special
arteries connected with digestion and so leads to sclerosis of the
vessels of the stomach, pancreas, and intestines. Personal habits
probably influence to great extent the production of this more or less
=localized= condition.
The organs supplied by the diseased arteries suffer from changes
analogous to those occurring in general or local malnutrition, such as
starvation, old age, or local anemias. These changes are atrophy with
hemachromatosis (brown atrophy) or fatty infiltration and degeneration.
Following the degenerative changes there result connective tissue growth
and further limitation of the functionating power of the affected
organs.
Pain is a more or less constant symptom of visceral sclerosis. In the
early stages there may be only a sense of oppression, of weight, or of
actual pressure in the abdomen or pit of the stomach. There may be only
recurring attacks of violent abdominal pain accompanied by vomiting. In
some cases symptoms of tenderness in the epigastrium, pains in the
stomach after eating, vomiting and backache may suggest gastric ulcer.
There may be dyspnea and a sense of anguish accompanied with a rapid and
feeble pulse. Hematemesis may make the symptom group even more like
ulcer of the stomach, and only the course of the disease with the
failure of rigid ulcer treatment and the substitution of treatment
directed toward relief of the arterial spasm with resulting betterment,
enables one to make a diagnosis. The condition may be present for years
and the symptoms only epigastric tenderness with dizziness and sweating
on lying down after dinner, as in one of Perutz's patients. The attacks
are probably due to spasmodic contraction of the sclerosed intestinal
vessels with a resulting local rise in blood pressure. The pains are
most probably due to the spasm of the intestinal muscles, and some think
they are located in the sympathetic and mesenteric plexuses.
This result of arteriosclerosis is not so uncommon, and by keeping this
cause of obscure abdominal pain in mind we are now and then enabled to
save a patient from operation.
An autopsy on a case which for many years had attacks of abdominal pain
and cramp-like attacks, with high blood pressure and heart hypertrophy,
showed extensive sclerosis of the abdominal aorta, superior mesenteric
and iliacs. These vessels were calcified. Hypertrophy of the left
ventricle was found. The kidneys were microscopically normal. There were
no changes in the ascending aorta but in the descending portion there
were scattered nodules and small calcified plaques.
The attacks of pain from which this patient suffered for many years, the
hypertrophy of the left ventricle and the increased blood pressure were
thought to be directly due to the sclerosis of the abdominal vessels.
=Cerebral=
It has been stated that arteriosclerosis is a general disease, yet
certain systems of vessels may be affected far more than others, and
indeed there may be marked sclerosis at one part of the body and none
demonstrable at another part.
In advanced sclerosis there may be one or more of a series of accidents
due to embolism, thrombosis, or rupture of the vessels. Such conditions
as transient hemiplegia, monoplegia or aphasia may occur. The attacks
may come on suddenly and be over in a few minutes; what Allbutt calls
"Larval apoplexies." They may last from a few hours up to a day, and are
very characteristic. A patient aged 64 years with pipe stem radials and
tortuous hard temporals would be lying quietly in bed when suddenly he
would stiffen, the eyes would become fixed and the breathing cease. In a
few seconds consciousness returned, the patient would shake himself,
pass his hand over his brow and ask, "Where am I? Oh, yes, that's all
right." He had as many as thirty of these attacks in twenty-four hours,
none of them lasting over one minute. To just what such attacks are due,
it is hard to say. Some have attributed them to spasm of the smaller
blood vessels of the brain, but there have never been demonstrated in
the vessels any constrictor fibers.
There is a well recognized form of dementia caused by arteriosclerosis.
In general paralysis of the insane and in senile dementia the blood
vessels are always diseased. Milder grades of psychic disturbances are
accompanied by such symptoms as mental fatigue, persistent headaches,
vertigo, memory weakness and fainting. Aphasia, periods of excitement
and mental confusion occur in some. Later stages are at times
accompanied by inclination to fabulate, loss of judgment,
disorientation, narrowing of the external interests, episodes of
confusion and hallucinatory delirium.
The hemiplegias, monoplegias and paraplegias may occur again and again
and last for one or two days. Unless there has been rupture of the
vessels, there is complete recovery as a rule.
In persons who have arteriosclerosis with high tension attacks of
melancholia are seen. There are at the same time fits of depression,
insomnia, irritability, fretfulness, and a generally marked change in
disposition. When the tension is reduced by appropriate treatment these
symptoms disappear, to recur when the tension again becomes high. On the
contrary, attacks of mania are accompanied by low blood pressure. The
dizziness and vertigo in cerebral arteriosclerosis are probably due to
the stiffness of the vessels which prevents them from following closely
the variations of pressure produced by position, and thus, at times, the
brain is deprived of blood and a transient anemia occurs.
Arteriosclerosis of the cerebral vessels is always a serious condition.
The greatest danger is from rupture of a blood vessel. Another of the
dangers is gradual occlusion of the arteries bringing about necrosis
with softening of the brain substance. The latter is more apt to be
associated with psychic changes, dementia, etc.; the former, with
hemiplegia. It is curious that a small branch of the Sylvian artery, the
lenticulo-striate, which supplies the corpus striatum, should be the one
which most frequently ruptures. Where the motor fibers from the whole
cortex are gathered together in one compact bundle, a very small
hemorrhage may and does cause very serious effects. A comparatively
large hemorrhage in the silent area of the brain may cause few or no
symptoms.
=Spinal=
It is conceivable that arteriosclerosis of the vessels of the spinal
cord might cause symptoms which would be referred to the areas of the
cord where the process was most advanced. The lesions would be scattered
and consequently the symptoms might be protean in character.
True epileptic convulsions dependent on arteriosclerotic changes are
also seen and are not so uncommon.
This is on the whole a rare condition, much less common than
arteriosclerosis of the cerebral vessels. Collins and Zabriskie report
the following typical case:
"H., a fireman, fifty-one years old, was in ordinary good health
until toward the end of 1902. At that time he noticed that his legs
were growing weak and that they tired easily. Later he complained of
a jerking sensation in different parts of the lower extremities and
at times of sharp pain, which might last from several minutes to two
or three hours. The legs were the seat of a heavy, unwieldy
sensation, but there was no numbness or other paresthesia. About the
same time he began to have difficulty in holding the urine, a
symptom which steadily increased in severity. These symptoms
continued until March, 1903, i. e., for three months, then he
awakened one morning to find that he was unable to stand or walk,
and the sphincters of the bowels and bladder relaxed. There was no
complaint of pain in the back or legs, no difficulty in moving the
arms, in swallowing or in speaking. He says he was able to tell when
his lower extremities were touched and he could feel the bed and
clothes. He was admitted to the City Hospital three weeks later and
the following record was made on April 21, 1903.
"The patient was a frail, emaciated man of medium height, who had
the appearance of being 55-60 years of age. He was unable to stand
or walk. When he was lying, he could flex the thigh and the legs
slowly and feebly. There was slight atrophy of the anterior and
inner muscles, more of the left than of the right side. The knee
jerks and ankle jerks were absent. Irritation of the soles caused
quite a typical Babinski phenomenon. The patient had fair strength
in the upper extremities, but the arms tired very soon, he said. The
grip was moderate and alike in each hand. The motility of the face,
head, and neck was not noticeably impaired. There was no difficulty
in swallowing, and articulation was not defective. Tactile
sensibility was slightly disordered in the lower extremities,
although he could feel contact of the finger, the point of a pin,
and the like. Sensibility was not so acute as normal; there was a
quantitative diminution. Sensory perception was not delayed. There
was a distinct zone of slight hyperesthesia about as wide as the
hand above the femoral trochanters. Above that, sensibility was
normal. There was no discernible impairment of thermal sensibility.
No part of the body was particularly tender on pressure. A bedsore
existed over the sacrum, and there was excoriation of the genitals
from constant dribbling of urine.
"Examination of the chest showed shallow respiratory movements. The
heart was regular, weak, there were no murmurs, the second sound was
accentuated. Examination of the abdomen showed that the liver and
spleen were palpable, but were not enlarged. The abdominal reflexes,
both upper and lower, were sluggish. The patient was slow of speech,
likewise apparently of thought. He did not seem to show an adequate
interest in his condition, still he was fully oriented and seemed to
have a fair memory. His mental reflex was slow. There were
indications in the peripheral blood vessels and heart of a moderate
degree of general arteriosclerosis. The peripheral vessels such as
the radial, were palpable, the walls thickened, the blood pressure
increased.
"The patient did not complain of pain while he was in the hospital,
a period of four weeks, nor was there any particular change in the
patient's symptoms, subjective and objective, during this time. His
mental state remained clear until forty-eight hours before death,
when he became sleepy, stuporous, and comatose, dying apparently of
cardiac weakness, which had set in simultaneously with the clouding
of consciousness."
At autopsy, except for a few small hemorrhages in the posterior
horns of the lower dorsal segments on the right side and a similar
condition of the left anterior horns, there was nothing noticed. On
microscopic examination, there was found widespread sclerosis of the
vessels of the cord to a marked degree with only slight thickening
of the vessels of the brain. There were secondary degenerations of
ascending and descending type particularly marked at the ninth
dorsal segment. They included portions of all the tracts, the
pyramidal tract as well. The symptoms in brief were: (1) weakness
and easily induced fatigue of the legs; (2) peculiar sensations in
the lower extremities, described as jerky, numbness, heaviness, and
occasionally sharp pain; (3) progressive incontinence of urine; (4)
progressive paraplegia.
Since one of the chief manifestations of syphilis is sclerosis of the
arteries, neurologic cases characterized by irregular symptoms and signs
which can not be placed in any of the definite system disease groups,
are possibly due to irregularly scattered areas of sclerosis throughout
the spinal cord caused by obliterating arteritis. Such cases are not so
very uncommon. Several have come under my observation. Further studies
of the spinal cords of these cases at autopsy are necessary before a
final opinion can be given as to their dependence on arteriosclerosis of
the spinal vessels.
=Local or Peripheral=
When the arteriosclerosis in the peripheral arteries reaches a stage
where endarteritis obliterans supervenes, there is usually no chance for
a compensatory or collateral circulation to be established. The area
supplied by the vessel undergoes dry gangrene. A portion of a toe or
finger or a whole foot or hand may shrivel up. It is more common to see
the spontaneous amputation take place in the lower extremities. The same
effect may be produced by the plugging of a vessel with a thrombus.
There may be much pain connected with the sudden blocking, whereas the
gradual obliteration of the blood supply of a toe or foot is not as a
rule at all painful. The condition is at times revealed more or less
accidentally when a patient injures his toe or foot and discovers that
there is no sensation in the part and that the wound instead of healing
is inclined to grow larger.
Other interesting vasomotor phenomena are frequently connected with
arteriosclerosis. Such a one is the curious condition known as Raynaud's
disease, a vascular disorder which is divided into three grades of
intensity: (1) local syncope, (2) local asphyxia, (3) local or
symmetrical gangrene. This is not the place to describe this condition
except to say that the condition called "dead fingers" is the most
characteristic feature of the first stage. Chilblains represent the
mildest grade of the second stage. The parts are intensely congested and
there may be excruciating pain. Any one who has ever had chilblains
knows how painful they can be. The general health is not impaired as a
rule, although the attacks are apt to come on when the person is run
down. The third stage may vary from a very mild grade, with only small
necrotic areas at the tips of the fingers, to extensive multiple
gangrene.
Another and very rare condition in which chronic endarteritis was the
only constant finding is the disease described by S. Weir Mitchell and
called by him erythromelalgia (red neuralgia). This is "A chronic
disease in which a part or parts--usually one or more extremities--suffer
with pain, flushing, and local fever, made far worse if the parts hang
down." (Weir Mitchell.)
Probably the most frequently seen result of arteriosclerosis in the leg
arteries is the remarkable condition, first described by Charcot, known
as intermittent claudication. Persons the subject of this disease are
able to walk if they go slowly. If, however, any attempt be made to
hurry the step, there results total disability accompanied at times by
considerable cramp-like pain. The condition is much more prone to occur
in men than in women, and Hebrews seem more frequently affected. The
cause is most probably to be sought in the anemia which results from the
narrowing of the channels through which the blood reaches the part. The
stiff, much narrowed arteries allow sufficient blood to pass along for
the nutrition of the part at rest or in quiet motion. Just as soon as
more violent exercise is taken, calling for more blood, an ischemia of
the part supervenes, for the stiff vessels can not accommodate
themselves to changes in the necessary vascularity of the part. A rest
brings about a gradual return of blood and the function of the part is
restored. Pulsation may be totally absent in the dorsal arteries of the
feet and when the legs are allowed to hang down there is apt to be deep
congestion.
In this connection a curious case reported by Parkes Weber will not be
out of place. The patient, a male, aged 42 years, complained of
cramp-like pains in the sole of the left foot and calf of the leg
occurring after walking for a few minutes and obliging him to rest
frequently. When the legs were allowed to hang over the side of the bed,
the distal portion of the left foot became red and congested looking.
No pulsation could be felt in the dorsal artery of the left foot or in
the posterior tibial artery. There was no evidence of cardiovascular or
other disease. An ulcer on the little toe had slowly healed, but
cramp-like muscular pains still occurred on walking. The disease had
lasted about five years without the appearance of gangrene.
Weber calls this case one of arteritis obliterans with intermittent
claudication.
=Pulmonary Artery=
In the symptomatology of sclerosis of the pulmonary artery the clinical
signs and symptoms are mostly referable to the obliterating endarteritis
of the smaller vessels, while the physical signs are more apt to reveal
the involvement of the main trunk. A history of severe infection in the
past is frequent, especially smallpox, and accompanying aortic sclerosis
with insufficiency of the mitral valve or stenosis of this valve is the
rule. Striking cyanosis is an early symptom, while there is little if
any dyspnea and edema. Intermittent dyspragia is common. There seems to
be no tendency to clubbed fingers. Repeated hemorrhages from the lungs
without the formation of infarcts may occur. There is usually an area of
dullness at the upper left margin of the sternum and nearby parts,
sensitive to pressure and to percussion, and the heart dullness extends
unusually far towards the right. The diagnosis of the right ventricular
hypertrophy may be substantiated by a fluoroscopic examination.