Every one has, of course, a general familiarity with the state and

actions of his own and other bodies in health, yet a more exact

knowledge of the movements of respiration, circulation, secretion,

etc., as well as the form, size, and relative location of all the

organs of the body, is needed. Physiology and medical anatomy furnish

such information. The more thorough this knowledge is appropriated,

the better fitted the student is for practical diagnosis. For its

application, however, cultivation of all the perceptive powers is very

important. Some men have a genius for quick and clear discernment of

symptoms and for their interpretation, as well as for that of physical

signs. But all can much improve their senses, and their sagacity in

using them, by experience. For this, if for no other reason,

scientific training, in field or laboratory studies, affords the best

introduction to the work of the medical student and physician. The

traits most needed for success in diagnosis are exactness and

comprehensiveness. First, to be sure precisely what each sign is that

comes under observation; next, to overlook no existing symptoms or

physical signs; and, last, so to combine them into a mental map,

diagram, or picture, as to make a coherent and rational whole. This

nosogram may then be compared with the descriptions of standard

authorities, to find its place (if it has one) in technical

classification. First, however, ascertain the thing, the morbid state

or combination of states; afterward the name, or morbid species, when

practicable. It is always to be remembered that complication of

diseases, or at least the existence of some irregular manifestations

along with those which are characteristic, is more common than the

occurrence of purely typical cases. The portraits of most diseases in

the books are averages, like the composite class-photographs of

Douglas Galton. Not nearly every case will correspond with such an

average in all respects. Moreover, so great is the possible variety of

alterations among the different organs of the body that the chances of

two instances of disease being precisely alike in every particular are

hardly greater than those in favor of every move being the same in two

games of chess with the same opening.

In an essay like the present it is not easy to decide upon the best

manner of treating the subject before us. Too much or too little may

be said. With advanced readers the whole history of symptoms and

physical signs might be left to the special discussions occurring in

articles upon different diseases. But it may be taken for granted that

those who consult the present work will do so either at a

comparatively early stage of their studies or when time has made

desirable a renewal of what may have been once known and then

forgotten. Since, then, it is impossible {150} to anticipate what may

be the exact needs of either class, a somewhat elementary statement of

main facts appears justifiable here.

Following the natural method, we may suppose a call to visit a

patient. Arriving in his presence, the first question (mostly left out

of view and rarely expressed) may be, Is it a case of real or only

imaginary indisposition? Army medical officers, more than most others,

can appreciate the possibility of this inquiry sometimes disposing of

the whole case.

Supposing it to be real, is it an illness or an accident or other

injury? Is it severe or of trifling account? Acute or chronic? We

observe the position of the patient, lying quietly in bed, sitting up,

or walking restlessly about the room. Then the countenance is

observed--pale or flushed, tranquil or excited in expression. We feel

the forehead, touch the cheek and hand. Is the skin hot or cold, dry

or moist? The pulse is felt; the breathing also is counted.

Of the patient himself or of another (in serious acute cases better of

his care-taker, in another apartment) we ask questions whose answers

give us the general history of the case. When not before known these

should include his antecedent personal history, even extending to that

of the family, as far as can be learned. What tendencies have they, or

has he or she, shown by previous attacks and their results?

So we come to the present attack: When did it begin, and how? What

have been its prominent symptoms since? Questions are then to be put

concerning the heat of the body, appetite, complaint of pain, sleep,

movement of the bowels, discharge of urine: in the female,

menstruation; if married, pregnancy or parturition, how often and when

occurring last. Thus the practitioner is enabled to get a clue to the

diagnosis, to be followed out through his own observation and closer

examination. If the patient be a child and the attack be acute and

febrile, an early question must be as to its having passed or not

through the different diseases of childhood--viz. the exanthemata,

mumps, and whooping cough, and also what exposure to any of these it

may have been recently subjected to.

Going farther into particulars, let us review some of the possible

developments obtained in the above questioning of symptoms.

When lying in bed the decubitus may be significant, as, upon the back

with the knees drawn up in peritonitis; with the hands pressing the

abdomen in colic; tossing to and fro in the delirium of fever or of

early cerebral inflammation; on one side constantly in acute

inflammation of the liver or in pleurisy. Or the patient may be

obliged to be propped in a sitting posture (orthopnoea) from

heart-disease, asthma, or ascites, or leaning forward upon the back of

a chair or a pillow with aneurism of the aorta. More remarkable still

may be the subsultus tendinum of low fever, the opisthotonos of

tetanus, the respiratory spasms of hydrophobia, or the clonic

movements of epileptic, hysterical, or occasional convulsions.

In the face we see pallor in syncope and in anæmia in any of its

varieties and with varied associations; a general redness in some

cases of apoplexy and in remittent fever; flushing of the forehead and

eyes especially in yellow fever; dusky redness in typhus, and a more

purple hue in typhoid fever; yellowness in jaundice, in some cases of

remittent and in most of yellow fever; sallowness in cancer; a bright

central glow upon each cheek in early pneumonia or the hectic of

phthisis; a blue or ashen appearance in the collapse of cholera, and

blackish-blue in {151} cyanosis or carbonic acid poisoning; bronzed in

Addison's disease; puffy about the eyelids in Bright's disease; the

surface swollen, yet resistant to the touch, in myxoedema. The eyes

(one or both) glare prominently in exophthalmic goitre; squint in

advanced cerebro-meningitis; roll to and fro often in the prostration

of cholera infantum and in convulsions; are clear and bright in

phthisis; yellowish in hepatic disorder; dull and clouded in low

fevers; without expression in imbecility and general paralysis.

Contraction of the pupil is observed in inflammation of the retina or

of the brain, narcotism from opium (until near death) or eserine, or

apoplectic effusion near the pons varolii. Dilatation of the pupil is

seen in most cases of hydrocephalus and of apoplexy; in

nerve-blindness (amaurosis), glaucoma, cataract, and narcotism from

atropia, duboisia, or hydrocyanic acid. Inactivity of the pupil

(Argyll Robertson) under changes of light and darkness is common in

locomotor ataxia. Different states of the two pupils under the same

light show disorder, either ophthalmic or cerebral in site, or may

indicate pressure on the cervical sympathetic ganglia, as from aortic

aneurism.

In elderly persons we ought always to look for the arcus senilis,

which is a sign of a tendency to fatty degeneration. It is a ring, or

part of a ring, with ill-defined edges, best seen by lifting or

depressing an eyelid, at the junction of the cornea and sclerotic coat

of the eye. In some quite healthy old persons there may be seen at the

same junction a clearly-defined circular line of calcareous nature.

This must be distinguished from the true fatty arcus senilis.

Of the face we may also notice the pinched nose, hollow eyes, and

falling jaw of the facies Hippocratica, presaging death; the square

forehead of the rickety child (not common in this country); ulcers on

the forehead, scars at the mouth-corners, or copper-colored eruptions

in syphilis; the full, flabby lips of scrofula. In peritonitis or

gastritis the mouth is apt to be drawn up with a peculiar expression

of suffering and nausea. Very striking is the characteristic one-sided

appearance in facial palsy, from lesion of the seventh nerve. There

may be a smile, a frown, or other expression on the sound side of the

face, while the paralyzed side is quite immovable. As the seventh

nerve (portio dura) supplies the orbicularis muscles, its paralysis

(so often temporary) may cause inability to close the eye upon the

affected side. Ptosis, or inability to open the eye, involving the

levator palpebræ, which is innervated by the third nerve (motor oculi)

is more significant of cerebral lesion.

Even the ears may have language, as when their lobes are full and

glistening red in the gouty diathesis, or wrinkled in prolonged

cachexiæ, or when they are running with discharges in the struma

(scrofula) of childhood. The hair becomes dry and lustreless in

phthisis, and falls out during convalescence from many acute diseases.

If we look at the gums in a case of lead-poisoning, we may expect to

find a blue line along their edges. Scurvy is betokened by a swollen,

spongy, and easily-bleeding state of the gums. Many scorbutic cases,

however, lack this so-called pathognomonic feature. It may be

remarked, by the way, that absolutely pathognomonic signs of

particular diseases, never absent and exclusively seen in them, are

very few. Albuminuria, for example, is not always present in Bright's

disease, and is {152} also met with in a number of other affections.

Sugar in the urine may follow inhalation of chloroform or an attack of

cholera, as well as diabetes mellitus. Rice-water discharges may be

absent in the collapse of cholera, and patients may die with yellow

fever without black vomit. Still, these symptoms have great diagnostic

value, and, taken with others associated with them, may often enable

us to attain to a diagnosis of much importance.

Perfect teeth in an adult in this country are rather the exception

than the rule. In the notched incisors of inherited syphilis, however,

there is something quite distinctive. The notches in Hutchinson's

teeth are vertical, not horizontal.

Old as medicine is the examination of the tongue in disease. It may be

protruded with difficulty, as in low fevers, in apoplexy, and in

cerebral paralysis (bulbar sclerosis, glosso-labio-pharyngeal

paralysis) or thrust to one (the paralyzed) side in hemiplegia. It is

pallid in anæmia; yellow in bilious disorder; red in glossitis (then

swollen also), in scarlet fever, and in gastritis; furred in

indigestion, gastro-hepatic catarrh, and the early stage of various

febrile attacks; dry, brown, cracked, or fissured in typhus or typhoid

fevers and in the typhoid state of malarial remittent fever; bare of

epithelium in advancing phthisis and in imperfect convalescence from

severe acute diseases. Coldness of the tongue is one of the worst

signs in the collapse of cholera.

As we examine the throat internally we look for signs of faucial

inflammation in redness and swelling, with or without enlargement of

the tonsils, or relaxation and elongation of the uvula, or ulceration,

or the gray or brown membranous deposit of diphtheria. In the mouth of

a child we may find the little white vesicular patches called aphthæ,

the curd-like exudations of thrush, or possibly the much worse grayish

ulcerations of cancrum oris, or the rarer ashen sloughs of gangrene of

the mouth.

Outside of the throat we must remember the significance of glandular

swellings or scars of suppurated glands in children; nor overlook, if

present, stiffness of the muscles, or torticollis, or goitrous

enlargement of the thyroid gland. Observation should be made also of

the site of the carotid artery on each side, and of the jugular veins,

since aortic regurgitation may be indicated by violent action of those

arteries or tricuspid regurgitation by pulsation of the veins in the

neck.

Long before vaso-motor physiology had any place in science the pulse

was known to afford valuable indications in disease. Either of the

accessible arteries will answer instead of the radial; its convenience

merely makes the wrist the common place of comparison. By careful

examination of the pulse something may be learned of several of the

factors concerned in its production. These factors are--1, the

muscular force of the walls of the heart; 2, the state of the cardiac

valves; 3, the muscularity of the arteries; 4, the elasticity of the

arterial coats; 5, the state of the capillary circulation; 6, the

qualities of the blood; 7, the condition of the nervous system as to

excitability or apathy.

A feeble heart must induce a feeble pulse. Moderate debility may be

attended by slowness of the pulse, but usually a weak circulation is

marked by frequent, small beats, like the vibrations of a short

pendulum. A strong heart-beat (other things being equal) is relatively

slow, with a proportionate pause after the second sound.

{153} Valvular lesions produce various effects upon the pulse. Most

notable are the irregularity connected often with mitral insufficiency

and the jerking pulse (Corrigan) of aortic regurgitation.

Believing, as the present writer does, in the existence of a true

arterial systole following and supplementing the ventricular

contraction,[38] it must be urged that a vigorous muscularity in the

arteries promotes strength in the pulse--not by resistance, but by

auxiliary propulsion of the blood. Another condition altogether is

tonic, spasmodic contraction of the arteries. This is not often met

with pure and simple, but a measure of it is seen in the corded or

wiry pulse of acute enteritis or peritonitis.

[Footnote 38: This view, although advocated by Sir Charles Bell,

Legros and Onimus, Hermann of Zurich, and others, is opposed to the

most prevailing vaso-motor physiology. Several complications and some

contradictions in pathological discussion at the present time would be

cleared up by the abandonment of the now commonly-held stopcock theory

of arterial function, which has really nothing whatever to support it

except the misinterpretation of some experiments upon arteries made

many years since.]

Deficient elasticity of the arteries is not easily separated in

observation from muscular relaxation. When arteries undergo

degeneration (atheromatous, fatty, or calcareous), their middle coat

suffers the deterioration of both elastic and muscular tissues, these

being substituted by materials either more or less yielding, and

always less resilient, than the natural fabric of the vessels.

The influence of the condition of the capillary circulation upon that

of the arterial system and the heart is manifest in inflammations. By

reflex excitation the arteries are made to contract actively and impel

the blood more forcibly than in the normal state toward the centre of

impeded nutrition (stasis). This has been abundantly proved by the

comparison of the amount of blood flowing through the arteries of a

sound limb and those of its fellow, when the latter is the seat of a

violent acute inflammation.

Blood-states also affect the pulse by the differences in direct

stimulation to which the heart and arteries are subjected according to

the qualities and composition of the blood. It is probable that the

fever-pulse of typhus, typhoid, the exanthemata, septicæmia, and

pyæmia has its origin in morbid conditions of the blood, acting in a

twofold manner--directly upon the heart and arteries themselves, and

mediately through the vaso-motor ganglia.

Lastly, the nervous system stands in an important relation to the

action of the heart and arteries, and thus to the pulse. In a nervous,

excitable person, changes in the rate of the pulse may take place,

with slight significance, which in a different constitution might be

of serious import.

To understand the language of the pulse care must be taken in several

respects:

1. Both wrists should be felt. Sometimes there is an abnormal

variation in the course of the main radial trunk which may pass over

the thumb. Again, an aneurism may cause a great difference between the

two radial pulses, or, possibly, an embolus may occlude one of the

radial vessels, annulling its pulsation.

2. Other arteries also, especially the carotids, should be

examined--in all obscure cases at least. Visibly beating, distended,

and tortuous temporal arteries are occasionally met with. They are not

pathognomonic of any one malady, although often referred to the gouty

diathesis. They {154} may attend irregular malarial attacks, or may be

connected simply with a hyperæmic state of the brain.

3. The heart's impulse should always be compared with the arterial

pulsation. The former may be strong and regular, while the latter is

small, feeble, or intermittent. Something must then be wrong, either

in the aortic valves or in the arterial system.

5. On account of possible nervous agitation, the pulse should usually

be examined more than once, during each visit to the patient.

6. Sex, age, position of the body, and time of day must all be taken

account of. In men the average rate of the pulse is between 65 and 75

per minute; in women, between 70 and 80. The pulse-rate of early

infancy varies from 100 to 120, and is very easily hurried. That of

old persons is commonly between 60 and 70, until, at a very advanced

age, with debility, its frequency may be increased, especially upon

exertion. Lying down, we find the slowest pulse; sitting, somewhat

more rapid; and most so in the standing position. In health the time

of day makes no constant difference apart from the effects of food and

exercise. In disorders attended by fever there are important changes

to be regularly observed. Excepting the variable paroxysms of

remittent and intermittent, which are a law unto themselves, in

febrile affections the pulse may be expected to be slowest in the

morning and most excited in the early part of the night. A diminution

of this difference is a favorable sign. Sleep generally slows the

pulse decidedly. The ordinary statement is, that the pulse is always

slower during sleep, but I have several times found that in states of

exhaustion without fever it may be considerably more rapid while the

patient is asleep. Nothing is more sure to increase the strength and

rapidity of the pulse than high temperature.

7. Very important is the relation between the pulse and respiration.

Normally, four pulsations occur to each respiratory act. In pulmonary

affections, while the circulation is often disturbed pari passu with

the breathing, it may be quite otherwise. Great acceleration of the

rate of breathing, with little increase in the rapidity of the pulse,

should lead us to suspect disease involving the respiratory organs.

Conversely, a much hurried or otherwise perturbed pulse, with little

or no change in the breathing, points toward the heart as either

functionally or organically the seat of disorder.

Let us further consider, briefly, the kinds of pulse to be met with

and interpreted in practice.

A natural pulse is always, per se, a good sign. Yet in the history of

a disease usually so well marked as yellow fever some fatal cases have

been recorded (walking cases) in which the pulse, almost to the last,

was natural.

Strength of the pulse, to a certain degree, belongs to it normally.

But this is often exaggerated, and we may have the strong, hard, full,

perhaps bounding, pulse of an inflammatory affection (of the brain,

for example, or of the joints in acute rheumatism) in a person of

vigor. A bounding pulse often accompanies mere palpitation of the

heart, whose source may be the sympathetic influence of indigestion or

nervousness. A similar pulse is apt to be constantly present in

hypertrophy of the heart. In this case it is made more forcible as

well as more rapid by {155} active exertion; while palpitation,

without organic trouble, is usually diminished by moderately active

exercise.

A full pulse is not always strong, nor is a small pulse necessarily

weak. Mention has been made already of the tense, corded pulse met

with in acute peritonitis, and sometimes in enteritis. Gastric

inflammation, with nausea, may exhibit a depressed pulse, weak and but

little accelerated. Under still other circumstances we may find a full

pulse which is soft, easily compressible, even gaseous. Most

frequently a feeble pulse is rapid, and a very rapid pulse is weak.

Slowness, in marked degree, attends apoplexy, opium narcotism, and

fracture of the skull compressing the brain. Functional disturbance of

the heart may occasionally exceed in effect these causes of

retardation. I have met, under such circumstances, with a pulse of 20

in the minute; one of 18 has been recorded. A few apparently healthy

persons have habitually a pulse with but 40 or 50 beats in the minute.

Quickness in each beat may occur, while a long interval makes the rate

per minute slow. The jerking pulse of aortic regurgitation is the most

remarkable example of this. Galabin asserts that without imperfection

of the valves of the aorta a decidedly abrupt pulse may attend great

lowering of arterial tension. Something of the same kind may be

noticed in the temporarily excited pulse of very nervous subjects

under agitation.

Dicrotism, or reduplication of the pulse-beat, is not uncommon in

typhus and typhoid fever. Here relaxation of the heart as well as of

the blood-vessels appears to allow a momentary interruption in the

succession of the arterial upon the cardiac systole.[39]

[Footnote 39: An exceptional phenomenon, noticed by a few observers,

is the recurrent pulse; _i.e._ a pulsation felt below the finger,

whose pressure interrupts the flow of blood through an artery. It may

be explained by supposing unusual fulness of the vessels (local, if

not general) with, at the same time, relaxation of their walls;

bearing in mind, also, the manner of anastomosis of the radial and

ulnar branches which favors recurrence.]

Intermittence and irregularity of the pulse are not exactly the same

thing. Occasional intermittence may be merely a nervous symptom or a

muscular twitch of the heart, like the twitches now and then occurring

without significance in voluntary muscles. Persistent intermittence,

with feebleness of the pulsations (these being generally somewhat

rapid), is among the signs of dilatation of the heart.

It is possible for intermittence of the radial pulse to accompany

regularity in the heart-beat. This usually results from narrowing

(stenosis) of the aortic valvular outlet from the left ventricle. Only

a certain number of impulses fairly reach the more distant arteries.

This symptom may result also from fatty degeneration of the heart.

Absence of pulse in one radial vessel, while it is present in the

other, shows the presence of an obstacle to the circulation on one

side, which may be an aneurism, or an embolus plugging the artery.

Irregularity of the pulse, a total derangement of its rhythm, while

not often important in young children, is a serious symptom at other

times of life. In one disease most common in childhood, acute

hydrocephalus, the pulse in the first stage is apt to be hard and

rapid, in the middle stage slow and tolerably full, in the third

rapid, feeble, and often irregular. Mitral disease frequently presents

considerable irregularity of the pulse; and so does dilatation, even

without mitral lesion. Brain trouble, especially late in life, whether

structural or functional, may produce the {156} same symptom. B. W.

Richardson has pointed this out as one of the effects of the excessive

use of tobacco, even in young persons.

The pulse of continued, relapsing, and remittent fevers is, during the

febrile exacerbation, rapid (100 to 120); in the earlier part of the

attack full, but only moderately hard, or even soft and yielding. As

the attack passes its height and critical defervescence occurs, the

pulse grows slower, unless great prostration has supervened; in which

case it increases in rapidity, while it fails more and more in fulness

and resistance.

The pulse of the moribund state is nearly always small, very rapid

(130-150), and thready, without force or fulness. It may become

imperceptible before death. A pulse of 140 beats in the minute is

always alarming; if much beyond that rate the case is desperate. A

pulse of more than 150 beats in the minute is very difficult to count

accurately.

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