CHAPTER LVII.

AMPUTATIONS 1023

GENERAL SURGERY.

INTRODUCTION.

An ultimate analysis of the primary causes of disease, excluding

traumatisms, will permit their reduction to one or the other of the

following categories: _nutritional_ (functional) and _parasitic_. These

may co-exist, in which case each tends to modify the other more or

less, usually unpleasantly, or either may precede and perhaps pave the

way for the other. In general, it may be said that parasitism perverts

nutrition, locally or generally, and, _per contra_, that perverted

nutrition often prepares the way for parasitic infection, so that even

between these primary causes there may occur all possible combinations.

With traumatisms surgery alone is mainly concerned, but its conceded

scope is now widened to include an ever-increasing number of morbid

conditions, which, in time past, were treated medicinally--or not at

all. Thus it has come to pass that it is no longer possible to make an

abrupt distinction between medicine and surgery, nor even briefly to

define the words “surgery” and “surgeon,” nor yet to ascribe to either

the physician or the surgeon his exact functions as such. In centuries

past physicians were exceedingly jealous of their vested rights, and

with propriety, when the only surgeons were uneducated barbers. But

about one hundred years ago conditions were materially altered for the

better, and surgery, liberated from its medieval environment, and from

the restrictions imposed by the clergy, rapidly developed into both a

science and an art, while the surgeon came to take that position in

society to which his increasing attainments entitled him. During the

past thirty years surgery, thanks to earnest workers in the surgical

laboratories of the world, has made progress scarcely equalled by the

science of electricity, and the impossibilities of yesterday have

become the routine of today.

Thus has come about the earlier separation, and now, in some respects

at least, the closer appreciation of the respective scope and functions

of the physician and the surgeon. Between them lies yet what has been

felicitously called the “borderland,” where they meet on common ground,

too often as rivals and not often enough as co-workers. Nowhere do

comprehensive knowledge, wide experience, and trained judgment appear

to better advantage, nor lead to better results, than when exhibited

where co-operation in these respects is most hearty. Someone has most

happily said that “the surgeon is a physician who knows how to use his

hands,” yet to regard a course in surgery as one in manual training

would be a most lamentable conception of its purposes. Rather is

it to be regarded as a superstructure, to be built upon a thorough

familiarity with anatomy, physiology, pathology, and therapeutics. In

fact, the better general practitioner a man is, the better surgeon may

he thereby become, providing he possess the other necessary attributes.

John Hunter took this view, but too many since his day have forgotten

or never realized it.

In the pages which follow it has been impossible to do more than

epitomize our present-day knowledge of surgery, an early disavowal

which is intended to save too frequent repetition of the advice to

consult, as needed, other larger and more specialized works. The

attempt here has been rather to build up a framework upon which the

student and the investigator may build with such other material as they

may later select from the quarries which are accessible to them. Hence

it has been impossible to describe or even mention all the operations

which have been devised to meet various indications. Preference has

therefore been given to those which have best served the author in his

personal experience.

Because of the numerous interrelations between surgery and internal

medicine, so called, I have not hesitated to insert paragraphs and even

whole chapters on subjects hitherto omitted from the later works on

surgery. To teach a student how to recognize nasopharyngeal adenoids,

to appreciate the widespread harm they may cause and how to cope with

them, and at the same time to leave him quite unfamiliar with their too

frequent relation to the status lymphaticus and its dangers, and to

omit in such a work all reference to the latter, is to put knowledge

and instruments into his possession without teaching him how rightly

to employ them. A case of exophthalmic goitre affords another equally

apt illustration, as being one in which the physician and the surgeon

should heartily co-operate.

The surgeon and the physician have drifted too far apart. It is time

that they met again in the presence of the pathologist. Such a group,

when properly constituted, forms an almost invincible triumvirate.

It has been said that “the resources of surgery are rarely successful

when practised on the dying.” Throughout these pages the attempt has

been made to impress the fact that delay, in many of the borderland

cases, is dangerous, and, often fatal, and that it is not just to

charge to surgery the blame for such a result due to the physician’s

dilatoriness.

It may lead to a better understanding of the teaching contained in

the following pages if it is here made clear just what is understood

by the suffix “_itis_” in medical terminology. The old tendency was

to regard all morbid conditions as expressions of inflammation in

some of its protean manifestations. The attempt has been made in this

work to distinguish as clearly as possible between _inflammation,

as an expression of infection_, and the vascular, nutritional, and

other changes which may be brought about by perverted nutrition

without necessary participation of parasites. To describe “ostitis,”

for example, as “inflammation of bone,” is to revert to an obsolete

definition. Let us, then, always translate the termination “itis”

as implying an _affection_, not necessarily an inflammation, of

the structure named in the word to which it is affixed. With this

conception of the word or the term there can be no contradiction in

its use under various conditions, and one does not necessarily commit

himself, by using it, to any definite view concerning the pathology of

the affection which is thereby implied.

With regard to one other feature there has been also a departure from

previous nomenclature. The term “lymph glands” or “lymphatic glands”

has always seemed objectionable, because, although they belong to the

lymphatic system, they are in no sense glands, having no ducts, and no

distinct secretion to be discharged through passageways. Whether in any

sense they are to be regarded as furnishing an “internal secretion”

is not the question here, their most obvious function being to act

as filters. Throughout the work, then, the term “lymph gland” has

been carefully excluded and the more accurate and far preferable term

“lymph node” has been substituted. This seems to be a suitable place to

explain the substitution and the reason therefor.

PART I.

SURGICAL PATHOLOGY.

CHAPTER I.

HYPEREMIA: ITS CONSEQUENCES AND TREATMENT.

The reactionary results of injury to various tissues and the first

local appearances due to the surgical infectious diseases are indicated

by certain appearances, which, for a few hours at least, are in large

measure common to both. Their beginnings being pathologically similar,

their results depend not alone on the violence or intensity of the

process, but also, and in predominating measure, upon the primary

influences at work. The consequences of mere mechanical injury--such as

strain, laceration, etc.--are in healthy individuals promptly repaired

by processes which will be taken into consideration in the ensuing

chapters. They are throughout conservative and reparative, and are

directed toward restoring, as far as possible, the original condition.

The consequences, on the other hand, of the surgical infections are

more or less disastrous from the outset, although the extent of the

disaster may be localized within a very small area, as after a trifling

furuncle, or they may be so widespread as to disable a limb or an

organ, or they may even be fatal. It is of the greatest importance, not

alone for scientific reasons, but also because treatment must in large

measure depend upon the underlying conditions, to differentiate between

these two general classes of disturbance, which we speak of as--

A. _Those produced by external or extrinsic disturbances_, _i. e._,

traumatisms, sprains, lacerations, etc.; and

B. _Those produced by internal and intrinsic causes_, which, for the

main part, are the now well-known microörganisms, such as cause the

various surgical diseases.

These latter disturbances may be imitated or _simulated_ in the

presence of certain irritants within the tissues, such as the poisons

of various insects and plants; the irritation produced by foreign

bodies, minute or large; and possibly the presence within the system

of certain poisons whose nature is not yet known, such as that of

syphilis, or certain others whose chemistry is fairly well understood,

but whose presence cannot be easily explained, as uric acid, etc.

Clinically, all these disturbances are manifested by certain phenomena

common to each, which may present themselves at one time more

prominently, at another less so. These significant appearances have

been recognized from time immemorial as the _calor_, _rubor_, _dolor_,

_tumor_, _et functio lesa_ of our ancestors, or as the heat, redness,

pain, swelling, and loss of function of our common experience. When one

or more of these are present, the surgeon cannot afford to disregard

the fact, while he should, moreover, be able to account for each on

general principles which should to him be well known.

To their more exact study we must, however, make some preface in the

way of general remarks concerning a phenomenon everywhere easily

recognized, but as yet incompletely understood. This phenomenon has

reference to an undue supply of blood to a part, and is commonly known

under two terms which are practically synonymous, namely, _congestion_

and _hyperemia_. To begin with these, then, we must note, first of all,

that congestion and hyperemia may be--

A. _Active_; and

B. _Passive_.

They may also be spoken of as--

1. _Acute_; and

2. _Chronic_.

Considering first the two latter distinctions, it will be found that

the acute hyperemias are met with most often in consequence of sharp

mechanical disturbances. The chronic hyperemias, on the contrary, are

conditions which in many individuals are more or less permanent. Note

accurately here the proper significance of certain terms. Hyperemia

means, in effect, an oversupply of blood to the given part; the term

should have only a local significance. When the entire body seems to be

too well supplied with blood, the condition is known as _plethora_, the

counterpart of which term is usually _anemia_. The direct counterpart

of the term _hyperemia_ should perhaps be _ischemia_, meaning a

perverted blood supply in reduced amount. With plethora and anemia

as terms implying general conditions, with hyperemia and ischemia

implying local conditions, there should be little room for confusion in

phraseology.

The active form of hyperemia used to be called “fluxion,” a term now

rarely used. _Active hyperemia_ means an increased supply of _arterial_

blood. In _passive hyperemia_ the oversupply is rather of _venous_

blood. In the former case the condition seems due to overactivity of

the heart, with such local tissue changes as permit it to occur. In

passive hyperemia the blood current is slower--there is a tendency

toward, and sometimes an actual, stagnation; all of which is usually

due to obstruction of the return of blood to the heart. The conditions

permitting these two results may be widely variant.

=Active Hyperemia.=--Active hyperemia may be produced by purely

nervous influences, even those of emotional origin. The flushing of

the face which is known as “blushing” is, perhaps, the most common

illustration of this fact. It is well known also that this is, in

some degree at least, the result of division of certain nerves which

have to do with the regulation of the blood supply. The cervical

sympathetic is the best known and most often studied of these, and the

consequences of division of this nerve in the neck are stated in all

the text-books on physiology. So also by electrical stimulation of

certain nerves the parts supplied by them can be made to show a very

active hyperemia, which will subside shortly after discontinuance of

stimulation, providing this has not been kept up too long. In active

hyperemia there is absolute increase of intra-arterial tension, and

under these circumstances pulsation may be noted in those small vessels

in which commonly it is not seen nor felt. This is the explanation

of the throbbing pain complained of under many actively hyperemic

conditions. This hyperemia affords the explanation of the clinical

signs to which attention has already been called. The increased heat

of the part is the result of greater access of blood, which prevents

cooling by radiation and evaporation; the peculiar redness is due to

the greater filling of the capillaries with the blood, which gives the

peculiar hue to the skin and visible textures; while to the increased

pressure upon sensory nerves is also due the pain. The minuter changes

occurring within the congested part call for more accurate description.

Whether or not there is actual dilatation of capillaries under these

circumstances is a matter still under dispute, but of the dilatation of

the larger vessels there can be no possible question.

As hyperemia is to such a great extent brought about by action

of the nervous system, it is well to divide it more accurately

into the hyperemia of paralysis, or _neuroparalytic congestion_,

which is the result of a paralysis of the constrictor fibers of

the vasomotor system, and into the hyperemia of irritation, or

_neurotonic congestion_, which is due to the irritation of the dilators

(Recklinghausen). Physiologists are fairly well agreed that as between

the dilating and the constricting apparatus of the vasomotor system

there is ordinarily preserved a certain degree of equilibrium; to which

fact is probably due that normal condition of affairs inaugurated after

temporary disturbance, since overaction in one direction succeeds

reaction in the other. As Warren has illustrated this, our common

treatment of frostbite by cold applications is a concession to this

fact, since by the cold applications we endeavor to limit the reaction

which would otherwise follow after thawing out the frozen part.

The best examples of the _hyperemia of paralysis_ are perhaps to be

met with after certain injuries to nerves, as, for instance, flushing

of the face and hypersecretion of nasal mucus, tears, etc., after

injury to the cervical sympathetic. Such, too, in its essentials is

that form of shock known as brain concussion, which is often followed

by nutritive disturbances among the brain cells, with consequent

perversion of brain function.

Waller’s experiment of placing a freezing mixture over the ulnar

nerve at the back of the elbow is also significant, the result being

congestion and elevation of surface temperature of the fingers supplied

by this nerve. Congestion and swelling have also been observed after

fracture of the internal condyle of the humerus, by which this nerve

was pressed upon; and similar phenomena may be noted in fingers or toes

as the result of injuries of other nerves.

Hyperemia due to _paralysis of the perivascular ganglia_ is observed

sometimes in transplanted flaps, in the suffusion of a limb after

removal of the Esmarch bandage, in the congestion of certain sac walls

after tapping, in the hyperemia of, perhaps even hemorrhage from, the

bladder wall after too quickly relieving its overdistention, and in

the swelling of the extremities when they begin to be first used after

having been put at rest because of injury.

The _hyperemias of dilatation_ are more acute in course and

manifestation. Along with them go sharp pain, hypersecretion of

glands, edema, and sometimes desquamation of superficial parts. The

facial blush due to effusion; the temporary flushing due to indulgence

in alcohol; the suffusion of the conjunctiva, perhaps the face,

with hyperlacrymation, accompanying facial neuralgia or hemicrania;

and the hyperemia consequent upon herpes zoster, urticaria, etc.,

are illustrative examples of this form. The erythema due to nerve

irritation or injury, the swelling of the joints which appears

after similar lesions, and that condition described by Mitchell as

_erythromelalgia_, probably also belong here. In fact, almost all the

reflex hyperemias are hyperemias of dilatation.

The forms of hyperemia considered above belong mainly to the

designation of _active_.

=Passive Hyperemia.=--Passive hyperemia is most often a mechanical

consequence of obstruction of the return of blood, which can be

imitated at will, and which is not infrequently the result of

carelessness, as when an injured limb is bandaged too tightly.

Experiment shows that when such mechanical obstruction has taken

place there is temporary increase of intravenous pressure, which soon

returns to the normal standard, such readjustment meaning that blood

has found its way back by collateral circulation. Only when such

rearrangement is possible do we have anything like permanent passive

hyperemia. In organs with a single vein, such as the kidneys, the

question of obstruction may assume a very important aspect. Under these

circumstances the appearance of the involved part, when visible, is

spoken of as _cyanotic_, while its surface, instead of being abnormally

warm, is the reverse, due to impeded access of warm blood and more

rapid surface cooling. The blood under such conditions is often darker

than natural, because, remaining longer in the part, it absorbs more

carbonic dioxide, or at least gives up more of its oxygen. As long as

actual gangrene is not threatened, the blood column has a communicated

pulsation, at least in the large veins. Escape of corpuscular elements

may occur after the phenomena above noted have been present for some

time; but the corpuscles rarely, if ever, escape until there has

been more or less copious transudation of the fluid portion of the

blood--_i. e._, the serum. When anatomical changes can be grossly, yet

carefully, observed, as in the fundus of the eye, it is seen that under

these circumstances the arteries become smaller, although whether this

is a primary or secondary change is not to be determined. Discoloration

of the integument is the frequent result of leakage of blood corpuscles

and their pigmentary substance into the tissues, and is consequently a

frequent accompaniment of chronic passive edema. It is seen often in

connection with varicose veins of the legs.

Another form of passive congestion or hyperemia is that due to

enfeeblement of the heart’s action by serious injury or wasting

disease. When under these circumstances the lung has become more or

less infiltrated with fluid, with hemorrhagic extravasation, the

condition is known as _hypostatic pneumonia_--a misnomer, nevertheless

indicating a condition which is only too frequent in the aged and

feeble.

RESULTS OF HYPEREMIA AND CONGESTION.

These may be--

1. Speedy subsidence of all hyperemic phenomena--resolution.

2. Acute swelling.

3. Chronic swelling.

4. Gangrene.

5. Nutritional changes--atrophy and hypertrophy.

1. =Resolution.=--The speedy subsidence of hyperemic phenomena is known

as _resolution_--a term which has also been applied to the retrograde

phenomena after a genuine inflammation. For present purposes it

implies, first, the subsidence into inactivity of the exciting cause

or its complete removal. This may include the passing of an emotion,

the removal of an irritant, the loosening of a bandage, the resort to

certain applications or to constringing or astringing measures by which

the effect is counteracted. A particle of dust in the conjunctiva may

within a few moments produce an active congestion of the conjunctival

vessels, which, ordinarily scarcely visible, becomes prominent and

easily noted. The removal of the offending substance permits a return

to their original size in perhaps a half-hour. This is an example of

the speedy subsidence of the hyperemia of dilatation after removal of

the cause. Should the hyperemia not subside promptly, it is well to use

cold applications, or in this instance an astringent collyrium, or some

agent whose physiological effect it is to produce vascular contraction,

as cocaine, adrenal extract, etc.

2. =Acute Swelling.=--When the effusion above referred to takes place

into loose connective tissues the condition is spoken of technically

as _edema_, while when it occurs into a previously existing cavity,

such as that of a joint, it is known as an _effusion_. The amount of

blood thus effused will be influenced by the anatomical and mechanical

conditions existing about the part. It may be presumed, as a general

rule, that when the extra vascular pressure equals the intravascular

pressure little or no more fluid may escape. As a matter of fact, it is

seldom that the former rises to the degree of the latter. Conversely,

one method of treating such edemas and effusions is by some device

which shall make the extravascular pressure exceed the intravascular,

when the fluid is, as it were, forced back into the vessels, and is

made to resume its proper place within the same. This is often done by

taking advantage of elastic compression, as when a rubber bandage is

applied about the part. In certain parts of the body it may be done by

pressure brought about by some other device. Pressure may be used for

two purposes:

_A._ To so increase extravascular pressure as to limit the possible

amount of an effusion, as when it is put on early after an injury; or,

_B._ When it is used as a later resort for the purpose of reducing

swelling which has already occurred.

3. =Chronic Swelling.=--This is something more than the swelling

alluded to under _Acute Swelling_. Chronic swelling implies either

a continuous passive hyperemia, or, what is more common, a positive

increase in tissue elements as the result of an oversupply of

nutrition brought by the blood, which itself was furnished to the part

in a degree far in excess of its needs. The result is a more rapid

reproduction of cell elements, with result in the shape of tissue

thickenings or tissue enlargements, known as _hypertrophy_, or, more

properly speaking, _hyperplasia_, of a part, and to the laity as

“overgrowth.” This chronic swelling or chronic enlargement is in some

degree also connected with the phenomena of escape of white corpuscles

from the bloodvessels and mitotic division of certain tissue cells,

which have up to this time been usually regarded as a feature of the

true inflammatory process.

4. =Gangrene.=--This may be the result of hyperemia--for the most part

the passive forms--though most instances of gangrene due to intrinsic

causes are inseparable from the presence of infectious microörganisms.

The gangrene which is spoken of here includes that due to the pressure

of tumors, tight dressings, or any natural or intrinsic agency, and

that due to pressure from without when not so pronounced as to produce

immediate and total loss of circulation in a part. It includes the

formation of many bed-sores and so-called _pressure-sores_, which may

be due to an enfeebled heart, to an obstructed pulmonary circulation,

or to external pressure in conjunction with cardiac debility. While

insisting, then, that gangrene should be recognized as a possible

result of hyperemia, it may be added that it is in effect a tissue

death, and that dead tissue is always and everywhere practically the

same thing, no matter by what causes brought about. Consequently, the

subject of gangrene will be considered under a separate heading.

5. =Nutritional Changes= will be considered later.

_The consequence of persistent hyperemia is transudation_--i. e.,

_escape of blood plasm from the vessels into body cavities and tissue

interspaces_. This leads to consideration under a distinct heading of--

TRANSUDATES AND EXUDATES.

Exudation may occur in vascular and non-vascular, in firm and soft

tissues, in, under, and upon membranes. With respect to location,

exudates are described as _free_, when found upon free surfaces or

within natural cavities; _interstitial_, when found between the tissues

or parts of tissues; and _parenchymatous_, when they are situated

within the tissues themselves, particularly in epithelial and glandular

cells of any kind.

Exudates are _serous_, _mucous_, _fibrinous_, or _mixed_, the mixed

forms including the so-called _seropurulent_, the _mucopurulent_, the

_croupous_, and the _diphtheritic_.

When any exudate contains red globules in sufficient quantity to stain

it, it is called _hemorrhagic_.

Serous transudates from free surfaces are sometimes spoken of as serous

_catarrhs_; when into cavities, as _dropsies_; when into tissues,

as _edema_; when occurring beneath the epidermis they form _serous

vesicles_ or _blebs_ or _bullæ_.

_Fibrinous_ exudation refers to the fluid which coagulates soon after

its exit from the vessels within those spaces into which it has

oozed. When flocculi of coagula float in serous fluid it is known as

a _serofibrinous_ exudate. Pure fibrinous exudate occurs rarely, save

in and upon mucous membranes. The extent to which exposure to the air

is responsible for the firm coagulation of the fibrin previously held

in solution is uncertain. The most potent factors in producing such

coagulation are bacteria, but it is not yet disproved that coagulation

may occur without their aid. When such coagulation occurs upon the

surface of a mucous membrane it has been spoken of as _croupous_. When

the epithelial covering as well as the basement membrane, and often

the submucous tissues, are involved, so that the membrane cannot be

stripped off without tearing across minute bloodvessels, the exudate

has been known as _diphtheritic_. These terms may possibly be still

retained in an adjective sense as implying the exact location of a

surface exudate, but are scarcely to be used in any other significance.

The following table illustrates significant differences whose full

importance cannot be impressed before a study of inflammation has been

carefully entered upon:

_Hyperemic Transudates._ _Inflammatory Exudates._

Poor in albumin. Rich in albumin.

Rarely coagulate in the tissues. Usually coagulate in the tissues.

Contain few cells. Contain numerous cells.

Low specific gravity. High specific gravity.

Contain no peptone. Contain peptone (product of cell

disintegration).

TREATMENT OF CONGESTION AND HYPEREMIA.

These disturbances are to be combated, first of all, by insisting upon

_physiological rest_. This, perhaps, is the most important measure of

all. The profession is indebted to Hilton for the decided advance which

he made in the treatment of congestive and inflammatory affections

by insisting upon this principle in his celebrated work on _Rest and

Pain_, which every young practitioner should read. Aside from this

first and underlying principle, the treatment must, in some measure

at least, be based upon the time at which we are called upon to treat

the case. If seen at once, before exudation has been excessive or the

other disturbances marked, we may carry out a certain line of treatment

for the purpose of limiting all these unpleasant features. On the other

hand, if seen late, when exudation has been copious and when pain and

other disturbances are due to its presence, a distinctly different

course will be adopted.

Toward the end first mentioned--namely, the limitation of hyperemia--we

may adopt local and general measures. Local measures include graduated

pressure, providing this is not intolerable to the patient, so

equalized that outside of the vessels it shall equal that inside. This

may be done by careful bandaging, extreme care being taken that the

pressure be applied from the very extremity of the limb; otherwise,

passive exudation might be augmented and gangrene be precipitated.

Elevation of a limb will often accomplish the same purpose. Cold, which

is in effect an astringent and which tends to contract bloodvessels,

is another measure in the same direction, and if applied early will

do much to limit the degree of the attack. This may be applied as dry

or moist cold, and should be gradually mitigated as the congestion

subsides. It acts through the vasomotor system, and is a measure to be

resorted to with caution. An efficient way of applying dry cold can be

extemporized by a few yards of rubber tubing, held in place by wire

or sewed in place to a piece of cloth, through which a stream of cold

water is permitted to pass.

Heat is another efficient means, acting, however, in a rather different

way. Heat is a measure to be employed to hasten the disappearance of

exudation--in other words to quicken resorption, which it does by

equalizing blood pressure, dilating the capillaries, stimulating the

lymphatic current, and in every way helping to clear the tissues of

that which has left the bloodvessels.

It is necessary also, at least in extreme cases, to employ some

detergent or derivative measures, including _bloodletting_, to which we

do not resort sufficiently often. When used for this purpose, depletion

should be applied at the area involved, if possible. This may be done

either as venesection, by leeching, either with the natural or the

artificial leech, or by a series of minute punctures or incisions,

which give relief to tension, permit the rapid escape of fluid exudate,

and often save tissues from the disastrous effects of strangulation. In

some cases of deep-seated congestions these measures are inapplicable,

and venesection at the point of election--say the cephalic vein in the

arm--may be followed by great benefit. Another method of depletion

is by administration of cathartics, such intestinal activity being

stimulated as shall lead to copious watery evacuations. The salines

rank high as measures directed to this end, but in emergency much

stronger and more drastic drugs may be administered, such as jalap,

calomel, elaterium, etc. Diaphoretics and diuretics help to reduce

temperature and in some degree to deplete, but their action is usually

slow. When exudation is considerable in amount and confined to some one

of the body cavities, it is often best combated, if at all obstinate,

by the method of _aspiration_. This includes any suitable suction

apparatus by which the fluid may be withdrawn through a small needle

or cannula, the operation being trifling in difficulty, but one to be

performed under strictest aseptic precautions, lest infection of an

exudate already at hand be permitted.

Certain individuals, especially the neurotic, will need more or less

anodyne, particularly when local applications fail to give relief.

Sometimes a small dose of morphine administered hypodermically will

act magically in making efficient those measures which would otherwise

be inefficient. In little children some anodyne or hypnotic will be of

great service. Under all circumstances it is well to keep the lower

bowel empty, and certain elderly individuals with weak and enfeebled

hearts will need the stimulation to be afforded by digitalis, quinine,

and alcohol, or preferably strychnine administered subcutaneously.

In cases of chronic hyperemia and its consequent hyperplasias

(induration, thickening, etc.) there is no one measure so generally

applicable and effective as the continued use of cold-water dressings.

These are generally spoken of as “cold wet packs,” and may be

continued--constantly or intermittently--for many days.

Massage is also an invaluable agent in the reduction of swelling and

tissue overproduction. It promotes absorption, even of acute effusions,

by equalizing the blood and hastening the lymph circulation, and under

its scientific application it is surprising how firm exudates and old

adhesions seem to disappear.

ATROPHY AND HYPERTROPHY, AND THE CONSEQUENCES OF ALTERED, DIMINISHED,

AND PERVERTED NUTRITION.

As a consequence of increase of nutrition we have a condition

known commonly as _hypertrophy_, more accurately as _hyperplasia_.

Hypertrophy literally means overgrowth, whereas hyperplasia more

accurately describes that which constitutes hypertrophy--namely,

numerical increase of constituent cells. Common usage has made the

more inaccurate name “hypertrophy” cover nearly all these conditions.

_Hypertrophy_, or hyperplasia, _means enlargement of a part or of an

organ beyond its usual limits_, and as the result of increased function

or increased nutrition. It is to be distinguished from _gigantism_,

which means inordinate enlargement as the result of a congenital

tendency or condition. Hypertrophy is--

A. _Physiological_ {1. Compensatory;

{2. From deficient use.

{3. Local;

B. _Pathological_ {4. General;

{5. Senile;

{6. Congenital.

[Illustration: FIG. 1

Congenital hypertrophy: gigantism of both lower extremities. (Case of

Dr. Graefe [Sandusky].)]

A. =Physiological Hypertrophy.=--1. This includes many of the

compensatory enlargements of an organ or a part when extra work is

put upon it, owing to deficiency of some other organ or part. This

is spoken of as _compensatory_ enlargement. Illustrative examples

may be seen in the heart, which becomes larger and stronger when the

bloodvessel walls are diseased and their lumen narrowed, or when other

obstructions to circulation are brought about; again, in enlargement

of one kidney after extirpation of the other, or of the wall of the

stomach when the pylorus is constricted or obstructed; again, of the

fibula after weakening or more or less destruction of the tibia, or

of the shaft of any bone when it has been weakened at some point by

not too acute disease; or, again, of the walls of bursæ after constant

friction.

2. The best examples of physiological hypertrophy owing to deficient

use are perhaps seen in some of the lower animals; as, for instance,

in the teeth of such rodents as beavers when kept in captivity and

prevented from natural use.

B. =Pathological Hypertrophy.=--3, 4. Instances of this are

everywhere and every day are met in the results of so-called _chronic

inflammation_, a term which is a complete misnomer and should be

expunged from text-book use. So-called chronic inflammation simply

means increase of nutrition owing to a certain degree of hyperemia,

which may have been produced in the first place as the result of

traumatism, which may have come from chemical irritants circulating

in the fluids of the part--as, for example, uric acid, etc.--or which

is brought about as the result of perverted trophic-nerve influence.

Instances of local pathological hypertrophy may be seen in the

thickened periosteum after injury, in the enlargement of a phalanx

known as the “baseball finger,” and in numerous other places; or they

may be general, in which case they are brought about mainly by some

irritating material in the general circulation. The unknown poison of

syphilis generally provokes such nutritive disturbances.

5. _Senile hypertrophy_ is connected with nutritional disturbances

characteristic of old age, as to whose remote causes we are still

uncertain. Instances of senile hypertrophy, however, are common,

particularly in the prostates of elderly men, which are liable to

undergo extensive enlargement.

6. Of _congenital_ hypertrophy and that of unknown origin we see, for

instance, examples in certain rare cases of hypertrophy of the breast,

in leontiasis, perhaps even in acromegaly, etc.; and these are to

be distinguished from _gigantism_, because in most instances of the

former type the hypertrophic tendency is not manifested until youth or

adult life, whereas gigantism is a condition in which the tendency was

apparent even before the birth of the individual.

ATROPHY.

_Atrophy implies impaired nutrition, and means diminution in the

size of an organ or part_, and is the converse of hypertrophy. It is

necessary to make plain that in atrophy nutrition is only impaired and

not arrested, since complete arrest of nutrition means necrosis--_i.

e._, gangrene or disappearance of parts. It may be--

{1. From disuse without disease;

A. _Physiological_ {2. Biological or developmental;

{3. Senile.

{4. Result of acute tissue losses;

B. _Pathological_ {5. Result of phagocytic activity;

{6. Result of continuous pressure;

{7. Specific.

A. =Physiological Atrophy.=--1. This is always the result of disuse

or impaired function from any cause. Its evidences are generally seen

in the fatty structures and muscles--_i. e._, in the soft parts. It

is true, however, even of the bones, or, of greater interest, even in

the brain cells. We see evidences of it also in minute organs; as,

for example, in the digestive glands in certain cases where diet is

restricted. Again, we see it in the diminution of the size of the heart

after hip amputation, less being required of that organ, and also in

the entire structure of the rectum after colostomy.

2. Examples of the _developmental type_ are best seen in the natural

disappearance of the hypogastric arteries, the ductus arteriosus,

the vitelline duct, the Wolffian bodies, and in the various

generative ducts (Gärtner’s, etc.) shortly after the birth of the

human individual. We sometimes see it also in the prostate after

orchidectomy. Equally illustrative is the disappearance of the tail

and gills of the tadpole, the eyes of animals living in caverns, and,

in a general way, of organs which become useless owing to a different

environment.

3. _Senile_ atrophy is seen equally well in the hair follicles, the

teeth, the bones, and the sexual organs of elderly people--in fact, in

all their tissues, even in the brain.

B. =Pathological Atrophy.=--4. Acute atrophy of surrounding tissues

is the necessary accompaniment of destruction by suppurative or other

disturbances; that is, parts disappear by absorption which have not

been interfered with by pyogenic organisms. So complete may atrophy

occur under these circumstances as to cause disablement of an organ

or part. This kind of senile disappearance is merely an expression of

phagocytic activity, although not now a question of bacteria.

5. The same is true of that variety spoken of above as _biological_ or

_developmental_, since phagocytes are the active agents in producing

the disappearance of the tadpole’s tail.

6. A more slow form of pathological atrophy is seen in the _gradual

disappearance_ of tissues in the neighborhood of advancing tumors,

enlarging cysts, etc. This is perhaps but another expression of atrophy

from continuous pressure. But a still better illustration is the

atrophy which comes from immobilization of a part without pressure.

This is usually the case when splints or orthopedic apparatus have to

be kept in place for some time.

7. _Specific_ forms of pathological atrophy are largely connected with

disturbances in the central nervous system. They are often referred

to as _trophoneurotic_. Their exact mechanism is not yet understood,

and cases may be confused under this head whose remote causes are

widely different. Here should be included, for instance, the atrophy

of a deep bone which occurs after extensive burn of the surface; also

that peculiar form of atrophy of tissues in the stump which produces

the so-called _conical stump_. These cases are of a more complicated

character, for if pressure is removed from the bone end, especially

in young people, the bone tends to grow faster than it should, while

the soft parts disappear, partly as the result of mere disuse or loss

of function. In this way conicity is produced, which sometimes calls

for subsequent re-amputation. Under this head might also be included

the so-called “trophic inflammation” (misnomer) of some writers,

such, for example, as ulceration of the cornea after division of the

trigeminus. The general subject of _atrophic elongation_ also belongs

here, referring to the fact that as a result of disuse, or sometimes

of active disease, the bones, while showing atrophic changes in other

respects, actually increase in length. Should such increase occur in

one bone of those portions of the limbs which are supplied with two,

the result would be posture deformity and displacement of the terminal

portion.

CHAPTER II.

SURGICAL PATHOLOGY OF THE BLOOD.

The part played by the constituent elements of the blood in

inflammation, suppuration, and other still more disastrous conditions

is so great and so important that, before proceeding to discussion of

these lesions, it seems necessary to set forth a _resume_ of facts

illustrating the importance of accurate knowledge concerning this most

important fluid.

The total amount of blood in the human body has been variously

estimated at from one-eleventh to one-twenty-fifth of the body weight,

the average being about one-sixteenth. The amount which the body may

lose and still retain vitality is very vague and differs not only with

individuals, but very greatly under various conditions. Severe loss

of blood is one to be atoned for as quickly as possible, and is to be

prevented as far as it can be after accidents or during operation. For

this reason the so-called bloodless method of operating upon limbs, by

the use of the rubber bandage, constituted a great advance in surgery.

For the same reason the use of hemostatic forceps is of equal value

in operating upon other parts of the body; other things being equal

the quickest and most satisfactory recoveries follow the bloodless

operations, and it is an advantage to conserve this vital fluid as far

as possible.

It has been roughly estimated that the blood is divided about as

follows, between the different parts of the body: the heart, lungs,

and large vessels holding one-fourth, the skeletal muscles one-fourth,

the liver one-fourth, the remaining quarter being distributed over the

balance of the body.

The blood varies within wide limits in its coagulability, and this

variation occurs apparently even within conditions of health. In some

patients the blood may be seen to coagulate almost as rapidly as it

collects upon the surface, while in others the exposed parts continue

to ooze, and the checking of hemorrhage is a difficult, sometimes

almost impossible, matter. There are certain diseases in which the

blood is known to have reduced power in this direction; for example,

in the toxemias, especially those connected with biliary obstruction

and jaundice. There were not a few of these cases of slow bleeding to

death in days gone by, simply because the capillary hemorrhage could

not be controlled. Recently, it has been shown that calcium chloride

administered internally has a marked effect in favoring coagulation,

and when opportunity is afforded it should be given for several days

previous to operating and as part of the necessary preparation. It may

be administered in doses of from 1 to 2 Gm., and should be given three

or four times, at least, in twenty-four hours.

A test of the coagulation time, normally three to five minutes, but

lengthened under circumstances like those mentioned above, even to an

hour, will often prove of great value.

There are certain albumoses whose effect on coagulation of the blood

is very suggestive and very mysterious. A very minute dose of cobra

poison, for instance, will make the blood of an experimental animal

remain fluid for days, unless this animal has been previously immunized

against it, in which case coagulation takes place even more rapidly

than normally. A trace of serum from an immunized rabbit is enough

to prevent the fluidifying effect of the cobra poison, but quite

insufficient to neutralize its toxic effects. The surgeon practically

never desires to reduce coagulability of the blood, but frequently to

increase it. When it is increased by natural conditions or those not

easily controlled, then it may lead to thrombosis and produce trouble

in that way.

=Fibrin.=--Increase of fibrin, _hyperinosis_, accompanies the

leukocytosis of inflammation and suppuration. It may be approximately

estimated on the cover-glass by noting the closeness of the network

resulting after fifteen minutes’ exposure. The inflammatory indication

of leukocytosis may, therefore, be inferred from its determination,

while the leukocytosis of malignant disease will not be so accompanied.

Hyperinosis is most marked in pyogenic processes, pneumonia and

rheumatism. Its opposite, _hypinosis_, is met with in pernicious

anemia. There is no change in the percentage of fibrin in the ordinary

anemias or chlorosis. In hemophilia and purpura hemorrhagica the

coagulation time is greatly increased.

=The Formed Elements of the Blood.=--The specialized elements of the

blood which are of particular interest to the surgeon are the red and

the white corpuscles. These may both vary in relative size within

certain physiological limits. The red cells especially are not of

uniform size and vary from 6 to 9 microns in diameter. There are also

present in normal blood a small number of red cells having a diameter

of only 6 microns, which are known as microcytes. In infancy there

are present also so-called giant corpuscles, or megalocytes, with

a diameter of 10 microns or more. Considerable variation occurs in

disease, especially in the severe anemias. Red corpuscles ordinarily

stain with acid dyes, which facilitate their examination and a

computation of the number present. When present in unusually large

number the condition is spoken of as a _polycythemia_; when in reduced

number as _oligocythemia_. In several of the anemias variations in

size, shape, and color occur, and in certain of them many of the red

corpuscles are found to be nucleated. Red cells which are nucleated are

known as _erythroblasts_, and according to their size are spoken of as

_microblasts_, _normoblasts_, and _megaloblasts_. Again, under certain

diseased conditions the ordinary discoid form of the cells becomes

irregular and crenated, and to those which are thus altered is given

the name of _poikilocytes_.

There is another form of degeneration which consists in death or

necrobiosis of the cell, whereby it loses its capacity for staining,

or, at all events, stains irregularly and abnormally. This is seen also

in cases of severe anemia and in conditions where the blood has been

altered by the addition of toxic material, such as chloroform, etc.

Occasionally also the red cells show a tendency to a granular change,

which is probably entirely degenerative.

The red corpuscles have a certain degree of elasticity which helps

them to pass through capillaries which are smaller even than their

own diameter; after escaping from these the corpuscles regain their

original form. In the presence of carbon dioxide they lose this

elasticity and become distorted or crenate. The influence of high

altitudes in increasing the number of corpuscles is known, but

unexplained. For instance, a residence of less than a month in the

mountains will cause an increase of from 2,000,000 to 3,000,000

corpuscles per cubic millimeter. It has been surmised that under the

influence of oxygen red corpuscle formation is stimulated to greater

activity; in other words, that the red marrow becomes more active in

the production of the hematoblasts.

In general terms it may be said that the blood of a normal adult male

contains 5,000,000 red corpuscles per cubic millimeter, and that of an

adult female 4,500,000. These figures are, of course, approximate and

variable. When the number is reduced to 3,000,000 by common consent the

case will be regarded as oligocythemia, and when increased to 6,000,000

as one of polycythemia.

The latter condition is most evident in cases of newly born infants.

The excess rapidly diminishes during the first week of extrauterine

life. It is to be explained by the loss of fluid suffered by the

infant upon the establishment of respiration. The proportion of red

cells also varies according to the nutrition of the individual, the

season of the year, the altitude (as above), and climate, and varies

during menstruation, pregnancy, lactation, and at the climacteric.

With the loss of red cells the number is reduced in proportion to

the hemoglobin, although the change in one respect is not exactly

proportionate to that in the other.

That the _colorless corpuscles_, or leukocytes, are not all of one kind

has been recognized for nearly sixty years, and long ago they were

divided into granular and nucleated cells. A vast impetus to the study

of hemocytology was given by Ehrlich, in 1878, when he introduced the

use of aniline dyes. The reader must be reminded that some of these,

like eosin, are acid in reaction, and others, like methyl blue, are

basic; while a third group has been supposed to be neutral in reaction,

like a mixture of methyl blue and acid fuchsin; but it has been found

that the so-called neutral dyes have really a slightly acid reaction.

We may, therefore, divide the cells according to the reaction of the

dyes with which they usually are distinguished into the acid and basic,

or, more technically, into oxyphile, which includes neutrophile, and

basophile.

This is not the place in which to go into any minute discussion of

this subject nor further than should be of practical interest to the

surgeon; nevertheless an examination of the blood by some common and

routine procedure is so necessary in many surgical conditions that it

is impossible to entirely avoid the subject in a work like this. I have

accordingly condensed it and put the salient facts about leukocytes

into the following table:

_Classification of Leukocytes._

_Granular._ _Non-granular._

{ A. With fine granules C. Hyaline. Transiti-

{Oxyphile. (polynuclear) 60- onal (large mono-

{ 70 per cent. nuclear) 4-8 per

{Neutrophile. cent.

Normal. {The so-called B. With coarse

{neutral stain granules (eosino- D. Lymphocytes (small

{being slight- philes) 2-5 per mononuclear) 20-30

{ly acid. cent. per cent.

{

{ E. Fine and coarse G. Atypical hyaline

{ granules (baso- (myelocytes).

Patho- {Basophile. philes, mast-

logical. { cells, etc.).

{

{Oxyphile. F. Atypical (myelo-

{ cytes).

In normal blood by far the greater part of the leukocytes consists of

A and D. _Lymphocytosis_ means a relatively high percentage of C and

D. _Eosinophilia_ means an increase in the proportion of B. Basophile

cells are not absolutely pathological, for they may be present in very

small numbers in normal blood.

The number of leukocytes in normal blood will average about 7000 to

10,000 per cubic millimeter, the percentage of each variety being

given in the above table. Leukocytes are sometimes diminished in

number; under diseased conditions they are often increased, and these

are then included under the term leukocytosis. Variations occur daily

and almost hourly under normal conditions. Increase naturally occurs

after digestion, when the number of leukocytes may be almost doubled,

the same being due principally to lymphocytes which are washed into

the blood system from the lymph nodes by the flow of lymph or chyle.

In starvation, however, the number may be remarkably reduced and in

the case of the fasting man, Succi, the leukocytes were reduced at

the end of the first week to 860 per cubic millimeter. The rather

unusual condition of reduction of the number of corpuscles is called

_leukopenia_.

Leukocytosis is usually the rule in carcinoma, with increase in A and

F; the more rapid the growth, the greater this increase. In sarcoma

this is even more pronounced; when occurring without hyperinosis the

probability of malignancy is greater. Non-malignant tumors produce no

such changes.

The blood _platelets_ or _plaques_ first described by Bizzozero, in

1882, have no small interest for physiologists and pathologists, but

little for the practising surgeon. They number perhaps 5,000,000 per

cubic millimeter and sustain a fairly constant ratio to the red cells.

Their surgical interest is limited to the role which they may play in

the formation of thrombus.

The term _phagocytosis_ has to do in a general way with those

leukocytes which act as scavengers by removing from the blood its

noxious elements, presumably by a process of ingestion and digestion

(see Chapter III).

Examination and estimation of the various formed elements of the blood

are very valuable to the surgeon in the study of the anemias, of acute

inflammation when the presence of pus is suspected, in the presence of

suspected cancer, and in the presence of such conditions as Hodgkin’s

disease, the various disorders of the spleen, etc. The so-called

_primary anemias_ include only the pernicious anemias and chlorosis;

all others are designated as _secondary_. This distinction is not for

convenience only, but serves a useful purpose.

_Pernicious anemias_ produce a reduction both of the red corpuscles

and the hemoglobin, the former usually in a greater degree than the

latter, so that the _color index_ (see below) is usually plus. Many of

the cells become nucleated and, in general, their size is increased. In

chlorosis the reduction of the hemoglobin is relatively large and the

color index is extremely low. In the secondary anemias the red cells

and hemoglobin are reduced disproportionately, so that the color index

is minus. There may or may not be a relative increase of leukocytes and

of the nucleated red cells, but these latter are not so likely to be as

large as those seen in primary anemias. The _color index_ is obtained

by dividing the percentage of the hemoglobin present by the percentage

of the red cells.

Leukocytosis becomes pathological in conditions of acute inflammation

where the neutrophiles (A) show the greatest relative increase. The

degree of leukocytosis depends on two different factors: the intensity

or the virulence _of the infection_, and the _vitality_ or resisting

power _of the individual_. These vary within such wide limits that it

is hard to predicate anything definite in a given case. In general

the increase is supposed to be proportionate to the severity of the

infection, though the greater the reactionary ability of the patient

the larger the number of white cells. Where vitality is very low

leukocytosis is less pronounced. It is possible to have toxemia to such

a degree that the activity of the leukocytes seems to be destroyed. The

following summary from Cabot puts things in very distinct form.

Infection mild, vital reaction good--small leukocytosis.

Infection less mild, vital reaction less good--moderate leukocytosis.

Infection severe, vital reaction good--very marked leukocytosis.

Infection severe, vital reaction poor--no leukocytosis.

From this it will appear that the absence of leukocytosis in cases

where it naturally would be expected is a serious indication and

justifies an unfavorable prognosis; or else it may be interpreted in

evidently favorable cases as indicating infection of very mild grade.

There are but few diseases in which leukocytosis by itself (or for that

matter any other indication which the ordinary examination or blood

count may give) is wholly sufficient for diagnostic purposes. But a

blood count and estimate of the amount of hemoglobin present will often

be of such advantage to the surgeon that he may well afford to wait in

order to secure them. This is rarely necessary in acute cases, but in

chronic cases, and especially the anemias, he may gain great benefit by

such investigation. In _trichinosis_, for example, eosinophilia is most

pronounced, B forming even as high as 70 per cent. of the leukocytes

present.

The anemias which are of particular interest to the surgeon may be

classified as follows:

1. _Anemias without marked leukocytosis._

A. Characterized by oligocythemia.

B. Characterized by diminution of hemoglobin.

2. _Anemias with marked leukocytosis._

A. Leukemia (leukocythemia).

B. Pseudoleukemia (Hodgkin’s disease).

1. A. Anemias due to hemorrhage may assume one of two forms, that

resulting from sudden and extensive loss of blood or that resulting

from constant oozing. Example of the former is seen in hemorrhages

of the stomach or intestines after perforating ulcer, etc. Examples

of the latter are met with in hemophilia and in uterine hemorrhages,

or in excessive menstruation where the loss of blood extends over

a considerable length of time. It is known, moreover, that certain

entozoa in the intestines will produce a chronic anemia. Thus the

red corpuscles may be reduced to even less than 1,000,000 per cubic

millimeter. Immediately after acute hemorrhage the hemoglobin

percentage is still normal, but after a short time it becomes reduced.

If such cases do not speedily end fatally, nucleated red corpuscles

appear in the blood and the observer will recognize both normoblasts

and megaloblasts. At the same time the bone-marrow, which is normally

yellow, becomes red, vascular, and richly cellular, and seems to

furnish these cells just mentioned. Certain drugs, like potassium

chlorate and glycerin, affect also the number of red corpuscles,

but such poisons as these cause not only disintegration of the red

cells, but produce also jaundice and hemoglobinuria. Pernicious anemia

sometimes interferes with or fatally complicates surgical treatment.

It is characterized by the extreme changes already mentioned, with

which it marches steadily to a fatal termination. Quincke has reported

an instance in which their number was reduced to 43,000 per cubic

millimeter, while the hemoglobin was reduced to 20 or 25 per cent. of

the normal amount.

1. B. The best example of anemia which depends upon diminution of the

hemoglobin content of the red cells is that known as _chlorosis_. In

this there are few recognizable signs of destruction of corpuscles,

even under chemical microscopic examination; consequently the blood

picture is very simple. The color index is very low, yet similar

conditions may also be seen in syphilis, tuberculosis, and cancer. The

underlying feature of all of these cases is malnutrition.

Within a few years a peculiar form of intense anemia has been described

by Banti and others, and is often spoken of as _splenic anemia_ or

_Banti’s disease_. It is characterized by three stages: first, of

splenic enlargement and anemia; second, a transitional stage; third,

a stage of ascites which increases up to death. It is quite closely

allied to Hanot’s hypertrophic cirrhosis of the liver. It is quite

generally regarded as an example of an infection by some as yet

unknown organism. It is of interest to the surgeon because if the

spleen is removed early there are fair prospects of recovery.

2. A. _Anemias with marked leukocytosis_ include especially those

first spoken of by Virchow as _leukemia_. Originally he applied the

term to a particular alteration of the blood, but it is now made to

cover a group of diseases, all of which are characterized by peculiar

and more or less similar increase of white corpuscles. Sometimes these

are increased to such an extent as to make the blood grossly resemble

a mixture of blood and pus. This resemblance led some of the earlier

observers to speak of the condition as “suppuration of the blood.” The

number of leukocytes is sometimes enormously increased; 1 to 10 of the

red cells is quite common and 1 to 5 not exceedingly rare. Cases have

been known in which the white cells outnumbered the red. In well-marked

cases of leukemia, the red cells will be somewhat diminished, while

the white will number from 100,000 to 500,000 per cubic millimeter.

Accompanying this change in the blood there are alterations in

the spleen, the lymph nodes, and the bone-marrow, sometimes one

predominating, sometimes another. It has been customary in fact to

speak of splenic, lymphatic, and medullary leukemia, but these forms

are not sharply differentiated and a pure type of either form is rare.

In this country we speak mainly of _lymphatic_ and _splenomedullary_

forms, the latter being much more common. The latter is accompanied

by enlargement of the spleen, while in the lymphatic form the lymph

nodes are involved and may become as large as walnuts. In the lymphatic

form over 90 per cent. belong to C and D; in the splenomedullary or

splenomyelogenous form the increase of F and G is most marked, while

A will be reduced to 50 per cent. and D to about 10 per cent. The red

corpuscles are decreased in number, but not necessarily in an inverse

ratio; their number may be reduced even to 2,000,000 in extreme cases.

In these cases, besides the change in number and form of the leukocytes

already described, there are frequently found in the blood very minute

crystals first described by Charcot. These are small, often adherent

to the leukocytes, and most frequently found when eosinophile cells

predominate; their exact significance is not known. The pathology

of leukemia is too remote from the purpose of this work to receive

consideration here. Without asserting its germ character one may say

that it is under suspicion, and that various observers have described

appearances supposed to indicate a specific cause, probably a protozoön.

2. B. _Pseudoleukemia._--This has, in time past, gone under many

different names, of which the most common is _Hodgkin’s disease_ (_q.

v._). Many speak of it as _malignant lymphoma_. This is doubtless a

disease with a specific cause, as yet unrecognized, which produces

very significant changes in the blood, especially in the white

corpuscles. The spleen and lymph nodes are both involved, mainly the

latter. The general blood changes are quite variable and one may find

many types. As a rule, these comprise not so much an increase in the

number of leukocytes as a decrease in the number of red cells by

which an apparent leukocytosis is brought about; hence the expression

_pseudoleukemia_. Many cases, however, will present a certain degree

of actual leukocytosis, the proportion of the whites to the reds being

about 40 to 50.

_What interpretation in general is to be given to leukocytosis?_ A

condition deserving this name is, first of all, essentially temporary.

In acute infectious diseases it shows itself during the febrile stage

and the principal increase is in the finely granular oxyphile cells. In

such diseases as erysipelas, as well as pneumonia, it lasts but a short

time after the crisis has been reached and the temperature has fallen.

In diseases like acute appendicitis and acute peritonitis from any

cause a marked leukocytosis may be regarded as indicating the presence

of pus; it should be emphasized, however, that _pus may be present

without this indication_, and it has been previously stated that such

a fact is to be interpreted either as an example of a mild degree of

infection or an exceedingly reduced vitality.

=Differential Leukocyte Count.=--It seems to be now quite clearly

demonstrated that the mere establishment of a certain degree of

leukocytosis does not furnish the surgeon a reliable guide for

determining the presence of pus, it being an index of reaction rather

than of actual severity of any particular kind of infection. A much

more reliable guide is found in the proportion of polynuclear cells to

the total number of leukocytes counted, _i. e._, by what may be called

a differential count. In order to make this reliable, the normal ratio

should first be determined. This is put at a point between 68 and 80

per cent. by various writers. As Gibson (_Annals of Surgery_, April,

1906) says, 75 per cent. may be considered the best working average.

This average should be maintained as the total number of leukocytes

increases, or else there is a disproportion which becomes significant.

With a moderate leukocytosis there is a notable increase in polynuclear

cells, and it may be estimated that there is either a severe form of

lesion or less resistance to absorption, or both.

[Illustration: PLATE I

_Fig. I._

_Fig. II._

_Fig. III._

_Fig. IV._

_Fig. V._

_Fig. VI._

_Fig. VII._

_Fig. VIII._

_DRAWN BY J. N. Z. CHASE_]

PLATE I.

BLOOD.

(Ehrlich triple stain.)

(Prepared by DR. I. P. LYON.)

Fig. I. TYPES OF LEUCOCYTES.

_a._ Polymorphonuclear Neutrophile. _b._ Polymorphonuclear

Eosinophile. _c._ Myelocyte (Neutrophilic). _d._ Eosinophilic

Myelocyte. _e._ Large Lymphocyte (large Mononuclear). _f._ Small

Lymphocyte (small Mononuclear).

Fig. II. NORMAL BLOOD.

Field contains one neutrophile. Reds are normal.

Fig. III. ANÆMIA, POST-OPERATIVE (secondary).

The reds are fewer than normal, and are deficient in hæmoglobin and

somewhat irregular in form. One normoblast is seen in the field,

and two neutrophiles and one small lymphocyte, showing a marked

post-hæmorrhagic anæmia, with leucocytosis.

Fig. IV. LEUCOCYTOSIS, INFLAMMATORY.

The reds are normal. A marked leucocytosis is shown, with five

neutrophiles and one small lymphocyte. This illustration may also

serve the purpose of showing the leucocytosis of malignant tumor.

Fig. V. TRICHINOSIS.

A marked leucocytosis is shown, consisting of an eosinophilia.

Fig. VI. LYMPHATIC LEUKÆMIA.

Slight anæmia. A large relative and absolute increase of the

lymphocytes (chiefly the small lymphocytes) is shown.

Fig. VII. SPLENO-MYELOGENOUS LEUKÆMIA.

The reds show a secondary anæmia. Two normoblasts are shown. The

leucocytosis is massive. Twenty leucocytes are shown, consisting

of nine neutrophiles, seven myelocytes, two small lymphocytes, one

eosinophile (polymorphonuclear) and one eosinophilic myelocyte.

Note the polymorphous condition of the leucocytes, _i. e._, their

variations from the typical in size and form.

Fig. VIII. VARIETIES OF RED CORPUSCLES.

_a._ Normal Red Corpuscle (normocyte). _b, c._ Anæmic Red Corpuscles.

_d-g._ Poikilocytes. _h._ Microcyte. _i._ Megalocyte. _j-n._

Nucleated Red Corpuscles. _j, k._ Normoblasts. _l._ Microblast. _m,

n._ Megaloblasts.

Gibson has suggested the formation of a chart where the number 10,000

of leukocytes shall appear upon the same line with 75 per cent. as the

average normal proportion of polynuclears. Then drawing a parallel

line, which shall indicate on one side each 1000 in increase of the

former and each advance of one in the percentage, it will be seen that

15,000 leukocytes will correspond to 80 per cent. of polynuclears,

20,000 to 85 per cent., etc. When upon this chart there is drawn a line

between that dot which represents the total leukocytosis on one side

and that on the other which indicates the percentage of polynuclears,

then the more horizontal this line the less the disproportion, while

the more marked the angle it makes with the base line the greater the

disproportion appears. It furnishes an admirable graphic record which

the eye appreciates at once.

It would appear, then, that a differential blood count made in this

way, and thus recorded, affords the most valuable diagnostic and

prognostic aid in acute surgical diseases, indicating especially the

presence of suppuration or of gangrene.

=Glycogen in the Blood and the Iodine Reaction.=--Glycogen occurs in

the blood especially in three classes of cases: those where there is

marked respiratory disturbance in certain of the anemias, and, what is

of especial interest to the surgeon, toxemias, either of chemical or

bacterial origin. It is usually present in the secondary and pernicious

anemias as well as in acute and late leukemias. It is considered

by some that in these cases it really indicates the occurrence of

some bacterial infection. Especially is glycogen present in cases

of suppuration and surgical sepsis, _i. e._, in those cases where

leukocytosis is usually, but not invariably, present; indeed, it would

seem to be a most significant indication. While the iodine test is

more easily carried out than is a blood count, the latter affords more

information. The reaction is reliable and its relative intensity gives

an idea of the intensity of the inflammatory process. In many cases

with obscure symptoms and without leukocytosis its presence will afford

much aid in diagnosis. It is of great assistance also in distinguishing

between a deep-seated pneumonia and serous pleurisy, since in the

latter there is no reaction, or in distinguishing between pleurisy with

effusion and empyema; again, in distinguishing gonorrheal arthritis

from true rheumatism. In a case of strangulated hernia the presence

of the iodine reaction would indicate that pressure had produced

gangrene, whereas its absence would indicate a relatively lesser degree

of destruction. It has been aptly said that the presence of iodine

reaction indicates that the patient is seriously sick.

It is easily obtained by staining a cover-glass with a blood smear in a

gummy solution of iodine and potassium iodide. When the blood is normal

all the cells take on a uniform, bright-yellow color, while the white

cells stain more lightly than does their protoplasm. When the glycogen

reaction is present, brown granules are seen in the protoplasm of the

polynuclear leukocytes, which may often take on a different brown tint.

Frequently brown particles are to be seen outside of the corpuscles,

while occasionally the other forms of leukocytes show also the reaction.

The value of a careful blood examination is well illustrated by

Plate I, prepared by Dr. Irving P. Lyon, in which are displayed the

alterations of greatest interest to the surgeon.

HEMOGLOBIN.

The principal interest of the red blood corpuscles for the surgeon,

aside from their relative number and shape, inheres in their relation

to hemoglobin, and hemoglobin is of particular interest here because

much can be learned by estimating the proportion in which it is

present. Hemoglobin has, furthermore, an interest which reaches

beyond the mere blood appearance, since it is considered to be the

apparent source from which both the urinary and biliary pigments are

produced. That the amount contained in the blood varies within wide

limits under different conditions has long been known. When notably

reduced in amount the condition is referred to as _oligochromemia_. The

ideal normal standard is present in but a small proportion of cases,

even in strong young men in the third decade of life. The average

is considerably lower and can scarcely be placed above 90 per cent.

Females show a smaller amount than males--3 or 4 per cent. less. In

anemia its reduction is not usually proportionate to that in the number

of red cells. After hemoglobin loss, as after surgical operations,

much can be gained in the matter of prognosis by estimating the speed

of its regeneration. With regard to how much actual hemoglobin loss

a patient can bear, it seems to be more important to determine how

much still remains in the body. The minimum is apparently 20 per

cent. In three cases dying of collapse after operation, Mikulicz

found only 15 per cent. remaining. The rapidity of regeneration is

a fairly accurate indication of improvement in every other respect.

Regeneration is interfered with by constitutional syphilis, and, on

the other hand, is often apparently favored in cases of tuberculosis.

In malignant tumors the average of hemoglobin is reduced to about 60

per cent., and in these cases also complete regeneration is materially

retarded. Incomplete removal or recurrence of cancer prevents typical

regeneration or restoration, while, after successful or radical

removal, complete restoration to the previous standard, often with

positive gain, is obtained. Thus, a woman who had gained thirty

pounds after resection of a cancerous pylorus, showed, after three

months, hemoglobin repair to the amount of 65 per cent. A prognostic

significance often attaches to the accurate estimation of hemoglobin at

intervals after removal of malignant tumors.

A very convenient method for the ready estimation of hemoglobin is

afforded by the Tallquist color scale. It can be practised at the

bedside and is sufficiently accurate for the surgeon’s general purposes.

THROMBOSIS.

Thrombosis is a term applied to the formation of a _thrombus_--_i. e._,

a clot within the cavity of the heart or one of the bloodvessels--the

term being limited to coagulation of blood within these natural

cavities, and without specifying the exciting cause of the same. A clot

so formed is called a thrombus. To be accurate, a distinction should

be made between a thrombus, which is caused always before death--or,

rather, during life--and the _clot_, which is essentially a postmortem

affair. Our application, then, of the terms “thrombosis” and “thrombus”

refers solely to that which takes place during life. In order to

appreciate the conditions which lead to thrombosis it is necessary

to fully appreciate the reciprocal conditions which must normally be

maintained between the circulating blood and the walls of the vessels

in which it flows. Fluidity of blood depends always upon integrity

of the vessel wall. As long as its lining membrane is absolutely

undisturbed and normal, moving blood will never coagulate within it,

and the only thrombi that may be met within it are those which are

propagated from a distance. Coagulation of blood is, for the main part,

associated with the peculiar properties of fibrin.

Fibrin is produced from _fibrinogen_, a globulin which is held in

solution under ordinary circumstances, which has certain peculiarities

of its own. When the change occurs it is entirely consumed and none

remains in the blood serum. Fibrinogen is split up by a peculiar

ferment called _thrombin_ into what we ordinarily speak of as fibrin

and a small amount of a soluble globulin, which remains in solution in

the serum. Thrombin is not a normal constituent of the blood, but is

formed when it escapes, as the result of the reaction between certain

calcium salts and a nucleoproteid, which has been called _prothrombin_.

The latter arises from the disintegration of the leukocytes, especially

the polynuclear, and the blood plaques, after the blood leaves the

bloodvessels. Calcium salts seem absolutely necessary for coagulation;

hence the value of the administration of calcium chloride in certain

cases previous to operation. Another essential feature seems to be

the absolute integrity of the endothelial lining of the bloodvessels,

although for this fact there is no satisfactory explanation. If a

portion of a vein is removed from the body after double ligation

its contained blood will not coagulate for a long time. Blood which

is kept circulating through the lungs and heart alone soon loses

its coagulability; hence the liver seems to be concerned in some

way in maintaining it. Certain other substances also seem to retard

coagulation, such as the albumoses of snake venom, and certain

synthetic, colloid, proteid-like substances, which can be introduced

very gradually. If, however, they are introduced rapidly, or in large

quantities, thrombosis occurs promptly. We have much to learn about the

coagulation of the blood, but the above facts are at least suggestive

to the surgeon.

[Illustration: PLATE II

FIG. 1

Small Vein showing Diapedesis of Leukocytes. (Engelmann.)

_a_, leukocyte escaping between endothelial cells; _b_, _c_, leukocytes

escaped; _f_, leukocytes migrating toward centre of attraction.

FIG. 2

Septic Thrombosis of Pulmonary Capillaries after Puerperal Septicemia,

showing Rapidly Increasing Colonies of Streptococci. (Klebs.)]

=Causes.=--The underlying _cause_ of all _thrombi_ is, then,

_alteration of the endothelium_. In consequence, when it is desirable

to produce coagulation artificially, advantage may be taken of this

fact, and mechanical injury to the vessel walls may be quickly followed

by the desired results. Advantage is also taken of this fact in

surgery, especially in certain methods of treating aneurysm, by rude

handling, by needling, by the introduction of horsehairs, fine wire,

etc. A venous thrombosis is certainly favored by the thinness of the

venous walls, by which poorer protection is afforded to their lining

endothelium, and infection more easily occurs. Arterial thrombosis is

favored when cardiac vigor is impaired and vessel walls are thickened

so as to obstruct the blood current. This occurs particularly in

syphilitic endarteritis, where the intima suffers most, and final

occlusion is due to the thrombus thus formed. Arteriosclerosis does

not, by itself, often produce this trouble; it comes rather with

atheromatous and calcareous degenerations. The local ischemia which

is occasioned by ergotism, by pellagra (due to use of certain kinds

of maize), by the vasomotor spasm of Raynaud’s disease (see under

_Gangrene_), by too long-continued constriction, or by frostbite,

causes results comparable to those produced experimentally in parts

supplied by a terminal artery, _e. g._, in the kidney after temporary

occlusion of its artery. All the tissues involved undergo profound

alterations, in which thrombosis figures very largely and may lead to

gangrene.

While such endothelial lesions are essential, there are, nevertheless,

numerous other accessory causes which should be mentioned. These

comprise:

A. _The presence of foreign bodies_, as, for example, needles, hooklets

of echinococci, parasites, particles of tumors, fragments from the

heart valves, and, most of all, that which is essentially a foreign

body, a clot which has come from some other point. Around such foreign

particles will quickly group themselves a relatively large number of

leukocytes, thus affording another example of phagocytosis, soon to be

described. Mere slowing of blood stream without some such mechanical

irritation is not sufficient to produce coagulation. If, for instance,

a section of vein is isolated between two ligatures, the ligation being

aseptically done and the surroundings of the vein wall disturbed as

little as possible, the blood thus shut up within the vein remains

fluid indefinitely. If, however, the vessel wall is separated from its

surroundings, so that its nourishment is compromised, the contained

fluid quickly coagulates.

B. _Necrosis_, _gangrene_, etc., lead to quick involvement of the

endothelium of the vessels contained within the involved part, and

consequently to quick coagulation of the blood which they contain.

C. _Temperature_ has also an influence in the same direction, and

extremes in either direction, or drying of vessels which may happen to

be exposed to the air for some time, lead to the same results.

D. _Inflammatory and degenerative processes_ occurring in and about the

vessel walls tend always to produce coagulation. This is well seen in

the influence exerted by the so-called _atheromatous ulcers_--_i. e._,

the degeneration of certain areas in the walls of large vessels.

E. _Microörganisms and their products_ are perhaps the most frequently

effective of all the accessory causes of thrombosis. In other words,

in all the surgical infectious diseases we may expect to find more or

less, sometimes extensive, thrombosis in the vessels of the affected

part. This may so far shut off circulation as to produce temporary or

permanent edema, or it may lead to gangrene, which may be local or may

terminate the life of the patient.

_Thrombi are classified_ as:

1. _Primary_; and

2. _Propagated_.

The _primary_ thrombus is one which has originated at the spot where

it has been first produced, and is usually co-extensive with its

cause. The propagated thrombus may be one which has been carried to

a considerable distance, and is met with at a point widely different

from that where it originated, or one which has extended along the

vascular channel in which it was first formed, but far beyond the

limits of its prime cause. When a thrombus attaches itself to a part

of the vessel wall it is called _parietal or valvular_, because it

does not completely occlude the vessel; when it involves the entire

circumference of the vessel, but does not completely occlude it, it

is spoken of as _annular_. The _obstructive_ thrombus is that which

completely fills a given vessel and shuts off all circulation through

it.

The _propagated_ thrombus extends usually in both directions, and

always much farther in veins than in arteries. Thus, thrombi may be

met with extending from the ankles even into the inferior vena cava.

The venous valves may on one hand excite coagulation, or on the other

tend to fix the coagula more firmly in their place. In arteries thrombi

usually extend only to the first collateral channel on the cardiac

side, but occasionally they spread farther. The _cause of a primary

thrombus_ is to be _sought at the site of its lodgement_; the _cause

of propagated thrombi_ is often observed _at a wide distance from the

effect_.

Thrombosis is, again, to be spoken of as--

_a. Marasmic;_

_b. Mechanical or traumatic;_

_c. Infective._

_a._ The _marasmic_ forms are due to essential alterations in the

constituents of the blood, which are due mainly to starvation or

wasting disease. Marasmic thrombi seldom give rise to serious

disturbance during life until the condition is so complex and grave

that the patient is at death’s door. Postmortem evidences of marasmic

thrombi, however, are often found, and yet have but little surgical

significance. They are seen perhaps as often in the cranial sinuses as

anywhere.

_b._ Thrombi of _mechanical or traumatic_ origin are those, for

instance, which are due to the presence of foreign bodies, to

stagnation of blood as the result of ischemia or local anemia, to

compression by tumors, etc.

_c._ _Infective_ thrombi are those distinctly due to the injurious

effects of micro-organisms, and are those mainly concerned in the

various manifestations of sepsis which are of interest to surgeons.

While the ordinary evidences of thrombosis are most often looked for

in the veins of the extremities, in the lungs, and in the cranial

sinuses, it must not be forgotten that thrombosis may occur equally

easily in the portal system of vessels; in which case we find the most

marked expressions in this system and in the liver. In cases also of

pyemia proceeding from lesions in the rectum or in the bowels there are

evidences of infection, abscess, etc., in the liver, but not in the

lungs, to which point infective thrombi from other sources are promptly

carried.

The _ultimate fate of a thrombus_ depends entirely upon the presence or

absence of bacteria. If septic, it invariably breaks down. If aseptic,

it may undergo one or more of the following metamorphoses:

A. _Decolorization._--This is noted particularly in the red thrombi,

and is due to disintegration of the red corpuscles, their coloring

matter being diffused and resorbed or transformed into hematoidin. It

would be a mistake, however, to suppose that all light-colored thrombi

are those which, originally red, have been decolorized. The possibility

of white thrombi must always be remembered.

B. _Organization._--This is the result of time, and means a

metamorphosis into solid vascular connective tissue. Newly formed,

minute, vascular loops project from the vasa vasorum into the thrombus,

and it becomes thus vascularized, while the completion of the

organization is due, in the main, to spindle-cell connective tissue,

which is formed by wandering cells that penetrate into the thrombus

from without. This gives the organized thrombus a certain resemblance

to a sponge, and makes the original vein resemble a cranial sinus,

since its interior is spanned by bands of connective tissue. Typical

illustrations of this kind are seen, for instance, where the iliac

veins join to form the inferior cava, by which a certain amount of

obstruction to venous return is produced without its being total. The

length of time required for these changes is indefinite. They begin,

however, within a short time after ligature of a vein, and proceed with

a rapidity varying according to circumstances.

C. _Calcification._--Calcium salts are occasionally deposited in

thrombi, usually not until they have undergone considerable contraction

and alteration; as the result of which we have formation of small

masses, essentially minute calculi, to which the name of _phleboliths_

has been given. These phleboliths are not infrequently found in more or

less occluded and much distended varicose veins of the extremities, and

they prohibit the occurrence of softening.

D. _Softening._--This is the most serious termination of the thrombotic

accident, and is usually due to the agency of infecting organisms.

A non-infectious form is, however, recognized, by which there is a

metamorphosis of original clot into an oily or pulpy fluid, usually

dark colored, but in the white thrombi often yellowish white,

reminding one crudely of pus. The discovery of such material under

these circumstances has led in time past to the supposition that pus,

as such, was found floating in the blood--a condition that does not

exist except under extraordinary circumstances. It is with infection

of thrombi and consequent softening, however, that surgeons have most

to deal, and the paramount importance to them of such disturbances is

emphasized in the article under Pyemia.

A closely allied topic to that above considered is the subject of

_thrombophlebitis_. This means, in effect, inflammation of one or

more veins, which is directly due to the presence therein of thrombi.

Such a condition is, in its strict sense, an inflammation, since it

is always an infectious process. If in the veins of a non-infected

region simple thrombi form, they may be occluded by organization of the

included masses, but such a process never extends beyond the immediate

area involved. On the other hand, if the process is essentially an

infectious one, either from without or from within, then both vessel

and its contained thrombi succumb completely to the infectious process,

which is also essentially a spreading one; and this is limited only

by mechanical barriers, by conservative suppuration, or often only by

the life of the individual. Excellent examples of thrombophlebitis are

seen in the involved uterine sinuses in cases of puerperal septicemia,

and in the cranial sinuses after infected compound fractures, or

particularly after disease originating in the middle ear has extended

to them.

Thrombosis is, at times, a distinctly surgical condition, and often

a surgical complication of febrile and other diseases, especially

typhoid, in which it constitutes a serious complication and prolongs

convalescence for a period of several months. If foreseen it can

scarcely be prevented, and when present calls for treatment varying

with the location of the lesion and the exciting causes. In the earlier

stage anything like rude manipulation or massage is very unfortunate,

since soft clots might thus be broken up and distributed to other parts

of the body. Absolute physiological rest combined with the application

of silver ointment, of ichthyol-mercurial ointment, which should be

covered with some non-absorbent material, will probably give the best

results. If the lower limbs are affected it may be well to elevate the

feet so as to favor return of blood through vessels not yet obstructed.

After a certain length of time the thrombi may be regarded as at least

adherent if not organized, and massage will prove an important remedy,

since by it the lymphatics will be better enabled to take up the

fluids which have leaked from the bloodvessels and produced the edema

which always characterizes these cases. Sluggishness of circulation

is nearly always followed by more or less laxness of tissue, or

actual hypertrophy, and a limb thus involved may never regain its

original size or flexibility. Veins once compromised, if not occluded,

frequently become varicose, or varicosities develop in adjoining veins

and still further complicate the case. For such difficulty the measures

discussed in the chapter on the Veins may be later required.

In every fresh case of thrombosis or thrombophlebitis great care should

be taken in order that by no means shall the clots be disengaged and

float away. The dangers correspond to those existing in variocele and

nevi, often treated by the older methods of injection of coagulating

material. In one instance reported, a child died within half an hour

after the injection of an iron salt into a small nevus of the face.

Coagulation was excited to a point far beyond the limits intended.

_Thrombophlebitis is essentially a surgical condition_, occasionally

terminating favorably by suppuration and spontaneous evacuation,

but calling for surgical intervention whenever it can be recognized

and the parts are accessible. The principles of treatment of these

conditions are positive and unmistakable. They comprise evacuation

of the infective material and disinfection of the involved cavities

and tissues. Thus, in sinus phlebitis--_i. e._, thrombophlebitis of

the lateral sinus--it has been made practicable not only to open the

sinus in the mastoid region, but to expose the jugular vein in the

neck, to ligate it, and to wash through from one opening to the other,

effectually getting rid in this way of a long mass of infected thrombi.

Only by such bold and radical measures in many of these instances may

life be saved.

EMBOLISM.

Embolism means the _transportation of any material by which a

bloodvessel can be occluded or plugged_ from one part of the vascular

system to some other. The underlying idea is that of _transportation_

or carriage. An _embolus_ is anything so transported, without implying

its exact character. The name is even applied to so unsubstantial an

affair as a minute bubble of air, which, however, in a tube containing

a circulating fluid is a possible source of considerable disturbance.

A single bubble thus carried would, by itself, be a trifling affair,

but when numerous bubbles are thus transported the result is such local

disturbance as may lead to loss of function. Thus, _air embolism_,

so called, may provoke profound, even fatal, disturbances, as, when,

with the returning blood stream through the cranial sinuses or one of

the large veins in the neck, when opened by accident or operation,

air is sucked in, it is carried to the right side of the heart, whose

action is perhaps completely perverted because of the new and strange

substance which thus enters it, so different from that for which its

lining membrane is prepared and to which it reacts. The _entrance of

air into veins_, which constitutes in effect air embolism, has been

in time past a bugbear to surgeons, but nevertheless is a source of

probable danger when large venous trunks in proximity to the heart are

thus exposed. Air embolism is certainly a rarity. On the other hand,

those substances which figure most often as emboli are _vegetations

from the valves of the heart_; _drops of fat_; _fragments of tumors_;

_pieces of softened and disintegrated thrombi_; _foreign bodies_, as

hooklets of echinococcus cysts; and, perhaps most often of all, the

_microorganisms_ clinging to some minute fragment of thrombus which

has been dislodged. Embolism is also produced experimentally by the

artificial introduction into the circulating blood of cinnabar or

small particles of pith or other material. Emboli differ in number and

size from the smallest appreciable up to the largest, which may be

met with in the larger venous trunks. They are _dislodged_ from their

primary site sometimes by _accident_, as by rude manipulation, injury,

etc.; sometimes by _undue cardiac activity_, as when detached from a

valve wall; sometimes by the _process of softening_ of thrombus and

a subsequent introduction into the blood stream as a result of some

trifling motion; or even by _spontaneous processes_. Emboli also differ

in numbers according to the nature of the primary lesion. In cases of

so-called fat embolism fluidified fat is taken into the returning blood

stream, carried to the heart, churned up with the contained blood,

and distributed to the lungs in such a way that myriads of minute fat

masses are distributed throughout the capillaries of the lungs, and

free circulation of blood through them is thereby impeded.

It will thus be seen that the relations between thrombosis and embolism

are most intimate, but that either one may occur without the occurrence

of the other.

Among the viscera, with the exception possibly of the brain, the

disastrous consequences of such processes as those just described

are more apparent and indicative than in _thrombosis and embolism

of the mesenteric bloodvessels_--a condition not so rare as journal

articles would imply, yet, nevertheless, one seldom recognized either

during life or after death. Its principal symptoms consist of intense

abdominal pain, bloody diarrhea, subnormal temperature, sometimes with

vomiting, perhaps in the latter stages vomiting of blood. Shock is

usually also extremely marked. The consequence of this condition is

almost inevitably gangrene of the intestine supplied by that particular

portion of the mesenteric vessels. The pain comes on within a short

time after the occurrence, and under the peculiar circumstances

gangrene may be practically determined within a few hours. Some two

hundred and fifty cases of this kind are now on record, and the

condition is one well worth the prompt attention of the surgeon,

because only by surgical intervention--_i. e._, by resection of the

necrotic mass of intestine--can life possibly be saved. That when a

limited portion of the intestine is involved the gangrenous part may be

successfully removed has been proved by several operators. (See Chapter

LII.)

It will thus be seen that embolism constitutes often a distinctly

surgical condition for which unfortunately only radical measures are

suitable. Many cases of gangrene of the toes and feet, extending to the

legs, are produced by embolism of the femoral and popliteal arteries,

similar conditions being noted less often in the upper extremities.

Amputation offers the only resource in such instances, at the same

time affording no guarantee against any similar embolic disturbance

elsewhere. In only most exceptional instances is it possible, by

resorting to moist heat, position, etc., to encourage circulation to

such an extent as to obviate the necessity of amputation. (See Chapter

V.)

=Fat Embolism.=--Fat embolism as a distinct, sometimes fatal, surgical

condition has received of late so much study as to be entitled to

consideration by itself. By this term is meant a plugging of small

arteries by minute drops of fat, which, having been set free somewhere

about the periphery, are carried into the venous circulation and thence

distributed to various parts of the system. Inasmuch as the capillaries

of the lungs are often their first lodging place, fat embolism here

is most often met with, and consequently recognized and studied. But

it may occur in the brain, the choroid, the kidneys, or other parts,

provided only that there has been sufficient _ris a tergo_ on the

part of the heart to force the fat globules through the pulmonary

capillaries and into the systemic circulation.

[Illustration: FIG. 2

Fat embolism of lungs. Large branching pulmonary artery filled with

spherical, oval, cylindrical, and branching masses of fat. Fresh mashed

preparation in potassium hydrate. (Kaiserling.)]

Fat embolism occurs frequently, and to a slight extent in nearly every

case of fracture and laceration. So common is it, and so closely

allied are some of its most prominent symptoms to those of shock,

that as a matter of fact many cases heretofore considered shock are

to be regarded as instances of this condition. Indeed, even in a

miscellaneous series of 260 dead bodies fat embolism was found in 10

per cent. The injuries most likely to be followed by it are simple,

and particularly compound fractures of bones; laceration of soft

parts, especially of adipose tissues; certain surgical operations;

acute infections of bone and periosteum; rupture of fatty liver; and

certain pathological conditions where the phenomena are not so easily

explained, _e. g._, icterus gravis, diabetes, etc.

Drops of fat may be seen floating on fluid or semifluid blood after

many operations and compound injuries, and the possibility of escape of

fat--or, more accurately, its suction into the vessels from which this

blood has escaped--is easily appreciable. But it has also been shown

that absorption of fat is possible even from serous surfaces, and that

fat embolism may occur when fluid fat has been passed into the heart

through the thoracic duct, although more slowly. Oil drops are also

found in the interior of the tissues, while in a piece of lung spread

out in water in the visible vessels highly refracting fatty material

may be noted. _Fatty infarction_, particularly in the lower lobes, is

sometimes plainly visible to the naked eye. Under a low objective,

especially with osmic-acid staining, the presence of fat is easily

demonstrated.

The essential danger in case of fat embolism is of so clogging the

pulmonary capillaries that oxygenation shall become so imperfect as

to lead to absolute asphyxiation from carbonic dioxide poisoning.

When this fact is understood, the cyanosis, the rapid breathing, the

overaction of the heart, etc., are easily and correctly interpreted.

Fat embolism by itself cannot cause inflammation nor infection, nor

sepsis in any sense. It may, however, lead to ecchymoses in conjunction

with fatty infarcts in the organs most affected. The minute hemorrhages

are easily explained by the bursting of the capillaries in the attempt

to force blood through them. Fatty emboli, however, take the same

course as do septic--are carried first to the right side of the heart

and distributed over the lungs; are, if the patient lives, forced

through the lungs into the systemic circulation, and are then carried

to the brain, kidneys, etc. The first symptoms are referable to the

plugging of the pulmonary capillaries; the secondary symptoms to the

systemic disturbance.

=Symptoms.=--Pallor of countenance with facial expression of anxiety

and distress, followed by cyanosis and contracted pupils, are seen.

Patients are usually first excited, sometimes more or less disturbed,

then become somnolent, and, finally, comatose in the fatal cases. The

respiration rate increases from normal up to 50 or 60, and breathing is

sometimes stertorous. Dyspnea, increasing in intensity until it becomes

agonizing, sometimes marks these cases. Occasionally foam, possibly

blood, proceeds from the mouth, as in edema of the lungs. Sometimes

hemoptysis occurs. The pulse becomes weak, frequent, and irregular,

while toward the close it is fluttering. Temperature is not notably

disturbed, at least not typically.

These symptoms set in usually within thirty-six to seventy-two hours

after the lesion which has caused them. I have, however, known death

to occur in one or more cases within eighteen hours after reception of

injury.

After fat has been forced through the lungs and carried to the kidneys

it will be eliminated with the urine, and may be found floating upon it

in the shape of oil-like drops. Discovery of this condition is positive

evidence of fat embolism. It is to be distinguished from shock in that

by the time the symptoms of embolic disturbance are at their height,

all or nearly all symptoms of pure shock have subsided. Furthermore,

cyanosis and embarrassment of respiration are not indicative of shock;

and, finally, the discovery of fat in the urine will be corroborative.

A mild degree of fat embolism may be noted, if looked for, after almost

all serious fractures. It will give rise to slight embarrassment of

respiration and cyanosis and to the elimination of fat by the kidneys.

=Prognosis.=--Prognosis varies according to the extent of the injury

and the proximity of the lesion to the heart and lungs; also to the

possibility of continuous entrance of fat, _i. e._, from its continual

absorption. Prognosis really depends upon whether the heart can be

given sufficient vigor and endurance to continue pumping blood with its

burden of fat through the pulmonary circulation. A secondary danger

may come from the circulation of this fat-ladened blood through the

capillaries of the brain. Should the source of motive power thus become

paralyzed with resulting general enfeeblement, death may ensue. When

well-marked evidences of fat embolism are present, but are followed by

recovery, the worst of the trouble is usually over within forty-eight

hours after it begins.

=Treatment.=--Obviously treatment is mainly directed toward the

heart, so that we may stimulate it to carry its load of fat through

from the venous into the arterial system. If it can do this, the fat

is disposed of by oxidation or is saponified by the alkalies in the

blood. Physiological rest of the injured part is the first indication,

however, and if this occurs in a patient, say with delirium tremens,

powerful mechanical restraint may be necessary. The most effective

cardiac stimulants are called for--alcohol, adrenalin, strychnine. In

other respects treatment is largely symptomatic. Next to giving the

heart vigor in this way, inhalations of oxygen give the most promise,

because of the crying need of the system during this ordeal for this

life-giving gas.[1]

[1] See paper by the author. New York Medical Journal, August 16,

1884.

PHYSICAL PROPERTIES OF THE LEUKOCYTES.

=Phagocytosis.=--All leukocytes have the power of shifting their

location. The lymphocytes, so called, being the youngest of the white

corpuscles, show it less than the older forms. The eosinophile cells

are less able to manifest the peculiar activities of the other forms.

It is particularly the mononuclear and polynuclear corpuscles which

are endowed with most pronounced activity. These have the power,

like the ameba among the lowest forms of life, to not only spread

themselves around inert bodies, like granules of carmine or other

particles used for experiment, or the particles of coal-dust found in

certain conditions in the human body, but they also have the power to

englobe many living organisms, for the main part vegetable (bacteria).

Under the microscope it is possible to see living bacilli, performing

active movements, although enclosed in the nutritive vacuoles of

the leukocytes, in some of the lower animals. This _ameboid_ power

possessed by these cells of thus attacking and disposing of foreign

bodies or irritants has been demonstrated and proved, especially by

Metchnikoff, and has been called by him _phagocytosis_. His views

were for a long time disputed, and are perhaps not yet absolutely and

generally accepted. Nevertheless, they fulfil every demand made upon

them for explanation, and are susceptible of such demonstration under

the microscope that we now have practically a new and apparently a

correct theory of the inflammatory process. (See Chapter III.) Any

cell which has this property is known as a _phagocyte_. It is shared

by some of the leukocytes with certain other cells to be spoken of

later (wandering tissue cells). Cells which possess this power do not

attract all microbes indiscriminately, and it is often the case that

the leukocytes of an animal peculiarly susceptible to a certain kind

of bacteria do not attract them at all, even though they are directly

in contact. It is plausible that an explanation of the peculiar

susceptibility of certain animals to certain diseases is furnished by

this fact (Fig. 3).

[Illustration: FIG. 3

Phagocytosis in anthrax pustule. (Gaylord.)]

On the other hand, leukocytes may and do englobe virulent microbes.

In man the mononuclear forms do not take up either the streptococcus

of erysipelas or the gonococcus; whereas these two organisms are

readily attracted by the polynuclear neutrophile cells. The bacillus

of leprosy, on the other hand, is never attacked by the polynuclear

forms, but is speedily devoured by the mononuclear cells. This shows

that the various leukocytes may exercise a marked selective ability.

This inclusion of minute bodies within ameboid cells seems to be an

evidence of a peculiar tactile sensibility upon the part of the latter.

In fact, this is clearly established, and seems to be inseparable from

the peculiar attraction between leukocyte and bacterium, to which the

name _chemotaxis_ has been given, and which is described in an ensuing

chapter. If the included organism is, as is usually the case, killed,

it is disposed of by a true process of intracellular digestion in a

neutral or alkaline protoplasmic medium, and its inert portions are

again extruded. On the other hand, if the leukocyte is poisoned or die

in this phagocytic attempt, it presents usually as a so-called _pus

cell_ or _corpuscle_, and the solid part of pus is made up in large

measure of cells which have perished in this way. (See Inflammation and

Suppuration.)

_To regard phagocytosis as an affair mostly of certain tissue cells and

invading bacteria_ would be altogether too narrow a view to take of

it. It is really a process of the greatest importance and of constant

performance in our systems. By virtue of it disintegrated muscle

fibers and other tissue cells are disposed of, sloughs are separated,

certain absorbable foreign bodies (catgut, etc.) taken away--_i. e._,

absorbed--cellular tissue reduced in numerical strength (progressive

atrophy), and a great variety of changes, either normal, as those

pertaining to health and advancing years, or abnormal, like those

incident to many diseases, are actually the product of this kind of

phagocytic activity. The protective power, then, which the phagocytes

exert as against bacteria is only one part of their normal functions,

by virtue of which they become, in effect, perhaps the most important

cells within our bodies. Their powers are limited, however, as will be

seen when describing pus, for the so-called pus corpuscle is nothing

but a phagocyte which has perished in its self-assumed task. It is

known also that in certain instances phagocytes, which are incapable

of defence as against the mature bacterial organism, are nevertheless

capable of englobing its spores and preventing their development.

This is true, for instance, in case of anthrax in animals ordinarily

immune, as, for instance, the frog and fowl. If, however, in these very

animals the vitality of the phagocytes be affected--as by cooling in

fowls or heating in frogs--phagocytosis is so far interfered with that

the spores germinate within the enfeebled leukocytes and the entire

organism is infected.

CHAPTER III.

INFLAMMATION.

_Inflammation is an expression of the effort made by a given organism

to rid itself of or render inert noxious irritants, arising from within

or introduced from without_ (Sutton, modified).

After having duly considered hyperemia as a phenomenon having an

identity and termination of its own, we are prepared to study the more

complex processes included under the term _inflammation_, the first

of which is the hyperemia already considered. The characteristic of

the truly inflammatory process is that it does not stop with mere

congestion nor with any of its previously mentioned terminations, but

goes on to something more complex. It must be understood, therefore,

in this consideration that hyperemia is the first act of the vessels,

resulting from peculiar stimuli which will shortly be considered.

Even the hyperemia seems to be now more distinct than under other

circumstances, and, along with the dilatation of vessels and the

stagnation of blood current, the capillary vessels seem crowded with

blood corpuscles to an abnormal degree, the rapidity of their motion

is checked, and there occurs accumulation of blood cells along the

walls of the small veins, to which they seem to adhere as if by some

new cohesive property. The result is that before long the vessel wall

appears to have received a new coating of white corpuscles, this being

more marked in the veins than in the arterioles, while in the latter

the red are more numerously mingled with the white than in the veins,

in which the distinction between the two classes of cells is better

maintained.

Next comes the phenomenon whose clear recognition and description

is inseparably connected with Cohnheim’s name. This is known under

different names as _migration_ or _diapedesis of the leukocytes_. The

program is about as follows: A little protrusion of the vascular wall,

a marked alteration in the shape of a leukocyte, which yet adheres

to this point of its lumen, and then the curious fact so often seen

under the microscope--the gradual passage of this cell through the

vascular wall, from its inner to its outer side, by what is generally

known as its _ameboid movement_. This migration of the leukocyte is

not confined to its mere escape from the restriction of the vessel

lumen, but goes on to an indeterminate extent after it has detached

itself from the outer surface of the vessel. This seems to occur by

virtue of the same ameboid characteristic which it exhibited in passing

through between the cells of the vessel itself. If this occurs at one

point, it occurs at innumerable points, in consequence of which a large

number of leukocytes escape into the tissues of the part involved.

This diapedesis occurs most markedly from the smaller veins, to a

less extent from the capillaries. The cells which escape from the

latter are usually accompanied by red cells, the consequence being

that the exudate which necessarily occurs at the same time is more or

less tinged with the coloring matter of the blood, and is known as a

hemorrhagic exudate.

The above phenomenon, described in so few words, is in its minutiæ

a really complex one, depending on a variety of causes not easily

appreciated; but it is at least positive and well known, because it

can be observed at will in the mesentery or web or tongue of certain

animals which can be confined upon the stage of the microscope. The

_phenomena of inflammation_, therefore, comprise, first, _hyperemia_,

and then _escape_ from the bloodvessels of the _corpuscular_ and

_fluid_ elements of the blood. The former may be due, as already seen,

to various irritations of a non-specific character; while, as we shall

learn, the latter practically never take place save when the irritation

has been, as pathologists say, specific or infectious.

The phenomena of true inflammation comprise practically the roles

played by the three elements which conspire to produce those

changes--namely, the _tissues_, the _blood_, and the _specific

irritants_ which are the primary cause of the entire lesion. Each of

these should be considered separately.

All observers agree that in actively inflamed tissues the number of

cells is very greatly increased. A certain increase may be accounted

for by that which has already been described--namely, the escape into

the tissues of the wandering cells from the bloodvessels. But neither

this alone nor the products of their rapid proliferation are sufficient

to account for all the cells found in the truly inflammatory condition.

It is now well established that in connective tissue there are two

varieties of cells--the fixed and the wandering--the former concealed

in the trabeculæ of the intercellular substance, while the latter are

small, ordinarily round in shape, much resembling the white corpuscles,

possessed of ameboid characteristics, and having the power of changing

position. These are known as the wandering cells, which meander through

the lymph spaces of the tissues or back and forth into and out of

the blood-vascular system, their migration being regulated by causes

not yet known. Under natural conditions their number is relatively

small. Once given a true inflammatory disturbance they are reproduced

with amazing rapidity; and their numbers, added to those produced by

diapedesis of leukocytes, with the combined proliferative activity

of both forms, serve to account for the new cells whose presence

characterizes phlegmonous and other similar disturbances. That these

wandering connective-tissue cells have much to do with these changes

is shown by the unmistakable evidences of excessive activity known as

_karyokinesis_ (_i. e._, _nuclear activity_).

Karyokinesis is common not only in inflammatory disturbances, but in

new-growths of rapid formation, especially sarcomas, which are formed

from mesoblastic cells, the same which have to do with connective

tissue. Endothelial cells also undergo the same changes.

The peculiar characteristics of the leukocytes have already been

described at considerable length in the preceding chapter. It must

suffice, then, here to say that during the _inflammatory_ attack the

leukocytes are _increased in number_, _i. e._, there is a temporary

leukocytosis which is the usual accompaniment of suppuration. For

instance, this is regularly present in purulent, but not in catarrhal,

forms of appendicitis. The recognition of this fact may be of great

value in diagnosis. For instance, leukocytosis is rarely present in

tuberculous disease unless suppuration complicates the case. It is

met with in suppurative osteomyelitis and in all cases of pocketing

of pus. Moreover, when leukocytosis is present coagulability of the

blood is increased. Of the various leukocytes, it is the mononuclear

and polynuclear forms (see Chapter II) which are endowed with the

most pronounced activity and which play the principal role among the

blood cells or phagocytes. That phagocytosis plays a most important

part in the inflammatory process is a matter to be emphasized in more

than one way and in more than one place. The account of the process

already given should suffice for descriptive purposes; the importance

of the act, however, should be made most prominent in considering

inflammation and suppuration. That the phagocytic properties of these

cells are limited will be remembered when we recall that in certain

instances phagocytes, which are incapable of defence as against the

mature bacterial organism, are yet capable of englobing the spores and

preventing their development. Nevertheless, the activities of even the

most lively phagocytes are capable of being influenced and repressed

by extremes of heat and cold to which patients may be exposed, either

locally or generally.

CHEMOTAXIS AND OPSONINS.

Having considered briefly the cells which take prominent part in the

inflammatory process, and the escape along with them of the fluid

portions of the blood, whether these coagulate or not, it is necessary

before referring to specific factors to discuss that which induces

the above cells to act in this way. That there is a peculiar, even a

mysterious, attraction which brings specific irritant and phagocyte

together has been for some time recognized, but it remained for Pfeffer

to study it carefully and to give it the name by which it now passes,

_i. e._, _chemotaxis_, while others have widened our knowledge of

it, especially by a recognition of the _opsonins_ or material which

“prepares food,” _i. e._, prepare microbes for ingestion by the

phagocytes.

Chemotaxis is a term implying a peculiar property of _attraction and

repulsion between cells_, both animal and vegetable. It mainly pertains

to vegetable cells alone, and has been offered as the explanation of

the sporulation of ferns, for example; but as it interests us most in

this place it is manifested between the animal cells of the human body

and the bacteria, which are vegetable cells. As a result the former,

_i. e._, the phagocytes, having power of migration, are drawn toward

the latter. To be more accurate, this mutual or peculiar attraction

is known as _positive chemotaxis_, it being also known that exactly

the reverse prevails under certain circumstances, and that mobile

cells will move away as rapidly as possible from certain organisms or

substances for which they seem to have a repugnance, this being known

as _negative chemotaxis_.

SPECIFIC IRRITANTS.

These are essentially living organisms, bacteria, fungi, and the

protozoa, the first named being by far the most frequent. Before a

lesion can assume the type of inflammation as here understood some

one or more of these organisms must have secured an entrance into the

tissues, the circumstances determining such invasion being considered

a little farther on. It is these living organisms which, having once

invaded the tissues, determine that most active congregation and

proliferation of certain cells which we have just described under the

head of Phagocytosis. When once the irritants are present there begins

that very active conflict which Virchow has so graphically alluded to

as the _battle of the cells_. Now the mysterious chemotactic properties

of the component substances manifest themselves, and now phagocyte is

drawn toward bacterium, or the reverse, while the tiny war goes on

with sometimes varying results, it being a question which can prove

victor in the conquest. This is no fiction of the imagination, but is a

contest which may be seen under the microscope in certain of the lower

animals, while its results may be seen in the examination of pus from

any human source. In another place I have also likened this conflict

to that in which certain of the enemy resort to poisoned weapons,

because modern biological chemistry has now shown very evidently that

it is a part of the life history of many of these microörganisms to

produce, probably as excretory products, albuminoid or other substances

having sometimes extremely toxic properties. And so it comes about

that in many of the surgical infections, while the local destruction

is produced by the actual death of tissues which have been invaded by

microörganisms, the general or systemic symptoms, generally referred to

as the _toxic_ symptoms, are literally due to poisons generated in the

infected area, dispersed throughout the system, and often proving fatal.

The _local effect of these specific irritants_, when they are not

promptly attacked, devoured, and removed by phagocytes, is _pus_, which

means cellular death, or gangrene, which is death of masses of cells

which have not had time to separate from each other. Pus, then, is

the ordinary consequence of the contest above alluded to, and _each

pus cell represents the dead body of a phagocyte_ which has perished

in the attempt to protect the parent organism from harm. That it has

died valiantly can almost invariably be determined, because within its

dead body may be seen one or more of the minute invaders which it has

attacked. This, then, is the light in which inflammation and infection

should be viewed.

In other words, we may have escape of fluid portions of the blood,

which may or may not coagulate; we may even have some escape of

corpuscular elements with some activity in the extravascular cells,

which shall lead to temporary or even permanent enlargement of a part;

all of which may be provoked by injury or by the presence of certain

chemical irritants within the blood or tissues; for example, alcohol,

uric acid, etc. But the factors which provoke the greatest activity on

the part of intravascular and extravascular cells, and which determine

the richness in albumin of fluid exudates, or their prompt coagulation

as soon as blood serum has escaped from the vessels, and which

particularly determine the furious rush of phagocytes and that kind

of intercellular conflict which leads many of the contestants on both

sides to death, are living organisms which are introduced from without,

whose presence at the point of inflammation is abnormal and injurious,

which are offending substances in every respect, while the whole

phenomenon of inflammation is an expression of an effort to rid the

system thereof. Taking this view of the subject, there is an important

distinction between hyperemia and its consequences, which is absolutely

a non-infectious condition, and inflammation with its consequences,

which is always an infection and is always followed by more or less

death of cells, the same being often extruded in a semifluid mass known

as _pus_.

CIRCUMSTANCES WHICH FAVOR INFECTION.

1. =The Virulence of the Infecting Organisms and the Amount

Introduced.=--There is the widest difference between various forms of

microörganisms in the matter of virulence; and it is true that there

are very great differences between the same species under different

circumstances, these differences depending on conditions as yet

absolutely unknown. With certain organisms it is enough to infect an

animal with one alone in order to bring about a fatal result, this

meaning that the organism itself is extremely virulent and the animal

extremely susceptible.

In a guinea-pig, for instance, a single virulent anthrax bacillus

will produce death, whereas in a more resistant animal many are

required, and in still others there is absolute immunity against the

disease. Man is much more susceptible to the pyogenic organisms than

most of the lower animals, which is one reason why wrong deductions

have been drawn from many experiments, and why veterinary surgeons,

who are so careless of all antiseptic precautions, as a rule have

good results in work which, done after the same fashion on the human

being, would be inevitably fatal. It is one reason also why one may

draw false inferences from experimental work, for instance, upon dogs,

which survive many an operation which can scarcely be successfully

repeated upon a human being. The influences which affect the vitality

and virulence of microörganisms are most numerous and widespread.

Temperature, sunlight, moisture or dryness, association with other

bacteria, are but a few of the conditions known to be more or less

operative. Inoculation with a small number of certain bacteria may

be harmless; up to a certain number it may produce only a local

disturbance, like abscess, while a still larger dosage may produce

fatal results. This is not the case with all, however, but only with

some organisms. Bacteria which have been repeatedly passed through

the animal body become more virulent than those cultivated for many

generations in test-tubes in the laboratory. This variable virulence is

especially characteristic of the colon bacillus, the anthrax bacillus,

and the micrococcus of erysipelas. Nor does it always follow that the

most virulent organism is necessarily cultivated from the most toxic or

serous manifestation of its activity.

2. =Association.=--Bacteria are seldom found in pure cultures under

natural conditions. By mutual association remarkable changes are

produced, sometimes in the direction of enhanced virulence, sometimes

in the direction of attenuation of effect. Certain organisms, extremely

dangerous alone, lose their power when combined with others, while

still others have their virulence increased to a rapidly fatal degree.

In fact, these effects are so strange and so contradictory that no law

governing them has yet been formulated, it being necessary to establish

each case by experimental investigation. The virulence of the anthrax

bacillus under ordinary circumstances is well known, as is also that of

the streptococcus of erysipelas in man. Yet, when these two organisms

are introduced simultaneously, the mixture is apparently wellnigh

harmless. On the other hand, the simultaneous inoculation of certain

other species greatly increases the danger from either alone. The

diplococcus pneumoniæ when combined with the anthrax bacillus seems to

have a greatly augmented power.