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THE
PRINCIPLES AND PRACTICE
OF
MODERN SURGERY

BY

ROSWELL PARK, A.M., M.D., LL.D. (Yale)

PROFESSOR OF THE PRINCIPLES AND PRACTICE OF SURGERY AND OF CLINICAL SURGERY IN THE MEDICAL
DEPARTMENT OF THE UNIVERSITY OF BUFFALO, BUFFALO, NEW YORK; MEMBER OF THE
GERMAN, ITALIAN AND FRENCH SURGICAL SOCIETIES; EX-PRESIDENT OF THE
AMERICAN SURGICAL ASSOCIATION AND OF THE MEDICAL SOCIETY OF
THE STATE OF NEW YORK; SURGEON TO THE BUFFALO
GENERAL HOSPITAL, ETC.

WITH 722 ENGRAVINGS AND 60 FULL-PAGE PLATES IN COLORS
AND MONOCHROME

LEA BROTHERS & CO.
PHILADELPHIA AND NEW YORK
1907

Entered according to Act of Congress, in the year 1907, by
LEA BROTHERS & CO.
in the Office of the Librarian of Congress. All rights reserved.

PREFACE.

A new work on Surgery enters a field of literature already rich in excellent books differing widely in plan and viewpoint. Fortunately nothing else is possible in representing so vast a subject, for it is obviously advantageous that the reader should have the benefit of the personal equation of his author as reflected in his knowledge, experience, and assimilation from the writings of others. When Surgery can be represented by a conventional and well-settled type of book it will have ceased to advance. There is still room for many a serious effort to place the subject before students and practitioners in a way to instruct from the beginning through to the operative and postoperative treatment. This has been the object of the present volume, upon which the author has brought to bear the experience of many years as a teacher and surgeon, and into which he has also endeavored to infuse the most advanced knowledge gleaned from the surgical literature of America and Europe.

To the extent of the author’s ability the work therefore represents the net Surgery of to-day, obsolete and obsolescent material having been excluded, and the pages being devoted to sound principles and practice, stated as clearly and succinctly as possible. The author has been free to employ illustrations wherever a point could be so explained to the eye. In the pictorial department utility and effectiveness have been considered of more importance than extreme and unusual cases. Simple drawings and even diagrams are often most instructive, and such have been accordingly liberally used.

With every effort at conciseness it has not been practicable to cover the subject in less than the equivalent of about fifteen hundred ordinary octavo pages. By adopting a larger form the publishers have presented this material in a convenient volume. In justification of the size of the work it should be borne in mind that its scope is very extensive, for it aims to cover the Principles as well as the Practice of Surgery, thus supplying the needs of students and general practitioners, and, the author hopes, also interesting his surgical confrères.

He takes this opportunity to extend his warmest acknowledgments to his fellow-collaborators of the Treatise on Surgery by American Authors, who on the exhaustion of the third edition most kindly consented to allow it to be succeeded by this individual work, placing their material and illustrations freely at his command. He also wishes to acknowledge the kindness of Dr. H. R. Gaylord, who has contributed certain material utilized in the chapter on Tumors, the assistance of Dr. E. R. McGuire, who has helped in many ways during the preparation of the book, and that of other colleagues who have furnished illustrations that are duly credited in their proper places.

R. P.

Buffalo, N. Y.
1907.

CONTENTS.

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:

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—

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—

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.

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.

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.

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.

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]).

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.

3. Hereditary Influences.

—The fact that immunity against certain infections and susceptibility to other conditions are transmitted from parent to offspring is one which admits of no dispute. The explanation, however, is almost as remote from us today as it ever was. But the recognition of the fact is of the greatest importance to all practising surgeons. That bacteria frequently enter through wounds and bruises is self-evident, but we all know that such wounds are more likely to suppurate in some than in others, and the causes of infection in some are, to a certain extent, connected with the hereditary habit of tissues. The same causes influence not merely liability to infection, but its severity and character. There are undoubtedly also local as well as general variations, and it is very certain that among these the results of bruising or contusion are by far the most prominent. There is also undoubted experimental evidence that under certain circumstances bacteria produce only local lesions, whereas under others they produce general and even fatal infection.

4. Local Predisposition.

—Local predisposition is a factor of almost equal importance. Once given a distinct infection, and hyperemia is sometimes a contributing cause of inflammation. Per contra, anemia of tissues seems to be also a favoring condition. In parts involved in chronic congestion the blood flows more slowly, while the vessels are dilated and apparently susceptibility is increased. Infection here produces a type of disease mentioned as hypostatic inflammation. Conspicuous exception as to the occasional value of an artificial passive hyperemia is seen, however, in the so-called congestion treatment (Bier’s) of tuberculous joints, where the more or less constant flooding of the tissues with venous blood seems to render them uninhabitable for living bacilli, which apparently die and disappear (by phagocytosis), thus permitting a slow return to the normal condition. General anemia, again, is a predisposing cause, while toxemias, including diabetes, etc., are still more so. The liability of diabetic patients to suppurative and even gangrenous infection is proverbial. The presence of foreign bodies has much to do also, and, infection once having occurred along with its introduction, the presence of a foreign body will nearly always excite suppuration; otherwise it will ordinarily remain inert. The withdrawal of trophic nerve influences also apparently permits infection, as is instanced by the ease with which bed-sores form in paralytic patients. Obstruction to the circulation or to escape of secretions more easily permits infection; for example, in the appendix, in the kidney, in the gall-bladder, the salivary glands, etc. Furthermore, one may formulate a quite comprehensive statement and say that all such lesions as solutions of continuity, hemorrhages, degenerations, vascular stasis produced by strangulation, etc., and all perforations, increase more or less the liability to infection.

5. Pre-existing Disease.