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—

They may also be spoken of as—

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. Resolution.

—The speedy subsidence of hyperemic phenomena is known as resolution—a term which has also been applied to the retrograde phenomena after a genuine inflammation. For present purposes it implies, first, the subsidence into inactivity of the exciting cause or its complete removal. This may include the passing of an emotion, the removal of an irritant, the loosening of a bandage, the resort to certain applications or to constringing or astringing measures by which the effect is counteracted. A particle of dust in the conjunctiva may within a few moments produce an active congestion of the conjunctival vessels, which, ordinarily scarcely visible, becomes prominent and easily noted. The removal of the offending substance permits a return to their original size in perhaps a half-hour. This is an example of the speedy subsidence of the hyperemia of dilatation after removal of the cause. Should the hyperemia not subside promptly, it is well to use cold applications, or in this instance an astringent collyrium, or some agent whose physiological effect it is to produce vascular contraction, as cocaine, adrenal extract, etc.

2. Acute Swelling.

—When the effusion above referred to takes place into loose connective tissues the condition is spoken of technically as edema, while when it occurs into a previously existing cavity, such as that of a joint, it is known as an effusion. The amount of blood thus effused will be influenced by the anatomical and mechanical conditions existing about the part. It may be presumed, as a general rule, that when the extra vascular pressure equals the intravascular pressure little or no more fluid may escape. As a matter of fact, it is seldom that the former rises to the degree of the latter. Conversely, one method of treating such edemas and effusions is by some device which shall make the extravascular pressure exceed the intravascular, when the fluid is, as it were, forced back into the vessels, and is made to resume its proper place within the same. This is often done by taking advantage of elastic compression, as when a rubber bandage is applied about the part. In certain parts of the body it may be done by pressure brought about by some other device. Pressure may be used for two purposes:

A. To so increase extravascular pressure as to limit the possible amount of an effusion, as when it is put on early after an injury; or,

B. When it is used as a later resort for the purpose of reducing swelling which has already occurred.

3. Chronic Swelling.

—This is something more than the swelling alluded to under Acute Swelling. Chronic swelling implies either a continuous passive hyperemia, or, what is more common, a positive increase in tissue elements as the result of an oversupply of nutrition brought by the blood, which itself was furnished to the part in a degree far in excess of its needs. The result is a more rapid reproduction of cell elements, with result in the shape of tissue thickenings or tissue enlargements, known as hypertrophy, or, more properly speaking, hyperplasia, of a part, and to the laity as “overgrowth.” This chronic swelling or chronic enlargement is in some degree also connected with the phenomena of escape of white corpuscles from the bloodvessels and mitotic division of certain tissue cells, which have up to this time been usually regarded as a feature of the true inflammatory process.

4. Gangrene.

—This may be the result of hyperemia—for the most part the passive forms—though most instances of gangrene due to intrinsic causes are inseparable from the presence of infectious microörganisms. The gangrene which is spoken of here includes that due to the pressure of tumors, tight dressings, or any natural or intrinsic agency, and that due to pressure from without when not so pronounced as to produce immediate and total loss of circulation in a part. It includes the formation of many bed-sores and so-called pressure-sores, which may be due to an enfeebled heart, to an obstructed pulmonary circulation, or to external pressure in conjunction with cardiac debility. While insisting, then, that gangrene should be recognized as a possible result of hyperemia, it may be added that it is in effect a tissue death, and that dead tissue is always and everywhere practically the same thing, no matter by what causes brought about. Consequently, the subject of gangrene will be considered under a separate heading.

5. Nutritional Changes

will be considered later.

The consequence of persistent hyperemia is transudation—i. e., escape of blood plasm from the vessels into body cavities and tissue interspaces. This leads to consideration under a distinct heading of—

TRANSUDATES AND EXUDATES.

Exudation may occur in vascular and non-vascular, in firm and soft tissues, in, under, and upon membranes. With respect to location, exudates are described as free, when found upon free surfaces or within natural cavities; interstitial, when found between the tissues or parts of tissues; and parenchymatous, when they are situated within the tissues themselves, particularly in epithelial and glandular cells of any kind.

Exudates are serous, mucous, fibrinous, or mixed, the mixed forms including the so-called seropurulent, the mucopurulent, the croupous, and the diphtheritic.

When any exudate contains red globules in sufficient quantity to stain it, it is called hemorrhagic.

Serous transudates from free surfaces are sometimes spoken of as serous catarrhs; when into cavities, as dropsies; when into tissues, as edema; when occurring beneath the epidermis they form serous vesicles or blebs or bullæ.

Fibrinous exudation refers to the fluid which coagulates soon after its exit from the vessels within those spaces into which it has oozed. When flocculi of coagula float in serous fluid it is known as a serofibrinous exudate. Pure fibrinous exudate occurs rarely, save in and upon mucous membranes. The extent to which exposure to the air is responsible for the firm coagulation of the fibrin previously held in solution is uncertain. The most potent factors in producing such coagulation are bacteria, but it is not yet disproved that coagulation may occur without their aid. When such coagulation occurs upon the surface of a mucous membrane it has been spoken of as croupous. When the epithelial covering as well as the basement membrane, and often the submucous tissues, are involved, so that the membrane cannot be stripped off without tearing across minute bloodvessels, the exudate has been known as diphtheritic. These terms may possibly be still retained in an adjective sense as implying the exact location of a surface exudate, but are scarcely to be used in any other significance.

The following table illustrates significant differences whose full importance cannot be impressed before a study of inflammation has been carefully entered upon:

Hyperemic Transudates.Inflammatory Exudates.
Poor in albumin.Rich in albumin.
Rarely coagulate in the tissues.Usually coagulate in the tissues.
Contain few cells.Contain numerous cells.
Low specific gravity.High specific gravity.
Contain no peptone.Contain peptone (product of cell disintegration).

TREATMENT OF CONGESTION AND HYPEREMIA.

These disturbances are to be combated, first of all, by insisting upon physiological rest. This, perhaps, is the most important measure of all. The profession is indebted to Hilton for the decided advance which he made in the treatment of congestive and inflammatory affections by insisting upon this principle in his celebrated work on Rest and Pain, which every young practitioner should read. Aside from this first and underlying principle, the treatment must, in some measure at least, be based upon the time at which we are called upon to treat the case. If seen at once, before exudation has been excessive or the other disturbances marked, we may carry out a certain line of treatment for the purpose of limiting all these unpleasant features. On the other hand, if seen late, when exudation has been copious and when pain and other disturbances are due to its presence, a distinctly different course will be adopted.

Toward the end first mentioned—namely, the limitation of hyperemia—we may adopt local and general measures. Local measures include graduated pressure, providing this is not intolerable to the patient, so equalized that outside of the vessels it shall equal that inside. This may be done by careful bandaging, extreme care being taken that the pressure be applied from the very extremity of the limb; otherwise, passive exudation might be augmented and gangrene be precipitated. Elevation of a limb will often accomplish the same purpose. Cold, which is in effect an astringent and which tends to contract bloodvessels, is another measure in the same direction, and if applied early will do much to limit the degree of the attack. This may be applied as dry or moist cold, and should be gradually mitigated as the congestion subsides. It acts through the vasomotor system, and is a measure to be resorted to with caution. An efficient way of applying dry cold can be extemporized by a few yards of rubber tubing, held in place by wire or sewed in place to a piece of cloth, through which a stream of cold water is permitted to pass.

Heat is another efficient means, acting, however, in a rather different way. Heat is a measure to be employed to hasten the disappearance of exudation—in other words to quicken resorption, which it does by equalizing blood pressure, dilating the capillaries, stimulating the lymphatic current, and in every way helping to clear the tissues of that which has left the bloodvessels.

It is necessary also, at least in extreme cases, to employ some detergent or derivative measures, including bloodletting, to which we do not resort sufficiently often. When used for this purpose, depletion should be applied at the area involved, if possible. This may be done either as venesection, by leeching, either with the natural or the artificial leech, or by a series of minute punctures or incisions, which give relief to tension, permit the rapid escape of fluid exudate, and often save tissues from the disastrous effects of strangulation. In some cases of deep-seated congestions these measures are inapplicable, and venesection at the point of election—say the cephalic vein in the arm—may be followed by great benefit. Another method of depletion is by administration of cathartics, such intestinal activity being stimulated as shall lead to copious watery evacuations. The salines rank high as measures directed to this end, but in emergency much stronger and more drastic drugs may be administered, such as jalap, calomel, elaterium, etc. Diaphoretics and diuretics help to reduce temperature and in some degree to deplete, but their action is usually slow. When exudation is considerable in amount and confined to some one of the body cavities, it is often best combated, if at all obstinate, by the method of aspiration. This includes any suitable suction apparatus by which the fluid may be withdrawn through a small needle or cannula, the operation being trifling in difficulty, but one to be performed under strictest aseptic precautions, lest infection of an exudate already at hand be permitted.

Certain individuals, especially the neurotic, will need more or less anodyne, particularly when local applications fail to give relief. Sometimes a small dose of morphine administered hypodermically will act magically in making efficient those measures which would otherwise be inefficient. In little children some anodyne or hypnotic will be of great service. Under all circumstances it is well to keep the lower bowel empty, and certain elderly individuals with weak and enfeebled hearts will need the stimulation to be afforded by digitalis, quinine, and alcohol, or preferably strychnine administered subcutaneously.

In cases of chronic hyperemia and its consequent hyperplasias (induration, thickening, etc.) there is no one measure so generally applicable and effective as the continued use of cold-water dressings. These are generally spoken of as “cold wet packs,” and may be continued—constantly or intermittently—for many days.

Massage is also an invaluable agent in the reduction of swelling and tissue overproduction. It promotes absorption, even of acute effusions, by equalizing the blood and hastening the lymph circulation, and under its scientific application it is surprising how firm exudates and old adhesions seem to disappear.

ATROPHY AND HYPERTROPHY, AND THE CONSEQUENCES OF ALTERED, DIMINISHED, AND PERVERTED NUTRITION.

As a consequence of increase of nutrition we have a condition known commonly as hypertrophy, more accurately as hyperplasia. Hypertrophy literally means overgrowth, whereas hyperplasia more accurately describes that which constitutes hypertrophy—namely, numerical increase of constituent cells. Common usage has made the more inaccurate name “hypertrophy” cover nearly all these conditions. Hypertrophy, or hyperplasia, means enlargement of a part or of an organ beyond its usual limits, and as the result of increased function or increased nutrition. It is to be distinguished from gigantism, which means inordinate enlargement as the result of a congenital tendency or condition. Hypertrophy is—

A.Physiological- 1.Compensatory;
2.From deficient use.
B.Pathological- 3.Local;
4.General;
5.Senile;
6.Congenital.

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- 1.From disuse without disease;
2.Biological or developmental;
3.Senile.
B.Pathological- 4.Result of acute tissue losses;
5.Result of phagocytic activity;
6.Result of continuous pressure;
7.Specific.
A. Physiological Atrophy.

—1. This is always the result of disuse or impaired function from any cause. Its evidences are generally seen in the fatty structures and muscles—i. e., in the soft parts. It is true, however, even of the bones, or, of greater interest, even in the brain cells. We see evidences of it also in minute organs; as, for example, in the digestive glands in certain cases where diet is restricted. Again, we see it in the diminution of the size of the heart after hip amputation, less being required of that organ, and also in the entire structure of the rectum after colostomy.

2. Examples of the developmental type are best seen in the natural disappearance of the hypogastric arteries, the ductus arteriosus, the vitelline duct, the Wolffian bodies, and in the various generative ducts (Gärtner’s, etc.) shortly after the birth of the human individual. We sometimes see it also in the prostate after orchidectomy. Equally illustrative is the disappearance of the tail and gills of the tadpole, the eyes of animals living in caverns, and, in a general way, of organs which become useless owing to a different environment.

3. Senile atrophy is seen equally well in the hair follicles, the teeth, the bones, and the sexual organs of elderly people—in fact, in all their tissues, even in the brain.

B. Pathological Atrophy.

—4. Acute atrophy of surrounding tissues is the necessary accompaniment of destruction by suppurative or other disturbances; that is, parts disappear by absorption which have not been interfered with by pyogenic organisms. So complete may atrophy occur under these circumstances as to cause disablement of an organ or part. This kind of senile disappearance is merely an expression of phagocytic activity, although not now a question of bacteria.

5. The same is true of that variety spoken of above as biological or developmental, since phagocytes are the active agents in producing the disappearance of the tadpole’s tail.

6. A more slow form of pathological atrophy is seen in the gradual disappearance of tissues in the neighborhood of advancing tumors, enlarging cysts, etc. This is perhaps but another expression of atrophy from continuous pressure. But a still better illustration is the atrophy which comes from immobilization of a part without pressure. This is usually the case when splints or orthopedic apparatus have to be kept in place for some time.

7. Specific forms of pathological atrophy are largely connected with disturbances in the central nervous system. They are often referred to as trophoneurotic. Their exact mechanism is not yet understood, and cases may be confused under this head whose remote causes are widely different. Here should be included, for instance, the atrophy of a deep bone which occurs after extensive burn of the surface; also that peculiar form of atrophy of tissues in the stump which produces the so-called conical stump. These cases are of a more complicated character, for if pressure is removed from the bone end, especially in young people, the bone tends to grow faster than it should, while the soft parts disappear, partly as the result of mere disuse or loss of function. In this way conicity is produced, which sometimes calls for subsequent re-amputation. Under this head might also be included the so-called “trophic inflammation” (misnomer) of some writers, such, for example, as ulceration of the cornea after division of the trigeminus. The general subject of atrophic elongation also belongs here, referring to the fact that as a result of disuse, or sometimes of active disease, the bones, while showing atrophic changes in other respects, actually increase in length. Should such increase occur in one bone of those portions of the limbs which are supplied with two, the result would be posture deformity and displacement of the terminal portion.

CHAPTER II.
SURGICAL PATHOLOGY OF THE BLOOD.

The part played by the constituent elements of the blood in inflammation, suppuration, and other still more disastrous conditions is so great and so important that, before proceeding to discussion of these lesions, it seems necessary to set forth a resume of facts illustrating the importance of accurate knowledge concerning this most important fluid.

The total amount of blood in the human body has been variously estimated at from one-eleventh to one-twenty-fifth of the body weight, the average being about one-sixteenth. The amount which the body may lose and still retain vitality is very vague and differs not only with individuals, but very greatly under various conditions. Severe loss of blood is one to be atoned for as quickly as possible, and is to be prevented as far as it can be after accidents or during operation. For this reason the so-called bloodless method of operating upon limbs, by the use of the rubber bandage, constituted a great advance in surgery. For the same reason the use of hemostatic forceps is of equal value in operating upon other parts of the body; other things being equal the quickest and most satisfactory recoveries follow the bloodless operations, and it is an advantage to conserve this vital fluid as far as possible.

It has been roughly estimated that the blood is divided about as follows, between the different parts of the body: the heart, lungs, and large vessels holding one-fourth, the skeletal muscles one-fourth, the liver one-fourth, the remaining quarter being distributed over the balance of the body.

The blood varies within wide limits in its coagulability, and this variation occurs apparently even within conditions of health. In some patients the blood may be seen to coagulate almost as rapidly as it collects upon the surface, while in others the exposed parts continue to ooze, and the checking of hemorrhage is a difficult, sometimes almost impossible, matter. There are certain diseases in which the blood is known to have reduced power in this direction; for example, in the toxemias, especially those connected with biliary obstruction and jaundice. There were not a few of these cases of slow bleeding to death in days gone by, simply because the capillary hemorrhage could not be controlled. Recently, it has been shown that calcium chloride administered internally has a marked effect in favoring coagulation, and when opportunity is afforded it should be given for several days previous to operating and as part of the necessary preparation. It may be administered in doses of from 1 to 2 Gm., and should be given three or four times, at least, in twenty-four hours.

A test of the coagulation time, normally three to five minutes, but lengthened under circumstances like those mentioned above, even to an hour, will often prove of great value.

There are certain albumoses whose effect on coagulation of the blood is very suggestive and very mysterious. A very minute dose of cobra poison, for instance, will make the blood of an experimental animal remain fluid for days, unless this animal has been previously immunized against it, in which case coagulation takes place even more rapidly than normally. A trace of serum from an immunized rabbit is enough to prevent the fluidifying effect of the cobra poison, but quite insufficient to neutralize its toxic effects. The surgeon practically never desires to reduce coagulability of the blood, but frequently to increase it. When it is increased by natural conditions or those not easily controlled, then it may lead to thrombosis and produce trouble in that way.

Fibrin.

—Increase of fibrin, hyperinosis, accompanies the leukocytosis of inflammation and suppuration. It may be approximately estimated on the cover-glass by noting the closeness of the network resulting after fifteen minutes’ exposure. The inflammatory indication of leukocytosis may, therefore, be inferred from its determination, while the leukocytosis of malignant disease will not be so accompanied. Hyperinosis is most marked in pyogenic processes, pneumonia and rheumatism. Its opposite, hypinosis, is met with in pernicious anemia. There is no change in the percentage of fibrin in the ordinary anemias or chlorosis. In hemophilia and purpura hemorrhagica the coagulation time is greatly increased.

The Formed Elements of the Blood.

—The specialized elements of the blood which are of particular interest to the surgeon are the red and the white corpuscles. These may both vary in relative size within certain physiological limits. The red cells especially are not of uniform size and vary from 6 to 9 microns in diameter. There are also present in normal blood a small number of red cells having a diameter of only 6 microns, which are known as microcytes. In infancy there are present also so-called giant corpuscles, or megalocytes, with a diameter of 10 microns or more. Considerable variation occurs in disease, especially in the severe anemias. Red corpuscles ordinarily stain with acid dyes, which facilitate their examination and a computation of the number present. When present in unusually large number the condition is spoken of as a polycythemia; when in reduced number as oligocythemia. In several of the anemias variations in size, shape, and color occur, and in certain of them many of the red corpuscles are found to be nucleated. Red cells which are nucleated are known as erythroblasts, and according to their size are spoken of as microblasts, normoblasts, and megaloblasts. Again, under certain diseased conditions the ordinary discoid form of the cells becomes irregular and crenated, and to those which are thus altered is given the name of poikilocytes.

There is another form of degeneration which consists in death or necrobiosis of the cell, whereby it loses its capacity for staining, or, at all events, stains irregularly and abnormally. This is seen also in cases of severe anemia and in conditions where the blood has been altered by the addition of toxic material, such as chloroform, etc. Occasionally also the red cells show a tendency to a granular change, which is probably entirely degenerative.

The red corpuscles have a certain degree of elasticity which helps them to pass through capillaries which are smaller even than their own diameter; after escaping from these the corpuscles regain their original form. In the presence of carbon dioxide they lose this elasticity and become distorted or crenate. The influence of high altitudes in increasing the number of corpuscles is known, but unexplained. For instance, a residence of less than a month in the mountains will cause an increase of from 2,000,000 to 3,000,000 corpuscles per cubic millimeter. It has been surmised that under the influence of oxygen red corpuscle formation is stimulated to greater activity; in other words, that the red marrow becomes more active in the production of the hematoblasts.

In general terms it may be said that the blood of a normal adult male contains 5,000,000 red corpuscles per cubic millimeter, and that of an adult female 4,500,000. These figures are, of course, approximate and variable. When the number is reduced to 3,000,000 by common consent the case will be regarded as oligocythemia, and when increased to 6,000,000 as one of polycythemia.

The latter condition is most evident in cases of newly born infants. The excess rapidly diminishes during the first week of extrauterine life. It is to be explained by the loss of fluid suffered by the infant upon the establishment of respiration. The proportion of red cells also varies according to the nutrition of the individual, the season of the year, the altitude (as above), and climate, and varies during menstruation, pregnancy, lactation, and at the climacteric. With the loss of red cells the number is reduced in proportion to the hemoglobin, although the change in one respect is not exactly proportionate to that in the other.

That the colorless corpuscles, or leukocytes, are not all of one kind has been recognized for nearly sixty years, and long ago they were divided into granular and nucleated cells. A vast impetus to the study of hemocytology was given by Ehrlich, in 1878, when he introduced the use of aniline dyes. The reader must be reminded that some of these, like eosin, are acid in reaction, and others, like methyl blue, are basic; while a third group has been supposed to be neutral in reaction, like a mixture of methyl blue and acid fuchsin; but it has been found that the so-called neutral dyes have really a slightly acid reaction. We may, therefore, divide the cells according to the reaction of the dyes with which they usually are distinguished into the acid and basic, or, more technically, into oxyphile, which includes neutrophile, and basophile.

This is not the place in which to go into any minute discussion of this subject nor further than should be of practical interest to the surgeon; nevertheless an examination of the blood by some common and routine procedure is so necessary in many surgical conditions that it is impossible to entirely avoid the subject in a work like this. I have accordingly condensed it and put the salient facts about leukocytes into the following table:

Classification of Leukocytes.

Granular.Non-granular.
Normal.- Oxyphile.A.With fine granulesC.Hyaline. Transitional (large
Neutrophile. The so-called(polynuclear) 60-70 per cent.mononuclear) 4-8 per cent.
neutral stain beingB.With coarse granulesD.Lymphocytes (small
slightly acid.(eosinophiles) 2-5 per cent.mononuclear) 20-30 per cent.
Pathological.- Basophile.E.Fine and coarse granulesG.Atypical hyaline
(basophiles, mast-cells, etc.).(myelocytes).
Oxyphile.F.Atypical (myelocytes).

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. 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:

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. 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.

—Here are reckoned, first, previous and long existent toxemias, e. g., syphilis, diabetes, scurvy, etc. Other conditions, like lithemia, cholemia, acetonemia, and the various conditions represented by oxaluria, or in which acetone, peptone, and excess of uric acid are found in the urine, also come under this head. One need never be surprised to find suppuration occurring in those cases in spite of due observance of all ordinary precautions, since by their existence immunity is destroyed and vulnerability increased. (See chapter on [Auto-infections].)

Recent toxemias also have important bearing in this same respect. For instance, after typhoid fever and other acute wasting diseases, including the exanthemas, surgical operations are sometimes followed by failure, and should always be postponed until complete recovery, except in cases of emergency. The condition to be hereafter described as enterosepsis, and which has previously been known under many different names, as fecal anemia, stercoremia, etc., is one which makes the performance of all operations dangerous, and which certainly predisposes to septic disturbances of all kinds. The postpuerperal state is also one in which operations are to be avoided if possible.

Certain anatomical changes peculiar to the various ages also belong in this category. Old age, with its accompanying arterial sclerosis, its cardiac debility, and other well-known tissue alterations, favors sluggishness of wound repair and leads not infrequently to sloughing or to bed-sores. Amyloid changes betoken impaired vitality. Children are much more liable to acute osteomyelitis than adults. Nursing infants are apparently exempt from many of the infectious diseases, but possess relatively small power of vital resistance to surgical operations. General anemia and impaired nutrition of the body predispose to most infections and to acute starvation.

6. Personal Habits and Environment.

—Diet has much to do with tissue resistance. Rats fed on bread are more susceptible to anthrax than those fed on meat. Hunger makes pigeons highly susceptible to the same disease, and artificial immunity induced in various animals is quickly destroyed by starvation. Prolonged thirst seems to have the same result. Excessive fatigue generally reduces immunity, as already mentioned. The various drugs which destroy red corpuscles impair immunity, and even by injection of water into the circulation the bactericidal power of the blood is reduced. White mice fed with phloridzin, which produces artificial diabetes, become highly susceptible to glanders, from which they are ordinarily exempt. In this connection may also be mentioned the various toxemias alluded to under the previous heading, which may proceed from the intestine, from the genito-urinary tract, and probably also from other sources. Climate has more or less to do, as also extremes of weather, with power to resist infection or to survive serious operations. Dark habitations, poorly ventilated, constitute surroundings which manifestly predispose to infection of all kinds. Rabbits inoculated with tuberculosis and confined within a dark cell, badly ventilated, become rapidly diseased, while others similarly inoculated, but allowed to roam at large, present but slight evidences of the affection. Certain occupations predispose to certain diseases. This is pre-eminently the case, for example, with workers in mother-of-pearl, who are exceedingly liable to a particular form of osteomyelitis; and with those who make phosphorus matches, who are prone to suffer from a peculiar necrosis of the lower jaw. Prolonged suppuration may produce such changes in the blood and tissues that vital processes of repair, cell resistance, and chemotaxis may be so far interfered with as to facilitate subsequent infection.

Finally, the influence of local injury to tissues, particularly of contusions which cause tissues to lose their vitality, is strenuously insisted upon by all, and is spoken of repeatedly in other places in this work. Many tissues will succumb to inoculation after bruising, ligature en masse, etc., which before such injury are not in the least disturbed.

7. Fetal Infection.

—It is only in a very limited class of cases that infection can be transmitted from mother to fetus, but there are instances of this kind in which the surgeon is deeply concerned. As Welch has stated, syphilis is the only infection capable of direct transmission through the ovum or spermatozoön; but intra-uterine infection may occur in many ways, and many diseases may be thus transmitted. The placenta is usually regarded as a perfect filter; nevertheless, it is occasionally passable to microörganisms. These may be caused by preëxisting lesions in the placenta or by the virulence and activity of bacteria. It is known that in animals the bacilli of chicken cholera (inoculated into the mammalia), of symptomatic anthrax, and the pyogenic cocci, frequently traverse this barrier. In mankind infection in utero has been observed in smallpox, measles, scarlatina, relapsing fever, syphilis, tuberculosis, croupous pneumonia, typhoid fever, anthrax, and surgical sepsis.

SOURCES OF INFECTION.

That the effects of bacterial invasion may be anticipated and guarded against most effectually it is necessary that the practitioner should be thoroughly familiar with the sources from which they come, and the localities in and about the body which they most commonly inhabit or where they are met with in largest numbers.

Skin and Mucous Membranes.

—Of all possible sources of infection, the skin itself is probably the most fertile. It is exposed to contamination by air and by everything which may come in contact with the body, and there is perhaps no organism met with in disease which may not be found upon its surface or within its recesses. In fact, these recesses, such as the crevices beneath the nails, the spaces between the toes, and the various pockets like the tonsils, the axillæ, etc., are those most commonly inhabited by microörganisms.

Bacteria may penetrate the skin by means of three different routes, namely, the sweat glands, the hair follicles, and the sebaceous glands, by means of their regular openings. The hairy appendages of the skin are even greater sources of danger than the skin itself, since a direct path of infection into the depths of the skin is afforded by their follicles. Experimentally it has been shown that when bacteria are rubbed into the skin where there are no follicles, there is freedom from infection, whereas the reverse is equally true, and it is clinically generally recognized that furuncles and carbuncles form almost exclusively in those parts provided with hair and sebaceous glands.

The mucous membranes are in constant contact with microörganisms and furnish conditions in many respects favorable for their rapid development. Nevertheless, the latter is interfered with and often inhibited by certain mechanical and chemical influences which afford protection. The conjunctiva is an extremely exposed membrane, which harbors, however, but a relatively small number of bacteria under ordinary circumstances. The tears before escaping from the conjunctival sac are sterile, and are probably saline enough to act as an antiseptic bath for the cornea. Moreover, by free escape of secretion through the nasal duct the conjunctival sac is kept constantly irrigated, to which is mainly due its ordinary healthy condition, as it is well known how commonly lesions follow obstruction to the lacrymal duct. The horrible results of Egyptian ophthalmia, i. e., the pyogenic form of conjunctivitis, are familiar to travellers in Egypt. Howe and others have shown that this disturbance is due to flies, which are carriers of infection, and are attracted toward the eyes of infants, while the superstitious notions of the parents restrain their children from instinctive protection of the eyes when thus irritated. There is probably no greater common carrier of pyogenic infection than the common house-fly, and nowhere is this agency more demonstrated than in the hot climates of the Orient.

PLATE III

FIG. 1

Artificial Dental Caries in Cross-section. Tubules Filled with Bacteria. (Miller.)

FIG. 2

Putrid Tooth Pulp. Infection of Dental Tissue. × 1000. (Miller.)

FIG. 3

Dental Caries. Disappearance of Dental Tissues as Result of Presence of Bacteria. (Miller.)

FIG. 4

Dental Caries. Tubule Filled with Cocci. (Miller.)

FIG. 5

Dental Caries. × 500. (Miller.)

FIG. 6

Dental Caries. Tubules Plugged with Cocci. × 500. (Miller.)

Upper Respiratory Tract.

—The oral cavity and pharynx are seldom free from bacteria. Miller has studied over one hundred species that he has found under various circumstances in the human mouth. Some of these are pathogenic; others are apparently absolutely innocent. Many of the forms which grow in saliva will not grow in ordinary media. (See [Plate III], illustrating infection of the teeth.) Miller has also shown that many forms of dental caries are but expressions of bacterial invasion even of those apparently most solid structures, the teeth; and of late we have been taught more fully that such invasion may extend far beyond the confines of the teeth alone, and may spread to various, even to distant parts, and produce possibly fatal mischief. Abscesses in the brain and extensive septic infections have been traced to invasion along the line of the dental tubules. One of the most virulent of all the common inhabitants of the mouth is the pneumococcus of Fränkel, known also as the micrococcus lanceolatus of Stebernrg. In virulence it is a variable organism, but it is present in a virulent state in only 12 or 15 per cent. of cases of infection due to it. This is the organism which is the cause of lobar pneumonia, and frequently of bronchopneumonia, as well as of numerous phlegmons and other inflammations of the throat, and which, getting into the general circulation through the tonsils or other possible ports of entry about the mouth, causes serious septic and inflammatory disturbances in widely distant regions. Aside from dental caries, a widely opened port of entry is often afforded by those ulcerations around the margins of the gums which are produced by accumulations of tartar. Disease in the antrum of Highmore, for instance, and many other local destructions, are frequently caused in this way.

The next most common port of entry is the tonsils, faucial, lingual, and pharyngeal, which contain a variety of crypts which are often filled with secretions or retentions loaded with bacteria. One of the most common sources of an involvement of the cervical lymph nodes in tuberculous disease is an infection springing first from the tonsils or the teeth.

In spite of the fact that myriads of bacteria are swept into the nasal cavities with the air we breathe, few are seen in the nose. A peculiar capsule bacillus, closely allied to that described by Friedländer, has been found in a number of cases of ozena, while the pneumococcus of Fränkel is also often found there, and is known to produce abscesses of the brain. One specific organism—namely, that of rhinoscleroma—concerns the nose almost solely, its first ravages being met with in this location.

Alimentary Canal.

—Probably more microörganisms enter the alimentary canal than gain access in any other way, these coming both from food and drink as well as air. Once within its confines, few of them are capable of prolonged existence. Welch states that the meconium of newborn infants is sterile, but that within twenty-four hours it usually contains abundant bacteria. That bacterial infection through this passage-way is a fertile source of non-surgical lesions is well known. The possibility of surgical infections being produced in the same way is both more remote and less demonstrable. Naturally, anaërobic organisms find here more favorable conditions, and even extremely acid or extremely alkaline conditions do not serve to destroy all such life. Pyogenic cocci are often present and are frequently found in peritoneal exudates. In the intestines of herbivorous animals the tetanus bacilli and those of malignant edema are regularly found. The fungus of actinomycosis also finds its way into the bowel along with ingested food. Under ordinary conditions the bile in its natural reservoirs is free from bacteria, but the colon bacilli and pyogenic cocci often invade these precincts.

Genito-urinary Tract.

—Even the healthy urethra may contain bacteria. While these may wander upward to an indefinite extent, it is believed that the urine contained within the bladder in a condition of perfect health is free from bacteria, and that if such gain entrance they do not long remain. The same is true of the female bladder and urethra. The vagina contains organisms of many species, some of which do not grow on ordinary culture media, but are to be recognized by the microscope. While it is generally acknowledged that the vaginal secretion is, as a rule, possessed of bactericidal properties, there is as yet no satisfactory nor comprehensive explanation of this fact, its normal acidity not being sufficient to account for the fact.

The Milk in the Lacteal Ducts.

—In a condition of perfect health milk secreted from the ideal mammary gland is sterile, but may easily become contaminated upon its exit from the nipple. Conversely, under many favoring conditions organisms may travel into the lacteal ducts from the skin without, and thus contaminate the milk. In all probability the breast corresponds in behavior to other glands whose ducts open upon the surface, and, while such openings invite entrance of bacteria, their migrations do not extend far from the surface unless some of the other conditions already mentioned predispose to further infection or extension.

In summarizing the general topic of possible sources and paths of infection bacteria may enter and exert deleterious action:

A. From within they may enter the tissues either through the inspired air, through food and drink, i. e., ingesta, or by means of more direct inoculation, e. g., by foreign bodies or by venereal contact. The danger through infection by inspired air is very small, and concerns probably a limited number of organisms, of which the tubercle bacillus is the most important. Foul air and air which emanates from sewers, cesspools, etc., while most unpleasant to breathe and deleterious in many other ways, do not necessarily contain any microörganisms which can be injurious. This fact, in opposition to general belief, is, nevertheless, proved by recent investigations. The ingesta furnish the most fertile source of contagion from within, but the diseases thereby produced fall for the most part into the domain of medicine rather than that of surgery.

B. Infection from without the body may come by actual contact with previous skin or mucous lesions, and particularly from noxious insects and certain parasites. Among surgeons the principal sources of contact infection to be enumerated and guarded against are:

While insisting here upon the recognition of these sources of danger, the precautions to be taken against them are to be considered under another heading, to which the reader is referred.

One of the greatest sources of possible infection has of late been shown to be the presence of flies and other noxious insects, which act as carriers of infection. The Egyptian ophthalmia, which ruins the sight of 30 per cent. of the inhabitants of Egypt, has been shown by Howe and others to be due to infection by this mechanism; and a simple bacteriological experiment will suffice to show that the foot-tracks of a single fly across a wound furnish abundant opportunities for infection with organisms which are presumably virulent. In fact, the danger of carriage of infection by this means is greater than from almost all other sources, except the use of improper materials during surgical operations.

CLASSIFICATION OF INFECTIONS.

We speak of infections as primary, secondary, and mixed; and it is necessary, for purposes of accuracy at least, to make a reasonably clear distinction between them.

Primary Infection.

—By primary infection is meant infection with a single form of organism whose effects are prompt and speedy. Of this, erysipelas or syphilis may serve as illustrations. Most of the acute infections belong to the primary type.

Secondary Infection.

—Secondary infection means that after certain disturbances due to a primary infection, i. e., one of a given type, there occurs at some later period and from a distinct source another infection whose results may be more or less disastrous, and cause the case, at least for the time being, to assume a different aspect. We have an illustration of this in the case, for example, of primary tuberculosis with distinct infection of a number of lymph nodes, which, acting as filters, have caught in their tissue net a large number of tubercle bacilli that, lodging there, have produced the usual well-known results and have practically converted the infected nodes into granulomata. In these infected masses well-known changes, such as those which follow tuberculous infection—atrophy, caseation, calcification, etc.—may be occurring, when suddenly there comes infection of a pyogenic type from another source, and suppuration of the granuloma is the result. It is possible even to have a tertiary infection, of which the following may be a hypothetical instance: Primary infection with scarlatina or measles, by which vital susceptibility is in some instances lowered; as the result of this, secondary tuberculous infection in an individual previously resistant; and, third, a suppurative infection, as above described.

In contradistinction to these distinct events, separated by an appreciable, sometimes a considerable, length of time, we recognize a mixed infection, where two or more organisms are implanted at or about the same time. An illustration of this is seen in most cases of gonorrhea in which there is a synchronous attack made by the gonococcus, which is a specific microörganism, accompanied by staphylococci or streptococci, whose effect will complicate the case and make it assume a less particulate type of infection. Mixed infections may often occur in other ways, as syphilis and chancroid, chancroid and gonorrhea, etc. Most cases of mixed infection belong rather to surgery than to general medicine, and constitute an apparent violation of the rule to which physicians often point—that two distinct infectious diseases are seldom communicated or acquired at the same time. Nevertheless, the facts remain as above.

Terminal Infections.

—Terminal infections constitute an apparent paradox, perhaps oftener in medical than in surgical cases. Few people, as Osler has shown, die of the diseases from which they suffer. The final exitus is due to a more or less rapid infection which terminates life. These terminal infections are mainly due to a few well-known microbes, such as the streptococcus, staphylococcus aureus, pneumococcus, bacillus proteus, gonococcus, bacillus pyocyaneus, and the gas bacillus. In surgery such infections are, perhaps, most often seen in malignant lymphoma, diabetes, tuberculosis, syphilis, cancer, and in the so-called surgical kidney.

BACTERIA OF PUS FORMATION.

Bacteria which act as agents in the formation of pus are collectively known as pyogenic organisms. These are divided into two groups:

Obligate pyogenic organisms are those whose activity is manifested in the direction of pus formation, which seem to produce it if they produce any unpleasant action whatever. On the other hand, the facultative organisms are those which are known occasionally to be active in this direction, and yet which are not always nor necessarily so. The members of group A are fairly well known and catalogued, and are not numerous. On the other hand, there is reason to believe that many organisms may have the occasional effect of producing pus, as it were, by accident or at least in a way not absolutely natural or peculiar to themselves, but still are frequently found when there is no pus present. A suitable list of the facultative organisms, therefore, can hardly be made, and will not be here attempted, the effort being only to mention the more common organisms which play this facultative role. It may be mentioned also that even the adjectives “obligate” and “facultative” are to be accepted with some mental reservation, since staphylococci, for instance, may be met with even in the absence of pus, although nearly all that we know about these organisms implies that pus would be the result of their presence. Furthermore, there are certain other organisms, not, strictly speaking, bacteria, which also have the power of producing either pus or pyoid material. These also will be mentioned in their place. Some of them belong not only to the vegetable, but also to the animal kingdom.

Obligate Pyogenic Organisms.
A. The Staphylococcus Pyogenes Aureus, Albus, Citreus, the Staphylococcus Epidermidis, etc.

—One of the characteristics of the staphylococci as a group is the powerful peptonizing action which they exert. Moreover, the chemical products of their life changes seem to be more potent in a local than a general way, leading to greater destruction of tissue in their immediate vicinity, with greater inhibition of the chemotactic powers of the leukocytes; that is, with more interference with phagocytosis, by which their progress would be interfered with. Their presence is recognized by a peculiar odor, as of sour paste, which should lead to a prompt change of dressings and disinfection of the wound (by irrigation, spraying with hydrogen dioxide, etc.).

B. Streptococcus Pyogenes and Streptococcus Erysipelatis.

—These two organisms do not differ in morphology nor characteristics, and, while for some time considered as distinct from each other, are now by most observers regarded as identical. The streptococci grow in chains of variable length, and individual cocci vary in size. They grow with and without oxygen, in all media, at ordinary temperatures, do not liquefy gelatin, stain readily, sometimes but not invariably coagulate milk, and vary in longevity. They differ extraordinarily in virulence according to their sources.

Fig. 4

Staphylococci in pus. × 1000. (Fränkel and Pfeiffer.)

Fig. 5

Streptococci in pus. × 1000. (Fränkel and Pfeiffer.)

There are many streptococci not included under the above head which are indistinguishable morphologically and in other respects, and yet which are partly or entirely free from pathogenic activity in man. A biological study reveals remarkable and unexplainable transformation between the different members of this species, a part of which may be referable to conditions pertaining to the organisms infected, but part of which apparently pertains to the bacteria. It is held by some that scarlatina is an invasion by certain organisms of this class; this, however, is not yet definitely established. When found in the stools of children with summer diarrheas they are regarded as indicating ulceration of the intestinal mucosa.

In contradistinction to the staphylococci, the streptococci manifest a predilection for lymph vessels and lymph spaces, along which they extend with great rapidity. They have less peptonizing power than the staphylococci (except in the absence of oxygen); hence streptococcus infection assumes usually the type of widespread infiltration rather than of circumscribed and distinct edema. One sees remarkable instances of this in cases of phlegmonous erysipelas. It is suggested also that the peculiar manner of growth of the streptococci, in long chains which may coil up and entangle blood corpuscles, has much to do with the formation of fat emboli and with pyemic disturbances.

Both these bacterial forms have the power of producing lactic fermentation in milk; and lactic-acid formation sometimes takes place with suppuration in the human tissues, causing acidity of discharge, sour odor, and watery pus. It appears also that these two pyogenic forms have less power of ptomain or toxin formation than many others, and, consequently, that the pyrexia attending suppuration or purulent infiltration is not always to be ascribed to this cause alone, for fever may in some measure be due to tissue metabolism attending their growth, the metabolic products being pyretic. This is in a measure substantiated by the fever attending trichinosis, where the question of ptomain poisoning has not yet been raised.

C. Micrococcus Lanceolatus.

—Micrococcus lanceolatus is also known as the diplococcus pneumoniæ or the pneumococcus of Fränkel and Weichselbaum, and as the micrococcus of sputum septicemia of Pasteur and of Sternberg. It is of interest to surgeons because it causes many localized inflammations and is a frequent factor in causing septicemia; it is often present in the mouths of healthy individuals. It may produce the various forms of exudates as the result of congestion set up by its presence; also otitis media, meningitis, osteomyelitis, and suppurative disturbance in the periosteum, the salivary glands, the thyroid, the kidney, the endocardium, etc.

Fig. 6

Diplococcus pneumoniæ of Fränkel. (Karg and Schmorl.)

D. The Micrococcus Tetragenus.

—Suppurations produced by these organisms are prolonged, mild in character, not painful, but accompanied by much brawny induration of tissues.

E. The Micrococcus GonorrhϾ.

—The micrococcus gonorrhœæ, or gonococcus, is found constantly in the pus of true gonorrhea, in many cases the pus being a pure culture of this organism. These cocci are generally seen in pairs (biscuit-shaped), while their inclusion within the leukocytes or their attachment in or to epithelial cells is characteristic. Unlike other pyogenic cocci, they do not stain by Gram’s method, being decolorized by iodine, by which fact they may be distinguished. They are cultivated with difficulty, and are known rather by their clinical effects than by their laboratory characteristics; are human parasites, other animals, so far as known, being practically immune. The gonococcus may also produce abscesses, and may be carried to distant parts of the body, where its effects are commonly noted as pyarthrosis, although endocarditis, pericarditis, pleurisy, etc., are known to be due to it, and fatal pyemia has been produced in consequence. In some way it is probably the explanation of the post gonorrheal arthritis, wrongly spoken of as gonorrheal rheumatism.

F. The Bacillus Coli Communis or Colon Bacillus.

—This is an inhabitant of the intestinal canal; varies extremely in virulence and somewhat in morphological appearances; coagulates milk; is often associated with other organisms; migrates easily both along the alimentary canal and from it into the surrounding tissues or channels. It is a disturbing element in the production of kidney and hepatic disease, also in the production of appendicitis and peritonitis. Ordinarily its pyogenic properties are not virulent; occasionally, however, it becomes extremely virulent.

G. The Bacillus Pyocyaneus.

—The bacillus pyocyaneus, a widely distributed organism, often observed in the skin and outside of the body; a motile, liquefying bacillus, growing at ordinary temperatures, seldom seen alone, but occasionally producing pus without association with other organisms; it stains the discharges and dressings a bluish-green and imparts sometimes an offensive odor. Suppuration caused by this bacillus is usually prolonged, but characterized by little constitutional disturbance.

Facultative Pyogenic Organisms

—i. e., those which have the power of provoking suppuration, but which have other and more distinct pathogenic activities as well.

A. Bacillus Typhi Abdominalis.

—This is found in many pus foci, developing during or after typhoid fever. It is occasionally met with alone, though most of these abscesses are really mixed infections. It is generally found in the bone or beneath the periosteum. Such abscesses are frequently seen in the ribs, and may not be noticed until months after convalescence from the fever. The pus contained within them is not always typical in appearance, but may be unduly thin or unduly thick.

B. Bacillus Proteus.

—Under this name are included three distinct forms, which were originally described by Hauser as distinct species, but which are now regarded as pleomorphic forms of the same organism. It is a motile bacillus, met with in decomposing animal and vegetable material, and occasionally found in the alimentary canal. It has been known to produce pus, especially in the peritoneal cavity and about the appendix. It may even cause general infection and peritonitis.

C. Bacillus Diphtheriæ.

—A non-motile bacillus, varying considerably in size and shape, changing the reaction in sweet bouillon from acid to alkaline; produces a dangerous infective inflammation of exposed surfaces, with tenacious exudate amounting to a distinct membrane. As a part of its life history it also produces a toxalbumin, which is one of the most powerful cell poisons known, the disintegration of the cell constituents due to its action being rapid and pronounced. This accounts for the heart failures which are often reported in connection with the disease.

D. Bacillus Tetani.

—More will be said about this organism when considering [tetanus], and to that subject the reader is referred. The tetanus bacillus is occasionally found in pus which comes from the area through which the original infection was produced. But these bacilli do not travel to any distance in the human body, and are seldom found away from the area involved. Under most circumstances the pus is the product of a mixed infection.

E. Bacillus Œdematis Maligni.

—This organism will be more fully considered under a different heading. (See [Malignant Edema].) It is a long, anaërobic bacillus, widely distributed in the soil and the feces of animals. It is believed that this, like the tetanus bacillus, may occasionally lead to formation of pus.

F. Bacillus Tuberculosis.

—This organism likewise will receive fuller description in an ensuing chapter. (See [Tuberculosis].) The pus of old cold abscesses in which the more obligate pyogenic organisms have long since died usually contains this organism in mildly virulent form. On the other hand, fresh suppurations occurring in connection with tuberculous disease are mixed infections. There is reason to believe, however, that this organism is capable of producing pus even when none of these are present; for example, in that form of acute miliary tuberculosis which is occasionally met with as bone abscess it may be found.

G. Bacillus Anthracis.

—This is one of the most malignant and resistant organisms known, being in the highest degree poisonous for the smaller animals, man being less susceptible. One of its characteristic lesions in the human body is a form of pustule commonly known as malignant pustule, the pus in which is usually a pure culture of this organism. (See [Anthrax].)

H. Bacillus Mallei.

—This is the organism which produces glanders in the lower animals and in man. That form of the disease known as farcy, in which the infected nodules rapidly break down, is likely to contain pus which will be more or less a pure culture of this organism.

I. Bacillus Lepræ.

—This is the microörganism which produces leprosy, closely resembling the tubercle bacillus. It is constantly and exclusively present in the lesions of leprosy, which are often of the suppurative type, the bacilli being enclosed within pus cells; it is also found in the fluid surrounding them. Although suppuration in these cases may be in a large measure due to secondary infection, it is positive that the leprous bacilli deserve to be grouped in this place.

J. The Bacillus Pneumoniæ of Friedlander.

—The bacillus pneumoniæ of Friedländer was at one time regarded as the cause of croupous pneumonia, which is now known to be due to the micrococcus lanceolatus. The Friedländer bacillus, however, is capable of producing bronchopneumonia, and is occasionally met with in empyema, suppurative meningitis, and inflammations about the nasopharyngeal cavity, of which it is known to be an occasional inhabitant.

K. The Bacillus of Rhinoscleroma.

—A distinctive organism has been described for this disease and given this name. It has such wide morphological differences, however, that it is possible that it is only the bacillus of Friedländer above mentioned. At all events, an organism of this general character is constantly found in this disease in the thickened tissues from the nose ([Fig. 8]).

L. The Bacillus of Bubonic Plague.

—This was recently discovered by Kitasato, and, in view of the recent ravages of the disease in the Orient, has assumed considerable importance. It grows upon most media, and is found in the blood, in buboes, and in all internal organs of patients suffering from this disease. The smaller animals are susceptible upon inoculation. Animals fed with inoculated foods die also, showing the possibility of infection through the intestine. When exposed to direct sunlight for a few hours the bacillus dies. The general symptoms of the disease are those of hemorrhagic septicemia and its consequences.

M. The Bacillus of Rauschbrand.

—This is seldom, if ever, seen in this country. It is known in England as “the black-leg” or “quarter-evil.” It is an anaërobic organism, frequently met with in cattle, which causes a peculiar emphysema of subcutaneous tissue, spreads deeply, and is followed by a copious exudate of dark serum with gas formation. The smaller animals are not ordinarily inoculable; but if to the culture material there is added 20 per cent. of lactic acid, their insusceptibility is overcome and they succumb to the disease. So, also, as in the case of the tetanus bacillus, by addition of the bacillus prodigiosus or of proteus vulgaris the disease may be produced in otherwise insusceptible animals.

N. The Bacillus Aerogenes Capsulatus.

—The bacillus aërogenes capsulatus seems capable sometimes of causing pyogenic and even fatal infection. Its presence is associated with gas formation. It grows as an anaërobe.

O. The Bacillus of Chancroid.

—The bacillus of chancroid identified by Ducrey, and briefly described in the chapter on that subject.

Fig. 7

Rhinoscleroma: infiltration of tissues about the nose. (Case reported by Dr. Wende, Buffalo.)

Fig. 8

Bacilli of rhinoscleroma. × 1000. (Fränkel and Pfeiffer.)

YEASTS.

Busse was the first to call attention of clinicians and pathologists to the role played by yeasts in certain infections. Since the original observations of Busse in a case in which the organism produced a general infection, the lesions of which were a combination of tumor and abscess formation, various observers have noted the presence of pathogenic yeasts, usually in skin lesions. Gilchrist and Stokes were the first in this country to determine the nature of these organisms, and their observations have been followed by the detection of a large number of similar cases. In the skin lesions the organisms are found in minute abscesses; in the subcutaneous tissue and in the infections similar to those of Busse large abscesses surrounded by extensive masses of granulation tissue characterize the infection. The organisms can be detected in the pus by means of an examination of the fresh unstained fluid ([Fig. 9]).

FUNGI.

Besides the micro-organisms everywhere grouped as bacteria, there are other minute organisms which have also the power of engendering pus. One of these is the ray fungus, known as the actinomycis, which causes the disease known as lumpy jaw or actinomycosis. Suppuration is always a concomitant of the advanced lesions of this disease, and, while it may be in many instances a mixed infection, it is not necessarily so. Moreover, the pus produced under these circumstances contains minute calcareous particles which are pathognomonic, by which a diagnosis can sometimes be made off-hand.

Besides these fungi, others, belonging rather to the class of vegetable molds, which are yet pathogenic for human beings, may be occasionally met with under these circumstances—e. g., the fungus of Madura foot, the leptothrix, and other molds from the mouth, while the different varieties of aspergillus may be found in pus about the ear or even in that from the brain.

PROTOZOA.

The protozoa have the power of producing, if not absolute ideal pus, something so nearly resembling it that we may include them among the facultative pyogenic organisms. The best known of these protozoa are the amebæ, which are met with in the intestinal canal in some countries, occasionally in the United States, especially as the exciting causes of a peculiar type of dysentery often accompanied by abscess of the liver. In these abscesses the amebæ are found, and no other organisms. Another group of the protozoa, known to biologists as the coccidia, are also capable of causing pus formation, more particularly in some of the lower animals. Numerous other parasites, belonging higher in the animal kingdom, are undoubted exciters of pus formation, though it is not necessary to lengthen the list beyond those already mentioned.

Fig. 9

Blastomycetic pus (fresh). × 1000. (Gaylord.)

Protozoa have recently been established as the active agents in the production of smallpox and probably also of scarlatina. They have been seen so generally in and around cancer cells as to make it extremely probable that cancer is a protozoan infection. In syphilis also they are found as the spirochetæ, now regarded as its cause.

Protozoa are as ubiquitous as bacteria, but their recognition is as yet more difficult, as but little is known of them. The numerous stages through which they pass in completing their life cycles only complicate the subject, while the difficulties encountered in cultivating them are still to be overcome. As we become more familiar with them we shall more frequently find them to be pathogenic organisms.

CLINICAL CHARACTERISTICS OF PUS FROM DIFFERENT AGENCIES.

Staphylococcus.—Dirty white, moderately thick, with sour-paste odor.

Streptococcus.—Thin, white, often with shreds of tissue.

Colon Bacillus.—Thick, brownish, with fetid odor, or thin, dirty white, with thicker masses.

Micrococcus Lanceolatus.—Thin, watery, greenish, often copious.

Bacillus Pyocyaneus.—Distinctly green or blue in tint.

Bacillus Tuberculosis.—Thick, curdy, white paste, or thin, greenish, with small, cheesy lumps or even with bone spicules.

Actinomycis.—Thick, brownish white, with small, firm, gritty or chalky nodules of yellow color.

Ameba Coli.—Thick, brownish red.

BACTERIAL DETERMINATION AS AN INDICATION IN TREATMENT.

There is a practical side of great importance pertaining to the recognition of the nature of the infectious organism in many cases of suppuration and abscess. For instance, pus which is due to streptococcus invasion indicates a collection which should be freely evacuated and carefully drained. This is also true in essential respects of staphylococcus pus, particularly that due to the streptococcus aureus. Putrid pus from any source requires disinfection and free drainage, the former preferably perhaps by hydrogen dioxide. Pus which is due to the colon bacillus is not often extremely virulent, which accounts for so many cases of appendicitis recovering with or without operation. A collection of this pus needs little more than mere drainage and opportunity for escape. Pus from a recognizable tuberculous source may still contain living tubercle bacilli. This means either that the cavity whence it came should be completely destroyed and eradicated, or else that the margins of the incision or opening through which it has escaped should be so cauterized that infection of a fresh surface is impossible. The same is true of abscesses due to glanders bacilli and to certain cases of suppurating bubo following chancroid, where the whole course of events shows the virulent character of the organisms at fault.

SUPPURATION.

Although it may be possible to produce in certain laboratory experiments metamorphosed material which very closely simulates pus, or, in fact, by injection of chemical irritants, to sometimes imitate the suppurative processes, nevertheless, the student should be brought face to face with the statement, to which for surgical purposes there is no practical exception, that suppuration, i. e., formation of pus, is due to the presence in the tissues of the specific irritants already catalogued and described, and of the peculiar peptonizing or other biochemical changes which bacteria exert upon living animal cells.

Coagulation Necrosis.

—Coagulation necrosis is the term applied to the characteristic changes occurring in the tissue cells when thus attacked, which may be summarized as a fading away of cell outlines, diminution in reaction to reagents, and a merging of cells and intercellular substance. Coagulation necrosis is not the only result of bacterial activity, but may be produced by other causes. Nevertheless, pyogenic bacteria do not exert their deleterious action upon the tissues without occasioning changes included under this term. In an area thus infected, as already described, leukocytes, i. e., phagocytes, are present in increased number for purposes already mentioned. As we approach the centre of activity phagocytes are more numerous than cells, and intercellular barriers completely break down. When bacteria are found in greatest number, there also occurs the greatest phagocytic activity, and there also will be found the evidence of suppuration, i. e., pus. As already indicated, the polynuclear leukocytes are most active in the process of defence. Where coagulation necrosis is most marked there has been the greatest activity of conflict with the greatest death of cells. Around these areas bacteria and cells are found in indiscriminate arrangement. Tissue vitality is impaired by intoxication of the cells by the excretory products of the bacteria, i. e., the so-called ptomains, toxins, etc., and their power of resistance is thus weakened. From the mechanical results of pressure tension around the centre of activity is increased, by which tension vitality is still more impaired and more rapid tissue death occurs. Thus there occurs migration or burrowing of pus; or, to state it more clearly, the tissues break down in front of the advancing destruction, and in the direction of least resistance. This is known as the pointing of pus, which brings it many times to the surface, and often in other and less desirable directions.

Abscess.

—An abscess is a circumscribed collection of pus. The term is used in contradistinction to purulent infiltration, in which the collection is not circumscribed, but is exceedingly diffuse and extends itself in various directions, the amount at any spot being almost inappreciable. Purulent infiltration is regarded as the more serious of the two conditions, as it is more difficult for pus to escape under these circumstances than when it can be evacuated through a single opening. The term phlegmon is one now generally used to indicate a suppurative process, usually of the general character of purulent infiltration rather than of abrupt abscess, but generally employed to include both conditions. The adjective phlegmonous is coupled with the names of other surgical infectious diseases to indicate that it is complicated by suppuration, e. g., phlegmonous erysipelas. Pus is a product of bacterial activity usually formed rapidly rather than otherwise, and abscess formation or phlegmonous activity of any kind is a question of but a few days. Empyema means a collection of pus in a preëxisting cavity.

The significance of this condition is well described in the story of inflammation and suppuration, to paraphrase Sutton, read zoölogically, as though it were the story of a battle: The leukocytes (phagocytes) are the defending army, the vessels its lines of communication, the leukocytes being, in effect, the standing army maintained by every composite organism. When this body is invaded by bacteria or other irritants, information of the invasion is telegraphed by means of the vasomotor nerves, and leukocytes are pushed to the front, reinforcements being rapidly furnished, so that the standing army of white corpuscles may be increased to thirty or forty times the normal standard. In this conflict cells die, and often are eaten by their companions. Frequently the slaughter is so great that the tissues become burdened by the dead bodies of the soldiers in the form of pus, the activity of the cells being proved by the fact that their protoplasm often contains bacilli in various stages of destruction. These dead cells, like the corpses of soldiers who fall in battle, later become hurtful to the organism which, during their lives, it was their duty to protect, for they are fertile sources of septicemia and pyemia. This illustration may seem romantic, but is warranted by the facts.

Around the margin of the site of an acute abscess a barrier is formed by condensation and cell infiltration of the surrounding tissues. This is not a distinct wall nor membrane, yet, nevertheless, serves as a sanitary cordon to confine the mimic conflict within reasonable bounds. This is the zone of real inflammation; within it there are tissue destruction and coagulation necrosis. By virtue of the peptonizing power of the pyogenic organisms the parts involved in this necrosis gradually liquefy the intercellular substance dissolving first. It is this which in the main forms the fluid portion of the pus. Various tissues show widely differing resistance to this softening process. In true glands the interlobular septa seem to break down first, and in this way suppuration extends around the acini or gland lobules, and thus pus may contain masses of easily recognizable size. These masses are ordinarily known as sloughs.

It is by virtue of the so-called lymphoid cells, which are those principally involved in producing the barrier or boundary of the acute abscess as above described, that granulation tissue is formed, which takes up the effort of repair as soon as pus is evacuated. This boundary has no sharp limit, but shades off into healthy surrounding tissues.

Under the term “abscess” is meant that which is described as acute abscess. Under certain circumstances, especially when they are produced by the facultative pyogenic organisms rather than the obligate, abscesses form more slowly, and may be spoken of as subacute. These are terms used in contradistinction to the so-called cold abscesses, which, although clinically bearing a certain resemblance to the acute, are in almost every pathological respect different from it. Cold abscesses will be considered under the head of Tuberculosis. It is possible to have an acute pyogenic infection of a cold abscess; in such case we have acute manifestations. Gravitation abscesses are those where pus forming in one part tends to migrate, usually in the direction in which gravity would take it, extending into portions deeper or lower. Perhaps the best illustration of this is the pointing of a psoas abscess below Poupart’s ligament. Metastatic abscesses are those which are formed as the result of embolic processes, each one being in miniature a repetition of a lesion which has occurred at some other part of the body. The underlying fact concerning metastatic abscesses is that the primary process has occurred in some other portion of the body, whence it has been distributed as above. These will be considered in the chapter treating of Pyemia.

The product of all acute suppurative lesions is pus. This is an opaque fluid of creamy consistence and whitish or grayish appearance, varying in density, met with in amounts from a minute drop to half a gallon or more. Under ordinary circumstances it is odorless, and its reaction, either acid or alkaline, is very faint. It is, like the blood, composed of a fluid and a solid portion. The solid portion consists of so-called pus corpuscles and other debris of tissue, which vary with the site of the disease and the parts involved. The source of the pus corpuscles has been cited and the statement made that they are in effect the bodies of phagocytes which have perished in the biochemical fight for existence of the parent organism. Cocci or bacilli are found in pus corpuscles and also in the surrounding fluid.

Pus should be without odor, but under certain circumstances it possesses an odor which will vary in character according to the source of the pus or the nature of its principal bacterial excitant. Pus from the upper end of the alimentary canal frequently has the sour smell of gastric contents; that from the neighborhood of the lower end, the fetid odor which is for the most part due to the action of the colon bacillus. Inasmuch as colon bacilli are found in widely distant parts of the body, they may also give an unpleasant odor to pus even from a brain abscess. When the pus has become contaminated with the ordinary saprophytic organisms, it may smell like any other decomposing material. The older writers called it ichorous pus, while sanious pus was supposed to be that more or less mixed with blood, undergoing ammoniacal decomposition or else strongly acid. Pus sometimes has a well-marked blue or bluish-green tint. This is due to the presence of the bacillus pyocyaneus, already described. An orange tint is sometimes given by the presence of hematoidin crystals, due to the original hemorrhagic character of the infected exudate. The former appearance indicates usually a slow course to the suppurative lesion, while the latter has been regarded by some as affording an unfavorable prognosis. Distinctly red pus, whose tint is due to the presence of a bacillus giving bright-red cultures on blood serum, has been noted in other instances. This can readily be distinguished from blood, because upon dressings it does not change color.

Pus may form superficially, when it is called subcutaneous suppuration, in which case there is a minimum of pain, because tension is not great and the distance to the surface is short. Collections which form beneath the fasciæ, especially the deeper fasciæ of the limbs and trunk, give rise to much more extensive disturbance, both locally and generally, and frequently do not point for many days; or, instead of pointing, burrow deeply and find their outlet at some undesirable point. These are known as subfascial collections. Subperiosteal abscesses give rise to still more pain, because of the unyielding character of their limiting structures, and the symptoms caused by them are acute and distressing.

An illustration of the pain which may follow deep suppuration may also be seen in the ordinary panaritium, or bone felon, where the path of infection is from without, but the destructive lesion is confined within absolutely unyielding tissues, at least at first. Along certain tissues infection spreads with rapidity. This is particularly true of the delicate areolar tissue seen between tendons and tendon sheaths, and the infectious process may follow this tissue wherever it shall lead, even along complex courses.

The question often arises, Can pus be resorbed? There is no question but that small amounts of pus are disposed of by phagocytic activity, and the disappearance of purulent infiltration, under the influence of favoring remedies, or even when let alone, is not infrequently noted. True pus resorption is a question of phagocytic possibilities, and can occur only in very limited degree, as a result upon which it is not safe to count, and which is capable of encouragement only up to a certain point.

One inevitable law seems to govern collections of pus, that when they advance or migrate in any direction it is in that of least resistance. This causes them to take peculiar and sometimes disastrous courses, but it is a law which is never violated. It leads to the bursting of abscesses into the brain, into the pleural cavity, into the peritoneal cavity, the bowel, and elsewhere; it leads to a condition where pus may travel along a path even a foot or more in length, rather than come to the surface, a distance of perhaps an inch, and affords one of the best reasons for early operative interference so that the disastrous effects of burrowing may be obviated. When the pus is limited to a drop or fraction thereof the abscess is called a furuncle, especially when in the skin. The average “boil” of the layman is a subcutaneous or subfascial abscess. When the infiltration is pronounced, and when there has been more or less extensive destruction of tissue, with perhaps formation of numerous outlets for the escape of pus and detritus, it is known as a carbuncle. (See [Chapter XXVI].) In certain conditions small superficial furuncles or boils form, sometimes in great number and almost synchronously, or, as it were, in crops. This condition is known as general furunculosis.

Signs and Symptoms of Abscesses.

—The appearances by which pus may be suspected or detected are those of congestion and hyperemia, more or less abruptly circumscribed and markedly accentuated. Along with these there is more or less edema or edematous infiltration of the skin and overlying tissue, which permits of that peculiar appearance known as “pitting on pressure.” Often, too, there is a distinctly edematous swelling of the parts, especially around the margin, with brawny infiltration of the centre of the infected area. Numerous vesicles occasionally are noted upon the skin, which may be filled with reddish serum. When softening and pus formation occur, there is a condition which to the palpating fingers gives the characteristic sensation known as fluctuation. Fluctuation simply points out the presence of fluid beneath; but when in an area marked as thus described fluctuation is noted, it means the presence of pus. It is detected by manipulating in a direction parallel to and concentric with the axis of the limb or part. The pain is also in most instances significant; patients speak of it as having an intense and throbbing character. With these local signs occur symptoms indicating some degree of septic intoxication, i. e., pyrexia, chills, malaise, sweats, etc., which are corroborative indications, their intensity being a reasonably correct index of the severity and gravity of the local infection.

When a deep-seated abscess is suspected a careful blood count will often permit a diagnosis to be made. This is conspicuously true of cases of appendicitis. If leukocytosis is established there should be immediate operation. (See [Chapter II].)

It is seldom that a superficial collection of pus can be mistaken for anything else. In small and superficial abscesses (boils, furuncles) as pus approaches the superficial layer (epidermis) of the skin it may be discovered through its thin covering. In deep lesions there is often a doubt, even on the part of the most experienced. The measure now usually resorted to for purposes of diagnosis and exact recognition is the exploring or aspirating needle. The old exploring needle was one of good size, having a groove along which, after introduction, pus might pass. Since the almost universal use of the hypodermic syringe, a small aspirating needle attached to the ordinary syringe is the measure commonly adopted. Such a needle may be introduced into the brain, into the liver, or into almost any and every soft tissue without danger, and if properly manipulated is almost sure to facilitate detection of pus. Exploration done with either of these means and for this purpose should always be conducted as an aseptic, even if a minor operation, in order that no extra infection may be added from without. The skin should be carefully washed, the needle sterilized, etc.

It is good surgery to resort to the knife either for the above purpose or in order that by a longer incision or by opening the cavity deep exploration may be made. Such explorations are of benefit even though a circumscribed collection of pus is not found, since by relief of tension and local abstraction of blood they act in a revulsive way and do much good. Acting upon the same principle the trephine or the bone chisel may be used for the purpose of opening the cranium and exploring for pus, or of opening into the medullary canal of the long bones and hunting there for that which is suspected.

Treatment.

—As soon as suppuration threatens speedy measures should be adopted, either for the purpose of bringing about resorption, or of favoring and hastening suppuration. In theory antiseptic applications are demanded; in practice they are sometimes of benefit. These may consist of mere soothing applications, as a lead and opium wash, or some other wet or dry astringent applied upon the surface; or they may consist of cold applications, which by their astringent action will limit the amount of exudate and prevent its further infection. Or advantage may be taken of the properties of moist heat, and the application of hot poultices or fomentations may encourage exudation, but particularly quicken superficial breaking down, and thus hasten the time when the phlegmon shall point, or come sufficiently close to the surface to show that its contents are pus and permit of evacuation. Such local applications, therefore, give relief from pain and hasten favorably the suppurative process. In cases of phlegmonous infiltration, the application of an ointment composed of resorcin 5, ichthyol 10, mercurial ointment 35, and lanolin 50 parts, or else the Credé silver ointment, is beneficial. Under the influence of these antiseptic and sorbefacient preparations, and of moist heat, many phlegmonous infiltrations assume a kindlier type, and may secure the actual resorption of pus.

Finally in almost every case pus must be evacuated. Here the universal rule may be applied, to which there are practically no exceptions, and which should be stamped on the mind of every student and young practitioner. It is—that pus left to itself will do more harm than will the knife of the surgeon if judiciously used for its evacuation. Action taken in accordance with this rule may be considered wise and timely. The operation of evacuation may at one time be a mere puncture, or possibly the aspirating needle alone will be enough; at other times it requires extensive and careful dissection and entails no little responsibility. This is particularly true in such deep-seated suppurations as those around the appendix and in the brain, while in the deep-seated bone lesions of this character the use of the bone chisel or the cutting forceps may be of use. But the rule holds good, no matter where the pus may be, and as long as good judgment is shown in the operative procedure nothing but good can come from recognition of this law. After the evacuation of pus the cavity should be cleansed and disinfected with hydrogen dioxide, perhaps even with caustic pyrozone, or, if these are not at hand, with other suitable antiseptic solutions.

Ordinary judgment should be exercised in evacuating every abscess, in order that opening be made at that point which in the common position of the body shall be most favorable to drainage by mere gravity alone. If circumstances compel opening when advantage cannot be taken of gravity, then one or more counteropenings should be made at points selected where drainage may be best effected, and where anatomical conditions do not make it injudicious to incise. Drainage should be favored by the introduction of a drainage tube or of other aids, such as gauze, strands of catgut, bundles of horse-hair, etc. Finally, a dressing should be applied which is both protective and absorbent, and in quantity sufficient to make compression of the walls of the abscess cavity—not sufficient to obstruct drainage, but enough to favor prompt adhesion of surfaces, which by speedy granulation shall ensure prompt healing.

Abscesses are found in proximity to large vessels or dangerous anatomical regions, when care must be exercised in opening them. Here careful dissection should be made under an anesthetic. This is true of abscesses in the neck and of those around the appendix, for example, where the general peritoneal cavity is shut off only by more or less delicate adhesions, and where the surgeon must literally feel his way with great precaution lest adhesions be torn and the previously protected cavity infected. At other times, especially in abdominal abscesses, it is necessary to pack sponges or absorbent gauze in and about the parts, so that any fluid which may escape may be absorbed by these dressings.

Accompanying Disturbances.

—The disturbance of function which accompanies all congestion and exudation, whether provoked by specific irritants or not, has been alluded to; but in cases of surgical infections, especially those which produce local suppuration, disturbance of function is much greater, while there are other disturbances which sometimes constitute the worst feature of these cases. The presence of pus is often indicated, especially when deeply seated, by one or more chills, and the occurrence of a chill is always marked to varying degree by pyrexia. It is conceded that the chill is an expression of a general septic disturbance; but it is necessary also not to forget that general septic disturbance is a frequent accompaniment of pus which is not evacuated as soon as formed. Moreover in certain cases suppuration and septic infection seem to occur synchronously, one being local, the other general.

Pus may also be suspected beneath a surface which is red, tender, swollen, edematous, and pitting on pressure. When fluctuation is added to these indications any element of doubt is thereby dissipated.

Other indications of the presence of pus are a well-marked leukocytosis, coupled with the iodine reaction indicating the existence of glycogen in the blood, the presence of indican in the urine, and the positive results frequently obtained by making cultures from the blood. When pyogenic bacteria are found in the blood the inference is very plain, and both treatment and prognosis are influenced. In such a case the introduction into the blood of an antiseptic such as Credé’s soluble metallic silver or of the antistreptococcus serum, is plainly indicated. The absence of bacteria from the blood, under these circumstances, does not disprove the presence of pus, but their presence gives a very serious character to the disease, and should lead to a most guarded prognosis. Invasion of the blood by staphylococci is nearly twice as serious as when streptococci gain entrance. Suppuration of the bones and of the tendon sheaths is liable to produce such invasion.

The other disturbance with which suppuration is so often complicated is septic infection. In fact it may be questioned whether pyrexia is not an expression of this condition. Any collection of pus, no matter how small, may show signs of septic infection; and, on the other hand, large collections may be formed without serious septic symptoms—in other words, suppuration and expressions of septic infection may be blended in almost every conceivable way. Sepsis as a distinct condition will be described in another chapter.

It is important to summarize what may become of pus when once it has formed and is not promptly evacuated. Pus when long present may be—

A. The possibility of the absorption of pus, or, what is equivalent to it, its spontaneous disappearance, has been mentioned. While it does not usually take this course, it may thus disappear; as, for instance, in the anterior chamber of the eye in cases of hypopyon, or in various other localities, particularly when present only in small amounts. The absorption of pus is purely a matter, as far as we know, of phagocytic activity plus the power of the tissues to take up various fluids.

B. Encapsulation.—This occurs only when pus has been present for some time and when the virulence of the pyogenic organisms is not intense. We may get encapsulation of pus in any part of the body, the most typical illustration naturally being within the bones. Around the purulent focus, as around any other irritating foreign body, the capsule is formed by condensation of surrounding tissue. This is the way in which most cold abscesses with their limiting membranes are produced, those produced by tubercle bacilli having slight irritating properties. Inasmuch, then, as the biological activity in such a focus is small, there is time for such encapsulation; while by the membrane thus formed, or the sanitary cordon, already referred to, protection is afforded to the surrounding tissues. In such a collection fresh infection may incite acute disturbances again, and many abscesses which thus lie latent for a considerable length of time are fanned, as it were, into a conflagration, when a new and acute inflammation is produced.

C. Of the various metamorphoses and chemical changes that occur in that which was originally pus, the caseous and the calcific are the most common. These also are connected largely with the tuberculous process, although calcareous particles are found in the pus of actinomycosis. Under their respective heads these degenerations will be more particularly described.

Certain names have been given to collections of pus in different localities or under peculiar circumstances. A collection of pus in the anterior chamber of the eye is known as hypopyon; when in any preëxisting cavity, it is known as empyema of that cavity, the distinction between empyema and abscess being that “abscess” means a circumscribed collection where previously there was no cavity, while “empyema” implies a normal cavity, without respect to size or location, filled with this abnormal fluid. The term empyema, when not used in connection with some particular cavity, is understood to refer to a collection of pus in the pleural cavity. Other names also are used which are particulate and distinctive; in these the prefix pyo is used while the suffix indicates the part involved; thus we have pyothorax, pyopericardium, pyarthrosis, etc.

SINUS AND FISTULA.

These are terms applied to more or less tubular channels abnormally connecting various parts of the body, or connecting some cavity with the surface of the body in a way anatomically quite abnormal. Or they may be regarded as tubular ulcers, or ulcerated tunnels, connecting as above. A more exact distinction between the two terms would imply that a sinus connects the surface with some deeper portion where a cavity is not normally present—i. e., with a focus of disease—whereas a fistula properly refers to a tubular passage connecting natural or preëxisting cavities in an abnormal manner. Thus we speak of buccal, rectal, vesicovaginal fistulas, etc., whereas a passage leading down to an old abscess or to a focus of disease in bone, for instance, is properly referred to as a sinus. It is possible for the margins of a fistula to become more or less cicatrized and cease to be ulcerous, whereas the entire track of a sinus is practically a continuous ulcer, only tubular in arrangement.

Causes.
A. Congenital.

—There are numerous points about the body where, as the result of arrest of development or failure to grow, fistulous passages which are comprised within the normal fetal arrangements, but which should close later, either before or at birth, fail to do so. Thus we have congenital fistulas of the neck, persistent urachus, persistent omphalomesenteric duct, etc. These are in no sense primarily connected with diseased conditions, but may become so secondarily.

B. Pre-existing Abscess with Unhealed Channel of Escape

—e. g., rectal, fecal, and other fistulas and sinuses which connect with tuberculous foci in any part of the body.

C. Previous Traumatic or other Destruction of Normal Tissues

—e. g., vesicovaginal fistulas due to tissue death from pressure, buccal fistulas from gangrene of the cheek, as in noma.

D. Foreign Bodies

—bullets, ligatures, etc.—which prove irritating or infectious enough to prevent absolute healing. More or less tortuous sinuses will generally be found leading down to the irritating material.

E. The Presence of Necrosed or Necrotic Material

—e. g., a sequestrum in bone, which is usually evidenced by the presence of one or more sinuses.

Treatment.

—If the determining cause is still acting, the treatment is to remove the cause. Consequently, when the sinus leads down to diseased bone or other dead or dying tissue, the complete evacuation of the cavity is necessary before the sinus may heal. If the cause is a foreign body, its removal should be at once insisted upon.

An excellent suggestion is to stain all fistulous tracks with methylene-blue; the blue trail after doing this may be followed, no matter how irregular its course (Fergusson). If the color is mixed with a little hydrogen dioxide, and this forced into a sinus mouth or a fistulous opening, it will carry the dye to all parts of the cavity. This may be used even in dealing with fecal fistulas or those extending deeply into the interior of the body or among the viscera.

Fistulas of congenital origin and those which connect two normal cavities of the human body are usually due to a cause which has ceased to act. Consequently we should endeavor solely to atone for the result. The direction and the course of a sinus may be learned by the use of a probe curved to suit and manipulated by a gentle hand, force never being required. Or sometimes, when the silver instrument fails to pass, a flexible bougie or catheter may be introduced. The character of the passage can be judged for the most part by the appearance of the discharges. With sinuses of recent origin leading down to recent suppurative foci it may be sufficient to enlarge the opening and to wash the cavity thoroughly. If a particle of gauze, tube, or sponge has been left therein, its removal is necessary to secure prompt healing. In cases of long standing antiseptic and stimulating substances should be injected or the interior should be cauterized with strong solutions of zinc chloride or silver nitrate, or with these melted upon the end of a probe. The chronic sinus, as well as the chronic rectal fistula, is usually an expression of local tuberculous disease. Accordingly these passages may be found lined with the same dense, fungating membrane which lines a cold abscess cavity—the membrane, protective in its purpose, to which I have given the name pyophylactic. Whenever such tissue and such membrane are met with they should both be extirpated thoroughly, since in this way only can absolute eradication of the tuberculous infection be relied upon. After such complete excision—which means usually laying open the entire sinus—the parts may be brought together with sutures (this, at least, is usually possible about the rectum) to secure primary union; otherwise, the whole sinus, as well as the cavity to which it has led, must heal by the granulating process, both being kept packed with gauze or some other desirable foreign body acting as an irritant, thereby provoking more rapid formation of granulation tissue. When it is necessary thus to pack a cavity, or when it is desired to keep its upper exit open lest it heal before the lower part, ordinary white beeswax, as suggested by Gunn, makes a serviceable material. This can be molded in hot water to fit the cavity; can be tunnelled or bored for drainage; can be diminished in size as the cavity heals, and is absolutely non-absorbent.

Finally there are numerous plastic methods which have been resorted to in various parts of the body, most of which are made to comprise, first, the absolute eradication of the diseased tract, and, later, the closure of the wound thus made by transplantation or sliding of flaps, or any other plastic expedient which may be considered best. These, as well as the special treatment made necessary for particular forms of sinus and fistula, will be dealt with under their proper headings.

CHAPTER IV.
ULCER AND ULCERATION.

The term ulcer pertains to surfaces, and should be defined as a surface which is or ought to be granulating, i. e., healing.

While an ulcer may be the result of ulceration, it is not necessarily so, the term ulceration being one of very loose significance and applied to many different processes. The idea underlying ulceration is infection, and, when limited to its proper significance, the term should never be used for a process in which infection and consequent breaking down of tissue do not virtually comprise the whole process. Therefore, it is to be distinguished from certain disappearances of tissue alluded to under the head of Atrophy or Interstitial Absorption. It is not correct to say that the sternum ulcerates away, making room for a growing aortic aneurysm, the question of infection here not being raised. These distinctions should be accurately maintained and constantly borne in mind.

ULCERS.

The causes of ulcers may be—

A. Traumatic.

—This includes all surfaces which are granulating and healing more or less rapidly, or are displaying a disposition toward healing, and which may have been produced by wounds, burns, frostbites, etc. These include also ulcers due to pressure, as from splints, bandages, orthopedic apparatus, or from external friction. Ulcers which form around foreign bodies may also be included under this head, their essential cause being traumatic. It should include also destruction of the surface by various chemical agencies, such as strong caustics, and the consequences of intense heat or cold, including burns and frostbites.

B. Local.

—1. Among local causes may be mentioned local infections, with tissue death in consequence, such as occur in tuberculous, cancerous, leprous, syphilitic, and other specific manifestations where surfaces are involved.

2. Tumors, either benign or malignant, whose blood supply is cut off and whose surface is thereby predisposed to infection.

3. Perverted surface nutrition, for example, in connection with varicose veins of the extremities, where, aside from any perverted trophoneurotic influence, there is stagnation of blood, saturation of tissues with serum, and final leakage of the same, even to the surface. Varicose veins of the leg which lie near or underlie ulcerating surfaces become thrombosed and obliterated, so that such ulcers rarely bleed. On the other hand, a passive hyperemia here leads to edema, perversion of nutrition, failure to repair trifling surface injury, and a surface is left which of itself rarely, if ever, heals.

4. So-called pressure sores or bed-sores, which in some cases may be regarded as having a traumatic origin, but which, nevertheless, would not occur from purely traumatic influences without predisposing tissue changes. The bed-sore is probably the best illustration of this. Simple ulcer is known as bed-sore, while a sloughing ulcer of this kind is frequently alluded to as decubitus. Such ulcers are usually found over those regions of the body made most prominent by bony projections, upon which undue pressure is made when debilitated patients have lain for a long time in bed.

5. Ulcer is the frequent result of numerous skin diseases, into whose etiology as yet bacteria have not been introduced—e. g., pemphigus, eczema, etc.

6. Ulcer is the occasional result of embolic or other disturbance of the principal artery of the part, by which nutrition is cut off and tissue death results.

7. Bites of insects or other parasites or of noxious animals frequently lead to ulceration.

8. Certain more specific forms of ulcer are described by some writers, apparently with more or less reason, among them being chancroid, perforating ulcer of the foot, etc. (Chancroid is described in Chapter X.) Trophic ulcers of the fingers or hand are also seen, particularly after injury to or division of nerve trunks in the arm or forearm. Perforating ulcer of the foot is a circumscribed circular ulcer with thickened edges, often nearly concealed by overhanging skin. It may be found in any part of the sole of the foot, but is most common near the first joint of the great toe. The borders of the ulcer are usually anesthetic. It is frequently seen in diabetics. By some it is associated with trophic nerve disturbance; by others it is regarded as having a specific etiology of its own. The probability, however, is that it is simply a subvariety of pressure sore.

9. Since the introduction of the Röntgen or x-rays into surgical therapeutics a new local cause of painful and intractable ulcers should be enumerated. A too prolonged or injudicious exposure of a part to this peculiar influence induces first a dermatitis, which is not always immediate, but may be tardy in appearance, and which may be followed by desquamation or exfoliation that may proceed to absolute surface destruction and sloughing. These lesions are popularly spoken of as x-ray burns. The superficial ulcers thus produced may be extensive and are nearly always excessively sensitive and painful. The very structure of the surface vessels is affected and they undergo a species of sclerosis. A strong preparation of radium has been known to produce a similar effect.

C. Constitutional.

—1. Ulcers are frequently met with in certain constitutional conditions which are characterized by tendency to local manifestation at points of least resistance. Among these may be mentioned scurvy.

2. There are ulcers of apparently distinctive trophoneurotic origin, of which that mentioned above as B, 8—perforating ulcer of the foot—may possibly be one. These accompany certain nervous disorders of central origin, prominent among which are locomotor ataxia and tabetic disease of all forms.

3. Ulcers are produced sometimes as the result of specific or selective action of certain drugs, among them mercury and phosphorus being the most prominent. These manifestations are usually perceived in the mouth, and may be regarded as infections at points of least resistance. Nevertheless, they are commonly associated with the tendency of these drugs.

4. There are many constitutional conditions in which vitality is so lowered that a special liability to ulcer—i. e., infection and production of ulcer at many points—is noted. It is well, however, to mention that the common diseases in which this tendency is most often noted are typhoid, diphtheria, diabetes, and syphilis.

With this summary of the common causes of ulcer it is again stated that ulcers may be due to direct consequence of traumatic loss of substance or to the process of ulceration—i. e., as a consequence of previous infection, or as permitted by trophoneurotic disturbance and ischemia. Ulceration is a process of molecular death, in which cells die successively and more slowly, as distinguished from gangrene, in which there is simultaneous death of large aggregations of cells, by which a slough or its equivalent is produced.

Ulcers are referred to as healthy when the process of granulation is proceeding with average rapidity; indolent, when the reverse prevails; sloughing, when there is actual visible tissue death in connection with the ulcerative process; phagedenic, when the gangrenous tendency is well marked and the process exceedingly rapid; irritable or erethistic, when the surface is exquisitely sensitive; hemorrhagic, when bleeding easily; fungous or fungoid, when the granulations have risen above the surface and are increasing at too rapid a rate. There is a peculiar form of ulcer, seen mostly upon the face, to which the name rodent ulcer (also lupus exedens) has been given. This is now known to be a slowly growing form of epithelioma, and is described in Chapter XXV.

The best examples of the indolent ulcer are seen in connection with varicose veins of the extremities; of the phagedenic ulcer, in certain cases of chancroid; of the irritable ulcer, in ulceration of the cornea, when the pain and photophobia are intense; or in fissured ulcer of the anus, where the pain and sphincter spasm are sometimes agonizing.

Ulcers are described according to their shape as regular or irregular; as fissured, when they extend more or less deeply and abruptly into the surface involved; as fistulous when they have a tubular arrangement; as rodent, when they spare nothing in their course.

The borders of ulcers are described as healthy, indurated, tumid, edematous, undermined, livid, inflamed, etc., these adjectives explaining themselves.

The surfaces of ulcers are described as healthy when they have normal color and appearance, inflamed, excavated, covered with sloughs, callous, etc. The callous ulcer is one which exhibits little change from month to month; its surface is dirty, and its secretion thin and mucopurulent. It is usually sunk considerably below the surrounding level, while its border is firm and nodular. The best examples of this form are those accompanying varicose veins.

In size or area ulcers may vary from the slightest local destruction of tissue to an area covering an entire limb or a large part of the trunk. In depth they vary within lesser limits; while an external ulcer may connect with some deep lesion by means of a tubular passage or sinus. It thus appears that the term ulcer may be applied to the result of a natural effort to repair loss of substance without introducing the element of disease, or that it may be the consequence of local infection with local tissue disaster.

The character of the material discharged from an ulcer will vary according to the category in which it belongs. The healthy, healing, or granulating surface, often spoken of as ulcer, discharges a material in gross appearance much resembling pus from an acute abscess; in consistency, color, and other appearances it is the same. Nevertheless, its origin is essentially distinct. This material represents simply the waste of reparative material, sent up to the surface for the purpose of hurrying the process. Its fluid, like that of pus, comes from the serum of the blood; its corpuscular elements, like those of pus, are leukocytes or wandering tissue cells, which have been furnished in great numbers—in fact, in excess. As it comes to the surface—or as, rather, it is rejected from the surface, being superfluous in amount—it is likely to become contaminated with bacteria by contact infection, and consequently may be seen under the microscope to contain various microörganisms. This contamination, however, has been final, accidental, and irrelevant. This material is not pus; has no infectious properties, except those which may accidentally be conveyed to it; represents no warfare of cells, only excess of supply or overdemand; and should be spoken of as pyoid or puruloid material, and never confused with pus. In amount it will vary according to the activity of the reparative endeavor, and somewhat according to the amount of irritation of the surface by dressings which may be applied. If a granulating surface is absolutely protected from possibility of contact infection, it will never contain microörganisms; while this pyoid, if allowed to remain too long, especially when infection is permitted, may decompose and become irritating, and is a material to be gently dislodged by a spray or an irrigating stream with each dressing, which dressing should be made once in twenty-four to sixty hours.

PROCESSES OF REPAIR.

An ulcer having been defined as a surface which is or ought to be granulating, it becomes necessary to define the granulation process and to show how healing is thereby achieved. Granulation tissue is a name applied to a new and temporary tissue of embryonic type, which acts as a scaffolding or temporary structure, permitting the construction of more permanent tissue. It is produced entirely by the activity of cells, which are the mononuclear and polynuclear leukocytes and the wandering cells already mentioned. They are frequently known as embryonal cells when performing this function; sometimes as formative cells. They have a distinct nucleus, which stains readily, and, having this resemblance to epithelial cells, they are often referred to as epithelioid cells—sometimes as fibroblasts, because they may later assume the dignity of connective-tissue cells. They assume a multitude of shapes. Between these cells as they are drawn toward the point at which they are most needed, perhaps by chemotactic activity, there is an intercellular substance which later becomes fibrillated. As these fibers develop the remaining cells become entangled between them, and in this way a new connective tissue is formed of cells of originally mesoblastic origin. Of such tissue the solid part of granulation tissue is built. This tissue is essentially different from the epithelium which it is expected will subsequently cover it. If a normal granulating surface is scanned with a magnifying glass of small magnifying power, it will be seen to consist of numerous minute projections, each of which is known as a granulation, consisting of the tissue above described, formed as a minute eminence around a budding capillary bloodvessel, from which a projection has arisen upon the exposed surface. This capillary bud is the result of karyokinetic activity on the part of the endothelium—namely, the hypoblastic cells of which it is essentially composed. In each of these cells, under certain circumstances, the karyokinetic threads already mentioned develop and become loosely coiled, while the chromatin in the nucleus increases in amount and the nucleolus disappears. The chromatin threads become thicker, arrange themselves equatorially around the poles of the nucleus, and gradually turn so as to point toward it, while a new membrane forms around each separate coil, and two nuclei are thus made out of one. While this is taking place within the nucleus the cell protoplasm undergoes active rotary motion, is finally segmented, and by the time the nucleus is divided is nearly ready for complete division of the cell. While nuclear division is usually bipolar, it may be multipolar; if a rearrangement of the protoplasm is delayed, the result becomes a multinuclear cell, known as a giant cell.

The consequence of this endothelial activity is new cell formation and the construction of a projection from the capillary which soon attains the dignity of its parent vessel, and, as connective-tissue cells form around it, soon becomes a granulation by itself, each granulation being marked by a capillary loop of its own. Healing by granulation or the granulation process, no matter how set up or caused, is essentially the formation of hundreds or thousands of these tiny structures, a new one being formed on top of those which precede it, while those first formed and deeper down undergo condensation and metamorphosis of tissues, by which they are converted into something higher in the tissue scale. Under ideal conditions true granulation building proceeds pari passu with epithelial reproduction around the margin of the granulating surface, so that by the time granulation tissue has completely filled the defect, no matter how caused, epithelial covering has been completely constructed and the healing process thus completed. These two processes, however, do not necessarily keep pace with each other. Should surface repair take place relatively early, we may have a depressed scar; while, on the other hand, should it not proceed rapidly enough, or, to state it in another way, should the granulating process be too rapid, we have such excess of granulations as shall rise considerably above the surrounding level, and may, under certain circumstances, become so exuberant that nutritive material cannot be formed rapidly enough, and those granulations farthest away from the centre of supply may die. Such exuberant granulation is often spoken of as fungoid, and constitutes that great bugbear in the eyes of the laity which is termed by them proud flesh. It has no further significance than that the supply has exceeded the demand and that the granulating process has been overdone. Such luxuriant granulations may be cut away with scissors or knife, may be burned away with caustic agents or the actual cautery, or may be disposed of in any other manner without harm and only with benefit; in fact, it is often necessary to suppress this exuberant tendency by caustics and pressure, in order that the desired epithelial covering may be properly formed.

Epithelium, being an epiblastic structure and capable of no other origin save from its kind, can only be supplied from those regions where it has preëxisted. Consequently, ulcers involving the external surface of the body demand a lively epithelial reproduction in order that they may have a normal covering. Epithelial activity sometimes becomes retarded, and is much slower toward the termination of the healing process than at the beginning. The epithelial covering of a healing ulcer is always marked by a delicate whitish or pinkish film, which proceeds from the periphery as well as from any little island of original epithelial structure left. It is well known that after a certain amount of this repair the process sometimes comes to a complete halt, and the various expedients for stimulating and promoting it, as sponge grafting and the different methods of skin grafting, have been devised solely to atone for such sluggishness or inability.

Ulcers of small size, which are more or less exposed to the air in healthy individuals, while also exposed to possibility of infection, nevertheless seem to escape it, owing to the defensive power of the blood serum and the active cells. Such discharge as naturally comes from them, when not excessive, undergoes evaporation until a point is reached where a dry crust or scab is formed. Under this scab granulation proceeds to a point where the pressure of the scab itself, presumably on the level of the surrounding parts, checks its activity, while at the same time epithelial reproduction goes on until it has been completed. Then the scab, being no longer of use, drops off or is detached by slight friction.

Such is granulation tissue: at first a mere trelliswork of temporary and delicate cell structure, traced in a certain amount of intercellular, homogeneous substance, into which the budding vessels project, the whole mounting, nearer and nearer to the surface, day by day, with variable rapidity, diminishing in this regard as the days go by, so that frequently the granulation process comes to an apparent halt before enough new tissue has been formed. While the superficial granulations preserve the characteristics above noted, those deeper down undergo firmer and more complete organization, and the delicate embryonic structures show the same tendency which they do in the growing embryo, by virtue of what Virchow has called metaplasia, to become converted into something higher and more dignified in the tissue scale. These cells do not specialize themselves to the extent of permitting complete repair of organs of special sense. Thus, while a wound in the cornea or retina may be completely healed, it heals by cicatricial tissue, and not by repair of the special structures involved. On the other hand, tissues of more common connective type—fibrous, bone, cartilage, etc.—are capable of regeneration; and it seems to be a part of the privilege of these new granulations to merge themselves into that kind of tissue necessary for filling the gap. Nevertheless the most common result of granulation is its metablastic conversion into fibrous tissue, which has the special characteristic of contractility without elasticity. As a result the scars contract, in consequence of which disfiguring results are sometimes the almost inevitable consequence of healing of extensive losses of substance. In certain instances it is possible by constant effort to overcome the unpleasant effect of this cicatricial contraction. For example, after extensive burn of the anterior part of the arm, the forearm will be gradually and permanently flexed upon the arm by virtue of contraction of the scar in front of the elbow unless some forcible means is practised for maintaining extension of the limb for at least a part of the time. So with many other injuries and the various mechanical or other expedients required to prevent the untoward result. Nowhere are the after-effects more disfiguring or serious than about the face, where the eyelids are drawn out of shape, the contour of the mouth altered, and where, sometimes, there are other extensive manifestations ([Figs. 10] and [11]).

Fig. 10

Cicatricial deformity following burn. (Original.)

Fig. 11

Cicatricial deformity following burn: side view of same case.

Fig. 12

Epitheliomatous degeneration of chronic ulcer, necessitating amputation. (Original.)

As a result of healing of the granulating surface there is what is known as a cicatrix or scar. This is composed of fibrous tissue, probably more or less distorted by virtue of its contractility, and of epithelial covering furnished from the margin of the original ulcer, constituting a thin, glistening membrane, applied closely to the scar tissue beneath, without intervening fat or tissue which permits of the play of the one upon the other. When this epithelial surface is abraded it is repaired with difficulty, and a raw or ulcerating scar is difficult to heal. Manifestation of perverted epithelial outgrowth is frequently provoked at these points by the action of continuous irritation. In consequence there is what is generally recognized as the transformation of a chronic ulcer, or the site of one, into an epithelioma, or possibly, by similar irritation of the connective-tissue elements, into a sarcoma. This is the so-called cancerous degeneration of previous ulcers, and is noted occasionally. The lesion is one which often requires disfiguring, or even mutilating operations in order to get rid of the malignant disease ([Fig. 12].) All the scars thus resulting are liable to undergo a fibrous and degenerative change to which is given the name cicatricial keloid. It is marked by increase in size and density, by reddening which denotes increased vascularity, and extension into surrounding previously healthy tissue. By these changes a given scar is made much more prominent and disfiguring. It cannot be prevented by any ordinary treatment, and is often the bête noir of surgeons. (See also under [Fibroma], and chapter on [Diseases of the Skin].)

The surface of a superficial scar while thus covered with epithelium shows a complete lack of all the other skin elements. No hair grows upon such a surface, because the original hair follicles are destroyed; neither is it moistened by perspiration nor anointed by sebaceous material, because the secretory glands have also disappeared. It is a surface which often needs more or less protection, especially when in exposed situations.

Treatment.

—Here, as in all other instances, the first effort of the surgeon should be to remove the cause. This may be done by local, or may require constitutional measures. If a definite local cause can be established, its removal may be a slight or may entail a more or less serious surgical operation. Aside from this disposal of the exciting agent, treatment should be divided into the general and the local. General treatment is scarcely called for when dealing with healthy ulcers; but in all those instances where the constitutional condition of the patient is below par, or where there is a general poisoning or infection underlying the ulcer itself, prompt and energetic constitutional treatment should be at once instituted. In scurvy, for instance, the diet and hygienic surroundings of the patient should be rectified immediately. In syphilis no lasting nor deep impression can be made on local manifestations without general constitutional treatment. In tuberculosis and the other surgical infections much will be accomplished by internal medication, by proper hygiene, as well as by local applications or operation. The importance of these general measures is likely to be underestimated, and many fail to realize the advantage of combining suitable internal and external therapeutic measures.

Local Treatment.

—First of all may be mentioned the insistence upon repose which induces physiological rest. The ulcer may then show a tendency to heal. This may necessitate wearing a splint or restraining apparatus, or confinement in bed, depending upon the location of the ulcer. Physiological rest will be enforced sometimes by stretching a sphincter in order to temporarily paralyze it in cases of irritable rectal ulcer, where the principal pain is produced by the reflex spasm of its fibers. Again, the eye with irritable ulcer of the cornea is sometimes kept so tightly closed by the same kind of spasm there that it may be necessary to divide the lids, or the orbicularis muscle at the angle of the lids, in order to make access to the part. This is carrying out the principle of physiological rest, because it permits proper exposure and treatment.

The healthy and healing ulcer needs no treatment except protection. Epithelial covering will probably keep pace with filling of the depression by granulations, and all that is necessary to do is to prevent external irritation. Should there be excess of discharge, the simplest absorbent dressing, with enough antiseptic material to prevent putrefaction by contamination with the bacteria of the surrounding air, should be employed. The ulcer which is becoming tardy in its repair may be stimulated by silver nitrate, zinc chloride, or other caustic applications, which act as a spur to the sluggish granulations, destroying those with which it comes in contact, but stimulating those below to do their duty more promptly.

The conventional applications to ulcers fall usually under two categories—the watery solutions and the unguents.

Fig. 13

Cicatricial deformity following specific ulcer. (Original.)

Investigations in the laboratory have led to the employment of peptonized preparations, among which are peptonized cod-liver oil and some of the partially or predigested foods, such as bovinine, etc. These appear to have the power of digesting sloughs and of causing a speedy separation or disposal of everything necessary in the endeavor to secure a healthy condition of the ulcerating surface and give most satisfactory results. When sloughs are present it is an advantage to dust over them papoid, caroid, etc., which have the power of catalytic disposition of decomposing material without reference to the action of bacteria. Under their use there seems to be a solution and disposition of these dead products. With a foul ulcer—one from which the discharge is more or less offensive, due usually to decomposition of sloughing masses, not yet separated—the method of continuous immersion in hot water, when it can be performed, is always valuable. But nothing seems to equal brewers’ yeast for this purpose. It may be applied on absorbent cotton (which should be soaked in it) and covered with oiled silk. Its curative property may be ascribed to the nuclein which it contains in a nascent state. It will, when fresh, clean off a sloughing surface better than anything I ever used.

Many ulcers are surrounded with such firm, indurated borders that it seems impossible that any active regenerative process can arise from such source. Hence, incisions have been practised for centuries. These have been made radially from the centre or have been made parallel to the margin of the ulcer, or sometimes the firm, dense tissues have been minced or chopped by a series of cross-cut stabs or incisions; as the result of which renewed activity has arisen, and an impetus given to the healing process. These methods, however, have yielded to that alluded to above. The ulcer in which granulation has come to a standstill is often treated with the sharp spoon or curette. The result of this has been to provoke again a speedy renewal of granulation efforts, and treatment by curetting is standard and often useful. Actual cauterization of the ulcer with a view to such complete destruction of its covering and border as shall lead to their separation by the sloughing process is occasionally practised. This is perhaps best performed with the actual cautery. It lacks, however, the valuable features of the operative method, to be described below. Modern methods have made it plain that it is often an absolute waste of valuable time to resort to the older expedients of stimulation, incising the edges, etc., and that one can accomplish by an operation in perhaps three weeks what ten times that length of time would fail to do by older methods. The most effective method, therefore, in dealing with old and chronic ulcers is to anesthetize the patient, to excise the entire affected area—i. e., the surface which ought to be granulating and the firm border and tissue in its neighborhood—and then to cover the surface either with skin grafts, pared off with a razor according to the Thiersch method, or with a strip of skin whose full thickness is raised, which is taken from surrounding parts by some autoplastic or heteroplastic method. This line of treatment is so far preferable to all others that, except in case of refusal of the patient to submit to it, it is the one which must hereafter commend itself. It may afford opportunity for extensive plastic operations or for the exercise of the best discretion and knowledge of experienced men; yet cases are rare in which it cannot be successfully performed. These methods of skin grafting have so far supplanted the older method of sponge grafting that the latter is now seldom practised. It may possibly have a sphere of usefulness in certain ulcerated cavities, but under all other circumstances it must take a position far below the plastic methods in practical value.

Finally, ulcers of specific type—syphilitic, tuberculous, leprous, glanderous, etc.—need methods in which the first effort should be not so much to arrange for healing as to dispose of infectious material. The knife, the scissors, the sharp spoon come first into use here, the surgeon bearing in mind that almost all this material is more or less infectious, and that inoculation of his own hands is possible as the result of carelessness. After taking away with instruments all the granulation tissue, with its surroundings, which seems to expose to danger, it is well to cauterize the part with the actual cautery, nitric acid, bromine, or zinc chloride.

The markedly hemorrhagic ulcer, whose surface bleeds on the slightest contact or disturbance, is often a cancerous ulcer, though not necessarily so. This ready bleeding is usually the effect of the fragility of the walls of the new-formed bloodvessels. In many instances it is sufficient to scrape until harder or more resisting tissue is encountered. Hemorrhage may be profuse for the moment, but it is easily controlled. Caustics may then be applied or not, according to the judgment of the surgeon.

Another method is to treat such a surface with the actual cautery. Another is to operate, even in the presence of incurable disease, in order to check a tendency to fatal hemorrhage before the disease has expended itself. In a general way, in regard to small, ulcerating, cancerous surfaces, it may be said that if they bleed excessively or are unduly irritable, it is preferable to attack them by operative measures in spite of the impossibility of effecting a cure.

There are other methods of treating ulcers, but they have mainly been abandoned for those mentioned.

CHAPTER V.
GANGRENE.

Gangrene is known also as necrosis, although this term is usually limited to gangrene of bone. It is known also as mortification, and to the older writers, especially when soft parts die and separate in sloughs, as sphacelus. Gangrene means death of tissue in visible and more or less circumscribed masses. It is distinguished from ulceration not on account of molecular disintegration, particle by particle, but because of death in toto and synchronously of a large, perhaps innumerable, number of cells. Gangrene is described as due to causes which may be:

A. Traumatic

, including the so-called thermal causes as essentially mechanical injuries. Under this head are included cases where injury is the primary cause, whether this injury is the crushing of a limb, the separation or occlusion of its main bloodvessels, the division of its main nerves, or the crushing or pulpefying of its entire structure by machinery or accident; also those so-called thermal cases which are due to intense heat or intense cold. To these might be added the chemical causes, comprising injuries by powerful caustics, alkalies, or acids, which are known to cause speedy death of every living tissue with which they come in contact.

Gangrene from frostbite is often of the moist type. There is scarcely a limit to its extent, either in area or depth. It is due primarily to thrombosis, which is followed by a purplish color of the skin, by loss of local warmth, and numbness. Naturally it involves the ears, nose, fingers, and toes. But after alcoholism and exposure one or more entire limbs may be involved. With moist gangrene there is danger of [septic infection] (q. v.). After formation of a line of demarcation the line of amputation may be made to follow it closely, but the best results are obtained by higher division, at points of election, where tissues are less sensitive and less infiltrated.

B. Local Causes.

—These are largely connected with ischemia. Gangrene from edema—itself the result of passive hyperemia and exudation—is not infrequent, the most common expression of this condition being seen perhaps in the external genitals of the male. Embolism due to valvular heart disease, thrombosis due usually to a preceding phlebitis, but possibly to marasmic origin, especially met with after confinement, with disturbance in the uterine sinuses, shutting off the circulation by endarteritis, which thus assumes the form obliterans, are some of the local causes which concern the bloodvessels alone. In fact, the majority of cases of spontaneous gangrene are probably due to changes in the vessels, endarteritis being the cause of a condition known as atheroma of vessels, in which fungoid outgrowths, or, rather, ingrowths into the vessel lumen, are common. Any one of these, if detached, may serve as an embolus. The degenerative excavations in the thickened walls of the bloodvessels, which discharge more or less cholesterin and other debris, and which have been known as atheromatous abscesses (misnomer), are frequently the precursors of the disease under consideration. As the result of these changes alone, without reference to formation of emboli, vessels may become completely occluded, especially when slightly injured.[2]

[2] Intermittent claudication, when recognized, may be regarded as a precursor of that arteriosclerosis which may proceed to gangrene. The term implies temporary anemia of one or more of the extremities, with numbness, burning, or prickling sensations in the skin, occasional cramps in the muscles, with loss of power, tenderness of the nerve trunks, weakening or loss of pulse in the affected part. When these symptoms occur in the feet they are not infrequently followed by terminal gangrene or other evidences of angioneurotic necrosis, including even those forms known as erythromelalgia and Raynaud’s disease. Its treatment, of course, is relaxation of vasomotor spasm, best accomplished by the use of the nitrites, among which nitroglycerin is perhaps most valuable.

Extravasation of blood is another cause connected with the bloodvessels, this coming usually from traumatic rupture, possibly from idiopathic causes. At any rate, the tension in the part may threaten its life because of the pressure which overcomes the circulation of blood. Ligation of the main trunk of an artery is sometimes followed by gangrene, no matter how carefully done, collateral circulation being insufficient to sustain the nourishment of the part. In certain fractures, simple as well as compound, the blood supply of a part is rudely broken off by injury to a bloodvessel in such a way as to cause local or general death, either of a bone or of the entire limb. Flaps made for plastic purposes, arranged without sufficient regard to their proper blood supply, or so dressed after operation as to sustain undue pressure, are often so shut off from the heart as to die for want of blood. Finally, gangrene may be the result of pressure either from splints, bandages, etc., or from tumors increasing in size, or possibly, as in certain pressure sores, etc., from the mere weight of the body. Here, too, chemical agents must be mentioned, referring now to the peculiar action of certain foods or drugs, particularly ergot. Thus antiseptic solutions, particularly carbolic acid, may be made strong enough to destroy the vitality of certain tissues. Carbolic gangrene (Warren) is a possibility not to be forgotten.

Extravasation of urine, unless promptly recognized and appropriately treated, or especially as occurring when the urine is peculiarly toxic (ammoniacal) and the patient’s vitality reduced, as in confirmed alcoholics, is almost sure to produce gangrene which may easily terminate fatally.

Fig. 14

Raynaud’s disease: digiti mortui. (Original.)

Fig. 15

Raynaud’s disease: perforating ulcer of foot. (Original.)

C. Constitutional Causes.

—Among these are to be mentioned particularly that symptom-complex ordinarily known as diabetes or glycosuria. This means a depraved condition of the system in which gangrene is threatened or permitted under circumstances which otherwise would have little or no disastrous effect. Thus diabetic gangrene has come to be one of the recognized manifestations of the general disease. That the trophic nerves have a more or less pronounced effect in determining gangrene in certain cases seems to be now quite well established. It is well known how quickly bed-sores form after injuries to the spine, while in certain nervous affections a minimum of friction of the skin may determine its death, particularly about the labia or scrotum. It is said that the insane, when made to sleep by chloral, may develop decubitus from pressure in a single night. There is also a well-known form of symmetrical gangrene, known sometimes as Raynaud’s disease, which is characterized by symmetry of lesions and absence of definite pathological changes ([Figs. 14] and [15]). The so-called digiti mortui, or dead fingers, and erythromelalgia are examples of this character. A condition almost leading up to gangrene, but perhaps not absolutely terminating in such a way, has been known as local asphyxia, which seems to be a condition of arterial spasm with venous congestion and slight edema. While the aged will often recover from a legitimate surgical operation without disturbance, it is, nevertheless, true that senile gangrene commencing in the toes has for its cause some very trifling injury or lesion, such, e. g., as paring of a corn, or the like. This shows a weakened local and general resistance, as well as the wisdom of redoubling aseptic precautions in operations upon such patients.

As constitutional causes also should be included the deleterious effects of certain drugs, particularly ergot, mercury, and phosphorus.

D. Infectious Causes.

—In the instances already mentioned reference to the infectious microörganisms has been avoided. There remain to be considered types of gangrene due to the activity of certain microörganisms—hospital gangrene, phlegmonous erysipelas, malignant edema, gangrenous emphysema, noma, ainhum, etc.

Gangrene as the result of infectious processes is seen in phlegmonous erysipelas, where death of tissue seems to be due to the combined influence of the invading organisms and of mechanical agencies—i. e., tension produced by stasis and exudation, with such stretching of tissues or overcrowding with inflammatory products as to virtually strangle them, in consequence of all of which they die. Gangrene of an entire hand may thus result, or, more commonly, the gangrene is limited in extent to the more superficial parts, so that sloughs separate. A specific form of gangrenous inflammation known as malignant edema, due to a peculiar anaërobic bacillus, will be treated of separately under a distinct heading. Quite like it in several respects is the gangrenous emphysema of certain writers, known also as the fulminating form, or, as the French call it, the “gangrène foudroyante.” More or less emphysematous condition may accompany malignant edema; yet that we do have gaseous forms of gangrene without the specific bacillus of malignant edema is established. At least sixteen cases of so-called gaseous gangrene due to infection by the bacillus aërogenes capsulatus are on record, of which twelve were fatal. Most of them followed surgical injuries—e. g., compound fracture.

Fig. 16

Noma. (Original.)

Hospital gangrene, so called, has been in years past the terror of military surgeons and camp hospitals. As a type it has almost completely disappeared from observation, and, in its old manifestations at least, is now practically never seen.

Noma, known also as gangrenous stomatitis, cancrum oris, and gangræna oris, is a term applied to a form of tissue necrosis affecting the cheeks or parts about the face of young children, occurring frequently as a complication of the exanthemata. A similar condition occasionally involves the external genitals. From the fact that it seldom passes across the middle line, it has been regarded by some as of neurotic origin. Naturally bacteria are always found in the decomposing tissues; but whether there as cause or as result is not yet established. The probability is, however, that we have to deal with a specific form of infection. The loss of substance is usually so great as to determine complete perforation of the cheek, so that the jaw bones may be laid bare. The gums and alveolar processes also frequently share in the process, and the teeth occasionally drop out. Death of tissue is rapid, and septic infection may accompany it to such an extent as to cause the death of the patient in a few days. While most vigorous measures are necessary for combating it, the patients are often so reduced as to preclude the possibility of doing much, and death is the termination of noma. Free incision, even complete excision, is called for, perhaps with combined resort to the actual cautery or such remedies as bromine (strong or diluted). Antistreptococcic serum has also been used with success. Obviously it must be used early if success is expected. Should patients recover, there is extensive deformity as the result of cicatricial contraction.

Along the coast of Africa and in the West Indies there occurs among the negroes a peculiar gangrenous affection of the toes known as ainhum. This may assume either the moist or the dry type of gangrene, but the result is gradual separation of the part, usually by the dry process, as if it had been strangulated by a ligature. The disease is slow and may extend over ten years. The cause is unknown.

Finally, gangrene is the termination of the infectious process in several other zymotic diseases, among the best illustrations being that afforded by diphtheria. The formation of diphtheritic ulcers in the mouth and the vulva, about the eyes and elsewhere, as the result of separation of sloughs, is too frequent to pass unnoticed, yet at the same time does not essentially differ from the separation of sloughs due to any other specific cause. All these acute zymotic diseases, therefore, need to be regarded as among the possible causes of gangrene by infection of tissues.

The symmetrical gangrene, often paroxysmal, affecting the fingers and toes, described by Raynaud and often called by his name, is due to vasomotor spasm, and is accompanied by neuralgia and sensory disturbances, with coldness of the part and discoloration suggestive of impending gangrene. (See above.)

Billroth and others have also described a spontaneous or angioneurotic gangrene of the extremities, occurring during youth, in abrupt distinction to senile gangrene, whose course is tedious and painful, which will usually necessitate amputation. The cause of this condition has been found to be a well-marked arteriosclerosis and thrombosis, both in the arteries and veins. This form of gangrene occurs most often in the frigid zone—e. g., in Northern Russia.

There are also forms of visceral gangrene, traumatic and non-traumatic, which often constitute fatal maladies. The latter are mainly due to thrombotic or embolic lesions, for example, the gangrene of the mesentery, already alluded to when discussing [thrombosis] (q. v.), clinically described under Surgical Diseases of the Mesentery.

Gross Appearances.

—In a general way tissue death, known as gangrene, assumes two opposite types—the moist and the dry. In moist gangrene, aside from those appearances which indicate commencing putrefaction of tissues, and the loss of heat due to stoppage of the blood supply, one of the most characteristic features is the formation of a so-called line of demarcation, i. e., a line which separates the dead from the living tissues. While this is usually plainly indicated by a red line which abruptly separates the discolored, usually dark, dead portion from the bright red, congested appearance of the living tissues, it is noted that this area of redness shades out into a more and more natural appearance as we pass upward, while below the line is seen a surface, usually covered with blisters, from which exudes a foul-smelling, altered serum, while the gangrenous portion assumes a dark, finally an almost black appearance, retaining only the crude outlines of its original shape. Along with this the objective evidences of putrefaction are unmistakable, appearances and odor being characteristic. With all there are more or less constitutional disturbances, and a recognizable, often a profound, condition of septic infection, due to the fact that along the line of demarcation absorbents are still active and that the poisonous products of putrefaction are being absorbed into the general system. Consequently collapse, profuse perspiration, septic diarrhea, etc., are noted. In gangrene from frostbite the process is slower than in the traumatic forms. In gangrene from extravasation of urine the separation of sloughs is extensive, and sloughing of the scrotum with exposure of the testicles is a frequent result. In decubitus, or bed-sore, the process is still more slow, but always of the moist type. After a variable length of time there is separation of slough and a resulting large, often foul, ulcer.

Dry or senile gangrene presents a very distinct contrast to the moist type. It occurs generally in patients over fifty, often as the result of causes which are slow of action. As a result of the shrinking and corrugation of the tissues, with the dryness of the same by evaporation, there is a peculiar appearance known as mummification, the foot, for instance—the feet are usually first involved—resembling the foot of a person who has been embalmed, except that it is discolored. It is possible sometimes to have a combination of moist and senile gangrene, especially when there has been infection by which putrefaction is permitted. When from the outset putrefactive processes are prevented, the gangrene of this type is almost invariably dry. In practically all of the cases of this character there will be found evidences of vascular disease, usually in the femoral artery and its branches. Gangrene of the foot alone is most commonly due to endarteritis, while gangrene of the foot and leg together are usually due to embolism or thrombosis.

While disease of the vessel walls is usually of the type either of endarteritis or arterial sclerosis, peculiar to the closing years of life, and commonly affecting the lower extremities, gangrene due to embolism of arteries or thrombosis, or both, may occur in the young, and in the upper extremities as well, in the latter case the emboli being detached from the heart, while thrombosis may be caused by a tight splint or bandage, or even the use of crutches. I have repeatedly amputated the arm as well as the leg for gangrene of this type.

Signs and Symptoms.

—The appearance and the odor of a part will indicate impending or actual traumatic gangrene. The pallor, the coldness, the dryness of senile gangrene are also characteristic. In the latter form constitutional symptoms are not indicative nor essentially of septic type. As soon, however, as a process of spontaneous separation begins putrefaction is inevitable and sepsis unavoidable. In moist gangrene there is seldom acute pain. This is one of the predominating subjective features of the senile form. Hemorrhages occur, sometimes terminating fatally, in the moist forms when large vessels are eroded. This is particularly true of the phagedenic or hospital form. A recognition of their possibility may enable us to avoid sudden death from this source.

Treatment.

—Threatening gangrene should be attacked and the cause removed. Threatening bed-sores may be avoided by equalizing surface pressure, which can be done with the water-bed; by protecting the skin or by stimulating and toughening it with alcoholic and astringent lotions; by frequent changes of position; by attention to the heart, which should be stimulated to a point that may make it capable of forcing or distributing blood equally over the entire body. So, too, with limbs which are enveloped in dressings or splints; it is well to leave exposed the tips of the toes or fingers in order that discoloration of the same may be recognized and the threatening disasters averted. Local gangrene as the result of pressure by tumors, aneurysms, etc., cannot always be averted.

For gangrene there is but one relief, the removal of the dead and dying tissue. The method and location of the operation must be determined by the general character of the cause. For a case of acute traumatic gangrene amputation at the nearest point of election above the injury will often suffice. In case of gangrene from frostbite the tissues in the neighborhood of the line of demarcation are so affected or their vitality so compromised that to separate the tissues along the lines at which nature is endeavoring to remove them is not enough, and to go an inch or so above this line is to operate in tissues which bleed readily and heal badly. Consequently it is often advisable to select a point at some distance above. It is especially in diabetic and senile gangrene that surgeons have laid down the rule that if amputation is done at all it must be high. For gangrene of the toe, as the result of disease of the vessels, it is best to amputate above the ankle; whereas if any greater portion of the foot is threatened, amputation should take place above the knee. The tibial arteries have been found so brittle as to snap under a ligature, and the femorals so disorganized as to require handling and ligating with the greatest caution. These high amputations are therefore necessitated by the condition of the vessel walls. While amputation for traumatic and acute cases is, in the majority of instances, if not too long delayed, successful in saving life, in the senile and particularly in the diabetic forms it is, in the majority of cases, a disappointment.

PART II.
SURGICAL DISEASES.

CHAPTER VI.
AUTO-INFECTION, ESPECIALLY IN SURGICAL PATIENTS.

One of the greatest advances made in pathology has been the establishment of the fact that a great many of the morbid conditions from which the human race suffer are those due to causes arising entirely from within their own systems and in consequence of deficiencies of elimination or of perverted physiological processes which, in large degree, are themselves the result of errors and indiscretions in diet, in manner of life, in habits, etc. That these general facts have been recognized for centuries is perhaps a credit to the powers of observation of practitioners of past generations. Exact knowledge, however, has come only with exact laboratory methods of research and most painstaking study of the secretions and excretions, both under normal and morbid conditions. The subject of auto-intoxication has been too commonly relegated to the domain of internal medicine, and has been supposed to be one in which the surgeon need take only passing interest.

The alkaloids are by no means the only poisonous products which the human body may produce and retain. That most important excrementitious material of all—i. e., carbon dioxide—could not be retained in the organism for more than a few moments without death as the inevitable consequence. The various soluble ferments elaborated by certain glands may exert deleterious influence, both local and general; and in the saliva are also found products which are not ferments. The biliary acids also, if they do not find free escape, may produce fatal poisoning. So also leucin, tyrosin, and all the excrementitious products which arise from insufficient liver activity, are capable of producing forms of intoxication—such, for example, as eclampsia, etc. The character of the solvent has much to do with toxicity. Thus aqueous extract of putrid matter is more poisonous than that of fecal matter, while alcoholic extract of fecal material is more toxic than that of putrid. All the alkaloids produced within the body are not poisonous. Some are found in the normal tissues, and they are, perhaps, only one of the results of the disassimilation of animal cells. Nor are all these poisons of bacterial origin, although many are formed only in the presence of microbes.

From these constantly menacing sources of intoxication man escapes by virtue of his intestinal, cutaneous, pulmonary, and renal emunctories. For instance, the usefulness of the perspiration is shown by the odor which it assumes under the influence of certain disorders. Among hypochondriacs and the inactive fatty acids are eliminated by the skin. Hence the odors of hospital wards, asylums, prisons, etc. So, too, in the case of many who suffer from deep-seated, indolent ulcers, the odor of the skin is suggestive of the presence of pus. During twenty-four hours there is eliminated from the lungs 1100 grams of carbon dioxide, water, etc., which sometimes contain ammonia and various volatile fatty acids; all of which will explain fetor of breath when it is the result of incomplete nutrition and destruction of food. Of the organs of elimination, the most important is the kidney, which does not reabsorb a part of its own products, as does the intestine. The kidneys eliminate fluids and solids, not gases. The most important of the toxic principles contained in the urine are:

1. Urea, which plays an important and useful role in the economy, since it possesses the property of forcing the renal barrier and removing along with itself the water in which it is dissolved and other toxic matters. Urea is toxic, but only in the sense that any other substance, even water, may be—i. e., it is toxic only in large doses, less than sugar, and no more than the most inoffensive salts. This is contrary to generally received views, but is established by the researches of Bouchard.

2. A narcotic substance, and

3. A sialagogue substance, whose composition is unknown;

4, 5. Two substances having the property of causing convulsions, one having the power of contracting the pupils. The composition of both is unknown.

6. A substance which produces heat by diminishing heat production—possibly a coloring matter. That coloring matters are absorbed by charcoal and that urine thus decolorized is rendered less toxic are no proof that the coloring matters themselves are responsible for this toxic action. There is no doubt that numerous alkaloidal bodies possessing a high molecular weight are precipitated by means of carbon or charcoal, and to these bodies may be attributed a portion of that toxic action previously considered as due to coloring matters.

7. Potassium salts, which are really convulsing agencies, are the most toxic perhaps of any of the poisons contained in the urine. Chloride of potassium, for instance, is toxic at 18 Gm. for every kilo of animal.

Salivation and myosis, as well as diarrhea, are often noticed in so-called uremia. In that form known as hepatic uremia, when the liver no longer forms urea, the kidneys scarcely act. In other words, if urea is no longer present in the body, the kidneys are deprived of their principal stimulation to physiological activity. Consequently urea, for so long a time the bugbear of physicians, is shown to be most dangerous when absent. When urea is deficient, blood serum or water in which the other toxic substances are dissolved should be withdrawn. This is best done by venesection, whose value in so-called uremia experience amply corroborates. When kidney activity ceases, intoxication is likely to be produced by potassium salts. Ptomains, amido bases, etc., are proved to be present in normal urine and are known to produce toxic effect. These ptomains increase enormously in pathological urines, and to this increase, rather than to that of potassium and coloring matters (which remain fairly constant), may be attributed the higher toxicity of pathological urine. In certain cases, however, as in that of jaundice, the toxicity of the urine is partly due to decomposition of tissue cells, whereby potassium salts and organic decomposition products are liberated and excreted in the urine. The toxicity of the urine also increases with the increase of indican, which is indirectly a product of intestinal fermentation.

The osmotic pressure of the blood has much to do with the general subject of auto-intoxication, since it surrounds and permeates all the organs of the body, which are necessarily in equilibrium with it. Their individual cells functionate, then, in accordance with it, and variations in such pressure must affect their activities. It is a special function of the kidneys to eliminate enough of the accumulated metabolic products in the blood to keep this osmotic pressure at its normal. Should investigation or symptoms of disease show a wide divergence from this standard, the inference is plain, i. e., that there is renal insufficiency from impairment.

This test may be made with a small amount of blood by cryoscopy (determination of freezing point). So, too, a determination of electrical conductivity may, in a similar way and for a similar purpose, be made of clinical value. Unfortunately, these investigations are not exactly simple in character, and are not available outside of well-equipped hospitals.

Correct performance of hepatic function is also necessary that surgical cases may progress without disturbance. Bile escapes direct absorption by the blood, but not all contact with it, since in the intestine it is in contact with mesenteric capillaries, but must pass again through the liver, which takes it up again and pours it once more into the intestine.

Bile in the blood is always dangerous, although its toxicity is much smaller than has been supposed. Of all the bile thrown out into the duodenum, we are only able to account for about one-half. Its coloring matter and biliary salts are metamorphosed. Yet in certain morbid conditions bile, as such, may be reabsorbed in the liver along the margin of the hepatic cells. In these cases, if the kidneys remain permeable, auto-intoxication is simply threatened; if they have ceased to be permeable, actual auto-intoxication is the result.

Putrefaction of intestinal contents affords another source of auto-intoxication. This comes both from imperfect metamorphosis of food and from bacterial infection. Here the conditions are most favorable. Nitrogenous substances become peptonized, and peptones form the best culture media for microbes. Water is present in sufficient quantities, and a constant temperature of 37° C. is maintained. The digestive tube is always open, and invaded at frequent intervals. By such mechanism are formed those products whose effects are revealed in the so-called putrid fever of Gaspard. Brieger has shown that alkaloids are developed during the act of peptonization. Fecal matter contains also excretin, whose toxicity has been amply proved, and several other alkaloidal substances, soluble in various media, varying in toxicity. The potassium and ammonium salts contribute largely to the toxicity of feces; bile also, but in lesser degree. It has been shown that the aqueous extract of putrid matter is very toxic, while that of fecal matter is otherwise.

The most serious features of the conditions grouped under the heading of Bright’s disease are their so-called uremic features. These happen at the period when retention of toxic products is peculiarly harmful. As long as the urine is ample in amount and density—i. e., containing enough toxic materials in solution—there is no danger of intoxication. But when it no longer eliminates in twenty-four hours what it should, then we see the chronic and paroxysmal nervous accidents, the edemas, fluctuations of temperature, etc. Oliguria with urine of increasing density and general edema of the tissues may be noticed, although the other secretions continue natural and the tongue moist. As long as the normal amount of solids is eliminated, this form of “uremia” may be due to mere accumulation of water and may not be serious. Ordinarily, uremic patients are those whose urine has lost its toxicity. Usually on the day in which so-called uremic accidents happen the urine quite ceases to be toxic and is scarcely more so than distilled water. Urea alone is not to be held guilty for this condition. In order to kill a man with urea it would require the quantity which he makes in sixteen days. Nevertheless, it may become harmful after undergoing transformation into ammonium carbonate or other substances.

Among the most poisonous substances in the urine are the extractive and coloring materials. Normal urine loses one-half of its toxicity by decoloration; bile acts in the same way. Urea alone represents about one-eighth of the total toxicity of urine. Ammonia is toxic, but present in small amounts. The coloring matters of the urine cause two-thirds of its toxicity, the remainder of which is to be ascribed to its mineral salts, which it contains in the following proportion: A liter of urine ordinarily contains 44 Gm. of solid matter, of which 32 are organic, 12 mineral. Of the latter, potassium salts constitute 3 Gm., sodium salts 7.5 Gm., and other earthy salts constitute the remainder.

In these conditions physicians have relied largely upon purgatives, hoping thereby to remove urea from the blood. But intestinal elimination has no elective affinity for it, and removes it only in its normal proportion with the balance of the blood. Purgatives, however, help, first, by dehydrating the tissues—i. e., removing water with toxic material in solution. But they should be followed by restoring to the tissues pure water. By bleeding more extractives are removed than by any other channel, except by the kidneys. A bleeding of 32 Gm. removes from the body as much toxic matter as would 280 Gm. of a liquid diarrhea or 100 liters of perspiration. This much may be removed by two leeches. It is especially in the subacute nephritis of scarlatina, etc., that bleeding finds its greatest indication. If the kidneys are chronically diseased, the utility of bleeding is doubtful. Between the arterial capillaries of the bowels, however, and the liver is found a mass of blood accumulated in the portal vessels. This may be regarded as a reserve which can be thrown into the general circulation when needed, in order that thereby arterial tension may be augmented and the function of the kidney increased. Cold injections into the bowels will often accomplish this, and serious anuria frequently disappears after their use. It is advisable, also, to make use of urea by subcutaneous administration, as the most powerful diuretic known, surface friction, caffeine, digitalis, etc., being far behind it in efficiency. In the form of intoxication noted in the eclampsia of puerperal patients inhalations of chloroform are valuable. Potassium salts should, under these circumstances, never be employed. An exposure of urine in compressed air will diminish its toxicity, on account of contact with the oxygen; the most toxic bacteria are those which grow without oxygen. Consequently patients inhaling this gas may overcome this kind of auto-intoxication.

The value of an active liver is not appreciated by most surgeons to the full extent. The blood of the portal vein is so much more toxic than that of the hepatic vein that it is evident that the function of the liver is to purify and remove the toxic material from the blood that comes from the intestines. This has been called by Flint and others the depurative action of the liver. The activity of the liver also may be proved by grinding up a freshly removed liver with alkaloids, whereby the latter are chemically changed.

That the facts above stated, or others related thereto, have not been lost sight of by surgeons is shown by such expressions as septic enteritis, enterosepsis, etc., which are used by various writers. In previous publications the writer has made a separate topic of so-called intestinal toxemia, which he has preferred to introduce here as one of the many possible auto-intoxications. It is a condition not always permitting of exact definition, nor, still less, can the exact toxic agency be indicated in a given case. Nevertheless, it has been made plain that there is perhaps no condition which so predisposes to sapremia, septicemia, or even pyemia as this vague condition of intestinal toxemia, which, notwithstanding, is so often present. Many surgical patients present forms of blood poisoning in which the poison has not proceeded from the wound, for which the surgeon is not responsible, except that he may have neglected to avail himself of certain precautions.

The auto-intoxications, then, which have peculiar interest for the surgeon may be conveniently classified as follows:

1. Those caused by failure in the function of particular organs; e. g., myxedema, cretinism, and cachexia strumipriva from thyroidal failure; pancreatic diabetes, where the islands of Langerhans are invaded ([interstitial pancreatitis], q. v.); Addison’s disease from adrenal failure (this being at present the prevailing belief).

2. Those caused by general disturbance of metabolism, where its incomplete or abnormal products reach the general circulation, e. g., oxaluria, gout, diabetes. (See [Diabetic Gangrene].)

3. Those caused by retention in particular organs or tissues of disturbed metabolic products, e. g., the toxemias following serious burns and many septic conditions.

4. Those due to excessive formation of more or less normal products, e. g.:

(a) Hydrothionemia, i. e., the presence of hydrogen sulphide in the blood. This results from one form of gastro-intestinal putrefaction and causes violent symptoms with evidences of hydrogen sulphide poisoning. It is seen in some cases of gastric dilatation, especially those caused by [pyloric obstruction] (q. v.).

(b) Acetonuria and Acetonemia.—The former sometimes follows chloroform anesthesia, and occurs especially in diabetes (particularly after removal of the pancreas in experimental animals). Acetone per se is nearly or quite harmless, but its congeners, diacetic and beta-oxybutyric acids, are very toxic. The danger in so-called acetonuria is from acid intoxication by these acids, which has been described as “excessive acidosis,” and its co-existence with glycosuria makes diabetes certain, while prognosis is grave in proportion to its presence. Prominent among the symptoms produced by it are delirium and coma.

When either or all of these three substances are present in the blood its alkalinity is reduced and its ability to absorb carbon dioxide impaired; hence, acetonemia is evidenced by carbon dioxide poisoning. To the brain symptoms above noted is added a peculiar odor in the breath—sweetish or ethereal. This has been noted in pyemia. This condition may set in after various operations, but whether due to disease, the traumatism itself, or to chloroform may not always be determined.[3]

[3] See paper by Brewer, Annals of Surgery, 1902, vol. xxxvi, No. 4, p. 481.

(c) Cystinuria.

(d) Coma of cancerous cachexia (coma carcinomatosum).

(e) Exophthalmic goitre, from excess of thyroidal activity (thyroidism).

Besides the above there is auto-intoxication proceeding especially from the gastro-intestinal and hepatic systems. Of the former, the best surgical examples are seen in the tetany which occasionally takes its rise from a dilated stomach, and which may be cured by a pyloroplasty or a gastro-enterostomy; in the nephritis which follows stercoremia of intestinal obstruction; and in oxaluria, with its painful, serious, and often deforming or crippling joint affections. Of the latter we have examples in the cholemia of acute atrophy or of biliary obstruction, and in the uremia of hepatic origin which occasionally terminates a surgical case.

In addition to the above there should also be mentioned the auto-intoxications of pregnancy, with the consequent salivation, peripheral neuritis, pigmentations of the skin, icterus, and pruritus, which are mainly attributed to perverted action of the liver or kidneys.

The practice of preparing patients for operation by a course of purgatives, emetics, etc., is based upon the recognition of certain principles. The general symptoms included under the name enterosepsis, stercoremia, copremia, are due to the activity of the colon bacillus, which seems to be made more virulent by certain conditions of diet or retained fecal excretions, and to such an extent that it wanders widely from its normal habitat and may be found in distant parts of the body. Enterosepsis may be mistaken for surgical fever, and is to be distinguished from it, perhaps, only by the study of the excretions of a case and establishing the fact that they are free, and that consequently pyrexia, etc., cannot be due to diminished elimination. Aside from the migrations of the colon bacillus, it is also possible for auto-intoxication to occur. Thus that which is stercoremia one day may later become a genuine septicemia, vital resistance being so lowered as to permit of local infection. The various conditions are so often merged that it is difficult to separate and identify them. Nevertheless, enterosepsis differs from sapremia in that in the one instance the putrefying material is contained within a normal cavity, whereas in sapremia it is contained within an abnormal cavity, in either case corresponding to a septic suppository, varying, however, in the place of insertion, also in the nature of the surrounding tissues, which in the latter case are more capable of absorption and of becoming infected than in the former.

A determination of indol and indican is often of the greatest value, both in determining the extent of infection and the presence of pus. Indol is set free under the following circumstances: (a) Suppuration in a closed cavity. (b) Continued suppuration in a cavity with an outlet. (c) Ulceration or necrosis of tissue. The degree of indicanuria will depend on the length of time pus has been present, the possibility of absorption from the tissues surrounding it, and its degree. When pus is fully formed in a serous sac the indican reaction becomes intense according to the length of time pus has been present. This is particularly true in the empyemas of childhood. In continued suppuration with a free outlet the production of indol will be great; but the amount finally eliminated will depend upon the character of the surrounding tissue. When solid tissue, like bone, becomes affected, the elimination of indol is intense. Rapid biogenic degeneration of tissue causes an increased amount of indol to be deposited in the liver, and it is possible at postmortem, by simple extraction with absolute alcohol, to take from the liver this excess deposit in the shape of its oxidation product, indigo blue. Lardaceous degeneration is characterized by marked and persistent elimination of indol, which seems to be a product of tyrosin. It occurs frequently in the liver, in which indol is notably deposited. Its primary factor is deposited by the blood, in which latter indol circulates and is oxidized. Lardaceous material gives a red or blue color with oxidizing agents, which latter yield with indol an indigo red or blue.

The practical outcome of such a chapter as this is, then, to insist as strongly as possible on the preparation of patients, whenever this is feasible, for an ordeal which comprises the combined effect of anesthesia and consequent disturbance of secretion and elimination, with loss of blood and of strength, and subsequent confinement in bed, with, moreover, all that this entails in further impairment of activities of important organs. It is not always possible, practically rarely so in emergency cases, to adopt these precautions; in which cases they must be atoned for, as far as possible, by extra attention in the same directions after the emergency is passed or has been met. In the former case, however, the functions of the skin, the kidneys, and the abdominal viscera should be regulated, the first by hot-air baths; the second by this same measure in conjunction with copious draughts of pure water, the correction of hyperacidity of the urine, and the administration of whatever drugs may be of benefit as diuretics, etc.; and the third by a course, perhaps covering several days, of gentle or active purgation, by which the alimentary canal will be entirely emptied of all that may serve to act as a source of poisoning. In addition to this, in certain cases careful massage will dislodge from the muscles and other tissues material which they ought not to retain, and which will be washed away, as it were, by the extra amount of fluid which this preparation, necessitates. Again, the activity of the heart should be stimulated, perhaps by digitalis, but preferably by that best of all tonics, strychnine, which is to be administered hypodermically in average doses of a thirtieth or twenty-fifth of a grain, morning and night. When these precautions are taken, patients will successfully pass through trying ordeals without anything which may give rise to alarm. When they are not possible, the risk of operating, even in a small way, is materially enhanced. So, too, after operations when these precautions have not been taken, it is necessary to give careful attention to atoning for their lack by such active purgation as a now reduced patient may bear—by hot-air baths, if feasible, and by the administration of such intestinal antiseptics as charcoal, naphthalin, corrosive sublimate, bismuth salicylate, salol, etc., for the purpose of reducing to the lowest possible minimum the opportunity for formation of poisons which will disturb the proper repair of injury.

CHAPTER VII.
THE SURGICAL FEVERS AND SEPTIC INFECTIONS.

SURGICAL FEVER, KNOWN ALSO AS TRAUMATIC FEVER, OR ASEPTIC WOUND FEVER.

Formerly the surgical fevers were all grouped together, and a certain amount of febrile disturbance was looked for after any injury. But with the introduction of antiseptic methods and the healing of wounds by primary union, with absence of all septic phenomena, and the use of the clinical thermometer, it is noted that there is a certain rise of temperature more or less quickly after an operation or reception of a wound, with fever of mild grade, persisting for several hours or two or three days, and with other accompaniments. This phenomenon has been carefully studied, and so separated from the septic fevers as to deserve a distinct recognition under the names above given, of which the most common in this country is surgical fever.

As long as this fever is free from indications of septic character it is without significance and needs only symptomatic treatment. It begins usually within the first twenty-four or thirty-six hours, after which the temperature may rise, progressively or with a morning remission, to a height of 102° or possibly 103°. In children we are more likely to get extremes in this regard than in healthy adults. It will be followed by some disturbance of alimentary function, glazing or drying of the tongue, deficiency in urinary secretion, and subside generally spontaneously—invariably so if cathartics, diuretics, cool sponge baths, etc., are used. It is usually due to the retention of blood clot, ligatures, etc., or tissues which have been ligated and whose stumps remain; in all instances there is some foreign material to be removed. This means unusual phagocytic activity, perhaps temporary leukocytosis, with active metamorphosis of clot and other material, of all of which the elevated temperature is an accompaniment and expression. It is not unlikely that the antiseptic materials used may sometimes occasion this pyrexia.

Iodoform and carbolic acid are among the drugs in common use which are known to be irritating and capable of producing toxic symptoms. Often after the use of the latter the urine will be discolored and will furnish the clue to the fever. In young children particularly, and not infrequently in adults, mental disturbance, even active delirium, may characterize the case. This is not always to be explained by cerebral anemia due to loss of blood during the operation or accident, but is probably due to drug toxemia or to intoxication from materials furnished by the altered tissues.

Surgical fever of strict type may merge into a more or less continuous fever as the result of intestinal toxemia permitted by failure to evacuate the bowels, and this intestinal toxemia may be a predisposing cause of genuine septic infection. Consequently a surgical fever which does not disappear within two days is to be viewed with suspicion, especially if it does not subside after the administration of cathartics.

Some surgical fevers are accompanied by eruptions, a number of which may be due to drugs and some to intrinsic poisons. Thus carbolic acid and iodoform give rise occasionally to erythematous eruptions, and the concomitant administration of drugs like potassium iodide, quinine, antipyrine, and copaiba may produce urticarial or other manifestations. Again, it is known that certain toxins—produced, e. g., by the bacillus pyocyaneus—are capable of causing dilatation of the superficial vessels and various flushes or eruptions. To one of these, which dilates the capillaries, Bouchard has given the name of ectasine. Consequently it by no means follows that every eruption or rash following operations or injuries is of a specific character. On the other hand it seems to be established by numerous observers—among whom Paget is perhaps the most prominent—that surgical patients, particularly the young, are particularly liable to infection by scarlatina; and in the experience of Thomas Smith, of forty-three children whom he cut for stone, ten had scarlet fever. Therefore, in spite of the fact that a certain number of cases of eruption may have been mistaken for scarlet fever, it is undoubtedly true that in surgical and puerperal cases patients are more than usually liable to this invasion. The use of antitoxins or serums is also occasionally followed by intense urticaria.

The subject of surgical fever may then be epitomized as consisting of elevation of temperature with certain accompanying disturbances, which appear to be essentially due to the results of tissue metabolism, including also metabolism of blood clot, ligatures, etc. It is not a necessary nor conspicuous accompaniment of all surgical cases, and in some individuals, even after grave operations, it will scarcely be noted. It is more likely to be extreme in children than in adults. As a result of excessive loss of blood it may be postponed. It may be complicated and prolonged by any one of the auto-infections, particularly that already mentioned in the preceding chapter as intestinal toxemia, as a result of which septic infection may ensue, and that which was at first a legitimate surgical fever may thus become merged into a septic condition. In the absence of auto-infection, and with appropriate treatment, surgical fever should quickly subside until it becomes indistinguishable about the second or third day.

Proceeding then in the order of pathological complexities, the first of the surgical infectious fevers to be considered is sapremia.

SAPREMIA.

The term sapremia will be used here as indicating a condition which is often likened to an intoxication produced by a supposititious septic suppository. The term was first used by Duncan, and was largely confined to puerperal cases. Some of the most ideal cases of sapremia are those of puerperal origin.

In each of the three conditions comprised under the general term of septic infection it is not now a question of particular organisms, but of intoxication by products which are more or less common to at least several of them. In a general way, they are mainly due to the activity of the organisms already grouped as pyogenic. Those which produce pus are capable of causing septic infection. In addition to these, it is probable that certain of the saprophytes or ordinary putrefactive organisms may produce the same effect.

Symptoms.

—In sapremia the symptoms begin promptly, depend for their intensity upon the dosage of poison, and recede quickly as soon as the source of poisoning is removed or its activity subdued. An instance of the possible causes of sapremia will perhaps best illustrate its pathology. Take, for example, the act of delivery of the full-term fetus. At the completion of this operation there is left a fresh, bleeding wound of large area which is more or less exposed to putrefactive agencies. This is reduced with the contraction of the uterine walls to a comparatively small cavity containing more or less freshly coagulated blood. As long as this clot does not putrefy it is disintegrated inoffensively, to be discharged in large part with the lochia. If germs of putrefaction enter, either during the act of labor or afterward, and linger, putrefactive processes are set up in the clot with the prompt production of certain toxins and ptomains. There is here then a septic suppository with conditions favorable for absorption by the containing tissues. How quickly the poisoning may show itself, and how soon it may subside after removal of the putrefying clot, daily experience may tell.

Sapremia then is intoxication produced by absorption of the results of putrefaction of a contained material within a more or less closed cavity, whose walls are capable of absorption of noxious products as they form. As long as putrefaction is essentially limited to the contained mass, and does not spread to and involve the containing or surrounding tissues the case is one of sapremia. As soon as the process spreads from the containing tissues the case merges from one of sapremia into one of septicemia. That this may occur in any case without prompt intervention will be readily understood. Sometimes patients may die of sapremia, though rarely, and in such case ordinarily as the result of gross neglect. Once the septicemic process is begun, however, its spread cannot always be checked, and the case which one day is sapremic and redeemable may later become septicemic and practically lost.

The symptoms of sapremia are not essentially different from those common to septic infection, save that ordinarily they are, at least at first, milder. There are flushing of the face, dry tongue, mental disturbance, pyrexia, while usually all the symptoms are ushered in by a chill, which may have been preceded only by slight malaise. These are followed by nausea and vomiting, with headache, and often, later, by diarrhea or active purging. Later delirium may occur, possibly even fatal coma. On postmortem examination there are few changes revealed; alterations in the blood, a failure to coagulate, and some softening of the spleen and liver would probably be the only ones.

Treatment.

—The treatment should be prompt and the cause removed. In puerperal sapremia the uterus should be emptied, antiseptic douches given, irrigating as often as necessary to prevent offensive odor to the discharge, and combating general signs of poisoning by plainly indicated measures. Heart depression should be overcome by diffusible stimulants and hypodermic injections of strychnine in doses of ¹⁄₂₅ grain or more. The bowels should be unloaded by a mercurial followed by a saline cathartic; suppression of urine treated by venesection and hot-air baths or sweats; diuretics should also be prescribed, and fluids administered copiously. If the patient is restless, an opiate should be given; if delirious, necessary restraint should be resorted to.

Essentially the same measures should be pursued in a surgical wound or in a case of compound fracture, or any injury where retained material may be undergoing changes already alluded to. General measures should be the same. Purgatives are advisable in these cases.

Chronic Sapremia.

—Chronic sapremia is a better name for what used to be known as hectic fever. It is characterized by rapid, feeble pulse, a temperature but little elevated in the morning and rising to 102° or 103° in the latter part of the day, with profuse perspiration, or sometimes colliquative sweats that leave patients exhausted. There is usually a distinctive flushing of the cheeks. Emaciation is a marked feature in most instances. Hectic means simply habitual fever. It is met with particularly in tuberculous cases, whether of lungs or bones or joints, in empyema, psoas abscess, and most all chronic pyogenic infections. It is frequently followed by or associated with amyloid or waxy degeneration of the liver, kidneys, and spleen. This process commences in the walls of the bloodvessels and by its spread to the surrounding connective tissue leads to notable enlargement of these organs, with albuminuria, edema, ascites, and the usual associated phenomena.

Treatment.

—Treatment, in addition to that already indicated above, should be addressed to removal of the cause. In all instances it should comprise attention to elimination, digestion, nutrition, and fresh air. By such measures even distinct amyloid changes may be arrested, or possibly improved.

Cryptogenetic or Spontaneous Septicemia.

—Cryptogenetic or spontaneous septicemia is a term applied to those cases in which the port of entry of the germs is no longer visible—e. g., a hypodermic puncture—or cannot be positively determined. On careful study this may be found to consist of a small focus where pus is forming within narrow confines and under great pressure. Under these circumstances, as Kocher has shown, toxic virulence is rapidly augmented. This is doubtless one reason why the septic features of many cases of osteomyelitis and appendicitis are so pronounced.

SEPTICEMIA.

According to the views thus enunciated, the difference between sapremia and septicemia is not one of character as much as of location. In septicemia the putrefactive action is no longer confined to material enclosed by (yet not of) the tissues themselves, but has spread from this to the surrounding living cells, which are being attacked by bacterial enemies; in other words, we deal with infection of living tissues rather than with mere intoxication. This is a progressive invasion of tissues by continuity, with a constantly proceeding systemic intoxication by poisons produced in larger quantities. So rapid may this action be—as may be seen in malignant diphtheria—that the individual speedily succumbs before evidences of abscess or local gangrene appear. On the other hand, providing that the toxic action is less pronounced or the patient’s vitality more enduring,—i. e., his tissues more resistant—abscess, phlegmon, or local gangrene may result in the destruction of tissue being limited to the environs of the parts first involved. Bacteria are also found in the blood.

While septicemia then may be a direct continuance of an original sapremia, it is not intended to intimate that it may not originate de novo; that is, many cases may begin as a pronounced septicemia from a local infection. This is the case, for instance, with the majority of dissecting wounds, etc.

Symptoms.

—In septicemia there is a period of incubation, usually two or three days, often longer. If this follows an operation, the mild fever which would indicate the slumbering fire is usually regarded as surgical fever. But when this rises and is followed by prostration, with alimentary disturbance, loss of appetite, headache, etc., followed by typhoidal symptoms, the alarm is sounded and should be quickly heeded. Usually, but not always, there is a preliminary or premonitory chill, after which prostration will be more marked than before. The severity of the symptoms cannot be foretold from the size, location, or character of the wound. The character of the fever is essentially continued, usually with morning remissions. Gussenbauer has called attention to a class of cases in which subnormal temperature is caused by the absorption of ammonia compounds. To these he has given the name ammoniemia. This condition may be seen in connection with gangrenous hernia, and has even been mistaken for shock (Warren). (See also [acetonemia], in previous chapter.)

In septicemia from infection of a visible portion of the body there are usually seen evidences of lymphangitis and perilymphangitis of septic character. These will be evidenced by tender and purplish lines, extending subcutaneously along the course of the known lymphatics or in connection with the more prominent subcutaneous veins. The lymph nodes, into which these visible vessels as well as the deeper ones empty, become enlarged and tender; the whole lymphatic system participates; the spleen in aggravated cases becomes notably enlarged, and even the bone-marrow more or less involved. Diarrhea is commonly an early but controllable symptom. A hematogenous icterus of mild degree is another frequent accompaniment. The conjunctiva becomes discolored and the skin slightly so. Should the blood be examined marked leukocytosis will be noted, and should cultures be made from it, in many instances at least, the organisms at fault can be detected and recovered from it. The vigor of the heart muscle is seriously impaired; the pulse becomes rapid and weak. In scarcely any form of septic infection is this more prominent than in diphtheria; and microscopic examination shows the rapid disintegration of the cells of the heart muscle, as well as those of other parts of the body, even to the almost complete molecular disintegration of the nuclei. Erythematoid, pustular, and even hemorrhagic eruptions are met with upon the skin, some of which are probably to be explained by thrombosis of the dermal capillaries. Certain complications are not infrequent, among which inflammations of the pericardium and endocardium—e. g., ulcerative endocarditis—are frequent. As the case becomes aggravated the temperature rises irregularly; the hot, dry skin becomes cold and clammy; prostration and indifference more marked; diarrhea more colliquative; icterus more pronounced; urine more reduced in quantity or suppressed; and these symptoms are succeeded by indifference, mental apathy, stupor or delirium, and finally death, the patients being comatose and collapsed.

While these are the general indications of septicemia, the wound or site of injury has undergone changes which are also characteristic. They comprise the edema and redness of wound margins, which may be seen even in sapremia, followed by increasing tumefaction, escape of foul-smelling discharge, and finally by sloughing and gangrene of the parts involved. On microscopic examination the capillaries are filled with infective thrombi and vessel walls infiltrated with microörganisms, which abound also in the lymph spaces. Bacterial infection can be traced in microscopic sections from the infected area, from the point in the neighborhood of the wound where microbes infest the tissues to points remote from it, where they are sparsely found, if at all. The same evidences of infection may be traced along the lymphatic vessels, and often the veins.

Postmortem Evidences.

—The postmortem evidences of septicemia are indicative on first sight: the blood is of the consistency of tar and does not coagulate; evidences of putrefaction are plain to sight and smell; the serous membranes, particularly the pia mater, are often extravasated; the muscles are discolored and of a darker hue than natural, edema of the lung is frequent; the intestines reveal a gastro-intestinal catarrh, the duodenum and rectum showing punctate hemorrhages; the spleen is darkened, enlarged, and softened; the liver shows similar signs, less marked, and at times an emphysematous condition due to putrefactive gases. Cultures can be made from the fluids and tissues of organs thus affected. It is also of importance to emphasize that such material is powerfully and often fatally infectious; some of the worst forms of dissecting wounds and instances of fatal infection have come from carelessness in making these postmortem examinations.

So far as concerns the character of the wound, which is most likely to be followed by septicemia, there is but little to be said. Wounds made by infected tools, the butcher’s knife, the anatomist’s scalpel, etc., are the most dangerous. All forms of phlegmonous erysipelas, many cases of gangrene following frostbite, nearly all instances of traumatic gangrene, most cases of carbuncle, and, in fact, all similar lesions, are likely to be followed by septicemia. The so-called spontaneous cases have an equally infectious origin, though one which is concealed. In unrecognized instances of appendicitis, for instance, and in many other conditions, although the path of infection may not be easily traced, it is, nevertheless, always present, and can be found if diligent search is made. The nasal cavity, the tonsils, the teeth, the middle ear, the deep urethra, and the rectum are often overlooked as offering possibilities for septic infection which may follow this general type.

Treatment.

—This should be both local and general. Local treatment should consist in complete and absolute removal of the active cause. This comprises the reopening of wounds, evacuation of clot, cutting or scraping away of sloughs and gangrenous tissue, with cauterization of the exposed living tissue, in order that absorption may be prevented, and will often include amputation or extirpation of a part. For tissues which are not too completely riddled by disease, and lost beyond possibility of redemption, continuous immersion in hot water offers the best possible prospect. By it putrefaction seems checked, the separation of dead from living tissues is accelerated, relief of pain or discomfort is afforded, and disinfection of material which is foul and infectious is guaranteed. An excellent local application is the mixture of resorcin 5 parts, ichthyol 10 parts, ung. hydrarg. 40 parts, and lanolin 45 parts, already mentioned in Chapter IV, or the application of brewers’ yeast. (See chapter on [Ulcers].) Of great value also will be found the silver ointment of Credé (Unguentum Credé). This permits of absorption of silver through the unbroken skin (as in the case of ung. hydrarg.), and the dissemination throughout the system of the antiseptic virtues of the silver itself. To ensure its greatest efficiency this ointment should be thoroughly rubbed in, especially over parts which are not too tender. Many cases of septic infection promptly yield under the influence of the argentine preparations which Credé has lately introduced.

In suitable cases also the subcutaneous injections of antistreptococcic serum will be followed by beneficial effects. The earlier the injection is given the better the prospect of benefit. Evidence is strongly in favor of this serum as a prophylactic measure, especially before operations, when septic pneumonia or other septic accidents are feared.

Another measure of great utility in selected cases is the intravenous infusion of a solution of Credé’s soluble silver, made with 1 gram of silver in 1000 Cc. of sterilized water at a temperature of 105° to 110°. In cases of profound toxemia a small amount of blood may be withdrawn (50 to 400 Cc.), for reasons stated in Chapter VI. No hesitation need be felt in introducing 500 Cc. or even 1000 Cc. of this solution. It is the ideal way of bringing a powerful non-toxic antiseptic into immediate contact with pathogenic microbes.

There have been recent suggestions as to the intravenous injection of very dilute formalin solution, in order to take advantage of its remarkable germicidal activity; it has been employed in a few cases, especially of puerperal sepsis, with success, 1 Cc. of standard formalin solution is mixed with 800 Cc. of sterilized salt solution. It has been shown that if 50 Cc. of this is thrown into the veins of an average adult it will form with the 5000 Cc. of blood a mixture of 1 to 200,000, in which strength it may be expected to prove an efficient bactericidal agent. Indeed, a smaller amount or a weaker preparation would probably suffice. Barrows has reported success following two infusions, two days apart, of first 500 Cc., then 750 Cc. of a 1 to 5000 formalin solution. Still, these injections may be followed by cramps in the arms, cardiac discomfort or distress, and blood (or blood cells) in the urine. It would probably be well to limit this use of formalin to those cases at least in which the presence of cocci in the blood can be demonstrated by culture or other method.

An excellent method in the local treatment of parts which admit of it (hands and feet) is their exposure to dry hot air in the Kelly heater or some similar apparatus. Hot air will be borne at a temperature of 210° to 220°, which may be destructive to germs while still tolerable for a short time by the tissues. Clinton, of Buffalo, with whom this method is original, reports that the temperature within the tissues thus treated is raised to about 107°, which is above the thermal death point of the ordinary pyogenic organisms, and that this method gives better results than any other of treatment of septic infection of those parts which can be subjected to it.

The general treatment of septicemia is, in the main, stimulant and tonic. Fever is not to be treated with arterial sedatives nor often with antipyretics. It is a symptom of poisoning, and its too prompt suppression prevents both the recognition of the intoxication and the measure of its degree. Pyrexia then is best combated with cool sponge baths and stimulant measures of a general character. The principal reliance must be upon nutrition and stimulants. Assimilation may be impaired when gastro-intestinal catarrh is as prominent a feature as it is in many of these cases. Consequently the simplest and most assimilable food, often that which is predigested, should be administered. Milk, eggs, beef peptonoids, and fruits are among the most appropriate. The best stimulants and tonics are alcohol and strychnine. Strychnine is preferably administered hypodermically in doses of ¹⁄₂₅ grain from two to four times a day. Heart depression is best combated by this measure, or by quinine in large doses, while digitalis and atropine may be added. For internal use alcohol is, par excellence, the remedy. This is administered in doses only to be measured by their effect. In fact, the administration of alcohol in these cases is a matter of effect, and not of dosage. Aside from these measures the intestinal antiseptics should be administered, among these being corrosive sublimate, ¹⁄₁₀₀ grain, every three or four hours, salol in large doses, bismuth salicylate, or naphthalin—any or all of these in connection with powdered charcoal. Intestinal pain and frequency of stool can be more or less controlled by opium, while disinfection of the alimentary canal is only to be accomplished by the above remedies, in connection with flushing of the colon with saturated boric acid solution or something of that kind. Pain is to be controlled by morphine administered subcutaneously.

No special attention need be given to the so-called septicopyemia. It represents a mixed condition of septic intoxication, local infection, and destruction, with metastatic abscess, and is a term appropriately applied to cases which combine the significant features of each type.

PYEMIA.

The derivation of the term pyemia, which came into general use in 1828, is misleading. Although septic fever always accompanies suppuration, it is not certain that pus as such circulates in the blood, as the term pyemia implies, the error having arisen originally from mistaking the contents of breaking-down thrombi for pus from ordinary sources. While a recognition of the etiology of the disease is new, the disease itself has been recognized for many centuries.

Pyemia is only met with in connection with suppuration, as far as known, never without it. In those cases which appear to be free from suppuration pus will be found. Pyemia may be described as septicemia plus thrombotic and embolic accidents, which lead to distribution of infectious material to all parts of the body. This distribution is made by the bloodvessels, although to some extent the lymphatics undoubtedly participate. When pyogenic organisms reach bloodvessel walls they tend to set up a mycotic phlebitis, which, by virtue of the coagulating blood, becomes soon what is known as thrombophlebitis. Infection proceeding through the vessel walls, the endothelial lining is loosened, while to these rotting spots leukocytes adhere and coalesce into a more or less homogeneous mass. This so-called white thrombus becomes also infected with bacteria; portions of it, loosened and dislodged, are carried by the returning blood stream to the right side of the heart, whence they are distributed through the lungs. Dislodgement may be made by mere force of the blood stream, or may be assisted by movements of the part or handling of the same. These particles of thrombi are loaded with the infectious organisms which began the disease, and wherever one settles a reproduction of the original thrombophlebitis is rapidly produced. In this way numerous infected thrombi are formed within the vessels of the lungs, which, again, loosen, and are now swept into the left side of the heart, whence they are distributed with arterial blood in all directions. While it is true that they are equably distributed, it is also positive that certain tissues seem more capable of lodging and being attacked by the contained organisms than are others. When it is once appreciated that each particle of infected clot is capable of setting up, either in the lungs or in the other tissues, upon the second distribution, other abscess formations analogous in etiology to that from which came the first disturbance, then the fundamental idea of metastatic abscess is fully impressed. The term metastasis may be regarded as synonymous with transportation, and metastatic abscesses are those produced by transportation of infected particles from one part of the body to another. Wherever they lodge similar trouble will result. Contiguous minute metastatic abscesses quickly coalesce, and in this way large collections of pus are formed. The blood also contains organisms not attached to thrombi, and from the blood of the pyemic patient cultures can at almost any time be made. Until this is done it will be virtually impossible to incriminate any particular organism as the one at fault. Thrombo-arteritis is the equivalent in the arteries of thrombophlebitis in the veins, and is accompanied by the same detachment of endothelium, adhesion of leukocytes, etc. Whenever such a lesion occurs in artery or vein, coagulation necrosis takes place and suppuration occurs around it. The metastatic abscess is thus the result of breaking down of this affected tissue, and is often called miliary abscess. Particles of infective thrombi cling also to the valves of the heart and a septic endocarditis may result.

The possibility of so-called spontaneous or idiopathic pyemia is occasionally discussed. This means a pyemia whose cause is concealed. The explanation will be found sometimes in an acute infectious osteomyelitis, sometimes in ulcerative endocarditis, or inflamed appendix or other portion of the peritoneal cavity. Again, it may proceed from middle-ear disease, in which there is so little discharge as scarcely to attract attention. Thus causes which predispose to suppuration (see [Chapter III]) come into play here, and the influence of exposure, fatigue, starvation, etc., is not to be ignored in furnishing an explanation for the so-called idiopathic cases.

In the majority of instances, however, pyemia follows surgical operations and injuries, among which are compound fractures, deep injuries with small superficial evidence thereof, compound injuries of the skull, and injuries by which veins are exposed. Inasmuch as the typical pyemic manifestations require a certain length of time for their development, the onset of this disease is more delayed than in the case of septicemia. While the case may be manifestly one of septic infection of unrecognizable type, the characteristic indications of pyemia seldom appear in less than ten days, and frequently not for several days longer.

Symptoms.

—The symptoms of pyemia do not essentially differ from those of other septic infections. The principal difference is in the frequency of chill and range of temperature. Chills are more common at the inception of the condition, and more frequent throughout its continuance than in other septic conditions. The chill may be slight or assume the proportions of a rigor, and each chill is followed by colliquative sweat and exhaustion. In other words, chills which are infrequent in septicemia are common in pyemia. There is reason to believe that with each fresh distribution of emboli we have one or more chills as the objective evidence thereof. Distinctive also of pyemia is the temperature curve, which much resembles that of intermittent fever, without the regularity of change characteristic of malarial fevers. It is without regular remissions, and has been referred to as irregularly intermittent. The first rise is abrupt and usually excessive, while with each fresh chill or series of chills similar abrupt alterations will be noted. These occur so frequently and fluctuate so irregularly that in order to note them accurately the temperature should be taken at least every two hours. The temperature seldom drops to normal.

As the lungs fill with the first crop of infected emboli, and the first series of metastatic abscesses form there, there is more or less dyspnea and sense of oppression; there may be also pulmonary complications—pleurisy, bronchitis, etc., even pulmonary edema. Frequently there is expectoration of frothy and discolored sputum; occasionally there is blood in the sputum. A peculiar sweetish odor of the breath has been noted by many observers in this disease, and is supposed to be idiopathic and characteristic. (See [acetonemia] in previous chapter.) With the dispersion of the second crop of emboli from the lungs there is apt to be icterus, with evidence of metastatic abscess in the liver, and collection of pus as the result of coalescence of small abscesses. The sensorium is not so affected in pyemia as in septicemia, and in the former disease patients are more likely to be alert and active in mind. General hyperesthesia and restlessness are common. Colliquative sweats are also a feature of pyemia. There is the same liability to eruptions, etc., which may mislead or complicate the diagnosis. A dermatitis is seen sometimes in pyemia, the lesions assuming a papular or pustular form, due to local infections of the skin. Purpuric spots are also seen, and vesication is not infrequent. Within the mouth sordes collect upon the teeth or gums; the tongue becomes dry and brown and heavily coated. Diarrhea is less common in pyemia. The urine is usually scanty and high colored, containing solids in excess; albumin is sometimes found therein, as well as peptone. The presence of peptone in the urine is probably an indication of the breaking down of pus corpuscles in various parts of the tissues.

A significant objective evidence of pyemia is met with in the metastatic collections of pus within the joints, which occur relatively early, and which, if multiple, may lead to a correct diagnosis. One of the earliest joints to be involved is the sternoclavicular, although none of the joints are free from the possibility of invasion. The articular serous membranes seem to have the property of carrying and holding the infective thrombi better than any other tissue in the body. The pyarthrosis of pyemia is for the most part painless, yet implies loss of function of the affected joints. The distention of these is usually evident to the eye, the fluctuation pronounced, tenderness not extreme, but the swollen part merges into tissues which are edematous and reddened. When pain in the limb is extreme, it is usually because of metastatic abscess within the bone-marrow cavity. In other words, we now have a metastatic osteomyelitis.

In all cases of pyemia prostration is marked, yet the pulse is seldom weak, at least until toward the close of life. As cases progress from bad to worse subsultus tendinum is often noted.

The appearance of the wound or site of operation does not differ essentially from that already described under Septicemia. There is usually, however, less discharge, granulations are smoother and dryer, and if tissues are gangrenous they are not as wet and nauseous as in the other case. Evidences of thrombophlebitis and lymphangitis will proceed from the wound toward the body, as in other instances of septic infection.

Prognosis.

—Prognosis is usually bad. While recovery may follow where metastatic infiltration has not been too general, the ordinary case of pyemia will die within twelve to fourteen days after diagnosis. Sometimes the entire process is much slower, and isolated cases occur which can be designated as so-called chronic pyemia, which differs but little from the acute form. A case of pyemia should not fail of recognition because there is no evidence of infection from without. A fatal case of pyemia has been known to occur from a suppurating soft corn which was not discovered during life; also from peridental abscess, etc., which had been overlooked. Death is the result of tissue destruction and septic intoxication.

Postmortem Appearances.

—In the vessels these consist essentially of thrombosis, examples of which may be seen, for instance, in the cranial sinuses and in the large veins. Aside from these, with the enlargement and softening of the spleen, the liver, and lymphatic structures, already described under Septicemia, the principal objective evidences consist in the discovery of metastatic abscesses in many or all parts of the body. As stated above, there is no tissue or organ in which they may not be found. The mechanism of their production has been already described. Infarcts may also be met with, in the kidneys especially, the liver and spleen as well, and indicate areas already cut off from blood supply by thrombo-arteritis, in which abscess formation would have occurred had time been given. In the liver large abscesses may be found; joint cavities may be filled with pus; the lungs are usually the site of innumerable small abscesses. The other postmortem changes commonly noted are not difficult of explanation, but are not so characteristic or pathognomonic as to call for further mention. In a joint which has become filled with pus there usually has been loosening of the cartilage and more or less disorganization of all the joint structures, which appear to have undergone rapid ulcerative destruction and putrefaction.

Treatment.

—Treatment of pyemia is in large degree unsatisfactory. That which used to be the terror of surgeons in the pre-antiseptic era is now, thanks to Lister and others, almost abolished. Pyemia is a rare disease in modern surgical practice. Its possibility should be borne constantly in mind, however, and the necessity for careful antiseptic or for a rigid aseptic technique is in large degree based upon fear of pyemic consequences.

When once established, the disease is to be treated on lines nearly similar to those laid down for septicemia, including resort to the ichthyol or silver ointments, and to intravenous infusion of silver solution. (See [p. 89].) Amputation or extirpation of the part from which infection has first proceeded may be of avail. Among the most successful measures for surgical treatment of this disease is to expose the infected area, open the involved veins, and either excise them or scrape them out and disinfect them. This treatment has been successful in cases of cranial infection following middle-ear disease, etc. (See chapter on [Cranial Surgery].)

Disinfection of the infected area and immersion in hot water should be practised. Metastatic abscesses should be opened and drained, and every accessible collection of pus evacuated, either by the knife or aspirator needle—e. g., in the liver.

The medicinal treatment is practically the same as in septicemia, while the surgeon’s mainstays are alcohol and strychnine. These, with cathartics and intestinal antiseptics, will practically sum up the drug treatment, the surgeon meantime not neglecting the matter of nutrition, crowding it in every assimilable form.

ERYSIPELAS.

Erysipelas is an acute infectious disease characterized by its tendency to involve the skin and cellular structures, to extend along the lymphatic vessels, to involve wounds and injuries under certain conditions, accompanied by more or less fever of septic type, leading frequently to septic disturbances of profoundest character, yet tending in the majority of instances to spontaneous recovery. It has been observed probably from prehistoric times, but has not found a proper description nor appreciation until perhaps within the past century. It occurs in so-called traumatic and idiopathic form—which latter means that the site of infection is not discovered—and also in a virulent and contagious type, which leads to the appearance of a number of cases over a large territory; it often appears in the epidemic form. On account of the reddening of the skin it goes by the name of the rose among the German laity. It may assume the type of an infectious dermatitis, subsiding without suppuration, or a similar lesion of exposed mucous membrane may be noted, or, occasionally, its virulence seeming greater, its lesions are met with in more deeply seated parts, accompanied by suppuration or even gangrene, and it is then called phlegmonous. In a small proportion of cases the infectious organism appears to be transported from one part of the body to another, and thus we have metastatic expressions of this disease. The most common examples of this are seen in erysipelatous meningitis after erysipelas of the face or scalp, and erysipelatous peritonitis after the disease has manifested itself on the truncal surface. It is of a type which makes itself almost interchangeable with puerperal fever; and when epidemics of erysipelas have involved certain states or areas, it has been noted also that nearly every obstetrical case developed puerperal septicemia.

Etiology.

—There is more than passing interest connected with this last statement. It is now definitely established that the infectious organism is a streptococcus which is allied to, if not identical with, the streptococcus pyogenes, the ordinary pyogenic organism of this form. This specific organism has been separated, studied, and its role assigned by Fehleisen, and the organism is frequently called Fehleisen’s coccus. Preserving always its morphological characteristics, it acts, as do many other pathogenic organisms, within wide limits in virulence. Cultivated from some cases, it scarcely seems infectious, while from others it is fatal.

Pathology.

—The disease manifests a tendency to travel via lymphatic routes. As long as it is confined to the skin and superficial tissues it has the appearance of an acute dermatitis. When it migrates deeper it generally leads to suppuration, another reason for believing that the streptococci of erysipelas and of pus production are the same. In the affected and infected area the minute lymphatics will be found crowded with the cocci, which are seen much less often in the small bloodvessels; also in the tissues beyond the apparently infected area they may be found dispersed less freely. The bacterial activity seems most active along the advancing border of the superficial lesion. Here the phenomena of hyperemia and phagocytosis are most active. Even in the vesicles that are characteristic of the disease the organisms may be found.

The discharges from this region are infectious, and caution should be observed in dressing such cases. A finger pricked by a pin from a dressing may subject the individual to loss of life. The dressings containing the discharges should be burned immediately.

The path of infection is usually through a wound, and as soon as discovered a case of erysipelas should be separated from all surgical cases, or if the erysipelatous patient cannot be isolated, he should be removed from proximity of other wounded individuals.

Erysipelas which follows injury, however slight, is termed traumatic. The terms “idiopathic” or “spontaneous” should be restricted to those cases in which the path of infection is not discovered.

Symptoms.

—With the exception of the local appearances, they are essentially the same in both of the above-mentioned forms. The characteristic feature of the disease is a dermatitis with its peculiar roseate hue, which it is impossible to describe in words. In tint it differs slightly from that noted in certain cases of erythema. It is, however, accompanied by an infiltration of the structures of the skin, so that the area which is reddened is at the same time elevated above the surrounding surface. Its edges are often irregular. As exudate takes the place of blood in the tissues, the red tint merges into a yellow. At this time there is more induration of the skin and tendency to pit on pressure. Vesication of this involved area is now frequent, the vesicles often coalescing and forming large blebs and bullæ, which fill with serum that may become discolored or purulent. When exposed to the air, unless the tissues become gangrenous, this serum usually evaporates and forms scabs. This disturbance of the skin is always followed after a number of days by desquamation. This infectious dermatitis shows a constant tendency to spread in all directions. Its most characteristic appearances are limited to the margin of the enlarging zone, while in its centre there may be evidences of recession of the disease. If it commences in the vicinity of a wound it will probably spread in all directions from it. Beginning in the face, it usually spreads upward; in the trunk, in all directions; if on the extremities it tends to migrate toward the trunk. Wandering erysipelas is a term often applied to these phenomena. The metastatic expressions of the disease have been described.

When this affection attacks a recent wound the local appearances are not essentially distinct from those mentioned under Septicemia. The wound margins separate to a greater or less extent, the surfaces slough, and a characteristic seropurulent discharge occurs. Granulating surfaces usually become glazed—often covered with a membrane resembling that of diphtheria; deep sloughs may occur, undermining of wound edges, even hemorrhages from destruction of vessel walls. In rare instances, however, under the influence of the microbic stimulation granulations proceed faster than normal.

Whether the disease proceeds from an injury or not, the constitutional symptoms vary but little. There is usually a period of malaise with nausea, followed by alimentary disturbance, coating of the tongue, elevation of temperature, sometimes with occurrence of chill. Complaint of pain or unpleasant sensation will lead to examination of the area involved, when the above symptoms will be noted, with evidences of lymphangitis and enlargement of lymph nodes. When chill occurs it is followed by pyrexia. Temperature fluctuates, with a tendency to assume the remittent type. When the disease subsides spontaneously it is by a gradual process of betterment and subsidence of temperature. In other instances the constitutional symptoms assume more or less of the septicemic or typhoid type, and it is seen that the patient’s condition is practically one of mild septicemia, which often proves fatal.

When the disease assumes the phlegmonous type the constitutional symptoms become more and more typhoidal and the septicemia becomes most pronounced. Locally exudation goes on to the point of threatening, even of actual, gangrene, unless tension is relieved by incisions. Pain is usually intense, partly because of confined exudates beneath resisting structures. More or less rapidly the local and constitutional signs of pus formation are noted, and unless these are observed and acted upon early there will not only be suppuration, but more or less actual gangrene, so that not only pus, but sloughs of tissue will be discharged through the incision, or will, when this is delayed, make their escape by death of overlying textures.

In all phlegmonous cases there is practically coincidence of septicemia, already described, and of the local appearances above noted. In proportion to the extent of the lesion in these phlegmonous cases, and failure to afford relief, will be the opportunity for septic intoxication.

The mucous membrane does not always escape, and even in the nose, the pharynx, the vagina, and the rectum a distinctive erysipelatous lesion may be found. The disease may travel from the pharynx through the nose and involve the face, or through the Eustachian tube to the ear and thence to the scalp, or vice versa. Erysipelatous laryngitis is to be feared on account of edema of the glottis, which would soon be fatal unless overcome by intubation or tracheotomy. An infectious exudation into the lungs is also known to follow erysipelas, and has been considered an erysipelatous pneumonia. The cellular tissue of the orbits may also be involved, when abscesses will occur, which should be opened early; the parotid and other salivary glands may become involved, usually in suppuration.

Many cases are accompanied by much gastric irritation, which it is difficult to explain. Ulcers are sometimes found in the intestines, as after burns. These usually give rise to bloody diarrhea. The cerebral symptoms may be simply those of delirium from irritation or of meningitis from infection. Strange phenomena have followed the disease in certain instances—cessation of neuralgic and of vague, unexplainable pain, improvement in deranged mental condition, spontaneous disappearance of tumors, etc. Advantage has been taken of this last in the treatment of these cases. (See [Cancer].)

It is quite likely that some of the worst forms of phlegmonous erysipelas are due to mixed infection. To inject the bacillus prodigiosus together with the streptococcus of erysipelas will greatly enhance the virulence of the latter, so that reaction may proceed even to gangrene.

Postmortem Appearances.

—These are not distinctive, but are a combination of local evidences of suppuration and gangrene, with the deterioration of the blood, the softening of the spleen, etc., which are characteristic of septic poisoning. Only in the skin, and then under microscopic examination, can any pathognomonic appearance be discovered. This will consist in the crowding of the lymphatic vessels and connective-tissue spaces with cocci, in the evidences of rapid cell proliferation, in the quantity of exudate, in vesication, sloughs, etc.

Diagnosis.

—Diagnosis of erysipelas should be made mainly from various forms of erythema, from certain drug eruptions, and from other forms of septic infection which do not assume the clinical type of erysipelas. The gastric symptoms of this disease are sometimes produced by certain poisonous foods or the distress which is produced by medicines, such as quinine, antipyrine, etc.

Prognosis.

—The majority of instances of idiopathic erysipelas run a certain limited course, although the eruption may spread to almost any distance upon the body. When the disease attacks surgical cases, and especially when it involves wound areas, the prognosis is not so good. When the disease assumes an epidemic type and involves cases of all kinds, it will be found to have a virulence that may make it a most serious affair. In proportion to the extent to which it assumes the phlegmonous type it will be found locally, if not generally, destructive. The ordinary case of facial erysipelas will recover with almost any treatment. Nevertheless meningitis may develop, and even a mild case is to be treated with care and caution.

Treatment.

—Danger comes from two sources—septic intoxication and local phlegmons or gangrenous destruction. Each is therefore to be combated. Treatment should consist of isolation. There is no specific internal treatment for this disease. Tincture of iron, which was long vaunted as such, has proved unsatisfactory, and is of benefit only as a supporting measure in a limited class of cases. Constitutional measures should be employed: First, for the purpose of maintaining free excretion by bowels and kidneys; second, for the purpose of supporting and maintaining strength; third, for tonic and stimulant measures in prostrated and debilitated patients; and, fourth, for the purpose of combating intestinal sepsis or intoxication from any other source. The robust patients with this disease need no particular tonic. The aged, the enfeebled, the dissipated, the prostrated individuals, and the confirmed alcoholics are those who need vigorous stimulation, partly by alcohol and quinine, and partly by strychnine, preferably given hypodermically, and by the other diffusible stimulants by which they may be kept alive. Pilocarpine, given subcutaneously and pushed to the physiological limit, has been praised by some. If along with prostration there occur restlessness and delirium, then anodynes and hypnotics are serviceable, and should be administered to meet the indication—morphine hypodermically and any of the agents which produce sleep are now most beneficial. Finally, if there is any drug which can be administered in doses sufficient to saturate the system with an antiseptic which shall at the same time not prove fatal because of toxicity, this is the ideal medicament for constitutional use only. Such a drug is not known, but it will be well to give some near approach to it internally, as by administering corrosive sublimate, salol, naphthalin, or something else of this character in doses as large as can be tolerated.

Should patients become violent it may be necessary to resort to mechanical restraint—a strait-jacket, a restraining sheet, a camisole, etc.

Nourishment must be kept up by the administration of the easily assimilable and predigested foods.

Locally the number of remedies that have been resorted to is legion. In a mild case of spontaneous erysipelas—i. e., where no infection can be traced—it will sometimes be sufficient to put on a soothing application, like a lead-and-opium wash. It often gives relief to have the part protected from air contact, which may be done by a soothing ointment or by dusting the part with a powder, such as bismuth oleate or subnitrate, zinc oxide, etc., these being rubbed up with powdered starch; or by a film of rubber tissue or of oiled silk. Brewers’ yeast applied on compresses and covered with oiled silk is efficacious.

Even before the bacterial origin of the disease was accepted it had been suggested to use antiseptic applications, either in watery solution or combined with oil or some unguent; this is now the ideal method of local treatment, the difficulty being only to find that which shall be efficacious as an antiseptic, yet not injurious in other ways. Compresses wrung in solutions of various antiseptics are often serviceable. The following preparation has given satisfaction: Resorcin (or naphthalin) 5, ichthyol 5, mercurial ointment 40, lanolin 50. The proportions of these ingredients may be varied, and the amount of ichthyol sometimes increased, especially when the skin is not too tender. The affected parts are anointed with this, and then covered with oiled silk or other impermeable material, simply to prevent its absorption by the dressings; the parts are then enveloped in a light dressing and bandaged. Credé’s silver ointment has also proved useful. As the disease becomes mitigated the ointment may be reduced with simple lard, and discontinued when local signs have disappeared. Absorption of any of these preparations may be hastened by scratches over the affected area with the sharp point of a knife.

Treatment of threatening phlegmon, or phlegmonous erysipelas, must be more radical, and consists of free incision down to the depth of the deepest tissues involved. In treating dissecting and other septic wounds of the fingers incision should be made to the tendon sheaths, even to the bone. It is only by such radical measures that worse disaster may be avoided. Some aggravated local cases are treated by a series of deep incisions with the use of the curette, the surface after careful clearing being kept buried under an antiseptic solution (silver lactate 1 to 500) or ointment.

RELATION OF LYMPH NODES AND GRANULATION TISSUE TO INFECTION.

In connection with erysipelas and the role of the lymphatics, it is advisable to consider the relation and behavior of the lymph nodes and granulation tissue to infecting agents. Depending on the virulence of the infectious material, the site of infection, and the variety of the microbe will be its arrival in these protective filters. Then follows a series of cycles of maximum and minimum activity in the nodes, during the former the bacteria almost disappearing. The more pathogenic the microörganism the more certain the destruction of the lymph node, or perhaps of the individual. The well-known enlargement of the nodes is due almost solely to an increase in their lymphoid elements. Halban, who demonstrated these cyclic variations in the contents of the lymph nodes, is inclined to insist on an intimate relation between them and the temperature variations noted in cases of septic infection.

When granulations are present the lymph sacs are closed, as by a sanitary cordon. Unless this tissue is broken they are proof against ordinary infection. It is well known that erysipelas will appear about an old wound or sinus that has been rudely probed. Even virulent organisms spread upon healthy granulating surfaces fail to infect. Strong carbolic and other toxic agents can be used in and about such granulating cavities with an exemption from poisoning that otherwise would produce dangerous effects.

CHAPTER VIII.
SURGICAL DISEASES COMMON TO MAN AND DOMESTIC ANIMALS.

TETANUS.

Synonyms: Trismus, Lockjaw.

Tetanus is an acute infectious disease, of relatively infrequent occurrence, invariably of microbic origin, characterized by more or less tonic muscle spasm with clonic exacerbations, which, for the most part, occurs first in the muscles of the jaw and neck, involving progressively, in fatal cases, nearly the entire musculature of the body. Certain races of people seem predisposed, and in certain climates and geographical areas the disease is exceedingly prevalent. Negroes, Hindoos, and many of the South Sea Islanders show a peculiar racial predisposition, and, in a general way, inhabitants of warm countries are less resistant. This is shown partly by the fact that in various European wars the Italians and French have suffered more than the soldiers of more northern climes. Tetanus is by no means confined to adult life, since infants are far from exempt, and in the tropics the trismus of the newborn is the cause of a high mortality rate. In Jamaica one-fourth of the newborn negroes succumb within eight days after birth, and in various other hot countries the proportion is at times equally great. One plantation owner states that fully three-fourths of the colored children born upon his plantation succumbed to the disease. The peculiar reason for this infection will appear later when speaking of tetanus neonatorum. Men seem more commonly affected than women, probably because of their occupations, by which they are more exposed. Military surgeons have had to contend with the disease in its most virulent form, and it has been noted that soldiers when worn out by fatigue or suffering from the disaster of defeat seemed more liable to the disease. In 1813 the English soldiers in Spain suffered from tetanus in the proportion of 1 case to 80 wounded men. In the East Indies, in 1782, this proportion was doubled. Quick variations of heat and cold, such as warm days and cold nights, coupled with the other exposures incidental to military life, seem to exert a great effect. Curiously enough, the wounded in many campaigns who have been cared for in churches have suffered more from the disease than those cared for in any other way. Tetanus, however, is by no means necessarily confined to any one clime or race, but may be met with anywhere, at any time, providing only that infection has occurred. A celebrated Belgian surgeon lost by tetanus ten cases of major operations before he discovered that the source of the infection was his hemostatic forceps. As soon as these were thoroughly sterilized by heat he had no further undesirable complications. If the disease can be conveyed by the instruments of a careful surgeon, how much more so by the dirty scissors of a careless midwife, etc.

It is true, also, that the popular notions of the laity concerning the liability to tetanus after certain forms of injury are not ill-founded. Small, ragged wounds of the hands and feet are those which ordinarily receive little or no attention, and are among those most likely to be followed by this disease. The toy pistol, which, a few years ago, was such a prevalent and widely sold children’s toy, was the cause of many a small laceration of the hand, due to careless handling and the peculiar injury produced by the explosion of a small charge of fulminating powder in a paper or other cap. It was not the character of the laceration or injury thereby produced, but the fact that such injuries occurred in the dirty hands of dirty children, which were most likely to become infected, that has caused the so-called toy-pistol tetanus to be raised almost to the dignity of a special form of this disease. During the month of July, 1881, in Chicago alone, there were over 60 deaths from tetanus among children who had been injured in this way by these little toys. This led to their sale being suppressed by law.

Etiology.

—Two theories have had strong advocates, one being that which would account for the disease by irritation of nerves; while the second, the humoral, would explain the disease by alterations in the blood. Each has had its most ardent defenders, but both have now completely yielded to the investigations of a few observers, among whom Kitasato and Nicolaier are the most prominent. These ardent workers were, in 1885, able to clearly establish the parasitic nature of this disease, and to isolate and investigate the organisms by which it is produced.

Fig. 17

Tetanus bacilli, showing spore formation. (Kitasato.)

The bacillus of tetanus is a somewhat slender, rod-shaped organism, with a peculiar tendency to spore formation at one end, which gives it a drumstick appearance. It is essentially an anaërobic organism, and can never be cultivated in contact with the air. In laboratory experiments it is grown in the depths of a solid culture medium or else in fluids and on surfaces in an atmosphere of hydrogen gas. It is one of the apparent contradictions of bacteriology that this organism, which can only be grown as an anaërobe, nevertheless abounds in earth, particularly the rich, black loam which best supports luxuriant vegetable life, and that it practically inhabits the upper layers of the soil, which accounts for the fact that so many contaminations and infections have occurred from stepping upon planks or boards with nails projecting, or from introduction of splinters, or from lacerations of the hands and feet which are so often followed by contact with such materials. There is nothing about a rusty nail wound which, by itself, predisposes to tetanus, but the rusty nail upon which a person steps is either itself infected or leaves a rent or wound which may become infected within the next few moments, and which is not likely to receive the careful attention which it should. Verneuil has of late laid stress upon the fact that in localities where horses are kept tetanus is more prevalent, and that the infectious organism abounds in and upon stable floors, about barn-yards, and wherever the excretions of a horse may be found. Bacteriologists are aware that in the intestines of herbivorous animals the bacilli (anaërobic) of tetanus and malignant edema are often found. Verneuil has further shown that almost the only instances of tetanus which occur on shipboard are upon those ships which are used for transportation of horses and cattle. His statements are at least interesting, if not absolutely well-founded. At all events, tetanus is certainly of telluric origin.

A French veterinary surgeon of twenty-five years’ experience had not seen a single case of tetanus until 1884, when he “removed a tumefied testicle from a horse, with the ecraseur, and it died of tetanus; in the following six months he castrated five, and all died; another castrated fifteen in one day, and all died but one; another in ten days castrated six bulls and operated on three fillies for umbilical hernia, when five of the bulls and one of the fillies died.” This will illustrate how the infectious agent may be conveyed by instruments, etc.

The tetanus bacillus manifests other peculiar properties, for some of which it is most difficult to account. Upon susceptible animals it is violently infectious, but is rarely found at any distance from the tissues in which it has first lodged. In laboratory investigations the period of incubation is seldom longer than forty-eight hours. Another peculiarity of the organism is that it generates certain poisons of active properties which may be separated from pure cultures, by whose injection the peculiar spasms of the disease itself may be reproduced. These have been isolated, especially by Brieger, who has given to them the names of tetanin, tetanotoxin, spasmotoxin, etc. It has been estimated that about ¹⁄₃₀₀ Gm. of the pure toxin of tetanus would be a fatal dose for a man. This toxin seems to have a specific affinity for the ganglion cells of the anterior horn of the spinal cord, with which it unites with great force. Herein lies the secret of its disturbing power.

It is peculiar that some time may elapse after its injection before the appearance of the first symptoms. Diphtheria toxins appear to be prompt in their action, and thus display quite opposite characteristics. Experiment would seem to show, moreover, that the tetanus toxins do not reach the cord through the blood stream, but appear to slowly pass along the axis cylinders. Sensory nerves do not transport the toxins to the cord. The toxin enters the nerve termination, first of all, at the site of the infection, where it is most concentrated, which will explain why the spasms most frequently begin in the vicinity of the infection, or are the most marked there. Most of the toxin is taken up by the blood and lymph and distributed all over the body, and then passing along the motor fibers it enters the cord and leads to general convulsion. When the toxin is injected directly into the cord the symptoms begin at once. Therefore, for protective purposes, much may be expected from the administration of the antitoxin in cases of suspicious injury or those where experiment has shown there is reason to fear the development of tetanus. There does not appear to be on record a single instance in which a person who had been given antitoxin soon after receiving such a wound has developed tetanus, nor does the antitoxin by itself seem to have done any harm. Obviously, then, the earlier antitoxin is used in the case the better. It may be recalled that there are no diagnostic symptoms of tetanus until the first spasm develops, usually after the expiration of from five to twelve days. By this time the nerve cells are thoroughly saturated with the poison and considerable time may elapse before the antitoxin can reach these cells by a more indirect route.

Tetanus Neonatorum.

—Tetanus neonatorum, or tetanus of the newborn, a condition already alluded to, is a remarkably fatal affection, very prevalent among the negro race, especially in hot climates. It nowise differs from traumatic tetanus, but is such in effect, since the infection in these instances always follows the division of the umbilical cord, which is usually effected with dirty scissors in the hands of a dirty midwife, while the thread with which the cord is tied is itself a possible source of infection, as well as the rags which are used to cover the umbilicus in the first dressing. It is generally fatal, because of the weakness and lack of resistance of these little patients. It occurs usually within a week after birth, if at all.

Tetanus Cephalicus.

—Tetanus cephalicus, called also tetanus hydrophobicus and head tetanus, is only a peculiar manifestation of this same affection, confined mainly to the head and usually following injuries to this region. The muscle spasms are mostly confined to the facial, pharyngeal, and cervical muscles, sometimes extending to the abdominal. These manifestations may be reproduced in animals by inoculating them on the head rather than upon the extremities. It is the least fatal form of the disease.

Symptoms.

—There is always a period of incubation, usually three or four days, occasionally a week in length, but rarely longer.

It is generally held that the longer the period of incubation the more hopeful the prognosis. While for the great part the disease assumes an acute type, a chronic tetanus is described and occasionally seen. The first warning of the disease usually comes as more or less stiffness of the cervical and maxillary muscles, which is likely to be referred to by the patient as a “sore throat,” because of the consequent difficulty in deglutition. A complaint to this effect should be regarded as a warning, especially if on inspection no visible reason for it can be detected in the pharynx. This complaint is usually made in the morning after an ordinary night’s rest. This muscle stiffness will be followed by increasing tonic spasm in the muscles of the jaw, making it difficult to open the mouth, while the head and neck gradually become stiffened and fixed by spasm of the cervical muscles. These muscles may now be felt more or less rigidly contracted, as if by voluntary effort, and the condition, which is at first not painful, becomes after some hours a source of discomfort, perhaps of actual pain, to the patient. If the disease pursues the usual course, the other muscles of the body become gradually affected, usually in the order of their proximity, but not necessarily so. The abdominal muscles are firm and board-like, and the dorsal muscles more or less contracted, sometimes to an extent which causes arching of the spine. Should the original wound or port of entry for infectious germs have been in the hand or foot, the muscles of this limb become contracted, more or less rigidly, holding it in a position which is not easily changed, even by efforts of the attendant. Sensation is also often more or less perverted. In this condition of tonic rigidity the muscles remain, to relax usually only with death.

The most characteristic features of the disease, however, are the peculiar clonic exacerbations, which convert spastic rigidity into violent and convulsive muscle activity, so that the limbs and even the frame of the patient are more or less contorted, the muscle exertion being sometimes painful to witness. Notable effects are thus produced; the mouth is peculiarly puckered, and its corners drawn upward and backward by the risorius muscles, giving to the face that peculiar expression known as the “sardonic grin.” When the abdominal and flexor muscles of the thighs are involved, and the body is more or less curved forward, this condition is known as emprosthotonos; when the muscles of the back especially are involved, with the extensor muscles of the thighs, as opisthotonos; and when the body is bent to one side or to the other it is called pleurosthotonos. It is said that opisthotonic convulsions occur to such an extent in some instances that the heels touch the head. At all events, the patient’s body is frequently raised from the bed, so that he rests upon the head and feet.

Another characteristic feature of the disease is the reflex irritability, or hyperesthesia, by which these convulsive attacks apparently are produced. Into this condition the patient falls more or less rapidly within the first day after the inception of the disease, and to such a height may it be augmented that the slightest movement in the room, jarring of the bed, or displacement of clothing, even noise or a flash of light, may immediately bring on a convulsion. Rupture of muscles has been reported during some of these violent convulsions.

Fig. 18

Characteristic tetanic spasm in a rabbit twenty-six hours after inoculation with pure culture of tetanus bacilli. (Tizzoni and Cattani.)

During the course of this disease the jaws are so fixed that patients speak with extreme difficulty and the tongue cannot be protruded. The mind is clear until the end. The pain is rather the acute soreness due to intense muscle strain. There is spasm of the sphincters, by which urine and feces are often retained. There is nothing characteristic about the temperature, which is seldom much augmented. Attempts to swallow give pain, and are resisted because of the renewed muscle spasm which is likely to follow the irritation inseparable from the act itself. As the result of spasm of the glottis peculiar respiratory sounds may be noted.

Until the last only the voluntary muscles are involved. Finally, however, there are spasms of the accessory respiratory muscles and of the diaphragm. Death is usually produced by involvement of these muscles analogous to those of the others, and results usually from apnea or suffocation. During the last hour or two perspiration may be copious and the temperature may rise.

Chronic tetanus is characterized throughout by a milder and much more prolonged series of symptoms. The period of incubation is much longer, and, while the general program of the acute form is adhered to, it is of less severe degree and is spread over a longer time; in fact, cases covering two months or more are reported. In chronic tetanus the prognosis is much more hopeful than in the acute form.

The wound is but slightly, if at all, affected. In some cases it will be found to have healed before the onset of the disease. If suppurating or open, its evidences of repair will be found unsatisfactory and some indications of septic infection may be noted. Pricking or needle sensations may be subjective phenomena.

Prognosis.

—Prognosis is almost invariably bad; if patients live more than five or six days it is thereby improved.

Postmortem Appearances.

—These are rarely distinctive. In most instances there are evidences at least of hyperemia, if not of more active changes, in the upper portions of the cord. Less often slight changes have been noted in the brain, consisting, in some measure, of disintegration and softening. Evidences of ascending neuritis in the nerve trunks leading to the injured area have been claimed in some instances. Few if any distinctive postmortem changes can be described as due to this disease.

Diagnosis.

—The diagnosis should be made as between strychnine poisoning, hysteria, hydrophobia, tetany, and, in the beginning, from pharyngitis, tonsillitis, etc. When the disease is fully developed it is not likely to be mistaken for anything else.

Tetanus may be simulated by hysteria, but in this event the phenomena will be so uncertain, and the evidences of organic disease so essentially lacking, that it is not likely that mistake can occur.

Treatment.

—If any case can be imagined in which efficient treatment is most urgently demanded it is one of tetanus. In scarcely any disease, however, is drug treatment so unsatisfactory. In the rare instances in which patients have recovered it is questionable whether it is not due to individual resistance rather than to medication. Treatment may be subdivided into local, constitutional, and specific. If there is still an open suppurating or discharging wound, it is, of course, essential to cleanse this out, basing this advice in some measure upon general principles—largely upon the fact, already stated, that ordinarily only the immediate surroundings of such a wound are found infected by the bacilli themselves. Consequently thorough scraping, excising, and cauterization, either with powerful caustics or the actual cautery, are indicated. Since the specific germ is an anaërobe, hydrogen dioxide may be used locally with great advantage, mainly because it oxidizes the albuminous material upon which the bacilli thrive. If it is in a finger or toe, amputation may be the simplest method of eradicating the local lesions.

Constitutional treatment may be divided into nutrition and medication. The tendency too often in these cases is to be careless or indefinite with regard to the excretions and the nutrition of the patient. If, for instance, each attempt at catheterization throws him into convulsions, the bladder may become overdistended and burst. So, too, there is apprehension usually in regard to fecal evacuations. At the same time these patients are allowed to almost starve because of the difficulty of feeding them. It is advisable to resort to chloroform to permit the introduction of the stomach tube—through the nostrils, if necessary—by which nutrition may be introduced into the stomach without causing the violent convulsions that would occur without an anesthetic. At the same time the catheter may be used.

In the way of active medication there is no agent so efficacious for controlling the tetanic spasms as chloroform, which may be administered occasionally, or more or less continuously, according to the wishes of the attendant. By its use the severest spasms can be kept in abeyance, and the horrible character of the disease somewhat mitigated. Of the other medicaments used, most of them are of the nature of nerve sedatives, such as chloral, the bromides, Calabar bean, cannabis indica, opium, etc. Hot-air baths or diaphoretics, by which copious perspiration may be induced, have yielded good results.

Specific treatment means in these instances taking advantage of the well-known properties which the blood serum of an animal artificially immunized against the disease possesses. This is in accordance with experimental labors with a number of different diseases, of which tetanus is one. It is, in effect, similar to the serum therapy of diphtheria.

The most hopeful of remedies is antitoxin. More lives can be saved by this preparation, if used early and freely, than by any other known remedy. Moschcowitz, in 1900, collected 338 cases, with a mortality of 40 per cent. In many of these cases it was not used early. It is of importance, however, to use it at the very outset, and to repeat its use as soon or as often as may be indicated by any exacerbation of symptoms. In one instance under my observation twenty-three phials of antitoxin were used before muscle rigidity subsided; in another case double this amount was used. Without quoting figures it is safe to say that the former great mortality rate of tetanus has been reduced at least 50 per cent. by its use, and that further reduction can be effected by its early and prolonged use.

The use of antitoxin nowise takes away the necessity for proper physical care of the laceration or the wound. Every particle of affected tissue should be cut away, all the principles of physical cleanliness adhered to, and proper antiseptics used.

When the antitoxin is used in the presence of the disease it should be injected into the spinal canal, as it is known that the cerebrospinal fluid may contain a considerable amount of the toxin and is of itself highly poisonous. Therefore after inserting the needle into the canal it is well to withdraw a considerable amount of the fluid before injecting the antitoxin. If this method is pursued the material is brought into more immediate contact with the anterior horns of the cord than could be effected in any other way. After withdrawing all the fluid that will run through the needle without applying the syringe—probably 150 to 200 Gm.—10 to 15 Cc. of the antitoxin may be slowly injected, the process consuming from three to five minutes. Then a further injection should be made along some of the large nerve trunks, preferably those leading to the part involved. This injection should be made with a finer needle, such as that with which cocaine solution is injected during anesthesia for the prevention of shock. This is a more effective and less serious matter than trephining the skull for the injection of fluid upon the surface of the brain. This may be done while the patient is under the influence of the anesthetic administered for the purpose of giving proper attention to the wound. The antitoxin should be injected into the nerve trunks after their exposure. At the same time it is well to make intravenous saline injections at more than one point. After from twelve to fifteen hours the injection of antitoxin and perhaps of saline solution should be repeated, if necessary, under such light anesthesia as can be produced by ethyl chloride. Recently a substitute for antitoxin has been suggested in an emulsion of brain tissue which has been shown to have a specific affinity for the tetanus toxin. It has been seen that when these two substances have been thoroughly shaken together the toxin is removed from the fluid and confined in harmless form within the brain-tissue cells.

In injecting the antitoxin into the spinal canal no harm will ensue if a little blood flow through the needle, showing that the cord itself has been touched.

When there is need to employ this material the brain of a freshly killed small animal should be removed under antiseptic precautions. 10 Gm. or 15 Gm. should be emulsified in about 30 Cc. of sterile salt solution, which should then be strained through a sterile cloth under light pressure. This is then injected as near the wound as possible and the procedure repeated every day as long as indicated. This method can only be expected to neutralize toxin that has not yet entered the nerve cells. Nevertheless, Russian observers have reported thirteen recoveries out of sixteen instances in which the method was practised.

When no other means are at hand a 1 per cent. carbolic acid solution may be injected after the same fashion, using such an amount that about five grains are administered during twenty-four hours to an adult. This is the method especially favored by the Italians, and is due especially to Baccelli.

Matthews has devised a method which seems quite effective in experimental animals. It consists of the use of a solution of the following: Sodium chloride 4 Gm., sodium sulphate 10 Gm., sodium nitrate 3 Gm., calcium chloride 14 Cgm., water 1000 Cc. This is intended for intravenous injection, and must be introduced very slowly. The performance should be repeated twice during the first twenty-four hours and once each succeeding twenty-four hours. It produces profound diuresis, i. e., a washing out of tissue cells, as he calls it.

HYDROPHOBIA.

Hydrophobia is an acute specific or infectious disease, as far as known never originating in man, but transmitted to him, usually through the bite or by inoculation from the saliva of a rabid animal—in this country usually the dog, although the wolf, the cat, the skunk, and even certain of the domestic poultry, are capable of conveying the disease. Chickens are said to be immune save when their vital resistance is lowered by starvation. Chicken blood injected into other animals seems to antidote the virulence of the virus. It can also be inoculated in other animals, like rabbits. The virus is ordinarily conveyed in the saliva of the rabid animal. This may be wiped off as the teeth of the animal pass through the clothing of the injured individual; consequently, infection does not certainly follow such bites. But those upon exposed portions of the body, where animals generally bite, are almost invariably followed by infection. Hydrophobia is frequently spoken of as rabies, sometimes as lyssa. While rare in this country, it is by no means uncommon in Central Europe, especially perhaps in Russia, where bites from infuriated wolves are common. In the United States infection comes almost invariably from the rabid dog, in which this disease presents two types.

The so-called furious form is that which is marked by frenzy and canine madness, the objective symptoms being more pronounced and alarming, though not less dangerous than the other variety. After the period of incubation, which varies considerably, these animals show depression and uneasiness, and even thus early their saliva is infectious. Their sense of hunger becomes perverted; they exhibit unusual tastes, secrete saliva abundantly, which becomes very tenacious and even frothy, exhibit a dry and edematous condition of the faucial mucous membranes; the character of the bark is altered, while they are usually infuriated at the sight of other dogs. In this stage there is usually insensibility to pain. Finally, come more or less paralysis of deglutition, quickened respiration, dilated pupils, and frenzy and madness of manner, by which they attack indiscriminately men and other animals. To this stage of furious excitation succeeds one of paralysis, and death follows from exhaustion. These manifestations usually last about a week.

Dumb hydrophobia is the more common form. Here paralysis appears much earlier and involves especially the lower jaw; the tongue falls out of the mouth; and the posterior extremities are quickly paralyzed. This form is much more quickly fatal than the other.

Animals thought to have hydrophobia should be kept by themselves in a secure enclosure and carefully watched, especially those known to have bitten men or other animals. If a suspected dog have been killed before the suspicion has been confirmed, the head and upper part of the neck should be removed for examination. Veterinarians claim that what they call the plexiform ganglion permits an almost certain diagnosis to be made. The presence of foreign bodies in the stomach of the animal is a corroborative feature. Diagnosis by subdural inoculation requires two or three weeks, and in at least one case a human patient died while waiting for diagnosis to be thus established.

Hydrophobia in man is rare in this country, yet is occasionally observed. Its etiology is as yet obscure. That a contagion vivum is present is positive, but its nature is uncertain. Negri, of Pavia, has recently described certain bodies observed in the nervous system of animals dead of hydrophobia which may offer the solution of the problem that has so long been sought. They are found in the protoplasm of nerve cells, but not in their nuclei. They are round or oval in shape, vary in size from 25 microns down to those which can be barely seen with the highest powers. They take ordinary stains.

Negri maintains that these bodies are parasites and he has invariably failed to find them in animals which did not have rabies. His work has been confirmed by a number of his colleagues, and bids fair to furnish a reliable and rapid means of diagnosis. The fact that the virus of hydrophobia will pass through a porcelain filter nowise contradicts the view that these bodies may be parasitic, for it is quite possible that they undergo different stages of development, in some of which they are small enough to pass even barriers of porcelain.

In fact it seems to have been positively demonstrated that these bodies described by Negri, in 1903, are diagnostic for rabies. They are most likely to be found in the horns of Ammon or the cerebellum. When found here, careful examination must be made of the Gasserian ganglion, where may be found the lesions first described by Van Gehuchten and Nelis, which consist of a proliferation of the endothelial cells to such an extent that the ganglion cells are first invaded and then destroyed, their places being taken by the new cells.

The Negri bodies have been generally regarded as protozoa and the specific cause of the disease. At all events, it seems possible always to successfully reproduce the disease in rabbits or guinea-pigs by inoculation with these bodies.

If examination shows neither the Negri bodies nor the lesions in the ganglion the presence of the disease can scarcely be suspected, and could only be proved by animal inoculations, which, however, would be advisable in doubtful cases where human beings have been bitten.

Symptoms.

—The period of incubation in man is variable, ten weeks being perhaps the average. It is shorter in children, as also when the bites are numerous. It is even stated that it may be as long as a year or more, during which time the poison seems to lie latent. When the active symptoms supervene there are, locally, discomfort about the wound, itching, heat, and peculiar unpleasant sensations. It is said also that vesicles may make their appearance in the neighborhood of the original lesion. As in animals, so in man, the disease may assume either the furious or the paralytic type. These cases are nearly all marked by mental depression and apathy, with complete loss of courage. The earlier symptoms are connected perhaps with the respiration, which is infrequent, while inspiration is halting and speech is interfered with. The facial appearance is often changed to one of anxiety, even despair. The muscles of deglutition are next involved in a combination of spasm and paralysis, and the act of swallowing is interfered with, sometimes made almost impossible. Although patients can swallow their own saliva, they find it difficult to swallow any foreign substances, such as water, etc. This is not due to the fear of water, as the term “hydrophobia” would imply—this being an absolute misnomer—but is due to reflex spasm excited by the attempt. It is accompanied by more or less sense of suffocation and palpitation of the heart. Indeed, a paroxysm of this kind may be precipitated by the attempt to swallow, so that the patient instinctively refuses water or any other fluid. Reflex excitability is also very great, and a breath of air or a trifling disturbance may precipitate a paroxysm, almost as in extreme cases of tetanus. As the case progresses the saliva becomes more tenacious and viscid, faucial irritation more marked, and the attempts to expel the secretion, along with the disturbed respiratory efforts, have given rise to the foolish lay notion that these patients bark like dogs. The paroxysms, as the case progresses, become more marked, the patient more restless, until, later, furious mania or muttering delirium is present, to be followed by prostration and paralytic phenomena, muscle tremor, etc., and death.

The paralytic form in man, as in dogs, is marked by the much earlier paretic phenomena, anesthesia, and, finally, respiratory paralysis which terminates the case. Curtis and others have insisted that the hydrophobic paroxysms are not convulsions in the ordinary sense of the term, but are due to temporary inhibitions of the most important respiratory and cardiac centres as the result of peripheral impressions. He likens them to the shock of a shower bath.

Postmortem Changes.

—Postmortem changes are indistinct and only suggestive. They consist for the greater part of a sort of vacuolous degeneration of the ganglion cells of the nerve centres—most prominently in the medulla, next in the hemispheres, and then in the spinal cord. There is hyperemia, with minute ecchymoses, with infiltration of the adventitia of the vessels and perivascular extravasation. The changes met with in the other viscera bear no constant relation to symptoms. Nevertheless, Gowers holds that because of the location of the lesions and their intensity in the neighborhood of certain nerve nuclei we have here a distinguishing anatomical character of the disease.

The toxin (as we may call it for the lack of a better term) seems to be transmitted much as is that of [tetanus] (q. v.), along the afferent nerves to the cells of the anterior horns of the cord.

Diagnosis.

—As between hydrophobia and tetanus diagnosis is not difficult, as already described. In certain hysterical individuals nervous paroxysms, largely due to fright, may be precipitated by dog-bites and other incidents or accidents. In these cases there is rarely such a period of incubation, and in a true hysterical case there will be no such mimicry of this awful disease. A condition known as lyssophobia (fear of hydrophobia) has been described. It is seen in hysterical subjects. It is said to have even been fatal, but this must have been from other complications.

Treatment.

—There is no authenticated case on record of recovery after medication by drugs. It is probable that recovery has never followed anything but the modern inoculation treatment.

The only successful treatment for this disease has been elaborated as the result of the labors of that indefatigable French savant, Pasteur, and is among the glorious triumphs of laboratory research, against which it is so often charged that it is not practical in its results. It is in some respects a curious commentary on the study of infectious disease that we can secure and work with the peculiar virus of hydrophobia, and at the same time be utterly unacquainted with its true character. To this fact is due the modern cure. It is based upon the fact that the virus is not only in the saliva, but also in the nervous system of animals suffering from this disease, and that its effects are intensified and hastened by inoculation directly into the cerebral substance. Accordingly, when a diagnosis of hydrophobia can be reasonably well established, no time should be lost in sending the patient to one of the “Pasteur Institutes,” to be found now in most of the great centres, there to undergo a regular course of treatment. It was reported that in the Institute in Paris, between the years 1886 to 1894, there were treated a total of 13,817 cases, and that the mortality was 0.05 per cent. Of course but a small proportion of these really had or would have developed the disease.

Virus obtained from the brain or cord and inoculated into the dura of another animal quickly precipitates the disease. It is, moreover, modified in virulence as it passes through successive animals of certain species—for example, monkeys. It is increased by passage through rabbits, and the period of incubation thereby shortened. The weakest virus can by proper handling and manipulation in this way be so intensified as to produce disease within seven days after inoculation. Desiccation reduces the virulence, and preparations from the cord of an infected animal may be attenuated to almost any desired extent by drying. By inoculating a dog or a rabbit with virus prepared from this weakened source, and daily making injections from stronger and stronger preparations, it is in the course of a couple of weeks rendered practically immune to the disease. Animals thus made immune are trephined and the virus injected beneath the dura, by which more certain results are obtained. The treatment consists in using a section of a rabbit’s spinal cord, 0.5 Cm. in length, rubbed up in 6 Cc. of sterile salt solution. Half of this amount is injected each day into the flank of the patient. The cord first used is one that is thirteen or fourteen days old, which has been kept suspended in a sterile flask, over caustic potash, in order to assist in its desiccation. The next day a cord one day younger is used, and so on until by the twelfth day of treatment the cord is one only two days old, and at the end of two weeks a fresh cord can be used which would convey the disease had it been used first. If this course of treatment can be carried through before the first symptoms of the disease appear, the antidote has gained complete mastery over the infecting agent and the patient is saved.

GLANDERS AND FARCY.

Glanders as it is known in man is a specific infectious disease, transmitted usually from the horse, characterized by rapid formation of specific granulomas, particularly in the skin and mucous membranes, which quickly break down into ulcers, and by the general toxemia characteristic of any acute infection. In German it is known as Rotz, in French as morve, while its old Latin name was “malleus” (hence we speak of the bacillus mallei). It was also known in former days as equinia. In horses the disease has also been known as farcy, because of the peculiar subcutaneous nodules which farriers and hostlers, almost from time immemorial, have called “farcy buds.” The disease, while capable of transmission from man to man, is generally produced by contagion from some of the domestic animals, most commonly the horse, although sheep and goats are known to occasionally have it, and dogs are susceptible, though seldom showing manifestations of it.

Like some of the other infectious diseases glanders appears to be variable in its manifestations. While infection occurs probably through some superficial abrasion, it is almost certain that it may also occur through the unbroken mucous membrane of the respiratory organs. It is said to be also capable of transmission from mother to fetus in utero. So far as known in man, infection occurs practically invariably through some slight abrasion, either of the skin or the mucous membrane of the nose, the eye, or the mouth. The discharges from the nostrils of affected animals are extremely virulent, and infection comes usually from this source. It is said to have been communicated from one patient to another by eating from the same dish or by drinking from a pail used by a diseased horse.

Glanders is due to the specific bacillus known as the bacillus mallei. It is shorter and plumper than the tubercle bacillus, in length about one-third the diameter of a red corpuscle. It is a non-motile organism, occasionally spore-bearing, not very resistant, belonging to the facultative anaërobic forms, growing best at blood temperature, taking stains easily, and losing them in the same way.

Symptoms.

—Glanders is seen usually in workers and hangers-on in stables. The acute—the common—form has a period of incubation of from three to seven or eight days, after which both local and general symptoms supervene. About the infected region a form of cellulitis appears, assuming often a more or less phlegmonous type, with implication of the adjacent lymphatic nodes and evidences of periphlebitis and perilymphangitis. Over the affected area vesicles appear, which become hemorrhagic and later suppurate. A wound which has healed may reopen. Almost always there are accompanying constitutional disturbances of septic type, occasionally chills, pyrexia, etc. It is rather characteristic of glanders to have severe pain in the muscles and extremities, with epistaxis and formation of metastatic tumors and edematous swellings in various parts of the body. Frequently, later in the disease, appears a somewhat distinctive eruption, papular in character, merging into pustular. Hemorrhagic bullæ are also often seen. Pustulation and edema of the face change its appearance. There are also edema of the eyelids and mucopurulent discharge from the conjunctivæ and the nose. This latter discharge is often ozenous in character. Upon inspection of the nasopharynx and oropharynx a similar condition will be noted. In connection with these local signs more or less general furunculosis also will be observed. Obviously, as these local conditions intensify and multiply, septic disturbance will be increased, and the patient dying of acute glanders dies generally of septicemia or intoxication and exhaustion combined.

A chronic form is known, distinguished mainly by slowness or tardiness of lesions, though the local changes are not particularly different in character. There is perhaps more tendency to suppuration and less to lymphatic complications. The nodule which breaks down will leave a foul ulcer, the discharge from these lesions being extremely infectious.

Diagnosis.

—This is not always easy, but may be based in suspicious cases to some extent upon the occupation of the patient. The presence of multiple lymphatic lesions and subcutaneous nodes, especially when breaking down as above described, and accompanied by ozenous discharge from the nose, should at least be suggestive, and will serve to distinguish between this disease and, for instance, typhoid fever. The chronic type of glanders might be mistaken for syphilis, and here is where the real difficulty of diagnosis will probably occur. In doubtful cases the crucial tests are the microscopic examination of discharges, after staining for bacilli, and the cultivation test.

Prognosis.

—A generalized attack of glanders is a matter of gravest import, especially when acute. Scarcely more than 10 or 15 per cent. of such cases recover. In the more chronic manifestations the prognosis is more favorable, half of the patients making a final recovery.

Treatment.

—All infected animals should be isolated and destroyed, their carcasses being burned. If possible, the infected wound or abrasion should be induced to bleed freely, and then cauterized with an active caustic. By prompt interference with the first manifestations it may be possible to cut short the disease. This would necessarily be done by excision, cauterization, packing, etc. Bayard Holmes has reported a case in which, during two and a half years of chronic manifestations of this disease, he anesthetized the patient twenty times for the purpose of opening new foci or scraping out old ones, finally obtaining a permanent cure. There is no specific treatment, but the septic symptoms should be combated as indicated in the chapter on Septicemia.

By making a glycerin extract from the filtered and evaporated culture of the glanders bacillus it is possible to prepare a toxalbumin analogous to tuberculin, which reacts in a similar way. By it animals may be fortified against inoculation, and by its use a peculiar reaction is produced in those affected by the disease. It is known as mallein, and by it are tested all horses used for the preparation of the diphtheria antitoxin, in order that all possibility of glanders may be eliminated. It is probable that it might be made of therapeutic value in treating the disease when actively present in man.

ANTHRAX.

Anthrax is more commonly known as splenic fever, malignant pustule, or woolsorters’ disease; in Germany as Milzbrand, and in France as charbon. It is an infectious disease of cattle, which has devastated many parts of Central Europe, and has been frequently met with on the Continent among men, though but rarely in the United States. All the domestic and nearly all the experimental animals are subject to it. Gronin has stated that in the district of Novgorod, in Russia, during four years more than 56,000 cattle and 528 men perished from anthrax. Poultry and dogs are not strictly immune, but possess a low susceptibility to the disease. It generally prevails in low districts and in marshy grounds.

The disease is the result of the invasion of the bacillus anthracis, which is a relatively large-sized bacillus, varying in breadth from 1 to 1¹⁄₂ and in length from 5 to 20 microns. It is easily cultivated outside the body, and multiplies with great rapidity in the bodies of susceptible animals; it is the type of spore-bearing bacilli, and is so readily recognized and worked with that it is commonly used in laboratory investigations. The demonstration of its specificity we owe to Davaine, in 1873, although he had described it in 1850.

PLATE IV

FIG. 1

Anthrax Bacilli. Spore Formation. (Karg and Schmorl.)

From an agar culture twenty-four hours old. About the margin of the photograph are a number of free spores, × 600.

FIG. 2

Anthrax Pustule. Removed from Arm of Man. (Karg and Schmorl.)

Marked edema of the skin, causing elevation and separation of the papillæ. In the edematous exudate a large number of anthrax bacilli and leukocytes. × 50.

Anthrax bacilli may enter the body through the respiratory organs, through any abraded surface, and possibly even through the alimentary canal. They may also pass through the placenta and affect the fetus in utero. They are too large to pass through the walls of the capillaries of ordinary size; consequently they plug them and produce a mechanical stasis which is rapidly followed by gangrene. From the kidney structures and capillaries, however, they may escape, as bacilli are found in the urine in certain cases of anthrax. (See [Plate IV].)

In man the disease occurs usually as the so-called malignant pustule, or woolsorters’ disease, the latter name being given because of the liability of those individuals who come in contact with the carcasses and hides of diseased animals or their immediate products. The period of incubation is brief—on the average two or three days. The first lesion appears usually on the face, hands, or arms, and is characterized by local discomfort with formation of a small papule, which rapidly becomes a vesicle with an areola of cellulitis about it. This is rapidly followed by induration and infiltration, and these by local gangrene, the result being the separation of a core-like mass, similar to that of carbuncle. The affected area is usually discolored, often quite black. The process is not usually accompanied by suppuration, nor is there the pain of true carbuncle. The lesions tend to spread peripherally, but there is more or less vesication of the surrounding skin. On account of the local ischemia there will always be edema of the affected region, and sometimes the swelling and local disturbance become extreme. These peculiar lesions have given rise to the common name malignant pustule, which is well deserved. At last a line of demarcation becomes manifest, and if the disease progresses favorably the included area is sloughed out, leaving a surface which it is hoped will soon become covered with reasonably healthy granulations.

Absence of pain, and usually of pus, are significant features of anthrax. Should mixed infection occur, however, we are likely to see pus formation. When the disease partakes less of the characteristics of malignant pustule and more of a general infection, the local symptoms may not predominate, but, on the contrary, septic indications may become serious and even fatal. The evidence of more or less toxemia is usually at hand, however, and the toxin of anthrax is almost as destructive of muscle cell integrity as is that of diphtheria.

The local lesions may be single or multiple, but will be met with almost always upon exposed areas of the body.

Postmortem Appearances.

—These will depend upon the clinical course of the disease. In the sloughing tissues the bacilli are very numerous, while around the margin more than one bacterial form will probably be met—i. e., mixed infection. Should saprophytic organisms complicate the case, they may have replaced the anthrax bacilli by the time the examination is made. The latter abound, however, in the blood, and may usually be found occluding the capillaries of the liver, spleen, kidney, etc. In intestinal infection, particularly in animals, the mesenteric nodes are involved. Inasmuch as septic features accompany all fatal cases, putrefaction will be found to begin early, and the changes in the blood and the gross changes in the other organs will resemble sepsis rather than anthrax.

Prognosis.

—Prognosis for man is not usually unfavorable, the majority of cases recovering with more or less local destruction of tissue. Should, however, infection become generalized, the case will probably terminate fatally. Cases assuming the type of splenic fever are of much more serious character, and their prognosis graver.

Treatment.

—This should be both local and constitutional. The former should consist of the most radical possible attack and include complete excision of the infected area, with the use of active caustics or the actual cautery. In fact, the latter instrument offers a most valuable means for combating the destructive tendency of the disease. Sloughing and separation of the cauterized mass may be hastened by warm antiseptic poultices. Subcutaneous injections of 5 per cent. carbolic solution have been given, with apparent benefit, in a number of cases, but should only be relied upon in the treatment of the milder manifestations.

Benefit will accrue from the use of the ichthyol-mercurial ointment whose formula was given under treatment of Erysipelas. It has been suggested to treat these cases by the employment of the bacillus pyocyaneus, since it is known that this organism when injected with the anthrax bacillus materially attenuates its effect.

Prophylaxis.

—Prophylaxis is most important. The bodies of all infected animals should be burned, not buried, since the resistant bacilli are often brought to the surface of the soil by earth-worms. Every discoverable source or medium of infection should be destroyed or sterilized.

MALIGNANT EDEMA.

This disease has been recognized for some time, mainly by French and Continental clinicians, and under such names as gangrène foudroyante, gangrène gazeuse, gangrenous septicemia, and gangrenous emphysema. The name malignant edema was given by Koch, who identified the infecting organism. It is one of the most dangerous forms of gangrenous inflammation, and occurs sometimes after serious injuries, and, again, after most trifling lesions, such as those inflicted by the dirty pointed implements of the gardener, etc., or even the stings of insects. Two cases are on record where the disease followed a puncture of the hypodermic needle for the administration of morphine. In one of these the organism was found in the solution; in the other it probably had been deposited upon the skin.

Malignant edema is essentially a specific form of gangrene (see [Chapter V]), and is mentioned here rather because of its specific character. It is characterized by rapidity of spread and the specific nature of the exudate, as well as by the speedy destruction of the tissue involved, and by more or less gas formation. It is not the same as the gaseous phlegmons described by some German surgeons, yet partakes of their general character. Gas phlegmons have been rarely noted, their peculiarity being formation not only of pus, but of more or less offensive gases, which escape when the phlegmon is incised. The gases are mainly due to the presence of bacillus aërogenes capsulatus, and gas phlegmons, as such, are to be regarded as instances of mixed or rarely pure infection.

Malignant edema is known by the brownish discoloration of the overlying skin, which is streaked with blue where the overfilled veins show through it, while the underlying tissues are sodden with fluid and more or less inflated by the gaseous products of decomposition, so that the finger detects a firm crepitus, as is common in subcutaneous emphysema. From the wound, if there is one, flows a thin, foul-smelling secretion, which may also be expressed from the deeper layers. That the neighboring lymph spaces and nodes are actively involved is evident from the enormous swelling of the latter, as well as from the general condition of the patient. The rapid elevation of temperature with but trifling remissions remains constant until shortly before death. The tongue early becomes dry and cleaves to the palate, its surface being covered with a thick, foul fur. Patients early become apathetic, complaining only of pain and burning thirst. Delirium and coma usually precede death, which may occur in fifteen to thirty hours. After death the cadaver bloats quickly and putrefaction goes on with amazing rapidity.

Postmortem Appearances.

—At the seat of the lesion even muscles and tendons will be found macerated, bone denuded and surrounded by a putrid fluid, the entire region presenting a notable swelling and infiltration of soft parts with reddish fluids and stinking gases. The overlying skin will be stretched, and superficial blisters may deepen the intensity of the process. The veins are clogged with decomposed blood and broken-down thrombi, and in the heart and large vessels will be found putrid liquid as well as gas, to whose presence early and sudden death is probably due.

Prognosis.

—This is unsatisfactory, especially when the bacillus of malignant edema is alone at fault. Patients may escape with their lives, but always at the expense of more or less tissue destruction.

Treatment.

—This should consist of extensive incision to permit escape of fluids and gases and relieve tension; of such antiseptic applications as can be made available; of immersion of the affected part in a hot antiseptic bath; and of such vigorous stimulation by the most powerful measures—strychnine, alcohol, etc.—in order to support the patient through the period of profound depression characteristic of the disease.

PLATE V

Actinomycosis. Ray Fungus in Man. (Gaylord.)

ACTINOMYCOSIS.

This also is a subacute but always destructive infection by a specific microörganism, though not a bacterium. Known always as actinomycosis in man, the disease, which is most common in cattle, is called lumpy jaw or swelled head, and years ago was usually regarded as cancer or as a malignant affection.

Many museum specimens labelled as cancer of the tongue, jaw, etc., have been shown to be instances of actinomycosis of these parts. It is occasionally met with in man, so that there are at least four hundred cases on record in this country and in Europe. The organism was recognized a half-century ago by Langenbeck and Lebert, but was not scientifically described until many years later. The names of Bollinger, Israel, and Ponfick will always be connected with these researches.

The organism belongs among the ray fungi, is known as the actinomycis, and occupies an uncertain place in classification. It is large enough, when entire, to be perceived by the naked eye, has ordinarily a yellowish tint, a tallowy consistence, and may be seen under the microscope to consist of a cluster of branching prolongations, club-shaped at the end, radiating from a common centre. They give it a sunflower appearance. It is stained with difficulty, the best stain being a combination of picrocarmine and an aniline dye. In tissue sections the Gram stain is the best. It is cultivated with difficulty, but can be grown upon solid media and may be inoculated. (See [Plate V].)

As met with in tissue or in pus these fungi constitute small granulations, giving usually a gritty sensation to the finger, which is due to the presence of calcium salts. The recognition of this calcareous material is of importance, since it may enable a diagnosis to be made offhand, in a case which otherwise might puzzle one.

The disease is very common among cattle in certain regions, and causes the condemnation of many animals in every large stockyard establishment where inspection is careful and scientific. It occurs oftener in young than in old animals, and most frequently in those which come from valley regions and marshes. In animals infection occurs almost invariably through the mouth, which is easily explained by the fact that, in grazing, the lips, tongue, and gums are likely to be irritated and infected at any time from soil containing these fungi along with growing grain. The path of infection is usually by the mouth, while accident seems to determine whether the infection shall manifest itself mainly in the intestinal canal or the respiratory tract. In animals there is less tendency to suppuration than in man, the infection in man being usually a mixed one. The name lumpy jaw, so generally given to the affection, is indicative of the most conspicuous lesion in cattle, for the organism, having once invaded the gum, for instance, passes quickly to the bone, or, having involved the tongue, is not slow to infect the lymphatics of that region. In consequence we have tumors, often of inordinate size, which may involve the bones or the soft parts and cause great disfigurement, along with necrosis, leading eventually to the death of the animal. These tumors are essentially granulation tumors due to the presence of a specific irritant—the actinomycis—which acts here as do the tubercle bacillus, the lepra bacillus, etc., in other infectious granulomata.

In man the disease is generally accompanied by abscess formation, the pus containing the distinctive yellow gritty particles which are found in no other disease. The strong resemblance between the lymphoid cells of this form of granuloma and the embryonal cells of sarcoma has permitted the perpetuation of confusion between these two neoplasms.

Fig. 19

Actinomycosis in man. (Lexer.)

Large abscesses form as the result of the coalescence of small ones, and by the time the disease is recognized extensive destruction and loss of substance may have taken place. In man it is not alone about the mouth that the disease is noted, although primary lesion here is by no means infrequent. It leads to affections similar to that already spoken of in cattle, with a progressive infiltration and breaking down, including actual necrosis of bone, etc. The pus will escape at various points, and may give to the surface an appearance as of many craters with a central cause. When the disease has involved the lung, either directly or indirectly, the fungi and the calcareous particles may be found in the sputum. Should there be suspicion of this involvement, the sputum should always be examined. Even in the heart substance tumors of this same character have been found. The first case noted in man had undergone extensive vertebral caries. Intestinal infection is possible, in which case multiple lesions will form in the intestinal walls, which may contract adhesions to the abdominal parietes and discharge externally through them. The appendix has been found involved in such lesions. Infection of the skin has also been described, though this occurs more rarely.

Diagnosis.

—Actinomycotic lesions have been mistaken for cancer, sarcoma, tuberculosis, syphilis, etc. In man it will always be characterized by more or less suppuration, and in the purulent discharge from the infected focus the yellow calcareous particles should enable recognition of this disease at once.

Prognosis.

—As long as the focus is accessible it is a purely local matter, and prognosis is as favorable as in local tuberculosis; but, inasmuch as in many cases infection has proceeded to a point where the surgeon cannot safely follow it, prognosis must be guarded. Actinomycosis is free from acute manifestations, for the main part free from pain, pursues a chronic course, and is characterized, as are the other slow infections, by progressive emaciation, prostration, etc. As it is essentially a chronic condition, time is afforded for careful study in doubtful cases, for microscopic examination, etc.

Treatment.

—This must consist of extirpation of all infected tissues and areas. If this can be done thoroughly there is a prospect of positive cure. Free incision, wide dissection, the use of the actual cautery, etc., are always called for in these cases. If it involves the tongue alone, there is an excellent prospect; if but a portion of the jaw is involved, a complete excision of one-half or more may be followed by excellent results. If, however, the lung, liver, vertebrae, or other vital and inaccessible parts are involved, surgical measures may afford amelioration, but can hardly be expected to cure.

Iodine, alone or in combination, has been found efficacious in the therapy of actinomycosis. In diluted solutions used locally, or as potassium iodide given internally or injected into tumors, it doubtless has a beneficial effect during the period of its administration. Recent reports and experiences show that great value attaches to the use, as suggested by Bevan, of copper sulphate in the treatment of actinomycosis, its use having been suggested by the fact that copper is used to destroy rusts (fungi) on grain. One-half grain (3 Cg.) may be given internally three times a day, while the sinuses are irrigated with a 1 per cent. solution. I have seen apparently complete cure of an aggravated case follow its use. Incidentally it may be stated that Bevan advises its use also in cases of blastomycosis.

MADURA FOOT.

While madura foot is not a disease from which domestic animals suffer, its general characteristics make it a proper subject for brief consideration. It is essentially a disease of the tropics and subtropics, and is often seen in some of our new possessions.

It commences as a painless swelling upon either aspect of the foot, in which hard nodules form, which later soften, ulcerate, and discharge puruloid material containing granules in which the microscope reveals mycelia of the peculiar fungus that produces the disease. In some cases these particles are black, in others colorless. The disease is of slow progress, and the lower limbs become weak, atrophied, and finally useless Death results from exhaustion or some terminal infection.

The principal lesion is the slowly growing gumma or granuloma, whose presence is unmistakable. This is due to the presence of a fungus, called by Vincent the streptothrix maduræ. Thus in its pathology the disease much resembles actinomycosis. The habitually bare feet of most of the inhabitants of the tropics and the habitat of the fungus explain the site of the primary lesion.

Treatment.

—The only treatment is extirpation of the growth—i. e., amputation.

PLATE VI

Tuberculosis of Testicle.

Miliary Tubercle with Caseation and Giant Cells. (Gaylord and Aschoff.)
a, seminal tubules; b, giant cells; c, caseated tubercles.