=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.

[Illustration: 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.

[Illustration: 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.

[Illustration: 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.)