The toxic group of causes is closely allied to the chemical variety of

the traumatic agencies. It includes chemicals whose action is

indirect, through absorption in a diluted form rather than from direct

application in a concentrated condition. Such chemicals are derived

from without, as arsenic, phosphorus, and antimony; or may be formed

within the body, and the latter include the chemical products of

putrefactive changes--in the urine, for instance--and, with

considerable probability, certain of the active agents of

blood-poisoning in septic diseases. It is not unlikely that some of

the inflammatory affections met with among the so-called

constitutional diseases, as rheumatism and gout, may owe their origin

to the production of chemical substances within the body, excessive in

quantity if not changed in quality.

{45} The parasitic causes of inflammation are both animal and

vegetable, and act upon the surfaces of the body or within its

deeply-seated parts. Some of the animal parasites act locally at their

place of entrance, while others produce but slight disturbances in

this region, their effects usually resulting from the transfer of

their offspring to remote parts of the body. The vegetable parasites

are for the most part the various fungi, which act locally upon the

skin or on those transitional surfaces lying between skin and mucous

membrane. The resulting parasitic inflammations are known as favus,

sycosis, ringworm, thrush, etc. The border-line between such parasitic

diseases and those included among the infective diseases is somewhat

arbitrarily drawn. Parasites in the limited sense act chiefly as

foreign bodies, while the effect of minute vegetable organisms is

rather that of ferments, in virtue of their products. Such a

distinction is of relative value merely, as the micrococci and

bacteria are capable of acting in other ways than by the production of

septic material.

The infectious causes of inflammation are for the most part parasitic

in their nature, although the discovery and identification of the

parasite are in most of these inflammations assumed rather than

demonstrated. The relation of the anthrax bacillus to malignant

pustule no longer admits of a doubt, mainly in consequence of the

researches of Koch. This investigator has been enabled to establish a

definite etiological relation between the septicæmia of certain

animals and accompanying minute vegetable organisms. His recent

discovery of the bacillus of tuberculosis definitely removes the

tubercular process from the group of dyscrasic or constitutional

affections to that of the infective diseases. The constant presence of

minute organisms in relapsing fever, leprosy, malaria, typhoid fever,

diphtheria, erysipelas, and numerous other affections associated with,

if not characterized by, inflammatory conditions, renders extremely

probable the closest pathological relation between such diseases and a

microscopic organism. That an inflammatory process may be regarded of

infectious origin, it is necessary, according to Koch,[14] that a

characteristic organism should be found in all cases of the disease,

and in such numbers and distribution as to account for all the

phenomena of the disease in question.

[Footnote 14: _Untersuchungen über die Aetiologie der

Wundinfectionskrankheiten_, 1878, 27.]

These organisms may act in virtue of their growth and the consequent

demand for oxygen, as seems probable in certain cases of malignant

pustule, where the affected individual dies with symptoms of asphyxia.

Their operation may also be like that of ferments, which produce

chemical material whose effect may be remote from the immediate

presence of the minute organism. They may likewise, in connection with

their colonization in various parts of the body, act more immediately

upon the walls of the blood-vessels, and produce that increased

porosity which is so essential a factor in inflammation.

The discovery of the immediate cause of the various infective

diseases, as measles, scarlatina, variola, cholera, dysentery, mumps,

whooping cough, cerebro-spinal meningitis, and numerous other epidemic

and endemic affections, still remains a question for the future. The

constant association of microbia with any or all of such diseases is

but one fact in connection with them, and such a discovery is to be

regarded merely as a step forward, to be followed by others, each of

which represents not only an advance, but confirms the position

attained.

{46} The dyscrasic or constitutional causes of inflammation are those

which, though long established, appear less demanded as our knowledge

advances. Regarded as the result of an alteration in the composition

of the blood, it is obvious that such changes may arise from the

introduction, from without, of wholly foreign material. The dyscrasia

may also represent modifications in the relative proportion of the

normal constituents of the blood. In the former series are included

what, for the most part, have already been referred to under the toxic

and infectious causes of inflammation. The dyscrasiæ from lead,

alcohol, and the like belong to this series. Still more important are

the poisons, the virus of tuberculosis and scrofula, of leprosy and

syphilis. The dyscrasiæ known as anæmia, leucæmia, uræmia, icterus,

and diabetes are to be regarded less as inflammatory causes than as

predisposing conditions which favor the action of other groups of

causes.

The trophic causes of inflammation are those whose action is supposed

to take place through the influence of nerves. Although, as has

already been stated, a faulty innervation of tissues is an important

element in favoring the action of various inflammatory causes, there

remain certain forms of inflammation where the disturbance of nervous

action seems to be the essential feature. The occurrence of an acute

peripheral gangrene soon after certain traumatic or inflammatory

lesions of the brain or spinal cord, of articular inflammation

following chronic affections of the cerebro-spinal axis, are instances

in point. The origin and distribution of herpes zoster, the occurrence

of sympathetic ophthalmia and symmetrical gangrene, suggest a

predominant disturbance of innervation as the exciting cause. At the

same time, it is desirable to call attention to the recent

observations of MacGillavray, Leber, and others,[15] which suggest

that a sympathetic ophthalmia is due to the extension of a septic

choroiditis along the lymph-spaces of the optic nerve. It is further

apparent that in certain so-called trophic inflammations, as the

pneumonia after section of the pneumogastric, and the inflammation of

the eye following paralysis of the trigeminus, the paralysis of the

nerve is a remote, rather than an immediate cause, of the

inflammation. There still remain, however, a number of localized

inflammations whose origin is so intimately connected with nervous

disturbances as to demand, for the present at least, a corresponding

classification.

[Footnote 15: Wadsworth's "Report of Recent Progress in

Ophthalmology," _Boston Medical and Surgical Journal_, 1882, cvi.

517.]

The course of an inflammation is often indicated by the predominance

of certain symptoms, which, for the most part, indicate a condition of

the individual acted upon rather than a peculiarity of the cause. The

sthenic inflammations take place in robust individuals with powerful

hearts and an abundant supply of blood. In such persons a strong

pulse, high fever, and an injection of the superficial blood-vessels

suggested, in former times, the necessity of bloodletting as the

essential therapeutic agent. The sthenic form of inflammation was most

commonly associated with pneumonia, where the obstruction to the

passage of blood through the lungs was an important cause of the

superficial injection of the blood-vessels.

The asthenic inflammations, on the contrary, are those occurring in

feeble individuals, debilitated in consequence of pre-existing

disease, exposure, or habits. A weak heart, low febrile temperature,

and {47} superficial pallor, characterize the asthenic inflammations,

which show a frequent tendency to become localized in the more

dependent parts of the body, the force of the circulation being too

feeble to overcome the effect of gravitation.

In the typhoidal inflammations are associated those symptoms which are

so prominent in the severe varieties of typhoid fever. These are the

predominant symptoms: hebetude or low, muttering delirium, picking at

the bed-clothes, involuntary evacuations, stertor, and the like. The

nervous disturbances are associated with a feeble pulse and a dusky

hue of the skin.

The constituents of an inflammatory exudation are frequently used as a

basis of classification, and characterize the inflammation from the

anatomical point of view. As the exudation is complex in its

composition, the predominant element is made use of to designate the

variety, and in doubtful cases a combined adjective indicates the

presence of the two most abundant constituents. As the exudation is

directly derived from the blood and contains serum in addition to

white and red corpuscles, the serous, purulent, and hemorrhagic

varieties of exudation naturally arise. The fibrinous and diphtheritic

inflammations relate to the presence of membranes or false membranes.

Finally, there are the productive inflammations, resulting in the new

formation of tissue, and the destructive inflammations, where losses

of substance occur.

Serous inflammations are most frequent in those parts of the body

where the structure contains the largest lymph-spaces. The so-called

serous cavities of the body offer the most favorable opportunities for

the accumulation, as well as for the exudation, of the inflammatory

product; then follow the regions of the larger lymph-spaces, according

to the size and number of the latter.

The serous inflammations may also arise from the epithelial coverings

of the body, as the cutaneous, alimentary, and respiratory surfaces.

The serous exudations of the skin are those present in vesicles,

blisters, or bullæ, which owe their limitation to the resistance

offered to the spreading of the liquid inflammatory product by the

coherent epidermis. Serous inflammations of the alimentary canal may

assume a vesicular character, although, from the structure of its

mucous membrane and the macerating influence of its contents, the

vesicles are apt to be of an extremely transitory character.

The more important serous inflammations of the intestines are those

manifested by profuse watery evacuations, the extreme form of which is

to be found in cholera.

Serous inflammation of the lungs accompanies the more severe forms,

and usually represents but a limited and circumscribed affection,

associated with more abundant cellular and fibrinous products.

Serous inflammations of the peritoneum, pleura, pericardium, tunica

vaginalis, and central ventricles often give rise to the presence of

enormous quantities of fluid, whose partial removal from many of the

cavities concerned by operative measures frequently represents a most

beneficial result of treatment.

The smaller lymph-spaces of the connective tissue in various parts of

the body are the frequent seat of the inflammatory oedema, so called,

whose presence is an important indication of the direction assumed by

a {48} spreading inflammation, as well as a suggestion of the frequent

virulence of its cause.

In general, the serous inflammations are to be regarded as less severe

than other varieties, or as representing an early stage of what later

may be otherwise characterized by a change in the nature of the

products.

The purulent variety of inflammation is present when the exudation is

abundantly cellular. As has already been stated, such cells are, for

the most part, white blood-corpuscles. The purulent exudation, like

the serous variety, may appear either on surfaces, when the term

secretion is applied, or within the lymph-spaces of the connective

tissue over a considerable space, when the pus is said to be

infiltrated. When the infiltration is more circumscribed and the walls

of the affected lymph-spaces are destroyed, so that adjoining cavities

are thrown into larger holes, an abscess is present, from whose wall

pus is constantly derived, while the inflammation is progressive.

The attention of the surgeon, in particular, has been directed to the

isolation of the immediate cause of suppurative inflammation, and the

modern, antiseptic, treatment of wounds is essentially based upon the

view of the infectious origin of pus. The frequent presence of

microbia in purulent exudation where no precautions are taken to

exclude their admission, and their frequent absence or presence in

minute quantities where such precautions are taken, have suggested

that through their influence an inflammatory exudation is likely, if

not actually compelled, to become purulent.

Whether the microbia or their products are the cause of most

suppurative inflammations may be regarded as an open question. It is

generally admitted, however, that, as a rule, an inflammation becomes

purulent in consequence of the presence of an infective agent; in

other words, that most pus is of an infectious origin and possesses

infectious attributes. The labors of Lister in insisting upon the

exclusion of all possible putrefactive agencies in the treatment of

wounds have met with universal approval, and the basis of his

treatment remains fixed, although different methods have been devised

for its enforcement. His researches, and those stimulated by his work,

have resulted in the establishment of principles which affect the

whole field of theoretical as well as practical medicine.

Although most pus may be considered as due to the action of a virus

introduced from without, and capable of indefinite progressive

increase within the body, all pus is not to be regarded as of

infectious origin. There are pyrogenetic agencies, like petroleum,

turpentine, and croton oil, which, introduced into the body, produce

suppurative inflammation without the association of microbia.

A bland pus is usually in a state of beginning putrescence, so that it

is only relatively bland, and acquires extreme virulence when long

exposed to putrefactive agencies. It is possible that those agencies

producing an ichorous pus are the same or different from those present

in bland pus. The ichorous exudation contains less corpuscles than

bland pus, is more fluid, less opaque, strongly alkaline, of a

greenish color, and of offensive odor.

In hemorrhagic inflammation the exudation contains large numbers of

red blood-corpuscles. The occurrence of this form is sometimes

associated {49} with peculiarities of the cause, as is obvious from

the epidemics of hemorrhagic small-pox, measles, scarlatina, and

cerebro-spinal meningitis. It is also associated with peculiarities of

the individual, as in such epidemics all cases are not equally

hemorrhagic, and in scurvy the hemorrhages are attributable to the

abnormal conditions to which the sufferers are exposed. Hemorrhagic

exudations are also met with in those inflammations of serous surfaces

accompanying the outcropping of tubercular and cancerous or

sarcomatous growths. In all cases a hemorrhagic exudation represents a

grave complication, and when found in serous cavities has a certain

diagnostic, as well as prognostic, importance.

Fibrinous inflammations are characterized by the presence in the

exudation of considerable quantities of fibrin. As the prevailing

theory of the formation of fibrin demands fibrino-plastic as well as

fibrinogenous material, both are to be sought for in the exudation.

The latter is present in the liquid portion of the exudation; the

existence of the former, as well as that of the ferment, is dependent

upon the presence of the white blood-corpuscles. The more numerous

these, within certain limits, the more abundant the formation of

fibrin. As their death appears essential for the fibrinous

coagulation, the latter is most constantly met with in those parts of

the body where the white blood-corpuscles are quickest separated from

influences favoring their life. The farther removed they are from the

blood-vessels, the more likely is their early death. Fibrinous

exudations are therefore frequent and abundant in cellular and serous

(sero-cellular) inflammation of the great serous cavities of the body.

The clotted fibrin appears as false membrane lying upon the serous

surface, either smooth or rough, tripe-like, or as villosities

projecting above the surface, and again as bands, fibrinous adhesions,

stretching across the cavity and uniting opposed surfaces.

The frequent occurrence of fibrinous exudations on the mucous

membranes of the larynx and trachea, accompanied by the suffocative

symptoms known as croup, has led to the use of the term croupous

inflammation as synonymous with fibrinous inflammation, and its

application to various parts of the body where croupous--_i.e._

suffocative--symptoms are not in question. Croupous inflammation, when

used, is to be considered as an anatomical term, indicating merely the

production of fibrin, and, for the avoidance of confusion, it is

preferable to substitute fibrinous for croupous when such

inflammations are described.

The disease, croup, it is well known, may exist without a

croupous--that is, fibrinous--inflammation, as is familiarly

recognized in the constant use of the terms spasmodic, membranous, and

diphtheritic croup.

Fibrinous inflammation of the mucous membrane of the larger

air-passages is much more frequently met with than that of mucous

membranes elsewhere, as of the intestines, uterus, and bladder. The

pseudo-membranous inflammations of the latter tracts are more commonly

the result of the catarrhal and diphtheritic varieties than of the

fibrinous form. Fibrinous exudations on mucous surfaces, according to

Weigert, can only take place when the epithelium is destroyed. Hence

those causes which give rise to the destruction or detachment of the

epithelium are alone capable of producing a fibrinous inflammation of

mucous membranes, and a fibrinous laryngitis, trachitis, and

bronchitis may result from {50} the local application of such

irritants as steam or ammonia, as well as occur in the diseases croup

and diphtheria.

Fibrinous exudations may also be present within tissues, especially in

those whose meshes are wide, provided the essential elements of

coagulation are present. The coagulative necrosis of various organs,

to be more fully mentioned hereafter, is closely allied to fibrinous

clotting, the fibrino-plastic element being derived from the death of

the parenchymatous cells of the part.

In the existence of a fibrinous pneumonia the conditions are somewhat

analogous to those present in the fibrinous inflammation of serous

surfaces and of the areolar connective tissue. There is present an

abundantly cellular exudation, held in the place of its origin, the

cells undergoing rapid death and surrounded by a wall whose

superficial cells resemble in structure, if not in origin, the

endothelial cells lining the smaller lymph-spaces of connective

tissue, as well as the larger cavities within the same, known as

serous cavities.

The diphtheritic inflammation is no more to be confounded with the

disease diphtheria than is the fibrinous inflammation with the disease

croup. Although diphtheria owes its name to the frequent presence of

an apparent membrane, it may be said that the latter is not essential

to the existence of the former. Diphtheria, like croup, is an

affection in which various exudations may be present, and the

anatomical product alone does not suffice in all instances for the

recognition of the disease. In croup there may be a swollen mucous

membrane, with a slight superficial mucous exudation, or a more

abundant exudation of desquamated epithelium and mucus, as well as a

fibrinous false membrane. In diphtheria the same varieties of

exudation may occur, and in addition the diphtheritic exudation may

also be present. The latter, however, is not limited to the disease

diphtheria, for its presence is apparent in other mucous membranes

than that of the air-passages, and in the pharyngeal mucous membrane

in other diseases than diphtheria. A diphtheritic conjunctivitis,

enteritis, cystitis, and endometritis are recognized. The cutaneous

surfaces of the body may also furnish a diphtheritic exudation. The

diphtheritic inflammations of wounds and of variolous eruptions are

instances in point.

The characteristics of a diphtheritic inflammation are the presence

within the tissues of a clotted exudation, which is associated with a

defined swelling and death of the part. The exudation contains not

only dead leucocytes and interlacing fibres, but is also provided with

abundant granular material, much of which presents the well-known

peculiarities of microscopic organisms. The apparent false membrane is

thus dead, infiltrated tissue, which may be torn away from the

continuous unaffected tissue, leaving a raw, rough surface, but not

peeled from a comparatively smooth surface, as in other forms of

pseudo-membranous inflammation.

The frequent association of a superficial false membrane,

corresponding in area with that of the deeper-seated changes, in which

cells and fibres may be present, is to be recognized. The diphtheritic

process, however, is localized within, and not upon, the tissues

affected. The diphtheritic exudation represents a local death, a

necrosis, of the part concerned, and the result has frequently been

compared with the death consequent upon the action of a caustic.

{51} The immediate cause of a diphtheritic inflammation is now

generally attributed to the action of microbia which enter the tissue

from without, and in their growth beneath the surface produce not only

the local, but also the remote, constitutional disturbances which are

associated with a diphtheritic inflammation. The investigations of

Wood and Formad[16] point to ordinary putrefactive organisms as a

sufficient cause for the diphtheritic inflammation of diphtheria,

while other observers demand a specific organism as the exciting

cause. The occurrence of diphtheritic inflammations in various parts

of the body, in regions, as the intestine, where putrefactive

processes are constantly present, and in the bladder and uterus, where

the phenomena of putrefaction are often associated with diphtheritic

inflammation, suggest the efficacy of ordinary putrefactive agencies

in producing the latter. As all microbia found in putrefaction are not

alike, and as the properties of certain, differ from those of others,

and as our knowledge of the effects of all is but fragmentary, the

characteristics of specific germs for a diphtheritic inflammation of

one part of the body, or of all parts of the same, must still be

regarded as not proven.

[Footnote 16: _Research on Diphtheria for the National Board of

Health_, 1880, Supplement No. 7.]

Productive inflammations are those which result in the new formation

of tissues. One of the frequent products of inflammation is fibrous

tissue, which, at first abundantly cellular, later becomes more

vascular, and is finally transformed into a tissue whose fibres

predominate over its cells. This formation of a cicatricial tissue

demands further recognition when the termination of inflammation is

considered.

A system of practical medicine. By American authors. Vol. 1 · 第 2 / 149 段