when multiple circumscribed new formations, as cancer, sarcoma,
tubercle, and the like, arise in connection with the ordinary products
of inflammation. Such new formations are of frequent occurrence in
serous membranes, and a tuberculous pericarditis or a cancerous
peritonitis, indicates that a growth of tubercles or cancerous nodules
has taken place, in addition to a more or less abundant exudation with
various proportions of serum fibrin and cells. This association of
ordinary and transitory inflammatory products with the formation of
more permanent tissues may be found within organs as well as upon
surfaces. A tubercular arachnitis or lepto-meningitis presents the
various products of an inflammation of the pia mater with an abundant
formation of tubercles. In like manner, a tubercular pneumonia, or a
tubercular nephritis suggests an association of neoplastic growth and
inflammation, in the lung and kidney. Such a relation offers a basis
for the theory in favor of the inflammatory origin of tumors, and is,
in part at least, a cause for the frequent consideration of tubercles
as mere inflammatory products, wholly cellular or cellular and
fibrous, subject to the same modifications as take place during the
course of ordinary inflammations.
Even if tuberculous and scrofulous inflammations are regarded as
inflammatory processes, modified by a specific cause and by
peculiarities of the individual, the cancerous and sarcomatous
inflammations are still to be considered as representing an
association of inflammatory disturbances and specific new formations,
the cause of the latter not being the cause of the former. As ordinary
inflammations of the regions concerned may take place in the absence
of the neoplasms, so may the {52} specific growth appear in the same
regions without anatomical or clinical evidence of inflammation.
The classification of inflammation as to its products is supplemented
by distinctions drawn with reference to the seat. The exudations may
be superficial or deep-seated; they may lie within the cells,
parenchyma, of an organ, or within the interstitial tissue of the
same.
The product of superficial inflammations may lie on the surface, as in
the case of inflamed mucous membranes, or immediately below the
surface, as in numerous cutaneous inflammations, of which erysipelas
may serve as the type. The term catarrhal, applied to superficial
inflammations, carries with it the idea of displacement, flowing, of
the exudation. The product of a catarrhal inflammation must be largely
liquid, that such a displacement may readily take place, and the
catarrhal exudation is chiefly composed of an excess of those elements
which are present in the normal, physiological secretion from the
membrane concerned. Mucus therefore represents a frequent constituent
of the catarrhal exudation, and mucous as well as muco-purulent
catarrhs of the gastro-intestinal, bronchial, genito-urinary, and
other mucous membranes are recognized. The catarrhal inflammation of
the respective membranes usually represents the mildest form, as it
demands an intact epithelium, and a ready removal of the inflammatory
product.
As the cause of a catarrhal inflammation may occasion a destruction of
the epithelium or a necrosis of the mucous membrane, the frequent
association of catarrhal with fibrinous or diphtheritic inflammations
is obvious. In such cases the clinical importance of the latter
varieties gives them the precedence in the designation of the
inflammation. The retention of the catarrhal products is the frequent
cause of permanent disturbances of a more or less serious nature.
These result in part from the mechanical obstruction offered to the
function of parts beyond the seat of obstruction, as pulmonary
atelectasis; and in part from the changes taking place in the retained
product. Purulent otitis media with its dangerous or fatal results,
and gangrene of the lung terminating in septic pleurisy, are not
infrequent instances of severe disturbances from putrefaction of the
retained products of a primarily catarrhal inflammation. A cheesy
degeneration of the catarrhal cells leads to a surrounding fibrous, or
destructive, inflammation, with a corresponding diminution in the
function of the organ affected.
Of the deep-seated varieties of inflammation, that requiring special
mention is the phlegmonous form. This runs its course within the less
dense fibrous tissue known as the areolar or cellular tissue. The term
cellulitis is usually employed by English writers to indicate the seat
and nature of the process, and although the use of the term cellular
tissue is rapidly becoming obsolete, the convenience of cellulitis
favors the retention of the latter name.
The exudation lies within the larger lymph-spaces, and is therefore
sometimes designated as the result of a lymphangitis, the deep-seated,
wider lymph-spaces being concerned rather than those more superficial.
Certain forms of phlegmonous inflammation are of decidedly infectious
origin, and, when seated subcutaneously, are known as phlegmonous
erysipelas, being thus distinguished from the simple erysipelas, whose
seat is defined by the small superficial lymph-spaces of the skin.
{53} Infective forms of cellulitis are also frequently met with in the
loose, sub-peritoneal tissue of the pelvis. The infectious element
usually proceeds from the uterus, and excites the malignant oedema of
the broad ligament, the septic parametritis, or the pelvic cellulitis,
according as the lymph-spaces inflamed lie nearer the fundus or
cervix, and as the direction of the current is upward toward the
spine, or outward toward the sub-peritoneal lymphatics of the pelvic
wall.
Parenchymatous inflammation is present when the exudation is taken
into the cells of an organ, or when the changes dependent upon
inflammation of an organ take place within its functionally important
cells. Virchow originally used the term parenchymatous inflammation in
contradistinction to secretory inflammation, the changes in the former
occurring within the elements of the tissues, while in the latter the
exudation made its appearance on the surface of the organ.
Parenchymatous inflammation is manifested by a degeneration of the
cells affected. This may terminate in their destruction through the
conversion of their protoplasm into fat-drops, fatty degeneration;
although more frequently a simple accumulation of albuminoid granules
(granular degeneration) occurs. The latter represents a transitory
condition, from which a return to the normal state readily takes
place. This form of inflammation is met with in those organs which
present a sharply-defined contrast between the functionally important
cells and the connective tissue which surrounds them. The liver,
kidneys, heart, spleen, pancreas, and glands in general, are
consequently the most frequent seat of parenchymatous inflammation.
Opposed to this variety is the interstitial inflammation. The
exudation of the latter remains within the connective-tissue framework
of the organ. It is essentially cellular in character, and the number
of cells is comparatively small. With their presence and the
possibility of their nutrition a permanent increase in the quantity of
the fibrous tissue of the organ is permitted. This becomes relatively
greater in the course of time, and the parenchymatous cells become
degenerated and absorbed. Interstitial inflammations are likely to
become chronic in character, and, from the outset, are usually
associated with parenchymatous changes.
An important clinical distinction is drawn with reference to the
duration of an inflammation. Acute inflammations are those whose
course is rapid, whose progress is associated with graver disturbances
of function, and with a greater prominence of the cardinal symptoms.
The chronic forms occupy more time in their progress, the functional
disturbances, though severe, are injurious more from their protracted
persistence, than their temporary violence, while redness, swelling,
heat, and pain are symptoms of trifling prominence.
The exudation in acute inflammation, if recovery takes place, is
rapidly removed from the place of its origin, while in the chronic
variety it tends to become a part of the region in which it lies, or,
if removed, slowly disappears, and may be constantly replaced. Acute
inflammations may become chronic, and the chronic variety is liable to
acute exacerbations.
The distinction between acute and chronic inflammations is essentially
one of convenience, and, when considered from the anatomical point of
view, relates rather to the persistence of the results. These may be
{54} present as a variously modified exudation or as a degenerated
condition of the parenchyma of the organ or tissue affected.
Inflammation terminates in resolution, production, or destruction.
For resolution to occur it is necessary that the causes of
inflammation cease to act, either by their removal or their isolation,
and that their results be removed. With the removal of the results
there is often associated the removal of the cause. That such may take
place it is necessary that the function of the vessel walls be so
restored that the exudation ceases to escape. Inflammatory products
already outside the vessels, if present on surfaces with external
outlets, are carried along in the course of the excretions. If they
lie within the cavities of the body not opening externally, their
removal is accomplished through the medium of the circulating lymph
and blood, by absorption. The liquid portion of the exudation becomes
a part of the circulating fluids of the body. The fibrin is converted
into a granular detritus, which eventually disappears from the place
of its formation. The leucocytes may return to the blood-vessels or
enter the lymphatics; the latter course probably being the one taken
by the larger number of the corpuscles. Many undergo a fatty
degeneration, and as they lie in lymph-spaces their conversion into an
emulsion permits a removal of the mechanical obstruction to the flow
of lymph through the spaces in which they were accumulated. The red
blood-corpuscles are destroyed, their pigment being dissolved by the
surrounding fluid and removed in the course of the circulation and
excretions, or it becomes transformed into granules or crystals, which
may remain in the place of their formation, or be transferred, within
amoeboid cells, to remote parts of the body.
When the exudation is abundant, as in the great lymph-sacs of the
body--the several serous cavities--and especially when the openings in
the walls of these sacs are obstructed or the currents within them are
feeble, absorption takes place with great difficulty, and demands a
long interval of time. The fibrinous and cellular portion of such an
exudation frequently becomes converted into a caseous mass, from a
partial fatty degeneration and inspissation. This mass becomes
isolated from the cavity in which it lies, usually at the most
dependent portion, by the formation of a capsule of connective tissue.
It may subsequently become infiltrated with lime salts, calcified, and
thus remain comparatively inert throughout the life of the individual.
The productive termination of inflammation is manifested by the new
formation of connective tissue. This tissue is variously designated,
as the inflammatory process is limited to the surfaces of the body
exposed to the air, or the surfaces of cavities and organs, or as it
lies within organs or the deep-seated parts of the body. In numerous
instances it becomes a permanent constituent of the body, and, as time
is usually essential for its formation, its occurrence is indicative
of a chronic, rather than an acute inflammation. Certain chronic
inflammations are progressive in character, the production of
connective tissue being continuous, with perhaps occasional
intermissions, as in the chronic interstitial inflammations of organs
and tissues. The new-formed tissue, which at the outset is rich in
cells, becomes in time more fibrous, and associated with this change
in structure is a physical modification, manifested by its shrinkage.
This new formation may fill a gap resulting from the destruction of
tissue in {55} the progress of an inflammation, when it is present as
cicatricial tissue--the scar which is usually met with upon the
surfaces of the body or of certain of its organs. When opposed
surfaces are united by the new-formed tissue, the term adhesion is
applied; the adhesions being present as fibrous bands, cords, or
membranes. The pericardial milk-spots and thickenings, the tendinous
or semi-cartilaginous, indurated patches of serous membranes and of
the intima of arteries, are all regarded as manifestations of a
chronic inflammation of these tissues. With the localization of the
inflammation in the outer walls of the bronchi and blood-vessels a
thickening of the external sheath results, called a peri-bronchitis,
arteritis, or phlebitis, as the case may be.
The new formation of blood-vessels is essential for the production and
preservation of this connective tissue, and both arise from
pre-existing tissues. Pus-corpuscles represent the simple cellular
product of an inflammation, and their existence is but transitory.
With the new formation of blood-vessels imbedded in abundant cells
there exists a granulation-tissue, likewise transitory, but out of
which arises the permanent fibrous tissue. The question is still
mooted as to the part played by exuded white blood-corpuscles in the
production of the permanent results of inflammation. It is generally
conceded, especially since the observations of Ziegler, that they are
capable of transformation into lasting constituents of tissue, into
blood-vessels as well as into cells and fibres. Whether all the
resulting permanent products of inflammation are dependent upon their
activity, or whether the pre-existing fixed elements participate, is
still to be considered undecided.
What, at present, appears most probable is, that from exuded
leucocytes there arise, in the course of several days, larger
cells--epithelioid or endothelioid--which are eventually associated
with still larger cells, more irregular in shape, and provided with
projecting filaments, giant-cells. Both varieties may result from the
enlargement of leucocytes by fusion or by the assimilation of
nutriment. The epithelioid cells eventually become fusiform or
stellate, and their projections, as well as those of many of the
giant-cells, become fibrillated. The fibrils of adjoining cells,
becoming united, are thus transformed into a meshwork of fibrous
bundles enclosing irregular spaces, while the nuclei of the cells,
with the immediately surrounding protoplasm, remain upon these bundles
as the permanent cells of the new-formed tissue. The blood-vessels
arise from pre-existing vessels, chiefly capillaries, and probably are
also formed from the cells present in the exudation. The former method
is indicated by the projection of solid sprouts from the wall of a
capillary, which may unite, forming arches, and communicate with
sprouts from neighboring capillaries, thus forming bridges. Both
arches and bridges then become hollowed and admit the circulating
blood. Ziegler maintains that the projections of the larger
epithelioid cells and giant-cells become elongated, and eventually
fused with capillaries, or the projections from capillaries. When this
fusion is accomplished the cells become hollowed, their cavities
communicating with those of the blood-vessels. These epithelioid
cells, whose formation and transformation are of such importance in
the history of productive inflammation, are designated by Ziegler as
formative cells, and are frequently derived from the exuded white
blood-corpuscles, though not identical with them.
{56} The inflammations not terminating in resolution or production,
end in the destruction of the part. This result occurs when the
nutrition of the inflamed territory is so diminished, by the changes
in and around the vessels, as to become insufficient for its
preservation. As the nutriment is derived through the blood-vessels,
the more complete and the more permanent the stagnation in them the
more likely is death to result. This event also depends upon the
quantity and quality of the exudation. The more abundantly cellular
the latter, the more likely is an abscess or ulcer to result.
As most abundantly cellular exudations are considered to be dependent
upon the presence of putrefactive agencies, those inflammations of a
predominant putrid character (gangrenous inflammations) are those
terminating in destruction. The dead product is present as a slough or
sequestrum, when dead soft or hard tissues are detached, entire or in
part, from the living; or as a granular detritus contained in a more
or less abundant liquid. The inflammatory process producing the slough
and sequestrum is characterized as a gangrenous inflammation of soft
parts or a caries of bone, while the process resulting in the
formation of the granular detritus, and which has no necessary
connection with putrefactive agencies, is called a softening, from the
physical condition of its result.
Thrombosis and Embolism.
A blood-clot formed within a blood-vessel during life is called a
thrombus. The entire process of which the thrombus is the essential
element is designated thrombosis.
These terms were introduced by Virchow[17] to avoid the confusion
which resulted from regarding the process and result as synonymous
with inflammation of the vessel. All writers, even at present, do not
adhere to this strictness of meaning. For a thrombus of the vulva
indicates a clot of extravasated blood within the connective tissue of
the labium; in like manner, a vaginal thrombus is the effused and
clotted blood in the loose connective tissue surrounding the vagina.
These exceptions are gradually disappearing, and the word hæmatoma,
tumor composed of clotted blood, is being substituted in both
instances. A cancerous thrombus represents a mass of cancerous tissue
whose growth is extended along the course of a vessel, its wall having
been penetrated. In general, however, the term thrombus, unless
otherwise qualified, is used as first stated.
[Footnote 17: _Handbuch der Speciellen Pathologie und Therapie_,
Erlangen, 1854, i. 159.]
Although thrombosis is commonly a morbid process, it is not uniformly
so. Its physiological significance is illustrated by the part it takes
in the closure of the umbilical and uterine vessels, after childbirth.
The surgeon makes use of it in his efforts to overcome certain of the
ill effects of amputation, and to accomplish a cure of such local
diseases as aneurism, where it is deemed important to diminish the
supply of blood.
The thrombus being a blood-clot, it is composed, like the latter, of
fibrin and blood-corpuscles. It is presumable that the fibrinous part
of a thrombus owes its origin to the same conditions which determine
the presence of fibrin in blood removed from the vessels during life
or in that within the vessels after death.
{57} According to A. Schmidt,[18] the blood and other fluids, in which
clotted fibrin makes its appearance, contain two generators, called
fibrino-plastic and fibrinogenous. The former is considered to be
paraglobulin, a substance contained mainly in the white
blood-corpuscles, while the fibrinogenous generator is held in
solution in the plasma of the blood. When these materials are acted
upon by a third, the fibrin ferment, clotting takes place and fibrin
is formed. It is thought that the ferment is intimately connected with
the white blood-corpuscles, for with the microscope coagulation is
seen to advance as these become destroyed, and where the leucocytes
are most abundant, there coagulation advances most rapidly. The
elements of clotted fibrin are always present in circulating blood,
but Brücke has shown that blood remains fluid, under ordinary
circumstances, because of its constant contact with the normal
vascular wall.
[Footnote 18: Rollett, _Hermann's Handbuch der Physiologie_, Leipzig,
1880, iv. 1, 114.]
The general causes of thrombosis are those which produce an abnormal
condition of the endothelium, a rapid destruction of the white
blood-corpuscles, or a stagnation of the blood. With the presence of
one of these causes there is often conjoined another, and the
conditions under which they are present are conveniently used in the
classification of thrombi.
Although stagnation of the blood is often an important immediate cause
of its coagulation, it is apparent, from the investigations of
Durante[19] and others, that stagnant blood clots in the living
vessels only when their endothelium is in an abnormal condition. With
the co-existence of abnormal endothelium and stagnant blood, thrombi
form with greater frequency and become more voluminous in a given
interval of time.
[Footnote 19: _Wiener Medizinische Jahrbucher_, 1871, 321.]
The importance of the death of white blood-corpuscles in the formation
of thrombi is generally admitted, and is especially insisted upon by
Weigert. According to the observations of Zahn, the nucleus of certain
thrombi is the result of the death of these leucocytes and their
accumulation upon an altered intima. The experiments of Naunyn,
Köhler, and others show that a thrombus may be rapidly produced by the
injection into the blood of fibrino-plastic substances, and of those
through which free hæmoglobin is admitted into the circulation. The
former may be expressed from a fresh blood-clot; the latter may be
obtained by thawing frozen blood, or by injecting such material
(bile-acids, for instance) into the circulating blood as rapidly
destroys the red blood-corpuscles. Although Weigert lays special
stress upon the destruction of white blood-corpuscles in the formation
of the thrombus, it appears, from the experiments above referred to,
that indirectly the destruction of the red corpuscles is also of
importance.
Although largely made up of fibrin, a thrombus also contains
blood-corpuscles, both red and white, and the appearance of the mass
is modified according to the variations in the relative proportions of
these constituents.
Zahn[20] divides thrombi, according to their color, into red, white or
colorless, and mixed varieties. The red owes its color to a large
number of red blood-corpuscles, while the white and mixed forms
contain various proportions of white blood-corpuscles and fibrin and a
diminished number {58} of red corpuscles. The cause of this difference
in the color of thrombi is to be sought for in their method of origin.
When blood clots slowly in a dish, the heavier red corpuscles settle
to the bottom, and the lighter white corpuscles form a superficial
layer. Stagnant blood clotting rapidly furnishes a uniformly red mass.
The red thrombus, like the red clot, is the result of the rapid
coagulation of stagnant blood. The white thrombus, on the contrary,
largely composed of white blood-corpuscles, represents a constantly
increasing deposition of these from flowing blood. The mixed thrombi
arise from a combination of both conditions, and are usually white at
the outset. Thrombi formed in the heart and larger arteries are
usually white, those in the auricular appendages and on venous valves
are mixed, while red thrombi are more common in arteries and veins,
since the conditions favoring their origin are more frequently met in
such vessels.
[Footnote 20: _Virchow's Archiv_, 1875, lxxii. 85.]
Thrombi are frequently stratified, in consequence of the successive
deposition of new layers of blood-corpuscles and fibrin upon a
pre-existing thrombus. Circulating blood is therefore necessary for
the stratification, and such thrombi are likely to be mixed in color.
Unstratified thrombi are usually white or red, the former largely
composed of agglomerated white blood-corpuscles so moulded and
situated as to prevent a stagnation of blood in their vicinity, while
the red thrombus is rarely stratified, since its formation demands a
stoppage of the blood-current. Stratification is intimately connected
with the enlargement or growth of the thrombus, which takes place from
the surface exposed to the flowing blood, and which is greater or less
according to the seat of the thrombus.