=Death of cells and tissue.= By the application of an irritant (acid,
heat, etc.,) a certain thickness of tissue with its enclosed cells is
killed, and a thin layer of necrosis is usually produced. This does not
constitute inflammation, but it acts as a foreign body, often septic, in
producing inflammation in the parts adjacent.
=Cloudy Swelling, Granular Degeneration.= This may occur in the inflamed
area surrounding the necrosed tissue in the seat of a burn or other
injury, it is exceedingly common in the cells of inflamed parenchymatous
tissue (liver, kidney), in the muscle of the heart, in the
gastro-intestinal mucosa, in febrile affections and in poisoning with
arsenic, phosphorus, or mineral acids. The gross appearance of the
tissue is that of swelling, with a dull grayish color and a loss of its
normal translucency. The cells of the affected organs are seen under the
microscope to be filled with small albuminous granules which may be so
abundant as to completely conceal the cell structure. The granules are
insoluble in ether, but disappear under acetic acid. This condition of
the cells is often associated with the exudative forms of inflammation.
=Cell Proliferation and Change.= In the nonvascular organ attacked by
inflammation the multiplication of tissue cells and their resumption of
amœboid movements is a constant phenomenon. Virchow insisted on the
fundamental relation of the cell to the morbid process, and Goodsir and
Redfern showed the rapid increase of the cells of articular cartilage in
attacks of arthritis. There is first a sensible increase of the nucleus
of the cartilage cell which shows a more extended and deeper staining in
carmine or aniline; then by a special method of division (karyokinesis)
the cell and nucleus divide in two; by a similar process these divide in
four and so on in regular order. Meanwhile the cartilaginous substance
becomes softened and finally dissolves and disappears, leaving in the
place a mass of closely aggregated cells.
In the nonvascular transparent cornea, the membrane of Descemet, the
epithelium of serous membranes and in the epidermis a similar cell
multiplication occurs, also in the lateral cartilages of the horse’s
foot.
To follow the indirect cell division by karyokinesis, we must note the
cell as a semi-solid mass, formed of protoplasm and nucleus, each having
as its framework a network of exceedingly fine inter-crossing filaments,
much finer in the nucleus than in the cell protoplasm. The nuclear
filaments stain with hæmatoxylon and safranin and are called _chromatin_
threads. The intervening non-staining material is _achromatine_. The
nucleus has a membranous envelope in two layers, of which the inner only
stains. When about to divide two poles are formed in the cell protoplasm
opposite to each other and near the nucleus the filaments concentrating
to the poles. The chromatin threads in the nucleus thicken, become
convoluted, split and multiply, and draw into their substance the
chromatin layer of the envelope. Next the chromatin threads form long
loops directed toward an achromatine centre or pole like a star, and
this is followed by the progressive division of the star-shaped mass
into two equal parts.
Finally they separate, together with the cell protoplasm, forming two
daughter cells.
This cell proliferation under the action of an irritant is common to the
vegetable kingdom in which galls, and tumors are formed in this way. It
is a remarkable feature of these multiplying cells that they not only
lose their power of developing the tissue in which they formerly lay,
and have all their vital powers devoted to proliferation, but they
acquire the amœboid power of their ancestors, the embryonic cells, which
they further resemble in size. Indeed these cells are freely spoken of
as embryonal cells, and the tissue formed by their massing together as
embryonal tissue, and there is a widespread impression that they revert
entirely to the form and characters of the embryonic cell. In some
respects, however, they are unlike. The modified tissue cell of
inflammation presents a nucleus of horseshoe outline, or after division
of the nuclei they together retain this semi-circular outline; it has
the power of actively digesting the adjacent tissues as the embryonic
cells do not, and again it does not possess the power of differentiation
into widely different tissues as does the early embryonic cell. It may
be called a reversion, in the direction of the embryonic cell, however,
since it reacquires a number of its functions.
=Migration of white blood cells.= This is another, and in vascular
tissues the main source of the great cell accumulation in the inflamed
tissue. This process was observed by Waller in 1846, but was given its
true importance through the later observations of Cohnheim. The
migration takes place through the walls of the capillaries and veins
only, and the migrating cells are largely of the polynuclear variety of
leucocytes. These remaining adherent to the inner wall of the blood
vessel may be seen to have a small portion of their substance projected
through the wall and appearing as a small buttonlike projection on the
outer side. This gradually increases, while the remaining portion of the
cell on the inner side of the wall correspondingly decreases until the
whole cell is lodged in the tissue outside the vascular wall. The time
occupied in passing through is very varied. It may be wholly
accomplished in half a minute, and again hours may be required for the
complete passage of a single leucocyte. The explanation of this
migration has been sought in the supposed existence of stigmata
(openings) in the vascular walls (Arnold), in the effect of the blood
pressure within the inflamed vessels, in softening of the vascular walls
and, in the contractility of the leucocyte which is strongly attracted
by the pressure of certain bacteria and other irritants (chemiotaxis).
The migrated leucocyte assumes in the tissues the same habit as the
altered tissue nucleus. It multiplies rapidly, assists in the solution
and removal of the inflamed tissue, contests the ground with infective
microbes (phagocytosis), and subserves the purpose of assisting in
building up new tissue, or of degenerations.
=Red Cells.= The red blood globules follow the active current in the
centre of the blood vessel, yet a few of these also become adherent to
the softened walls and pass through them (diapedesis). When stasis of
blood takes place in the vessels, they become packed more closely with
red globules which then pass outward into the tissues in much larger
numbers.
=Changes in innervation.= As shown under hyperæmia the vaso-motor system
of nerves exerts a potent influence on the circulation and is largely
instrumental in bringing about circulatory disorders. The increase in
the number and force of the contractions of the heart, and the rigid
contraction of the walls of the arteries proceeding to an inflamed part,
are distinctly the result of a reflex nervous action. The implication of
the second eye when one has been violently inflamed from a mechanical
injury is another example of this kind. The loss of power of the
vaso-motor nerves is however even more characteristic. Experimentally
the cutting of the cervical sympathetic or crushing of the superior
cervical ganglion causes congestion and finally inflammation of the
structures on that side of the head; the crushing of the semilunar
ganglion similarly affects the abdominal viscera; and the cutting of the
pelvic plexus, the structures of the hind leg. The contraction and
dilatation of the inflamed capillaries is largely a nervous phenomenon.
A certain number of irritants, like warm water, mustard, or ammonia
cause contraction followed by dilatation of the capillaries, while
others like dilute mineral acids, alkalies, chloroform, or sodium
chloride and sugar in concentrated solution produce dilatation at once.
Some poisons act variously on different parts, eucalyptol causing
dilatation of the arteries and contraction of the veins, while corrosive
sublimate causes contraction of the arteries and dilatation of the
veins.
So with certain microbian toxins. Introduced into the general
circulation they produce active congestion or inflammation in the seat
of colonization of the microbe from which they were derived, as
witnessed in the use of tuberculin or mallein. Finally the chill and
febrile reaction which attends on extensive inflammation is essentially
a nervous phenomena in its inception and progress.
=Changes in the circulation.= The usual changes in the bloodvessels of
the inflamed part may be thus succinctly stated: 1. Contraction of the
capillary vessels of the affected part and hastening of the current of
blood through them. 2. The succeeding dilatation of the capillaries and
the slowing of the blood stream, which still flows uniformly throughout
the diseased tissue. 3. The flow of blood becomes irregular, at points
tardy, and at others oscillating or even recoiling between the pulse
beats when it has been forced into a vessel already blocked by coagulum.
4. In the still pervious vessels the red blood globules occupy the
centre of the vessel where the current is rapid, while the white
globules roll slowly along the inner surface of the walls where the
current is slow and become adherent to the walls and stationary, while
the general current rolls on. This is a direct abstraction of the white
globules from the circulating blood and greatly favors the coagulation
of the blood in the capillaries. The blood plates equally collect in the
periphery of the vessel and escape. 5. The adherent white globules
migrate in large numbers through the capillary and venous walls into the
tissues. The red globules migrate to a less extent at first. 6. Small
coagula form in the affected capillaries, forming minute red points
which cannot be pressed out by the finger. 7. The red globules in the
area of stagnation back of these capillary emboli adhere to each other
by their flat surfaces and form rolls which pack into the vessel and are
enveloped in a fibrinous clot. 8. The liquid part of the blood rapidly
exudes into the tissues leaving the red globules relatively much more
abundant in the liquid which remains inside the vessel. 9. The walls of
the capillaries become softened and allow a readier transudation of
liquor sanguineous, and escape of the globules through the walls of the
vessels. 10. The arteries leading to the inflamed part have their
muscular coats more rigid and unyielding and transmit much more blood
than the corresponding artery leading to the healthy part. 11. The heart
is equally roused to more rapid and often more forcible contractions,
which modify the pulse both in number and rhythm. 12. The circulating
blood is found to have received a great increase in the fibrine formers,
the fibrine in the shed blood amounting to 6, 8, or 10 parts per 1000 in
place of 3 parts as is normal. The contraction of this causes a
depression on the surface of the clot. 13. The red globules become
viscous and adhere together by their flat surfaces to form rolls, which
precipitate much more rapidly than single globules and leave the
coagulated blood with a straw-colored upper stratum (buffy coat). 14.
Increase of waste products, urea, uric acid, hippuric acid, etc.
Other changes in the blood are alleged, like lessening of the albumen,
as balancing the increase of fibrine, and lipæmia, but the constancy of
these in all cases of inflammation is uncertain.
By way of comment and explanation of the above changes in the
circulation the following may be advanced: The primary contraction of
the capillaries is by no means a necessary condition of inflammation,
and contractions and dilatations within certain limits occur in health
and as a purely physiological act. The dilatation of the capillaries and
the increased flow of blood to the part are related to each other as in
part cause and effect, yet both are due to a reflex act from the seat of
irritation which inhibits contraction in the capillaries and determines
a more rigid contraction in the walls of the arteries running to the
part. A rigid inelastic vessel of the same calibre and under the same
pressure transmits more liquid than the one with elastic walls. The
movement of the white globules to the walls of the vessel depends in
part on their levity, light bodies passing into the outer slow moving
layer, which is less dense, from the central stream where the force and
density are greater. The epithelial cells of the intima undergo cloudy
swelling and are often detached, allowing the readier migration of the
globules through the openings of the lymphatics and the softened and
friable walls. When the capillaries are blocked the pressure necessarily
increases on the arterial side, favoring laceration of the friable walls
and the escape of minute masses of blood. The formation of the buffy
coat is characteristic of the normal equine blood; in inflammation it
becomes more abundant. In the other genera a buffy coat apart from
inflammation may be shown in: (a) anæmia or oligocythæmia in which the
blood is deficient in red globules; (b) in plethora in which there is an
excess of blood solids; (c) in pregnancy in which there is an excess of
white and small red globules; (d) in violent exertion or
over-excitement, in which the blood has circulated with extraordinary
rapidity. The all-sufficiency of the tissue cells in determining
inflammation may be deduced from the following experiment. A ligature is
tied around a frog’s thigh so tightly as to arrest circulation, and the
leg amputated above the ligature; mustard is then applied to the web of
the foot and a blister rises precisely as though circulation continued.