O.O.

Bogomolets National
medical university

Titova Yuliia Pavlovna

Blood
Lymph
Tissue fluid
 disturbances of blood filling or
disturbances in the volume of the
circulating blood (hyperemia and
ischemia)
 disturbances of blood vessel wall
permeability (hemorrhage,
lymphorrhage, plasmorrhagia)
 disturbances of blood rheology
(stasis, sludge,thrombosis, embolism)
disseminated intravascular
coagulation (DIC)
thromboembolic syndrome
Shock
Acute or chronic cardiac
insufficiency
Hyperemia
Ischemia
arterial
and venous
general or local
An excess of blood
contained within blood
vessels in a part of the body
due to an active process
 Physiologic: in response to
increased demands for nutrients
because of work being done
 Pathologic: in response to
certain vasodilator chemicals
and neurogenic stimuli
associated with irritation of tissue
 bright red
 warmer than usual
 swollen
 pulse may be felt readily
 due to the elastic recoil of
arterioles, hyperemia is dissipated
after death in skin and mucous
membranes and is usually not
apparent post-mortem
 capillaries and
occasionally arterioles
are dilated and
engorged with blood
 Develops at increase of
circulating blood volume or at
increase of erythrocyte
amount. Clinically, general
arterial hyperemia manifests
by elevation of arterial
pressure and skin reddening.
 Physiological arterial hyperemia is due to
increase in the organ function or as a
result of shame and rage.
 Pathological arterial hyperemia may be:
 1) angioneurotic
 2) collateral
 3) postanemic (hyperemia after anemia)
 4) vacant
 5) inflammatory
 6) caused by arteriovenous fistula
 Angioneurotic hyperemia is caused
by irritation of vasodilatory nerves or
by paralysis of vaso-constrictory
nerves.
Caused by obstruction to the blood flow
in the main arterial trunk (thrombosis,
embolism). In this case the blood gains
entry to the collateral vessels
and they dilate.
Vacant hyperemia is observed at
reduction of barometric pressure. It
may be general (in divers)
or local (on the
place of medical
cups).
Inflammatory
hyperemia is
caused by
inflammation.
 Observed when the factor causing
anemia (tumor, fluid in the cavity) is
eliminated. The vessels of anemic
tissue are overfilled which may cause
their rupture and hemorrhage as well
as anemia in the brain. That is why
manipulations aimed at removal of a
tumor, fluid or ligature should be
performed slowly.
 Hyperemia caused by
arteriovenous fistula is observed
at injury, when anastomosis
between an artery and vein is
formed and the arterial blood
enters the vein.
increased filling with blood of
the organ or tissue due to
difficulties with blood outflow
(passive process) when blood
supply is not changed or
decreased.
 General venous hyperemia develops
in acute or chronic cardiovascular
insufficiency
 Local venous hyperemia develops
when there are difficulties with
venous blood outflow from the organ
or a part of the body (tumor,
thrombus, embolus)
 dark blue-red
 swollen
 cooler than normal
 after death the color becomes
even more dark blue
 if chronic, the tissue may have a
brown color
 capillaries and veins are
engorged with blood
 excessive hemosiderin in
tissues (especially lungs)
 fibrosis in the walls of veins and
the parenchyma
 peripheral (local)
 obstructive - thrombus or embolus
 constrictive - organ twists, collapsing veins
 central - due to heart failure, which may be
caused by
 conditions associated with weakened
ventricular muscle
 conditions causing ventricles to pump against
increased resistance (valvular stenoses,
hypertension)
 conditions that increase volume of blood
delivered to ventricles (leaky valves, septal
defects)
Acute
Chronic
Left
Right
 Ischaemia/infarction
 Myocarditis
 Cardiomyopathy
 Increased workload
 Pulmonary hypertension due to: left ventricle failure
chronic lung disease
 pulmonary thromboembolism
 pulmonary and tricuspid valve disease
 Systemic hypertension
 Aortic and mitral valve disease
 Coarctation of the aorta
 Anaemia
 Thyrotoxicosis
isa manifestation of a
syndrome of acute cardiac
insufficiency and is
characterized by edema,
plasmorrhagia,
hemorrhage and
degeneration (necrosis).
 develops in chronic cardiovascular
insufficiency. It is accompanied by tissue
hypoxia development which increases
vascular permeability, which in turn results in
development of edema, plasmorrhagia,
diapedesis of erythrocytes, degeneration in
surrounding parenchymatous cells, with
outcomes like necrosis and sclerosis,
hemosiderosis. It results in congestive brown
or cyanotic induration of the organs.
Edematous contents of pink
color, single cells are in the
lumen of the alveoli. The
blood vessels are sharply
enlarged with the
phenomena of plethora.
 The organs are dense, brown with
multiple hemorrhages, besides sclerosis is
observed.
The pigment hemosiderin stains blue
(the formation of Berlin's
azure) in the cytoplasm of cells
(sideroblasts and siderophages). Perls reaction
 a) pulmonary hypertension
 b) hypoxia
 c) reflective spasm of arteries and arterioles
 d) vascular sclerosis,
 e) dilatation and plethora of capillaries
 f) diapedesis
 g) hemosiderosis
 h) plasm proteins exiting into the tissues
 i) pneumosclerosis
 j) insufficiency of the lymphatic system
Acute left ventricle failure -
Pulmonary edema
Chronic left ventricle failure
- «Brown induration» of the
lungs
edema, plasmorrhagia,
hemorrhage and
degeneration (necrosis) in
lever, kidneys, spleen
 «Nutmeg» liver
 Cyanotic induration of kidneys
 Cyanotic induration of spleen
 Ascytes
 Anasarca
 it is enlarged, dense, its borders are
rounded, it has «nutmeg» appearance. In
this case you can see
gray-yellow and dark-red
areas.
 The central veins are greatly expanded. In
the centers of the lobules the sinusoidal
capillaries are dilated, filled with blood.
Hepatic beams are narrowed (atrophy
from pressure). On the periphery of the
lobes the congestion is much less
pronounced, the liver beams and
capillaries have a normal
appearance, hepatocytes
with the phenomena of
fatty dystrophy.
Morphogenesis of cyanotic
induration in the kidney and spleen
is similar to liver one.
originates from Greek ischo
— delay) is decreased filling
with blood of the tissue,
organ, part of the body due
to insufficient blood flow.
 1) angiospastic caused by arterial spasm
because of irritation, pain;
 2) obturation, due to closure of the artery
lumen with a thrombus or embolus or
growth of connective tissue in
inflammation, arteriosclerosis;
 3) compression, squeezing of the artery
with a tumor, fluid, tourniquet;
 4) ischemia as a result of blood
redistribution in case of postanemic
hyperemia.
 Ifthe duration of ischemia is
short, the structure and the
function of tissue may be
restored.
 When the lesion is continuous,
infarct, atrophy or sclerosis
may develop.
Hemorrhage
Lymphorrhage
Plasmorrhagia
Hemorrhage is exit of the
blood from the lumen of the
vessel or from the heart
cavity.
Hemorrhage is also defined
as accumulation of blood in
the tissues.
 external (to the environment)
such as from the nose (epistaxis),
vomiting of blood (hemotenesis)
 internal (in the body cavity) such
as hemoperi-cardium,
hemothorax, hemoperitoneum
 by degree of vascular injury
 by size and form
 by location
1) rupture of the vessel (per
rhexin);
2) corrosion of the vessel
(per diabrosin);
3) diapedesis (per
diapedesin).
-Inflammation of vessel wall (vasculitis)
-Abnormal coagulation of blood
-Nutritional deficiency
-Toxic injury
-Hypoxia and
anoxia
There are hyperemia, edema,
hemorrhages, vacuolation of cells of the
cortical layer, focal necrosis -
karyopicnosis
and karyolysis.
 Petechial hemorrhage (petechiae) is
derived from Latin for "freckle"; petechiae
are spots of hemorrhage that are pinpoint
or less than 2mm in diameter.
 Ecchymotic hemorrhage (ecchymoses) is
from the "ek" for out and "chymos" for juice,
so think of it as squeezing juice out! These
are hemorrhages 2 to 20mm in diameter.
 “Paint-brush” hemorrhage refers to when
the purpuric hemorrhage forms streaks.
 Heart ecchymosis

Conjunctival ecchymosis
 Trauma
 Vessel wall necrosis (local tissue death) –
 Vascular disease
 Rupture of an aneurysm
 Elevated pressure in systemic hypertension
(hyalinosis)
Small foci of erythrocytes are
around the blood vessels, the
substance of the brain is swollen.
The ascending arch and descending aorta from
a 26-year-old man, who died of a dissecting
aneurysm. A transverse intimal tear is present just
above the aortic valve and there is narrowing
(coarctation) of the aorta , visible at the apex
of the aortic arch.
The lumen of the coronary artery is
blocked by an intramural
haematoma. This is an example of
spontaneous coronary artery
dissection with intramural haematoma
 Massive or submassive
hemorrhage is hemorrhage
involving all or most of a particular
anatomic site.
 A hematoma is a collection of
blood in the tissue that produces
a tumor-like swelling.
 Vessel wall invasion by neoplasm (tumor) –
Tumors growing into a blood vessel can
cause sufficient physical disruption of the
wall that significant hemorrhage happens.
 Vessel wall errosion by stomach ulser (Hcl)

Hypopharynx tumor
 Epistaxis – blood from nares
 Hematuria – blood in the urine
 Hemarthrosis – blood in a joint
 Hemothorax – blood in the thorax
 Hemopericardium – blood in the
pericardial sac
 Hemoperitoneum – blood in the
abdominal cavity
 Hemorrhagic saturation -
accumulation of the blood in the
tissue when its entity is preserved
 Hemosalpinx – blood in a tube, usually
refers to oviduct
 Hyphema – blood in the anterior chamber
of the eye
 Hemoptysis – coughing up blood
 Hematemesis – vomiting blood
 Hematochezia – presence of blood in the
stool
 Melena – presence of tarry blood in the
stool
 severityof consequences is
generally proportional to the
amount of blood loss
 -Hypovolemic shock and death
 -Local outcomes
 -Acute or chronic aneamia
 Blood resorption (red blood cells
are phagocytized by
macrophages)
 Cyst formation (brain)
 Encapsulation (hematoma)
 Organization (Solid portions of
the clot organized by
connective tissue)
 Suppuration
Exit of plasma from the circulatory system. This
can be caused by vascular spasm, tissue
hypoxia, immune pathology. As a result,
vascular permeability increases, plasma
saturates the vessel and the surrounding
tissues, plasma saturation occurs resulting in
fibrous edema, fibrous necrosis and sclerosis.
Plasmorrhagia is significant in morphogenesis
of hypertension, infectious and allergic
diseases, autoimmune diseases.
spasm
tissue
hypoxia
immune pathology
 Vascular permeability increases
 Plasma saturates the vessel and the
surrounding tissues
 Plasma saturation resulting in fibrous
edema
 Fibrous necrosis
 Sclerosis
Morphogenesis of
hypertension
Infectious
Allergic diseases
Autoimmune diseases
Stasis
Sludge
Thrombosis
Embolism
(stasis — stop) is arrest of blood
flow in the vessels of
microcirculatory system
(capillaries). It is preceded by
slowing the blood flow which is
called prestasis.
 Type of stasis.
 It is characterized by sticking
of erythrocytes, leukocytes
and thrombocytes to each
other, which is accompanied
by blood viscosity increase.
 Stasis may be discirculatory as a result of
venous hyperemia or ischemia. It develops
due to:
 1) physical factors (temperature elevation,
cold);
 2) chemical factors;
 3) infection;
 4) infectious-allergic factors;
 5) autoimmune factors.
 exchange between the blood and tissue.
Pathology of microcirculatory system is formed of
vascular, intravascular and extravascular
changes.
 Vascular changes are those in the thickness and
shape of the vessels, angiopathies with
disturbance of vascular permeability as a result of
hypoxia.
 Intravascular changes manifest as different
disturbances of blood rheology (sludge, prestasis,
stasis). They are observed in shock of different
origin.
 Extravascular changes are perivascular edema,
hemorrhage, lyphostasis on the lymph vessels.
(originates from Greek thrombus —
blood clot) is a pathologic
manifestation of homeostasis, i.e.
intravital coagulation of blood with
formation of a blood clot called
thrombus in the lumen of the
vessel.
thrombocytes agglutination
fibrinogen coagulation and
fibrin formation
erythrocyte agglutination
plasma protein precipitation
 Includes local and general factors
causing thrombus formation. Local
factors are changes in the vascular wall,
slowing the blood flow and disturbance
of turbulent motion. General factors
include disturbances of regulation of
coagulation and anticoagulation
systems and changes in the blood
composition.
Parietal thrombi develop in
large arteries and heart
cavities
Obstructive thrombi most
commonly develop in small
arteries and veins
 The thrombus is attached to the vascular
wall, it is dense, with corrugated surface.
It is composed of branching bars of stuck
thrombocytes and bands of fibrin with
erythrocytes and leukocytes located
between them.
 White
 Red
 Mixed Red thrombus (femoral vein)
 Hyaline
  consists of
precipitating
plasma proteins,
destructed
erythrocytes,
leukocytes and
Hyaline thrombus (lung) thrombocytes. They
do not contain
fibrin. They
resemble hyaline
and are located in
the microcirculatory
bed
Cross-section of a coronary
artery in which there is an
occlusive
thrombus blocking the vessel,
leading to sudden death in this
patient.
A saccular atherosclerotic aneurysm of
the descending aorta in the typical
position above the iliac, and below the
renal, arteries. Its lumen contains soft
thrombus.
Section of kidney showing fibrinoid
necrosis and thrombosis
of arterioles (stained red)
 Main factor in morphogenesis of
disseminated intravascular coagulation
(DIC) syndrome
 The basis of thromboembolic syndrome
 The thrombus may partially or
completely close the lumen and cause
serious disturbances of blood circulation.
 Homeostasis is a protective mechanism
and it becomes active at the vessel
rupture
 Favorable
 Aseptic thrombus autolysis
 Organisation (Growth of connective
tissue from vascular intima)
 Canalization (formation of clefts and
channels
 Vascularization (canals turn into vessels
with restored blood flow)
 Calcification of thrombus with stones
(phlebolith) formation
Organized thrombus
The occluding thrombus is in the lumen of the vessel. A
significant part of the thrombotic masses is replaced by a
connective tissue that grows from the side of the intima.
You can see the cracks in which the elements of the
blood are determined - canalization of the thrombus.
Thromboembolism
Septicthrombus autolysis
Thrombobacterial vascular
embolism in sepsis
Large embolus derived from a lower extremity
deep venous thrombosis and now impacted in
a pulmonary artery branch
originates from Greek emballein
— to cast into, circulation in the
blood or lymph of particles
which do not normally occur
and obstruction of the vessels
with them. These particles are
called emboli
 1) orthograde (with the flow):
 • from the veins of general circulation to the
vessels of pulmonary circulation,
 • from the left part of the heart, aorta, large
arteries to the arteries of the heart, brain,
kidneys, spleen, etc.,
 • from the veins of the portal system to the
portal vein of the liver;
 2) retrograde embolism, movement of embolus
against the flow with his own weight (e.g.
through inferior vena cava to femur vein);
 3) paradoxical embolism, in defect of atrial or
ventricular septum when the embolus enters
the arteries from the general circulation.
1) thromboembolism
2) air embolism
3) gas embolism
4) fat embolism
5) tissue embolism
6) foreign bodies
 The most frequent form
occurring when a thrombus or
its part separate. It may be
either venous or arterial.
 Outcomes – infactions in
organs
 Thromboemboli formed in the veins of the
general system and in the right heart and
enter the pulmonary artery. They may enter
small branches of the pulmonary artery
causing hemorrhagic lung infarction. If the
embolus enters a large branch of the
artery, the patients die suddenly because
of pulmonocoronary reflex. This condition is
characterized by spasm of bronchial tree,
branches of pulmonary artery and
coronary arteries.
The valve leaf is thickened due to sclerosis and
hyalinosis; on the periphery of the valve -
mucoid swelling and fibrinoid necrosis; in the
necrosis zone,
the endothelium is destroyed with an attached
mixed thrombus
 occurs in bone injuries when the fat is
crushed and turned into emulsion

Fat embolism (lung)

(toluidine blue)

Bone marrow embolism

(lung)
(silver stain)
The lumen of the blood
vessel is filled with fat
cells, the cytoplasm of
which has an "optically
empty" appearance.

Most of the blood

vessels of the lung
are filled with fat
drops, painted in
red-orange.
A section of kidney tissue from a patient who died
after multiple long bone fractures. It shows two renal
glomeruli stained to reveal fat (red). The glomerular
capillaries are plugged with fat globules which, being
fluid at body temperature, have passed through the
pulmonary capillaries.
 Caused by the air entering the venous
system in injuries of the veins located near
the heart. Air embolism may be caused by
injection of air to the uterine cavity at
criminal abortion, at intravenous injections if
the air has not been evacuated from the
syringe.
 Diagnosis: at autopsy, the right heart is
punctured without taking it out. The cavity
of the cardiac sac should be preliminary
filled with water. Air discharge and foamy
blood are observed
 Occurs during delivery if amniotic fluid
and chorion enter the veins of the uterus.
The other examples are tumor cells and
septic thrombus

Echinococcal hydatid
embolism (lung)
In a blood vessel there are the basophilic
homogeneous masses - colonies of
microorganisms.
  fragments of shells, bullets, embolism with
lime, cholesterol crystals

Cholesterol embolism
 occurs as a result of exudation
of bubbles of the gas
dissolved in the blood, e.g. at
rapid transition from high
atmospheric pressure to
normal in caisson disease, gas
gangrene, in pilots
 is separation of a thrombus or a part of it
and circulation of these particles in the
blood of general system with obstruction of
lumina of different arteries accompanied by
multiple infractions.
 Causes - rheumatic and bacterial
endocarditis, atherosclerosis, cardiac
aneurysm, heart defects
 Thromboembolic syndrome may complicate
infectious, cardiovascular, and oncological
diseases, it may occur after different
operations.
consumption coagulopathy
defibrination
thrombohemorrhagic syndrome or
phenomenon
 pathologicalsyndrome which is
characterized by formation of
disseminated blood clots in the
micro-circulatory bed (often in
combination with simultaneous
reduction of blood coagulability)
causing hemorrhages
 complicated pregnancy,
profuse uterine bleedings,
Cesarean section, large injuries,
anemias, thrombocytopenias,
leukosis, in 36—50% of cases of
asphyxia in premature children
 Acute:
 shock
 sepsis
 placental abruption
 severe trauma and burns
 severe hypoxia
 acute pancreatitis
 fat embolism
 intravascular haemolysis
 Chronic:
 adenocarcinomas
 acute myeloid leukaemia
 malignant hypertension
 1. Massive formation of thromboplastin or
its activators. It may be thromboplastin of
erythrocytes in intravascular hemolysis
(hemolytic disease of newborn, massive
blood transfusions, poisoning, infections)
or thromboplastin of amniotic fluid at
massive aspiration of amniotic fluid by
the fetus, tissue thromboplastin in injury
(especially that of brain and lungs).
 2. Generalized disturbance of
microcirculation accompanied by changes in
blood rheology and its clotting which is
observed in hypoxia and shock of different
origin. Bacterial toxins and immune complexes
act similarly. They activate factor XII which
plays the most important role both in blood
coagulation and anticoagulation activation.
The same mechanism regulates disseminated
intravascular coagulation syndrome in
thrombosis of large arteries or at severe loss of
fibrinogen at formation of hyaline membranes
in the lungs of newborns.
 3. Reduction of the number of
thrombocytes (consumption
thrombocytopenia in Kasabach-
Merritt syndrome).
 4. Generalized angiopathy in
infectious diseases and
hemolytic disease of newborn
also causes disseminated
intravascular coagulation
syndrome.
 1. generalized increase of blood
coagulation in the microvessels. Large
number of fibrin clots are formed. They
close the vessel (fibrinoembolism).
 2. the amount of thrombocytes,
fibrinogen, protrombin in the blood
decreases sharply because they have
already been used at the first stage with
the resultant consumption
coagulopathy. Thus, hemorrhagic
syndrome develops.
 3. fibrinolysis activation takes place in
response to generalized increase of
coagulation occurring at the first stage
which makes hemorrhagic syndrome more
severe.
 4. In severe cases the three stages develop
simultaneously. Disturbance in blood
clotting is accompanied by stasis, opening
of arteriovenous shunts, capillary paralysis,
decrease in arterial pressure. Degenerative
and necrotic changes develop in
parenchymatous organs.
 1) large amount of fibrin thrombi and
emboli in the small vessels of the liver, red
pulp of spleen, adrenals, brain, lungs,
kidneys, placenta, thymus,
 2) mucoid swelling, fibrinous swelling
and fibrinous necrosis with endothelium
desquamation in the walls of small
arteries,
 3) thromboses of large vessels are
possible. Often the thrombi occur in the
sinuses of the dura mater, hepatic veins,
aorta,
 4) in thrombosis of microcirculatory bed,
vital processes of blood-tissue metabolism
stop. Under these conditions organ
pathology is not distinct, general changes
(like toxicosis or shock) develop,
 5) in thrombosis of larger arteries, organ
pathology prevails, i.e. acute renal or
hepatic insufficiency, shock lung, brain
edema, myocardial infarction,
 6) DIC (disseminated intravascular
coagulation) results in hemorrhages in
different organs.
 DIC A sectioned lung
showing spontaneous
pulmonary
haemorrhage
DIC: Microthrombosis in
lung vessels
(PAS)
Shock is failure of the
circulatory system to
adequately perfuse
vital organs.
 Shock is nonspecific clinical syndrome
caused by reduction in tissue perfusion
with blood. Shock believed to be
based not so much on the primary
disturbance of central neuro-
regulatory mechanisms as disturbance
of autoregulation in microcirculatory
system due to the release of abundant
biologically active substances.
 Shockis initiated by anything that
severely and usually relatively
suddenly decreases cardiac
output, blood volume, and/or
peripheral vascular resistance.
 1. Hypovolemic (blood loss).
 2. Cardiogenic (caused by the reduction in
cardiac output).
 3. Bacterial (caused by endotoxins).
 4. Anaphylactic (immediate reaction of
hypersensitivity).
 5. Neurogenic (in intoxication with hypnotic
preparations, ganglioblockers, narcotics).
 6. Shock developing as a result of obstruction to
the blood flow (pulmonary thromboembolism).
 7. Shock developing in hormonal insufficiency
(thyrotoxic shock, myxedema, adrenal
insufficiency).
 Myocardial infaction
 myocarditis, such as might occur with a
septicemia or viral infection
 cardiac tamponade, which occurs
when fluid (usually blood) accumulates
rapidly in the pericardial space and
impinges on the ability of the cardiac
ventricles to dilate and fill with blood
 electrolyte imbalances (hyperkalemia)
that negatively affect heart rate
 acute hemorrhage involving loss of greater
than ¼ - ⅓ of total blood volume. The blood
may be lost externally or into internal spaces
such as the peritoneal cavity or the
alimentary tract.
 loss of fluid (intravascular and extravascular),
which may occur with water deprivation,
vomiting, diarrhea
 increased vascular permeability leading to
loss of intravascular fluid, proteins, and
sometimes blood cells. These insults include
infections, toxicities, and immune reactions
that injure vessels.
 is caused by a sudden severe decrease
in peripheral vascular resistance that
causes extensive pooling of blood within
the venous system and subsequent
decreased venous return to the heart.
Some authors classify these types of
shock as varieties of hypovolemic shock
 results from a bacterial infection
(localized or systemic) in which
large quantities of endotoxin are
released into circulation.
Endotoxins are complex
components of the cell wall
bacteria and are released only
upon death of the bacteria and
degradation of the cell wall
 is a systemic manifestation of an acute
hypersensitivity (allergic) response. This is an
idiosyncratic reaction that occurs in certain
predisposed individuals upon exposure to
certain antigens (substances, usually proteins,
to which the individual is allergic) such as
insect stings, foods, medicines, etc. Histamine
and other chemicals are released from cells
such as mast cells. Histamine and the other
substances bind to receptors, causing
vasodilation and increased vascular
permeability with loss of intravascular fluid.
 can occur following severe emotional
stress, severe pain, or electrical shock
(e.g., lightning strike, biting through the
electrical cord). This type of shock is not
related to cytokine release, but rather is
a result of massive autonomic discharges
that cause extensive peripheral
vasodilation, venous pooling, and tissue
hypoperfusion
 1.
Non-progressive (initial
compensated reversible) shock.

 2.
Progressive decompensated
shock.

 3.
Decompensated (irreversible)
shock.
 1. Non-progressive (initial compensated
reversible) shock. In the early stage of
shock, an attempt is made to maintain
adequate cerebral and coronary blood
supply by redistribution of blood. This is
achieved by activation of various
neurohormonal mechanisms causing
widespread vasoconstriction and by
fluid conservation by the kidney.
 2. Progressive decompensated shock. This is
a stage when the patient suffers from some
other stress or risk factors besides persistence
of the shock so that there is progressive
deterioration.
 3. Decompensated (irreversible) shock.
When the shock is so severe that in spite of
compensatory mechanisms and despite
therapy and control of etiologic agent,
which caused the shock, no recovery takes
place it is called decompensated or
irreversible shock.
 Microscopically it is characterized by
generalized spasms of the vessels,
microthrombosis, signs of increased
vascular permeability in microcirculatory
system, hemorrhages, degenerations,
necroses connected with hypoxia and
damaging effect of endotoxins.
Pale cortex
 degeneration and necrosis in proximal
canals with development of necrotic
nephrosis (or symmetrical cortical
necroses are possible) which
results in acute
renal insufficiency

Shock kidney
(Weigert’s stain)
 glycogen amount in the hepatocytes
decreases, hydropic degeneration and
centrolobular necroses resulting in acute
hepatic insufficiency develop.
Combination of renal
and hepatic
insufficiency is called
hepatorenal
syndrome
atelectasis foci, serous-hemorrhagic
edema
atelectasis foci, serous-hemorrhagic
edema, stases and thromboses in the
microcirculatory bed resulting in acute
respiratory insufficiency
Hyaline membne
 Shock heart degeneration and necrosis in
cardiomyocytes, reduction in glycogen
amount, fat degeneration, necrosis foci.
 Stomach and intestines: congestion,
edema (particularly severe in the equine
colon), and mucosal necrosis with
hemorrhage (all of these changes are
grossly visible)
 Brain: edema and anoxic cerebral laminar
necrosis (both changes grossly visible if
severe)
 Endocrine systems
 Immune organs
Spontaneous serosal haemorrhages in
a case of meningococcal
shock with disseminated intravascular
coagulation.
 It often leads to death. The end result is
inadequate tissue perfusion and here are some
of the augmenting mechanisms that help
shock progress from reversible to irreversible
(and death).
 Anoxic injury to endothelial cells leads to
increased vascular permeability and further
loss of intravascular fluid, aggravating the
hypovolemia and anoxia.
 Insufficient renal and muscular perfusion
results in metabolic acidosis, which further
suppresses cardiac output.
 Insufficient myocardial perfusion causes
anoxic injury to myocytes, further decreasing
cardiac output.
islymph congestion due to
mechanical, resorption or
dynamic insufficiency of
lymph circulation.
 Mechanical insufficiency is caused by
increase in venous pressure, compression
or obstruction of the lymph vessels.
 Dynamic insufficiency is due to
discrepancy between the abundance
of the fluid in the interstitial tissue and the
rate of its outflow.
 Resorption insufficiency is due to
disturbances in lymphatic capillaries
permeability or changes in tissue protein
composition.
 Lymphostasis results in lymphedema,
edema accompanied by chylosis when the
fluid becomes milk white. There are
mesothelial or tumor cells in chylous ascites.
Prolonged lymphostasis results in
lymphogenic sclerosis, e.g. elephantiasis of
the extremities. In contrast to inflammatory
sclerosis, lymphosclerosis develops without
formation of granulation and inflammatory
infiltration, it is called «non-cellular».
Hyalinosis often develops in the connective
tissue.
 Interstitial fluid is located in the
intercellular substance. The amount of
interstitial fluid is controlled by
neurohumoral system (aldosterone and
pituitary antidiuretic hormone). It
depends on the state of blood and
lymph circulation as well as the level of
vascular-tissue permeability.
increase (edema)
reduction (dehydration,
exicosis)
 Edema develop in the patients with
cardiovascular, kidneys, liver, allergic
diseases, infections, pathologic
conditions of pregnancy (hestosis), in
vein thrombosis, lymph congestion,
disturbances of nervous trophism
 Oncotic edema results from reduction in
colloid-osmotic pressure in the blood
plasma.
 Membranogenic edema is associated with
the increase in capillary permeability which
results in plasma protein exit and its
accumulation in the tissues.
 Electrolyte edema results from retention of
water and electrolytes.
 Lymphogenic edema is caused by lymph
congestion.
 1. increased hydrostatic pressure
(transudate; edema may be localized or
generalized)
 2. increased vascular permeability
(exudate; edema may be localized or
generalized)
 3. decreased colloidal osmotic pressure of
plasma (transudate; generalized edema)
 4. lymphatic obstruction (transudate;
edema may be localized or generalized)
 Edema when transudate (which
contains not more than 2% of protein)
accumulates in the tissues or the cavities
of the body
 in subcutaneous fat - anasarca
 in the heart cavity – hydropericardium
 in the pleural cavity – hydrothorax
 in the abdominal cavity – ascites
 in the testis - hydrocele.
 Lymphangiectasia: edema

Cutaneous edema

Peripheral edema
(subcutaneous
tissue)
oedema of the lower legs demonstrated
clinically.
 1. Congestive (in thrombophlebitis, vein
compression, lymphostasis). Most
frequently edema is local. This is due to
venous congestion resulting in increase
in venous pressure, hypoxia, damage of
endothelium and basement membranes
of the capillaries, increase in vascular
permeability, transudation of some
amount of blood to the tissue.
 2. Cardiac (in cardiac
decompensation). This case edema is
characterized by combination of
pathogenesis of congestive edema as
well as accompanying blood
redistribution, increase in aldosterone
secretion and reduction in its destruction
by the liver. Aldosterone is known to
retain Na and water resulting in edema.
 3. Hepatic. The pathogenesis consists of
oncotic factor and Na retention.
 4. Degenerative. Protein deficiency.
Hypo-proteinemia develops and oncotic
blood pressure reduces.
 5. Inflammatory edema develops in the
focus of inflammation where vascular
permeability increases.
 Favorable - the fluid resolves
 Degeneration
 Atrophy
 Sclerosis
Reduction in interstitial fluid
amount may occur in rapid
loss of great amount of fluid
(cholera, prolonged
diarrhea)