Transcript Kribriformní adenokarcinom jazyka

Disorders of vascular flow:
edema, congestion,
hemorrhage, thrombosis,
embolism. Shock. Infarction.
2011
EDEMA
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abnormal accumulation of fluid in the
intercellular space or in the body cavities
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Edema may occur
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Localized
generalised
Severe and generalised oedema, with marked
swelling of the subcutaneous tissue- anasarca
edematous collection in body cavities:
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hydrothorax - chest cavity
hydropericardium - pericardial cavity
hydroperitoneum (ascites) - abdominal cavity
pathogenesis of edema
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increased hydrostatic pressure
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may results of the impaired venous outflow, caused
by thrombosis- most common in legs- thus localized
oedema
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generalised increase in venous pressure- occurs in
right-sided congestive heart failure
reduced osmotic pressure
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results from the excessive loss or reduced synthesis
of serum albumin.
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the most important cause of plasma protein lossnephrotic syndrome (increased permeability of
glomerular membranes)
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causes of decreased synthesis of plasma proteinsin liver cirrhosis, in severe malnutrition
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lymphatic obstruction
 impaired lymphatic drainage results in lymphedema
(due to obstruction-inflammatory, neoplastic)
 filariasis-parasitic infection- often causes massive
fibrosis of the lymph nodes and lymphatic channelsexcessive lymphedema of legs and external genitalia elephantiasis
 cancer of the breast- sometimes treated by removal
also axillary lymph nodes- may cause severe
postoperative oedema of the arm
sodium retention -water retention
 in acute reduction of renal function- in acute renal
failure
Edema
MORPHOLOGY OF THE EDEMA
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changes are evident grossly
 edema is encountered most often at three sites = lower
extremities, lungs, brain
subcutaneous oedema of the lower extremities- manifestation of
heart failure (of right ventricle)- legs are subject to the highest
hydrostatic pressures.
 Distribution of oedema fluid in heart failure is influenced by
gravity, it is termed „dependent„.
 in contrast, oedema in acute renal failure-results of proteinuria
and sodium retention, tends to be generalised, more severe than
cardiac oedema, affects all parts of the body equally, manifests
mostly in loose connective tissue matrices-periorbital oedema
pulmonary oedema-is a prominent feature of left ventricle heart
failure, alveolar spaces are filled with eosinophilic fluid
oedema of the brain- is encountered in a variety of clinical
circumstances, such as brain trauma, meningitis, hypertensive crisis
In case of pulmonary edema the alveoli are filled with
eosinophilic edematous fluid
HYPERAEMIA OR CONGESTION
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local increase of volume of the blood - caused by
dilatation of the small vessels
active hyperemia: results from an augmented arterial
inflow
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in muscles during exercise
in inflammation
passive hyperemia: results from diminished venous
outflow, is always accompanied by oedema
 in cardiac failure
 in obstructive venous disease
 chronic passive congestion and edema of the lung
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indicator of left ventricular cardiac failure
chronic passive congestion of the liver, kidney, spleen
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represents an indicator of right ventricular failure
Chronic congestion
In case of passive chronic congestion the lung is heavier, stiffer and
dark red to brown in color (so-called brown induration)
Chronic congestion
The brown color results from accumulation of siderophages, i. e. macrophages
containing iron that stains blue with Perls stain
Chronic congestion
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Causes of impaired hepatic venous outflow
Chronic passive congestion: very common, results from chronic
right-sided heart failure
Budd-Chiari syndrome (thrombosis of the major hepatic veins):
hematologic disorders, use of contraceptive, tumors, intrahepatic
infections, idiopathic
Venoocclusive disease (wall thickening, sclerosis and even
occlusion of multiple small and central veins ): consequence of drug
administration, including some anti-cancer agents, or may be caused
by radiation
Chronic congestion
Nutmeg liver
Histology may show various regressive changes (e. g. steatosis, atrophy or
necrosis) mainly in the centrilobular region and in severe long-standing congestion
even fibrosis
HEMORRHAGE
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hemorrhage results from rupture of a blood vessel
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Haemorrhages may be
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rupture of large artery or vein- caused by some type of injury, such as trauma,
atherosclerosis, inflammatory or neoplastic erosion of a blood vessel wall
rupture of small arteries-in systemic diseases
external-may cause exsanguinating
internal- is referred to if blood is trapped in tissues
hematoma – haemorrhage
Petechiae- minor multiple hematomas in the skin,
mucosal and serosal surfaces
Purpura- multiple slightly larger hematomas
Ecchymoses- large subcutaneous or subserous
hematomas (more than 1-2 cm in diameter)
blood collection in body cavities:
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hemothorax= the blood accumulates in
pleural cavities
hemopericardium= in pericardial cavity
hemoperitoneum
hemarthros
A: Punctate petechial hemorrhages of the colonic mucosa- thrombocytopenia.
B: Fatal intracerebral hemorrhage.
CLINICAL SIGNIFICANCE:
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depends on the volume of blood lost by
hemorrhage and on the site of hemorrhage
larger and acute blood loss - may cause
posthemorrhagic shock
site- when located in brain- even smaller
hemorrhage may cause death
repeated external hemorrhages- may result in
severe lack of iron- iron deficiency anemia
THROMBOSIS
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thrombosis= the formation of clotted mass of blood, the clotted
mass itself= thrombus
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thrombus may flow downstream in blood vessel system= embolism
the process of clotting and embolism- closely related=
thromboembolism
potential consequence of embolism and thrombosis= ischemic
necrosis= infarction
thromboembolic infarctions of heart, brain, lungs, are dominating
causes of death
pathogenesis of thrombosis =inappropriate activation of normal
hemostasis
Normal hemostasis :there are three major contributing aspects of
normal hemostasis- platelets, endothelial cells and coagulation
system
Thrombosis
Virchow triad in thrombosis
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1 intact endothelial cells serve to protect blood
platelets and coagulation protein from highly
thrombogenic subendothelial substance (collagen)
 injury - loss of anticoagulative mechanism
 thrombi appear often on ulcerated plaques in
atherosclerotic arteris (mostly the aorta), at sites of
inflammatory or traumatic injury to arteries (the walls
have been infiltrated by cancer)
 thrombi appear regularly in heart chambers when
there has been injury to endocardium (due to
hypoxia) adjacent to myocardial infarct or in any form
of myocarditis
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2 stasis and turbulence of blood
 constitutes the second major thrombogenic influence
 in normal lamelar flow- blood cells are separated from
the endothelial surface
 Stasis, turbulance, and decrease of rate of blood flowpermits erythrocytes and platelets to come to contact
with endothelial cells
 prevents dilution of clooting factors in plasma
 decreases inflow of clotting factor inhibitors
 promotes endothelial cell hypoxia and injury
Stasis play dominant role in thrombosis in veins - low
speed of blood flow in veins - origin of venous thrombi in
sinuses behind venous valves in deep vein in low
extremities
 similar phenomen- in auricular appendices of heart
chambers - in atrial fibrillation
 stasis and turbulence contribute to thrombosis in
arterial aneurysmal dilatations
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3 hypercoaguability of the blood
thrombotic diathesis
 nephrotic syndrome
 late pregnancy
 disseminated cancer
 use of oral contraceptives- increase in plasma level
of prothrombin, fibrinogen and other coagulative
factors can be demonstrated
 trauma, surgery, burns
 cardiac failure
 advanced age, immobilization and reduced physical
activiy increase the risk of venous thrombosis
Thrombosis
Coronary
thrombosis
occurs mainly in the
setting of
atherosclerosis
Thrombosis of coronary artery
MORHOLOGY OF THROMBI
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arterial and cardiac thrombi: arise at sites of endothelial injury,
atherosclerosis- often at the site of branching of the artery- white or
mixed thrombi- composed of fibrin white blood cells and
erythrocytes
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mural thrombus- thrombus attached to one wall of the artery- mural
thrombi also develop in abnormally dilated arteries-aneurysms
occlusive thrombi - thrombus completely obstructs the lumen- in
smaller arteries
most commonly affected arteries: coronary, cerebral, femoral, iliac,
mesenteric, popliteal
venous thrombi: also known as „phlebothrombosis„- mural or
occlusive
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in slower-moving blood in veins- red coagulative or stasis thrombi composed mostly of fibrin and erythrocytes
most commonly affected veins: veins of lower extremity (deep calf,
femoral, popliteal, iliac), periprostatic plexus, portal vein etc
Mural thrombi
A: Thrombus in the left and right ventricular apices, overlying white fibrous scar.
B: Laminated thrombus in a dilated abdominal aortic aneurysm
DEVELOPMENT OF THROMBUS:
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thrombus may continue to grow into adjacent vessels
thrombus may embolize
thrombus may be removed by fibrinolytic activities
it may undergo organization- when thrombus persists in
situ for several days- it may be organized= ingrowth of
granulation tissue and mesenchymal cells into the
fibrinous thrombus
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thrombus is populated with spindle mesenchymal cells and
capillary channels are formed within thrombus
the surface of thrombus becomes to be covered by endothelial
cells
capillary channels anastomose- recanalization = reestablishing
the continuity of original vessel
CLINICAL SIGNIFICANCE of
thrombosis
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cause obstruction- lead to infarction
may provide the source of embolism
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superficial veins-varicosities, such thrombi may cause
local edema and congestion and pain, rarely give rise
to emboli, local edema predispose to infectionvaricous ulcers difficult to heal
deep veins of the leg (popliteal, femoral, iliac)- the
most important source of emboli, they also may cause
edema, pain, tenderness but approximately half of
the patients with deep vein thrombosis are
asymptomatic
EMBOLISM
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Embolism refers to occlusion of some part of the
cardiovascular system by the impaction of embolus
transported to the site of occlusion by the blood stream.
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most emboli represent parts of thrombi, thus the term
thromboembolism,
much less commonly- other material such as fat droplets, gas
bubbles, atherosclerotic debris, tumor fragments
TYPES OF EMBOLISM:
1. pulmonary embolism
2. systemic embolism
3. paradoxical embolism
TYPES OF EMBOLISM
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1. pulmonary embolism
2. systemic embolism
3. paradoxical embolism
Embolism
Recent pulmonary embolia
Postembolic fibrous bridge
PULMONARY EMBOLISM
thrombus originates in deep venous
system of legs
 occasionally from right side of heart
 embolus or emboli are transported
into right heart ventricle and to
pulmonary arteries
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Consequencies of PE
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multiple small emboli in peripheric branches of pulmonary artery
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smaller emboli impact in medium-sized arteries- if
cardiovascular circulation is normal, the vitality of lung tissue
is maintained, but alveolar spaces are usually filled with
erythrocytes= pulmonary hemorrhage
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with compromised cardiovascular status (in congestive heart
failure)- hemorrhagic infarction
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Pulmonary infarction is sharply circumscribed necrosis of
triangular shape with apex pointing towards the hilus of the
lung
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pleural surface is covered with fibrinous exudate
large snake-like emboli-large emboli impact in main pulmonary
arteries-death
saddle embolus- massive embolism in main pulmonary artery,
death suddenly from hypoxia or right ventricle heart failure
(acute cor pulmonale) - no time to develop morphologic
changes in lung tissue
Pulmonary embolism
Pulmonary hemorrhagic infarct
Pulmonary hemorrhagic infarct
Normal lung parenchyma
Infarct
SYSTEMIC EMBOLISM
to systemic arteries -brain, kidney, spleen, etc
Severe consequencies- necrosis
Sources of the emboli
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intracardiac mural thrombi (in myocardial infarction)
atherothrombotic fragments from the aorta and the
large arteries
heart valves
left heart atrium - in atrial fibrillation
left ventricle aneurysm
PARADOXICAL EMBOLISM
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most common source- clots in deep leg
veins, and most common target organsarteries of the brain, kidney, spleen
abnormal opening between right and left
atrium ( foramen ovale ), higher blood
pressure on right side than on left allows
embolization from systemic veins to
systemic arteries
FAT EMBOLISM
fatty droplets and minute globules of fat in blood capillaries
complication of bone fractures
about 90% patients with severe skeletal injuries fat embolism, but
very few have clinical course known as
fat embolism syndrom acute respiratory insufficiency,
neurological symptoms, anemia and thrombocytopenia - typically
syndrom appears about 2 - 3 days after injury
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fat embolism syndrome has mortality of about 10%
pathogenesis of fat embolism syndrom
not absolutely clear, both mechanical obstruction and chemical injury
are involved
microaggregates of fat cause occlusions in microcirculation of lungs
and brain and free fatty acids cause endotheial cell damage microglobules of fat are found in capillaries in many organs- most
important- brain
AIR EMBOLISM
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= is defined as entry of air into venous or arterial blood vessels
-in venous air embolism- small quantities are innoculous, but 100 ml and more
may be fatal
-in arterial air embolism- even small quantity may be fatal, most commonly complication of abortion, chest surgery
caisson disease is a particular form of gas embolism =decompression sickness
may appear in deep-sea divers who ascend rapidly to high altitudes, the gases within
pressurized air are dissolved in the blood, tissues and fat
if the diver then ascends up rapidly to the surface- the dissolved oxygen, nitrogen
and carbon dioxide come out of solution in the form of small bubbles
-most dangerous in this respect seems to be nitrogen, because of its low
solubility- nitrogen persists as gas bubbles
- mainly in the brain - brain necroses
-the same process may affect other highly vascularized tissues and organs,
such as heart and kidney, skeletal muscles, etc.
-in the lungs- sudden respiratory distress syndrom
TREATMENT: rapid placing of the affected person into the compression chamber- and
slow decompression
AMNIOTIC FLUID EMBOLISM
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is characterized by sudden onset, rapid dyspnea, cyanosis, collapse and coma with
convulsions
occurs rarely, is totally unpredictable, may be fatal - is one of major causes of
maternal death after delivery
typical findings:
in pulmonary arteries and capillaries- epithelial squames from fetal skin, lanugo
hairs,
fibrin thrombi indicative of DIC - in small vessels of uterus, lungs, kidney, thyroid,
myocardium pathogenesis of amniotic fluid embolism is unclear
the main cause of syndrom is infusion of amniotic fluid into the blood, such entry
may occur through cervical uterine veins, from the uteroplacental site , etc
it is suspected that vasoactive substances from the amniotic fluid are responsible
for pulmonary vasoconstriction
-thrombogenic substances from amniotic fliud- may cause intravascular
coagulation leading to DIC
hemorrhages and acute renal failure
DISSEMINATED INTRAVASCULAR
COAGULATION (DIC)
is characterized by activation of coagulation sequence that
leads to formation of multiple minute fibrin thrombi in
capillaries and small venules
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the thrombi are mostly composed of fibrin and aggregations of
platelets
leads to widespread thromboses with consumption of platelets
and of coagulation factors and with subsequent fibrinolysis
(secodary effect)- DIC is also called microvasculary thrombosis
thromboses cause focal ischemia - multiple foci of
necrosis mostly in the lungs, kidneys, brain, heart
increased bleeding tendency causes multiple
hemorrhages
main clinical disorders associated
with DIC:
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DIC is not primary disease, it is a complication of
some underlying diseases , such as
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amniotic fluid embolism
EPH gestosis
septic abortion
retained dead fetus or abruption placentae
severe infections (gram-negative sepsis for example)
neoplasms, such as carcinoma of pancreas, prostate,
lungs
massive tissue injury, burns
extensive surgery, etc
morphology of DIC
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widespread occurrence of fibrin thrombi in capillaries of
kidney, adrenal glands, brain, and other organs
-ischemia and multiple microinfarcts
-necrosis in adrenals may cause Waterhouse-Fridrichsen
syndrom
-necrosis in brain- severe neurologic complications
-DIC leads to hemorrhagic diathesis, because of
consumption of clotting factors in multiple microthrombi
increased bleeding tendency causes multiple
hemorrhages
INFARCTION
infarct is a localized ischemic necrosis in an organ or tissue
resulting from sudden occlusion of arterial supply
CAUSES OF INFARCTIONS:
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thrombotic or embolic occlusions
1. thrombosis = in situ formation of the blood clot that occluds
the lumen of the blood vessel
2. embolism = a portion of the thrombus in one area breaks off
and lodges into the blood vessel of the other area usually of
narrower lumen
less common causes of infarcts include:
3. atherosclerosis = narrowing of lumen or the total obstruction
of the lumen by atherosclerotic plaque alone- due to ulceration,
hemorrhage, or edema of the plaque
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4. spasm of artery = due to active pathologic
vasocontriction
5. hypotension - causes severe temporary impairments
of blood supply in an area of compromised circulation
6. twisting of the blood vessel with occlusion of both
arteries and veins
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in a hernial sac or under peritoneal adhesion
in cases of torsion of organs or tissues that have the blood
supply through a pedicle, such as ovaries, testes
7. pressure of blood vessel - caused by expanding tumor
or due to mechanical pressure in decubital ulcer
MORPHOLOGY OF INFARCTS:
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Infarcts can be divided into two types:
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the distinction is given only by amount of hemorrhage that occurs in
necrotic area, the difference is not principal
1. WHITE, PALE INFARCTS
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in solid organs (heart, spleen, kidney)- firm consistency of the organ does not
permit blood inflow into the necrotic area
2. RED, HEMORRHAGIC INFARCTS
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white (anemic)
red (hemorrhagic)
in loose, spongy tissues (lungs, intestine) permits blood to collect in necrosis
from the anastomosing capillary circulation hemorrhagic infarcts are also encountered if the venous outflow from the
necrotic area is limited -for example hemorrhagic venous infarction of intestine
in some intstances, spasm of vessels about clot subsequently relaxes
causing partial hemorrhagic infarction
A, Hemorrhagic, roughly wedge-shaped
pulmonary infarct (red infarct).
B, Sharply demarcated pale infarct
in the spleen (white infarct).
MORPHOLOGY OF DEVELOPING
INFARCT
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1- at the onset- all infarcts tend to be poorly defined and slightly
hemorrhagic due to anoxic leakage of residual blood from capillaries
in affected area - early infarcts are grossly red
2- at later stage- white infarcts in solid organs- (spleen, kidney)
become well circumscribed, progressively pale, sharply delimited
with hyperemic border 
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hemorrhagic infarcts in spongy organs - (lung, intestine), first the
infarct is cyanotic, later is firmer and brown (hemosiderin deposits), the
delimitation of infarcts- inflammatory reaction and hyperemia at the
margins of necrosis
in organs with excellent collaterals- the infarction remains red because
blood continues to be poured to the affected area
in venous occlusion- infarction is usually hemorrhagic
in heart- appearance may be mixed red and white, yellow color is due
to accumulation of leukocytes
in brain- cerebral infarction usually undergoes liquefaction
Infarction of the kidney
Slide 5
Coagulative necrosis
Myocardial infarct
Coagulative necrosis
Kidney infarct
Necrotic
tissue
Viable
tissue
necrosis
Demarcation line
Coagulative necrosis
Infarct of the spleen
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3 at last stage -in most organs, the infarcted area is
replaced by granulation tissue which is finally replaced
by a scar with deposits of hemosiderin
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in lungs- infarcts dry out, become paler eventually are replaced
by scars
in heart - a similar phenomen occurs, but solid consistency of
heart muscle does not permit great shrinkage and even
prominent scar is of normal size (myofibrosis)
in brain- scars do not from in the brain, and the necrotic area
liquefies. As a result, a speudocyst may be formed- smoothwalled, glia-lined cavity (postmalatic pseudocyst)
in intestine- infarction causes death if not removed surgically- no
development
FACTORS THAT INFLUENCE THE
DEVELOPMENT OF INFARCT
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1- nature of vascular supply
-the most important is an availability of alternative way of blood
supply in the affected area - role of collateral circulation
-in organs with abundant collateral circulation (notably the lungs)arterial occlusion leads to development of infarct only if preexisting
vascular disorders (usually congestive heart failure) is present
the lungs have dual arterial supply ( pulmonary system and
bronchial arterial supply )
-occlusion of small branch of pulmonary artery in young person with
normal bronchial circulation does not produce infarct
-embolism in older person with pulmonary hypertension and
pulmonary congestion, emboli often result in hemorrhagic infarcts
in liver- similar situation with dual circulation- hepatic and
portal arterial system
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upper extremity-double arterial supply through radial
and ulnar arteries- of the hand and forearm- prevents
development of infarction or gangrene of this extremity,
this is not true for legs
heart- collateral circulation- may operate even
in coronary circulation- important in preventing
myocardial infarction
-three major coronary arteries (left anterior
descending, left circumflex and right coronary artery)effective small anastomoses between these three trunks
2- rapidity of occlusion
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-slowly developing occlusions-usually
cause vascular atrophy, very seldom cause
infarct - since they provide opportunity to
improve or develop the alternative blood
supply,
-rapidly developing occusions-more
likely to cause infarct
3- vulnerability of tissue to hypoxia
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the susceptibility of a given tissue to hypoxia
influence the likelihood of infarction
neurons and nervous tissueirreversible damage even after 4-5 min of anoxia
myocardial cell also very sensitive to
hypoxia
in contrast, less sensitive are
fibroblasts, lipocytes, skeletal muscle
many epithelial cells- resistent to
hypoxia
4-oxygen-carrying capacity of blood
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patients with normal levels of oxygen
transport tolerate better disorders of
vascular supply, than those with anemia or
cyanosis
-thus, cardiac failure can contribute to
development of infarct through reduced
level of oxygen transport capacity
SHOCK
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acute circulatory deficiency caused by inadequacy or
maldistribution of blood supply resulting in circulatory
hypovolemia
-may develop following any massive insult to the
body, constitutes a widespread hypoperfusion of cells
and tissues due to reduction of blood volume or due to
redistribution of blood resulting in a considerable
decrease of effectiveness of circulation.
-leads to serious tissue ischemia, irreversible injuries
and may eventually cause the death of patient
TYPES OF SHOCK:
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CARDIOGENIC = shock related to cardiac
pump failure
-caused by heart muscle damage
(myocardial infarction, rupture of heart), or
rhythmic disorders, (arrhytmias), and
pulmonary embolism, cardiac tamponade, etc.
HYPOVOLEMIC- results from either internal or
external fluid loss
-both hypovolemic and cardiogenic shock
cause a drop in cardiac output and a decrease
in tissue perfusion
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HEMORRHAGIC SHOCK
-blood loss may be - external or internal
-may be initiated by trauma or endogenous
(spontaneous) resulting from ulcerating or necrotizing
lesions, such as- disruption of artery wall in peptic ulcer
-bleeding from arteries due to tumor invasion
-bleeding from varices- esophageal in liver
cirrhosis
-from dissecting or saccular arterial aneurysm
-fluid loss (excessive vomiting, diarrhea,
burns)
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BURN SHOCK= massive loss of fluid and blood cell into injured
tissue and from denuded surface
-Mechanisms underlying cardiogenic and hypovolemic
shock-low cardiac output, hypotension, decreased tissue
perfusion, tissue hypoxia
SEPTIC = shock related to severe bacterial infections, (particularly
gram-negative bacilli, such as Escherichia coli, Klebsialla
pneumoniae)gram-positive bacteria, such as streptococci, pneumococci
-endotoxemia secondary to sepsis causes increased vascular
permeability and internal loss of fluids from the circulation
Mechanisms underlying septic shock less obvious - in majority of
cases -endotoxins and DIC are most important in pathogenesis.
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ENDOTOXIC SHOCK
-cardiac output is not lower, but the capacity of arterial
system is abnormally incresed due to arterial dilatation
-septic shock is associated with defects of distribution
of blood- so called peripheral pooling, with endotoxinmediated activation of inflammatory responce and
direct toxic damage to the tissues
NEUROGENIC - after anesthesia, and in spinal cord
injury
major mechanism is peripheral vasodilatation with
pooling of blood
PATHOLOGY AND PATHOGENESIS
OF SHOCK
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-whatever the main cause leading to shock is, major pathogenetic aspect is
diminished volume of circulating blood
-due to loss of extracellular fluid or due to blood loss
- due to pooling of blood in certain areas, such as in the
abdominal viscera in abdominal trauma
STAGES OF SHOCK:
1- nonprogressive stage-reflex compensatory mechanisms are
activated and perfusion and blood supply to vital organs is preserved
2- progressive stage -is characterized by tissue hypoperfusion,
progressive tissue hypoxia due to arterial dilatation and stasis, function of
vital organs begin to deteriorate- the patient is confused
3- irreversible stage - is characterized by irreversible tissue injury of
hypoxia, condition no longer responsive to therapy
-the flow through the renal cortex is markedly reduced - renal tubular
necrosis develops, with consequent decrease in the urinary output- resulting
in metabolic acidosis
MORPHOLOGIC CHANGES DUE TO
SHOCK:
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tissue changes are essentially the same as those of hypoxic injury,
-late stages of shock are characterized by failure of multiple organs
brain-ischemic encephalopathy- changes due to ischemia and hypoxia changes depend on the duration of hypoxia
-in mild cases- transient confusional state, more severely affected
patients will be comatose with subsequent loss of part of cortical function
heart -variety of changes- myocardial infarction, subendocardial
hemorrhage,
lungs- so called shock lung - Adult respiratory distress syndrome ARDS,
-ARDS is a clinical syndrome not always but often associated with
shock,
-grossly. the lungs are firm, dark red, airless, heavy
-microscopically: capillary congestion, intraalveolar edema and hemorrhage,
fibrin thrombi may be presentin capillaries, diffuse alveolar damage, hyaline
membranes lining the alveolar surfaces,
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kidneys-acute tubular necrosis
adrenal glands- focal depletion of lipids in the
cortical cells-this loss of corticolipids does not
imply adrenal exhaustion, but more likely
activated state and increased production of
corticoids
gastrointestinal tract -focal mucosal
hemorrhages
liver-fatty change or centroacinar necroses
ARDS
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Acute (adult) respiratory distress
syndrome, shock lung
Diffuse alveolar damage (DAD)
Result of acute alveolar injury of various
etiology
Triggered by endothelial and/or
pneumocyte injury
Causes of ARDS
Infection
Chemical Injury
Sepsis*
Heroin or methadone overdose
Diffuse pulmonary infections*
Acetylsalicylic acid
Viral, Mycoplasma, and Pneumocystis pneumonia; miliary
tuberculosis
Barbiturate overdose
Gastric aspiration*
Paraquat
Physical/Injury
Hematologic Conditions
Mechanical trauma, including head injuries*
Multiple transfusions
Pulmonary contusions
Disseminated intravascular coagulation
Fractures with fat embolism
Burns
Ionizing radiation
Inhaled Irritants
Pancreatitis
Uremia
Cardiopulmonary Bypass
Oxygen toxicity
Hypersensitivity Reactions
Smoke
Organic solvents
Irritant gases and chemicals
Drugs
Pathogenesis of ARDS
„Shock lung“
„Diffuse alveolar damage“
Hyaline membranes