Disorders of vascular flow: Disorders of vascular flow: edema, congestion, edema, congestion,

hemorrhage, thrombosis, hemorrhage, thrombosis, embolism. Shock. embolism. Shock.

Infarction. Infarction. 20112011

EDEMA

abnormal accumulation of fluid in the intercellular space or in the body cavities Edema may occur

Localized generalised

Severe and generalised oedema, with marked swelling of the subcutaneous tissue- anasarca

edematous collection in body cavities: hydrothorax - chest cavity hydropericardium - pericardial cavity hydroperitoneum (ascites) - abdominal cavity

pathogenesis of edema

increased hydrostatic pressure may results of the impaired venous outflow,

caused by thrombosis- most common in legs- thus localized oedema

generalised increase in venous pressure- occurs in right-sided congestive heart failure

reduced osmotic pressure results from the excessive loss or reduced

synthesis of serum albumin. the most important cause of plasma protein loss-

nephrotic syndrome (increased permeability of glomerular membranes)

causes of decreased synthesis of plasma proteins- in liver cirrhosis, in severe malnutrition

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 channels- excessive 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

EdemaEdema

MORPHOLOGY OF THE EDEMA

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

local increase of volume of the blood - caused by dilatation of the small vessels

active hyperemia: results from an augmented arterial inflow 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

indicator of left ventricular cardiac failure chronic passive congestion of the liver, kidney, spleen

represents an indicator of right ventricular failure

Chronic congestionChronic congestion

In case of passive chronic congestion the lung is heavier, stiffer and dark red to brown in color (so-called brown induration)

Chronic congestionChronic congestion

The brown color results from accumulation of siderophages, i. e. macrophages containing iron that stains blue with Perls stain

Chronic congestionChronic congestion Causes of impaired hepatic venous outflowCauses 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 congestionChronic 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 hemorrhage results from rupture of a blood vessel

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 Haemorrhages may be

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:

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:

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

THROMBOSISTHROMBOSIS

thrombosis= the formation of clotted mass of blood, the clotted mass itself= thrombus

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

ThrombosisThrombosis

Virchow triad in thrombosis

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

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

flow- permits 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 appendicesappendices of heart

chambers - in atrial fibrillation stasis and turbulence contribute to thrombosis in

arterial aneurysmal dilatations

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

ThrombosisThrombosis

Coronary thrombosis

occurs mainly in the setting of

atherosclerosis

Thrombosis of coronary arteryThrombosis of coronary artery

MORHOLOGY OF THROMBI

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

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

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 thrombiA: Thrombus in the left and right ventricular apices, overlying white fibrous scar. B: Laminated thrombus in a dilated abdominal aortic aneurysm

DEVELOPMENT OF THROMBUS:

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 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

cause obstruction- lead to infarction may provide the source of embolism

superficial veins-varicosities, such thrombi may cause local edema and congestion and pain, rarely give rise to emboli, local edema predispose to infection-varicous 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

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. 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

1. pulmonary embolism 2. systemic embolism 3. paradoxical embolism

EmbolismEmbolism

Recent pulmonary embolia

Postembolic fibrous bridge

PULMONARY EMBOLISMPULMONARY 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

Consequencies of PE multiple small emboli in peripheric branches of

pulmonary artery 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

with compromised cardiovascular status (in congestive heart failure)- hemorrhagic infarction

Pulmonary infarction is sharply circumscribed necrosis of triangular shape with apex pointing towards the hilus of the lung

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 Pulmonary hemorrhagic infarctinfarct

Pulmonary hemorrhagic Pulmonary hemorrhagic infarctinfarct

Normal lung parenchyma Infarct

SYSTEMIC EMBOLISM SYSTEMIC EMBOLISM

to systemic arteries -brain, kidney, spleen, etc Severe consequencies- necrosis Sources of the emboli

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 PARADOXICAL EMBOLISM

most common source- clots in deep leg veins, and most common target organs- arteries 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 EMBOLISMFAT 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

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 EMBOLISMAIR EMBOLISM

= 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 AMNIOTIC FLUID EMBOLISM

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 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:

DIC is not primary disease, it is a complication of some underlying diseases , such as 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 DICmorphology of DIC

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

INFARCTIONINFARCTION

infarct is a localized ischemic necrosis in an organ or tissue resulting from sudden occlusion of arterial supply

CAUSES OF INFARCTIONS: 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

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 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:

Infarcts can be divided into two types: white (anemic) red (hemorrhagic)

the distinction is given only by amount of hemorrhage that occurs in necrotic area, the difference is not principal

1. WHITE, PALE INFARCTS in solid organs (heart, spleen, kidney)- firm consistency of the organ

does not permit blood inflow into the necrotic area 2. RED, HEMORRHAGIC INFARCTS

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 MORPHOLOGY OF DEVELOPING INFARCTINFARCT

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 -

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 kidneyInfarction of the kidney

Slide 5

Coagulative necrosisCoagulative necrosis

Myocardial infarct

Coagulative necrosisCoagulative necrosis

Kidney infarct

necrosis

Necrotic tissue

Viable tissue

Demarcation line

Coagulative necrosisCoagulative necrosis

Infarct of the spleen

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 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- smooth-walled, glia-lined cavity (postmalatic pseudocyst)

in intestine- infarction causes death if not removed surgically- no development

FACTORS THAT INFLUENCE THE DEVELOPMENT OF

INFARCT 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

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

-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

the susceptibility of a given tissue to hypoxia influence the likelihood of infarction

neurons and nervous tissue- irreversible 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

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

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:

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

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)

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.

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 endotoxin-mediated 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 PATHOLOGY AND PATHOGENESIS OF SHOCKPATHOGENESIS OF SHOCK

-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:

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,

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

ARDSARDS

Acute (adult) respiratory distress Acute (adult) respiratory distress syndrome, shock lungsyndrome, shock lung

Diffuse alveolar damage (DAD)Diffuse alveolar damage (DAD)

Result of acute alveolar injury of Result of acute alveolar injury of various etiologyvarious etiology

Triggered by endothelial and/or Triggered by endothelial and/or pneumocyte injurypneumocyte injury

Causes of ARDSCauses of ARDS

Infection

Sepsis*

Diffuse pulmonary infections*

Viral, Mycoplasma, and Pneumocystis pneumonia; miliary tuberculosis

Gastric aspiration*

Physical/Injury

Mechanical trauma, including head injuries*

Pulmonary contusions

Fractures with fat embolism

Burns

Ionizing radiation

Inhaled Irritants

Oxygen toxicity

Smoke

Irritant gases and chemicals

Chemical Injury

Heroin or methadone overdose

Acetylsalicylic acid

Barbiturate overdose

Paraquat

Hematologic Conditions

Multiple transfusions

Disseminated intravascular coagulation

Pancreatitis

Uremia

Cardiopulmonary Bypass

Hypersensitivity Reactions

Organic solvents

Drugs

Pathogenesis of ARDSPathogenesis of ARDS

„„Shock lung“ Shock lung“

„„Diffuse alveolar damage“Diffuse alveolar damage“

Hyaline membranes