Disorders of vascular flow: edema, congestion, hemorrhage by vRaGRt

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									 Disorders of vascular flow:
    edema, congestion,
 hemorrhage, thrombosis,
embolism. Shock. Infarction.
            2011
                           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
Edema
    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 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
   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
   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
                       THROMBOSIS
   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
Thrombosis




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 appendices 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
     Thrombosis


          Coronary
         thrombosis
        occurs mainly in the
             setting of
       atherosclerosis




Thrombosis 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 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:
   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
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
           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 infarct
 Pulmonary hemorrhagic infarct




Normal lung parenchyma   Infarct
            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

   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 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 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
   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 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
                         INFARCTION
       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
            INFARCT
   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 kidney




       Slide 5
Coagulative necrosis




    Myocardial infarct
Coagulative necrosis




     Kidney infarct
Necrotic
 tissue


                                         Viable
                                         tissue




           necrosis   Demarcation line
Coagulative 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 PATHOGENESIS
            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
                     ARDS

   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
                                                                 Barbiturate overdose
                        tuberculosis
                  Gastric aspiration*                                   Paraquat

                 Physical/Injury                            Hematologic Conditions
      Mechanical trauma, including head injuries*                Multiple transfusions
                Pulmonary contusions                     Disseminated intravascular coagulation
             Fractures with fat embolism
                                                                    Pancreatitis
                         Burns
                                                                       Uremia
                   Ionizing radiation

                Inhaled Irritants                          Cardiopulmonary Bypass
                    Oxygen toxicity                       Hypersensitivity Reactions
                        Smoke                                      Organic solvents

             Irritant gases and chemicals                                Drugs
Pathogenesis of ARDS
„Shock lung“
„Diffuse alveolar damage“




            Hyaline membranes

								
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