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By: Dr. Pamela Josefina T. Fabie
 The abnormal accumulation of fluid in
  the intercellular tissue of body cavities.
    It may be localized or systemic
• ANASARCA – when edema is
  sever and generalized; with
  diffused swelling of all tissues and
  organs in the body




• ASCITES – collection of
  edema fluid in the
  peritoneal cavity
• HYDROTHORAX – collection of
  edema fluid in the thoracic
  (pleural cavity)




  • PERICARDIAL EFFUSION –
    collection of edema fluid in
    the pericardial sac
FACTORS CONTRIBUTING TO EDEMA
               FORMATION

I.        Arteriolar Dilatation –
          inflammation, heat, toxins, neurohumoral excess
          or deficit


II. Reduced Effective Osmotic Pressure
     I.   Hypoproteinemia – malnutrition, cirrhosis, nephrotic
          syndrome, protein-osing gastroenteropathy
     II. Leaky Vascular Endothelium –
          inflammation, burns, trauma, allergy
     III. Lymphatic Obstruction
III. Increased Venous Pressure – congestive heart
     failure, thrombophlebitis, liver cirrhosis


IV. Sodium Retention – excessive salt intake,
    increased tubular reabsorption of sodium
MORPHOLOGY OF EDEMA

A. In Cardiac Failure – edema is most
   severe in the dependent parts of
   the body (“dependent edema”)



B. In Renal Failure – generalized, most
   manifested in loose tissues like the
   face, particularly the eyelids
“Pitting Edema” – finger
pressure over the edematous
subcutaneous tissue displace the
interstitial fluid from the skin to
leave pitted depressions




Edema of the brain and the lungs
are most life-threatening forms;
edema of the brain is encountered
with trauma, infections (meningitis,
brain abscess, encephalitis)
hypertensive crises, etc.
Pulmonary Edema – major manifestation of left
ventricular failure; also found in renal disease, shock, infection
within the lungs, hypersensitivity states
• HYPEREMIA – occurs when arterial and
  arteriolar dilatation produces an increased flow of blood
  into capillary beds, with opening of inactive capillaries

• Causes redness in the affected part;

• Active hyperemia of the skin is seen whenever excess body
  heat must be dissipated like in muscular exercise and high
  fever. “Blushing”
• CONGESTION (Passive Hyperemia)

• Results from impaired venous drainage
• Causes an intensified blue-red colored, accentuated
  when there is an increase of deoxygenated blood –
  “Cyanosis”

• Closely related with edema
Indicates exravasation of blood due to
       rupture of blood vessels
• HEMATOMA – significant
 amount of released blood
 accumulating within a tissue
 forming a massive clot; it may
 be relatively insignificant (as in
 bruise)or life-threatening
PETECHIAE – Minute (1-2mm), typically assoc. with
localized intravascualr pressure, low platelet
counts(thrombocytopenia), defective platelet function, or
clotting factor deficiencies




PURPURA – Slightly larger (3-
5mm), typically assoc. with many of
the same disorders that cause
petechiae, as well in
trauma, vascular inflammation
(vasculitis) or increased vascular
fragility
ECCHYMOSES – Larger (1-2cm), these
are subcutaneous hematomas (bruises)




The erythrocytes in these local hemorrhages are
degraded and phagocytosed by macrophages; the
Hemoglobin (red-blue color) is then enzymatically
converted to Bilirunin (blue-green) and eventually into
Hemosidirin (golden-brown) accounting for a
charateristic color changes in a hematoma
Formation of a solid mass in living blood
      vessels or in the heart from the
constituents of the blood; resultant mass
  is called “Thrombus”. A blood clot is
 formed by coagulation of extravascular
                    blood
DANGERS OF THROMBOSIS

        1.    Diminished or obstructed blood flow
                 ischemia to tissue/organ
             2. Becomes dislodged  Embolus


EMBOLUS – intravascular solid, liquid, or gaseous
mass carried in the bloodstream to some site
removed from its origin, or from its point of entry in
the CVS
INFARCTS – ischemic necrosis of tissues



Arterial Thrombi – dry, friable grey masses
composed of almost regularly arranged
alternating layers of fibrin and platelets with scant
amount of darker red coagulated blood resulting
to laminations known as “Lines of Zhan”.
Venous Thrombi – more gelatinous moist
appearance; called “Stasis or Red Coagulation” or
“Phlebothrombosis” (90% in in veins)




Post-Mortem Clot – cyanotic dark red “Currant
Jelly” or with supernatant portion of coagulated
clear plasma “chicken fat” overlying a portion of
darker hue where the red cells have settled
Detached intravascular solid, liquid or
gaseous mass that is carried by the blood
 to a site distant from its point of origin
SYSTEMIC EMBOLISM – travel through the arterial
circulation; thrombi from the left side of the heart;
affects the heart, lower extremity. Kidneys and spleen.
Almost always cause infarction of the affected parts




PULMONARY EMBOLISM – most common form
and one of the most lethal; 95% arise from the thrombi
withing the veins of the legs
   – SADDLE EMBOLUS – large thrombus lodged in the
     bifurcation of the main pulmonary artery
• AIR OR GAS EMBOLISM– sometimes happen
 after delivery or abortion when it is forced into
 ruptured uterine venous sinuses by the powerful
 contractions of the uterus
  – “Caisson Disease” or decompression
    sickness, bends, chokes – occurs in sudden
    changes in atmospheric pressure and deep-sea
    divers
• FAT EMBOLISM (Circulating fat Microglobules) –
  caused by severe trauma to fat-laden tissues such as
  fractures of bone containing fatty marrows or fat
  depots



• AMNIOTIC EMBOLISM (Amniotic Fluid Infusion)
  – fatal maternal obstetric complication; trauma in
  Labor
A localized area of ischemic
  necrosis in an organ or tissue
resulting from occlusion of either
   its arterial supply or venous
 drainage, either by thrombosis
         and/or embolism
TYPES OF INFARCT

1. ANEMIC (white) – encountered with
arterial occlusion and in solid tissues;
common in heart. Spleen and kidneys




2. HEMORRHAGIC (red) – with venous
occlusions in loose tissues, in tissues with
double circulation and in tissue with
previously congested; common in
lungs, ovarian pedicles, intestine and brain
Infarcts may either be “Septic” or “Bland”
 • Presence or absence of bacterial infection In the
   area of necrosis



Ischemic Coagulative Necrosis – characteristic
cytologic change in all infarcts
A constellation of syndromes, all characterized
    by low-perfusion circulatory insufficiency
 leading to imbalance in the metabolic needs of
 vital organs and the available blood flow; as a
result, oxygen and nutrient delivery to cells and
    removal of waste products are decreased
Signs and Symptoms:
Hypotension, weak thready pulses, cool clammy
skin, tachycardia, alterations in
respiration, sensorium, peripheral cyanosis and
oliguria
CLASSIFICATION OF SHOCK

1. HYPOVOLEMIC – reduction of blood
volume from external loss of blood plasma or
water; reduction in blood volume from internal
loss (internal haemorrhage); heart unable to
pump enough blood to the body


 2. CARDIOGENIC – inadequate circulation of blood due
 to primary failure of the ventricles of the heart to function
 effectively
3. SEPTIC– overwhelming gram-
negatve infections (endotoxemia);
overwhelming gram-positive infections
(endotoxic shock)



 4. NEUROGENIC – occurs in anaesthetic accident
 or spinal cord injury due to vascular tone and
 peripheral pooling of blood
5. ANAPHYLACTIC – initiated by a generalized
immunoglobulin E-mediated hypersensitivity
response; associated with systemic vasodilation and
increased vascular permeability
3 Most Causes of Shock
1. Loss of blood volume – hypovolemic shock
2. Pump Failure – cardiogenic shock
3. Action of Toxins on peripheral vessels – Septic
   and neurogenic shock
Fluid and Hemodynamic Derrangements

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Fluid and Hemodynamic Derrangements

  • 1. By: Dr. Pamela Josefina T. Fabie
  • 2.  The abnormal accumulation of fluid in the intercellular tissue of body cavities.  It may be localized or systemic
  • 3. • ANASARCA – when edema is sever and generalized; with diffused swelling of all tissues and organs in the body • ASCITES – collection of edema fluid in the peritoneal cavity
  • 4. • HYDROTHORAX – collection of edema fluid in the thoracic (pleural cavity) • PERICARDIAL EFFUSION – collection of edema fluid in the pericardial sac
  • 5. FACTORS CONTRIBUTING TO EDEMA FORMATION I. Arteriolar Dilatation – inflammation, heat, toxins, neurohumoral excess or deficit II. Reduced Effective Osmotic Pressure I. Hypoproteinemia – malnutrition, cirrhosis, nephrotic syndrome, protein-osing gastroenteropathy II. Leaky Vascular Endothelium – inflammation, burns, trauma, allergy III. Lymphatic Obstruction
  • 6. III. Increased Venous Pressure – congestive heart failure, thrombophlebitis, liver cirrhosis IV. Sodium Retention – excessive salt intake, increased tubular reabsorption of sodium
  • 7. MORPHOLOGY OF EDEMA A. In Cardiac Failure – edema is most severe in the dependent parts of the body (“dependent edema”) B. In Renal Failure – generalized, most manifested in loose tissues like the face, particularly the eyelids
  • 8. “Pitting Edema” – finger pressure over the edematous subcutaneous tissue displace the interstitial fluid from the skin to leave pitted depressions Edema of the brain and the lungs are most life-threatening forms; edema of the brain is encountered with trauma, infections (meningitis, brain abscess, encephalitis) hypertensive crises, etc.
  • 9. Pulmonary Edema – major manifestation of left ventricular failure; also found in renal disease, shock, infection within the lungs, hypersensitivity states
  • 10.
  • 11. • HYPEREMIA – occurs when arterial and arteriolar dilatation produces an increased flow of blood into capillary beds, with opening of inactive capillaries • Causes redness in the affected part; • Active hyperemia of the skin is seen whenever excess body heat must be dissipated like in muscular exercise and high fever. “Blushing”
  • 12. • CONGESTION (Passive Hyperemia) • Results from impaired venous drainage • Causes an intensified blue-red colored, accentuated when there is an increase of deoxygenated blood – “Cyanosis” • Closely related with edema
  • 13. Indicates exravasation of blood due to rupture of blood vessels
  • 14. • HEMATOMA – significant amount of released blood accumulating within a tissue forming a massive clot; it may be relatively insignificant (as in bruise)or life-threatening
  • 15. PETECHIAE – Minute (1-2mm), typically assoc. with localized intravascualr pressure, low platelet counts(thrombocytopenia), defective platelet function, or clotting factor deficiencies PURPURA – Slightly larger (3- 5mm), typically assoc. with many of the same disorders that cause petechiae, as well in trauma, vascular inflammation (vasculitis) or increased vascular fragility
  • 16. ECCHYMOSES – Larger (1-2cm), these are subcutaneous hematomas (bruises) The erythrocytes in these local hemorrhages are degraded and phagocytosed by macrophages; the Hemoglobin (red-blue color) is then enzymatically converted to Bilirunin (blue-green) and eventually into Hemosidirin (golden-brown) accounting for a charateristic color changes in a hematoma
  • 17. Formation of a solid mass in living blood vessels or in the heart from the constituents of the blood; resultant mass is called “Thrombus”. A blood clot is formed by coagulation of extravascular blood
  • 18. DANGERS OF THROMBOSIS 1. Diminished or obstructed blood flow  ischemia to tissue/organ 2. Becomes dislodged  Embolus EMBOLUS – intravascular solid, liquid, or gaseous mass carried in the bloodstream to some site removed from its origin, or from its point of entry in the CVS
  • 19. INFARCTS – ischemic necrosis of tissues Arterial Thrombi – dry, friable grey masses composed of almost regularly arranged alternating layers of fibrin and platelets with scant amount of darker red coagulated blood resulting to laminations known as “Lines of Zhan”.
  • 20. Venous Thrombi – more gelatinous moist appearance; called “Stasis or Red Coagulation” or “Phlebothrombosis” (90% in in veins) Post-Mortem Clot – cyanotic dark red “Currant Jelly” or with supernatant portion of coagulated clear plasma “chicken fat” overlying a portion of darker hue where the red cells have settled
  • 21. Detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin
  • 22. SYSTEMIC EMBOLISM – travel through the arterial circulation; thrombi from the left side of the heart; affects the heart, lower extremity. Kidneys and spleen. Almost always cause infarction of the affected parts PULMONARY EMBOLISM – most common form and one of the most lethal; 95% arise from the thrombi withing the veins of the legs – SADDLE EMBOLUS – large thrombus lodged in the bifurcation of the main pulmonary artery
  • 23. • AIR OR GAS EMBOLISM– sometimes happen after delivery or abortion when it is forced into ruptured uterine venous sinuses by the powerful contractions of the uterus – “Caisson Disease” or decompression sickness, bends, chokes – occurs in sudden changes in atmospheric pressure and deep-sea divers
  • 24. • FAT EMBOLISM (Circulating fat Microglobules) – caused by severe trauma to fat-laden tissues such as fractures of bone containing fatty marrows or fat depots • AMNIOTIC EMBOLISM (Amniotic Fluid Infusion) – fatal maternal obstetric complication; trauma in Labor
  • 25. A localized area of ischemic necrosis in an organ or tissue resulting from occlusion of either its arterial supply or venous drainage, either by thrombosis and/or embolism
  • 26. TYPES OF INFARCT 1. ANEMIC (white) – encountered with arterial occlusion and in solid tissues; common in heart. Spleen and kidneys 2. HEMORRHAGIC (red) – with venous occlusions in loose tissues, in tissues with double circulation and in tissue with previously congested; common in lungs, ovarian pedicles, intestine and brain
  • 27. Infarcts may either be “Septic” or “Bland” • Presence or absence of bacterial infection In the area of necrosis Ischemic Coagulative Necrosis – characteristic cytologic change in all infarcts
  • 28. A constellation of syndromes, all characterized by low-perfusion circulatory insufficiency leading to imbalance in the metabolic needs of vital organs and the available blood flow; as a result, oxygen and nutrient delivery to cells and removal of waste products are decreased
  • 29. Signs and Symptoms: Hypotension, weak thready pulses, cool clammy skin, tachycardia, alterations in respiration, sensorium, peripheral cyanosis and oliguria
  • 30. CLASSIFICATION OF SHOCK 1. HYPOVOLEMIC – reduction of blood volume from external loss of blood plasma or water; reduction in blood volume from internal loss (internal haemorrhage); heart unable to pump enough blood to the body 2. CARDIOGENIC – inadequate circulation of blood due to primary failure of the ventricles of the heart to function effectively
  • 31. 3. SEPTIC– overwhelming gram- negatve infections (endotoxemia); overwhelming gram-positive infections (endotoxic shock) 4. NEUROGENIC – occurs in anaesthetic accident or spinal cord injury due to vascular tone and peripheral pooling of blood
  • 32. 5. ANAPHYLACTIC – initiated by a generalized immunoglobulin E-mediated hypersensitivity response; associated with systemic vasodilation and increased vascular permeability
  • 33. 3 Most Causes of Shock 1. Loss of blood volume – hypovolemic shock 2. Pump Failure – cardiogenic shock 3. Action of Toxins on peripheral vessels – Septic and neurogenic shock