This document discusses hemodynamic disorders such as edema, thrombosis, embolism, and infarction. It focuses on edema, defining it as abnormal accumulation of fluid in interstitial tissues or body cavities. Edema fluid can be a transudate or exudate depending on its protein content. The document examines the pathogenesis of edema including increased hydrostatic pressure, decreased plasma oncotic pressure, lymphatic obstruction, sodium retention, and inflammation. It also discusses specific types of edema like pulmonary and cerebral edema.

1. Hemodynamic Disorders
P SUNIL KUMAR
Haematology & Transfusion Medicine
St.John’s Medical College
Bangalore
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2. Hemodynamic Disorders
 EDEMA
 THROMBOSIS
 EMBOLISM
 INFARCTION
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3. • Normal fluid homeostasis is maintained by vessel
wall integrity, intravascular pressure and
osmolarity with in certain physiologic ranges
• Changes in intravascular volume,
• Pressure, or
• Protein content, or
• Alterations in endothelial function will affect the
movement of water across the vascular wall.
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7. • Edema (increased fluid in the ECF)
• Hyperemia (INCREASED flow)
• Hemorrhage (extravasation)
• Hemostasis (opposite of thrombosis)
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8. • Hemostasis (opposite of thrombosis)
• Thrombosis (inappropriate clotting blood)
• Embolism (downstream travel of a clot)
• Infarction (death of tissues w/o blood)
• Shock (circulatory failure/collapse)
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9. Oedema
• Definition of Oedema
• Types of oedema
• Transudate & Exudate
• Differences B/w Trans .. & Exudate
• Pathogenesis of Edema
• Other types of oedema
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10. DEFINITION………OF
Edema/Odema
• The Greek word “oidema” means swelling.
• Odema/ Edema may be defined as abnormal
and excessive accumulation of ‘free fluid’ in
the interstitial tissue spaces and serous
cavities.
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11. Edema/oedema
• The presence of abnormal collection of fluid
within the cells…… is sometimes called
intracellular oedema or hydropic
degeneration.
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14. • Oedema can be….
• 1. Free fluid in body fluid cavities
• 2. Free fluid in interstitial space
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15. Free fluid in body fluid cavities …..
• Depending upon the body cavity in which the
fluid accumulates , it correspondingly known
as …..
• Peritoneal cavity…. ( Ascites)
• Pleural cavity ….(Pleural effusion/Hydrothorax)
• Pericardial Cavity ……(Pericardial effusion
/Hydro pericardium)
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16. Peritoneal cavity….
( Ascites)
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17. Peritoneal cavity…. ( Ascites)
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18. Radiological Features in Ascites
Normal US ABD Ascites…. Ultra Sound ABD
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19. Radiological Features in Ascites
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20. NORMAL CHEST X - RAY
NORMAL CHEST X- RAY
NORMAL CHEST X- RAY
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21. PERICARDIAL EFFUSION
OR
HYDRO PERICARDIUM
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22. Normal Pericardium VS Pericardial
Effusion
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23. PERICARDIAL EFFUSION
RADIOLOGICAL FEATURES
NORMAL CHEST X- RAY PERICARDIAL EFFUSION
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24. Pleural cavity
Pleural
effusion/Hydrothorax
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25. Pleural Effusion
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26. Pleural Effusion Radiological Features
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27. Free fluid in interstitial space…….
• The oedema fluid lies free in the interstitial
space between the cells and can be displaced
from one place to another.
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29. Types of oedema
• Mainly two types
• 1. Localised Oedema
• 2.Generalised Oedema
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30. 1. Localised Oedema
• Localised when limited to an organ or limb.
• Examples :
• 1. Lymphatic oedema.
• 2.Inflammatory oedema
• 3.Allergic oedema
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31. 2.Generalised Oedema
• Generalised Oedema ( Anasarca or dropsy)
• When it is systemic in distribution, particularly
noticeable in the subcutaneous tissues .
• Examples:
• 1.Renal oedema
• 2.Cardiac oedema
• 3.Nutritional oedema
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32. Other forms of Oedema
• Pulmonary oedema
• Cerebral oedema
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33. Depending upon fluid composition,
oedema fluid may be…..
• 1. Transudate
• 2. Exudate
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34. 1.Transudte
• A Transudate is a filtrate of blood.
• Transudate is extra vascular fluid with low protein
content and a low specific gravity (< 1.012).
• It has low nucleated cell counts
• It is due to increased pressure in the veins and
capillaries.
• That forces fluid through the vessel walls or to a low
level of protein in blood serum.
• Transudate accumulates in tissues outside the blood
vessels and causes edema (swelling).
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35. 2.Exudate
• An exudate is any fluid that filters from the
circulatory system into lesions or areas of
inflammation.
• a fluid with a high content of protein and
cellular debris
• That has escaped from blood vessels and has
been deposited in tissues or on tissue
surfaces, usually as a result of inflammation
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36. 10/13/2018 36SUNIL KUMAR P

37. Pathogenesis of Oedema
• Oedema is caused by mechanisms that
interfere with normal fluid balance…..
• of Plasma
• Interstitial fluid and
• Lymph flow
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38. Pathogenesis of Oedema
• 1.Decreased plasma oncotic pressure.
• 2.Increased capillary Hydrostatic pressure
• 3.Lymphatic obstruction
• 4. Sodium and Water retention
• 5.Inflammation
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39. Patho-physiologic Causes of Edema
• 1.Increased Capillary Hydrostatic Pressure :
Impaired venous return.
• Examples of oedema by this mechanisms …..
• 1.Oedema of cardiac diseases : congestive
cardiac failure
• 2.Ascites of liver disease : Cirrhosis of the liver
• 3.Passive congestion : Varicosities
• 4.Postural oedema
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40. 2.Reduced plasma osmotic pressure
( Hypo-proteinemia) :
• Examples of oedema by this mechanisms
• 1.Oedema of renal disease : Nephrotic
syndrome, acute glomerulonephritis
• 2. Ascites of liver disease: Liver cirrhosis,
• 3.Protein – losing enteropathy
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41. 3.Lymphatic Obstruction :
• Neoplastic,
• post surgical.
• Inflammation of the lymphatic's
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42. • 4.Sodium and water Retention :
Excessive salt intake with renal insufficiency
• 5.Inflammation :
– Acute inflammation, chronic inflammation
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43. Types of edema
• Peri orbital edema: is a characteristic finding
in severe renal disease.
• Pitting edema: finger pressure over
substantially edematous subcutaneous tissue
displaces the interstitial fluid and leaves a
finger shaped depression
• Pulmonary edema: most typically seen in the
setting of left ventricular failure
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44. Fetal Anasarca
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45. Subcutaneous Edema
• can be diffused but usually accumulates preferentially
in parts of the body positioned the greatest distance
below the heart where hydrostatic pressures are
highest
• Thus, edema typically is most pronounced in the legs
with standing and the sacrum with recumbency, a
relationship termed dependent edema.
• Pitting edema - a finger-shaped depression when the
finger leaves pressure over edematous subcutaneous
tissue that displaces the interstitial fluid
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46. “Pitting” Edema
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47. Periorbital Edema
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48. Pulmonary Edema
• Acute pulmonary oedema is the most
important form of local oedema as it causes
serious functional impairment but has special
features….
• Pulmonary oedema due to
• 1.Elevation in pulmonary hydrostatic pressure
• 2.Increased Vascular permeability
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49. Cerebral edema
• Cerebral oedema or swelling of brain is the
most threatening example of oedema.
• The mechanisms of fluid exchange in the brain
differs from elsewhere in the body …
• Since there are no draining lymphatic's in the
brain but instead the function of fluid
exchange is performed by the blood –brain
barrier located at endothelial cells of the
capillaries
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50. Cerebral oedema can be of 3 types
• 1.Vasoenic oedema
• 2.Cytotoxic oedema
• 3.Interstital oedema
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51. Renal oedema
• Generalised oedema occurs in certain diseases
of renal origin such as….
• In nephrotic syndrome,
• Some types of glomerulonephritis and
• In renal failure
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52. HEMOSTASIS AND THROMBOSIS
• Normal hemostasis comprises a series of
regulated processes that maintain blood in a
fluid, clot-free state in normal vessels while
rapidly forming a localized haemostatic plug
at the site of vascular injury.
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53. • The pathologic counter part of hemostasis is
thrombosis, the formation of blood clot
(thrombus) within intact vessels.
• Both hemostasis and thrombosis involve three
elements:
• the vascular wall,
• platelets, and
• the coagulation cascade.
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54. • Normal hemostasis result of a set of well-
regulated processes that accomplish two
important functions:
• (1)They maintain blood in a fluid, clot-free
state in normal vessels.
• (2)They are aimed to induce a rapid and
localized haemostatic plug at a site of vascular
injury
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55. Thrombosis:
• Thrombosis is the process of formation of
solid mass in circulation from the constituents
of flowing blood; the mass itself is called a
thrombus.
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56. PATHOPHYSIOLOGY
• Since the protective haemostatic plug formed
as a result of normal hemostasis is an example
of thrombosis.
• It is essential to describe the thrombogenesis
in relation to the normal haemostatic
mechanisms
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57. • Virchow described three primary events which
predispose to thrombus formation(virchow’s triad)
• Three primary causes for thrombus formation, the so-
called Virchow triad:
• 1.Endothelial injury
• 2.Altered blood flow
• 3.Hypercoagulability of blood.
• To this added the processes that follow these primary
events; activation of platelets & clotting sysytem
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58. Virchow triad in thrombosis.
• Endothelial integrity is the
single most important factor.
Note that injury to endothelial
cells can affect local blood
flow and/ or coagulability
;abnormal blood flow(stasis or
turbulence)can, inturn, cause
endothelial injury. The
elements of the triad may
actin dependently or may
combine to cause thrombus
formation.
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59. • 1.Endothelial injury
• 2.Role of platelets
• 3.Role of coagulation system
• 4.Alteration of blood flow
• 5.Hypercoagulability of blood
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60. 1.Endothelial injury
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61. 10/13/2018 61SUNIL KUMAR P

62. • Thrombi may develop any where in the
cardiovascular system, but stasis is a major
factor in the development of venous thrombi
• An area of attachment to the underlying
vessel or heart wall, frequently firmest at the
point of origin, is characteristic of all
thromboses.
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63. • The propagating tail may not be well attached
and, particularly in veins, is prone to
fragmentation, creating an embolus.
• Mural thrombi-arterial thrombi that arise in
heart chambers or in the aortic lumen, that
usually adhere to the wall of the underlying
structure
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64. 2. Role of platelets
• Following endothelial injury, platelets come to
play a central role in normal hemostasis as
well as thrombosis .
• The sequence of events are
• 1.Platelet adhesion
• 2.Platelet release reaction
• 3.platelet aggregation
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65. 3.Role of Coagulation System
• Coagulation mechanisms is the conversion of
the plasma fibrinogen into solid mass of fibrin.
• The coagulation system is involved in both
haemostatic process and thrombus formation.
• 1. In the intrinsic pathway
• 2.in the extrinsic pathway
• 3.in the common pathway
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66. 4. Alteration of blood flow
• Turbulence : meaning unequal flow
• Stasis : meaning slowing
• Turbulence and slowing occur in thrombosis in
which the normal flow of blood is disturbed.
• When blood is slows thrombi is facilitated by
turbulence in the blood flow,
• While stasis initiates the venous thrombi even
without evidence of endothelial injury.
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67. 5.Hypercoagulability of blood
• Hypercoagulablity of blood occur by the
following changes in the composition of
blood.
• 1.Increase in coagulation factors : eg;
fibrinogen, prothrombin, FVIIa, VIIIa nd Xa
• 2.increase in platelet count
• 3.Decreased levels of coagulation inhibitors :
eg; Antithrombin III , fibrin split products.
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68. Morphological features
• Thrombosis may occur in the heart, arteries,
veins and the capillaries.
• Arterial thrombi produce ischemia, and
infarction , whereas cardiac and venous
thrombi cause embolism.
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69. Thrombosis
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70. • Muralthrombi.
• Thrombus in the left and
right ventricularapices,
overlying a white fibrous
scar.
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71. Mural thrombi.
• Laminated thrombus in a
dilated abdominal aortic
aneurysm
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72. Fate of the Thrombus.
• 1. Resolution
• 2.Organisation
• 3.Propagation
• 4.Thromboembolism
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73. 1. Resolution
• Thrombus activates the fibrinolytic system
with consequent release of plasmin which my
dissolve the thrombus completely resulting in
resolution.
• Eg; of activators of fibrinolytic activity are
• 1.urokinase
• 2.streptokinase
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74. 2.Organisation
• 1. if the thrombus is not removed, it starts
getting organised.
• 2.Phagocytose cells appear and begin to
phagocytose fibrin and cell debris.
• 3.The proteolytic enzymes liberated by
leukocytes and endothelial cells start
digesting coagulum.
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75. 3.propagation
• The thrombus may enlarge in size due to more
and more deposition from the constituents of
flowing blood.
• In this way , it may ultimately cause
obstruction of some important vessel.
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76. 4.Thromboembolism
• 1. the thrombi in early stage and infected
thrombi are quite friable and may get
detached from the vessel wall.
• These are released in part or completely in
bloodstream as emboli which produce ill –
effects at the site of their lodgement.
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77. Clinical effects
• 1. cardiac thrombi
• 2.arterial thrombi
• 3.venous thrombi
• 4.capillary thrombi
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78. Embolism
• An embolus is a detached intravascular solid,
liquid, or gaseous mass that is carried by the
blood to as it distant from its point of origin.
• Emboli lodge in vessels too small to permit
further passage, resulting in partial or
complete vascular occlusion
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79. Pulmonary Thrombo-embolism
• 95% of venous emboli originate from deep
leg vein thrombi
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80. • Large embolus derived
from a lower extremity
deep venous thrombosis
and now impacted in a
pulmonary artery branch.
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81. Systemic Thrombo embolism
• Emboli traveling within the arterial circulation.
• •Most (80%) arise from intra-cardiac mural
thrombi,
• •Two thirds of which are associated with left
ventricular wall infarcts
• •The major sites for arteriolar embolizationare:
• 1. Lower extremities (75%)
• 2. Brain (10%)
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82. A-Fat Embolism
• Microscopic fat globules may be found in the
circulation after fractures of long bones
(which have fatty marrow) or, rarely, in the
setting of soft tissue trauma and burns.
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83. Amniotic Fluid Embolism
• •Underlying cause is the infusion of amniotic
fluid or fetal tissue in to the maternal
circulation via a tear in the placental
membranes or rupture of uterine veins.
• Characterized by sudden severe dyspnea,
cyanosis, and hypotensive shock, followed by
seizures and coma.
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84. Infarction
• An infract is an area of ischemic necrosis
caused by occlusion of either the arterial
supply or the venous drainage in a particular
tissue.
• Nearly 99% of all infarct result from
thrombotic or embolic events, and almost all
result from arterial occlusions
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85. Infarction
• Infarcts are classified on the basis of their
color (reflecting the amount of hemorrhage )
and the presence or absence of microbial
infection.
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86. Red(hemorrhagic)infarcts occur
• 1.withvenousocclusions (such as in ovarian
torsion)
• (2)in loose tissues(such as lung)
• (3)In tissues with dual circulations ( e.g./ lung
and small intestestine.
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87. White(anemic)infarcts occur
• 1. With arterial occlusions in solid organs with
endo arterial circulation (such as heart,
spleen, and kidney.)
• 2.Solidtissues
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88. Examples of infarcts.
• (A) Hemorrhagic, roughly
wedge-shaped pulmonary
infarct.
• (B) Sharply demarcated
white infarct in the spleen.
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89. • The dominat histologic characteristics of
infarction is ischemic coagulative necrosis.
• Most infracts are ultimately replaced by scar
tissue.
• The brain is an exception in to theses
generalizations ischemic injury in the central
nervous system results in liquefactive necrosis
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90. • Septic infarctions may develop when
embolization occurs by fragmentation of a
bacterial vegetation from a heart valve or
when microbes seed an area of necrotic
tissue.
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