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Thrombosis, Embolism and Shock Professor Arundathi P. Kurukulasuriya MBBS, Dip.Path,MD(Haem),FRCPA, AS THE, SFSEDA

Thrombosis Embolism and Shock

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Text of Thrombosis Embolism and Shock

  • Thrombosis, Embolism and Shock

    Professor Arundathi P. KurukulasuriyaMBBS, Dip.Path,MD(Haem),FRCPA, AS THE, SFSEDA

  • Fluid Homeostasis

    Cells and tissues need oxygen, removal of waste material and also an intact vascular system which carries these to and fro.

    Normal fluid homeostasis needs

    Normal :

    vessel wall

    Intravascular pressure


  • Altered Fluid Homeostasis

    Increased movement of water across the vessel wall is caused by :


    vessel wall/ function

    Intravascular pressure


    It is called oedema

  • Oedema

    Increased movement of water across the vessel wall in to interstitial spaces

    Swelling of legs : Oedema of lower limbs

    In the lungs : Pulmonary Oedema

    In the peritoneal cavity : Ascites

    In the thoracic cavity: Hydrothorax





    Congestion :

    Passive process. Collection of blood in vasculature due to poor venous return (has a cyanotic tinge)

    *What is the colour of cyanosis? Why?

  • Congestion in Organs

    Lungs : In Left ventricular failureAcute

    Capillaries engorged with blood, focal intra alveolar haemorrhage, alveolar septal oedema


    Alveolar septa are thickened, fibrotic, Haemosiderin laden macrophages maybe present.

    What are these haemosiderin laden macrophages called?

    Heart Failure cells

    Why are they laden with haemosiderin?

    Engulf extravasated red cells in the alveoli



  • Congestion in Organs cont

    Centrilobular necrosis -

    Central vein with necrosis

    of cells around it caused by

    passive congestion in

    hepatic vein

    Liver : Macroscopy and microsdcopy

    Why is it called the nutmeg (Saddika) appearance of liver?

  • Some Definitions


    Fluid which leaks out due to increased hydrostatic pressure. Spg 1.012

    Exudate :

    Fluid leaks out due to inflammation associated with increased vascular permeability, is protein rich

    Spg 1.012

  • Nephrotic syndrome

    Liver cirrhosis

    Protein malnutrition

    How does this cause oedema??

    Low Albumin causes

    low intravascular osmotic


    Fluid moves out in to

    interstitial tissue


    List conditions where there is

    low Albumin in the body

  • Lymphatic Obstruction

    Localised :


    Ca breast post surgical removal of lymph nodes

    What is Paud o range ??

  • Paud o range appearance due to tethering of skin in


  • Pathophysiologic Categories of oedema

    Increased Hydrostatic Pressure Impaired venous return Congestive heart failure Constrictive pericarditis Ascites (liver cirrhosis) Venous obstruction or compression Thrombosis External pressure (e.g., gravid uterus, enlarged lymph

    node) Lower extremity inactivity with prolonged dependency Arteriolar dilation Heat Neurohumoral dysregulation

  • Pathophysiologic Categories of oedema Cont

    Reduced Lymphatic Obstruction





  • Pathophysiologic Categories of oedema

    Plasma Osmotic Pressure (Hypoproteinemia)

    Protein-losing glomerulopathies (nephrotic syndrome)

    Liver cirrhosis (ascites)

    Malnutrition Protein-losing gastroenteropathy

  • Pathophysiologic Categories of oedema

    Sodium Retention

    Excessive salt intake with renal insufficiency Increased tubular reabsorption of sodium Renal hypoperfusion

    Increased renin-angiotensin-aldosterone secretion

  • Pathophysiologic Categories of oedema


    Acute inflammation

    Chronic inflammation


  • Quiz Time

    Give yourself 1 mark for answering correctly

    What is the oedema of peritoneal space of abdomen called?


    In the lung parenchyma?

    Pulmonary oedema

    In encephalitis which organ may show odema?


  • Quiz Time

    Where would you expect oedema to occur in congestive cardiac failure?

    Dependent lower extremities

    In renal failure?

    Areas with loose subcutaneous connective tissue ie. peri orbital tissue

    Whats your score??

  • Maintaining Blood In Its Fluid State; What happens when its not

    maintained Thrombosis : inappropriate clotting in the

    living body

    Migration of clots to distant sites : embolisation

    Obstruction of blood flow to tissues causing cell death: infarction

    Inability to clot when necessary leads to: haemorrhage

    Extensive haemorrhage may result in : Shock

  • Quiz Time Cont

    1. Define oedema

    2. Classify the different mechanisms / aetiology of oedema

    3. Draw a diagram of the circulatory system and explain how fluid homeostasis is maintained

  • List three main causes of haemodynamic disorders associated with high mortality in the western


    1. Myocardial infarction

    2. Pulmonary embolism

    3. Cerebrovascular accidents

  • Normal Haemostasis

    Fluid blood within the vascular system poised to clot rapidly at focal points of vascular injury, when necessary

  • Rudolf Virchow

    German Pathologist

    Virchow Triad

  • Axial (Laminar) Flow in Blood Vessels

    Vascular Endothelium

    Platelets and white

    blood cells

    Plasma layer between cells in

    axial stream and the endothelium

  • What Disturbs The Laminar Flow?



  • What Happens When Laminar Flow Is Disturbed?

    1. Platelets come in contact with vessel wall

    2. Prevent dilution of activated clotting factors

    3. Retard inflow of anti thrombotic factors

    4. Promote endothelial cell activation

  • What Factors Injure The Endothelium

    Direct injury especially in the heart & arterial system:

    Scars from myocardial ischaemia

    Damaged valves

    Atheromatous plaques


  • What Factors Injure The Endothelium Cont

    Haemodynamic stress of hypertension

    Bacterial endotoxins




  • Protective Mechanisms To Prevent Thrombosis

    Axial flow

    Intact Endothelium

    Inactive clotting Factors

    Inert Platelets

    Inert prothrombotic pathways

    Normal fibrinolysis

  • Thrombosis

    Inappropriate activation of haemostatic mechanism leading to clot formation in the living body

    Ie. in uninjured /injured vasculature

    HITTS (Heparin induced thrombosis, thrombocytopenia syndrome)

    Lupus anticoagulant induced thrombosis

    AV fistulae

  • Thrombus

    A mass formed from constituents of blood, within the vascular system, in the living body

  • Primary Haemostasis Vascular injury

    Exposure of subendothelium to platelets

    Tissue Factor (TF)release**

    Platelets are activated shape change

    Platelet adhesion aggregation

    Platelet plug formation (white clot)

    Primary haemostatic plug forms

    *Arterial system favour white thrombi formation due to high shear rates

  • Normal Haemostasis

  • Properties of Vascular Endothelium

    Related To Haemostasis

  • Thrombus Formation

  • Types of Thrombi

    Red In the venous circulation

    Contains fibrin, more red cells and platelets

    Forms in conditions where stasis of blood flow occurs

    White Arterial circulation

    Consists mainly of platelets and fibrin

    Forms because it is in high shear rate flow

  • Formation of a red thrombus

    Columns of Zahn

    Identify the different


  • This vessel has an acute thrombus

    with some faint lines of Zahn (platelet-

    fibrin columns (arrow)), transmural

    arterial inflammation

  • Columns of Zahn in a thrombus

  • What is this thrombus called?

    Where in the circulation do they form more often?

  • Activated Platelets

  • Mind Map

  • Fate of A Thrombus

    Propagation along vessel in the direction of blood flow





  • Fate of A Thrombus

  • Embolus

    Is detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin

  • Thrombus


    How an embolus


  • Types Of Embolisation





  • Pulmonary Embolism

    Emboli commonly arise in the veins above knee in the lower limbs

    Most emboli are small and resolve

    Are large and block arterioles

    When 60% or more of the circulation is obstructed sudden death, cardiac failure may ensue

    Multiple emboli over a period of time cause pulmonary hypertension

  • Fat Embolism

    Occurs with fractures of long bones /Soft tissue injury

    Occurs about 1-3 days after injury

    Tachypnoea, dyspnoea, confusion, irritability purpura, thrombocytopenia and anaemia

    ( Symptoms related to CNS, RS, Blood)

  • Fat Embolism



    Fat Embolism In The Brain

  • Air Embolism

    May occur during obstetric procedures

    Chest wall injuries

    Decompression sickness *

    >100cc of air is required to make any impact

    * When gas dissolves under high pressure like in deep sea divers and IF they ascend fast to the surface(depressurising) the nitrogen bubbles out of solution and form gas bubbles

    Home Work : Read Caisson Disease

  • Air Embolism Cont

    Rapid formation of gas bubbles within the vessels of skeletal muscles cause pain

    Arch their backs bends

    Focal ischaemia results in the brain, heart, in the lung focal haemorrhagic points may occur

    Treatment: compression chamber where the gas forced back in to solution and then allowed to dissolve out slowly instead of rapidly forming air bubbles

  • Amniotic Fluid Embolism

    Occurs during labour and immediate post partal period

    Mortality 20 - 40%

    sudden severe dyspnoea, cyanosis, hypotensive shock, followed by seizures and coma. If the patient survives the initial crisis, pulmonary edema typically develops, along with (in half the patients) DIC, owing to release of thrombogenic substances from amniotic fluid.

  • Squames

    Amniotic fluid embolism

  • Amniotic Fluid Embolism Cont


    Infusion of amniotic fluid or fetal tissue into the maternal circulation via a tear in the placental membranes or rupture of uterine veins.

    The classic findings : the presence in the pulmonary microcirculation of squamous cells shed from fetal skin, lanugo hair, fat from vernix caseosa, and mucin derived from the fetal respiratory or gastrointestinal tract.

  • Amniotic Fluid Embolism Cont

    marked pulmonary edema and changes of diffuse alveolar damage

    systemic fibrin thrombi indicative of DIC.

  • Clinical Correlation

    Emboli in the arterial system

    cause ischaemia

    Infarcts in brain, myocardium etc

    Emboli in the venous system

    Pain, swelling, tenderness, decolourisation of skin etc due to stasis and congestion.

  • Clinical Correlation Cont

    What is Deep Vein Thrombosis(DVT) ?

    Superficial Vein Thrombosis(SVT) ?

    When is DVT likely to occur?

    Give reasons

  • Secondary Haemostasis

    Formation of fibrin clot (red thrombus)

    Coagulation cascade

    Antifibrinolytic pathway

    In the venous system red thrombi formation occurs

  • Hypercoagulable States Primary (Genetic)


    Factor V Leiden

    Prothrombin gene mutation


    Protein C, S deficiency

    Anti thrombin deficiency

    Very Rare

    Defects in fibrinolysis

  • Hypercoagulable Statessecondary (Acquired) High Risk

    Prolonged bed rest

    Surgery, fracture, burns

    Myocardial infarction

    Prosthetic cardiac valves


    Lupus anticoagulant

    Antiphospholipid antibody syndrome

    HITTS (heparin induced thrombocytopenia thrombosis syndrome)

  • Hypercoagulable Statessecondary (Acquired) Low Risk



    Oral contraceptive use

    Nephrotic syndrome

    Treatment with cytarabine in acute leukaemia

  • Effects of Thrombi

    Reduces blood flow to organs


  • Difference Between Thrombus and A Postmortem Clot

    Thrombus Forms in the living body

    Is firmly lodged on the endothelial surface

    Columns of Zahn* can be seen microscopically

    Postmortem clot

    Forms in the dead body

    Can be dislodged easily, not attached to vessel wall

    Red cell precipitate to the bottom and chicken fat like jelly like plasma is on top

  • Coagulation


  • Antifibrinolytic Pathway

  • Platelet


    Blood vessel


    Activation of



    Formation of

    platelet thrombus

    Fibrin Clot


    Physiological inhibitors of

    coagulation and platelet

    activation Inhibting factors

    Vessel Injury

    In a nut shell

  • Defects in Coagulation Cascade


    Absence of

    defective function of coagulation factors


    Activation of coagulation

    Reduced antithrombotic mechanisms

  • Clinical Conditions Caused By

    Absence of Platelet Glycoproteins

  • Bleeding Disorders

    Defects in :



    Fibrinolytic Pathway

    Vascular endothelium

  • Hyphema commonly occurs

    after trauma

    A hyphema is an

    accumulation of

    blood in the anterior

    chamber of the

    eye. This is the

    space between the

    cornea (front clear

    surface of the eye)

    and iris (colored part

    of the eye).

  • Commonly caused by vascular or platelet defects

    1. Purpura

    2. Petichiae

    3. ecchymoses

  • Ecchymoses

  • Coagulation Defects

    Haemarthrosis in weight bearing

    joints in FVIII deficiency

    ( Haemophilia)

  • Queen victoria was a

    carrier of

    Haemophilia B

    Haemophilia has featured prominently in European royalty and thus is

    sometimes known as 'the royal disease'. Queen Victoria passed the

    mutation for Haemophilia B to her son and, through some of her

    daughters, to various royals across the continent, including the royal

    families of Spain Germany and Russia. In Russia, Tsarevich Alexei

    Nikolaevich son of Nicholas II was a descendant of Queen Victoria

    through his mother Empress Alexandra and suffered from haemophilia.

  • Microangiopathic haemolytic

    Anaemia : Disseminated

    intravascular coagulation (DIC)


  • Acquired haemophilia : Inhibitors to

    FVIII molecule

  • Balance Between Thrombosis