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Pathology Seminar
   October 2010
 Year 4 Medicine
Group 1 UST Sana’a
Introduction
                  
 DIC stands for Disseminated intravascular
  coagulation.
 It is the disturbance of the blood clotting mechanism.
 Several clots in some vessels  increase
  consumption of the blood clotting factors and
  platelets deficiency, lack or destruction of those
  factors in other body parts Several bleedings in
  other areas of the body.
DIC Presentation
Normal Hemostasis
            
 During vascular injury hemostasis normally occurs
  on the affected site. The hemostasis has four phases:
 1. Vasoconstriction then,
 2. Primary phase,
 3. Secondary phase,
 4. Tertiary phase,
VASOCONSTRICTION




After vascular injury occurs there are certain
factors of neurohumoral type released causing
transient vasoconstriction to the affected site.
PRIMARY HEMOSTASIS




Platelets adhere (via GpIb receptors) to exposed
extracellular matrix by binding to von Willebrand factor
and are activated, undergoing a shape change and granule
release. Released adenosine diphosphate and thromboxane
A2 lead to further platelet aggregation (via binding of
fibrinogen to platelet GpIIb-IIIa receptors), to form the
primary hemostatic plug.
SECONDARY HEMOSTASIS




Local activation of the coagulation cascade (involving
tissue factor and platelet phospholipids) results in
fibrin polymerization, "cementing" the platelets into a
definitive secondary hemostatic plug.
TERTIARY HEMOSTASIS




Counter-regulatory mechanisms, such as release of t-
PA (Tissue plasminogen activator, a fibrinolytic
product) and thrombomodulin (interfering with the
coagulation cascade), limit the hemostatic process to
the site of injury.
1)   Generation of a hyperthrombinemic state
2)   Alteration of the physiological anticoagulants
     levels
3)   Impaired fibrinolysis at the onset of the DIC:
4)   Activation and liberation of inflammatory
     cytokines in the pathogenesis of DIC
Generation of a
  1)

  hyperthrombinemic state
                           
 The exposing of the tissue factors thromboplastin and
  factor III during injury causes a cascade activation of a
  factor pathway that has a dominant role in the
  hyperthrombinemic state in DIC.
 Cytokines and bacterial endotoxin are all triggers to the
  formation of endothelial cell tissue factor.
 In severe trauma also tissue phospholipids initiates the
  clotting cascade.
cont.: The   cascade goes here as follows
                        
cont.: The   Thrombin in turn activates

                      
Alteration of the physiological
2)

anticoagulants levels
                               
      There are 3 most common Anticoagulants in the
       body:
        Antithrombin,
        Active Protein C
        Tissue factor pathway inhibitor (TFPI).
      In DIC:
        ↓Antithrombin
        ↓Active Protein C
cont.:   The cause of the decrease
                       
DIC Presentation
Protein C function
        
 Normally     In DIC
cont.:   Protein C’s Importance
                      
Impaired fibrinolysis at the onset of
3)

the DIC:
                            
      Plasminogen activator inhibitor 1 (PAI-1) is a
       neurohumoral compound released by the endothelial
       cells at the effected site.
      PAI-1 suppresses the normal fibrinolysis activity.
      Some DIC individuals have shown a mutation in the
       PAI-1 gene, leading to an increased plasma PAI-1
       levels.
DIC Presentation
Activation and liberation of inflammatory
4)

cytokines
                                
      Activation of Clotting sys.  Inflammatory cascade
       activation Induced pro-inflammatory cytokines
       (thrombin and other serine proteases).
      Pro-inflammatory cytokines + Protease-activated
       receptors (of the cell surface of the endothelial cells)
        Inducing an inflammatory and clotting reaction.
DIC Presentation
Signs & symptoms of DIC
                         
 Renal failure.
 Cough
 Confusion.
 Decreased platelets.
 Blood clots.
 Drop in blood pressure.
 Sudden bruising.
 Bleeding, possibly from multiple sites in the body.
 Fever
Sites of Thrombosis
          
     Site in decreasing
     order of frequency
     Brain
     Heart
     Kidney
     Adrenals
     Spleen
     Lungs
     Liver
DIC Presentation
DIC Is most likely to occur after sepsis, obstetric
 complications, malignancy, and major trauma
        (especially trauma to the brain)
Obstetric complications
            
 Abruption placentae
 Retained dead fetus
 Septic abortion
 Amniotic fluid embolism
 Toxemia
Infections
                   
 Sepsis (gram negative and gram positive)
 Meningococcemia
 Rocky Mountain spotted fever
 Histoplasmosis
 Aspergillosis
 Malaria
Neoplasms
                 
 Carcinomas of pancreas, prostate, lung, and stomach
 Acute promyelocytic leukemia
Massive Tissue Injury
            
 Trauma
 Burns
 Extensive surgery
Miscellaneous
                
 Acute intravascular hemolysis,
 Snakebite,
 Giant hemangioma
 Shock
 Heat stroke
 Vasculitis
 Aortic aneurysm,
 Liver disease
 Rejection of graft
1.   CBC
2.   Clotting times:
3.   Fibrin related markers important for the
     diagnosis of DIC:
4.   Coagulation factors:
Labinvestigations of DIC
CBC
thrombocytopenia is usually present
Clotting times:
                                     
Prothrombin time (PT) – prolonged (may be normal in early or chronic DIC)
Partial thromboplastin time (PTT) – prolonged (may be normal in early or
chronic DIC)
Thrombin time (TT) – may be increased due to consumption of fibrinogen
Fibrin related markers important for the diagnosis of DIC:
D-dimer – increased in acute and chronic DIC (best single test)
A normal d-dimer essentially rules out DIC
Elevated d-dimer levels are seen in a number of conditions in addition to DIC
(eg, pregnancy, acute thrombosis)
Coagulation factors:
Fibrinogen is usually decreased (in an acute phase of DIC, the fibrinogen may not
be decreased, only until DIC is severe)
International Society on
Thrombosis and Haemostasis
Scoring System for Diagnosis of
DIC

A score below 5 is
suggestive as a
diagnosis but not
definite; hence the
test must be
repeated.
1.   Underlying cause
2.   Supportive therapy
3.   Heparin therapy
Treatment
                     
 The most important fact in the management of DIC, is the
  treatment of the underlying cause.
 Supportive therapy may be given to patients with
  excessive bleeding:
  1) Fluid
  2) Blood transfusion
  3) Fresh frozen plasma
  4) Platelet concentrates
  5) Fibrinogen
 Patients with chronic DIC and thrombosis may need
  heparin therapy.

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DIC Presentation

  • 1. Pathology Seminar October 2010 Year 4 Medicine Group 1 UST Sana’a
  • 2. Introduction   DIC stands for Disseminated intravascular coagulation.  It is the disturbance of the blood clotting mechanism.  Several clots in some vessels  increase consumption of the blood clotting factors and platelets deficiency, lack or destruction of those factors in other body parts Several bleedings in other areas of the body.
  • 4. Normal Hemostasis   During vascular injury hemostasis normally occurs on the affected site. The hemostasis has four phases:  1. Vasoconstriction then,  2. Primary phase,  3. Secondary phase,  4. Tertiary phase,
  • 5. VASOCONSTRICTION After vascular injury occurs there are certain factors of neurohumoral type released causing transient vasoconstriction to the affected site.
  • 6. PRIMARY HEMOSTASIS Platelets adhere (via GpIb receptors) to exposed extracellular matrix by binding to von Willebrand factor and are activated, undergoing a shape change and granule release. Released adenosine diphosphate and thromboxane A2 lead to further platelet aggregation (via binding of fibrinogen to platelet GpIIb-IIIa receptors), to form the primary hemostatic plug.
  • 7. SECONDARY HEMOSTASIS Local activation of the coagulation cascade (involving tissue factor and platelet phospholipids) results in fibrin polymerization, "cementing" the platelets into a definitive secondary hemostatic plug.
  • 8. TERTIARY HEMOSTASIS Counter-regulatory mechanisms, such as release of t- PA (Tissue plasminogen activator, a fibrinolytic product) and thrombomodulin (interfering with the coagulation cascade), limit the hemostatic process to the site of injury.
  • 9. 1) Generation of a hyperthrombinemic state 2) Alteration of the physiological anticoagulants levels 3) Impaired fibrinolysis at the onset of the DIC: 4) Activation and liberation of inflammatory cytokines in the pathogenesis of DIC
  • 10. Generation of a 1) hyperthrombinemic state   The exposing of the tissue factors thromboplastin and factor III during injury causes a cascade activation of a factor pathway that has a dominant role in the hyperthrombinemic state in DIC.  Cytokines and bacterial endotoxin are all triggers to the formation of endothelial cell tissue factor.  In severe trauma also tissue phospholipids initiates the clotting cascade.
  • 11. cont.: The cascade goes here as follows 
  • 12. cont.: The Thrombin in turn activates 
  • 13. Alteration of the physiological 2) anticoagulants levels   There are 3 most common Anticoagulants in the body:  Antithrombin,  Active Protein C  Tissue factor pathway inhibitor (TFPI).  In DIC:  ↓Antithrombin  ↓Active Protein C
  • 14. cont.: The cause of the decrease 
  • 16. Protein C function  Normally In DIC
  • 17. cont.: Protein C’s Importance 
  • 18. Impaired fibrinolysis at the onset of 3) the DIC:   Plasminogen activator inhibitor 1 (PAI-1) is a neurohumoral compound released by the endothelial cells at the effected site.  PAI-1 suppresses the normal fibrinolysis activity.  Some DIC individuals have shown a mutation in the PAI-1 gene, leading to an increased plasma PAI-1 levels.
  • 20. Activation and liberation of inflammatory 4) cytokines   Activation of Clotting sys.  Inflammatory cascade activation Induced pro-inflammatory cytokines (thrombin and other serine proteases).  Pro-inflammatory cytokines + Protease-activated receptors (of the cell surface of the endothelial cells)  Inducing an inflammatory and clotting reaction.
  • 22. Signs & symptoms of DIC   Renal failure.  Cough  Confusion.  Decreased platelets.  Blood clots.  Drop in blood pressure.  Sudden bruising.  Bleeding, possibly from multiple sites in the body.  Fever
  • 23. Sites of Thrombosis  Site in decreasing order of frequency Brain Heart Kidney Adrenals Spleen Lungs Liver
  • 25. DIC Is most likely to occur after sepsis, obstetric complications, malignancy, and major trauma (especially trauma to the brain)
  • 26. Obstetric complications   Abruption placentae  Retained dead fetus  Septic abortion  Amniotic fluid embolism  Toxemia
  • 27. Infections   Sepsis (gram negative and gram positive)  Meningococcemia  Rocky Mountain spotted fever  Histoplasmosis  Aspergillosis  Malaria
  • 28. Neoplasms   Carcinomas of pancreas, prostate, lung, and stomach  Acute promyelocytic leukemia
  • 29. Massive Tissue Injury   Trauma  Burns  Extensive surgery
  • 30. Miscellaneous   Acute intravascular hemolysis,  Snakebite,  Giant hemangioma  Shock  Heat stroke  Vasculitis  Aortic aneurysm,  Liver disease  Rejection of graft
  • 31. 1. CBC 2. Clotting times: 3. Fibrin related markers important for the diagnosis of DIC: 4. Coagulation factors:
  • 32. Labinvestigations of DIC CBC thrombocytopenia is usually present Clotting times:  Prothrombin time (PT) – prolonged (may be normal in early or chronic DIC) Partial thromboplastin time (PTT) – prolonged (may be normal in early or chronic DIC) Thrombin time (TT) – may be increased due to consumption of fibrinogen Fibrin related markers important for the diagnosis of DIC: D-dimer – increased in acute and chronic DIC (best single test) A normal d-dimer essentially rules out DIC Elevated d-dimer levels are seen in a number of conditions in addition to DIC (eg, pregnancy, acute thrombosis) Coagulation factors: Fibrinogen is usually decreased (in an acute phase of DIC, the fibrinogen may not be decreased, only until DIC is severe)
  • 33. International Society on Thrombosis and Haemostasis Scoring System for Diagnosis of DIC A score below 5 is suggestive as a diagnosis but not definite; hence the test must be repeated.
  • 34. 1. Underlying cause 2. Supportive therapy 3. Heparin therapy
  • 35. Treatment   The most important fact in the management of DIC, is the treatment of the underlying cause.  Supportive therapy may be given to patients with excessive bleeding: 1) Fluid 2) Blood transfusion 3) Fresh frozen plasma 4) Platelet concentrates 5) Fibrinogen  Patients with chronic DIC and thrombosis may need heparin therapy.