disseminated intravascular coagulation n.
Skip this Video
Loading SlideShow in 5 Seconds..
Disseminated intravascular coagulation PowerPoint Presentation
Download Presentation
Disseminated intravascular coagulation

Loading in 2 Seconds...

play fullscreen
1 / 18

Disseminated intravascular coagulation - PowerPoint PPT Presentation

  • Uploaded on

Disseminated intravascular coagulation. Disseminated intravascular coagulation (DIC) is a state/syndrome which is characterized by accelerated intravascular coagulation associated with increased consumption of platelets and plasma clotting factors. . ETIOLOGY.

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about 'Disseminated intravascular coagulation' - tanginika

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
disseminated intravascular coagulation
Disseminated intravascular coagulation

Disseminated intravascular coagulation (DIC) is a state/syndrome which is characterized by accelerated intravascular coagulation associated with increased consumption of platelets and plasma clotting factors.

  • Bacterial (septic shock) : menningococcus, S. aureus, E. coli, protease, salmonella
  • Viral : measles, CMV, acute hepatitis
  • Fungal : Candida, histoplasmosis
  • Others : malaria, rickettsial
  • Tissue injury : head injury, multiple fracture, crush injury, shock, hypothermia, burns
  • Toxins: snake bite, insect bites
  • Hematological : incompatible blood transfusion, sickle cell anemia, acut iron toxicity
  • Neonatal causes: septicemia, RDS, birth asphyxia, necrotising enterocolitis, hypothermia
  • Obstetric complication: pre – eclampsia, septic abortion, maternal toxemia, retained fetus
  • Collagen vascular disease: JRA, SLE, acute vasculitis
  • Miscellaneous: major surgery, heat stroke, graft reaction, acute pancreatitis
  • There is intravascular activation of platelet adhesion, and the extrinsic and intrinsic systems of coagulation, initiated by any of the three major mechanism : -
    • 1. direct activation of factor V or X by proteolytic enzymes;
    • 2. activation of factor XII and
    • 3. activation of extrinsic pathway by release of tissue thromboplastin
  • Continuation of this clotting process is dependent upon consumption of clotting factors and platelets, thrombin formation, activation of fibrinolytic system.
  • Thrombin activates the fibrinolytic system by activating the plasminogen by splitting peptides A and B from fibrinogen to soluble fibrin monomers and D dimers.
  • Fibrin monomers and polymers along with fibrin are degraded to fibrin split products (FSP) by plasmin.
fibrinolytic system
Fibrinolytic system
  • Thrombin --------------- plasminogen --------

fibrinogen peptides A and B -------- soluble

fibrin monomers and D dimers ---------- fibrin split products (FSP)




  • Increased levels of D – dimers and FSP are the pathognomonic of DIC

Thrombin functions :

  • activates fibrinolytic system
  • activates factor XIII which acts on the fibrin polymers to form fibrin split products.
  • induces platelet adhesion and aggregation, leading to platelet consumption and thrombocytopenia.

Course of DIC is determined by :

  • 1. platelet production versus platelet destruction;
  • 2. fibrin deposition versus fibrinolysis and
  • 3. synthesis of coagulation factor versus their depletion

Process of DIC results in :

  • 1. increased thromboembolic phenomenon causing tissue ischemia and necrosis of multiple organs;
  • 2. depletion of clotting and antihemostatic effects of FSP resulting in bleeding and hemorrhages at multiple sites;
  • 3. red cell fragments
clinical features
Clinical features
  • Purpura, ecchymosis, easy bruising, and bleeding from gums and mucous membranes.
  • Shock
  • Hematuria, oliguria leading to acute renal failure, abdominal pain, vomiting and respiratory distress
differential diagnosis
Differential diagnosis
  • Acute fulminant liver failure
  • Hemolytic uremia syndrome
  • Renal failure
lab investigation
Lab investigation
  • Low platelet count
  • Low levels of fibrinogen, factor II, V, X, VIII and XIII
  • Prolonged PT, APTT and TT
  • Low levels of antithrombin III, heparin cofactor II, protein C
  • Increased level of fibrin split products and
  • Microangiopathic hemolytic anemia as indicated by the presence of red cell fragmentation.
  • Management of:
  • Acidosis, electrolyte disturbances, hypoxia, shock
  • Anemia (packed cells)
  • Hydrocortisone
  • Vitamin K

Replacement therapy :

  • Fresh frozen plasma (FFP) :
    • Fibrinogen level should be raised to over 150 mg/dL
    • 10 – 15 mL/kg of FFP along with ½ to 1 unit of platele concentrates every 12 – 24 hours
    • Platelat count should be maintained above 50,000/microL while fibrinogen level should be maintained above 75mg/dL.

Exchange transfusion :

  • Double volume exchange transfusion helps by providing the replacement factors and removing the
  • A. circulating fibrin split products (FSP)
  • B. activated procoagulant: and
  • C. toxins
  • Platelet concentrates should be administered after the exchange for the successful management of DIC.

Heparin :

  • Inhibits number of proteolytic enzymes and factors such as thrombin, IXa and Xa
  • Dose : 15 – 20 units/kg hour as continuous drip or 50 – 70 units/kg/6 hourly

Mortality :

  • Prolongation of PT (>1.5 times) and
  • APTT (>2,5 times) indicates poor prognosis.