05 disseminated intravascular coagulation

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  • 1. DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
  • 2.  DEFINITION  ETIOLOGY  PATHOPHYSIOLOGY  CLINICAL MANIFESTATIONS  LABORATORY FINDINGS  DIFFERENTIAL DIAGNOSIS  TREATMENT
  • 3. It is an acquired condition in which normal physiology of coagulation is disturbed leading to widespread intravascular coagulation process associated with injury to microvasculature which results in organ dysfunction, capillary leak & shock.
  • 4. MECHANISMS Occurs due to simultaneous action of the following 4 mechanisms 1) Increased thrombin generation 2) Suppressed physiological anticoagulant pathways 3) Activation & subsequent impairment of fibrinolysis 4) Activation of inflammatory pathways
  • 5. ETIOLOGY  INFECTIOUS: Meningococcemia- purpura fulminans Bacterial sepsis- staphylococcal, streptococcal, E coli Rickettsia- Rocky Mountain spotted fever Viral- CMV, varicella, arboviruses Malaria, Candida, Aspergillus  TISSUE INJURY: Multiple fractures with fat emboli, crush injury, head injury  MALIGNANCY: Acute promyelocytic leukemia, acute myeloid leukemia, neuroblastoma  VENOM OR TOXIN: Snake bites, insect bites
  • 6. Contd…  MICROANGIOPATHIC DISORDERS:     TTP, HUS, Kasabach-Meritt syndrome GI DISORDERS: Fulminant hepatitis, Inflammatory bowel disease, Pancreatitis HEREDITARY THROMBOTIC DISORDERS: Antithrombin III deficiency, Homozygous protein C deficiency NEWBORN: Maternal toxemia, Abruptio placentae, Necrotizing enterocolitis, Erythroblastosis fetalis MISCELLANEOUS: Acute graft rejection, Acute hemolytic transfusion reaction, Collagen vascular disorders, Heparin induced thrombosis, hyperpyrexia
  • 7. PATHOPHYSIOLOGY
  • 8. CLINICAL MANIFESTATIONS DIC NON OVERT DIC OVERT DIC ACUTE DIC CHRONIC DIC CONTROLLED UNCONTROLLED
  • 9. Non overt DIC: Stressed & compensated hemostatic system. Lab testsabnormal but no clinical manifestations. Overt DIC: Stressed and decompensated hemostatic system. Lab tests- abnormal with clinical bleeding or micro vascular thrombosis and organ dysfunction. Further divided into controlled and uncontrolled based on whether the process will resolve when the underlying condition is removed.
  • 10. Acute DIC:  Bleeding from vein puncture site, surgical wound.  Grayish discoloration of tips of fingers, toes & ears in a symmetrical distribution.  Meningococcemia(PURPURA FULMINANS)- bleeding from GI tract, gingival bleeding, epistaxis, pulmonary hemorrhage, hematuria.
  • 11. PURPURA FULMINANS
  • 12. Chronic DIC:  Superficial and extensive ecchymosis of extremities without petechiae which may be intermittent or can persist.  Recurrent episodes of epistaxis or internal mucosal bleeding.  Trousseau sign- Recurrent migratory thrombophlebitis in association with cancer.  Impairment of renal function, confusion, repeated episodes of cerebral thrombosis.
  • 13. CHRONIC DIC
  • 14. Specific features of DIC in neonates and infants  CAUSES:  Transplacental passage of thromboplastin or other procoagulant substances in neonates born of mothers affected with DIC owing to abruptio placenta, eclampsia or septicemia  Development of DIC in a twin fetus may be due to feto-fetal passage of thromboplastin.  DIC secondary to hemangioma .  PRECIPITATING FACTOR: Asphyxia, septicemia, eclampsia
  • 15.  CLINICAL FEATURES:  Symmetric ecchymosis of lower extremities and buttocks. Later these lesions become necrotic ultimately forming blood filled bullae.  Sharply circumscribed infarcts of skin and genitalia  Gangrene of extremities involves digits symmetrically.  Fever and prostration  Mortality 40-70%  TREATMENT: Heparin. Relapse common after cessation.
  • 16. BULLAE SEEN IN DIC
  • 17. LABORATORY FINDINGS  COMPLETE BLOOD COUNT: Severe thrombocytopenia(50000-100000/µl) with or without anemia  PERIPHERAL BLOOD SMEAR: Schistocytes- Microangiopathic hemolysis  PROTHROMBIN TIME & aPTT: Prolonged in early cases but may be normal or short in chronic cases  FIBRINOGEN LEVEL: Low
  • 18. SCHISTOCYTES IN PERIPHERAL BLOOD SMEAR
  • 19.  D dimer, FIBRINOGEN / FIBRIN DEGRADATION PRODUCTS: Increased >25µg fibrinogen equivalents/ml  PROTEIN C & S, ANTITHROMBIN: decreased  MARKERS OF ENDOGENOUS THROMBIN GENERATION: Prothrombin fragment 1.2 and Thrombin-Antithrombin complexes(TATs) are elevated
  • 20. Overt DIC Scoring System
  • 21. DIFFERENTIAL DIAGNOSIS  Primary fibrinogenolysis or Pathologic fibrinolysis: Platelet count is normal D dimer may be normal or minimally increased No hypoprothombinemia & No deficiency of coagulation factors (VII, IX, X, XI)  Severe liver disease: D dimer test is normal
  • 22. TREATMENT BLOOD COMPONENT THERAPY: INDICATIONS: Active bleeding Invasive procedure Risk of bleeding complication GOALS: To maintain Platelet count >50000/µl Fibrinogen concentration >1g/L Prothrombin values less than double the normal range
  • 23.  FRESH FROZEN PLASMA(FFP):  Constituents: 0.7-1.0 U/ml of factors II,V, VII, VIII, X, XI, XII, XIII and 2.5mg/ml fibrinogen.  Dosage: 15ml/kg  CRYOPRECIPITATE:  Constituents; fibrinogen 150mg/bag factor VIII 80-120units/bag factor XIII & vWB  Dosage: 1 bag/5kg body wt.
  • 24. PLATELETS:  Random donor platelets(RDP): • Constituents: 5.5×10¹° platelets  Dosage: 1 unit/ 10 kg  Single donor platelets:  Constituents: 3×10¹¹ platelets FRESH BLOOD: Indicated in severe trauma to replace acute massive blood loss.
  • 25. ANTICOAGULANT THERAPY: Heparin and other anticoagulant therapy to inhibit thrombin. Indicated in patients with clinically overt thromboembolism , chronic DIC and extensive fibrin deposition. Dosage: Weight < 30kg – 10U/kg/hr Weight > 30kg – 4U/kg/hr
  • 26. REPLACEMENT OF NATURAL ANTICOAGULANT PATHWAY Recombinant human activated protein c 24µg/kg/hr. Adverse effects include bleeding. ANTI-THROMBIN INDEPENDENT INHIBITORS desirudin gabexate mesylate
  • 27. COMPLICATIONS  Respiratory failure Renal failure Stroke Cardiac tamponade Hemothorax