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DISSEMINATED
INTRAVASCULAR
COAGULATION (DIC)
 DEFINITION
 ETIOLOGY
 PATHOPHYSIOLOGY
 CLINICAL MANIFESTATIONS

 LABORATORY FINDINGS
 DIFFERENTIAL DIAGNOSIS
 TREA...
It is an acquired condition in which normal
physiology of coagulation is disturbed leading to
widespread intravascular coa...
MECHANISMS
Occurs due to simultaneous action of the
following 4 mechanisms
1) Increased thrombin generation
2) Suppressed ...
ETIOLOGY
 INFECTIOUS:

Meningococcemia- purpura fulminans
Bacterial sepsis- staphylococcal, streptococcal, E coli
Rickett...
Contd…
 MICROANGIOPATHIC DISORDERS:








TTP, HUS, Kasabach-Meritt syndrome
GI DISORDERS:
Fulminant hepatitis, Inf...
PATHOPHYSIOLOGY
CLINICAL
MANIFESTATIONS
DIC

NON OVERT DIC OVERT DIC ACUTE DIC CHRONIC DIC

CONTROLLED

UNCONTROLLED
Non overt DIC:
Stressed & compensated hemostatic system. Lab testsabnormal but no clinical manifestations.

Overt DIC:
S...
Acute DIC:
 Bleeding from vein puncture site, surgical wound.
 Grayish discoloration of tips of fingers, toes & ears in...
PURPURA FULMINANS
Chronic DIC:
 Superficial and extensive ecchymosis of extremities

without petechiae which may be intermittent or can
pe...
CHRONIC DIC
Specific features of DIC in neonates

and infants
 CAUSES:
 Transplacental passage of thromboplastin or other

procoagu...
 CLINICAL FEATURES:
 Symmetric ecchymosis of lower extremities and

buttocks. Later these lesions become necrotic
ultima...
BULLAE SEEN IN DIC
LABORATORY FINDINGS
 COMPLETE BLOOD COUNT:

Severe thrombocytopenia(50000-100000/µl) with or
without anemia
 PERIPHERAL ...
SCHISTOCYTES IN PERIPHERAL BLOOD
SMEAR
 D dimer, FIBRINOGEN / FIBRIN

DEGRADATION PRODUCTS:
Increased >25µg fibrinogen equivalents/ml
 PROTEIN C & S, ANTITHROM...
Overt DIC Scoring System
DIFFERENTIAL DIAGNOSIS
 Primary fibrinogenolysis or Pathologic

fibrinolysis:
Platelet count is normal
D dimer may be nor...
TREATMENT
BLOOD COMPONENT THERAPY:
INDICATIONS:

Active bleeding
Invasive procedure
Risk of bleeding complication
GOALS...
 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 fibrin...
PLATELETS:
 Random donor platelets(RDP):
• Constituents:

5.5×10¹° platelets
 Dosage:
1 unit/ 10 kg
 Single donor plat...
ANTICOAGULANT THERAPY:
Heparin and other anticoagulant therapy to inhibit
thrombin.
Indicated in patients with clinically...
REPLACEMENT OF NATURAL

ANTICOAGULANT PATHWAY
Recombinant human activated protein c 24µg/kg/hr.
Adverse effects include b...
COMPLICATIONS
 Respiratory failure
Renal failure
Stroke
Cardiac tamponade

Hemothorax
05 disseminated intravascular coagulation
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05 disseminated intravascular coagulation

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05 disseminated intravascular coagulation

  1. 1. DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
  2. 2.  DEFINITION  ETIOLOGY  PATHOPHYSIOLOGY  CLINICAL MANIFESTATIONS  LABORATORY FINDINGS  DIFFERENTIAL DIAGNOSIS  TREATMENT
  3. 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. 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. 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. 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. 7. PATHOPHYSIOLOGY
  8. 8. CLINICAL MANIFESTATIONS DIC NON OVERT DIC OVERT DIC ACUTE DIC CHRONIC DIC CONTROLLED UNCONTROLLED
  9. 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. 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. 11. PURPURA FULMINANS
  12. 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. 13. CHRONIC DIC
  14. 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. 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. 16. BULLAE SEEN IN DIC
  17. 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. 18. SCHISTOCYTES IN PERIPHERAL BLOOD SMEAR
  19. 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. 20. Overt DIC Scoring System
  21. 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. 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. 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. 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. 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. 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. 27. COMPLICATIONS  Respiratory failure Renal failure Stroke Cardiac tamponade Hemothorax

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