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Disseminated intravascular coagulation (DIC)

Disseminated intravascular coagulation (DIC)

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Disseminated intravascular coagulation (DIC)

  2. 2. COAGULATION CASCADE Nawaf Abdullah Alosaimi 434029628
  3. 3. HEMOSTASIS • The term hemostasis means prevention of blood loss. Whenever a vessel is severed or ruptured, • hemostasis is achieved by several mechanisms: 1. Vascular constriction, 2. Formation of a platelet plug, 3. Formation of a blood clot as a result of blood coagulation, 4. Clot retracts (Fibrinolysis)
  4. 4. COAGULATION PATHWAYS • Intrinsic • Extrinsic • Common
  5. 5. FIBRINOLYSIS • The plasma proteins contains plasminogen (or profibrinolysin) that, when activated, becomes a substance called plasmin (or fibrinolysin). whenever plasmin is formed, it can cause lysis of a clot by destroying many of the clotting factors. • When a clot is formed, a large amount of plasminogen is trapped in the clot along with other plasma proteins. This will not become plasmin or cause lysis of the clot until it is activated. The injured tissues and vascular endothelium very slowly release a powerful activator called tissue plasminogen activator (t-PA) that a few days later, after the clot has stopped the bleeding, eventually converts plasminogen to plasmin, which in turn removes the remaining unnecessary blood clot.
  7. 7. PREGNANCY • Pregnancy is a hypercoagulable state because of an alteration in the thrombotic and fibrinolytic systems. There is an increase in clotting factors VIII, IX, X and fibrinogen levels, and a reduction in protein S and antithrombin (AT) III concentrations. The net result of these changes is thought to be an evolutionary response to reduce the likelihood of haemorrhage following delivery.
  8. 8. PREGNANCY • This is further exacerbated by venous stasis in the lower limbs due to the weight of the gravid uterus placing pressure on the IVC in late pregnancy and immobility. • Pregnancy is associated with a 6–10-fold increase in the risk of VTE compared to the non-pregnant situation.
  9. 9. COAGULOPATHY (CONGENITAL) ‫هليل‬ ‫بن‬ ‫مشعل‬ ‫بن‬ ‫عبدالرحمن‬‫المخلفي‬‫الحربي‬ 435031643
  10. 10. Disorders of Secondary Hemostasis • inability to form an adequate fibrin clot ■■ disorders of clotting factors or co-factors ■■ disorders of proteins associated with fibrinolysis • characterized by delayed bleeding, deep muscular bleeding, spontaneous hemarthroses
  11. 11. COAGULATIONACQUIRED Asem Mustafa Shadid 435032467
  13. 13. •Etiology • • drugs • ■■ vitamin K antagonist (e.g. Warfarin) – diminished production of functional Factors II, VII, IX, X, proteins C and S • ■■ antibiotics eradicating gut flora, altering vitamin K uptake • poor diet (especially in alcoholics) e.g. prolonged fasting or starvation • biliary obstruction • chronic liver disease (decreased stores) • fat malabsorption (e.g. celiac disease, disorders of bile or pancreatic secretion, intestinal disease, CF) • hemorrhagic disease of newborn Investigations • (PT) is elevated out of proportion to elevation of the aPTT • decreased Factors II, VII, IX, X (vitamin K-dependent)
  14. 14. • Treatment • • hold anticoagulant if vitamin K antagonist on board • • vitamin K PO if no active bleeding • • if bleeding, give vitamin K 10 mg IV (reversal may take up to 12 h) • • if life-threatening bleeding and vitamin K antagonist used, give prothrombin complex concentrate • (PCC) or FP if PCC contraindicated ■■ PCCs are contraindicated if there is a previous history of HIT (heparin is within the PCC product)
  15. 15. VITAMIN K DEFICIENCY HEMORRHAGIC DISEASE OF THE NEWBORN • Etiology • • hemorrhagic disease of the newborn due to relative deficiencies of vitamin K-dependent coagulation factors • ■■ generalized bleeding; GI/intracranial hemorrhage • • IM injection at birth, can also be given orally (3 doses: at birth, 2-4 wk, 6-8 wk) but infants at higher risk of HDNB • • reason for administration at birth: ■■ human milk contains small amounts of vitamin K, and infants require ingestion of large volumes of human milk to promote GI bacterial colonization ■■ until few days after birth, susceptible to vitamin K deficiency
  16. 16. LIVER DISEASE • Pathophysiology • • deficient synthesis of all factors except VIII (also made in endothelium) • • aberrant or diminished synthesis of fibrinogen (factor I) • • diminished synthesis of natural anticoagulants and altered regulation of fibrinolysis
  19. 19. DIC OUTLINES • Definition • Pathophysiology • Clinical Manifestations • Risk factors • Complications • Investigations • Treatment
  20. 20. DIC OUTLINES • Definition • Pathophysiology • Clinical Manifestations • Risk factors • Complications • Investigations • Treatment
  21. 21. DEFINITION • Consumption coagulopathy • Defibrination syndrome • Disseminated intravascular coagulation (ko-ag-u-LA-shun), or DIC, is a condition in which blood clots form throughout the body's small blood vessels. These blood clots can reduce or block blood flow through the blood vessels, which can damage the body's organs. • Disseminated intravascular coagulation is a disorder of hemostasis in which intravascular activation of both clotting and fibrinolytic systems leads to consumption of coagulation factors and platelets. Widespread endothelial damage causes release of tissue factor that activates these systems. Clinically, a patient will experience systemic hemorrhage concurrent with widespread microvascular thrombosis.
  22. 22. Acquired, acute and chronic
  23. 23. • In DIC, the increased clotting uses up platelets (PLATE-lets) and clotting factors in the blood. Platelets are blood cell fragments that stick together to seal small cuts and breaks on blood vessel walls and stop bleeding. Clotting factors are proteins needed for normal blood clotting. • With fewer platelets and clotting factors in the blood, serious bleeding can occur. DIC can cause internal and external bleeding. • Internal bleeding occurs inside the body. External bleeding occurs underneath or from the skin or mucosa. (The mucosa is the tissue that lines some organs and body cavities, such as your nose and mouth.) • DIC can cause life-threatening bleeding.
  24. 24. • DIC may occur in 30-50% of patients with sepsis, and it develops in an estimated 1% of all hospitalized patients. DIC occurs at all ages and in all races, and no particular sex predisposition has been noted. • A retrospective single-center Korean study of women with primary post- partum hemorrhage who presented to the emergency department found that 57 (22.4%) of the 255 patients had overt DIC. Of patients with DIC, 96.5% experienced major adverse events.
  25. 25. • The prevalence of DIC in pregnancy ranges from 0.03 to 0.35 percent in population-based studies, or 12.5 per 10,000 delivery hospitalizations (0.13 percent) in one study. • Although the overall prevalence of DIC is low in pregnancy, the frequency of DIC in women with specific pregnancy complications can be quite high. As an example, an evidence-based review noted that coagulopathy was reported in 22 to 83 percent of cases of amniotic fluid embolism in large series. In a series of 442 pregnancies complicated by hemolysis, elevated liver function tests, and low platelets (HELLP) syndrome, 92 had DIC (21 percent); the majority were associated with abruptio placentae.
  26. 26. PATHOPHYIOLOGY • 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
  27. 27. Thrombomodulin
  28. 28. Tissue factorSurface contact with collagen
  29. 29. IN PREGNANCY • Placental tissue (decidual cells) strongly expresses tissue factor, an integral membrane glycoprotein that is mostly functionally inactive under normal conditions. However, at sites of vascular endothelial disruption, placental trauma (eg, abruption), or fetoplacental necrosis (eg, retained fetal demise), tissue factor becomes activated and serves as the cofactor for the production of activated factor VII (VIIa).
  30. 30. CLINICAL MANIFESTATIONS • The symptoms of disseminated intravascular coagulation (DIC) are often those of the underlying condition. • In addition to the symptoms related to the underlying disease process, there is typically a history of blood loss through bleeding in areas such the gingivae and the gastrointestinal (GI) system. • Acutely presenting DIC often manifests as petechiae and ecchymosis, along with blood loss from intravenous (IV) lines and catheters. In postoperative DIC, bleeding can occur in the vicinity of surgical sites, drains, and tracheostomies, as well as within serous cavities.
  31. 31. ?
  32. 32. • Look for symptoms and signs of thrombosis in large vessels (eg, deep vein thrombosis [DVT]) and microvascular thrombosis (as in renal failure). • Bleeding from at least 3 unrelated sites is particularly suggestive of DIC. As many as 25% of patients present with renal failure. Patients with pulmonary involvement can present with dyspnea, hemoptysis, and cough. Comorbid liver disease as well as rapid hemolytic bilirubin production may lead to jaundice. Neurologic changes (eg, coma, obtunded mental status, and paresthesias) are also possible.
  33. 33. • With acute DIC, the physical findings are usually those of the underlying condition; however, patients with the acute disease (ie, the hemorrhagic variety associated with excess plasmin formation) have petechiae on the soft palate, trunk, and extremities from thrombocytopenia and ecchymosis at venipuncture sites. These patients also manifest ecchymosis in traumatized areas. • In patients with so-called chronic or subacute DIC, of which the primary manifestation is thrombosis from excess thrombin formation, the signs of venous thromboembolism may be present.
  34. 34. • Circulatory signs include the following: • Signs of spontaneous and life-threatening hemorrhage • Signs of subacute bleeding • Signs of diffuse or localized thrombosis • Bleeding into serous cavities
  35. 35. • Central nervous system signs include the following: • Nonspecific altered consciousness or stupor • Transient focal neurologic deficits
  36. 36. • Cardiovascular signs include the following: • Hypotension • Tachycardia • Circulatory collapse • Respiratory signs include the following: • Signs of acute respiratory distress syndrome (ARDS) • Gastrointestinal signs include the following: • Hematemesis • Hematochezia
  37. 37. • Genitourinary signs include the following: • Signs of azotemia and renal failure • Acidosis • Hematuria • Oliguria • Metrorrhagia • Uterine hemorrhage
  38. 38. • Dermatologic signs include the following: • Petechiae • Jaundice (liver dysfunction or hemolysis) • Purpura • Hemorrhagic bullae • Acral cyanosis • Skin necrosis of lower limbs (purpura fulminans) • Localized infarction and gangrene • Wound bleeding and deep subcutaneous hematomas • Thrombosis
  39. 39. Any question?
  40. 40. RISK FACTOR AND COMPLICATION Muteb Mousa Alharbi 435032375
  42. 42. RISK FACTORS • Abruptio placenta (most common): Maternal disseminated intravascular coagulation (DIC) can occur and is found in 10% to 20% of AP with stillbirth. • Severe preeclampsia • Amniotic fluid embolism. • Sepsis
  43. 43. • Trauma • obstetric complications • Malignancy • liver failure • renal failure • Acute fatty liver of pregnancy (AFLP) ( rare ) .
  44. 44. INTRAUTERINE FETAL DEATH (IUFD) • intrauterine fetal demise (IUFD), is the antenatal diagnosis of a stillborn infant after 20 weeks’ gestation. • Most common complication associated with IUFD was Disseminated Intravascular Coagulation (DIC). • Clinically, fetal death should be suspected when: • 1- absence of fetal movements. • 2 - uterus is small for date. • 3 - fetal heart tones are not detected using a Doppler device. • Sonography confirms the lack of fetal movement and absence of fetal cardiac activity
  46. 46. • Acute kidney injury. • Change in mental status. • Respiratory dysfunction. • Hepatic dysfunction. • Life-threatening thrombosis and hemorrhage (in patients with moderately severe–to–severe DIC). • Cardiac tamponade.
  47. 47. • Hemothorax • Intracerebral hematoma • Gangrene and loss of digits • Shock • Death
  48. 48. INVESTIGATIONS AND TREATMENT ‫دهمش‬ ‫بن‬ ‫عبدالمجيد‬ 435031658
  49. 49. INVESTIGATIONS OF DIC • Prothrombin Time (PT): Increased. • Partial Thromboplastin Time (PTT): Increased. • Fibrin Split Products (D-dimer): Increased.The Johns Hopkins Manual of Gynecology and Obstetrics
  50. 50. INVESTIGATIONS OF DIC • Platelet Count: Decreased. • Fibrinogen: Decreased. The Johns Hopkins Manual of Gynecology and Obstetrics
  51. 51. INVESTIGATIONS OF DIC • Peripheral Blood Smear: • RBCs: fragmented (i.e. schistocytes). • Platelets: Thrombocytopenia with large platelet. The Johns Hopkins Manual of Gynecology and Obstetrics
  53. 53. SUM UP • DIC is never primary diagnosis. • Most of the time its diagnosed in hospitalized patients. • Associated conditions • Sepsis, • Cancer, • Trauma, • Burns, • Conditions that lead to vascular stasis • Snake bites In pregnancy: • HELLP syndrome (haemolysis, • elevated liver enzymes and low platelets) • Sever pre-eclampsia (5-10%) • Placental abruption • Amniotic fluid embolism More in multiparous women
  54. 54. DIC MANAGEMENT Treat the underline cause The main goal of treatment should be to keep the platelets >20K/ml or >50K/ml if the there is bleeding Platelet, FFP, cryoprecipitate, packed RBCs and heparin are used in treatment as follows:
  56. 56. DEFINITIONS Faisal Eid Almutairi 435031637
  57. 57. BLOOD • Blood Product: Any therapeutic substance prepared from human blood. • Whole Blood: Unseparated blood. • Blood Component: Such as Red cell, Plasma and platlet.
  58. 58. CENTRIFUGE
  60. 60. USAGE
  61. 61. USE OF WHOLE BLOOD • Rarely used now a days. • Infrequently used in massive trauma. • Pediatric practice, mostly for neonatal exchange transfusion.
  62. 62. USE OF FFP IN DIC

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Disseminated intravascular coagulation (DIC)


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