This action might not be possible to undo. Are you sure you want to continue?
-also known as consumptive coagulopathy - a pathological activation of coagulation (blood clotting) mechanisms that happens in response to a variety of diseases which leads to the formation of thrombi in the microvasculature of the body. a complex systemic thrombohemorrhagic disorder involving the generation of intravascular fibrin and the consumption of procoagulants and platelets, and also because of systemic circulation of thrombin and plasmin that result to intravascular coagulation and hemorrhage.
DIC is a pathophysiological process and not a disease. It is when the body's natural ability to regulate blood clotting does not function properly because of excessive consumption of clotting factors and platelets within circulation. This causes the blood's clotting cells (platelets) to clump together and clog small blood vessels throughout the body. This excessive clotting damages organs, destroys blood cells, and depletes the supply of platelets and other clotting factors so that the blood is no longer able to clot normally. This often causes widespread bleeding, both internally and externally.
Pregnancy Hypercoagulability Pregnancy normally induces: ↑ concentrations of coagulation factors I (fibrinogen), VII, VIII, IX, X. ↑ plasminogen levels Plasma factors and platelets do not change so remarkably. Plasmin is normally decreased.
Pathological activation of coagulation I. Coagulation maybe activated via: a. extrinsic pathway by thromboplastin from tissue destruction b. intrinsic pathway by collagen and other tissue components when there is loss of endothelial integrity. II. Tissue factor is released and complexes with factor VII, which in turn activates tenase (factor IX) and prothrombinase (factor X) complexes.
Common inciting factors of DIC: Thromboplastin, endotoxin and exotoxins from placental abruption Direct activation of factor X by proteases Amniotic fluid contains abundant mucin from fetal squames which causes rapid defibrination with amniotic fluid embolism.
- Consumptive coagulopathy is almost always seen as a complication of an identifiable, underlying pathological process against which treatment must be directed to reverse defibrination. - With pathological activation of procoagulants that trigger consumptive coagulopathy, there is consumption of platelets and coagulation factors in variable quantities. - As a consequence, fibrin may be deposited in small vessels of virtually every organs system.
- Small vessels are protected because coagulation release fibrin monomers that contain with tissue plasminogen activator and plasminogen wich releases plasmin. - Plasmin lyses fibrinogen, fibrin monomers, and fibrin polymers to form a series of fibrinogen-fibrin derivatives. - Measured by immunoassay, these are known as fibrin degradtion products as split products.
Conditions associated with DIC in obstetrics
Abruptio placenta Amniotic fluid embolism Pre-eclampsia and eclampsia abortion
Etiology: the placenta breaks away, or abrupts, from the wall of the uterus too early, before the baby is born.
The hypertensive states of pregnancy are associated with 2.5 – 17.9% incidence of placental separation.
Predisposing factors: maternal age, multiparty, uterine distention (multiple gestation, hydramnios), vascular disease (DM, SLE), thrombophilias, uterine anomalies or tumors (leiomyoma), cigarette smoking, alcohol consumption (>14 drinks/day), coccaine use, possibly maternal type O blood
Amniotic fluid Embolism
a rare obstetric emergency in which it is postulated that amniotic fluid, fetal cells, hair, or other debris enter the maternal circulation, causing cardiorespiratory collapse. (http://emedicine.medscape.com/article/253068-overview) The etiology of coagulopathy associated with amniotic fluid embolism is incompletely understood, but it is known that amniotic fluid has a potent total thromboplastin and antifibrinolytic activity. Both of which increase with advancing gestational age. The response to amniotic fluid embolus in humans may be biphasic, initially resulting in intense vasospasm, severe pulmonary hypertension, and hypoxia
Pre-eclampsia and Eclampsia
Preeclampsia usually occurs with first pregnancies. May be seen:
• • • • •
with twins (or multiple pregnancies) in women older than 35 years, in women with high blood pressure before pregnancy, in women with diabetes in women with other medical problems (such as connective tissue disease and kidney disease).
Preeclampsia is also associated with: problems with the placenta (such as too much placenta, too little placenta) how the placenta attaches to the wall of the uterus. hydatidiform mole pregnancies
- Serious disruption of the coagulation mechanism as the consequence of abortion may develop in the folowing: Prolonged retention of a dead fetus Sepsis syndrome Medical induction with prostaglandin During instrumental termination of the pregnancy Intrauterine instillation of hypertonic saline or urea solutions ► thromboplastin is released from the placenta, fetus and decidua because of the necrobiotic effect of the hypertonic solutions, which then initiates coagulation within the maternal circulation.
• presentation in pregnancy may be more sudden and unexpected causing: > Generalized bleeding > Localized hemorrhage > Purpura > Petechiae > Fever > Hypertension > Proteinuria > Hypoxia • Widespread fibrin deposition may affect lungs, brain, kidney, liver • Chronic DIC may have minimal or absent clinical signs and symptoms
- The likelihood of life threatening hemorrhages in obstetrical situations complicated by consumptive coagulopathy depends not only on the extent of coagulation defects but on whether the vasculature is intact or ruptured - With gross derrangement of blood coagulation, there maybe fatal hemorrhage when vascular integrity is disrupted yet no hemorrhage as long as all blood vessels remain intact.
D-dimer test. This blood test helps determine whether a person's blood is clotting normally by measuring a substance (fibrin) Prothrombin time (PT/INR). This blood test measures how long it takes blood to clot. Fibrinogen. This blood test measures how much fibrinogen is in the blood. Fibrinogen is a protein that plays a part in blood clotting. Complete blood count (CBC). counting the number of red blood cells and white blood cells. CBC results cannot diagnose DIC, but they provide information to help the doctor make a diagnosis. Blood smear. The number, size, and shape of red blood cells, white blood cells, and platelets are recorded. Blood cells often look damaged and abnormal in people with DIC.
Practical markers of disseminated intravascular coagulation
MJ 2003;327:974-977 (25 October), doi:10.1136/bmj.327.7421.974)
Control of the underlying disease: because prolongation of exposure to the triggering factors worsens DIC, it is important to eliminate the etiologic factors as rapidly as possible. Elimination of the cause of DIC can be easily performed in obstetrics, for example, by cesarean section.
(Bruchim, Y. et al. Disseminated Intravascular Coagulation (2008)COMPENDIUM Vol. 30,No. 10)
***If not achieved, attempts of using anticoagulation
Prophylactic transfusion of platelets at delivery does not reduce the incidence of postpartum hemorrhage or hasten normalization of the platelet count.15 Patients with DIC should be given fresh frozen plasma and packed red blood cells.
(Padden, M.HELPP Syndrome: Recognition and Perinatal Management (2008) Compendium Vol30, No10)
Antithrombin Therapy AT is considered to be the primary inhibitor of circulating thrombin, and AT levels are considerably reduced in DIC.
Thrombomodulin Therapy may be beneficial in DIC as a sole treatment with no APC transfusion.119 Thrombomodulin had a beneficial effect on coagulation in humans and animals and appeared to reduce pulmonary vascular injury and leukocyte accumulation.94,120 These effects were not dependent on thrombomodulin’s thrombin-binding properties but were probably mediated through an increase in APC.94,119 Interleukin-10 and Anti–Tumor Necrosis Factor Antibodies Administration of recombinant interleukin-10, an antiinflammatory cytokine, has been shown to completely nullify the endotoxin-induced effects on coagulation. (Bruchim, Y. et al. Disseminated Intravascular Coagulation (2008)COMPENDIUM Vol. 30,No. 10)
Synthetic serine protease inhibitors: continuous infusion of gabexate mesilate (FOY) or nafamostat mesilate (FUT) is effective for DIC. Controlled multicenter trials showed a significant improvement not only in clinical response but also in platelet counts and prothrombin time (PT) in the AT group compared with the FOY group. Activated protein C (APC): can inhibit thrombin generation and accelerate fibrinolytic activity. APC (5,000 to 10,000 units) is administered for 2 days in patients with placental abruption complicated by DIC. APC is a very safe, effective, and useful agent for the treatment of DIC. (Thachil J, Toh CH. Disseminated intravascular coagulation in obstetric disorders and its acute haematological management. (2001)
Santos, Criselda Shih, Chun I Silla, Earica Sim, Samantha C Siquijor, Michel Analie V Solleza, Earl John Tamayo, James Tan, Irene Carmelle Tauro, Charlene Gayle