Coagulation Disorders in Obs

COAGULATION DISORDERS IN OBS/GYN
Presenters:
ACEN KEZIA
NAMAGEMBE JENNIFER
MBChB V
Tutor: DR. WASSWA WANGI ESAU

15-NOV-22
Outline
 Hemostatic changes in pregnancy

 Mechanism of coagulation.
 Disseminated intravascular coagulopathy
 Deep vein thrombosis
 Pulmonary embolism
Virchow’s triad of
thrombosis
Source: www.researchgate.net/figure/The-Virchows-triad-of-risk-factors-for-venous-
thrombosis
Cont……..
Source: https://www.researchgate.net/figure/Coagulation-changes-in-pregnancy
 Pregnancy affects both the coagulation and fibrinolytic systems
 Many clotting factors increase and anticoagulation factors decrease causing augmented
coagulation and decreased fibrinolysis.
 This leads to a state of hypercoagulability during pregnancy
 The physiological hypercoagulable state of pregnancy aim is to reduce risk of haemor-
rhage during pregnancy, labour and puerperium
 The hypercoagulable state however increases the risk of Venous thromboembolism and
Disseminated intravascular coagulopathy(DIC) among pregnant women.

 Disorders of coagulation in OBS/GYN can be classified into;
1. Clotting factor abnormalities
 Congenital coagulopathies(Von Willebrands disease, Haemophilia A&B, Antithrombin deficiency)
 Acquired coagulopathies(Pregnancy induced hypertension, Placenta abruption, retained dead fetus,
Amniotic fluid embolism, anticoagulant drugs like aspirin and heparin)
2. Platelet abnormalities
 Thrombocytopenia( DIC, HELLP syndrome)

MECHANISM OF COAGULATION
Source: DC Dutta textbook of obstetrics 7th edition

DISSEMINATED INTRAVASCULAR COAGULOPATHY\
(DIC)
 DIC is a clinical pathological syndrome characterized by systemic activation of pathways
leading to coagulation which results in the generation of fibrin clots with concomitant
consumption of platelets and coagulation factors that may result in clinical bleeding.
 Obstetric causes of DIC

 Placenta abruption(↑ release of tissue factor)
 Amniotic fluid embolism (↑ inflammatory reaction and activation of coagulation factors)
 Intrauterine fetal demise (around 3-5 weeks due to release of thromboplastin)
 Pre-eclampsia, HELLP syndrome/ eclampsia( Endothelial injury activating the intrinsic pathway)
 Septic abortion, chorioamnionitis, pyelonephritis (Endothelial injury )

Obstetric complications and trigger factors for DIC
Clinical manifestation of DIC
 Before delivery
 Bruising
 Prolonged bleeding at the injection sites (veno-puncture or intramuscular)
 Gum bleeding
 GI bleeding
 After Delivery
 Postpartum hemorrhage
 Bleeding from the suture sites (episiotomy wound)
 Hematoma formation in the abdominal wound following cesarean section
 Formation of a vulval hematoma following vaginal delivery

LABORATORY INVESTIGATIONS
Bedside tests
 Bleeding time (1-3 min)
 Coagulation time(3-7 min)
 Clot observation test(blood in the test tube clots within 6-12 minutes)
 Essential lab tests to assess specific defects in the coagulation mechanism
 Partial thromboplastin time(intrinsic coagulation)
 Prothrombin time(extrinsic coagulation)(11-17 sec)
 Thrombin time(10-15 sec)
 Fibrinogen levels(300-600mg)
 Fibrin degradation products(FDP)(0-5µg/ml)
 D-dimers(breakdown product of fibrin) (0-200mg/ml)
 CBC(Low platelets)
MANAGEMENT OF DIC
PREVENTION
 Early detection and management of predisposing factors
 Abruptio placenta
 Massive blood transfusion
 Expedite early delivery
 Emergency cesarean section
 Intrauterine death
 Avoid expectant management
 Labor induction to empty the uterus
 Proper management of pre-eclampsia, eclampsia and HELLP syndrome
 Better understanding of the pathophysiology of shock and early appropriate therapy
 Emptying the uterus and controlling the infection with antibiotics
 Inj Vit K(5-10mg IM ) to help replenish vitamin K dependent factors II, VII, IX and X
MANAGEMENT OF DIC
Actual Management
 Volume replacement
 Blood component therapy
 Heparin
 Fibrinolytic inhibitors
Actual Management
 Volume replacement should be by crystalloids (RL) or by colloids (haemacel, Human

albumin). Use 2 large bore IV cannulas. Dextran should be avoided as it adversely
affect platelet function and blood cross matching tests
 Blood component therapy (to provide coagulation factors); Whole blood transfusion,
FFPs, Platelet concentrates.
 Heparin; it helps prevent DIC for example if given in amniotic fluid embolism, retained
dead fetus. IV heparin 5000 units given 4-6 hours interval.
 Fibrinolytic inhibitors(tranexamic acid); mainly indicated in PPH following abruption

placenta and when blood fibrinogen level is 200mg% or more
VENOUS THROMBOEMBOLISM
 Pregnant women or in the postpartum period have a 4-5 fold increased risk of thromboembolism
compared with non-pregnant women.
 Although VTE can occur during any trimester studies suggest that VTE is more common during
the first half of pregnancy (RCOG 2015).
 The two manifestations of VTE are deep venous thrombosis (DVT) and pulmonary embolus (PE).
 DVT is approximately 3 times more common than PE in pregnancy.
Incidence of VTE
 VTE was the leading cause of direct maternal death in 2009-2012.

 Incidence declined after the publication of royal college of obstetrics and
gynecology Greentop guideline(2015) due to thromboprophylaxis during
pregnancy, labour and after delivery.
 The prevalence of DVT varied between 2.4% and 9.6% in post op patients and
between 380 and 448 per 100000 births per year in pregnant and post partum
women.
 PE prevalence varied between 0.14% and 6.15% with mortality rate of 40-
69.5%.
Pathophysiology
Pregnancy characterized by Virchow’s triad; stasis of blood, endothelial cell

injury and hypercoagulability. For example compression of pelvic veins and
inferior vena cava by enlarging uterus reduces lower extremity venous system
leading to stasis. Stasis can cause endothelial damage. Hypercoagulability due to
increased coagulation factors and resistance to antithrombotic factors.
Risk factors
 C-section
 Hyperemesis
 Immobility
 Multiple gestation
 Pre-eclampsia
 Puerperal infection
 Thrombophilia
Cont……..
 Sickle cell disease

 Oral contraceptive use
 Advanced maternal age
 Diabetes melitus
Deep vein thrombosis
Most DVTs are confined to the deep veins of lower extremities. Approximately
70% of cases are located in the ileofemoral vein without involvement of calf
veins. Most cases during pregnancy are left sided.
Signs and symptoms
 Pain
 Swelling of lower extremity
 Warmth around the affected vein0
Investigations
 Compression ultrasonography of the proximal veins

 Magnetic resonance
 dDimer screening test
 Contrast venography (gold standard)
Management
 Anticoagulants initiated at diagnosis incase of no contraindication. Common

anticoagulants used include;
 Indirect thrombin inhibitors eg heparin (UFH, LMWH), factor Xa inhibitors eg
rivaroxaban, apixaban. LMWH preferd in acute VTE (enoxaparin 1mg/kg
12hrly).
 Direct thrombin inhibitors eg argatroban, lepirudin
 Vitamin k antagonist eg warfarin but used postpartum.
Cont……….
 Temporary discontinuation of anticoagulants in regional anesthesia.

 Regional anesthesia should be withheld 12hrs following last prophylactic
LMWH to 24hrs following last therapeutic LMWH.
 Patients may be converted from LMWH to subcut UFH at 36 weeks if delivery
is expected earlier.
Postpartum
 Anticoagulants maybe restarted 4-6hrs following vaginal delivery or 6-12hrs

following c/s.
 Heparin or warfarin
 Patient remains on heparin 4-5days while warfarin titrated to a goal INR of
2.0-3.0 with close monitoring due to narrow therapeutic window.
Pulmonary embolism
 A condition in which one or more arteries in the lungs become blocked by a

clot.
 PE in most cases is secondary to DVT but it also occurs without any previous
clinical manifestation of DVT.
Signs and symptoms
 Dyspnea
 Chest pain
 Cough
 Tachypnea
 Tachycardia
 Hemoptysis
 In massive PE syncope, pulseless cardiac electrical activity and death occur.
Investigations
 CT pulmonary angiography.
 Magnetic resonance angiography
 Ventilation perfusion scintigraphgy lung scan
Management
 Immediate treatment for PE is full anticoagulant similar to that for DVT

though a number of complementary procedures may be indicated.
 Vena caval filters.
 Thrombolysis; compared with heparin thrombolytic agents provide more rapid
lysis of pulmonary clots and improvement of pulmonary hypertension eg
streptokinase.
 Embolectomy.
Prophylaxis for VTE
 Prevention of trauma, sepsis, dehydration in pregnancy and labour.

 Thromboprophylaxis with LMWH or warfarin for atleast 6 weeks postpartum
regardless of the mode of delivery for high risk mothers.
 Leg exercise, early ambulation following operative delivery.
References
 DC dutta’s textbook of obstetrics, 7th edition.

 William’s obstetrics, 24th edition.
 First aid for obstetrics and gynecology, 3rd edition.
.
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COAGULATION DISORDERS IN OBS/GYN

Tutor: DR. WASSWA WANGI ESAU

 Hemostatic changes in pregnancy

rhage during pregnancy, labour and puerperium

Disseminated intravascular coagulopathy(DIC) among pregnant women.

1. Clotting factor abnormalities

 Congenital coagulopathies(Von Willebrands disease, Haemophilia A&B, Antithrombin deficiency)

 Acquired coagulopathies(Pregnancy induced hypertension, Placenta abruption, retained dead fetus,

Amniotic fluid embolism, anticoagulant drugs like aspirin and heparin)

 Thrombocytopenia( DIC, HELLP syndrome)

Source: DC Dutta textbook of obstetrics 7th edition

 Obstetric causes of DIC

 Amniotic fluid embolism (↑ inflammatory reaction and activation of coagulation factors)

 Intrauterine fetal demise (around 3-5 weeks due to release of thromboplastin)

 Septic abortion, chorioamnionitis, pyelonephritis (Endothelial injury )

 Prolonged bleeding at the injection sites (veno-puncture or intramuscular)

 Bleeding from the suture sites (episiotomy wound)

 Hematoma formation in the abdominal wound following cesarean section

 Formation of a vulval hematoma following vaginal delivery

 Bleeding time (1-3 min)

 Coagulation time(3-7 min)

 Essential lab tests to assess specific defects in the coagulation mechanism

 Partial thromboplastin time(intrinsic coagulation)

 Prothrombin time(extrinsic coagulation)(11-17 sec)

 Thrombin time(10-15 sec)

 Fibrin degradation products(FDP)(0-5µg/ml)

 D-dimers(breakdown product of fibrin) (0-200mg/ml)

 Early detection and management of predisposing factors

 Expedite early delivery

 Emergency cesarean section

 Labor induction to empty the uterus

 Proper management of pre-eclampsia, eclampsia and HELLP syndrome

 Better understanding of the pathophysiology of shock and early appropriate therapy

 Emptying the uterus and controlling the infection with antibiotics

 Blood component therapy

 Volume replacement should be by crystalloids (RL) or by colloids (haemacel, Human

 Fibrinolytic inhibitors(tranexamic acid); mainly indicated in PPH following abruption

 VTE was the leading cause of direct maternal death in 2009-2012.

Pregnancy characterized by Virchow’s triad; stasis of blood, endothelial cell

 Sickle cell disease

 Compression ultrasonography of the proximal veins

 Anticoagulants initiated at diagnosis incase of no contraindication. Common

 Temporary discontinuation of anticoagulants in regional anesthesia.

 Anticoagulants maybe restarted 4-6hrs following vaginal delivery or 6-12hrs

 A condition in which one or more arteries in the lungs become blocked by a

 Immediate treatment for PE is full anticoagulant similar to that for DVT

 Prevention of trauma, sepsis, dehydration in pregnancy and labour.

 DC dutta’s textbook of obstetrics, 7th edition.

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