dr : hashmi hajrai mbbch, dgo, m’mas, mrcog consultant obstetrician & gynaecologist
TRANSCRIPT
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Dr : Hashmi Hajrai
MBBCh, DGO, M’MAS, MRCOG
Consultant Obstetrician & Gynaecologist
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The student should understand the alterations in coagulations & fibrinolysis associated with pregnancy
Refresh his mind about the normal coagulation cascade mechanisms and its triggers
Broad line classification of coagulation failure in pregnancy
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Understanding the pathogenesis of DIC syndrome, diagnosis, complications & management outlines
Brief knowledge on some other important causes of coagulation failure in pregnancy
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Bleeding during labour is dealt with effectively by
- increased production of coagulation factors during pregnancy - increased blood volume - myometrial contraction
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this hypercoagulable state with local activation of clotting system is associated with increased risk of not only VTE but also DIC
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The fibrinolytic system is responsible for disposing of fibrin after fulfilling its haemostatic function
Plasma proteases are responsible for controlling the speed and extent of coagulation & fibrinolysis
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Primary HemostasisPlatelet Plug Formation:dependent on normal
platelet number & function
Secondary HemostasisActivation of Clotting Cascade Deposition &
Stabilization of Fibrin Tertiary Hemostasis
Dissolution of Fibrin Clot:dependent on Plasminogen Activation
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Normal Artery
Endothelium
SmoothMuscle
Adventitia
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Vascular Damage
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Hemostasis
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Overview of blood coagulation
VesselInjury
PlateletActivation
TissueFactor
CoagulationCascade
PlateletAggregation
PlateletPlug
Thrombin
Clot
Vasocon-striction
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2D Medical Animation- Clot Formation and Clot Breakdown.flv
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Three phases
1. Intrinsic pathway2.Extrinsic pathway 3.Common pathway
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XII
XI
IX
XVIII
Prothrombin (II)
thrombin
fibrinogen fibrin
STABILISED FIBRIN
V, Ca, P/L
VII
Intrinsic pathway
Extrinsic pathway
XIII
APTT
PT
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Congenital coagulation failure disorders these are uncommon.....examples:
i. Von Willebrand’s disease...will be discussed
ii. Haemophilia A & B
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are far more commonly seen
a. Thrombocytopenic coagulopathies b. Disseminated intravascular
coagulation ..DIC c. Anticoagulant therapy
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Von Willebrand disease
• Factor synthesized by endothelial cells & megakaryocytes
• Forms a complex with factor VIII• Mediates platelet adhesion and collagen
• Inherited as autosomal dominant trait
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Von Willebrand diseaseDuring pregnancy
•Prophylactic treatment factor VIII level below 25%
•DDAVP is administered as labor begins – repeated every 12 hrs.
•FFP or cryoprecipitate (500-1,500 units of factor VIII activity)
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Von Willebrand diseaseDuring labor
• Factor VIII levels should be maintained at 50%
of normal• CS – factor VIII level to 80%of normal
• Check daily during the post partum period
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Other coagulation factor deficiencies
• Factor VIII ( hemophilia A)• Factor IX ( hemophilia B)
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• Autoimmune Thrombocytopenic Purpura• Idiopathic thrombocytopenic purpura• Immunoglobulin G (IgG)
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Diagnosis• Platelet count < 100,000/mm3• Increased numbers of megakaryocytes• Increased platelet volume• Diameter
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•Conservative management
• Corticosteriods – if platelet count <20,000/mm3 before the onset of labor or < 50,000/mm3 at time of delivery
• High dose IV immunoglobulin produces increase in platelet count
• Significant hemorrhage – immediate postpartum period platelet transfusion
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The theoretical risk of intracranial haemorrhage in the thrombocytopenic foetus has not been shown to be reduced by C/S therefore C/S should be performed for obstetric reasons
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An acquired syndrome characterized by systemic intravascular coagulation
Coagulation is always the initial event
SYSTEMIC ACTIVATION OF COAGULATION
Intravascular
deposition of
fibrin
Depletion of platelets
and coagulation
factors
Thrombosis of small and
midsize vessels
Bleeding
Organ failure
DEATHDEATH
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Falls into three categories conditions associated with release of tissue
thromboplastin that activates extrinsic pathway - placental abruption - dead foetus - molar pregnancy Conditions associated with endothelial damage
leading to activation of intrinsic & extrinsic pathways - pre-eclampsia & eclampsia
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Conditions having non-specific or indirect action
- amniotic fluid embolism - gram negative septicaemia - saline abortion
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Mechanism of DIC
Bick et al., 2002
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Those of the underlying cause
Those due to Complications of DIC
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Involving skin & mucus membranes Ecchymosis Petechiae Bleeding from the gum Haematuria GIT bleeding Venepunctur oozing Intracranial or intracerebral haemorrhage
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Neurologic with multifocal lesions , delirium & coma
Dermatologic with focal ischaemia & superficial gangreen
Renal with cortical necrosis and ureamia GIT acute ulceration with bleeding Vascular occlusion causing pulmonary
infarction or peripheral vascular gangreen
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Markedly decreased platelet count Markedly Increased fibrin degradation
products FDP’s Fragmented RBCs & microspherocytes
in peripheral blood film Low fibrinogen , factor II , V & VII Prolonged PT, PTT & TT
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Fragments Schistocytes Paucity of platelets
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๓ ธั�นวาคม ๒๕๕๑T. TATU 37
Fragmented RBC
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Treatment of DIC
• Remove underlying cause• Replenish depleted factors• FFP Provides source of most
factors• Cryoprecipitate provides
fibrinogen• Platelet and blood support• Cautious use of heparin
Up to date, emedicine
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Blood coagulation is a major component of haemostasis. Increased Coagulation factors levels in pregnancy is meant to minimize blood loss at time of delivery
This haemostatic mechanism could fail risking patient’s life
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Thrombocytopenic coagulation failure and DIC syndrome are the most commonly seen in obstetric practice
Congenital causes of coagulation failure are uncommon and usually already diagnosed prior to pregnancy
DIC syndrome is always secondary to an underlying pathology
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If diagnosis of DIC is missed or appropriate action is delayed it can cause serious maternal morbidity or even death
Platelet transfusion and coagulation factor replacement or fresh blood transfusion are the main stay of treatment besides other supportive therapy
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Use of heparin is controversial . Haematologist opinion should be sought before it’s use