Coagulation failure in pregnancy

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Dr : Hashmi Hajrai MBBCh, DGO, M’MAS, MRCOG Consultant Obstetrician & Gynaecologist

Transcript of Coagulation failure in pregnancy

Dr : Hashmi Hajrai

MBBCh, DGO, M’MAS, MRCOG

Consultant Obstetrician & Gynaecologist

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

Understanding the pathogenesis of DIC syndrome, diagnosis, complications & management outlines

Brief knowledge on some other important causes of coagulation failure in pregnancy

Bleeding during labour is dealt with effectively by

- increased production of coagulation factors during pregnancy - increased blood volume - myometrial contraction

this hypercoagulable state with local activation of clotting system is associated with increased risk of not only VTE but also DIC

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

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

Normal Artery

Endothelium

SmoothMuscle

Adventitia

Vascular Damage

Hemostasis

Overview of blood coagulation

VesselInjury

PlateletActivation

TissueFactor

CoagulationCascade

PlateletAggregation

PlateletPlug

Thrombin

Clot

Vasocon-striction

2D Medical Animation- Clot Formation and Clot Breakdown.flv

Three phases

1. Intrinsic pathway2.Extrinsic pathway 3.Common pathway

XII

XI

IX

XVIII

Prothrombin (II)

thrombin

fibrinogen fibrin

STABILISED FIBRIN

V, Ca, P/L

VII

Intrinsic pathway

Extrinsic pathway

XIII

APTT

PT

Congenital coagulation failure disorders these are uncommon.....examples:

i. Von Willebrand’s disease...will be discussed

ii. Haemophilia A & B

are far more commonly seen

a. Thrombocytopenic coagulopathies b. Disseminated intravascular

coagulation ..DIC c. Anticoagulant therapy

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

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)

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

Other coagulation factor deficiencies

• Factor VIII ( hemophilia A)• Factor IX ( hemophilia B)

• Autoimmune Thrombocytopenic Purpura• Idiopathic thrombocytopenic purpura• Immunoglobulin G (IgG)

Diagnosis• Platelet count < 100,000/mm3• Increased numbers of megakaryocytes• Increased platelet volume• Diameter

•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

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

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

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

Conditions having non-specific or indirect action

- amniotic fluid embolism - gram negative septicaemia - saline abortion

Mechanism of DIC

Bick et al., 2002

Those of the underlying cause

Those due to Complications of DIC

Involving skin & mucus membranes Ecchymosis Petechiae Bleeding from the gum Haematuria GIT bleeding Venepunctur oozing Intracranial or intracerebral haemorrhage

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

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

Fragments Schistocytes Paucity of platelets

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Fragmented RBC

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

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

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

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

Use of heparin is controversial . Haematologist opinion should be sought before it’s use