Bleeding disorders

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BLEEDING AND CLOTTING ABNORMALITIES

SUPREET KUMAR

BLEEDING

WHAT IS BLEEDING ???

Bleeding, technically called as HAEMORRHAGING is the loss or escape of blood from the circulatory system… BLEEDING CAN EITHER BE :-

1) EXTERNAL

2) INTERNAL

TYPES OF BLEEDING

A) CLASS I HAEMORRHAGE : 10-15 % of blood volume

B) CLASS II HAEMORRHAGE : 15-30 % of blood volume

C) CLASS III HAEMORRHAGE : 30-40 % of blood volume

D) CLASS IV HAEMORRHAGE : > 40 % of blood volume

CAUSES OF BLEEDING

A)TRAUMA - Lacerations - Incisions - Contusions - Crush injuriesB)UNDERLYING MEDICAL CONDNS - Anatomical defects - Cancer & infections - Disorders of hemostasis - Drugs & Anticoagulation therapy

A DELICATE BALANCE

HEMOSTASIS

HEMOSTASIS is the co-ordinated sequence of events that eventually stops the bleeding..

EFFECTIVE HEMOSTASIS :-

A) Response should be rapid

B) Response should be localised to the region of damage

C) Response should be carefully controlled

MECHANISMS THAT REDUCE BLOOD LOSS

THERE ARE 3 IMP MECHANISMS :-

1) VASCULAR SPASM

2) PLATELET PLUG FORMATION > Platelet adhesion > Platelet release action > Platelet aggregation

3) BLOOD CLOTTING

BLOOD CLOTTING

DEFINITION :

The process of formation of jelly like substance over the ends and within the walls of the blood vessels, with the resultant stoppage of blood flow ..

> Clotting involves a series or a cascade of chemical reactions that culminates in formation of FIBRIN THREADS.

> Clotting involves specific substances known as the CLOTTING FACTORS.

CLOTTING FACTORSNUMBER NAME OF FACTOR SOURCE ACIVATION

I FIBRINOGEN LIVER COMMON

II PROTHROMBIN LIVER COMMON

III THROMBOPLASTIN PLATELET EXTRINSIC

IV CALCIUM IONS PLATELET & BONE

ALL PATHWAYS

V LABILE FACTOR LIVER & PLATELET

EXTRINSIC AND INTRINSIC

VII PROCONVERTIN LIVER EXTRINSIC

VIII ANTIHEMOPHILIAC FACTOR A

LIVER INTRINSIC

CLOTTING FACTORSNUMBER NAME OF THE FACTOR

SOURCE ACTIVATION

IX ANTIHEMOPLHILIAC FACTOR B

LIVER INTRINSIC

X STUART-PROWER FACTOR / THROMBOKINASE

LIVER INTRINSIC AND EXTRINSIC

XI PLASMA THROMBOPLASTIN ANTECEDENT

LIVER INTRINSIC

XII HAGEMAN FACTOR LIVER INTRINSIC

XIII FIBRIN STABILISING FACTOR

LIVER AND PLATELETS

COMMON PATHWAY

THE CLOTTING CASCADECLOTTING is a complex cascade of enzymatic reactions in which each clotting factor activates many molecules of the next one in a fixed sequence…

CLOTTING CAN BE DIVIDED INTO 3 STAGES

1) THE 2 pathways : EXTRINSIC & INTRINSIC Leading to formation of PROTHROMBINASE

2) PROTHROMBINASE converts PROTHROMBIN into enzyme THROMBIN

3) THROMBIN converts soluble FIBRINOGEN into insoluble FIBRIN

SOME FAQs

1) WHAT IS THE NEED FOR 2 PATHWAYS ??

2) WHAT ARE THESE EXTRINSIC AND INTRINSIC PATHWAYS ??

3) WHY ARE THEY CALLED SO ??

4) HOW DOES THE INSOLUABLE FIBRIN FORMED IN THE LAST STEP OF THE CASCADE LEAD TO CESSATION OF BLEEDING ??

CLOT RETRACTION

ONCE the clot is formed

IT plugs the ruptured area of blood vessel & thus stops further bleeding

CLOT RETRACTION is the consolidation of the fibrin clot

AS the clot retracts , it pulls the edges of the damaged vessels close to each other and bridges the gap caused due to the trauma or injury and hence leads to arrest of bleeding

HEMOSTATIC CONTROL MECHANISMS

REGULATION of hemostasis is of optimum importance

The body has an in built mechanism to CONTROL AND REGULATE the process of hemostasis.

1) THE FIBRINOLYTIC SYSTEM

2) PROSTACYCLIN

3) NATURAL ANTI COAGULANTS IN BLOOD

WHY DOESN’T THE BLOOD CLOT WHILE FLOWING THROUGH THE VESSELS ??

1) THE ENDOTHELIAL LINING OF THE VESSEL

2) AXIAL FLOW OF THE BLOOD

3) VELOCITY OF THE BLOOD FLOW

4) NATURAL ANTICOAGULANTS

DYSREGULATION OF THE HEMOSTATIC MECHANISM …

> CLOTTING is a dynamic process that involves AMPLIFICATION and POSITIVE FEED BACK CYCLE.

> DYSREGULATION in the control mechanism can lead to uninhibited clotting and hence a large clot called THROMBUS is formed.

> THROMBUS has the potential to clog the vessels and impair the blood flow that has hazardous consequences.

THROMBUS FORMATION

VIRCHOW’S TRIAD

ENDOTHELIAL INJURY

STASIS OF BLOOD

HYPER COAGULABI

LITY

VENOUS THROMBI : INITIAL PHASE

MASSIVE THROMBUS IMPAIRING BLOOD FLOW

VESSEL OCCLUDED BY THE THROMBUS

AN APPROACH TO BLEEDING DISORDERS 1) HISTORY

* Site of bleeding * Duration of bleeding * Precipitating factors of the bleeding * History of previous operative procedures * Family history * History of drug intake

2) EXAMINATION

* Look for BRUISES,PURPURA,TELANGIECTASIA * Examination of joints ( HAEMOPHILIA ) * stigmata of liver diseases * SPLEENOMEGALY ( indicates thrombocytopenia )

MANAGEMENT OF BLEEDING DISORDERS

INVESTIGATIONS TREATMENT

INVESTIGATIONS IN CASE OF A BLEEDING DISORDER

* PLATELET COUNT* BLEEDING TIME* CLOTTING TIME* PROTHROMBIN TIME* ACTIVATED PARTIAL THROMBOPLASTIN TIME* FIBRINOGEN LEVEL* CLOT RETRACTION TIME* ACTIVATED CLOTTING TIME* PLASMA THROMBIN TIME

TREATMENT MODALITIES

* TREATMENT IS DEPENDENT ON THE TYPE OF BLEEDING DISORDER

* THE MAIN AIM OF THE TREATMENT IS TO REPLACE THE COMPONENT OR THE FACTOR WHOSE DEFICIENCY LEADS TO BLEEDING

AN APPROACH TO CLOTTING DISORDERS

1) HISTORY

* Careful history taking is important for evaluation * Family history should be enquired about

2) EXAMINATION

Careful evaluation of the signs and symptoms

* Pain * swelling * Redness at the site and other relevant symptoms

INVESTIGATIONS FOR ABNORMAL CLOTTING OR THROMBOTIC DISORDERS

1) BLOOD EXAMINATION

* D- DIMER* CBC* COAGULATION STUDIES BT,CT,APTT,FIBRINOGEN* LIVER ENZYMES

2) IMAGING STUDIES

* DOPPLER* ULTRASOUND* DUPLEX AND THERMOGRAPHY

TREATMENT MODALITIES FOR ABNORMAL COAGULABILITY

ANTI-THROMBOTIC DRUGS ARE THE DRUGS USED FOR TRAETMENT OF HYPER COAGULABILITY

ANTI THROMBOTIC DRUGS

ANTI PLATELET DRUGS

ANTI COAGULANTS

FIBRINOLYTIC AGENTS

ANTI PLATELET DRUGS

1) ASPIRIN

2) THIENOPYRIDINES

* CLOPIDOGREL * TICLOPIDINE

3) DIPYRIDAMOLE

4) GP II b / III a RECEPTOR ANTAGONIST * ABCIXIMAB * TIROFIBAN

ANTI COAGULANTS

1) HEPARIN

2) LMW HEPARIN

3) FONDAPARINUX

4) DIRECT THROMBIN INHIBITOR * LEPIRUDIN * BIVALIRUDIN * ARGATROBAN

FIBRINOLYTIC DRUGS

1) STREPTOKINASE

2) UROKINASE

3) ALTEPLASE

4) TENECTEPLASE

5) RETEPLASE

6) ANISTREPLASE

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