bleeding tendency for dentist

7/29/2019 Bleeding Tendency for Dentist

1/58

Bleeding tendency

Normal haemostasis

Factors involved in normal

haemostasis


2/58

Bleeding: Clinical Features

Local - Vs - General, spontaneous . . Hematoma & Joint bleed -

Coagulation

Skin/Mucosal Petechiae & PurpuraPLT

wound / surgical bleeding

Immediate - (PLT) Delayed - (Coagulation)


3/58

Hemostasis

BV Injury

Platelet

Aggregation

Platelet

Activation

Blood Vessel

Constriction

Coagulation

Cascade

Stable Hemostatic Plug

Fibrinformation

Reduced

Blood flow

Tissue

Factor

Primary hemostatic plug

Neural

Lab TestsCBC-PltBT,(CT)PTPTT

Plt StudyMorphologyFunction

Antibody


4/58


5/58


6/58

Primary Hemostatic Disorders

Vascular defect - fragilityPetechiae, purpura, ecchymoses

senile purpura

vitamin C deficiency (scurvy)

connective tissue disorders Osler-Weber-Rendu syndrome -

hereditary malformations


7/58

Senile Purpura


8/58

Primary HemostaticDisorders

Vascular defect - cont.

Infectious and hypersensitivity

vasculitides- Rickettsial and

meningococcal

infections

- Henoch-Schonlein purpura

(immune)


9/58


Platelet disorders: platelets (thrombocytopenia)

petechiae

spontaneous bleeding after

trauma

CNS bleeding (severe

plt) Platelet dysfunction -

mucocutaneous bleeding

Prolonged bleeding time (BT)


10/58

Bleeding Time Test

Timer is started uponincision

Bleeding time = time

to complete cessationof free blood flow fromincision


11/58

Thrombocytopenia -Causes

Marrow injury/failure- aplastic or myelophthesic

anemia

- drugs, infections

- megaloblastic anemia, PNH

Decreased survival- immune (ITP, drugs,

infections)

- nonimmune (DIC, TTP)


12/58

Idiopathic ThrombocytopenicPurpura (ITP)

Acute - children (post infection)

Chronic - adults ( females, 20-40yrs)- autoimmune disorder

- antiplatelet antibodies (IgG

against plateletglycoproteins)

- IgG coated platelets removed by

spleen ( platelet survival)


13/58


Platelet dysfunction:Inherited - autosomal recessive Bernard-Soulier disease

- large platelets

- lack of glycoproteins (1b-IXcomplex)

- failure of platelet adhesion

Glanzmanns thrombasthenia

- normal platelet morphology

- lack of glycoproteins (IIb-IIIa

complex)


14/58


Platelet dysfunction:Acquired - common

Aspirin and NSAID

- cyclo-oxygenase inhibitors

- lack of thromboxane A2 and

PGE- failure of platelet aggregation

Systemic disorders - i.e.


15/58

Primary Hemostatic Disorders

Plasma proteins required foradhesion to subendothelium:

von Willebrand disease

- quantitative or qualitative

deficiency of vWF molecule

- binds to exposedsubendothelial collagen

- mediates initial platelet

adhesion


16/58


17/58

Secondary Hemostasis

Consolidates initial plateletplug into stable clot

Disorders - deficiencies of

plasmaclotting factors

Clinical - bleeding from large

vessels into joints(hemarthroses), muscles, deepsoft tissues (hematomas, large

ecchymoses)


18/58

Secondary HemostaticDisorders

Laboratory findings: Normal bleeding time, platelet

count

Prolonged prothrombin time(PT)

deficiencies of II, V, VII, X

Prolonged activated partialthromboplastin time (aPTT)

all factors except VII, XIII

Mixing studies - normal plasma


19/58

Screening Tests of Blood Coagulation


20/58

Factor VIII Deficiency

Classic hemophilia (hemophilia

A)

X-linked disorder (affects 1males)

Most common hereditary

disease with severe bleeding

30% new mutations (not

hereditar


21/58

Factor VIII Deficiency

Classic hemophilia - cont. Clinically severe if


22/58

Factor IX Deficiency

Christmas disease(hemophilia B)

X-linked recessive disorder

Indistinguishable fromclassic hemophilia

Requires evaluation of factor

VIII and IX activity levels todiagnose

Treatment - factor IX

concentrate


23/58

Secondary HemostaticDisorders

Acquired coagulation disorder: Vitamin K deficiency

- neonates - decreased

intestinal

flora and dietary intake

- oral anticoagulants

(coumadin)

- fat malabsorption syndromes

Required for factors II, VII, IX, X


24/58

Combined Primary andSecondary Hemostatic

Disordersvon Willebrands DiseaseAutosomal dominant (or

recessive) Primary defect - platelet

adhesion

(prolonged bleeding time) Secondary defect - deficiency

of factor VIII; normally

stabilizes factor VIII in


25/58

Von Willebrands Disease

Clinical - often mild- excessive bleeding fromwounds- spontaneous bleeding from

mucous membranes Different types - quantity or

loss of selective multimers Diagnosis - ristocetin induced

plt aggregation or multimer


26/58

von Willebrand Factor multimeric analysis


27/58


DisordersDisseminated IntravascularCoagulation

Primary - platelet consumption( bleeding time, platelets)

Secondary - factor consumption

( PT, aPTT) Major pathologic processes -

obstetric complications,

neoplasms, infection (sepsis),


28/58

Disseminated IntravascularCoagulation

Multiple initiating

factorsTissue factorThromboplastic substances

Widespreadendothelial injury

platelet

aggregationActivates extrinsic pathway Activates intrinsic pathwa

Microvascular thrombosis

Clotting factorconsumptionFibrinolysis

plasmin

Fibrin split products Bleeding

Tissue injury,Hemolyticanemia


29/58

Disseminated Intravascular

Thrombosis (DIC)

Acute DIC - bleeding- i.e. major trauma

- give fresh frozen plasma Chronic DIC -

thrombosis

- i.e. cancer

- give heparin or

anticoagulant

C bi d P i d


30/58


DisordersSevere Liver Disease

Primary - dysfunctional platelets

and/or thrombocytopenia ( BT) Secondary - decrease in all

coagulation factors except vWF (PT, aPTT)

Vitamin K will promote synthesis of

factors II, VII, IX, X


31/58

Summary Hemostatic Disorders

BT Plt PTPTT

1

o

hemostasis

-

-

--

2o Factor VIII/IX

deficiency - - -2o Vitamin K

deficiency - -


32/58

Approach to bleeding disordersPersonal history of bleeding

With surgery Tonsillectomy, circumcision

Epistaxis

a

Immediate bleeding after trauma or surgerysuggest platelet or severe protein deficiency.

Bleeding 2-5 days post trauma or surgery suggestplasma protein deficiency .


33/58

Family history

X linked

Autosomal al

* Drug history Oral anticoagulant, Heparin,Aspirin

* Physical examination


34/58

Initial lab works

CBC : Platelet count

PT (INR)APTT

Bleeding time


35/58

Signs and Symptoms of

Coagulation Disorders Bleeding Ecchymoses

Petechiae Hemarthroses

Hematomas


36/58

Petechiae


37/58

Platelets versus Coags

Petechiaeplatelets low or dysfunctional

Ecchymoses, hematomas,

hemarthrosesseen more frequently with

low clotting factors or dysfunction

Bleeding can be seen with either


38/58

Hematom

a


39/58

Hemarthrosis


40/58

Hematom

a


41/58


42/58

Management :

Always be on the safe side

Dont do invasive procedures if you are in doubt.

Always check with haematology/ internal medicine.

Check the above tests if normal you can proceed

Remember some cases of bleeding tendency

might go first to you, like AML with gingival hypertrophy.

Always check Drugs


43/58

HEPARIN THERAPY

Enhances activity of AT III

Parenteral administration required

Onset of action immediate

Monitor aPTT

Lower dose may work in patients withoutactive thrombosis

HEPARIN THERAPY


44/58

HEPARIN THERAPYLow Molecular Weight Heparin-

Advantages

Less heterogeneous than heparin

Less inhibition of platelet function Longer half life - Can give 1-2x/day

Much less thrombocytopenia

? safer, equally effective

HEPARIN


45/58

HEPARINLow Molecular Weight Heparin-

Disadvantages

Bleeding-? Less than with heparin

(probably not) Most cross react with heparin RE:

thrombocytopenia

Each preparation is different Less overall experience with the drug

COUMADIN (warfarin)


46/58

COUMADIN (warfarin)Mechanism of Action

Inhibits Vitamin K dependent carboxylase activity

Prevents reduction of Vitamin K

Humans secrete des--carboxyglutamic acid, an

inactive protein DOES NOT AFFECT PROTEINS ALREADY

SYNTHESIZED

Monitor using prothrombin time

Multiple interactions with other drugs

Antidote-Vitamin K


47/58

What do if no help

if INR< 1.5 safe to do procedures, so if

patient on Warfarin , stop Warfarin 2 days

before surgery.

Heparin stop if unfractionated 2 hours before

SX. If low MW Heparin 4-6 hours stop

surgery


48/58


49/58

Systemic illnesses can predispose to

bleeding like liver diseases, Chronic renal

failure.


50/58

Depending on the underlying cause

abnormalities of the platelet should be

corrected before any procedure .

How to correct depends on the underlying

cause either with platelets transfusion or

other modalities to increase the count ,like

steroids , IVIg in ITP.


51/58

If on Aspirin please stop Aspirin at least

one week before SX. If urgent please

check bleeding time if prolonged please

give platelets. Which should be 1-2 hourbefore SX.


52/58

For congenital causes of bleeding please

contact haemtology.


53/58

leukaemias

Can predispose to bleeding due to

1- low platelets count

2- DIC

3-Hyerviscosity syndrome.

Oral manifestations of acute leukaemia

Includes : gingival hypertrophy, bleeding ,and ulcers.


54/58

Oral manifestations of leukaemia


55/58


56/58
http://www.google.jo/imgres?imgurl=http://img.medscape.com/pi/features/slideshow-slide/inflamed-skin/fig12.jpg&imgrefurl=http://reference.medscape.com/features/slideshow/inflamed-skin&usg=__ZGpHJY2Y1OXZJm9AbyVeA0r_zFo=&h=355&w=522&sz=173&hl=ar&start=4&zoom=1&tbnid=eMRXKloHEaVlTM:&tbnh=89&tbnw=131&ei=ZQgiUYeQCfDa0QXu14GADQ&prev=/search%3Fq%3Dhemorrhage%2Bmouth%2Bbullae%26um%3D1%26hl%3Dar%26safe%3Dactive%26sa%3DN%26rlz%3D1T4ADRA_enJO492JO492%26tbm%3Disch&um=1&itbs=1&sa=X&ved=0CC4QrQMwAwhttp://www.google.jo/imgres?imgurl=http://img.medscape.com/pi/features/slideshow-slide/inflamed-skin/fig12.jpg&imgrefurl=http://reference.medscape.com/features/slideshow/inflamed-skin&usg=__ZGpHJY2Y1OXZJm9AbyVeA0r_zFo=&h=355&w=522&sz=173&hl=ar&start=4&zoom=1&tbnid=eMRXKloHEaVlTM:&tbnh=89&tbnw=131&ei=ZQgiUYeQCfDa0QXu14GADQ&prev=/search%3Fq%3Dhemorrhage%2Bmouth%2Bbullae%26um%3D1%26hl%3Dar%26safe%3Dactive%26sa%3DN%26rlz%3D1T4ADRA_enJO492JO492%26tbm%3Disch&um=1&itbs=1&sa=X&ved=0CC4QrQMwAw


57/58
http://www.google.jo/imgres?imgurl=http://ars.els-cdn.com/content/image/1-s2.0-S1079210406000096-gr5.jpg&imgrefurl=http://www.sciencedirect.com/science/article/pii/S1079210406000096&usg=__92O1MhAllL6g7u4hg5yOTNHyuD4=&h=304&w=452&sz=77&hl=ar&start=3&zoom=1&tbnid=Ivr3sQPvlhFBtM:&tbnh=85&tbnw=127&ei=ZQgiUYeQCfDa0QXu14GADQ&prev=/search%3Fq%3Dhemorrhage%2Bmouth%2Bbullae%26um%3D1%26hl%3Dar%26safe%3Dactive%26sa%3DN%26rlz%3D1T4ADRA_enJO492JO492%26tbm%3Disch&um=1&itbs=1&sa=X&ved=0CCwQrQMwAghttp://www.google.jo/imgres?imgurl=http://img.medscape.com/pi/features/slideshow-slide/inflamed-skin/fig12.jpg&imgrefurl=http://reference.medscape.com/features/slideshow/inflamed-skin&usg=__ZGpHJY2Y1OXZJm9AbyVeA0r_zFo=&h=355&w=522&sz=173&hl=ar&start=4&zoom=1&tbnid=eMRXKloHEaVlTM:&tbnh=89&tbnw=131&ei=ZQgiUYeQCfDa0QXu14GADQ&prev=/search%3Fq%3Dhemorrhage%2Bmouth%2Bbullae%26um%3D1%26hl%3Dar%26safe%3Dactive%26sa%3DN%26rlz%3D1T4ADRA_enJO492JO492%26tbm%3Disch&um=1&itbs=1&sa=X&ved=0CC4QrQMwAwhttp://www.google.jo/imgres?imgurl=http://img.medscape.com/pi/features/slideshow-slide/inflamed-skin/fig12.jpg&imgrefurl=http://reference.medscape.com/features/slideshow/inflamed-skin&usg=__ZGpHJY2Y1OXZJm9AbyVeA0r_zFo=&h=355&w=522&sz=173&hl=ar&start=4&zoom=1&tbnid=eMRXKloHEaVlTM:&tbnh=89&tbnw=131&ei=ZQgiUYeQCfDa0QXu14GADQ&prev=/search%3Fq%3Dhemorrhage%2Bmouth%2Bbullae%26um%3D1%26hl%3Dar%26safe%3Dactive%26sa%3DN%26rlz%3D1T4ADRA_enJO492JO492%26tbm%3Disch&um=1&itbs=1&sa=X&ved=0CC4QrQMwAwhttp://www.google.jo/imgres?imgurl=http://img.medscape.com/pi/features/slideshow-slide/inflamed-skin/fig12.jpg&imgrefurl=http://reference.medscape.com/features/slideshow/inflamed-skin&usg=__ZGpHJY2Y1OXZJm9AbyVeA0r_zFo=&h=355&w=522&sz=173&hl=ar&start=4&zoom=1&tbnid=eMRXKloHEaVlTM:&tbnh=89&tbnw=131&ei=ZQgiUYeQCfDa0QXu14GADQ&prev=/search%3Fq%3Dhemorrhage%2Bmouth%2Bbullae%26um%3D1%26hl%3Dar%26safe%3Dactive%26sa%3DN%26rlz%3D1T4ADRA_enJO492JO492%26tbm%3Disch&um=1&itbs=1&sa=X&ved=0CC4QrQMwAw


58/58
http://en.wikipedia.org/wiki/File:Aphtha2.jpg

bleeding tendency for dentist

Documents