Bleeding and Haemostasis

Saman W.Boskani HDD, FIBMS

Maxillofacial Surgeon

1 Beeding

● Its escaping or extravasation of blood contents from blood vessels

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● Types: - Arterial - Venous - Capillary

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Differences between the types:

Arterial Venous Capillary● Bright red

● Eject out Synchronously

● Its control is difficult

● Avoidable

● Darker blood

● Has steady flow

● Its control is sometimes easier

● Common

● Bright red ●

● Shows as generalized ooze

● Its rapid & controlled much

easier

●Most common than others

Classifications:According to time of haemorrhage:

1. Primary: immediately 2. Reactionary: commonly within first 24

hours 3. Secondary: usually occurs 7-14 days

According to appearance: 1. Revealed (external) 2. Concealed (internal)

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Classifications: (cont.)According to size of haemorrhage:

1. Small haemorrhages (petechiae,purpura,ecchymosis)

2. Large or massive haemorrhages (appear as running, clotting or hematomas)

● According to different organs or systems named:

1. Epistaxis, hemoptysis, 2. Hematamesis & melena, 3. Hematuria Next

Compensatory reactions activated by haemorrhage:

➢Vasoconstriction ➢Tachycardia ➢Venoconstriction ➢Tachypnea- increased thoracic pumping ➢Restlessness ➢ Increased movement of intestinal fluid into

capillaries

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➢ Increased secretion of norepinephrine &epinephrine

➢ Increased secretion of vasopressin ➢ Increased secretion of glucocorticoid ➢ Increased secretion of renin& aldosterone ➢ Increased secretion of erythropoietin ➢ Increased plasma protien synthesis

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Clinical presentation:● Pale ,cold, wet skin ● Restlessness ,anxiety ,change in

conscious level ● Tachycardia ,with normal or even raised

BP at first but later on Hypotension if bleeding cont.

● Deep sighing breathing( air hunger), tachypnea

● Thirst in late stages ● Empty veins ● Shock

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Investigations1. Hematological

1. Hb, pcv, blood group 2. Bleeding& clotting studies

2. Radiological studies (including US) 3. Electrolyte, acid- base analysis 4. Blood gas analysis & monitoring 5. Renal function studies after few days 6. Liver function studies

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Management● In general managing of a case of

hemorrhage include: I. Primary assessment while resuscitating the

patient I. IV line, fluid, sending blood for group& cross match II. Send for blood if necessary III. Assessing of the amount of blood lost if possible IV. Stopping of bleeding if possible( external) V. CVP measurement

II. Secondary assessment Definitive treatment: including taking the patient to

theatre if indicated

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ManagementLocal Haemostasis: 1. Mechanical:

1. Positioning 2. Pressure

1. Finger 2. Hemostat 3. Bandage ,sterile gauze, tourniquet ( better to be avoided)

3. Packing 4. Ligation

2. Thermal 1. Electro cautery 2. Cryogenic surgery

3. Chemical 1. Epinephrine 2. Gel foam, oxycel, fibrin glue 3. Coagulation factors (regardingly )

4. Follow up of the patient

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2 hemostasis

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Can be define as : ● The process of arresting bleeding by repair

of vessel wall ● Maintaining a balance between

● Coagulation ● Fibrinolysis

Mature clot : is acombination of cross linked fibrin admixed with blood cells

and plasma

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Sub-endothelial matrix

PlateletsHemostatic plug

FibrinEndothelial cell

RBCWBC

WBC

CLOT

Fibrin

Red Blood CellPlatelet

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COMPONENTS OF HEMOSTASIS

● Vascular system ● Platelet System ● Coagulation System

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Hemostatic Mechanism● 2 phases

● PRIMARY- blood vessel (vascular) and platelet response to injured vessel

● SECONDARY- response of protein coagulation factors to the injury

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Vascular phase ● It provide by vasoconstriction due to local

contraction in smooth muscles of vessels by the effect of different stimuli (eg Thromboxane A2 which is a powerful vasoconstrctor) also (Serotonin , bradykinin )

● By this process : 1-reduces blood loss 2-prevents clot from washing out

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Platelet Phase

● Also platelet plays a great role as an injury to vascular walls ; expose endothelial collagen to which platelet adhere ,& this required vWf which is producing in the Sub-endothelium , it binds to Glycoprotein in the surface of platelets

● This phase pass through : 1- platelet adhesion 2-platelet activation 3-platelet aggregation

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Coagulation ● It is a stepwise pathway , which is stimulated

by platelet phase , ● The resultant system known as coagulation

cascade which consist of two paralleling routes (Intrinsic & Extrinsic pathways )

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Coagulation ● Intrinsic Pathway : all its components are found in blood so

its activated by exposure to negatively charged foreign substance

the Intrinsic Pathway include factors VIII , IX , XI , XII

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Coagulation ● Extrinsic pathway: refer to extrinsic because the factors that

activate it (tissue factor) is normally outside the vascular space and is exposed to vascular space only after damage to vascular endothelium

Extrinsic Pathway include factor ( III , VII )

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Coagulation ● Both intrinsic and extrinsic pathways connect

to forming common pathway ● Common pathway include factors I ,II , III ,X

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Contact Tissue Factor + VII

XIIIa

XIII

Thrombin

Fibrin (strong)

Fibrinogen Fibrin (weak)

IXXI

XIaIXa

XaVa

XIIaProthrombin

TF-VIIa

(Prothrombinase)

PL

PL(Tenase)

VIIIaPL

X

Intrinsic Pathway

HKa

Extrinsic Pathway

Common Pathway

TF Pathway

Coagulation Pathways

Protein C, Protein S, Antithrombin III

Important Note

● vWF which synthesized by vascular endothelial and attaches to both platelet receptors and collagen sp.

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Important Note

● BT : primary hemostasis ● PT : Extrinsic pathway ● PTT : Intrinsic pathway ● TT : Common pathway

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Important Note

● Some time case of vWF disease mistaken for hemophiliac case because the level of factor VIII are commonly low in vW disease because vWF acts as carrier protein for factor VIII

● but with normal PT ,PTT

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Important Note

● Bleeding time : reflects the time required to form the platelet

plug (primary hemostasis ) so it reflects platelet function rather than coagulation cascade

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Important Note

● Aspirin inhibits platelet function by irreversibly inhibiting the enzyme

cyclo-oxygenase which is normally function to synthesize thromboxane A2 ,

TXA2 normally acts to stimulate platelet aggregation and constriction of blood vessels

so aspirin lead to prolonging Bleeding Time Next

Important Note

● Heparin activates anti-thrombin III (ATIII) which is a potent inhibitor of factor II thrombin as well as some other factor in intrinsic pathway , it prolong PTT , no PT except in high dose ,

● it not affect BT because it not affect platelet function

It can be antagonized by protamine

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Important Note

● Warfarin inhibit the production of Vit. K dependant clotting factors X IX VII II so it affects common and extrinsic pathways and so it affects PT rather than PTT .

● Its effect can be antagonized by administering Vit K or fresh frozen plasma

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Important Note

● Desmopressin acetate DDAVP is useful in many case of bleeding disorder because it induces the hepatic production of plasma clotting factors , and it stimulate the release the vWF from the endothelial cells

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FibrinolysisPlasminogen

Plasmin

Fibrin, fibrinogen

ActivationExtrinsic: t-PA, urokinase

Intrinsic: factor XIIa, HMWK, kallikreinExogenous: streptokinase

Fibrin, fibrinogen degradation products Next

Fibrinolysis● Mechanism of action of tissue palsmogen

activator its enzyme that activate plasma enzyme plasmogen by converting it to active form plasmin and plasmin is an enzyme that protolytically cleave fibrin strands thereby degrading fibrin clots like streptokinase and urokinase

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References

● Baily & Love Short practice of surgery ● Textbook of General & Oral Surgery ● Clinician’s manual OMF surgery ● Internet articles

Thanks