Bleeding and Haemostasis. Saman W.Boskani HDD, FIBMS Maxillofacial Surgeon
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1 Bleeding and Haemostasis Saman W.Boskani HDD, FIBMS Maxillofacial Surgeon
2 1 Beeding
3 Its escaping or extravasation of blood contents from blood vessels
4 Types: - Arterial - Venous - Capillary
5 Differences between the types: Arterial Venous Capillary Bright red Eject out Synchronously Its control is difficult Darker blood Has steady flow Its control is sometimes easier Bright red Shows as generalized ooze Its rapid & controlled much easier Avoidable Common Most common than others
6 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)
7 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
8 Compensatory reactions activated by haemorrhage: Vasoconstriction Tachycardia Venoconstriction Tachypnea- increased thoracic pumping Restlessness Increased movement of intestinal fluid into capillaries
9 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
10 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
11 Investigations 1. 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
12 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
13 Management Local 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
14 2 hemostasis
15 Can be define as : The process of arresting bleeding by repair of vessel wall Maintaining a balance between Coagulation Fibrinolysis
16 Mature clot : is acombination of cross linked fibrin admixed with blood cells and plasma
17 Sub-endothelial matrix WBC Hemostatic plugendothelial cell Platelets Fibrin RBC WBC
18 CLOT Platelet Red Blood Cell Fibrin
19 COMPONENTS OF HEMOSTASIS Vascular system Platelet System Coagulation System
20 Hemostatic Mechanism 2 phases PRIMARY- blood vessel (vascular) and platelet response to injured vessel SECONDARYresponse of protein coagulation factors to the injury
21 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
22 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
23 This phase pass through : 1- platelet adhesion 2-platelet activation 3-platelet aggregation
24 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 )
25 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
26 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 )
27 Coagulation Both intrinsic and extrinsic pathways connect to forming common pathway Common pathway include factors I,II, III,X
28 Contact XIIa XI XIa Intrinsic Pathway HKa IX IXa Coagulation Pathways TF Pathway TF-VIIa PL VIIIa PL (Tenase) Protein C, Protein S, Antithrombin III Tissue Factor + VII X Xa (Prothrombinase) Extrinsic Pathway Va Fibrinogen Common Pathway Prothrombin PL Thrombin Fibrin (weak) XIII XIIIa Fibrin (strong)
29 Important Note vwf which synthesized by vascular endothelial and attaches to both platelet receptors and collagen sp.
30 Important Note BT : primary hemostasis PT : Extrinsic pathway PTT : Intrinsic pathway TT : Common pathway
31 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
32 Important Note Bleeding time : reflects the time required to form the platelet plug (primary hemostasis ) so it reflects platelet function rather than coagulation cascade
33 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
34 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
35 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
36 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
37 Fibrinolysis Plasminogen Extrinsic: t-pa, urokinase Activation Intrinsic: factor XIIa, HMWK, kallikrein Exogenous: streptokinase Fibrin, fibrinogen Plasmin Fibrin, fibrinogen degradation products
38 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
39 References Baily & Love Short practice of surgery Textbook of General & Oral Surgery Clinician s manual OMF surgery Internet articles
40 Thanks
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