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Haemostasis and Coagulation PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Haemostasis & Coagulation”.

This medical PowerPoint presentation is about haemostasis, the process of stopping bleeding from damaged blood vessels. It involves a complex interplay between platelets, blood vessels, and coagulation factors.

When a blood vessel is damaged, the bodys first response is to constrict the vessel to reduce blood flow to the area. This is followed by the formation of a platelet plug at the site of injury. Platelets are small cell fragments that circulate in the blood and are essential for haemostasis. They adhere to the damaged vessel wall and to each other, forming a temporary seal to prevent further bleeding.

The platelet plug is reinforced by the coagulation cascade, a series of enzymatic reactions that ultimately leads to the formation of a fibrin clot. Coagulation factors, which are present in the blood, are activated in a specific sequence to produce fibrin, a fibrous protein that forms a mesh-like structure around the platelet plug. This fibrin mesh consolidates the platelet plug and forms a stable clot that seals the damaged vessel.

Once the clot has formed, the body begins the process of fibrinolysis, which is the breakdown of the fibrin clot. This is important to prevent the formation of unwanted blood clots in the circulatory system.

Disorders of haemostasis and coagulation can lead to bleeding or thrombotic disorders. Bleeding disorders such as haemophilia are caused by deficiencies in coagulation factors, while thrombotic disorders such as deep vein thrombosis (DVT) are caused by an excessive formation of blood clots.

Tags : Haemostasis, Coagulation, blood vessels, platelets, blood vessels, coagulation factors, Hematology, Hematology PowerPoint presentation

Published on : May 29, 2023 | Views : 1983 | Downloads : 5

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Slide 1-

Haemostasis & Coagulation
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‘THE DOCTOR WAS IN SUCH A HURRY TO OPERATE ON MY FATHER, LIKE A CHILD WANTING A LOLLYPOP’
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When an incision is made , the blood clots
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A 68 year old woman with a history of a 12 kg weight loss over the past six months presents to the emergency room with a history of passing bright red blood per rectum. Her pulse is 95, her blood pressure 120/70. She has not seen a physician in 40 years. Study Questions: What history and physical exam information would you gather to assess this patient's coagulation system? If there is a problem present, what would be the most likely? What laboratory tests would you order to assess this patient's coagulation system?
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A 24 year old man is in the operating room for a massive liver injury sustained when his motorcycle hit a truck. After one hour of surgery he has received 15 units of packed cells and has developed diffuse oozing from the surface of his liver. Clots are no longer forming. His body temperature is 34oC. Study Question: What are the most common coagulation difficulties associated with massive transfusion? What is the management of each?
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HAEMOSTASIS
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OBJECTIVES Mechanism of coagulation Tests Abnormal thrombosis Abnormal bleeding
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HAEMOSTASIS Keeps blood in fluid state & in circulation Prevents blood loss
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Haemostasis Four interconnected mechanisms form the basis of hemostasis: (a) blood vessel contraction (b) platelet plug formation (primary hemostasis) (c) clot stabilization with fibrin cross-linking (secondary hemostasis) (d) endogenous fibrinolysis.
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What is involved in Haemostasis? Blood vessels Platelets Plasma coagulation factors Inhibitors Fibrinolytics
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Events in Haemostasis Vascular spasm Formation of platelet plug Formation of fibrin plug - Blood clot Re-establishment of endothelium
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Haemostasis Vasoconstriction Clean cut vessels > crushed vessels Partially transected > completely cut Veins are easily compressed Danger areas of bleed
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Haemostasis Platelet plug - White bodies or microthrombi Contact with subendothelial collagen swell irregular with pseudopods release ADP, thromboxane A2 , phospholipids , HMWK sticky & aggregate
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Haemostasis Fibrin clot: Severe trauma - 15-20 secs Minor trauma - 1-2 mts Retraction - 20-60 mts
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Haemostasis COAGULATION 3 steps: Prothrombin activator Prothrombin Thrombin Fibrinogen Fibrin
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Haemostasis Pathways Intrinsic - XII = slow Extrinsic - VII = fast Common pathway factor V Xa Prothrombin activator phospholipid, calcium
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Haemostasis Extrinsic Tissue extract factor VII factor X Intrinsic surface contact VII XII XII a XI a IX a X HMWK phospholipid calcium BOTH ARE ESSENTIAL
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COAGULATION FACTORS
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HAEMOSTASIS ACTIVATED PLATELETS Prothrombin activator {rate limiting factor} {THROMBOPLASTIN} CALCIUM PROTHROMBIN THROMBIN FIBRINOGEN FIBRIN MONOMERS CALCIUM XIII FIBRIN POLYMERS STABLE CLOT
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Haemostasis Clotting of 1 ml of blood: 3 mg of fibrinogen 100 microgram of prothrombin 10 microgram of factor X 0.1 microgram of factor VIII
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HAEMOSTASIS PRODUCTION OF CLOTTING FACTORS Fibrinogen liver II, VII, IX, X liver with vit K VIII, V, XII endothelium XIII platelets
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HAEMOSTASIS THROMBIN Intensely proteolytic Activates factor V ,VIII, XIII Releases phospholipid from endothelium & platelet Activates protein C
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HAEMOSTASIS Clot retraction serum plasma [fibrinogen + consumed clotting factors] Platelets
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HAEMOSTASIS CONTROL Fibrinolysin or Plasmin Plasminogen activator DIGESTS ACTIVATES fibrin factor XII fibrinogen kinin factor VII complement factor V,XII prothrombin Inhibited by- alpha 2 plasmin inhibitor .
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HAEMOSTASIS Why does not blood clot normally ? Endothelium Fibrin & Antithrombin smooth thrombin fibrin [85-90%] glycocalyx antithrombin thrombomodulin prostacyclin heparin sulfate tissue plasminogen activator ADP ase
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HAEMOSTASIS Why does not blood clot normally? Heparin Thrombin Alpha 2 macroglobulin Thrombin C 1 inhibitor XII a, Kallikrein Alpha 1 antitrypsin XI a, Elastase Protein C Va, VIIIa
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Tests of blood coagulation 1. Bleeding time: 2.Clotting time: {modified Ivy’s method} {Lee & White method} N = 1-6 mts N = 6-10 mts in glass platelet plug N = 20-60 mts in Prolonged in: siliconized tubes Thrombocytopenia Measures intrinsic & Thrombasthenia common pathway Von-Willebrand’s disease
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Tests of blood coagulation Prothrombin time: { Quick’s one stage test } calcium oxalated blood from patient clot tissue thromboplastin N = 12 secs extrinsic & common pathway
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Prothrombin time contd... Prolonged in: 1. Oral anticoagulant drugs 2. Liver disease, obstructive jaundice 3. Vit K deficiency 4. D I C 5. Deficiency of factor VII , X, V, II SPECIFIC FOR FACTOR VII [ With X & V APTT is also prolonged]
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PARTIAL THROMBOPLASTIN TIME[ activated ] Contact activation KAOLIN + of factor XII + pt’s = Clot CEPHALIN blood phospholipid Intrinsic & Common pathway
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Partial thromboplastin time[activated ] contd….. Prolonged in: 1. D I C 2. Liver disease 3. Massive transfusion of stored blood 4. Heparin 5. Circulating anticoagulants 6. Deficiency of clotting factors other than VII 7. Haemophilia
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THROMBIN TIME PLASMA + THROMBIN CLOT Assesses fibrinogen Prolonged in : 1. Hypofibrinogenemia DIC CONGENITAL 2. FDP 3. Heparin [ assess with REPTILASE test ] 4. Dysfibrinogenaemia
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PLATELET COUNT N = 150 - 300 x 10 9 / L 80 x 10 9 / L Bleeding may follow trauma < 40 x 10 9 / L Spontaneous haemorrhage < 10 x 10 9 / L Lethal haemorrhage
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PRIMARY SCREENING TESTS Bleeding time Platelet count P T A P T T Specific tests- Factor VIII, XIII, fibrinogen Tests for fibrinolysis
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ABNORMAL HAEMOSTASIS Normal haemostasis Disorder of platelet function. Mild coagulation disorder Factor VII deficiency Early oral Anticoagulation 12-36 hrs Factor VIII, IX, XI, XII deficiency Prekallikrein, HMWK Deficiency, vWD, circulating anticoagulant
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ABNORMAL HAEMOSTASIS Vit K deficiency Oral anticoagulants Heparin, Fibrinogen Deficiency, Liver disease, Fibrinolysis Thrombocytopenia Massive transfusion Liver disease DIC
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SURGICAL SCREENING
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HAEMOSTASIS In a patient who bleeds: LIVER IMMUNOLOGIC RENAL COMPLETE CARDIAC WORK UP SEVERE INFECTION DRUGS Best screening test - HISTORY
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NATURAL ANTICOAGULANTS Antithrombin III Protein C and protein S
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NATURAL ANTICOAGULANTS Antithrombin III This is an inhibitor of thrombin, its action being potentiated by heparin. Congenital antithrombin III deficiency is inherited as an autosomal dominant. Heterozygotes may suffer from recurrent DVT, pulmonary embolism, and mesenteric thrombosis. Homozygotes present in childhood with severe arterial and venous thrombosis.
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NATURAL ANTICOAGULANTS Protein C and protein S These are synthesised in the liver and are dependant on vitamin K. Protein C degrades factors Va and VIIIa and promotes fibrinolysis by inactivating plasminogen-activator inhibitor I. Protein S is a cofactor for protein C and enhances its activity. Hereditary protein C defciency may occur, patients being more susceptible to DVT, PE, superficial thrombophlebitis, and cerebral venous thrombosis
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ANTICOAGULANT DRUGS Warfarin Warfarin is a coumarin derivative which is administered orally. It is a vitamin K antagonist and in effect induces a state analogous to vitamin K deficiency. It interferes with the activity of factors II, VII, IX and X. It delays thrombin generation, thus preventing the formation of thrombi. Warfarin is usually administered for 3–6 months following DVT or PE Lifelong warfarin is required for recurrent venous thromboembolic disease,some prosthetic heart valves, congenital deficiency of antithrombin III, deficiency of protein C or protein S,
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ANTICOAGULANT DRUGS Heparin Heparin potentiates the action of antithrombin III. Standard unfractionated heparin is administered i.v. or s.c. and has a half life of about 1 h. Low molecular weight heparin is used subcutaneously and has a longer biological half life.. Heparin does not cross the placenta and is, therefore, the drug of choice when anticoagulation is required during pregnancy. Bleeding due to overdose is managed by stopping the heparin and administering protamine sulphate intravenously. Side effects of heparin include thrombocytopaenia,hypersensitivity reactions, alopecia, and osteoporoi
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DISORDERS OF HAEMOSTASIS AND COAGULATION
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CONGENITAL HAEMOPHILIA A and B. Von WILLEBRAND’S disease. Defencies of factorXI and XII,prekallikrien,HMWkininogen. Defencies of factorVII,V and thrombin. Disorders of fibrinogen like a or hypofibrinogenemia or dysfibrinogenemia. Factor XIII defeciency.
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ACQUIRED VITAMIN K DEFECIENCY. ANTICOAGULANT DRUGS. HEPATIC FAILURE. RENAL FAILURE. THROMBOCYTOPENIA. THROMBOCYTOPATHY. HYPOTHERMIA. DIC.
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APPROACH
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HISTORY H\O bleeding,easybruising. Frequent or unusual mucosal bleeding. Metromenorrahgia. Haematuria. Epistaxis. Previous h\o prolonged bleeding asso with invasive procedures. Positive family history. Drug history like intake of NSAIDS,aspirin,etc.
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EXAMINATION Ecchymotic patches or petechiae on skin. Joint deformities. Adenopathy. Hepatospleenomegaly. Hypermobility of joints. Increased elaticity of skin.
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SCREENING TESTS CBC. Platelet count. PT. aPTT. Bleeding time. Fibrinogen level. Thrombin time. Platelet function tests. Specific factor assays.
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PROTHROMBIN TIME Measures function of factor VII,X, prothrombin and thrombin,fibrinogen and fibrin. Prolongation occurs when levels of factor V,VII or X fall. Seen in warfarin therapy and vit.k defeciency.
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aPTT Detects decreased levels ofHMWkininogen,prekallikrien,XII,XI,IX,VIII,V,X. Increased in heparin therapy.
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CONGENITAL DISORDERS HAEMOPHILIA A
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HAEMOPHILIA A Deficiency of factor VIII. X linked recessive disorder with males being affected exclusively. Severe bleeding if factor level<2%.Moderate bleeding with levels b\w 2%-5%.Mild bleeding with factor levels b\w 5%-30%. Patient has large haematomas and haemarthroses. Bleeding is prolonged for hours or days after injury. Lab tests show a prolonged Aptt with decreased factor VIII level,normal PT,bleeding time and vWF levels.
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HAEMOPHILIA A Desmopressin may temporarily raise factor VIII levels in mild disease. Can be given intranasally or iv and is ineffective in treating severe disease. Antifibrinolytic therapy with EACA and tranexemic acid with or without desmopressin is also effective in dental extarctions or paediatric patients. CRYOPRECIPITATE is a good source of factorVIII. One bag contains 80 units of factor VIII and 1U\kg increases levels by2%. Specific factor VIII concentrates are more popular now. Give 50U\kg stat then 30U\kg every 8 hrs for the first 2 days after surgery or injury.
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CONGENITAL DISORDERS HAEMOPHILIA B
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HAEMOPHILIA B Xlinked bleeding disorder with a deficiency of factor IX. Patient presents with deep bleeding and haemarthroses. Lab tests show increased Aptt with decreased factor IX levels, normal PT, BT,platelet count and factor VIII. Tt is by prothrombin complex concentrate which contains factor IX and all of the vit k dependent factors. HighPurity factor IX concentrate is also available.
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CONGENITAL DISORDERS Von WILLEBRAND’S DISEASE
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Von WILLEBRAND’S DISEASE Most common congenital bleeding disorder. vWF is an important stimulus for platelet aggregation and carrier protien for factor VIII. Type 1 is inherited as autosomal dominant and is characterized by quantitative defect in vWF. Type 2 has variable inheritance and there is qualitative defect in vWF. Type3 is autosomal recessive disease with absent levels of vWF. Patients present with mucosal bleeding,petechiae,epistaxis and menorrhagia. Tt is by desmopressin or cryoprecipitate.
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ACQUIRED DISORDERS VITAMIN K DEFECIENCY
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Platelet disorders Thrombocytopaenia This may be due to a failure of platelet production or increased destruction or sequestration of platelets, and abnormal platelet function. Abnormal platelet function may cause bleeding despite a normal platelet count. Abnormal platelet function may occur with: drugs, e.g. aspirin, non-steroidal antiinflammatory drugs carbenicillin, and ticarcillin; uraemia;septicaemia; and von Willebrand’s disease.
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Blood vessel wall abnormalities Blood vessel wall abnormalities These are rare and may be due to scurvy, steroids, Cushing’s syndrome, or Henoch-Schonlein purpura.
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VITAMIN K DEFICIENCY Vit k is required for the reaction that attaches a carboxyl gp to glutamic acid. Causes of def are inadequate dietary intake, Malabsorption,obstructive jaundice,biliaryfistula, Oral antibiotics and TPN. Tt is parenteral administration of vit k if there is no active bleeding. Administration of FFP rapidly corrects the coagulation deficit and is given in patients with ongoing bleeding. Correction of the etiology.
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ACQUIRED DISORDERS HEPATIC INSUFFICIENCY
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HEPATIC INSUFFICIENCY Liver is the site of synthesis of all clotting factors except factorVIII,vWF. Hepatic failure will result in coagulopathy. Asso with platelet dysfunction. Tt is by giving vitk,FFP,cryoprecipitate and platelets.
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ACQUIRED DISORDERS HYPOTHERMIA
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HYPOTHERMIA Usually seen in a lengthy open surgery on the abdomen or thorax. The coagulopathy is because of defect in platelet function,fibrinolytic activity,coagulation cascade enzyme. Intraoperatively all efforts should be made to keep the temp normal by warming fluids,heated ventilation and warm environment.
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ACQUIRED DISORDERS MASSIVE TRANSFUSION
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MASSIVE TRANSFUSION Defined as more than 10 units of transfused blood or replacement of the pts total blood volume within 24 hrs. Pts have thrombocytopenia,low fibrinogen and prolonged PT. These changes result from low temperature of blood,increased citrate level,increased k level,low pH,decreased ca level. Tt is by infusion of FFP,PLATELETS.
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ABNORMAL HAEMOSTASIS
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Misappropriately applied haemostasis
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ABNORMAL THROMBOSIS CLINICAL FEATURE SCORE 1.Active cancer 1 2.Paralysis, paresis, plaster 1 immobilisation 3.Bed ridden, major surgery 1 4.Tenderness on deep veins 1 5.Entire leg swollen 1 6.Calf swelling > 3 cms 1 7.Collateral superficial veins 1 ( non-varicose) 8.Pitting edema 1 9.Alternative diagnosis likely - 2
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POST-OP THROMBOSIS WHY? 1. NO MUSCLE CONTRACTION 2. FIBRINOGEN , PLATELET,vWF, FACTOR VIII 3. DECREASED ANTITHROMBIN III 4. SEPSIS 5. DAMAGE TO VEINS
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POST-OP THROMBOSIS PREVENTION: Intermittent compression or electrical stimulation Aspirin, dextran, di-pyridamole Low dose heparin, low molecular weight heparin Early mobilization Hydration T E D stockings
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ABNORMAL THROMBOSIS Prophylaxis RISK PATIENTS RECOMMENDED LOW Age < 40 Early ambulation Surgery < 30 mts Leg exercises No added risk factors MODERATE Age > 40 Heparin 5000 u S/C 12 hrly Abdominal / Thoracic beginning 2 hr pre – op. surgery > 30 mts External pneumatic Neurosurgery compression RISK OF DVT 20 – 30 %
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ABNORMAL THROMBOSIS Prophylaxis RISK PATIENTS RECOMMENDED HIGH Hip # LMWH Hip replacement Knee replacement + Open prostatectomy Ext. pneumatic Gyanecologic malignancy compression RISK 40 – 70 %
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ABNORMAL THROMBOSIS Investigations: Phlebography Plethysmography Radionucleotide scanning I 125 fibrinogen uptake Ultrasound & Duplex scanning
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ABNORMAL THROMBOSISTreatment PRINCIPLES 1.Prevent embolism 2.Prevent progression 3.Restore patency 4.Preserve valve function 5.Prevent chronic venous insufficiency
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ABNORMAL THROMBOSIS Treatment Heparin L M W H Oral anticoagulants Thrombolytic therapy Thrombectomy Vein grafting I V C filter Angioplasty & Stenting
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Surgery in patients on anticoagulants DRUG BLEEDING ELECTIVE EMERGENCY RISK SURGERY SURGERY 1 .HEPARIN Low / Moderate Discontinue high dose Same as elective Give low dose heparin High risk Discontinue 6 – 12 hrs Discontinue before surgery Give Protamine sulphate 2. L M W H -- Discontinue 12 – 24 hrs before surgery especially in high risk group
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Surgery in patients on anticoagulants DRUG BLEEDING ELECTIVE EMERGENCY RISK SURGERY SURGERY 3. Warfarin LOW Adjust dose to I N R < 2.5 Discontinue warfarin MODERATE ‘’ Discontinue warfarin FFP to decrease INR to < 2.5. HIGH Discontinue & allow P T to Discontinue warfarin normalize. Substitute with FFP , Vit K to heparin . normalize PT.
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Surgery in patients on anticoagulants Aspirin: Discontinue 1 week before surgery. Platelet transfusion DDAVP In emergency surgery Fibrinolytics: Wait for half life 6 min for TPA 23 min for Streptokinase 16 min for Urokinase EACA: Only in emergency. Weigh benefit Vs risk
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ABNORMAL HAEMOSTASIS BLEEDING
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ABNORMAL HAEMOSTASISBleeding Liver disease: Causes 1.Varices, gastritis, haemorrhoids 2.P T prolonged 3.Reduced platelets 4.Increased fibrinolysis 5.D I C Treatment Vit K, F F P, plasma exchange, platelet transfusion, DDAVP
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ABNORMAL HAEMOSTASIS Bleeding: Haemophilia Christmas disease Von-Willebrand disease
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Haemophilia Haematologist & laboratory Comfortable surgeon Blood bank Rehabilitation team No inhibitor Schedule surgery on Monday or Tuesday
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Haemophilia Pre-op orders : No IM medications No ASA containing compounds MINOR SURGERY: Factor VIII to 100 % Post-op EACA for 7-10 days MAJOR SURGERY: Factor VIII to 100 % ( 40 – 50 u/kg ) Keep at 30-50 % for 10 – 14 days Mild haemophilia: DDAVP , Cryoprecipitate
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ABNORMAL HAEMOSTASIS Bleeding: Haemophilia Christmas disease Von-Willebrand disease
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Christmas disease Minor surgery - EACA or Tranexamic acid 20 – 50 % activity for 2-5days Major surgery – Factor IX to 100 % activity for 7 – 10 days DDAVP no use
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ABNORMAL HAEMOSTASIS Bleeding: Haemophilia Christmas disease Von-Willebrand disease
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Von-Willebrand disease Type I : DDAVP for 2-3 days ( 0.3 microgram / kg ) Type II : more need for blood products DDAVP: vWF in 30 mts from storage site
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ABNORMAL HAEMOSTASIS Thrombocytopenia safe surgery- 50,000 - 100,000 / micro litre maintain values for 1 week treat cause
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ABNORMAL HAEMOSTASIS Aids: Cautery Laser Topical absorbable haemostat Gelatin sponge Oxidized regenerated cellulose Collagen Thrombin Fibrin seal
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ABNORMAL HAEMOSTASIS Aids: Packing Pharmacologic agents Trasylol Epsilon aminocaproic acid Tranexemic acid Desmopressin acetate
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ABNORMAL HAEMOSTASIS BLOOD PRODUCTS: FFP Cryoprecipitate Platelets
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CONCLUSION The more exotic these approaches become, the more one is compelled to emphasize that gentle handling, precise dissection and accurately applied haemostasis constitute much the art of surgery. Injecting, burning, stuffing, and scorching wounds is not likely to lead to a higher plateau of accomplishment. John A Collins , M.D
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THANK YOU