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SURGERY
Hematologic principles
| Question | Answer |
|---|---|
| Waht is hemostasis | A complex process by which the loss of blood from the injured vessel is prevented. |
| Waht are the four main steps/process involved in hemostasis? | 1) Vascular constriction 2) Platelet plug formation 3) Fibrin formation 4)Fibrinolysis |
| Describe the first step in hemostasis | Vasoconstriction - It is the initial step in hemostasis. It is mediated by Thromboxane A2 (TXA2), Serotonin, Endothelin, Bradykinin, fibrinopeptides. |
| Role of platelets in hemostasis | Platelet adhesion Platelet aggregation Platelet plug formation |
| What is the life span of platelets and from which cells are they derived from?. Normal count of platelets? | Life span of platelets is 7-10 days and they are derived from megakaryocytes. Normal count - 150,000 - 400,000 |
| How are platelets removed from the circulation? | Spleen |
| First role of platelets in hemostasis | Platelet adhesion - The injury to the blood vessels exposes the subendothelial collagen to which the platelets adhere with the help of vWF |
| Second step in hemostasis? | Platelet aggregation - DP and serotonin are the primary mediators of this step. Arachidonic acid released from the platelets membrane along with the help of cyclooxygenase converts into TXA2(vasoconstrictor and platelet aggregator). |
| Reversible and irreversible ways by which cyclooxygenase can be blocked. | Platelet cyclooxygenase is irreversibly inhibited by aspirin and reversibly blocked by non-steroidal anti-inflammatory agents. |
| Explain the platelet plug formation | Fibrinogen is important in this step as it acts as a bridge for both GP2b/3a receptor on activated platelets. Platelet factor 4 which is a heparin antagonist is also released. |
| How can platelet plug formation be inhibited? | By aspirin, anti inflammatory drugs, by cAMP and nitric oxide. |
| Among platelet adhesion and aggregation which is reversible and which is irreversible step? | Reversible - Platelet adhesion Irreversible - Platelet aggregation |
| How is fibrin formed during hemostasis? | By the coagulation cascade. Intrinsic pathway and Extrinsic pathway. |
| Explain the intrinsic pathway | 12a will go activate 11, 11a will activate 9, 9a will activate 10 in the presence of 8a, 10A in the presence of 5a will activate 2. (Check) |
| Explain the extrinsic pathway | |
| Steps involved in Fibrinolysis | 1) Initiation (Tissue factor forms thrombin) 2) Amplification 3) Propagation |
| Explain amplification in fibrinolysis | Platelets adhere to extracellular matrix components at the site of injury and become activated upon the exposure to thrombin and other stimuli |
| Explain propagation in fibrinolysis | Tenase (factor 8a/9a) and prothrombinase (factor 5a/10a) assemble on the activated platelets and generate large scale thrombin and fibrin (thrombin burst) |
| Regulatory mechanism to prevent the propagation of the clot. | 1) Thrombomodulin (TM) - prevents the thrombin from cleaving fibrinogen 2) tPA - cleaves plasminogen to initiate fibrinolysis 3) Tissue factor pathway inhibitor (TFPI) and Antithrombin 3 - Blocks the TF-7A complex 4) APC system - Cleaves 5a and 8a |
| Role of plasmin in fibrinolysis | 1) Degrades fibrin polymers leading to the production of fibrin degradation products. 2) It is derived from the pro enzyme plasminogen. |
| What is TXA2? What is its role in hemostasis? | TXA2 is a vasoconstrictor and platelet aggregator. |
| Fibrinolysis regulatory mechanisms | 1)t PA activates plasminogen to plasmin. (When plasminogen binds to fibrin tPA activates it into plasmin) 2) α2-antiplasmin - protein that is crosslinked to fobrin by factor 13. |
| Fibrinolysis regulatory mechanisms (continued) | 3) Fibrin degradation products - they interfere with the normal aggregation . Larger fragments get incorporated in the clot which will result in unstable clot (Hyperfibrinolysis associated with trauma induced coagulopathy). |
| What can act as a marker for thrombosis? | D- dimer acts as a marker for thrombosis. |
| Name some congenital factor deficiencies | Factor 8 - Hemophilia A or vW disease Factor 9 - Hemophilia B or Christmas disease Factor 11 - Hemophilia C Factor 2,5, 7, 10, and 13 Platelet functional defects. |
| Hemophilia A & B | 1) Sex - linked recessive disorder 2 ) Hemophilia A treated with factor 8 and Hemophilia B treated with factor 9 |
| Severity of bleeding in Hemophilia A & B | 3) Severity - If the plasma factor levels MILD - 5-30% (minor bleeding after trauma or surgery) MODERATE - 1 -5% (severe bleeding after surgery) SEVERE - <1% (spontaneous bleeding) |
| Hemophilia C | 1) Autosomal recessive 2) Spontaneous bleeding is rare but bleeding may occur after trauma or surgery) 3) Fresh frozen plasma(FFP) - each ml of the plasma contains 1 unit of factor 11 activity |
| Platelet Functional Defects | 1) Thrombasthenia - Problem with glycoprotein 2b/3a 2) Bernard - Soulier Syndrome - Deficiency of GP 1b/9/10 receptors for vWF. 3) Intrinsic Platelet Defect/ Platelet Granule abnormality - Storage pool disease - Decrease in ADP release. |
| How can a decrease in ADP release be treated? | It can be treated with desmopressin (DDAVP), platelet transfusion. |
| AQUIRED HYPOFIBRINOGENEMIA | 1) Disseminated Intravascular Coagulation (DIC) 2) Primary Fibrinolysis |
| DISSIMINATED INTRAVASCULAR COAGULATION | a) Systemic activation of coagulation pathway causes excess thrombin production |
| What are the possible causes of DIC? | Traumatic embolization, malignancy, organ injury, liver failure, certain vascular abnormalities (aneurysms), snake bites, illicit drugs, transfusions reactions, transplant rejection and sepsis. |
| Diagnosis for DIC? | Thrombocytopenia, prolongation of the prothrombin time, low fibrinogen level, elevated fibrin markers. |
| Treatment for DIC? | Relieve the primary problem, FFP transfusion. |
| PRIMARY FIBRINOLYSIS. Waht is the treatment for this? | Urokinase release following prostate resection, Extracorporeal bypass. Treatment - Antifibrinolytic agents such as ε-aminocaproic acid, tranexamic acid. |
| Name myeloproliferative disease | POLYCYTHEMIA (Excess of RBC) - Causes spontaneous thrombosis. Complication of polycythemia vera - myeloproliferative neoplasm, increased platelet count, blood viscosity, increased tendency towards stasis.(stasis - reduce flow of blood). |
| Treatment of polycythemia | Low dose aspirin, phlebotomy (taking blood from the vein for testing), and hydroxyurea. |
| COAGULOPATHY OF LIVER DISEASE | Abnormalities of liver dysfunction are :- 1) Thrombocytopenia 2) Impaired humoral coagulation function manifested as prolongation of the prothrombin time and international normalized ratio (INR) - Cause - Vitamin K deficiency. |
| Treatment for liver diseases that leads to problems related to hemostasis | Usually done with FFP, If the fibrinogen is less than 200 mg/dL, administration of cryoprecipitate may be helpful. Cryoprecipitate is also a source of factor VIII for the rare patient with a low factor VIII level. |
| Treatment of coagulopathy | Treat the active bleeding and prophylaxis for invasive procedures and surgery. |
| COAGULOPATHY OF TRAUMA | While treating a trauma patient they undergo a triad - ACIDOSIS, HYPOTHERMIA and DILATION OF COAGULATION FACTORS. It is more or less related to the treatment of the patient. |
| DILUTIONAL COAGULOPATHY | dilutional coagulopathy is iatrogenic in which the doctors infuse a lot of crystallites to raise the blood pressure but in doing so it does more harm by diluting the coagulation factors leading to bleeding sol there is further blood loss |
| TRAUMA INDUCED COAGULOPATHY (TIC) | 1) Due to tissue injury of hemorrhagic shock. (High risk of mortality in the first 24 hours of injury) 2) Independent of iatrogenic hemodilution or DIC 3) Trauma without iatrogenic problems then it is known as intrinsic induced coagulopathy |
| TRAUMA INDUCED COAGULOPATHY (TIC) (continued ) | Decreased clotting factor activity, platelet dysfunction and hyperfibrinolysis. |
| ACQUIRED COAGULATION INHIBITORS | Antiphospholipid syndrome (APLS) ○ Lupus anticoagulant ○ Anticardiolipin antibodies In a APLS an individual is in an hypercoagulable state. |
| CQUIRED COAGULATION INHIBITORS can be seen in which conditions? | Seen in patients with systemic lupus, rheumatoid arthritis, Sjögren’s syndrome, infection, drug-induced APLS prolonged aPTT in vitro but an increased risk of thrombosis in vivo |
| HEPARIN | 1) Given in order to prevent thrombosis. Too much of it causes bleeding. 2) It has short half -life. It must be given continuous. 3) Reversal is by PROTAMINE SULPHATE. 4) It is monitored by blood test aPPT. |
| Administration of Heparin | In a person in whom the venous thromboembolism outweighs bleeding. Heparin should not be given 4-6 hours before the procedure and should be restarted within 10-24 hours after the procedure. |
| Who are at high risk for taking HEPARIN | People with mechanical heart valves, who had a recent MI (within 30 days) stroke, or pulmonary embolism. |
| LOW MOLECULAR WEIGHT HEPARIN | 1) It is more convenient than heparin as there is no need to check aPPT. 2) Therapeutic anticoagulation 3) MONITORING : Use an assay for anti 10a activity. |
| WARFARIN | 1) Used for long term anticoagulation 2) Reversal - Vit K, plasma, cryoprecipitate, recombinant factor 7a, prothrombin complex concentrate (PCC) 3) INR is less less than 1.5 reversal is not necessary. |
| Among which group of patients is Warfarin used? | Deep vein thrombosis, pulmonary embolism, valvular heart disease, atrial fibrillation, recurrent systemic emboli, recurrent myocardial infarction, prosthetic heart valves, and prosthetic implants. |
| DIRECT ORAL ANTICOAGULANTS (DOAC's) | 1) Not to be taken 36 -48 hours prior surgery 2) Direct thrombin inhibitors - DABIGATRAN REVERSAL - IDARUCIZUMAB 3)Factor 10a inhoibitors - RIVAROXABAN, APIXABAN, AND EDOXABAN). REVERSAL - four factor PCC ( factor 2,7,9,10) |
| LOCAL HEMOSTASIS | Significant surgical bleeding is caused by ineffective local hemostasis. The goal is to prevent further blood loss from a disrupted vessel that has been incised or transected. |
| How to prevent local hemostasis? | 1) Mechanical Procedure - Direct digital pressure, tourniquet, Pringle maneuver, ligature, transfixing suture, packing with gauze/ bone wax. 2) Thermal Agents - Electrocautery, Argon gas |
| TOPICAL HEMOSTATIC AGENTS | Absorbable agents - Gelatin foams (Gelfoam), oxidized cellulose (Surgicel), microfibrillar collagens (Avitene). Biologic agents - Topical thrombin, fibrin sealants (FloSeal), and platelet sealants (Vitagel) |
| Replacement Therapy | 1) Typing and cross matching 2) Banked Whole Blood (WB) 3) RBC's 4) Frozen RBC's 5) Leukocyte reduced / Washed RBC's 6) Platelet concentrates 7) Plasma 8) Tranexamic Acid |
| Replacement Therapy - Typing and cross matching | ○ In emergency situations, universal donor type O-negative red blood cells and type AB plasma may be transfused to all recipients ○ Platelets do not require cross matching |
| Replacement Therapy - Banked Whole Blood (WB) | ○ For acute traumatic hemorrhagic shock ○ This whole blood contains packed RBCs, platelets, and your plasma, these are not separated into components, best given for patients with massive blood loss in the acute setting |
| Replacement Therapy - RBCs | Shelf life - 42 days Stored RBCs progressively become acidotic |
| Replacement Therapy - Frozen RBCS | Shelf-life of 10 years at -80°C with improved cellular viability |
| Replacement Therapy - Leukocyte-Reduced/Washed Red Blood Cells. | ○ Removes about 99.9% of white blood cells and most of the platelets |
| Replacement Therapy - Leukocyte-Reduced/Washed Red Blood Cells. | ○ Prevents almost all febrile, nonhemolytic transfusion reactions (fever and/or rigors), alloimmunization to HLA class I antigens, and platelet transfusion refractoriness and cytomegalovirus transmission |
| Replacement Therapy - Platelet concentrates | Stored at room temperature and have a shelf-life of 5 days |
| Replacement Therapy - Plasma | ○ Usual source of vitamin K-dependent factors, the only source of factor V ○ Stored for up to 2 years at -18°C, but requires 20-30 minutes to thaw prior to use |
| Replacement Therapy - Tranexamic Acid | 1) Antifibrinolytic that inhibits both plasminogen activation and plasmin activity, thus preventing clot breakdown 2) Early administration of tranexamic acid to your trauma patients can give a benefit in survival 3) Hemostatic adjunct |
| INDICATIONS FOR REPLACEMENT OF BLOOD AND ITS ELEMENTS | 1) Improvement in Oxygen-Carrying Capacity - Primarily a function of the red blood cells 2) Treatment of Anemia: Transfusion Triggers 3) Volume Replacement |
| Treatment of Anemia: Transfusion Triggers | ○ Maintaining hemoglobin levels between 7 and 9 g/dl had no adverse effect on mortality ○ Symptomatic anemia should be transfused one RBC unit at a time |
| Volume Replacement | ○ The most common indication for blood transfusion in surgical patients is the replenishment of the blood volume. ○ As long as even if the hemoglobin is less than normal (7-9g/dL) if the patient is symptomatic no need to transfuse |
| Massive Transfusion | ≥10 units of RBCs in 24 hours |
| Critical administration threshold (CAT) positive status | ○ Transfusion of 3 units of red blood cells within a 60-minute period ○ Associated with a two-fold increase in risk of mortality |
| ABC Scoring - Early prediction of massive transfusion in trauma | 1. Penetrating mechanism 2. Positive FAST 3. SBP ≦ 90mmHg on arrival 4. Heart rate ≧ 120bpm on arrival Scoring ≧ 2 is 75% sensitive and 86% specific for predicting massive transfusion. |
| Damage Control Resuscitation | ○ Permissive hypotension ○ Minimizing crystalloid-based resuscitation ○ Immediate release and administration of predefined balanced blood products (red blood cells, plasma, and platelets) in ratios similar to those of whole blood (ratio 1:1:1) |
| What is component therapy? | (plasma and RBC) |
| Fibrinogen Replacement | Fibrinogen is the first coagulation factor to fall to critically low levels during major hemorrhage |
| Non-hemolytic transfusion reaction | Most common 1)Usually signs and symptoms are fever, which is caused by your preformed cytokines from your donor blood 2) You can also have bacterial infection and allergic reactions to blood treatment for this transfusion reactions |
| Transfusion-Associated Circulatory Overload | 1) large volume of blood transfused into older patients with congestive heart failure 2) Treatment is you increase transfusion time or lower transfusion weight administer diuretics minimize fluid in order to prevent congestion |
| Transfusion-Related Acute Lung Injury | This lung injury compared to TACO, these damage into your lungs in which there is no related heart problem symptoms are acute hypoxemia bilateral infiltrates, tachycardia, hypotension |
| Platelet Count | ○ 150,000 to 400,00/μL ○ >1,000,000/μL associated with bleeding or thrombotic complications ○ <50,000/μL associated bleeding with major operations ○ <30,000/μL associated bleeding with minor operations ○ <20,000/μL associated with spontaneous bleeding |
| PT or INR | ○ I, II, V, VII, X ○ Factor VII has the shortest half-life of the coagulation factors, and its synthesis is vitamin K dependent ○ INR=(measured PT/normal PT) IS |
| aPTT | ○ I, II, V, and VIII, IX, X, XII ○ Heparin therapy-therapeutic target range of 1.5-2.5 times the control value ○ Low molecular weight heparins-selective Xa inhibitors, does not need PTT monitoring |
| Viscoelastic Assays | ○ Thromboelastography (TEG) or rotational thromboelastometry (ROTEM) ○ Monitor homeostasis as a dynamic process ○ Better measure of coagulopathy |
| EVALUATION OF EXCESSIVE INTRAOPERATIVE OR POSTOPERATIVE BLEEDING | • Excessive bleeding may be the result of o ineffective hemostasis o blood transfusion o undetected hemostatic defect o consumptive coagulopathy o fibrinolysis |
| • Excessive bleeding from the operative field unassociated with bleeding from other sites usually suggests inadequate mechanical hemostasis | |
| • Hemolytic transfusion reaction-release of ADP from hemolyzed red blood cells, resulting in diffuse platelet aggregation • Transfusion purpura occurs when the donor platelets are of the uncommon HPA-1 group | |
| Thrombocytopenia has occurred as a result of | Gram-negative sepsis. |
Created by:
Ashritha.R
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