Hemostasis, surgical bleeding and transfusion
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Hemostasis, surgical bleeding and transfusion

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  • HEMOSTASIS : limits blood loss from an injured vessel
  • THROMBOXANE A2 (TXA2) : produced locally at site of injury via release of arachidonic acid from platelet membranes and is a potent constrictor of smooth muscle ENDOTHELIN : synthesized by injured endothelium SEROTONIN : released during platelet aggregation BRADYKININ & FIBRINOPEPTIDES : vasoconstrictors also involved in coagulation cascade more pronounced in vessels with medial smooth muscles & dependent on local contraction of smooth muscle
  • NOTE about 30% of platelets are sequestered in the spleen; ave life span of 7-10 days) Platelets play an integral role in hemostasis by forming a hemostatic plug and by contributing to thrombin formation Platelets do not normally adhere to each other or to the vessel wall but can form a plug that aids in cessation of bleeding when vascular disruption occurs. Injury to the intimal layer in the vascular wall exposes subendothelial collagen to which platelets adhere. NOTE this process involves the von Willebrand factor (vWF) which binds to glycoprotein I/IX/V on the platelet membrane NOTE called as primary hemostasis; heparin does NOT interfere & thus hemostasis can occur in the heparinized patient
  • Coagulation Cascade Extrinsic Pathway: initiated by tissue factor Intrinsic Pathway: initiated by contact of XII & platelet with collagen vascular wall The intrinsic pathway begins with factor XII and through a cascade of enzymatic reactions activates factors XI, IX, and VII in sequence. In the intrinsic pathway all of the components leading ultimately to fibrin clot formation are intrinsic to the circulating plasma and no surface is required to initiate the process. In contrast, the extrinsic pathway requires exposure of tissue factor on the surface of the injured vessel wall to initiate the arm of the cascade beginning with factor VII. The two arms of the coagulation cascade merge to a common pathway at factor X , and activation proceeds in sequence of factors II (prothrombin) and I (fibrinogen). Clot formation occurs after proteolytic conversion of fibrinogen to fibrin . elevated activated partial thromboplastin time (aPTT) is associated with abnormal function of the intrinsic arm of the cascade, whereas an elevated prothrombin time (PT) is associated with the extrinsic arm. Vitamin K deficiency and warfarin use affect factors II, VII, IX, and X.
  • Fibrin clot undergoes lysis, permitting the restoration of blood flow During the wound-healing process, the fibrin clot undergoes clot lysis, which permits restoration of blood flow. The main enzyme, plasmin, degrades the fibrin mesh at various places, which leads to the production of circulating fragments that are cleared by other proteases or by the kidney and liver. Fibrinolysis is initiated at the same time as the clotting mechanism under the influence of circulating kinases, tissue activators, and kallikrein, which are present in many organs, including the vascular endothelium. Fibrin is degraded by plasmin, a serine protease derived from the proenzyme plasminogen. Plasminogen may be converted by one of several plasminogen activators, including tPA and uPA. The tPA is synthesized by endothelial cells and released by the cells on thrombin stimulation as single-chain tPA. This is then cleaved by plasmin to form two-chain tPA. Bradykinin, a potent endothelium-dependent vasodilator cleaved from high molecular weight kininogen by kallikrein, causes contraction of nonvascular smooth muscle, increases vascular permeability, and enhances release of tPA. Both tPA and plasminogen bind to fibrin as it forms, and this trimolecular complex cleaves fibrin very efficiently. After plasmin is generated it cleaves fibrin, somewhat less efficiently, and it also will degrade fibrinogen. Fully cross-linked fibrin is also a relatively poor substrate for plasmin. Plasminogen activation may be initiated by activation of factor XII, which leads to the generation of kallikrein from prekallikrein and cleavage of high molecular weight kininogen by kallikrein. Several characteristics of the enzymatic reactions ensure that fibrinolysis occurs at a controlled rate and preferentially at the site of clot formation. The tPA activates plasminogen more efficiently when it is bound to fibrin, so that plasmin is formed selectively on the clot. Plasmin is inhibited by 2 -antiplasmin, a protein that is cross-linked to fibrin by factor XIII, which helps to ensure that clot lysis does not occur too quickly. Any circulating plasmin also is inhibited by 2 -antiplasmin and circulating tPA or urokinase. Clot lysis yields fibrin degradation products, including E-nodules and D-dimers. The smaller fragments interfere with normal platelet aggregation and the larger fragments may be incorporated into the clot in lieu of normal fibrin monomers. This may result in an unstable clot. Presence of D-dimers in the circulation may be a marker of thrombosis or other conditions in which a significant activation of the fibrinolytic system is present. The final inhibitor for the fibrinolytic system is TAFI, a procarboxypeptidase that is activated by the thrombin-thrombomodulin complex. The active enzyme removes lysine residues from fibrin that are essential for binding plasminogen.
  • The oldest mechanical method of halting bleeding is digital pressure digital pressure over a bleeding site often is effective and has the advantage of being less traumatic than a hemostatic clamp Simple ligature- When a small vessel is transected Direct pressure applied by packs affords the best method of controlling diffuse bleeding from large areas, eg trauma The device converts electrical energy into mechanical motion. The motion of the blade causes collagen molecules within the tissue to become denatured, forming a coagulum. No significant electrical current flows through the patient. The instrument has proved advantageous in performing thyroidectomy, hemorrhoidectomy, and transsection of the short gastric veins during splenectomy, and in transecting hepatic parenchyma
  • - Heat achieves hemostasis by denaturation of protein that results in coagulation of large areas of tissue. - With cautery, heat is transmitted from the instrument by conduction directly to the tissue. When electrocautery is used, heating occurs by induction from an alternating current source. The amplitude setting should be high enough to produce prompt coagulation but not so high as to set up an arc between the tissue and the cautery tip. A negative grounding plate should be placed beneath the patient to avoid severe skin burns. Use of direct current also can result in hemostasis. Because the protein moieties and cellular elements of blood have a negative surface charge, they are attracted to a positive pole, where a thrombus is formed. Direct currents in the 20- to 100-mA range have successfully controlled diffuse bleeding from raw surfaces, as has argon gas.
  • Topical hemostatic agents play an important role in common or complex general surgical procedures classified based on their mechanism of action and include physical or mechanical, caustic, biologic, and physiologic agents Some agents induce protein coagulation and precipitation that results in occlusion of small cutaneous vessels, whereas others take advantage of later stages in the coagulation cascade, activating biologic responses to bleeding. The ideal topical hemostatic agent  has significant hemostatic action, shows minimal tissue reactivity, is nonantigenic, biodegrades in vivo, provides ease of sterilization, is low in cost, and can be tailored to specific needs.
  • Thrombin Products: direct conversion of fibrinogen to fibrin  clot formation; avoids foreign body or inflammatory rxn, wound bed is not disturbed Fibrin Sealants: from cryoprecipitate; does not promote inflammation or tissue necrosis Gelatin Agents: provides hemostasis for operative fields with diffuse small vessel oozing
  • 0- and 0+ are equally safe for emergency transfusion risk for transfusing >4 u of blood  risk for hemolysis The use of autologous transfusion is growing. Up to 5 units can be collected for subsequent use during elective procedures Patients can donate blood if their hemoglobin concentration exceeds 11 g/dL or if the hematocrit is >34%. The first procurement is performed 40 days before the planned operation and the last one is performed 3 days before the operation. Donations can be scheduled at intervals of 3 to 4 days. Administration of recombinant human erythropoietin accelerates generation of red blood cells and allows for more frequent harvesting of blood.
  • - Banked whole blood, once the gold standard, is rarely available.
  • Concentrated suspensions of red blood cells  can be prepared by removing most of the supernatant plasma after centrifugation. This preparation reduces, but does not eliminate, reaction caused by plasma components. It also reduces the amount of sodium, potassium, lactic acid, and citrate administered. Leukocyte-reduced or Washed RBCs Removes 99.9% of WBCs & most of platelets Prevents almost all febrile, nonhemolytic transfusion reactions, alloimmunization to HLA class I Ag, platelet transfusion refractoriness & CMV transmission
  • One unit of platelet concentrate has a volume of approximately 50 mL. Platelet preparations are capable of transmitting infectious diseases and can provoke allergic reactions similar to those caused by blood transfusion C/I: ITP, TTP, Untreated DIC, thrombocytopenia with septicemia
  • FFP carries infectious risks similar to those of other component therapies FFP has come to the forefront with the inception of damage control resuscitation in patients with trauma-associated coagulopathy.
  • Is a frozen blood product prepared from plasma prepared by slowly thawing a unit of ffp at a temp above freezing  centrifuged to remove majority of the plasma  the precipitate is resuspended in the remaining plasma or sterile saline. - Each unit contains vWF, fibronectin, fibrinogen, CF VIII & XIII -
  • Refers to plasma from which cryoprecipitate has been removed Reduced levels of cf 8, vwf, 13
  • Volume Replacement : most common indication
  • Primarily related to blood-induced proinflammatory responses. Transfusion-related events occur in 10% of all transfusions, but <0.5% are serious. 16-22% : acute lung injury 12-15% : ABO hemolytic transfusion reactions 11-18% : bacterial contamination of platelets
  • Coombs + : indicates that the presence of transfused cells coated with patient antibody is diagnostic
  • NOTE preformed cytokines in donated blood & recipient antibodies reacting with donated antibodies are postulated causes Bacterial contamination  sepsis & death 25%
  • NOTE caused by the transfusion of antibodies from hypersensitive donors or the transfusion of antigens to which the recipient is hypersensitive
  • NOTE related to anti-HLA or anti-human neutrophil Ag Ab in transfused blood that primes neutrophils in the pulmo circulation - Risk factor: multiparity of donor
  • NOTE reactions to non-ABO antigens involve Ig G-mediated clearance by reticuloendothelial system
  • Malaria : all blood components; incubation of 8-100 days; shaking chills, spiking fever
  • PT: contains thromboplastin & Ca that when added to plasma  fibrin clot aPTT: phospholipid substitute + activator + Ca that when added to plasma  fibrin clot Ivy Test: placing a sphyg on the upper arm inflated to 40mmHg  stab 5mm incision on the flexor surface  bleeding stops in 7mins

Hemostasis, surgical bleeding and transfusion Hemostasis, surgical bleeding and transfusion Presentation Transcript

  • Mae Caridad R. Martinquilla VCMC- Surgery Department November 2012
  •  Complex process whose function is to limit blood loss from an injured vessel  4 Major Events  Vascular Constriction  Platelet Plug Formation  Fibrin Formation  Fibrinolysis
  •  Initial response to vascular injury  THROMBOXANE A2 (TXA2)  ENDOTHELIN  SEROTONIN  BRADYKININ & FIBRINOPEPTIDES  Extent of vasoconstriction varies with degree of vessel injury
  •  PLATELETS : anucleate fragments of megakaryocytes (150T – 400T/uL) - hemostatic plug and contribute to thrombin formation  Injury to the intimal layer  exposes subendothelial collagen platelets adhere  PLATELET ADHESION  recruits other platelets from the circulating blood to seal the disrupted vessel  PRIMARY HEMOSTASIS
  • I fibrinogen II prothrombin V proaccelerin, accelerator globulin, labile factor VII proconvertin, serum prothrombin conversion accelerator, stable factor VIII antihemophilic factor, antihemophilic globulin IX Christmas factor, plasma thromboplastin component X Stuart-Prower factor XI plasma thromboplastin antecedent XII Hageman factor XIII fibrinase, fibrin-stabilizing factor
  •  PT = prothrombin time - II,V, VII, X - Fibrinogen  aPTT = activated partial thromboplastin time - XII, High molecular weight kininogen, Prekallikrein, XI, IX, VII, X, V , II and Fibrinogen  
  • Goal is to prevent further blood loss from a disrupted vessel via direct closure of the blood vessel wall fefect
  •  Digital pressure  Extremity tourniquet to occlude a major vessel proximal to bleeding site  Pringle maneuver for liver bleeding  Simple ligature for small vessels  Direct pressure applied by packs  Harmonic scalpel: cuts & coagulates tissues via vibration 55 kHz
  •  Heat denatures CHON  coagulation of large areas of tissue  Cautery  Amplitude setting must be high enough to produce prompt coagulation but not so high as to set up an arc between the tissue & cautery tip
  •  Ideal topical hemostatic agent has:  Significant hemostatic action  Shows minimal tissue reactivity  Nonantigenic  Biddegrades in vivo  Provides ease of sterilization  Low cost  Tailored to specific needs
  • Human Blood Replacement Therapy
  •  “O-” Blood  Emergency situations  > 4 U transfused  increased risk of hemolysis  Autologous Transfusion: up to 5 U  1st U: 40 days before; last U: 3 days before  Blood donors:  Hgb > 11 g/dL or if Hct > 34%
  •  Banked whole blood - Shelf life: 6 weeks  Fresh whole blood - blood that is administered within 24 hours of its donation  70% of transfused RBCs remain in the circulation for 24hrs post-BT  During storage: reduction of ADP & 2,3-DPG  alters oxygen dissociation curve  decreased oxygen transport
  •  Usual product of choice  Shelf-life same as WB  Leukocyte-reduced or Washed RBCs  prepared by filtration that removes approximately 99.9% of the white blood cells and most of the platelets (leukocyte-reduced red blood cells), and if necessary, by additional saline washing (leukocyte-reduced/washed red blood cells).
  •  Prevents almost all febrile, nonhemolytic transfusion reactions, alloimmunization to HLA class I Ag, platelet transfusion refractoriness & CMV transmission  For:  Chronic anemias, bone marrow & liver failure  Pre-op and post-op surgery  CHF, uremia
  •  Shelf-life: 120 hrs after donation  1 U per 10kg BW (1 U = 50 mL = 5.5 x 10^10)  Apheresis = 4.4 x 10^10  For:  Massive blood loss  Nonbleeding: plt < 20T (chemo, tumor invasion)  Pre-op/invasive procedure: plt < 50T  Documented bleeding: plt < 50T  Documented abnormal plt function
  •  Usual source of Vit K-dependent factors  Only source of Factor V  For:  Liver disease, Warfarin overdose  DIC, TTP  ↓CF d/t large volume transfusions
  •  vWF, fibronectin, fibrinogen, CF VIII & XIII  For:  vWF deficiency, Hemophilia A  ↓fibrinogen, factor XIII  Bleeding related to renal failure
  •  Cryo-poor plasma, cryoprecipitate depleted  Factors II, VII, IX, XI  For:  Hemophilia B  Liver disease
  •  Improvement in oxygen-carrying capacity  Treatment of anemia  Hgb approaching 9 g/dL  Volume replacement  Blood loss can be evaluated by estimation in wound, drapes, sponges, suctioned
  • Reaction Acute (mins-hrs) Delayed (days-yrs) Immune mediated Hemolytic Febrile non-hemolytic Urticarial Anaphylactic Alloimmune Hemolytic GVHD Post-transfusion purpura Non-immune mediated Hemolytic TRALI Circulatory Metabolic Embolic Infectious Metabolic iron overload
  •  Symptoms in an AWAKE patient:  Pain at site of transfusion  Facial flushing  Back & chest pain  Fever  Respiratory distress  Hypotension  tachycardia
  •  Symptoms in an ANESTHETIZED patient:  Diffuse bleeding  Hypotension  Laboratory criteria:  Hemoglobinuria, hemoglobinemia  Serologic findings  Positive Coomb’s test  Jaundice  Low levels of haptoglobins
  •  FEBRILE NONHEMOLYTIC REACTION  Increase in temp >1°C associated with a transfusion (1% of transfusions)  Bacterial contamination of infused blood  Yersinia enterocolitica, Pseudomonas  Emergency!  Discontinue transfusion ASAP  Oxygen, adrenergic blocking agents, antibiotics
  •  1% of all transfusions  Mild rash, urticaria & fever within 60-90 minutes of the start of transfusion  Treatment:  Mild: Antihistamines  Severe: Steroids or epinephrine
  •  Associated with transfusion-associated circulatory overload  Occur with rapid infusion of blood, plasma expanders, crystalloids esp in older patients with heart disease  Rise in venous pressure, dyspnea, cough, rales in LLF
  •  TRANSFUSION-RELATED ACUTE LUNG INJURY (TRALI)  Noncardiogenic pulmonary edema related to transfusion  Occur with administration of any plasma- containing blood product  Fever, rigors, bilateral pulmonary infiltrates on CXR  Within 1-2 hrs after onset of transfiusion (before 6 hrs)
  •  ACUTE HEMOLYTIC REACTION  Administration of ABO-incompatible blood  Fatal in 6% of cases  Technical or clerical errors  Administration of blood of the wrong blood type
  •  IMMEDIATE HEMOLYTIC REACTION  Intravascular destruction of RBCs & consequent hemoglobinemia & hemoglobinuria  Acute renal insufficiency d/t toxicity associated with free Hgb in the plasma  tubular necrosis & precipitation of Hgb in tubules
  •  DELAYED HEMOLYTIC REACTION  Occur 2-10 days after transfusion  Extravascular hemolysis, mild anemia, indirect hyperbilirubinemia  Low antibody titer at time of transfusion but titer increases after transfusion d/t anamnestic response
  •  Malaria (P. malariae) , Chagas’ disease, brucellosis, syphilis, CMV infection
  •  Careful review of the patient’s history  Abnormal bleeding/bruising, drug use  Platelet count  Plt > 1M/uL  Bleeding o r thrombotic complications  Major surgical procedures: <100T/uL  Minor surgical procedures: <50T/uL  Spontaneous b;eeding: <20T/uL
  • PT aPTT INR BT For: Vit K def; warfarin therapy For: heparin therapy Measured PT divided by Control PT N: 2-3 Ivy test; Bleeding must stop in 7mins VII XII HMWK Prekallikrein XI IX VIII X V II (Prothrombin) Fibrinogen