HEMOSTASIS

Hemostasis, Surgical Bleeding, and Transfusion

SHIBASIS BEHERASUMANTA KUMAR DHADAREUBEN LALROSIAMACHIH JU CHEN

Biology of HemostasisPrevents or terminates blood loss from a disrupted intravascular spaceProvision of a fibrin network for tissue repair and its removal when no longer neededBiology of HemostasisEndothelial cells

interfere with platelet recruitment by inactivation of adenosine diphosphate (ADP)Provide an environment in which thrombin is inactivated by complexing with antithrombin III

Release of thrombomodulin that down-modulates the coagulation process

Biology of HemostasisFour Major Physiologic Processes

Vascular constrictionPlatelet plug formationFibrin formationFibrinolysis

Biology of HemostasisVascular ConstrictionInitial vascular response to injury, even at the capillary levelDependent on local contraction of smooth muscleOccurs before any platelet adherence at the site of the injuryAdherence of endothelial cells to adjacent endothelial cells may be sufficient to cause cessation

of blood loss from the intravascular spaceBiology of HemostasisVascular ConstrictionSubsequently linked to platelet plug and fibrin formationThromboxane A2 (TXA2)

Results from release of arachidonic acid from platelet membranes during aggregationPowerful vasoconstrictor

Biology of HemostasisVascular ConstrictionProstacyclin

Also secreted during platelet release reactionPotent vasodilator

Serotonin, 5-hydroxytryptamine (5-HT)Vasoconstrictor

Bradykinin and fibrinopeptidesCapable of contracting smooth muscle

Biology of HemostasisVascular Constriction

Lateral incision in a small arteryMay remain open due to physical forces

Complete transectionContraction to the extent that bleeding may cease spontaneously

Vascular response factorShould also include the contribution of pressure provided by surrounding tissues

Biology of HemostasisVascular Constriction

With low perivascular pressure, bleeding tends to be more persistent

Patients with muscular atrophy accompanying agingPatients on prolonged steroid therapyPatients with Ehlers-Danlos syndrome

Biology of HemostasisPlatelet FunctionPlatelets

2-μm diameter fragments of megakaryocytes200,000 to 400,000/mm3

Life span of 7 to 9 days

Normally do not adhere to each other or to the normal vessel wall, but forms a plug that stops bleeding when vascular disruption occurs

Biology of HemostasisPlatelet FunctionInjury to intima exposes subendothelial collagen – platelets adhere within 15 seconds of traumatic event

Requires von Willebrand factor (vWF)Platelets expand, develop pseudopodal processes and also initiate a release reaction that recruits other platelets

Biology of HemostasisPlatelet FunctionAs a consequence, a loose platelet aggregate forms, sealing the disrupted blood vessel

Aggregation up to this point is reversible and is not associated with secretionPrimary hemostasis

Administration of heparin does not interfere with this reaction

Biology of HemostasisPlatelet FunctionADP and serotonin

Principal mediators in this process of adhesion and aggregation

Arachidonic acidReleased from platelet membranesConverted by cyclooxygenase to prostaglandin G2 (PGG2) and PGH2, which in turn are converted to TXA2

(potent vasoconstrictor)Biology of HemostasisPlatelet FunctionPGI2 (prostacyclin) and PGE2 inhibit aggregation and act as vasodilatorsADP, released from damaged tissues and platelets, plus platelet factor 4 and trace thrombin on the platelet surface

in the face of Ca2+ and Mg2+, stimulate a platelet release reaction by which the content of the platelet and its granules is discharged Biology of HemostasisPlatelet FunctionFibrinogen required for this processThrombin plays central role – stimulates platelet degranulation and activating the generation of thromboxane A2

Platelet factor 4, β-thromboglobulin, platelet-derived growth factor, ADP, serotonin, and calcium – introduced into the plasma

Release reaction results in compaction of the platelets and the

formation of an “amorphous” plug, which is no longer reversible

Biology of HemostasisPlatelet FunctionProcess in inhibited by cyclic adenosine monophosphate (cAMP)As a consequence of the release reaction, platelet factor 3 is made available and contributes phospholipid to several stages of the coagulation cascadeBiology of HemostasisPlatelet FunctionLipoprotein surface provided by platelets – catalyzes reactions that are involved in conversion of prothrombin (factor II) into thrombinBiology of HemostasisPlatelet FunctionPlatelet factor 3

involved in reaction by which activated factor IX (IXa), factor VIII, and calcium activate factor X

Also involved in the reaction by which factor Xa, factor V and Ca2+

activate factor II

Biology of HemostasisPlatelet FunctionPlatelets may also play a role in

initial activation of factors XI and XIIFibrinolytic process by releasing an inhibitor of plasminogen activation

Platelet factor 4 and β-thromboglobulin are also made available during the release reaction, and may inhibit the activity of heparin and modify fibrin formationBiology of HemostasisCoagulationProcess by which prothrombin is converted into the proteolytic enzyme thrombin, which in turn cleaves the

fibrinogen molecule to form insoluble fibrin in order to stabilize and add to the platelet plugBiology of HemostasisCoagulationConsists of a series of zymogen activation stages in which circulating proenzymes are converted in sequence to activated proteasesIntrinsic and extrinsic pathwayBiology of HemostasisCoagulationIntrinsic Pathway

Involves components normally present in bloodFactor XII is activated by binding to subendothelial collagen

Prekallikrein and high-molecular weight kininogen amplify this contact phase

Activated factor XII (XIIa) proteolytically cleaves factor XI and also prekallikrein to form factor XIa and kallikrein

In the presence of Ca2+, factor XIa activates factor IX (IXa)

Biology of HemostasisCoagulation

This in turn complexes with factor VIII, which can be activated to a more potent form by thrombin, and, in the presence of Ca2+ and the phospholipid platelet factor 3, activates factor X

Biology of HemostasisCoagulationExtrinsic Pathway

The tissue phospholipid, thromboplastin, reacts with factor VII and Ca2+ to activate factor XActivated factor X (Xa), produced by the two pathways, proteolyses prothrombin (factor II) to form thrombin

Effects of thrombin limited to the area of endothelial disruption by several processes

Biology of HemostasisCoagulationThrombin activates the fibrin stabilizing factor (XIII) and cleaves fibrinopeptides A and B from fibrinogen (factor I) to form fibrin, a monomer that is cross-linked with factor XIIIa, to form a stable clotBiology of HemostasisCoagulationAll the coagulation factors except thromboplastin, Ca2+ and most of factor VIII are synthesized in the liverFactors II, VII, IX, and X require vitamin K for their productionBiology of HemostasisFibrinolysisNatural process directed at maintaining the patency of blood vessels by lysis of fibrin depositsCirculating antithrombin III (AT III) also involved in the maintenance of vascular patency

Neutralizes the action of thrombin and other proteases in the coagulation cascade

Biology of HemostasisFibrinolysisInitiated at the same time as the clotting mechanismDependent on the enzyme plasmin

Plasmin derived from plasminogenPlasminogen levels known to rise during exercise, venous occlusion, and hypoxiaActivation of plasminogen also initiated by activation of factor XIIPlasmin preferentially absorbed on fibrin deposits

Lyses fibrin and acts on other coagulant proteins as well, including fibrinogen, factor V, and factor VIII

Congenital Hemostatic DefectsPlatelet DeficienciesCongenital Hemostatic DefectsPlatelet DeficienciesVon Willebrand’s DiseaseVon Willebrand’s Disease

Most common congenital platelet deficiencyVon Willebrand factor (vWF) is missing or in profoundly decreased amounts

vWF is required for platelet adhesion to subendothelial collagen

Congenital Hemostatic DefectsPlatelet DeficienciesVon Willebrand’s DiseaseUsually transmitted as an autosomal dominant trait, but recessive inheritance may occurDiminution of level of factor VIII:C (procoagulant) activity that corrects the clotting abnormality in hemophilia A plasma Congenital Hemostatic DefectsPlatelet DeficienciesVon Willebrand’s DiseaseVariation in the level of circulating factor VIII:C activity may be noted

A given patient may have abnormal bleeding time on one occasion and a normal bleeding time on another

Vast majority of patients have a prolonged aPTTManifestations of bleeding – usually mild, often overlooked until trauma or stress of surgical treatment makes them apparentCongenital Hemostatic DefectsPlatelet DeficienciesVon Willebrand’s DiseaseCareful taking of clinical history of great importanceSpontaneous manifestations often are limited to bleeding into the skin or mild mucous membrane bleeding, along with epistaxis and menorrhagia

Serious bleeding after dental extractions and tonsillectomy are not uncommonCongenital Hemostatic DefectsPlatelet DeficienciesVon Willebrand’s DiseaseTreatment: Correcting the bleeding time and factor VIII R:vWF

replacement therapy should be begun 1 day before a surgical procedureAspirin must be avoided for 10 days before an elective operation

Congenital Hemostatic DefectsPlatelet DeficienciesBernard-Soulier SyndromeResults from the deficiency of the platelet membrane GPIb-IX complexes with a morphologically large spherical plateletCauses abnormalities of platelet adhesion

Treatment is by local control of hemostasis and judicious use of platelet transfusionCongenital Hemostatic DefectsPlatelet DeficienciesGlanzmann’s ThrombastheniaCaused by an abnormality of platelet membrane glycoprotein (GP) IIb-IIIIaDeficient platelet aggregationlife-long bleeding tendency because of prolonged bleeding timeNormal PT and PTTCongenital Hemostatic DefectsPlatelet DeficienciesStorage Pool DiseaseCongenital disorder of platelet secretionPlatelets lack the storage capability of ADP required for aggregationManaged with platelet transfusionCongenital Hemostatic DefectsCoagulation Factor DeficienciesCongenital Hemostatic Defects - Coagulation Factor Deficiencies

Factor VIII Deficiency

(Classical Hemophilia or Hemophilia A)Disease of MalesFailure to synthesize factor VIII in normal proportionsInherited as a sex-linked recessive traitSpontaneous mutations in almost 20% of cases

Congenital Hemostatic Defects - Coagulation Factor Deficiencies

Factor VIII Deficiency (Classical Hemophilia or Hemophilia A)Severity of clinical manifestations related to degree of deficiency of factor VIII

Spontaneous bleeding and severe complications when virtually no factor VIII is detected in the plasmaWhen concentrations are in the range of 5% of normal, no spontaneous bleeding, but may

bleed severely with trauma or surgical treatment – moderately severe hemophiliacsGreater than 5% of normal – mild hemophiliacs


Factor VIII Deficiency (Classical Hemophilia or Hemophilia A)Significant bleeding typically first noted when child is a toddlerIn addition to hemarthrosis, epistaxis and hematuria may be notedInjury to the tongue or lingual frenulum – may lead to bleeding that may be life-threateningCongenital Hemostatic Defects - Coagulation Factor Deficiencies

Factor VIII Deficiency (Classical Hemophilia or Hemophilia A)

Tracheal compression and retropharyngeal bleeding may follow tonsillar infectionIntracranial bleeding is responsible for ~25% of deathsTalipes equinus contracture deformity – secondary to bleeding into the calfCongenital Hemostatic Defects - Coagulation Factor Deficiencies

Factor VIII Deficiency (Classical Hemophilia or Hemophilia A)Deep soft-tissue bleeding may result from Volkmann’s contracture of the forearm and flexion contractures of the knees and elbows



Hemarthrosis – most characteristic orthopedic problem

May cause few symptoms until distention of the joint capsule occursLarge hemarthrosis – generally manifested by a tender, swollen, warm and painful jointMuscle spasm and pain around the joint – due to involvement of periarticular structuresMay mimic infectionSame orthopedic problems noted in association with severe factor IX deficiency (Christmas disease)



Retroperitoneal bleeding – may follow lifting of a heavy object or strenuous exerciseTreatment involves replacement therapy

For maintenance of hemostatic integrity - ~2-3% of factor VIII activity neededIf with serious bleeding, level of factor VIII activity of ~30% may be necessary



For joint and muscle bleeding and major hemorrhages, factor VIII levels of ~50% of normal may be requiredFor major surgery and life-threatening bleeding, levels of 80-100% should be reached preoperatively and maintained above 30% for 2 weeks post-op


Factor IX Deficiency (Christmas Disease)Clinically indistinguishable from factor VIII deficiencyX-linked recessive mode of inheritanceAccounts for ~20% of hemophiliacsCan occur in severe, moderate, or mild forms according to level of factor IX activity in the plasmaCongenital Hemostatic Defects - Coagulation Factor Deficiencies

Factor IX Deficiency (Christmas Disease)½ of afflicted patients have the severe form with factor IX levels less than 1%Patients have prolonged partial thromboplastin time (PTT)Treatment – replacement therapy on a regular basis

All patients require substitution threapy whenever minor or major surgery is performedGenerally based on administration of fresh frozen plasma or factor IX concentrates


Factor IX Deficiency (Christmas Disease)

Severe hemorrhage – plasma levels of factor IX must be 20-50% of normal for the first 3-5 days, then maintaining plasma level at 10-20% of normal for approximately 10 daysWhen an operation is required, ~50-70% of normal levels should be achieved

Acquired Hemostatic DefectsPlatelet AbnormalitiesAcquired Hemostatic DefectsPlatelet AbnormalitiesThrombocytopenia

Most common abnormality of hemostasis that results in bleeding in the surgical patientIn patients with thrombocytopenia, patients afflicted with conditions such as idiopathic thrombocytopenic purpura (ITP), thrombotic thrombocytopenic purpura (TTP), SLE, and portal hypertension usually demonstrate marrow with normal to increased number of megakaryocytesAcquired Hemostatic DefectsPlatelet AbnormalitiesThrombocytopeniaMegakaryocytes generally reduced in patients with leukemia, uremia or patients on cytotoxic therapyMay occur acutely as a result of massive blood loss followed by replacement with stored blood

Exchange of 1 blood volume (11 units in a 75 kg man) decreases platelet count from ~250,000/mm3 to ~80,000/mm3

Acquired Hemostatic DefectsPlatelet AbnormalitiesThrombocytopeniaMay be induced acutely by administration of heparin and may be associated with thrombotic and hemorrhagic complicationsAcquired Hemostatic DefectsPlatelet AbnormalitiesThrombocytopeniaOften accompanied by impaired platelet function

Impaired aggregation after the addition of ADP has been demonstrated in patients receiving a blood transfusion of more than 10 unitsA variety of drugs interfere with platelet function: aspirin, indomethacin, ibuprofen,

dipyrimadole, phenothiazines, penicillins, chelating agents, lidocaine, dextran, β-blockers, nitroglycerin, furosemide, and anti-histamines

Acquired Hemostatic DefectsPlatelet AbnormalitiesThrombocytopeniaTreatment depends on underlying cause:

If secondary to vitamin B12 or folic acid deficiency – associated with megaloblastic bone marrow

Supplying the appropriate nutrient will correct the thrombocytopenia in 2-3 days

Acquired Hemostatic DefectsPlatelet Abnormalities

ThrombocytopeniaWith ITP or lupus and a platelet count less than 50,000/mm3

may raise platelet count with steroid therapy or plasmapheresis

Platelet packs may be administered pre-op to rapidly increase platelet count in surgical patients with thrombocytopenia due to marrow depression or in association with massive bleeding and replacement with banked blood

Acquired Hemostatic DefectsPlatelet Abnormalities

ThrombocytopeniaIn patients refractory to standard platelet transfusions, the use of HLA-compatible platelets coupled with special processors has proved effectiveEvaluation of the Surgical Patient as a Hemostatic Risk

Evaluation of the Surgical Patient as a Hemostatic

Risk History: Pre-Op EvaluationProlonged bleeding or swelling after biting the lip or tongueBruises without apparent injuryProlonged bleeding after dental extractionExcessive menstrual bleedingBleeding problems associated with major and minor operationsEvaluation of the Surgical Patient as a Hemostatic

Risk History: Pre-Op EvaluationMedical problems receiving a physician’s attention within the past 5 yearsMedications including aspirin or remedies for headache taken within the past 10 daysRelative with a bleeding problemEvaluation of the Surgical Patient as a Hemostatic Risk

Evaluation of Excessive Intra-Op or Post-Op Bleeding

Excessive bleeding during or shortly after a surgical procedure may be due to one of more of the following factors:

Ineffective local hemostasisComplications of blood transfusionPreviously undetected hemostatic defectConsumptive coagulopathyfibrinolysis

Evaluation of the Surgical Patient as a Hemostatic RiskExcessive Intra-Op or Post-Op Bleeding

Ineffective HemostasisExcessive bleeding from the field of the procedure, unassociated with bleeding from other sites (e.g. CVP line, IV line, etc.) usually suggests inadequate mechanical hemostasis

Exception to the rule – operations on the prostate, pancreas, and liver

Operative trauma may stimulate local plasminogen activation and lead to increased fibrinolysis on raw surface

Evaluation of the Surgical Patient as a Hemostatic RiskExcessive Intra-Op or Post-Op Bleeding

Complications of Blood TransfusionMassive blood transfusionHemolytic transfusion reactionTransfusion purpuraEvaluation of the Surgical Patient as a Hemostatic RiskExcessive Intra-Op or Post-Op Bleeding

DIC and Disseminated FibrinolysisOccur intra-op or post-op when control mechanisms fail to restrain hemostatic process to area of tissue damageMay cause diffuse bleeding caused by trauma, sepsis, retained products of conception, etc.Evaluation of the Surgical Patient as a Hemostatic RiskExcessive Intra-Op or Post-Op Bleeding

DIC and Disseminated FibrinolysisDIC

Thrombocytopenia

Positive plasma protamine test for fibrin monomersDecreased fibrinogen levelIncreased level of FDP

Local HemostasisLocal HemostasisMechanicalThermalChemicalLocal HemostasisMechanicalDigital Pressure

Pressure applied to an artery proximal to an area of bleedingPringle maneuver

Occluding the hepatic artery in the hepatoduodenal ligament as a method of controlling bleeding from a transected cystic artery or from the surface of the liver

Local HemostasisMechanicalHemostatLigature

Permanent method of effecting hemostasis in a single vesselNon-absorbable sutures (silk, polyethylene) evoke less tissue reaction than absorbable materials (catgut, polyglycolic acid, polyglactin)

Local HemostasisMechanicalAbsorbable materials are preferred in the face of overt infectionPresence of non-absorbable material in an infected wound can lead to extrusion or sinus tract formation

Monofilament wire and coated sutures have advantage over multifilament sutures in the presence of infection

Local HemostasisMechanical

Multifilament sutures tend to fragment and permit sinus formation

Direct pressure applied by means of packs affords the best method of

controlling diffuse bleeding from large areasLocal HemostasisThermalHeat achieves hemostasis by denaturation of protein – results in coagulation of large areas of tissueWith electrocautery, a negative plate should be placed beneath the patient to avoid severe skin burns

Advantage: saves timeDisadvantage: more tissue is necrosed than with precise ligature

Local HemostasisChemicalVary in hemostatic action

VasoconstrictiveCoagulant properties

Hygroscopic properties – increase their bulk and aid in plugging disrupted blood vessels

Local HemostasisChemicalEpinephrine

Applied topically induces vasoconstrictionExtensive application can result in considerable absorption with systemic effectsGenerally used in oozing sites in mucosal areas, e.g., during tonsillectomy

Local HemostasisChemicalHemostatic FibrinProperties required

Handling easeRapid absorptionHemostatic action independent of the general clotting mechanismNon-irritating

Local HemostasisChemicalExamples include gelatin foam (gelfoam), oxidized cellulose (oxycel), oxidized regenerated cellulose (surgicel), and micronized collagen (avitene)Transmit pressure against wound surface and interstices provide a scaffold on which the clot can organizeTransfusion

Transfusion

Characteristics of Blood and Replacement TherapyBlood

Vehicular organ, perfuses other organsTransportation of oxygen, removes the by-product carbon dioxideTransport of chemical nutrients for, and waste products from, metabolic activityCarry hormones, coagulation factors, and antibodies

Transfusion

Characteristics of Blood and Replacement TherapyReplacement Therapy

Banked Whole BloodRarely indicated, rarely availableShelf life 40 + or - 5 daysChanges in red cells occur during storage

Reduction of intracellular ATP and 2,3 DPG – alters curve of oxygen dissociation for hemoglobin – decreasing oxygen transport function

Poor source of platelets – platelets lose ability to survive transfusion after 24 hours of storage

Transfusion

Characteristics of Blood and Replacement TherapyTyping and Crossmatching

Serologic compatibility is established routinely for recipients’ and donors’ A, B, O, and Rh groups

Transfusion

Characteristics of Blood and Replacement Therapy

Rh-negative recepients ideally should be transfused only with Rh-negative blood

Rh-negative group comprises only 15% of population – limitedIf recipient is an elderly male who has not been transfused previously, transfusion of Rh-positive blood is acceptable if Rh-negative blood is unavailableAnti-Rh antibodies form within several weeks of transfusionRh-positive blood should not be transfused to Rh-negative women shortly before or after childbirth - this precaution largely eliminates Rh disease in subsequent offspring

Transfusion


In a patient receiving repeated transfusions, serum drawn not more than 72 hours before crossmatching should be utilized for matching with cells of the donorEmergency blood transfusion – blood type OPatients with malignant lymphoma and leukemia – cryoglobulins may be present, and blood should be administered through a blood warmerTransfusion

Characteristics of Blood and Replacement TherapyAutologous Predeposit Transfusion

In healthy, non-anemic patients, up to 5-6 units of blood may be collected for use in elective surgical proceduresMay donate blood if hemoglobin level is more than 11 g/dL or if hematocrit concentration is greater than 34%First procurement – 40 days prior to planned operation and last collection, 3 days before

Transfusion

Characteristics of Blood and Replacement TherapyFresh Whole Blood

Refers to blood administered within 24 hours of donationRarely indicated

Packed Red Cells and Frozen Red CellsPacked red cells is the product of choice for most clinical situationsPreparation reduces but does not eliminate reaction caused by plasma components

Essentially provides oxygen-carrying capacityNot available for use in emergenciesRed cell viability is improved; ATP and 2,3-DPG concentrations are maintained

Transfusion

Characteristics of Blood and Replacement TherapyLeukocyte-poor Washed Cells

Prepared by aspirating the buffy coat and supernatant plasma and passing them through a specific white-cell filter; red cells then are washed with sterile isotonic solutionIndicated for patients with demonstrated hypersensitivity to leukocytes or platelets (buffy coat reactions)

Syndrome is manifest by fever, chilly sensations, and urticaria due to plasma proteins in the absence of hemolysis

Transfusion

Characteristics of Blood and Replacement TherapyPlatelet Concentrates

Indications: thrombocytopenia due to massive blood loss and replacement with platelet poor productsThrombocytopenia due to inadequate production and qualitative platelet disorders

Preparations should be used within 120 hours of blood donation

Transfusion


May transmit infectious diseases and account for allergic reactions similar to those caused by whole bloodFor thrombocytopenic bleeding or pre-op thrombocytopenic patients – platelets must be maintained at

50,000 to 100,000/mm3 for continued protection

TransfusionCharacteristics of Blood and Replacement Therapy

Frozen Plasma and Volume ExpandersFrozen Plasma provides factors V and VIIILactated Ringer’s (LR) Solution or Buffered saline solution administered in amounts 2-3 times the estimated blood loss is effective and is associated with fewer complicationsDextran or a combination of LR solution and normal human serum albumin are preferred for rapid plasma expansionTransfusionCharacteristics of Blood and Replacement Therapy

Frozen Plasma and Volume ExpandersCommercially available dextran preparations probably should not be administered in amounts exceeding 1L/day – prolongation of bleeding time; possible hemorrhage may occurTransfusionCharacteristics of Blood and Replacement Therapy

ConcentratesAntihemophilic concentrates are prepared from plasma and are available for the treatment of factor VIII deficiencyAlbumin

25 g may be administered and provide osmotic equivalent of 500 mL of plasmaHepatitis free product

Indications for Replacement of Blood or its Elements

TransfusionIndications for Replacement of Blood or its Elements

Improvement in Oxygen-Carrying CapacityAnemic patientsIf anemia can be treated by specific therapy (erythropoetin), transfusion should be withheldTransfusionIndications for Replacement of Blood or its Elements

Volume ReplacementMost common indication in surgical patientsMeasurement of Hgb and Hct levels used to interpret blood loss

Misleading in the event of acute blood loss – Hct may be normal in spite of severely contracted blood volume


Volume ReplacementAmount and rate of bleeding are factors in development of the signs and symptoms of blood loss

A healthy person can lose 500 mL in 15 minutes with only minor effects on the circulation and little change in BP or pulseLoss of 15-30% of blood volume is associated with tachycardia and decreased pulse pressureLoss of 30-40% may result in tachycardia, tachypnea, hypotension, oliguria, and changes in mental status


Volume ReplacementLoss of blood may be evaluated in the operating room by estimating the amount of blood in the wound and on the drapes and by weighing sponges

Loss determined by weighing sponges is only about 70% of true loss


Volume Replacement

In patients with normal pre-op blood values:

Blood loss up to 20% of total blood volume (TBV) is replaced with crystalloid solutionsBlood loss above 50% of TBV is replaced with crystalloids, RBCs, and albumin or plasma


Volume ReplacementIf electrolyte solutions are used to replace blood volume, an amount 3-4 times the lost volume is required because of immediate diffusion into the interstitial spaceTransfusionIndications for Replacement of Blood or its Elements

Replacement of Clotting FactorsIn treatment of certain hemorrhagic conditions, it must be noted that there may be multiple clotting defectsInitial volume of fresh frozen plasma needed for an effect on coagulation

ranges from 600-2,000 mL administered in 1-2 hoursTransfusionIndications for Replacement of Blood or its Elements

Massive TransfusionImplies a single transfusion greater than 2,500 mL, or 5,000 mL transfused over a period of 24 hoursComplications include:

Circulatory overloadDICDilutional thrombocytopeniaImpaired platelet functionDeficiencies of factors V, VIII, and XI may occur


Massive TransfusionCitrate Toxicity

Particularly in young children and patients with severe hypotension or liver disease

Related to excessive binding of ionized calcium and is usually corrected by spontaneous mobilization of calcium from bone


Massive TransfusionHeat exchanger may be used to warm the blood – hypothermia may cause a decrease in cardiac rate and output and a reduction in the blood pH

Warming the blood significantly decreases the frequency of intra-op cardiac arrests


Massive TransfusionDuring massive transfusions, pH, blood gases, and potassium should be measured regularlyTransfusion

Methods of Administering Blood Routine administration

Rate of transfusion depends on patient’s status5 mL/min is administered for 1 min, after which 10-20 mL/min may be administered to complete routine transfusionMarked oligemia – first 500 mL in 10 minutes, and second 500 mL may be given rapidly in most cases

Transfusion

Methods of Administering BloodOther methods

Instilled intraperitoneallyInto the medullary cavity of the sternum and long bones

PainfulRate of administration limited

Transfusion

Methods of Administering Blood

Intra-op autotransfusion

Approximately 250 mL of blood can be retrieved, washed or filtered, and returned to the patient overa 5-6 minute period

Transfusion Complications


Hemolytic ReactionsNon-fatal incidence: 1 per 6,000 units of blood administeredFatal incidence: 1 in every 100,000 units administeredReactions due to incompatibility of A, B, O, and Rh groups may result from lab or clerical error


Hemolytic ReactionsCharacterized by intravascular destruction of red blood cells and consequent

hemoglobinemia and hemoglobinuriaMost common symptoms are the sensation of heat and pain along the vein into which the blood is being transfused, flushing of the face, pain in the lumbar region, and constricting pain in the chestTransfusion Complications

Hemolytic ReactionsPatient may experience chills, fever, respiratory distress, hypotension, and tachycardia from amounts as small as 50 mLIn anesthetized patients – 2 signs may be seen:

Abnormal bleedingContinued hypotension despite adequate replacement


Hemolytic ReactionsTreatment

Transfusion must be stopped immediatelySample of recipient’s blood should be drawn and sent along with the suspected unit to the blood bank for comparison with the pretransfusion samplesSerum bilirubin must be determined in the patient

Each gram of hemoglobin is converted to about 40mg of bilirubinIncrease in the indirect reacting fraction


Hemolytic ReactionsUrine output must be monitoredDiuresis and alkalinization of urine


Febrile and Allergic Reactions

Relatively frequent, occurring in ~1% of transfusionsUsually are mild and manifested by urticaria and fever occurring ~60-90 minutes of the start of transfusionAllergic reactions are caused by the transfusion of antibodies from hypersensitive donors or the transfusion of antigens to which the recipient is hypersensitiveTransfusion Complications

Febrile and Allergic ReactionsTreatment consists of administration of antihistamines, epinephrine, or steroids, depending on the severity of the reaction Transfusion Complications

Bacterial Sepsis

Most common cause are gram-negative organisms, specifically the Pseudomonas species (capable of growth even at 4°C)Clinical manifestations include:

FeverChillsAbdominal crampsVomitingdiarrhea


Bacterial SepsisTreatment includes administration of adrenergic blocking agents, oxygen, and antibioticsTransfusion Complications

EmbolismAir embolism

Normal adult can generally tolerate an embolism of 200 mL of airSmaller amounts can cause alarming signs and may be fatal

:Transfusion Complications

EmbolismManifestations of venous air embolism include:

Rise in venous pressureCyanosis“mill wheel” murmur heard over the precordiumHypotensionTachycardiasyncope


EmbolismTreatment consists of placing the patient on the left side in a head-down position with the feet upArterial air embolism is manifested by:

Dizziness and faintingLoss of consciousnessconvulsions


ThrombophlebitisProlonged infusions into peripheral veins – superficial venous thrombosisIV infusions that last more than 8 hours are more likely to be followed by thrombophlebitisIncreased incidence in the lower limb as compared to upper limb infusionsTransfusion Complications

ThrombophlebitisTreatment consists of discontinuation of the infusion and local compressionTransfusion Complications

Overtransfusion and Pulmonary EdemaMay occur with rapid infusion of blood, plasma expanders, and other fluids, particularly in patients with cardiac problemsCentral venous pressure must be monitored in cardiac patients whenever large amounts of fluids are being given


Overtransfusion and Pulmonary EdemaCirculatory Overloading manifested by:

Rise in venous pressureDyspneaCoughRales may be heard over the lung bases

Treatment consists of stopping the infusion and placing the patient in a sitting positionTransfusion Complications

Overtransfusion and Pulmonary EdemaAcute Pulmonary Edema

Damaging factor is apparently carried by perfusing bloodImmature plasma cells are found in the interalveolar tissueRepresents and immune response to blood

Reduced by employing hemodilution technique of pump priming


Transmission of DiseaseMalariaChagas’ DiseaseBrucellosisSyphilisPosttransfusion viral hepatitis

Most common fatal complication of blood transfusionCaused either by hepatitis B or C

AIDS

HEMOSTASIS

Documents

platelet membranes

platelet surface

platelet adherence

platelet recruitment

platelet degranulation

plateletderived growth

vascular response factor

loose platelet aggregate