anemia bleeding
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Anemia and The BleedingPatient
November 1, 2005Eli Denney D.O.
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Definition of Anemia
Anemia a reduced concentration of redblood cells. Measured by Hct, Hgb and RBCcount.
Anything that reduces production or increases destruction will result in anemia if the processes are not corrected.
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Anemia - Causes
Most common causes in U.S.Iron deficiencyThalassemia
Anemia of Chronic Disease
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Physiologic Reactions to Blood Loss
Acute Peripheral vasoconstriction andcentral vasodilatation
If blood loss continues small vessel
dilatation with compensatory decreased PVR,resulting in increased CO.
Chronic - Increased plasma volume keepsintravascular volume normal
Erythropoietin released by kidneys reticulocytes in 3-7 days.
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Signs and Symptoms
Depend uponRate of blood loss
Amount of blood lost
AgeOverall HealthComorbid disease states
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Signs and Symptoms
WeaknessFatigueDyspnea
PalpitationsOrthostaticsymptomsLethargy
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Physical Exam Findings
+ Orthostatic BPs Tachycardia
Pallor Systolic ejc. murmur
Widened pulsepressure
GI bleeding/Uterinebleeding Altered Mental Status
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Diagnosis
Confirmed by lab values RBC count, Hgband Hct.CBC may not determine specific cause
need to obtain other labs to begin appropriateworkup
CBC-provides RBC indices (MCV)Reticulocyte countPeripheral smear Iron studiesFolate, B12 levels
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Treatment
In ED, anemia from hemorrhage is the mostcommon need for treatment
Symptomatic
Hemodynamically unstable Asymptomatic - can do outpatient work up -depends upon clinical situation.
Based on clinical situation, patients should betyped and cross-matched for transfusion
Admit Patients with ongoing blood loss for definitive care
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Increased Likelihood of BleedingDisorder
Spontaneous bleeding-multiple sitesBleeding from untraumatized sites
Bleeding several hours after traumaBleeding into deep tissues or jointsFamily history of bleeding disorder
Excessive bleeding after dental extractions or surgical proceduresLiver disease
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Increased Likelihood of BleedingDisorder
Drugs EthanolCoumadin
ASANSAIDS
AntibioticsPlavix
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Bleeding Site May Indicate SpecificAbnormalities Indicative of PlateletDisorder
Mucocutaneous BleedingPetechiae
EcchymosisEpistaxisGI/GU bleedingHeavy menstrual bleeding
Purpura are associated withthrombocytopenia and commonly indicates asystemic disease
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Coagulation Factor Deficiencies
Bleeding into joints, potential spaces,retroperitoneum and delayed bleeding
Mucocutaneous bleeding and bleeding intodeep spaces may be signs of DIC both
pathways of homeostasis are involved.
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Normal Coagulation
Platelet Plug (Primary Homeostasis)
Cross-linked Fibrin (Secondary Homeostasis)
Fibrinolytic system counter regulatory
system that prevents excessive clotformation.
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Primary Homeostasis
Depends upon platelet interaction withendothelium
Requires normal vascular endothelium,
functional platelets, von Willebrand factor, andnormal fibrinogenvon Willebrand factor connects platelets to theendothelium by glycoprotein Ia
Fibrinogen connects platelets by glycoproteinsIIB-IIIA.
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Secondary Homeostasis
See Fig 218-3 - Coagulation Cascade
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Fibrinolytic System
Purpose is to limit the size of fibrin clotsEndothelial cells release tPA which convertsplasminogen to plasmin which is already a
part of the fibrin clotPlasmin degrades fibrinogen and fibrinmonomer into fibrin degredation products andcross linked fibrin into D-Dimers
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Other Inhibitory Proteins
Antithrombin III inhibits clotting cascade.Inhibits function of XIIa, XIa, IXa andThrombin.
Heparin potentiates this interaction.
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Proteins C and S
Activated Protein C binds with cell surfacebound Protein S the bound proteins inhibitfactors Va and VIIa.
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Inhibitory Proteins
Deficiencies or dysfunction of proteins C,S or antithrombin III can cause a hypercoagulablestate.
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Initial Testing for Bleeding Disorders
CBCPT/INRPTTFurther testing as indicated (Table 218-4)
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Acquired Bleeding Disorders
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Acquired Platelet Defects
Quantitative DefectsDecreased productionIncreased destruction
Splenic sequestrationPlatelet levels less than 10-20,000 / microLincreases the likelihood of spontaneous
bleeding
especially intracranialLevels less than 10,000 transfusion of platelets will be necessary
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Decreased Production
Bone marrow infiltration Aplastic anemiaViral infections CMV, RubellaDrugs (Thiazides, Ethanol, Chemo-agents)Vitamin B12, Folate deficiencyRadiation
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Increased Destruction
ITPTTPHUSDIC
Viral infections HIV, Varicella, EBVDrugs
Heparin/Protamine
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Idiopathic Thrombocytopenic Purpura
Autoimmune disease involvingthrombocytopenia, purpura or petechiae,normal bone marrow function and no other
known cause for decreased platelets. Autoantibodies attach to circulating plateletsand are destroyed by the reticulendothelialsystem.Platelets function normally despite lownumbers and bound with antibodies
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ITP Acute and Chronic Course
Acute typically occurs in children, males =females, duration 1-2 months.Chronic typically occurs in adults, lasts
greater than 3 months, female > male,resolution unlikely even with treatment.Patients with chronic ITP more commonlyhave another disease or autoimmunedisorder.
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ITP PE and Lab
Commonly PE will show petechiae, epistaxis,gingival bleeding, bruising, and possiblemenorrhagia. Remaining PE may be normal.
Lab CBC - low platelets, otherwise normal.Peripheral smear-normal platelets, few innumber If history, PE, and above lab support thediagnosis of ITP, no further ED testing isnecessary.
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Treatment - ITP
Minimize bleeding risks Meds, falls,comorbid disease states and procedures.
Asymptomatic and healthy, with platelet
counts > 50,000 no treatment is needed< 50,000 and symptoms require treatment
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Treatment - ITP
Prednisone 60-100 mg/d tapered after plateletcount returns to normal ranges.If steroid therapy fails splenectomy producesremission in 65 percent of patients.If bleeding is life threatening local hemorrhagecontrol should instituted and high dosemethylprednisolone 1-2 g/d for 2-3 days used.Intravenous immunoglobulin as needed.Platelets transfused after steroids or immunoglobins.
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Drug Induced Thrombocytopenia Table 219-2
Common drugsHeparinSulfas
ASAEthanolThiazides
IndomethacinValproic AcidLasix
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Platelet Sequestration
Splenomegaly and thrombocytopenia withoutsignificant bleeding is not uncommon.
Another bleeding disorder is usually involved
if significant hemorrhage is present.
Splenectomy is the definitive therapy for patients with low counts and evidence of significant hemorrhage.
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Qualitative Platelet Abnormalities
Liver diseaseUremiaDIC
SLEITPCardiopulmonaryBypass
MyeloprolifertivedisordersDysproteinemiasVon WillebrandsdiseaseLeukemias
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Drug Induced Platelet Dysfunction
ASANSAIDSClopidogrelTiclopidine
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Liver Disease
Any disease that affects the hepatocytes canaffect the production of the clotting factorsMalabsorption of Vit. K by primary biliary
cirrhosis and intra and extrahepaticcholestasis will affect factor II, VII, IV, and XIn more severe liver disease, decreasedsynthesis of a2 plasmin inhibitor will cause ageneral state of fibrinolysis and increase D-Dimers and fibrin degradation products
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Lab
To evaluate coagulation in liver disease thefollowing labs will need to be ordered
Hematocrit
PTaPTTPlatelet countFDP and D-Dimer
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Treatment
Lab abnormalities without bleeding patientscan be observedBleeding or invasive procedure needed
treatment is necessaryVitamin K for liver diseaseFFP if prolongation of PT and aPTT
Cryopercipatate if fibrinogen levels < 100mg/dLPlatelet transfusion if indicated -
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Renal Disease
Dialysis related thrombocytopeniaToxin inhibition of platelet aggregation uremic toxins.
For life threatening bleeding, treatment isusually dialysis and transfusion for anemia,DDAVP and conjugated estrogens.Platelet transfusion and cryoprecipitatetransfusions as needed.
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Disseminated Intravascular Coagulation
DIC an acquired syndrome characterizedby activation of the coagulation systemresulting in fibrin formation. The fibrinolytic
system is also activated which breaks downclots, uses all coagulation proteins andresults in bleeding - TintinalliDIC is associated with many conditions Table 219-5
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Pathophysiology
Disease process begins by the activation of tissuefactor extrinsic pathway.Thrombin converts fibrinogen to fibrin leading toformation of small clots that are deposited in
capillaries causing tissue ischemia organdysfunction.Excessive activation of the coagulation system leadsto depletion of coagulation proteins and platelets.tPA is activated indirectly by thrombin and fibrin andthe fibrinolytic system is activated in DIC thesystem works in excess and can result inuncontrolled bleeding
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DIC Manifestations
Hemorrhage and thrombosis both take place,one form usually is dominate.Hemorrhage most dominate
PetechiaeEcchymosesGI/GU bleeding
Wounds/IV sites
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DIC Manifestation
ThrombosisPurpura fulminansMental Status Changes
MOFOliguria
ARDS
Tissue necrosisIn chronic DIC the liver produces enoughcoagulation proteins to compensate
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DIC - Lab
Increased PTThrombocytopenia most commonLow fibrinogen levels
Fibrinogen levels less than 100 mg/dL, - morelikely to see bleeding complications
D-Dimers are more specific than FDPs in
diagnosing DICIncreased LDH, decreased haptoglobin,schistocytes on peripheral smear
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DIC Treatment
Treatment of underlying disease triggering DICHemodynamic support as needed PRBCs, IVFs,vasopressors as needed.Supplementation of coagulation proteins, platelets
and fibrinogenCryoprecipitate in 10-unit doses to keep fibrinogen to100-150 mg/dLPlatelet transfusion if < 20,000 or < 50,000 withbleedingFFP transfused at 10-15 mL/kg to replace clottingproteinsVitamin K, Folate
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DIC Treatment
Heparin for thrombotic dominant DIC or chronic DIC and known clots purpurafulminans
Antifibrinolytic agents are withheld for provenhypofibrinogenemia and fibrinolysis. Heparinshould be infused before to decrease chanceof thrombosis
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HIV Bleeding Disorders
Thrombocytopenia is one of the earliest signsof HIV infectionBleeding problems are uncommon, the mostcommon problems being bruising, mucosalbleeding and petechiaeThrombocytopenia caused by
Increased destruction immune complex
related and HIV medicationsDecreased synthesis immune complexrelated and HIV medications
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HIV Bleeding Disorders
HIV patients commonly haveLupus anticoagulant increased aPTT, whichmay appear and disappear with infection
Anticardiolipin antibody rarely causes adisorder in itself
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Circulating Anticoagulants
Antibodies that affect coagulation factorsKnown inhibitors for each coagulation proteinexist but the two most common are
Factor VII inhibitors Antiphospholipid antibodies lupusanticoagulant and anticardiolipin antibodies.
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Factor VIII Inhibitors
Can develop at any time but usually affectpatients with hemophilia APatients at risk of developing factor VIIIinhibitors
ElderlyPostpartum patients
Autoimmune disorders SLE, RA, UC, Mult.
MyelomaHave drug reactions PCNs, Sulfas,Phenytoin
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Factor VIII Inhibitors
Signs and SymptomsLarge bruising without traumaEcchymoses
HematomasLabNormal PTNormal Thrombin clotting time
Prolonged aPTT does not correct after mixingFactor VIII assay will be low
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Factor VIII Inhibitors
Treatment of Bleeding EpisodesPressure to bleeding siteFactor VIII concentrates
Factor IX complex concentratesProthrombin complex concentratesRecombinant factor VIIIa concentrates
PlasmaphersisUltimately a hematologist should direct carefor life or limb threatening bleeding episodes
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Antiphospholipid Antibody Syndrome
Presence of lupus anticoagulant or anticardiolipin antibodies, plus one or both of the following: thrombosis and/or
complications with pregnancy (recurring fatalloss
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Antiphospholipid Antibody Syndrome
In reality SLE patients rarely have theantibody (5-15 percent) in vivo patientsdevelop clots rather than bleed.
Lupus anticoagulant more common in HIVpatients, cancer, drug reactions and other autoimmune disorders
Anticardiolipin antibodies commonly occur with lupus anticoagulant but both can occur separately
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Antiphospholipid Antibody Syndrome
Lupus anticoagulant lab abnormalitiesNormal or prolonged PTProlonged aPTT does not correct when mixedNormal Thrombin clotting timePatients may develop antibodies to prothrombincausing a deficiency suggested by markedlyprolonged PTFactor assays all factors will be mildly low
Russell viper venom time detects presence of lupusanticoagulant
Anticardiolipin antibodies detected by ELISA assay
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Antiphospholipid Antibody Syndrome
Signs and SymptomsThromboembolism venous > arterialPregnancy complications
ThrombocytopeniaPatients who develop thrombosis and remainpositive for lupus anticoagulant have a 50percent chance of another clot forming within
2 yearsRecurrent fetal loss most likely due tothrombosis of placental vessels
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Antiphospholipid Antibody Syndrome
Treatment Asymptomatic observation, reduce risks for Virchows triad.
Treat underlying disorder if knownCorticosteroids for both AAS and autoimmunedisease together Patients with episodes of thrombosis needlifelong anticoagulation
ASA alone is inadequateLMWHs good role for these medicines
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Bibliography
Tintinalli Judith E., Emergency Medicine AComprehensive Study Guide 6 th Edition.Chapters 218-219
Q i
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Questions
T/F Lupus Anticoagulant is always present inpatients with SLE?T/F von Willebrand disease is a disorder of the extrinsic clotting pathway?T/F Definitive treatment of DIC is heparinfollowed by coumadin therapy?T/F Defiencies of proteins C and S cause
thrombotic disorders?T/F This was a fun and interesting chapter?F, F, F, T, F