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Anesthesia Oral boards > Blood > Flashcards

Blood Flashcards

1
Q

How frequently are there transfusion reactions

A

1:10,000 to 1:50,000
- new data suggest 1:250,000
Acute hemolytic tranfusion reactions
- death rates 25% with < 100 ml transfused and 44% with > 1000 ml tranfused

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2
Q

Are all transufion reaction imemidate

A

Immediate occur within 24 hrs (acute hemolytic, allergic (mild, anaphylactic, anaphylactoid), febrile nonhemolytic, hypotensive, bacterica contaminated, TRALI, TACO
Delayed 24-3 months latera (GVHD, delated hemolytic, infectious)

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3
Q

Can all blood products cause transufions rxn?

A

Yes.
Only incompatible RBC cause intravascular hemolytic
Allergic (most common reactions 1-3%) - occur iwth RBC , plasma or platelet
- Usually result from preformed antiboides to plasam proteins
- IgE may mediate allergic rxn and anphylaxis may occur
-Febrile rxn may be procedue by stored leukocytes (IL-1 endogenous pyrogen) or anti-IgA abx by pts who are deficient in IgA

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4
Q

Immediate intravascular hemolytic tranfusion reaction

A

Destruction of donor RBC release free hemoglobin, elaborates cytokines and chemokines, activates completment, reduces O2 carrying capacity and caused electrolyte imbalances.
-Usually ABO incompatibility –> high IgM (anti A and B) attach to donor RBCs (can be Kell, Duffy, Rh (IgG and doesn’t do completment), Lewis, and Kidd)
-destruction of these cells and activation of completement lead to acute hemolysis
-Attachment of IgM leas to completment activation, cytokine and kine production, thrombin generation, and platelet activation.
- Completment leads to cell ysis and degranulation of mast cells, histamine release, free radical procection
-Macrophages degranulate and release histamine, serotonin, and cytokines and bradykinin –> hypotension and capillary leak
-DIC
Free hemoglobin –> renovasuclar vasocontstirciton and norepi release in response to hypotension makes this work

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5
Q

Extravascular hemolytic rx

A

Non-ABO groups –> more often Rh incompatibitlity

  • No RBC intravascular destruction
  • Removed in spleen or liver
  • Low grade fever, or hemoglobinemia or hemoglobinuria
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6
Q

Febrile nonhemolytic tranfusion rx

A

Most comon type of rxn –> donor leukocytes in transufsed blood products (usually RBC or platelets)

  • Increase by 1 degree C
  • Chilles, cold, rigors
  • Alloantibodies against donor leukocytes - cytokines
  • Leukoreduction reduced incidence
  • -> 12.5% chance of again if previous –> given leukocyte depleted
  • Tx with tylenol and NSAIDS
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7
Q

Allergic transfusion rxn

A

1% of transfusions

  • Usually mild (urticara, swelling, rash) –> sometimes anaphylactic or -toid
  • Release of histamine due to donor plasma protiens attach to preformed IgE or IgG antibtoids on mast cells in sensitized individuals
  • more likely with FFP
  • Anaphylactic usually with IgA deficient individuals
  • Anaphylatoid is related to how much is tranfused
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8
Q

Hypotensive rxn

A

SBp or DBP decrease at least 30 mmHg

  • Generation of bradykinin –> hypotension and fluid leaking from endothelial activation
  • More often in patients taking ACE inhibitors (ACE breaksdown bradykinin)
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9
Q

Bacteria contaminated transfusion

A

Mild fever or frank sepsis
Usually with a increase in Temp by > 2C
Absence of hemoglobiemia or -uria distinguishes from AIHTR
Higher incidence in platelets due to temp
Psudomonas, enterobacter, and yersinia can grow at cold temps though
-Transfusion of both bacteria and endotoxin and release of proinflammatory cytokines and IL
-Nitric oxide leads to refractory hypotension

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10
Q

TRALI

A

1: 1000- 1:4500 transfusions
- Leading cause of morbidity and accounts for 47% of deaths from transfusions
- More common with platelets and FFP and more from multiparous women
- Mortality 5-10%
- Noncardiogenic pulmonary edema within 6 hr of transfusion
- BIlateral pulmonary infiltrates –> 70% require intubation
- Lung injury usually transient and resolves in 72-96 hrs
- Two step process: preexsiting condition cause neutrophil priming along pulmonary vasculature –> transfused blood activates the leukocyte and causes cytotoxic granules to be released –> disrupt endothelium

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11
Q

TACO

A

Rapid admin of blood products
Esp in pts with preexisting heart dz or renal insufficency
-CHF with dyspnea, desat, overload, and JVD, increased CVP, increased PCWP and tachycardia
- Limit transfusion rates to 2-3 ml/kg/hr

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12
Q

Hyperkalemia

A

Usually if blood products near the end of their shelf life –> up to 45 mEq/L at end of life

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13
Q

Citrate toxicity

A

Citrate-phosphate-dextrose is the preservative

  • Eliminated in liver - large voles of reduced liver perfusion or fuction and hypothermia impair metabolism
  • Citrate binds Ca and Mg
    • leads to impaired cardiac function and coagulopathy
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14
Q

Delayed hemolytic reaction

A

3-10 days post-transfusion

  • From amnestic response (prior exposure but quiesent abx at time of transfusion –> slowly ramp up)
  • RBC taken via spleen
  • More often with Rh groups
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15
Q

GVHD

A

8-10 days post transfusion

  • usually with bone marrow transplants
  • close human leukocyte antigen haplotype – recipent sees donor leukocyte as own, but donor cells sees recipent as foreign –> attacking recipent and bone marrow
  • Death within a few weeks
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16
Q

Delayed infections from transfusions

A

Hep B - 1:137,000
Hep C - 1:1,000,000
HIV - 1: 1,900,000

17
Q

Tx of transfusion reactions

A

Stop blood product and send to lab with pt blood for re-crossmatch and culture
ABCs - ventilate with PEEP, vasopressors (phenyl, epi, norepi….maybe vasopressin and methylene blue for refractory hypotension)
Send labs: CBC, coags and platelets, free hgb levels and haptoglobin levels, cr, BUN, ABG, UA
Renal protection: Fluids (>2 ml/kg/hr), mannitol, furosemide and urine alkalinaztion (bicarb - 75 mEq in 1 L 0.5 NS and infuse at 125 ml/hr)
Allergic rxn: diphenhydramine (25 mg), famotidine (20 mg) –> both H1 and H2 together work better
Epi

18
Q

Preventing transfusion rxn

A

Proper pt and blood sample identification
Not from multiparous women
Leukoreduction to reduce febrile rxn, TRALI
Irradiation to reduce GVHD
Allergic rxn reduced with saline washed ?

19
Q

Preop coagulation evaluation

A

Gal: optimize pt safety by identifying porthrombotic and antithrombotic tendeniuws: Routing preop coag studies are not useful
Personal adn family bleeding hstiory, meds, and physcial exam
Also ask about homeopathic meds
Maybe get preop stuides in the absence of bleeidng hx if the scheduled procesure is associated with a catastrophic (intracranial surgery) or high (hepatic resection) risk of bleeding

20
Q

What lab tests are performed to dx preop coagulopathies

A

PTT - intrinsic (I, II, V, VIII, IX, X, XI, and XII) and heparin - also affected by hypothermia and hypofibrinogenemia
PT - vit K antagonist meds (warfarin – I, II, V, VII, and X)
Automated test can be affected by elevated hematocrit, lipemia, hemolysis, or elevated bilirubin….also VIII is very labile - so can degrade
Platelets are critical for hemostasis - tissue injury exposes extracelular matrix rpotein for binding using vo willebrand factor
-plts are actived releasing fibrinogen, facotr V, factor VIII, and vWF etc to recruit more plts
–Exposed glycoprotine IIb/IIIa receptors provide binding sites for fibrin cross-linking

21
Q

Platelet abnormalities

A

Quantitiative (platelet counts)
–If less than 10,000 or bleeding/periop and less than 50,000 - transfuse. above 100,000 is normal
Qualitative -uremia, vonwillebrand diseas, an antiplatelet therapy (may need dialysis, desmopressin, or waiting until antiplt drugs are gone)

22
Q

fibrinogen

A

a major factor in both intrinsic and extrinsic –> thrombin acts on fibnrinogen to form fibrin strand and create a fibrin clot

23
Q

mixing studies

A

differentiate between the presence of factor deficiency or inhibitor

  • correction of PT/PTT by mixing - factor deficiency
  • no correction - inhibitor (like lupus anticoagulent etc)
24
Q

Antithromobtic agents

A 
Warfarin (vitamin K antagonist)
Unfractionated heparin (clings to antithrombin III which then inactivates Xa)
25
Q

Factor Xa inhibitors

A

Mouth - rvaroxabn, apixaban
IV: low-molecular weight heparin (lovenox)
dalteparin, enoxaparin

26
Q

Direct thrombin inhibitors

A

mouth: dabigatran
IV: argatroban, bivalirudin, hirudin

27
Q

antiplatelet agents

A

Aspirin, NSAIDS, clopidogrel & ticlodipine (ADP blockers), abciximab (IIb/IIIa inhibitor)

28
Q

Dilutional coagulopathy with massive transfusion

A

> 10 units of PRBCs in 24 hrs or >6 units in 24 hrs
Multifactorial coagulopathy
Initially levels of VII and VWF are increased by stress and platelets are released from spleen
Fibrinogen doesn’t go below 1 g/L until loss of 150% blood volume
Initially the decrease of both procoag and anticoag keeps hemostatis balanced
Then the hemodilution favors fibrinolysis and hypothermia nd acidosis impair thrombin generation
Tx: FFp, cryo or fibrinogen concentrates, antifibrinolytics, plts, - consider PCC (prothrombin complex concentrate: II, IX, and X) or rFVIIa

29
Q

Platelet dysfunction

A

Acquired: hepatic or renal failure, antiplt meds, CPB, ECMO, HIT, colloid use - either thrombocytopenia or increased bleeding time
Congenital: vWD (1% of population) or bernard-soulier and glanzmann
TX: transfusion and DDAVP

30
Q

Congential or acquire factor deficiency

A 
Hemophilia A (VIII) and B (IX) (Normal PT, elevated PTT) - xlinked recessive (mild disease 5-40% nl, severe < 1% nl factor) - tx: Factor VIII and IX concentrates, factor eight inhibitor
Factor VII deficency (normal PTT, elevated PT) 
Dabigatran - tx: hemodialysis
Rivaroxabn - tx: PCC
Vit K antagonist/malnutrition (elevated PT and normal PTT) - tx: vit K, PCC, FFP, rFVIIa
Liver disease (II, V, VII, IX, X, XI, XIII and fibrinogen) - VIII is ok i think....: elevated PT and PTT (FFP, Cyro, fibrinogen concentrate)
Myeloproliferative dx: def of factor V/ 
Amyloidosis: factor X deficency
31
Q

Acquired factor inhibitors

A

Autoimmune dz, malignancy, postpartum - variety of factos, but factor VIII is most common inhibitors
Penicillins and phenytonin and sulfa too
May need steroid, IVIG, plasma exchange and replacement of inhibited factors

32
Q

Fibrinolysis

A

Dilutional, DIC, hepatic disease
Aminocaproci acid and tranexamic acid
Replace fibrinogen

33
Q

DIC

A

Systemic activation of coagulation leading to microvascular thrombosis, organ failure, consumption of clotting factors and plts, clinical bleeding
Sepsis, trauma, burns, OB, allergies
Proinflam cytokine release –> thrombin generation widespread and microvascular thrombosis with bleeding
tx: FFP, cryo, plts (goal > 50,000), maybe antifibrinolytics

34
Q

Thrombosis

A 
DIC, HIT (5-14 days after starting heparin - 5% of pts treated with heparin), anticoauglant deficiency, antiphospholipid deficiency, factor V leiden, malginancy, liver disae, immobilization
Fibrinolytic therapy
Anitcoagulant concentrates (antithrombin and protein C)

Anesthesia Oral boards (1 decks)

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