Case 47 - periop coagulopathies Flashcards

1
Q

How would you assess a patient’s coagulation status?

A
  • all preop coagulatoin evals begin with H&P, familiy hx of bleeding, med history.
  • consider surgical bleeding risk as well

History

  • known coagulpathy disorder
  • epistaxis
  • prolong bleeding (dental extraction)
  • hepatic dysfunction (decreaes clotting factor)
  • renal dysfucntion (PLT dysfunction)
  • stroke, cardiac disease, GI bleed

PE

  • brusing
  • bleeding from mucous membrane
  • petechiae
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2
Q

What is the difference between extrinisic and intrinisc pathway?

A

Intrinsic pathway

  • measured by PTT
  • Common pathway (1, 2, 5, 10) + factor 8, 9, 11, 12
    • Factor 1 = fibrinogen
    • Factor 2 = prothrombin

PTT

  • affected by common pathway deficiency and factor defiency ( hemophilia, hypofibrinogenmia)
  • hypothermia, heparin

Extrinisc pathway

  • measured by PT/INR
    • to overcome interlaboratory variation in PT cause by different reagents, INR arose
  • Tissue factor activates factor VII –> goes to common pathway
    *
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3
Q

Describe PLT mechanism of action in coagulation?

A

3 steps: adhesion, activation, aggregation

1) adhesion

  • tissue injury exposes subendothelial layer
  • Plt adhere to injured vessel wall using vWF as a bridge

2) activation

  • PLT secrete chemical messengers to activate additonal PLT to site of injury (ex TxA2)
  • also initiate coagulation cascade

3) aggregation

  • PLT aggregate and bind to each other via receptor binding sites
  • exposed PLT glyco iib/iiia recpetors allow for fibrin cross-linking
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4
Q

Indications for Platelet transfusion?

A

Indications for Platelet Transfusion

1) Active Bleeding

  • < 50,000/mm3 and not the result of immune mechanisms
  • > 50,000/mm3 and a condition which impairs platelet function is present
  • Do not give platelets for > 50,000/mm3 with normal function, or if thrombocytopenia is caused by antibody

2) Massive Transfusion
* < 50,000/mm3 and evidence of continued bleeding
3) Prophylaxis (without evidence of bleeding)

  • < 5000/mm3
  • < 20,000/mm3 and high-risk condition (ex. PUD, previous hemorrhage)
  • Do not give platelets for < 20,000/mm3 (but > 5000/mm3) if no risk factors for bleeding are present
  • < 50,000/mm3 and endoscopic biopsy, lumbar puncture, or major surgery are planned
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5
Q

Describe dilutional coagulopathy?

A

Etiology

  • massive transfusion
    • > 10 U of PRBC within 24 hrs
  • coagulation is multifactorial
    • hemodilution of coagulation factors
    • fibrinolysis favored by hemodilution of inhibitors to tPA
    • hypothermia and acidosis –> impair thrombin generation

Labs

  • hemodilutoin of everything
  • Inc PT/INR, Inc PTT, dec fibrinogen, dec Plt

Tx:

  • FFP
  • cryo (fibrinogen and Factor 8)
  • PLT
  • consider antifibrinolytics (aminocaproic acid)
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6
Q

Describe Platelet dysfunction

A

Etiology (congenital or acquired)

  • hepatic or renal failure
  • antiplatelet meds
  • CPB
  • ECMO
  • HIT
  • vWD defiency
  • Hextend

Labs:

  • normal PLT count (dec function) - vWD defiency
  • thrombocytopenia - ECMO, CPB
  • increase bleeding time - hextend, hepatic/renal dz

Tx:

  • first check bleeding vs no bleeding
  • consider transfusion if plt count < 50,000 and no immune mechanism
  • > 50,000 and a condition which impairs platelet function is present
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7
Q

Describe congential or aquired factor deficiency?

A

Etiology + lab + tx:

1) liver disease

  • L: increase INR and PTT
  • T: ffp, cryo, firbinogen concentrate

2) vit K antagonists (warfarin)

  • L: increase INR, normal PTT
  • Vit K, FFP

3) intrinisc pathway deficiency (hemophilia)

  • L: nomral INR, increase PTT
  • T: specific factor concentrate, FFP, cryo

4) Common pathway deficiency (hypofibrinogenemia)

  • involves both extrinsic and intrinsic pathway
  • L: inc INR, inc PTT
    *
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8
Q

Describe acquired inhibitors

A

etiology

  • antibodies that inhibit specific factor activity (can occur with eveyr factor)
  • autoimmune disease (SLE, RA)
  • malignancy
  • factor VIII inhibitor (hemo A)

Labs:

  • normal INR, increase PTT
  • FVII inhibitor - inc INR, normal PTT
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9
Q

Describe fibrinolysis

A

etiology

  • plasminogen activation 2/2 to decrease plasminogen inhibtors or decrease plasminogen activator clearance
  • dilutional coagulatipathy
  • DIC
  • liver disease

Labs:

  • inc PT, inc PTT

Tx:

  • maintain fibrinogen levels
  • antifibrinolytics (amicar, transexaminc acid)
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10
Q

describe DIC

A

etiology

  • consumptive coagulopathy –< systemic activation of coagulation leading to thrombosis, organ failure, consumption of clotting factors, oozing from sites
  • sepsis
  • trauma
  • burn
  • aortic aneurysm
  • allergic/immunologic rxn

Pathophys

  • proinflammatory cytokine release leading to widespread tissue factor expression and resultant thrombin generation via extrinsic pathway.
  • also assoc with deragnement of normal anticoagulant (C, S, AT III) –> leads to favoring thrombosis

Labs:

  • inc INR, inc PTT
  • dec PLT
  • dec fibrinogen
  • inc fibrin degrade products

tx:

  • give everything
  • maintain Plt > 50,000
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11
Q

Describe thrombotic events

A

etiology

  • typically manifest as DVT
  • congential or acquired
  • HIT
    • 5-14 days after heparin therapy
  • Protein C, S, AT III deficiency
  • immobilizatoin
  • pregnancy (hypercoag state)
  • malignancy

Labs:

  • decrease bleeding time

Tx:

  • thrombectomy
  • fibrinolytic therapy
  • anticoagulants
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12
Q

what are the pitfalls of intraop coagulation testing?

A

Pitfalls:

  • results unavailable for 30-60 min
  • Abnromal results (ex inc PTT) are not diagnostic of underlying mechanim of coagulopathy (factor defiency, fibrinogen defiency, hypothermia)
  • not detect effects of hypothermia because lab tests are performed at 37 C
  • do not show mechanical properties of clot over time b/c PT and PTT terminate at low thrombin level and before fibrin is polymerized
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13
Q

what does a thromboelastogram do?

A

TEG

  • measure coagulation (viscoelasticity) of whole blood
  • measures coagulation factor function (PT, PTT) as well as assess platelet function, clot strength, and fibrinolysis which these other tests cannot.
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14
Q

what does the R value in the TEG represent?

A

1) R value (Reaction Time)

  • Time from start of measurement until beginning of clot formation, initial fibrin formation.
  • result
    • Increase r value = factor deficency
  • Causes:
    • factor deficiency
    • heparin/anticoagulants
  • Tx:
    • FFP
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15
Q

What does K value in TEG represent?

A

K Value - clot kinetics

  • time from end of R time to an amplitude of 20 mm
  • reflects clot kinetics
  • k and alpha angle show fibrinogen and coagulation formation
  • result
    • increase K value -
      • Deficiency of thrombin formation
      • affected by any variable that would slow clot formation (factor defiency, heparin)
      • Lack of generation of fibrin from fibrinogen
  • Tx
    • Cryo
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16
Q

what does alpha angle in TEG mean?

A

Alpha angle - clot kinetics

  • tangent of curve made as K is reached at 20 mm
  • reflects kinetics of fibrin production and cross linking
  • result
    • decrease alpha angle = hypofibringonemia
  • Tx:
    • Cryo
17
Q

What is maximum amplitude in TEG represent?

A

MA (Maximum Amplitude) - clot strength

  • indication of clot strength
  • depends on both plt number and function, as well as adequate fibrinogen levels
  • Result
    • decrease MA -
      • Thrombocytopenia
      • Thrombocytopathy (function defect)
      • Hypofibrinogenemia
  • Tx:
    • PLTs
    • consider DDAVP

*

18
Q

what is MA 30 and MA 60 in TEG represent

A

MA 30+60 - Clot stability (clot lysis)

  • reflects degree of fibrinoloysis
  • 30 min vs 60 min after max amplitude (clot strength)
  • Result
    • decease in MA 30 or MA 60:
      • abnormal fibrinolysis / excess plasminogen activity
  • Tx:
    • Tx with FFP, cryo, platelets as indicated, possibly may need Factor VII, antifibrinolytic
19
Q

Review the following coagulation abnormalities and its corresponding TEG values

A

1) anticoagulants / hemophilia

  • factor deficiency
  • R & K - prolonged
  • MA & alpha angle - decreased

2) PLT blockers

  • thrombocytopenia/thrombocytopathy
  • R - Normal; K - Prolonged
  • MA - Decreased

3) Fibrinolysis

  • tPA
  • R - normal, MA - continuous decrease
  • MA 30 and 60 - decreased

4) Hypercoagulation

  • r & k - decrease
  • MA & alpha angle - increased

5) DIC

  • hypercoagulable state with secondary fibrinolysis
  • r and k - decrease
  • MA and alpha - increase
  • MA 30 + 60 - decrease
20
Q

Pros and cons of FFP

A

Pros

  • contains all components of coagulatoin found in pts plasma: factors, anticoagulants, natural antifibrinolytics

Cons

  • risk of TRALI, viral transmission, volume overload
  • in presence of factor inhibitors (heparin, direct thrombin inhibitor), FFp is infective to treat or prevent bleeding 2/2 inhibitor acting against FFP
  • inadeaquate to provide increase fibrinogen plasma conc
21
Q

what is prothrombin complex concentrate?

A
  • PCC contains factors II (prothrombin), IX, and X
  • eliminates disadvantages of FFP - volume overloaad, hemodilution, infection, and need for crossmatching
  • recommended - antagonize effects of warfarin and can tx specific factor deficiences
22
Q

what is recombinant activated factor VII (rFVIIa)?

A
  • rFVIIa - thought to bind to tissue factor at site of vascular injury and amplify thrombin gneeration
  • theoretical risk of thombotic complicatoins must be weighed against risk of ongoing hemorrhage
  • off-label use during life-threatening hemorrhage that is unresponsive to convential management
23
Q

What is DDAVP?

A
  • desmopressin
  • V-2 receptor agonist
  • stimulates release of vWF from endothelial cells & increases available FVIII
  • use: hemophilia A (FVIII deficient) & vWD
24
Q

how do antifibrinolytics such as tranexamic acid or aminocaporic acid work? (mech of action)

A
  • inhibit conversion of plasminogen to plasmin
  • inhibit activity of plasmin
  • Plasmin cleaves fibrin into fibrin degredation products