Case 47 - periop coagulopathies Flashcards
How would you assess a patient’s coagulation status?
- 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
What is the difference between extrinisic and intrinisc pathway?
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
*
Describe PLT mechanism of action in coagulation?
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
Indications for Platelet transfusion?
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
Describe dilutional coagulopathy?
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)
Describe Platelet dysfunction
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
Describe congential or aquired factor deficiency?
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
*
Describe acquired inhibitors
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
Describe fibrinolysis
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)
describe DIC
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
Describe thrombotic events
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
what are the pitfalls of intraop coagulation testing?
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
what does a thromboelastogram do?
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.
what does the R value in the TEG represent?
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
What does K value in TEG represent?
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
-
increase K value -
- Tx
- Cryo
what does alpha angle in TEG mean?
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
What is maximum amplitude in TEG represent?
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
-
decrease MA -
- Tx:
- PLTs
- consider DDAVP
*
what is MA 30 and MA 60 in TEG represent
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
- decease in MA 30 or MA 60:
- Tx:
- Tx with FFP, cryo, platelets as indicated, possibly may need Factor VII, antifibrinolytic
Review the following coagulation abnormalities and its corresponding TEG values
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
Pros and cons of FFP
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
what is prothrombin complex concentrate?
- 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
what is recombinant activated factor VII (rFVIIa)?
- 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
What is DDAVP?
- desmopressin
- V-2 receptor agonist
- stimulates release of vWF from endothelial cells & increases available FVIII
- use: hemophilia A (FVIII deficient) & vWD
how do antifibrinolytics such as tranexamic acid or aminocaporic acid work? (mech of action)
- inhibit conversion of plasminogen to plasmin
- inhibit activity of plasmin
- Plasmin cleaves fibrin into fibrin degredation products