emergent reversal of anticoagulants Flashcards
FFP
contains variable but near-normal levels of coagulation factors, coagulation inhibitors, albumin, and immunoglobulins
large volumes of plasma transfusions are not well-tolerated in patient with little CV/pulm reserve (overload, TRALI)
efficacy is assessed by PT/INR, PTT, fibrinogen, PLT count, viscoelastic test
cryoprecipitate
slowly thawing FFR leaves behind a cold-insoluble precipitate which containes fibrinogen, FVIII, vWF, and FXIII
factor concentrates
plasma-derived
recombinant
which product is it NOT okay to use a warmer?
platelets
KCentra
4 factor concentrate that has II, VII, IX, and X
approved for reversal of vit-K antagonists like coumadin with INR > 1.5 and experiencing acute major bleeding
**contains heparin and antithrombotic proteins C and S
at higher doses, may also help reverse factor Xa inhibitors like xarelto and eliquis
Riastap
fibrinogen concentrate
it is fractionated from blood and is stored at room temp for up to 30 months
can be quickly reconstituted and administered IV with no thawing or blood-type matching
standardized in each vial
as effective as cryo and more effective than FFP
profilnine
3 factor concentrate of II, IX, and X
also called factor IX complex
originally approved for treatment of patients with hemophilia B (factor IX deficiency)
reserved mainly for cardiac cases, not indicated for heparin or other factor X inhibitor reversal
recombinant factor concentrates
factor VIIa, factor IX
factor complex conentrates (kcentra and profilnine)
reverses the effect of significant vitamin K-antagonism coagulopathy (coumadin reversal)
contraindicated in DIC and HIT
dosing of profilnine
10-15u/kg - IBW
max 1000u
recombinant activated factor VII (novoseven)
used for hemophilia A (factor 7 deficiency) or B (factor IX deficiency) or congenital factor 7 deficiency
off label - postpartum hemorrhage, trauma, anticoagulant reversal, high risk surgery)
can be associated with increased thrombosis risk especially in patients without hemophilia
works by enhancing the extrinisic pathway (bypasses intrinsic, so good for people with factor VIII and IX deficiency
theoretically should be localized to site of injury because it requires tissue factor to work, which should only be at site of injury
factor VII dosing
single dose for 80kg pt is $8,000
90 mcg/kg IV bolus - redose every 2 hours as clinically indicated
supplied in 1mg, 2mg, and 5mg vials
factor VII additional considerations
high risk of thrombotic adverse event
will not stop surgical hemorrhage
should not be given instead of other blood products - adequate FFP, cryo, and platelets need to be on board for the full effect because it depends on the function of platelets and fibrinogen
half life is 2-2.5 hours and initial dose may require repeating until bleeding is controlled
FCC consideration (why choose it?)
they provide faster correction of coagulopathy as compared to FFP and vit K (30 mins as opposed to >3h)
less risk of overload, TRALI, other transfusion reactions)
antifibrinolytic medications MOA
prevents the lysis of fibrin - promotes clot formation
used to treat/prevent excessive bleeding
interferes with formation of plasmin which takes place in lysine rich areas on the surface of fibrin
what are the 2 types of antifibrinolytics
lysine analogues (tranexamic acid and aminocaproic acid) serine protease inhibitors (aprotinin) - no longer available
epsilon aminocaproic acid (AMICAR)
FDA approved for use in treatment of acute bleeding d/t elevated fibrinolytic activity
inhibits plasmin
clinical use: trauma, CPB, spinal fusion
dosing of amicar
bolus: 5-15g (peds 75-150mg/kg)
infusion: 1-2g/hr (peds 5-30mg/kg/hr)
TXA - tranexamic acid (cylokapron
synthetic analog of lysine that inhibits fibrinolysis by competitively binding to the lysine receptor sites on plasminogen, and this prevents plasmin from binding to and degrading fibrin
good for GI, surgical, Trauma bleeding
2 hour half life
8-10x more potent than amicar
dose of TXA
10-15mg/kg IV (up to 1g) followed by an a gtt of 1-5 mg/kg/hr
cost of 1g = $50
clinical uses of TXA
non-cerebral trauma (only beneficial within the first 3 hours)
pediatrics (spine fusions, craniosynostosis)
ortho (joint procedures)
cardiac (with or without CPB)
OB (massive transfusion algorithm)
CRASH-2 trial
20,011 adults with traumatic bleeding showed that TXA reduces death d/t bleeding with no increase in vascular occlusive events
strong evidence of time to treatment - TXA reduced death d/t bleeding by 1/3 when given within 3h but actually increased risk after 3h
TXA and post partum hemorrhage
WOMAN study showed that death d/t bleeding was significantly reduced in woman given TXA, especially in those given treatment within 3 hours of giving birth
contraindications of TXA
active intravascular clotting (PE, DVT, embolic stroke), anaphylaxis, SAH
precautions for TXA use
decrease dosing in renal patients because renally eliminated
UTI - ureteral obstruction d/t clot formation
hypotension with rapid injection
color vision defect - visual changes can indicated toxicity
seizure disorders - increase seizure risk
concomitant administration with factor concentrates
protamine
simple proteins obtained from salmon sperm
it is positively charged alkaline and combines with negative acidic heparin to form a stable complex without any anticoag activity
protamine dosing
1-1.5mg for every 100u of heparin (over last 2 hours), guided by ACT
protamine adverse responses
hypotension with rapid IV injection d/t histamine release
pulmonary HTN d/t complement activation and thromboxane release = constriction
allergic reaction
options for patients with allergic reaction to protamine
pretreat with histamine receptor antagonist, followed by a slow trial
completely avoid and wait for effect of heparin to wear off (takes hours)
administer alternative to heparin (bivalirudin)
what patients are at risk for a true allergy to protamine
prior protamine reaction allergy to true vertebrae fish exposure to NPH insulin allergy to any drug prior exposure to protamine
DDAVP d-amino-d-arginine vasopressin
aka desmopressin
causes release of endogenous store of vWF
increases platelet adhesion/improves platelet function
dose of DDAVP
0.3 mcg/kg IV infusion over 15-30min - platelet adhesion increases within 30 minutes
DDAVP vs arginine vasopressin
DDAVP is more potent than arginine vasopressin
the change in structure results in decreased ADH and vasopressor action on smooth muscle and increased function of increasing factor VII in patients with vWD
what is the most common side effect of DDAVP
paradoxical hypotension
contraindications for DDAVP
hypersensitivity, renal impairment, hyponatremia
why is hyponatremia a conraindication for DDAVP
overuse can lead to water retention and dilutional hyponatremia with consequent convulsion
can lead to water intoxication/hyponatremia which can be fatal
