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why are ESRD pts at increased bleeding risk at baseline
due to platelet dysfunction
ACs accumulate in ESRD
why are ESRD pts at increased thrombotic risk
chronic activation of clotting cascade
increasing homocysteine
decreased levels of protein C and S
are ESRD pts at increased bleeding risk, increased thrombotic risk, or both?
both
ESRD preferred (green) anticoags
A War Is Underway
apixaban
warfarin
IV UFH → minimal renal metabolism/elimination
ESRD cautious (yellow) anticoags
Lookout Soldiers
LMWH
SQ UFH
ESRD anticoags to avoid (red)
Avoid RED Flags
rivaroxaban
edoxaban
dabigatran
fondaparinux → CI! primarily renally cleared
monitoring for enoxaparin (LMWH) in ESRD - when is steady state
4-5 doses
monitoring for enoxaparin (LMWH) in ESRD - dose
0.7-1.0 mg/kg/qd
monitoring for enoxaparin (LMWH) in ESRD
check trough or peak?
when do you check ^?
goal for VTE tx?
check a trough level
check 30-60mins prior to next dose
trough goal for VTE tx: less than 0.5 u/mL
if we’re checking a trough level, what are we worried abt?
poor CL
if we’re checking a peak level, what are we worried abt?
efficacy
preferred (green) anticoags in pregnancy
Pregnant Lions Isolate
LMWH (enoxaparin)
IV UFH
anticoags to be cautious with in pregnancy (yellow)
Caution With Fetal Safety
SQ UFH
Warfarin
assess risks/benefits
max 5mg dose
fondaparinux
can cross placenta
only use if can’t take LMWH/UFH
anticoags to avoid in pregnancy (red)
DOACs (insufficient data)
enoxaparin monitoring in pregnancy - dosing
start off with 1mg/kg q12h
may need to increase to 8h dosing
enoxaparin monitoring in pregnancy
check peak or trough?
when do we check?
peak
~4 hrs after dose (steady state)
when is steady state for enoxaparin
4-5 doses
preferred anticoags in cancer (green)
(including which is preferred in pts with and without GI lesions)
Cancer Is Ugly; either it Applies, or you Lie
IV UFH
apixaban
preferred for pts without GI lesions
LMWH
preferred for patients with GI lesions
anticoags to be cautious with in cancer (yellow)
RED
rivaroxaban
edoxaban
dabigatran
as effective as rivar/edoxaban as VTE recurrence prevention
but increases GI bleeds
anticoags to avoid in cancer (red)
warfarin
if possible; may be cheapest option though :/
where are most coagulation cascade factors made
liver
which coagulation cascade factors are NOT made in the liver
factors VIII (8) and XIII (13)
factors that contribute to cirrhosis
coagulation factor deficiencies
vitamin K deficiencies → malnutrition
thrombocytopenia
reduced platelet function
decreased protein C, S
decreased AT
preferred anticoags in cirrhosis (green)
Cirrhosis Enters In Undetected
enoxaparin
IV UFH
anticoags to be cautious with in cirrhosis (yellow)
warfarin
if INR is not significantly elevated at baseline
fondaparinux
anticoags to avoid in cirrhosis (red)
DOACs
very limited evidence
CYP (liver) metabolism
VTE risk factors in obese pts
endothelial dysfunction
platelet dysfunction
stasis
inflammation
preferred anticoags in obesity (green)
Obesity Is Underestimated And Really Widespread
IV UFH
apixaban
rivaroxaban
warfarin
anticoags to be cautious with in obesity (yellow)
FEED
fondaparinux
enoxaparin
edoxaban
dabigatran
monitoring for LMWH (enoxaparin) in obesity - dosing & max dose
0.7-1.0 mg/kg/q12h
max dose = 120-150mg
monitoring for LMWH (enoxaparin) in obesity
check peak or trough level?
when do we check ^?
goal for VTE tx?
peak (worried abt efficacy)
check 4 hrs after dose (steady state 4-5 doses)
peak goal for VTE tx: 0.6-1 u/mL
why is there increased thrombotic risk in APS
APS ABs → endothelial damage
APS preferred (green) anticoags
APS Will Leave Us
warfarin
LMWH
IV UFH
anticoags to be cautious with in APS (yellow)
fondaparinux
limited data
anticoags to avoid in APS (red)
avoid DOACs
increased thrombotic risk