VTE/PE Flashcards
1
Q
Why is VTE and PE so important?
A
VTE is a major cause of morbidity & mortality
-more deaths than breast cancer, HIV, and vehicle accidents combined
-50% attributed to hospitalization
10% of hospital deaths due to PE
average cost per VTE=$10k-$30k
affects approximately 100,000 Canadians/yr
2
Q
True or false: VTE treatment and prophylaxis is the same as atrial fibrillation or secondary prevention of MI/stroke
A
false
not the same
3
Q
Provide some characteristics of veins.
A
returns blood to the heart for re-oxygenation
thinner walled than arteries
elastic (variably widens as blood passes through)
lower shear rate than arteries
one-way valves close to prevent backflow (damage=pooling)
4
Q
Differentiate between a venous thrombus and an arterial thrombus.
A
venous thrombus
-formed without damaging vessel wall
-held together mostly by fibrin, less platelet
-leads to VTE (DVT/PE)
arterial thrombus
-formed from rupture of atherosclerotic plaque
-held together by mostly platelets, less fibrin
-leads to ACS, stroke, or PAD
5
Q
What is a venous thromboembolism?
A
results from clot formation within venous circulation
mainly develops in lower extremities
-majority in calf veins
-minority in arms, brain, GI tract, liver
6
Q
After a venous thrombus is formed, what are some possibilities that could occur next?
A
lyse
obstruct venous circulation
embolize
combination of the above
7
Q
Briefly describe the physiology of coagulation.
A
central to the coagulation is the generation of thrombin
-factor IIa
thrombin is made from prothrombin by factor Xa
prothrombin–>thrombin–>fibrinogen–>fibrin clot
8
Q
What is Virchows triad?
A
risk factors for VTE
-stasis
-vessel wall injury
-hypercoagulability
9
Q
Describe circulatory stasis as a risk factor for VTE.
A
bed rest/immobility (prolonged)
heart failure (class III-IV)
varicose veins (controversial)
atrial fibrillation
10
Q
Describe vascular damage as a risk factor for VTE.
A
previous VTE
bacterial infection (sepsis)
prosthetic implants
peripheral vascular disease
trauma
surgery (mainly hips and knees)
11
Q
Describe hypercoagulability as a risk factor for VTE.
A
medications
use of oral contraceptives
malignancy
inherited thrombophilias (factor V leiden gene)
advanced age >60 (esp >75)
obesity (esp >50)
protein C or S deficiency
smoking
12
Q
Describe pregnancy as a risk factor for VTE.
A
5-10x increase during pregnancy
15-35x increase during early postpartum (6-12wks)
13
Q
What are some medications that increase the risk for VTE?
A
estrogen
-CHC has RR of 2 but ARI is 0.04% and NNH is 2500
SERMS (tamoxifen/raloxifen)
chemotherapy
older antipsychotics
erythropoeitin
14
Q
What is the clinical presentation of VTE?
A
often asymptomatic
symptoms are often non-specific
-diagnosis is difficult
-requires assessment of risk factors and lab/imaging
15
Q
What are the symptoms of DVT?
A
leg pain (90%)
tenderness
ankle edema
calf swelling
dilated veins
dusky discolouration
16
Q
What are the symptoms of PE?
A
sudden, unexplained SoB
tachypnea
tachycardia
unexplained chest pain/discomfort
cough
hemoptysis
fever
cyanosis
syncope
sense of impending doom
17
Q
What are the complications of VTE?
A
recurrence rates are high
post-thrombotic syndrome
venous ulcers
chronic thromboembolic pulmonary hypertension (CTEPH)
18
Q
Describe PTS as a complication of VTE.
A
sx: chronic pain, edema, fatigue, and leg ulcers
20-50% of DVT sufferers will develop within 3-6mo
possible treatment: compression stockings
-ankle to knee
-30 to 40mmHg at ankle at onset of DVT
-may decrease incidence of PTS
19
Q
Describe venous skin ulcers as a complication of VTE.
A
results from venous insufficiency, leading to pooling of blood
major cause of chronic wounds
lack of proper blood flow
20
Q
Describe CTEPH as a complication of VTE.
A
can occur after a PE
causes scarring in lungs
-narrows the arteries and leads to a permanent increase in pulmonary blood pressure, may lead to right-side HF
requires anti-coagulation for life
21
Q
What are the ways that VTE is diagnosed?
A
lab tests
-D dimer increase
-ESR and WBC count increase
clinical prediction score
-Wells criteria
imaging
-compression, ultrasonography
-CT scan
-ventilation/perfusion scan
22
Q
What are the goals of therapy for VTE?
A
prevent initial VTE
resolution of signs and symptoms
prevention of extension of VTE (prevention of PE in pts with DVT)
prevention of hemodynamic collapse and/or death
prevention of recurrence of VTE in select patients
prevent the development of CTEPH or PTS
reduce the risk of adverse effects from pharm treatment
23
Q
What is PT?
A
prothrombin time
-measures the extrinsic and common pathway for coagulation (factor 10, 5, 7, 2)
-tests heparin
24
Q
What is aPTT?
A
activated partial thromboplastin time
-measures the intrinsic and common pathways of coagulation
-longer time means less clotting
-tests heparin, not for LMWH
25
What does anti-Xa activity test for?
tests LMWH and heparin
26
What is the INR?
international normalized ratio
-standard measure of anticoagulant activity of warfarin
-only validated for warfarin, other anticoags will change it but does not accurately reflect it
-PT/PT reference
27
What is the difference between PT and aPTT?
both measure the intrinsic and common pathways but aPTT uses an activator to speed up clotting time, creating a narrower reference range to aim for (more sensitive)
28
What are the challenges of preventing and treating VTEs?
precise dosing of anticoagulants
monitoring properly
balance bleed risk vs clotting risk
bleeding is the predominant adverse event
-tends to increase with the intensity and duration of therapy
potential drug interactions
drug/disease interactions
patient issues: compliance, administration
clinician assessment and appropriate prophylaxis
29
What are the drugs used for VTE?
heparin
low molecular weight heparin
heparinoids (danaparoid)
glycosaminoglycan heparinoid (fondaparinux)
direct thrombin inhibitor (argatroban)
vitamin K antagonist (warfarin)
direct oral anticoagulants
30
What is the MOA of unfractionated heparin?
catalyzes antithrombin-->inactivates factor IIa and IXa, Xa, XIa & XIIa
prolongs aPTT
cannot bind to thrombin already in a clot
also binds to cells and other plasma proteins (unpredictable PK/PD)
31
What is the onset of effect for UFH?
IV: beings working immediately
SC: 30-60min
32
What is the duration of effect for UFH?
t1/2=1-2hrs
IV: continuous infusion to ensure level response
SC: 8hrs
33
What are the contraindications for UFH?
*not absolute CI*
active bleeding or conditions that increase bleed risk
-hemorrhagic stroke, severe HTN, active gastric ulcer, haemophilia
injuries and operations to brain, spinal cord, eyes/ears
severe thrombocytopenia
prior occurrence of HIT (this is an absolute CI)
34
Describe the dosing and administration of UFH.
IV or SC only
initial doses calculated using body weight
prophylaxis: 5000 units SC q8-12h
treatment:
-IV: LD 80 units/kg over 10min; then 18 units/kg/hr
-SC: 250 units/kg q12h
*both: adjust dose until aPTT is 1.5-2.5x baseline*
35
Does UFH have a wide or narrow therapeutic window?
narrow
36
How long is heparin used?
<7 days
-simultaneously given with warfarin
-discontinued once warfarin reaches target INR for 1-2 days
37
What are the common adverse effects of heparin?
minor bleeds
injection site reactions if subcut
transient, mild liver enzyme increase
38
What are the serious adverse effects of heparin?
heparin induced thrombocytopenia
major bleeds
hyperkalemia
skin necrosis
BMD decrease
39
What is the antidote to major bleeds from heparin?
IV protamine sulfate
-1 to 1.5mg neutralizes 100U of heparin if heparin was in last 29 minutes
-0.5 to 0.75mg neutralizes 100U of heparin if heparin was in last 30-120 minutes
-0.25 to 0.375mg neutralize 100U of heparin if heparin was given over 120 minutes ago
40
Describe heparin induced thrombocytopenia.
immune-mediated platelet aggregation reaction
-causes platelets to activate and stick together
-increased thrombotic and bleed risk
onset typically occurs 5-10 days after heparin initiation
depends on prior heparin exposure
41
Describe the 4T score.
thrombocytopenia:
-2 pts=>50% fall or nadir >20 x 10 to the 9/L
-1 pt=30-50% fall or nadir 10-19 x 10 to the 9/L
-0 pts=<30% fall or nadir <10 x 10 to the 9/L
timing of the decrease in platelet count:
-2 pts=days 5-10, or < day 1 with recent heparin (past 30d)
-1 pt=>day 10 or timing unclear, or <1 day if heparin exposure within past 30-100d
-0 pts=
42
What is the treatment of HIT?
discontinue all sources of heparin
begin alternate anticoagulation
-warfarin initially unsuitable
-argatroban, fondaparinux, danaparoid, bivalirudin
-transition to warfarin once platelets restored and minimum x 5 days
-DOACs in stable pts with medium risk of bleed (rivaroxaban 15mg BID until platelets restored, 15mg BID x 21d then 20mg daily thereafter)
43
What are the drug interactions of UFH?
ACE/ARBs (hyperkalemia)
antiplatelets (increased anti-coagulation)
ASA/NSAIDs (increased anti-coagulation)
estrogens/progestins (pro-thrombotic)
herbs (194 have anti-coagulant properties)
potassium salts/sparing diuretics
44
Describe monitoring for UFH.
effectiveness
-must monitor aPTT (VTE tx, not prophylaxis)
-see validated nomograms
safety
-platelet count (get baseline if possible, if >4d of therapy then check qod until finished, if prev UFH exposure check at baseline and q24h)
-Hgb and hematocrit (baseline and q3d)
-potassium (only if high risk of hyperkalemia; baseline & q3d x 1wk)
45
Which are examples of low-molecular weight heparin?
enoxaparin
dalteparin
tinzaparin
nadroparin
*all appear equal clinically in safety and efficacy*
*not interchangeable*
*different dosing regimens*
46
What is the MOA of LMWH?
same as heparin but higher affinity for Xa
can affect aPTT
cannot bind to thrombin already in a clot
more predictable PK compared to UFH (allows for fixed doses and adjustment based on labs)
47
Which LMWH is of choice in the SHA?
tinzaparin
-prophylaxis and treatment of VTE
-dialysis line patency
*enoxaparain used for acute ACS*
48
What are the contraindications of LMWH?
same as UFH
49
Describe dosing and administration of LMWH.
subcut administration
prophylaxis:
-tinzaparin 75 units/kg
-okay down to CrCl 20ml/min
treatment:
-tinzaparin 175 units/kg
-okay down to CrCl of 30ml/min
dialysis line patency:
-tinzaparin 2500 units
*no renal dose adjustment*
50
Describe LMWH use in pregnancy.
altered metabolism of LMWH throughout course of pregnancy, especially in the 3rd trimester
opinion differs:
-weight at the beginning and go
-weigh every trimester and adjust dose?
-anti Xa levels
-switch to UFH at 36 wks (SC q12h)
51
What is the onset of effect for LMWH?
starts in one hour
peak anti-coagulation response in 3-5h
52
What is the duration of effect for LMWH?
anti-Xa activity persists for 12-24h with a SC dose
half-life is only 3-6h
53
What are the common adverse effects of LMWH?
same as UFH, but much lower incidence
54
What are the serious adverse effects of LMWH?
same as UFH, but risk of HIT is dramatically lower
55
What are the drug interactions of LMWH?
same as UFH
56
Describe the monitoring for LMWH.
efficacy:
-cannot use aPTT
-monitoring anti-Xa levels not indicated unless obese, pregnant, renal insufficiency
safety:
-platelet count (baseline if possible, if on therapy for >4d then check qod until finished, previous heparin exposure get baseline and after 24h)
-Hgb and hematocrit
-potassium (only if high risk of hyperkalemia; baseline & q3d x 2 then weekly thereafter)
-renal function
57
What is the MOA of heparinoids (danaparoid), glycosaminoglycan (fondaparinux), and direct thrombin inhibitor (argatroban)?
inhibits factor Xa (fondaparinux, danaparoid) or directly inhibits thrombin (argatroban)
58
What is the indication for danaparoid?
prevention of DVT after surgery, or use in HIT
59
What is the indication for fondaparinux?
same as LMWH, plus use in HIT
60
What is the indication for argatroban?
anticoagulation in patients with HIT
61
What are the advantages of fondaparinux?
no cases of HIT reported
possibly superior in preventing recurrent events
even less variability with dose-response
no monitoring
obesity dose better studied
62
What are the disadvantages of fondaparinux?
possible increase in major bleeds with high doses
no antidote
longer half-life
can only use to CrCl of 30ml/min
63
What are the advantages of danaparoid and argatroban?
specifically studied to treat HIT
no cases of HIT
no adjustment in obesity needed
can use in severe renal impairment
64
What are the disadvantages of danaparoid and argatroban?
no antidote
limited pregnancy experience
65
What is the MOA of warfarin?
vitamin K antagonist
interferes with production of clotting factors dependent on vitamin K (X, IX, VII, II) and protein C and S
66
What is the onset of effect for warfarin?
not immediate (must clear vitamin K clotting factors from circulation)
takes 2-7 days (avg 3-5)
offset also takes a similar time
67
What are the contraindications to warfarin?
pregnancy
high risk of bleed where benefit of anticoagulation is less than risk of bleeding
previous skin reaction to warfarin
68
What are the options for initiating warfarin?
option 1: begin at 2-3mg OD x 2d
option 2: begin at 5mg OD x 2d
option 3: beging at 10mg OD x 2d
then adjust dose on day 3
69
How do we deal with subtherapeutic or supratherapeutic INRs?
step 1:
-determine indication and target INR
-any symptoms of high or low INR?
step 2:
-if no issues above; is the pt at risk of having those issues develop?
step 3:
-determine if sub/supratherapeutic INR is from a permanent or transient cause
70
Describe the bridge to warfarin therapy.
delayed onset
must assess how critical rapid anti-coagulation is needed
starting warfarin:
-initiate warfarin and UFH or LMWH simultaneously
-overlap for at least 5 days AND until INR is >2 for 2d
71
When do we bridge to warfarin therapy?
during initial treatment of VTE
for prevention of VTE after high-risk procedure
for a patient at high risk of VTE or arterial emboli undergoing surgery
72
Describe bridging off warfarin therapy.
warfarin has a delayed offset
must assess risk of thrombosis for stopping anticoagulation vs bleed risk for continuing during surgeries
-stop warfarin 3-5 days prior; wait until INR drops <1.5
-begin UFH or LMWH once INR <2
-->stop UFH 4-5h before surgery; LMWH 24hrs
-resume UFH or LMWH 24hrs after surgery, alongside warfarin
73
What are the common side effects of warfarin?
minor bleeds (gums, shaving, cuts, bruises)
abdominal cramps
diarrhea
nausea
skin reactions, hives (rare but not serious)
74
What are the serious side effects of warfarin?
major bleeds
-intracranial hemorrhage
purple toe syndrome
skin necrosis
75
What are the 8 major classes of interacting drugs for warfarin?
antibiotics
antifungals
antidepressants
antiplatelets
amiodarone
anti-inflammatory agents
acetaminophen
alternative remedies
corticosteroids
*any 2C9 inhibitor/inducer will have strong effect*
*648 documented food and drug interactions*
*acute drugs most risky*
76
Describe the antibiotic-warfarin interaction.
all impact warfarin by decrease in vitamin K
some also inhibit warfarin metabolism significantly
-ciprofloxacin
-clarithromycin
-erythromycin
-metronidazole
-TMP/SMX
77
How do we manage drug interactions for warfarin?
empiric dose adjustment to warfarin is often more risky and unpredictable than the DI
check INR again in 4-6 days and adjust dose in response
some warfarin DIs cannot be monitor for
-NSAID, antiplatelet, hormone therapy
-must balance risk of bleed or clot with benefit of therapy
78
Describe monitoring for warfarin.
safety/efficacy
-signs of major bleeds
-INR on day 3 & 5-->twice weekly x 1wk-->weekly until stable for 2 wks-->q2w until stable x 1 month-->monthly
-check in 4-6d after dose change or other issue
79
What are some clinical tips regarding warfarin?
warfarin thrives on consistency
-many DIs
-many food interactions
easiest piece of advice to give patients:
-dont start any new meds/OTC/herbals or make any drastic changes in your diet without consulting a pharmacist/MD
80
What is the antidote for warfarin?
vitamin K
-bleed or extremely elevated INR (>10), vitamin K IV or oral is given
-2.5-5mg orally will reduce INR in 24-48hrs
if serious bleed, regardless of INR
-hold warfarin
-give vitamin K 5-10mg IV q12h
-give factor IV prothrombin complex or FPP
81
What is the MOA of the DOACs?
rivaroxaban, apixaban, edoxaban
-inhibit factor Xa
dabigatran
-directly inhibits thrombin
82
What is the onset of effect for the DOACs?
all achieve peak anti-coagulation in about 2hrs
83
What is the duration of effect for the DOACs?
rivaroxaban: t1/2 9h
apixaban: t1/2 8-14h
dabigatran: t1/2 13h, up to 18h in renal impairment
edoxaban: t1/2 14h
84
True or false: there are renal dose adjustments for the DOACs
false
its all or none
85
What are the drug interactions of the DOACs?
antiplatelet properties (ASA, NSAIDs, antidepressants)
estrogens/progestins
strong 3A4 and P-gp inducers
-carbamezepine, phenytoin, rifampin, St Johns Wort
strong 3A4 and P-gp inhibitors
-ketoconazole, itraconazole, ritonavir, clarithromycin, fluconazole, dronedarone
strong 3A4 inhibitors
-HIV protease inhibitors
strong p-glycoprotein inhibitors
-cyclosporine
86
Which DOACs are unaffected by the CYP drug interactions?
dabigatran and edoxaban
87
True or false: dabigatran is unaffected by anything that raises pH
false
affected by anything that raises pH
88
What is the dosing of the DOACs for prevention of VTE after TKR/THR?
rivaroxaban: 10mg daily
-35 days (hip), 14 days (knee)
apixaban: 2.5mg BID
-35 days (hip), 14 days (knee)
dabigatran: 110mg STAT, then 220mg daily
-35 days (hip), 10 days (knee)
-reduce to 150mg OD if >75yo
edoxaban: N/A
89
What is the dosing of DOACs for VTE treatment?
rivaroxaban
-15mg BID CC x 3wks; then 20mg OD x 3-6months
apixaban
-10mg BID x 7d; then 5mg BID x 3-6months
dabigatran
-must receive 5-10d of SC anti-coag; then begin prevention dosing
edoxaban
-60mg OD (after bridging x 5-10d)
-<60kg: 30mg
90
What is the dosing of DOACs for prevention of recurrent VTE?
rivaroxaban
-6 months after tx dose; 10-20mg daily with food
apixaban
-6 months after treatment dose; 2.5mg BID
dabigatran
-150mg BID; consider 110mg BID if bleeding risk
edoxaban
-60mg OD (after bridging x 5-10d)
-<60kg: 30mg
91
Describe DOAC dosing in obesity.
BMI <40 or <120kg: standard dosing
BMI >40, or >120kg: can use, but patient must understand potential unknown risks
-avoid dabigatran & edoxaban
-avoid in acute setting after bariatric surgery
92
What are the common side effects of DOACs?
minor bleeding
GI upset and dyspepsia (dabigatran more)
diarrhea or constipation
itch
93
What are the serious side effects of DOACs?
bleeding
-mostly better or same as warfarin
94
What are examples of thrombolytics?
alteplase and tenecteplase
-strong clot busters
95
Where do thrombolytics fit in for DVT?
benefit
-more rapid and complete lysis of DVT, less PTS
risk
-more major bleeding
-other anticoagulation has similar rates of recurrence and overall mortality
only VTE indication: high risk PE
96
What is the duration of treatment for VTE provoked by a transient risk factor?
first: 3 months
second: same as for first
97
What is the duration of treatment for VTE associated with ongoing non-cancer related risk factors?
indefinite therapy with periodic reviews or as long as risk factor persists
97
What is the duration of treatment for unprovoked VTE?
first: minimum 3 months and then reassess
-with low-mod bleed risk: indefinite therapy
-with high bleed risk: 3 months
second: same as for first
98
What is the duration of treatment for cancer-associated VTE?
minimum 3 months then reassess
99
Describe the switch from heparin to the DOACs and LMWH.
apixaban: stop infusion and start apixaban at the same time
dabigatran: stop infusion and start dabigatran at the same time
edoxaban: stop the infusion and start edoxaban 4h later
rivaroxaban: stop infusion and start rivaroxaban at same time
LMWH: stop infusion and start LMWH at same time
100
Describe the switch from LMWH to DOACs.
apixaban: start at same time as next scheduled dose of LMWH is due
dabigatran: start 0-2h before the next dose of LMWH is due
edoxaban: start at same time the next scheduled dose of LMWH is due
rivaroxaban: start 0-2h before next dose of LMWH is due
101
Describe the switch from DOAC to parenteral.
apixaban:
-UFH: stop apixaban and start UFH at time next dose of apixaban is due
-LMWH: stop apixaban and give LMWH at time next dose of apixaban is due
dabigatran
-UFH: CrCl>30 wait 12hrs after last dose of dabigatran, CrCl <30 wait 24hrs after last dose of dabigatran
-LMWH: same as UFH
edoxaban:
-UFH: dc edoxaban and start UFH at next scheduled dose of edoxaban
-LMWH: dc edoxaban and start LMWH at next scheduled dose of edoxaban
rivaroxaban:
-UFH: stop rivaroxaban and start UFH at next scheduled dose of rivaroxaban
-LMWH: stop rivaroxaban and give LMWH at next scheduled dose of rivaroxaban
102
Describe the switch from warfarin to DOAC.
to rivaroxaban:
-stop warfarin, wait until INR <2.5
to dabigatran/edoxaban/apixaban:
-stop warfarin, wait until INR <2.0
103
Describe the switch from DOAC to warfarin.
from rivaroxaban/apixaban:
-use both concurrently, test INR on day 3, then each day prior to dose, once INR >2.0 can dc DOAC
from dabigatran/edoxaban:
-if CrCl >50ml/min, start warfarin 3d before dc
-if CrCl 30-50ml/min, start warfarin 2d before dc
104
What is the most important patient safety strategy in patients admitted to the hospital?
thromboprophylaxis
-PE is the leading cause of preventable in hospital death
-risk depends on medical vs surgical admission
105
What are the reasons for no VTE prophylaxis?
on therapeutic anticoagulation
fully mobile and expected length of stay less than 48hrs
palliative/compassionate terminal care/end of life care
no acute medical conditions and awaiting placement in LTC
psychiatric admission with no known VTE risk factors
106
What are the agents used for VTE prophylaxis in the SHA?
tinzaparin
heparin
mechanical
107
What are examples of mechanical devices for VTE prophylaxis?
graduated compression stockings
intermittent pneumatic compression device
108
What is the VTE risk for air travel?
0.5% for flights <12hrs
1.5-10% for flights >24hrs
risk is elevated for up to 2-8wks post-travel
*almost all who have a VTE during travel had many risk factors for VTE*
109
What are the recommendations for those who have VTE risk factors when travel is >6hrs?
compression stockings
frequent ambulation
flexion of ankles and knees
hydration
110
Is pharmacologic prophylaxis needed for air travel?
pharmacologic prophylaxis NOT needed
highest risk individuals may receive LMWH
other antiplatelets or anticoagulants have no proven value
111
Which anticoagulants cannot be used in pregnancy?
warfarin (teratogenic)
DOACs have not been studied
112
What are the treatment choices for VTE during pregnancy and post-partum?
UFH
LMWH
danaparoid/fondaparinux?
*multi-dose heparin preparations have benzyl alcohol as a preservative; must select preservative free options*
113
List some tips regarding VTE treatment in pregnancy and post-partum.
initiate treatment as soon as pregnancy occurs
if already on anti-coagulation, switch to safer alt
monitoring same as regular anti-coagulation
doses usually increase throughout pregnancy
114
What are the three types of dosing protocols for VTE and pregnancy/post-partum?
prophylactic dosing (low, fixed)
intermediate dosing (adjust upwards based on weight)
therapeutic dosing (full dose, weight adjusted)
*which dosing to use depends on clot risk*
115
Which agent should be used at 36-37 weeks of gestation?
switch to UFH
116
How long after delivery should anticoagulation be initiated?
4-6hrs
117
How long should anticoagulation continue for after delivery?
at least 6 weeks post-partum
118
What are the complications from VTE treatment during pregnancy and post-partum?
bleeds
HIT
-lower incidence in pregnancy
-platelets decrease in pregnancy
bone loss
119
What is the takeaway regarding malignancy and thrombosis?
malignancy poses pro-thrombotic factors as well as bleeding risks
120
What is the treatment for cancer associated thrombosis?
LMWH is the DOC historically
evidence for DOAC usage
-not in GI/GU malignancy
duration depends on provoking factors
121
What are some considerations for treatment of cancer associated thrombosis?
drug interactions with chemotherapy
renal impairment
thrombocytopenia
dosing in underweight cancer patients?
ICH risk in brain cancers
