This document discusses deep vein thrombosis (DVT) prophylaxis. It notes that the incidence of DVT in critically ill patients ranges widely from 10-80% depending on patient population and diagnosis methods. It identifies several risk factors for DVT including immobility, recent surgery/trauma, older age, sepsis, and central lines. The document describes primary and secondary prophylaxis methods, DVT risk scoring systems, pharmacological and non-pharmacological prophylaxis treatments, and considerations for prophylaxis duration and dosing in critically ill patients. It also discusses heparin-induced thrombocytopenia (HIT) diagnosis and treatment as well as the use of oral anticoagulants for prophyl

1. How to learn DVT
Prophylaxis like a Pro ….
Areej Abu Hanieh
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2. Epidemiology
 occurrence of DVT is 10%–80% Precise
incidence in the critically ill population is
challenging because of inconsistencies
in patient populations, different diagnosis
strategies.
 Rate of DVT , In the absence of
prophylaxis: 30% in medical-surgical
patients, 50%–60% in trauma patients,
up to 80% in orthopedic surgical
patients, and 20%–50% in neurosurgical
patients
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3. Risk Factors
 Malignancy,
 previous VTE
 Immobility
 known thrombophilia
 recent (1 month or less) surgery or
 Trauma
 older age (70 years or older)
 heart or respiratory failure
 sepsis, obesity (body mass index of 30 kg/m2 or more),
 pregnancy
 erythropoiesis-stimulating agents with hemoglobin of 12 g/dL or
more
 hormonal therapy,
 recent transfusions of concentrated clotting factors,
 central venous lines,
 long distance travel
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4. Types of Prophylaxis
 Primary prophylaxis — Primary prophylaxis, the
preferred method for VTE prevention, is carried out
using either drugs (eg, heparin) or mechanical methods
(eg, intermittent pneumatic compression boots) that are
effective for preventing deep vein thrombosis (DVT).
 Secondary prophylaxis — Secondary prevention
involves the early detection and treatment of subclinical
venous thrombosis by screening medical patients with
objective tests that are sensitive for the presence of
DVT. However, it is not commonly used as the efficacy
of available screening methods (eg, contrast
venography, venous ultrasound, MRI venography) is not
well established, used in pregnant women that has high
risk for thrombosis.
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5. DVT Scoring
 There is multiple scoring systems , but
in avarage :
 Score < 4 is low risk
 Score > 4 is high risk
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7. Non pharmacological
Treatments
 Intermittent pneumatic
compression (IPC)
 graduated compression stockings
(GCS)
 venous foot pumps (VFP)
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8.  Low risk patient , acute medical illness and
who are without obvious risk factors for VTE
(eg, young patients admitted for a 12 hour
observation following an episode of syncope
from hypoglycemia),pharmacological
treatments is not recommended .
 Moderate risk patient , an acute medical
illness, who have at least one risk factor for
VTE and do not have an increased risk of
bleeding, we recommend the use of
pharmacologic thromboprophylaxis rather
than mechanical methods or no prophylaxis.
 High risk patient , (eg, critically-ill, cancer,
stroke) and at low risk of bleeding, we
recommend the use of pharmacologic
thromboprophylaxis rather than mechanical
methods or both . 8

9. VTE prevention for non-
orthopedic surgery
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11. Heparin-induced thrombocytopenia
 HIT is a severe, immune-mediated
reaction potentially leading to life-
threatening complications such as
myocardial infarction, skin necrosis,
stroke, and VTE.
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12. Frequency of HIT
 Higher in patients receiving
unfractionated heparin compared with
low-molecular-weight heparin .
 Higher risk in cardiac or orthopedic
surgical patients receiving
unfractionated heparin (15%) than in
medical patients (0.1%–1%).
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13.  Alternative causes of
thrombocytopenia in critically ill
patients include extracorporeal
devices like dyalisis , intra-aortic
balloon pumps, sepsis, disseminated
intravascular coagulation caused by
sepsis , bleeding, and medications.
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14. Diagnosis of HIT
 Suspected when a patient has a decrease in
absolute platelet count to less than
150,000/mm3 or a relative decrease of at
least 50% from baseline, skin lesions at
injection sites, or systemic reactions after
intravenous boluses.
 Typical onset is 5–10 days after heparin
exposure, though onset can be delayed and
occur up to 3 weeks after therapy cessation .
 Recent heparin exposure may result in rapid-
onset HIT, occurring within hours after
rechallenge.
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15. Laboratory testing
 GTI-PF4 (Genetic Testing Institute, Waukesha,
WI) and ID-PaGIA.
 Antibody present if sample from patient binds to
the heparin-PF4–coated wells.
 High sensitivity (greater than 90%) and low to
moderate specificity
 (a) Clinically insignificant HIT antibodies are often
detected among patients who have received
heparin 5–100 days earlier.
 (b) Detects a range of immunoglobulin IgA and
IgM antibodies that are not pathogenic.
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16. Functional assays
 Heparin-induced platelet aggregation (HIPA) and
C14 serotonin release assay.
 Detect platelet activation in the presence of
heparin, Patient serum is mixed with washed
platelets from healthy volunteers and low and
high concentrations of heparin. In the presence
of HIT antibodies, platelets are activated in low
concentrations of heparin and detected using
radioactive serotonin (serotonin release assay)
or visually (HIPA).
 It is high sensitivity and specificity but not always
available and expensive .
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17. Treatment of HIT
 Immediately discontinue all sources of heparin, and
initiate an alternative non-heparin anticoagulant.
 Parenteral direct thrombin inhibitors (bivalirudin ,
Dabigatran) are the agents of choice for anticoagulation
in acute HIT because they have no cross-reactivity with
heparin.
 Some studies support the use of the factor Xa inhibitor
fondaparinux for the treatment of HIT, though there are
reports of fondaparinux-induced HIT.
 Parenteral direct thrombin inhibitors are associated with
a higher rate of major bleeding complications than is
unfractionated heparin
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18.  Initiate warfarin once the platelet count
has recovered and is within normal
limits (at least 150,000/ mm3 ) and
after at least 5 days of therapy with an
alternative anticoagulant. Alternatively,
conservative warfarin dosing may
begin once the platelet count is
recovering. If a patient is receiving
warfarin at the time of HIT diagnosis,
reversing with vitamin K is
recommended.
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19.  Argatroban dosing in the critically ill
population :
 i. Mean dose in critically ill patients was 0.24
± 0.16 mcg/kg/minute and 0.22 ± 0.15
mcg/kg/ minute in critically ill patients with
multiple organ dysfunction.
 ii. In patients with severe liver impairment,
consider 0.5 mcg/kg/minute.
 iii. Target aPTT is 1.5–3 times baseline.
 f. Bivalirudin dosing in the critically ill
population
 i. Dose reduced to 0.05–0.1 mg/kg/hour,
depending on renal function and bleeding
risks
 ii. Target aPTT is 1.5–2.5 times baseline. 19

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21. Duration of Prophylaxis
 VTE prophylaxis should ideally
continue until the patient is ambulatory
or discharged from the hospital.
 Thromboprophylaxis is typically not
administered in chronically
immobilized patients residing at home
or in a nursing home.
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22. In Critically ill patients TIPS
 Routine screening for VTE with
ultrasonography is not recommended.
 Dosing frequency of low-dose unfractionated
heparin (twice vs. thrice daily).
 The bioavailability of subcutaneously
administered drugs is reduced in critically ill
patients with the concomitant use of
vasoactive drugs or the presence of edema,
thereby potentially providing a reduced effect.
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23.  Patients at high risk of bleeding with a
moderate to high risk of VTE may be
considered for mechanical VTE
prophylaxis; however, pharmacologic
prophylaxis should be reassessed
when the bleeding risk is no longer
present.
 An inverse relationship between body
weight and anti-factor Xa (anti-Xa)
concentration may exist in patients
with obesity; however, the risk of VTE
and optimal anti-Xa concentrations to
achieve is unclear !! 23

24. Oral Anticoagulants for VTE
Prophylaxis
 No studies to date of critically ill ICU patients with direct
thrombin inhibitors (dabigatran) or factor Xa inhibitors
(rivaroxaban, apixaban, edoxaban)
 Rivaroxaban is noninferior to standard treatments in
other settings such as orthopedic surgery.
 Rivaroxaban 10 mg orally once daily was compared
with enoxaparin 40 mg subcutaneously daily for 10
days, increased bleeding rates occurred in the
rivaroxaban group.
 Low-molecular-weight heparin is preferred to vitamin K
antagonists such as warfarin for prophylaxis; however, it
may be used in patients who refuse injections.
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