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LWMH is superior on UFH Aspirin and warfarin should not be used as primary agents
A rare manifestation is delayed-onset HIT, affecting patients exposed to heparin in the recent past (prior 2 weeks) who present with a new thrombosis and low platelet counts
the meaning of high sensitivity and low specificity : they are good for catching actual cases of the disease but they also come with a fairly high rate of false positives
Deep Vein Thrombosis - DVT
How to learn DVT
Prophylaxis like a Pro ….
Areej Abu Hanieh
occurrence of DVT is 10%–80% Precise
incidence in the critically ill population is
challenging because of inconsistencies
in patient populations, different diagnosis
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
recent (1 month or less) surgery or
older age (70 years or older)
heart or respiratory failure
sepsis, obesity (body mass index of 30 kg/m2 or more),
erythropoiesis-stimulating agents with hemoglobin of 12 g/dL or
recent transfusions of concentrated clotting factors,
central venous lines,
long distance travel
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.
There is multiple scoring systems , but
in avarage :
Score < 4 is low risk
Score > 4 is high risk
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
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
HIT is a severe, immune-mediated
reaction potentially leading to life-
threatening complications such as
myocardial infarction, skin necrosis,
stroke, and VTE.
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%).
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.
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
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
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
(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.
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 .
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
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
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
Argatroban dosing in the critically ill
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
i. Dose reduced to 0.05–0.1 mg/kg/hour,
depending on renal function and bleeding
ii. Target aPTT is 1.5–2.5 times baseline. 19
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.
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.
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
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
Oral Anticoagulants for VTE
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
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.