HIT Flashcards

1
Q

HIT type 1

A

see acute drop in platelets within 48 hours and mild transient effect of heparin on platelets.

Plts rarely drop less than <100K and recovers spontaneously regardless of stopping heparin or continuing it.

normalization is quick and not tx is needed.

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2
Q

is HIT type 1 clinically significant?

A

no, because not associated with VTE

heparin should not be discontinued with HIT type 1

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3
Q

HIT type 2 is

A

clinically relevant and an immune mediated disorder that causes platelet aggregation and thrombosis and this disorder results in thrombocytopenia 5 to 10 days after heparin exposure

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4
Q

4 t score is based of probability for HIT type 2

A

worse things would be degree of thrombocytopenia (50% or nadir <20K)
timing of drop (onset 5-10 days or <1 day if prior heparin exposure in last 30 days)
thrombosis (confirmed new thrombosis, skin necrosis or reaction after IV heparin bolus)
AND most importantly no apparent cause for these symptoms

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5
Q

which antibiotic can cause thrombocytopenia?

A

ceftriaxone and zosyn

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6
Q

When does HIT 2 see changes in thrombocytopenia

A

5-14 days after heparin therapy or within 24 hrs of heparin re exposure (rapid onset HIT)

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7
Q

highest risk factors for HIT 2 is

A

type of heparin exposure (highest risk is unfractionated heparin)
duration of tx
gender (higher in women)
trauma severity (higher risk in surgical pts)

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8
Q

When to suspect HIT2?

A

platelets decrease >50% from baseline 5-14 days after starting heparin and new onset unexplained thrombocytopenia and thrombosis after heparin treatment

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9
Q

4T score for HIT evaluation stand for

A

thrombocytopenia
timing
thrombosis
and oTher causes

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10
Q

Diagnosis of HIT 2 is confirmed with

A

serotonin release assays (preferred) and heparin induced platelet aggregation assays and solid phase immunoassays with ELISA for heparin PF4 complexes.

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11
Q

Management of suspected HIT2

A

all forms of heparin must be stopped (including low molecular weight heparin like enoxaparin)

Should get alternate form of rapid acting AC as they are high risk for thrombosis like argatroban, bivalirudin or fondaparinux

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12
Q

Clinical observation without alternate AC therapy is only recommended in

A

high bleeding risk pts. HIT increases risk for thrombosis and compression stockings do not treat acute thrombus or effectively prevent future ones.

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13
Q

After HIT2 is done what should be done in terms of AC?

A

transition AC into a vitamin K antagonist or alternate AC for 3 months.

initial treatment with warfarin is usually contraindicated as rapidly dropping protein C can cause a prothrombotic state.

Usually hold off on warfarin until non heparin anticoagulant is started and recovers a platelet count of 150K

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14
Q

When to start warfarin after a suspected HIT pt?

A

Usually hold off on warfarin until non heparin anticoagulant is started and recovers a platelet count of 150K

initial treatment with warfarin is usually contraindicated as rapidly dropping protein C can cause a prothrombotic state.

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15
Q

what is delayed onset HIT

A

immune mediated due to high titer antibodies against heparin PF4 copmlexes in the absence of circulating heparin.

arise 5-19 dyas after heparin cessation and so most pts present as outpatinet

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16
Q

when do delayed onset HIT pts present?

A

present 5 to 19 days after heparin cessation and see these pts as outpatient with thrombocytopenia without life threatening arterial or venous thrombosis

17
Q

how long to treat someone with HIT and VTE as a result? How long to keep them on AC?

A

need to treat someone with active thrombosis for usually 6 months.

18
Q

Do we ever use IVC filters for someone with HIT?

A

no because generally associated with significant thrombotic complications and should be avoided.

19
Q

argatroban is ok to use in pts who have

A

renal failure

contraindicated in hepatic failure

20
Q

what effect does argatroban have on INR

A

will falsely elevate it. hepatically cleared