Supportive and Preventive Medicine
HEP (HIT Expert Probability) score
Incorporates more clinical features than the 4T score
ii.
More complex (time-consuming) and evaluation studies limited (not in ICU patients)
Laboratory testing
Antigen assays
Depends on the detection of antibody binding by enzyme-linked immunosorbent assays or
particle-based immunoassays
ii.
An automated latex immunoturbidimetric assay has been made available. This assay does not
require sample batching as is common with the enzyme-linked immunosorbent assays; thus,
results can be obtained within 20 minutes.
iii.
Antibody present if sample from patient binds to the heparin-PF4βcoated wells, leading to a
color-producing reaction. A higher antibody concentration leads to greater color production
and a higher optical density reading. Optical density readings of 0.4 or greater are considered
positive and indicative of HIT antibodies.
iv.
High sensitivity (greater than 90%) and low to moderate specificity
| (a) | Clinically insignificant HIT antibodies are often detected among patients who received |
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heparin 5β100 days earlier.
| (b) | Detects a range of immunoglobulin (Ig) A and IgM antibodies that are not pathogenic |
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Functional assays
Examples: Heparin-induced platelet aggregation (HIPA) and C14 serotonin release assay
ii.
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 either
visually (HIPA) or using radioactive serotonin (serotonin release assay).
iii.
Advantages: High sensitivity and specificity
iv.
Disadvantages: Technically challenging and not readily available; often send-out laboratory
tests with a turnaround time of several days
Treatment of HIT (Table 10)
An intermediate or high 4T score should prompt immediate discontinuation of all sources of heparin
and initiation of an alternative nonheparin anticoagulant until confirmatory testing is completed.
Parenteral direct thrombin inhibitors 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.
2007;41(5):749-754)
| (a) | Mean dose in critically ill patients was 0.24 plus or minus 0.16 ΞΌg/kg/min and was 0.22 |
|---|
plus or minus 0.15 ΞΌg/kg/min in critically ill patients with multiple organ dysfunction.
| (b) | A typical starting dose is 2 ΞΌg/kg/min; however, consider reduced dosing of 1 ΞΌg/kg/min |
|---|
in critically ill patients. In patients with severe liver impairment, consider 0.5 ΞΌg/kg/min.
| (c) | The target aPTT is 1.5 to 3 times baseline. |
|---|
ii.
| (a) | Dose reduced to 0.05 to 0.1 mg/kg/h, depending on renal function and bleeding risks |
|---|---|
| (b) | The target aPTT is 1.5 to 2.5 times baseline. |
iii.
Parenteral direct thrombin inhibitors are associated with a higher rate of major bleeding