More information needed on HIT in critical care: expert


By Tony James

19 Oct 2015

Better tools are needed to diagnose heparin-induced thrombocytopenia (HIT) and more information is required to guide the switch to alternative anticoagulants, according to Professor Chris Ward, head of haematology at the Royal North Shore Hospital in Sydney.

“There are special challenges in diagnosing and treating HIT in ICU patients,” he told delegates during an ASTH symposium on critical care and haemostasis.

“Thrombocytopenia is common in this setting for reasons including sepsis, coagulopathy, marrow failure and reactions to many drugs, and heparin use is also common, but HIT causes only a few per cent of cases.”

HIT can occur with low molecular weight heparin, but rates are ten-fold higher with unfractionated heparin.

The disease results from the formation of IgG antibodies against the complex of heparin and platelet factor 4 (PF4).

“In more severe forms of HIT, the antibodies trigger thrombosis by causing platelet and endothelial cell activation,” Professor Ward said.

Thrombocytopenia is not usually severe, with the platelet count typically >109/L, and thrombotic complications can occur when platelet count is within the normal range.

“The consequences can include DVT and other manifestations such as skin necrosis, digital gangrene and a need for limb amputation, with high morbidity and mortality.”

Identification of anti-heparin-PF4 antibodies is a useful screening tool but is not diagnostic, and ELISA assays are often difficult to perform in the urgent setting of ICU-associated HIT.

“Review of the case history by an experienced clinician is preferable to routine use of screening assays,” he said.

Confirmatory tests include whole blood impedance aggregometry and the serotonin release assay, but they are not widely available.

Once HIT is confirmed or even strongly suspected, switching to an alternative anticoagulant is mandatory.

Warfarin must not be used until platelet numbers are restored, so the options are currently limited to agents such as fondaparinux, danaparoid and bivalirudin.

“In theory novel oral anticoagulants should be ideal, but there is not yet any evidence to support their use,” Professor Ward said.

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