Structured clinical assessment of probability for HIT in children may save lives.

Heparin-induced thrombocytopenia (HIT) is a rare, but life-threatening adverse drug reaction. It can cause debilitating consequences (like stroke or pulmonary embolism), loss of a limb, or death. The key to treatment is stopping heparin as soon as possible and starting an alternative anticoagulant (usually fondaparinux, argatroban, or potentially one of the new oral anticoagulants). HIT is more commonly seen after cardiac surgery and with use of unfractionated heparin at therapeutic doses, but it may sometimes occur with low-molecular-weight heparin or with the small amount of heparin used to flush arterial and vein catheters. The critical steps in preventing serious consequences due to this condition are awareness and fast action once HIT is suspected.

Preliminary testing for HIT antibodies can be performed using onsite immunoassays; however, these assays are known to have low specificity (high false-positive rate). Reference standard tests that have high specificity for HIT, such as the serotonin release assay, are not always available. It may take days or sometimes weeks for a result to be reported, especially if the sample must be shipped to another laboratory. During that time, patients who have HIT will be at risk for developing thrombosis if not properly treated, whereas those who do not have HIT may be exposed to the bleeding risk of alternative anticoagulants without any benefit. For these reasons, a clinical tool that helps physicians decide which patients require reference laboratory testing and which ones do not would be extremely useful.

The 4Ts scoring system has been validated in adult patients and is recommended by experts in the field. The study by Obeng and colleagues tested its applicability in a pediatric population and reported results that are promising, but preliminary. Limitations of the study include retrospective calculation of the 4Ts score and use of an onsite HIT assay that has low specificity (detects all immunoglobulin types instead of just the IgG antibodies that cause HIT). Although a low 4Ts score excluded HIT, the total number of patients evaluated was small (n = 38) and more important, not all samples were tested with the reference assay (serotonin release assay). This raises concern that the prevalence of HIT may have been overestimated in this study (due to false-positive onsite immunoassay results).

What this study does well is illustrate the importance of using a structured clinical assessment of the likelihood of HIT before performing laboratory testing. Patients with a high 4Ts score should have heparin stopped and an alternative anticoagulant started without waiting for the test result. This approach has the potential to save lives by reducing the risk for HIT-associated thrombotic complications. As for patients with a low score, it may be possible to omit laboratory testing for HIT, but further data are needed to confirm the safety of this strategy.