Heparin induced thrombocytopenia (HIT), diagnostic test EBM!

Thanks Jeff for presenting a great case! This was a middle age patient with recent cardiac surgery presenting with arterial and venous thromboses found to be thrombocytopenic. This patient was ultimately diagnosed with HIT despite a negative anti-PF4 antibody.

Main points:

1) Heparin induced thrombocytopenia (HIT) is largely a clinical diagnosis and empiric treatment should be started in a patient with very high pretest probability prior to definitive diagnosis with a serotonin release assay, which usually takes days to a week to return. See this NEJM review article about HIT.

2) When applying a diagnostic test, we should use a Bayesian approach: derive a pretest probability and use likelihood ratios to generate a posttest probability. However, if we have an extremely high pretest probability we should consider not even ordering the diagnostic test if it would not change management. See this superb blog post on how to apply likelihood ratios and myths about sensitivity and specificity.

Want to learn more?

Thrombophilia testing

In the setting of an acute hospitalization for a provoked DVT, thrombophilia testing is usually advised against as it is (1) expensive (2) has a high false positive rate (given medications and the critically ill state can also affect test results) and (3) unlikely to change management. Here is a essay about this from JAMA Internal Medicine.

We discussed some settings where it may be appropriate to proceed or engage in shared decision making with some thrombophilia testing such as multiple unprovoked clots, a young person, critical illness that would change management, and knowing whether a woman of childbearing age has APLA.

Approach to thrombocytopenia

One way to look at true thrombocytopenia is underproduction vs. sequestration vs. destruction.

  • Underproduction – usually there are other cytopenias – think about marrow processes and nutritional deficiencies; MDS, B12/folate deficiency, 2/2 chronic inflammatory/ infectious processes, marrow infiltration, congenital conditions
  • Sequestration – splenic 2/2 liver disease
  • Destruction – think about DIC, TTP/ HUS, ITP, APLS; more severe conditions like CAPS
  • Other things to think about are postpartum causes eg. acquired factor VIII inhibitor (see the previous report for an excellent overview of this) and medication induced