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017 Preventing strokes from vasospasm and heparin induced thrombocytopenia type II: nicardipine, milrinone, angioplasty and Argtroban
  1. J Rabinov1,
  2. J Pryor2,
  3. R Nogueira1,
  4. A Yoo1,
  5. J Hirsch1
  1. 1Neuroradiology, Massachusetts General Hospital, Boston, Massachusetts, USA
  2. 2Neurosurgery, Massachusetts General Hospital, Boston, Massachusetts, USA

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Purpose: To investigate the use of Argtroban in patients at risk for heparin induced thrombocytopenia type II (HIT) during intra-arterial (IA) therapy for subarachnoid hemorrhage (SAH) related vasospasm.

Methods and Materials: In 2007, 33 patients underwent angiographic procedures for cerebral vasospasm following presentation to our institution with aneurysmal subarachnoid hemorrhage. 32 patients underwent pharmacologic IA therapy for SAH related vasospasm. The other patient underwent cerebral angiography and was treated with the Neuroflo aortic balloon catheter. The Neuroflo catheter was used in two patients, one as adjunctive therapy and one as the sole mode of therapy. 10 men and 23 women were included in this group with an average age of 47.9 (range 20–82). A total of 104 procedures were done, including IA administration of nicardipine, milrinone and/or angioplasty. All procedures were done under general anesthesia or monitored anesthesia care. Standard heparinized catheter flush system (4000 units/l) was used in all patients, with some patients receiving additional 1000–2000 unit intravenous heparin boluses. Selected patients were treated using Argtroban, a direct thrombin inhibitor, at 1–2 µg/kg/min. Data are compared with the 2006 and 2008 SAH related vasospasm cohorts.

Results: Seven of 33 SAH patients treated for cerebral vasospasm developed positive screening titers for HIT type II (HIT+) in 2007. Two of these seven patients with HIT+ screens developed strokes, one of whom died as a result. None of these patients developed a drop in platelets below 100 000 (normal 150 000–400 000/cc). Clot formation was also seen in seven other patients (not HIT+): three at the time of endovascular aneurysm treatment, three during vasospasm treatment and one with pulmonary embolism only. Subsequently, patients were selectively treated with Argtroban after their second or third time in the angiography suite as prophylaxis. No patients treated with Argtroban developed embolic strokes or further intracranial hemorrhages. The incidence of HIT type II was 21% in the 2007 SAH related vasospasm cohort, and the overall patient population of HIT+ or clot formation was 42%. In the year 2006 we identified two out of 32 patients with 68 IA vasospasm procedures who were clinically hypercoagulable. One of them was found to have a HIT+ screen. In 2008, two out of 16 patients with 39 IA vasospasm procedures were clinically hypercoagulable. One of them was found to have a HIT+ screen. Combining the 2006 and 2008 patients, the incidence of HIT type II positive screens was 4.2%, which is significantly lower than in 2007 (p = 0.0276).

Conclusion: The year 2007 was associated with a statistically significant increase in the incidence of HIT type II positive screens in SAH related vasospasm patients at our institution. In March 2008, the FDA discovered that over-sulfated chondroitin sulfate had been added to heparin produced for Baxter, Inc by Scientific Protein Laboratories, Changzhou, China. Selective use of Argtroban in patients undergoing multiple IA procedures for vasospasm can prevent strokes related to HIT type II. Use of Argtroban and improvement in heparin quality have decreased thromboembolic complications.

Competing interests: None.

Reference

  1. Hoh BL: HIT Type II in SAH patients. Neurosurgery 2005;57:243–8.