Vikas Pandey, MD
The treatment of intracerebral hemorrhage currently involves a lot of “watchful waiting” and blood pressure management, with the exception of those with devastating bleeds requiring surgery or those with intraventricular hemorrhages requiring intraventricular thrombolytics. The ultimate goal in these patients is to minimize hematoma growth which is thought to improve overall patient outcome. What if, instead of clinical dismay at not being able to treat with tPA when seeing a hemorrhage on CT scan during an acute stroke evaluation, there was an option to improve platelet activity and prevent further hematoma expansion. The authors of this article had a similar dream. Desmopressin, a vasopressin analogue, has been used for conditions such as nocturnal bed-wetting and central diabetes insipidus, however has also been used in coagulation disorders such as von Willebrand disease and Hemophilia A due to the interesting effect of stimulating release of vWF from endothelial cells and also increasing the survival of Factor VIII due to increased vWF complexing.
The authors prospectively enrolled 14 patients with either reduced platelet activity on point-of-care testing, or aspirin use, or both and they received desmopressin 0.4 mcg/kg intravenously over 30 minutes. The infusion was started 12.25 (5.7-23.1) hours after the symptom onset. They measured the change in platelet function assays and vWF antigen activity and found shortened Mean PFA-EPI results from 192 +/- 18 seconds to 124 +/- 15 seconds (improved platelet activity) one hour after infusion as well as increase in vWF antigen from 242 +/- 96 to 289 +/ 103 percent activity, both of which were significant results. Peculiarly, one patient had paradoxically increased PFA-EPI. Hematoma volume was found to be decreased with a range of -1.4 to 8.4 mL (two had hematoma growth). Median change in hematoma volume was -0.5 mL. Modified Rankin Scale at 3 months showed, out of 12 patients for whom follow-up was obtained, four had no disability, one had a mRS score of 3 and three had mRS of 4. Sodium decreases with the infusion were only in six patients and were in the range of 1-3 mEq/L. Of the seven patients who received the infusion within 12 hours of symptom onset, 2 had hematoma growth.
The article demonstrated safety and efficacy in improving measures of platelet activity and vWF antigen and, though with small numbers, demonstrated some effect of halting hematoma growth, especially if given within 12 hours of symptom onset. The article lacked measures of baseline hematoma volumes, GCS levels, hematoma location and intraventricular involvement. These “ICH score” markers should not be overlooked especially given their importance toward determining patient outcome. The obvious side effects of hypertension and hyponatremia due to water retention were not seen at high rates in this small trial but given the impact these may have toward hematoma expansion and herniation, larger trials are needed to determine if this will be a factor. The authors also allude to the PATCH trial testing platelet transfusions in intracerebral hemorrhage and if positive, this may be a possible co-therapy with desmopressin. The study provides the skeleton for a larger randomized prospective trial and the authors should be applauded for having the proper approach to an area where stroke neurologists feel somewhat helpless.