Evaluation of methylene blue in vasodilatory shock in non-mechanical circulatory support device patients Annette Lista, PharmD; Kevin Donahue, PharmD; Julin Thomas, PharmD; Kalliopi Fitousis, PharmD; David Putney, PharmD, MPH PURPOSE
The loss of vascular tone in vasodilatory shock is frequently due to a severe inflammatory response secondary to infection and is a major cause of morbidity and mortality in the intensive care unit. Vasodilation due to smooth muscle relaxation by nitric oxide is one cause of hypotension. Methylene blue is a selective inhibitor of guanylate cyclase, a second messenger involved in nitric oxide-mediated vasodilation. By inhibiting guanylate cyclase, methylene blue may minimize the effects of nitric oxide and subsequent vasodilatation. The purpose of this study to provide new knowledge on the effects of methylene blue across multiple shock etiologies and patient populations. METHODS
This was a single center retrospective descriptive study. Eligible patients were > 18 years of age and received methylene blue for vasodilatory shock from Jan. 1, 2011, to Sept. 31, 2015. The primary endpoint of this study was to determine clinical response to methylene blue, defined as a change in mean arterial pressure (MAP) > 10% without an increase in vasopressor requirements. RESULTS
Sixty-one patients met eligibility criteria. Baseline demographics as follows: mean age 13.5 (±14), 36 (59%) were male, 31 (51%) were Caucasian, and 42 (69%) were
admitted to the surgical and liver intensive care unit (ICU). The primary shock etiology was 38 (62%) septic, 18 (30%) cardiogenic, and 5 (8%) hemorrhagic. Methylene blue was ordered as a bolus and infusion in 33 (54%) patients, bolus alone in 27 (44%) patients, and infusion alone in 1 (2%) patient at a mean bolus dose of 1.25 mg/kg (±0.45) and infusion 0.5 mg/kg/hr (±0.30). There were 20 (33%) that met the primary endpoint compared to 41 (67%) of patients who did not meet the primary endpoint, p = 0.62. Preliminary results suggest that there is no difference in change of MAP by greater than 10% from baseline without any change in vasopressor support from baseline. Of those who responded to methylene blue, the time from ICU admission to methylene blue initiation was 6 (±6) hours compared to 11 (±15 hours), p = 0.06, which could suggest some benefit in earlier initiation of therapy. However, the overall mortality included 3 (15%) of responders that survived compared to 6 (15%) of non-responders that survived. CONCLUSION
There were no observed differences in association with methylene blue and improvement of mortality or increase in MAP as defined in this study with methylene blue utilization. Preliminary data suggests there is a lack of evidence to support methylene blue use.
PGY2 CRITICAL CARE RESIDENCY
Annette Lista, PharmD Annette earned her BS in Pharmaceutical and Healthcare Studies at the University of the Sciences in Philadelphia, PA. She earned her Doctor of Pharmacy at the University of the Sciences in Philadelphia, PA in 2014. She completed a PGY1 pharmacy residency at Einstein Medical Center in Philadelphia, PA. Annette has accepted a Clinical Specialist II in Critical Care position at Houston Methodist Hospital. Primary project preceptor: Kevin Donahue, PharmD, BCPS Presented at 2016 Midwest Pharmacy Residents Conference, Omaha, Neb.
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