Background: Persistent hypotension in patients affected by circulatory shock is a common barrier to discharge in the ICU. Even after these patients have been otherwise stabilized, low-level hypotension often ensures that they remain in the ICU on IV vasopressors. Midodrine, an oral α1-agonist, has shown promise as an adjunct therapy to wean patients off IV vasopressors and facilitate earlier discharge. According to a recent study at the Mayo Clinic ICU, Rochester, discharge on Midodrine was associated with a shorter ICU length of stay as well as decreased in-hospital mortality. However, it was also associated with an increased 1-year mortality rate. Additionally, the same study found that, among the patients discharged from the ICU on Midodrine, 50% were concomitantly started on some form of medication to lower blood pressure while still on Midodrine. This counterintuitive practice, coupled with the increased 1-year mortality rate seen with prescribed Midodrine, raises the question of why the medication is being continued at discharge.
Methods: In this retrospective chart review, data from patients with persistent hypotension treated with Midodrine, at the University of New Mexico (UNM) Hospital, was analyzed. Specifically, records were reviewed to obtain data regarding details of Midodrine treatment. Moreover, we examined the strategies used by different physicians to taper or discontinue Midodrine outside of the ICU. Our study has received IRB approval by the University of New Mexico.
Results: We have examined 35 charts. This included 21 males and 14 females with a mean age of 60. 58% of patients who survived their hospital stay were discharged on Midodrine. Additionally, of those discharged on Midodrine, 16.6% were concomitantly discharged on at least one anti-hypertensive medication. Our results also suggest that providers, on average, prefer a hard stop method of Midodrine discontinuation (65.6%) to a taper (34.4%). The most common indication for Midodrine use in the hospital was hypotension as a result of septic shock (31.4%), followed by chronic Midodrine use continued in hospital (17.1%), hypovolemic shock (8.6%), neurogenic shock (5.7%), renal failure (5.7%), cirrhosis (5.7%), and cardiogenic shock (2.9%). Other causes of hypotension accounted for 22.9% of Midodrine use. There was only one adverse event due to Midodrine use.
Conclusions: Midodrine, an oral α1-agonist, has been proposed as a therapy to wean patients from IV vasopressors, facilitate earlier ICU discharge, and maintain blood pressure outside of the ICU. However, the effects of Midodrine on patients discharged from the ICU is an area of active research and much is still unknown. We undertook a study to investigate the use of Midodrine at UNM and look for areas for improvement. Initial data indicated that a hard stop method of Midodrine discontinuation is preferred, the most common indication for Midodrine use in the hospital was hypotension secondary to septic shock, and patients are concomitantly being discharged on Midodrine and anti-hypertensives. The practice of discharging patients on antihypertensives and Midodrine is counterintuitive and an area for education and exploration. Another potential area for education could be notifying providers that a hard stop for Midodrine seems to be safe. Current data is preliminary, but can ultimately be published with the goal of serving as a guidance to physicians considering discharging a patient on Midodrine.
