In this case study, we will outline an adverse effect of midodrine that can lead to the prescribing cascade. SK is a 79-year-old male nursing home resident with a history of Parkinson’s disease, hypertension, and benign prostatic hyperplasia (BPH). Over the past few months, he has been struggling with worsening dizziness upon standing. Despite attempts to modify his antihypertensive regimen, SK continued to experience symptomatic orthostatic hypotension. After discussing options, the provider initiated midodrine 5 mg three times daily.
Within about a week, SK’s blood pressure readings had improved when transitioning from sitting to standing, and his dizziness had lessened. However, nursing staff began reporting that SK was increasingly uncomfortable, complaining of abdominal fullness and difficulty urinating. Recognizing his history of BPH and the potential for alpha-1 agonist–induced urinary retention, the provider trialed tamsulosin (Flomax) to help relax the bladder neck and improve urine flow.
Despite this intervention, SK continued to experience worsening difficulty and eventually was unable to void at all. He required catheter placement to relieve acute urinary retention, providing immediate relief of his discomfort. Urinary retention is a contraindication for the use of midodrine.
Midodrine, as an alpha-1 agonist, is useful in raising blood pressure by causing vasoconstriction. However, the same alpha-1 mediated activity also increases bladder sphincter tone, which can worsen or trigger urinary retention (excellent board exam question), particularly in older males with BPH. This case demonstrates how even with an attempted pharmacologic countermeasure like tamsulosin, midodrine can still precipitate significant urinary complications leading to catheterization.
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