Case Presentation: A 68-year-old Caucasian male with a history of hypertension, prediabetes (A1c 5.9), and chronic gout presented to the hospital with acute transient left-sided weakness and numbness. MRI confirmed a small acute CVA and CTA revealed complete occlusion of right internal carotid artery (ICA) and 75% stenosis of left ICA. Workup included a negative bubble study on echocardiogram with no shunt. The patient was discharged home on Eliquis and aspirin with a plan for scheduled carotid endarterectomy (CEA) as an outpatient in 2 weeks. However, he was readmitted less than 24 hours later for intermitted left-sided weakness. Hospital course: The patient developed increasing episodes of transient ischemic attacks (TIAs) that escalated in frequency and severity, known as “crescendo TIAs.” Due to new evolving stroke on repeat MRI brain complicated by significant bilateral carotid disease confirmed on cerebral angiogram, vascular surgery chose to proceed with transcarotid artery revascularization (TCAR) of the left ICA. Post-procedure course was complicated and prolonged, and the patient was in the hospital for a total of 18 days. He had persistent orthostatic hypotension which manifested clinically as fluctuating left-sided weakness, dysarthria, and difficulty ambulating. He was monitored in the ICU on phenylephrine drip with a target SBP >160mmHg as any lower than this, patient would have left-sided weakness and focal deficits. Eventually the patient was weaned off pressors, maintained on oral midodrine (10mg TID) with nursing instructions for permissive hypertension and gradual ambulation to prevent orthostatic hypotension. He was discharged on scheduled midodrine (5 mg TID) with a SBP goal of >140mmHg, DAPT and transitioned to a rehab facility.
Discussion: Interventions for Carotid Artery Disease such as CEA or TCAR can cause disruption of the nerve endings surrounding the baroreceptors resulting in increased baroreceptor sensitivity (BRS). This can lead to hemodynamic instability such as hypertension, hypotension or bradycardia. Although the overall risk of stroke after TCAR is similar in comparison with traditional CEA, data from the ongoing TCAR Surveillance project has shown that TCAR patients are more prone to develop hypotension post-procedure increasing the risk of watershed infarcts (1). Watershed infarcts occur at vulnerable junctions between two major arterial territories. These zones are sensitive to hypotensive insults (2) which explains why our patient had left-sided weakness every time his SBP dropped below 160mmHg. Some predictive risk factors to develop post-TCAR hypotension are older age, history of CAD, CHF and high-grade carotid stenosis (1). Our patient had complete unilateral right ICA occlusion making his right hemispheric perfusion extremely blood pressure dependent on collateral circulation from the left ICA. Hence his goal SBP was >160mmHg to support cerebral perfusion to avoid new watershed infarcts.
Conclusions: As hospitalists, we must be aware that post-TCAR baroreceptor dysfunction can lead to orthostatic hypotension, complicating recovery and increasing hospital stays that can result in frustration on the patient’s end. Early gradual mobilization with hydration, compression stockings and medication adjustments such as pressors and midodrine may be essential in mitigating the risks of recurrent neurologic deficits. By close collaboration with the vascular surgery team, we can improve patient satisfaction and outcomes.
