Postoperative Neurologic Deficits in a Veteran With Recent COVID-19

On the day of surgery, the patient was hemodynamically stable: heart rate 86 beats/min, blood pressure 167/93 mm Hg (baseline 120-150 mm Hg systolic pressure), respiratory rate 16 breaths/min, oxygen saturation 99% without supplemental oxygen, temperature 97.1 °F. He received amlodipine and clopidogrel, but not lisinopril, that morning. No focal neurologic deficits were appreciated on preoperative examination, and resolution of symptoms related to the 2 prior MIs was confirmed. Preoperative glucose was 163 mg/dL. Femoral and sciatic peripheral nerve blocks were done for postoperative analgesia. A preinduction arterial line was placed and 2 mg of midazolam was administered for anxiolysis. Induction of general anesthesia with oral endotracheal intubation proceeded uneventfully; he was positioned prone.

Given his stroke risk factors, mean arterial pressure was maintained > 70 mm Hg for the duration of surgery. No vasoactive infusions were necessary and no β-blocking agents were administered. Insulin infusion was required; the maximum-recorded glucose was 219 mg/dL. Arterial blood gas samples were routinely drawn; acid-base balance was well maintained, PaO₂ was > 185 mm Hg, and PaCO₂ ranged from 29.4 to 38.5 mm Hg. The patient received 2 units of packed red blood cells for nadir hemoglobin of 7.5 mg/dL. At surgery end, we fully reversed neuromuscular blockade with suggamadex. The patient was returned to a supine position and extubated uneventfully after demonstrating the ability to follow commands.

During postanesthesia care unit (PACU) handoff, the patient exhibited acute speech impairment. He was able to state his name on repetition but seemed confused and sedated. Prompt formal neurology evaluation (stroke code) was sought. Initial National Institutes of Health (NIH) stroke scale score was 8 (1 for level of consciousness, 1 for minor right facial droop, 1 for right arm drift, 3 for right leg with no effort against gravity, 1 for right partial sensory loss, and 1 for mild dysarthria). The patient was oriented only to self. Other findings included mild right facial droop and dysarthria. On a 5-point strength scale, he scored 4 for the right deltoid, biceps, triceps, wrist extensors, right knee flexion, right dorsiflexion, and plantarflexion, 2 for right hip flexion, and ≥ 4 for right knee extension. Positive sensory findings were notable for decreased pin prick sensation on the right limbs.

We obtained emergent head computed tomography (CT) that was negative for acute abnormalities; CT angiography was negative for large vessel occlusion or clinically significant stenosis (Figure). On returning to the PACU from the CT scanner, the patient regained symmetric strength in both arms, right leg was antigravity, and his speech had normalized. Prior to PACU discharge 2 hours later, the patient was back to his prehospitalization neurologic function and NIH stroke scale was 0. Given this rapid clinical resolution, no acute stroke interventions were done, though permissive hypertension was recommended by the neurologist during PACU recovery.

The neurology team concluded that the patient’s symptoms were likely secondary to recrudescence of previous stroke symptoms in the setting of brief postoperative delirium (POD). However, we could not exclude transient ischemic attack or new cardioembolism, therefore patient was started on dual antiplatelet therapy for 3 weeks. Unfortunately, elective confirmatory magnetic resonance imaging (MRI) was not sought to confirm new ischemic changes due hospital COVID-19 restrictions on nonessential scanning. Neurology did not recommend carotid duplex ultrasound given patent vasculature on the head and neck CT angiography. Finally, the patient had undergone surface echocardiography 3 weeks prior to surgery that showed a left ventricular ejection fraction of 50% without significant valvular abnormalities, thrombus, or interatrial shunting, so repeated study was deferred.

Formal neurology consultation did not extend beyond postoperative day 1. One month after surgery, the anesthesiology team visited the patient during inpatient rehabilitation; he had not developed further focal neurologic symptoms or delirium. His strength was equal bilaterally and no speech deficits were noted. Unfortunately, the patient was readmitted to the hospital for continued foot wound drainage 2 months postoperatively, though no focal neurologic deficits were documented on his medical admission history and physical. No long term sequalae of his COVID-19 infection have been suspected.

Discussion

We report a veteran with prior stroke and COVID-19 who experienced postoperative speech and motor deficit despite deliberate risk factor mitigation. This case calls for increased vigilance by anesthesia providers to employ proper perioperative stroke management and anticoagulation strategies, and to be prepared for prompt intervention with COVID-19-sensitive practices should the need for advanced airway management or thrombectomy arises.

The exact etiology of the postoperative neurologic deficit in our patient is unknown. The most likely possibility is that this represents poststroke recrudescence (PSR), knowing he had a previous left medullary infarct that presented similarly.¹¹ PSR is a phenomenon in which prior stroke symptoms recur acutely and transiently in the setting of physiologic stressors—also known as locus minoris resistantiae.¹² Triggers include γ aminobutyric acid (GABA) mediating anesthetic agents such as midazolam, opioids (eg, fentanyl or hydromorphone), infection, or relative cerebral hypoperfusion.^11,13,14 The focality of our patient’s presentation favors PSR in the context of brief POD; of note, these entities share similar risk factors.¹⁵ Our patient did indeed receive low-dose preoperative midazolam in the context of mild preoperative neurocognitive deficit, which may have predisposed him to POD.