What triggers intraoperative blood pressure/heart rate surges and postoperative hypertonia during unilateral biportal endoscopy?

Unilateral biportal endoscopy (UBE) is an increasingly utilized minimally invasive technique for lumbar degenerative disease. Dural tear is a recognized complication (incidence 1.9-5.8%), typically associated with cerebrospinal fluid leakage and intracranial hypotension. However, the unique irrigation dynamics of UBE - an open two-portal system permitting high-flow continuous irrigation - may produce a distinctly different pathophysiology when an occult dural defect is present. The anesthesiology literature contains few descriptions of the acute intraoperative hemodynamic manifestations of this phenomenon.

A 49-year-old woman (ASA physical status I) underwent UBE for L4-L5 and L5-S1 disc herniation under total intravenous anesthesia. The procedure was complicated by intraoperative wrong-level surgery (L4-L5 misidentified as L5-S1), necessitating complete portal withdrawal, re-localization, and re-establishment of the surgical field, which prolonged the operation to 4 h 23 min with a cumulative irrigation volume of 51,000 mL. Approximately 2.5 h after incision, progressive, treatment-refractory tachycardia (70 → 117 beats/min) and hypertension (up to 183/102 mmHg) developed; esmolol and urapidil produced minimal antihypertensive effect despite concurrent augmentation of anesthetic depth. On postoperative review, the scrub nurse recalled observing a suspected dural tear approximately 10 min before the hemodynamic escalation, which had not been communicated intraoperatively. Following extubation, the patient exhibited impaired consciousness, persistent tachypnea (40-50 breaths/min), and generalized hypertonia with decerebrate posturing. Multidisciplinary evaluation excluded epileptic seizure, metabolic encephalopathy, malignant hyperthermia, and intraoperative awareness. Suspected acute intracranial hypertension secondary to massive irrigation fluid entry into the subarachnoid space via the unrecognized dural defect was considered the most likely diagnosis. The patient was reintubated and managed in the intensive care unit with osmotic diuresis (furosemide, mannitol), corticosteroids, and sedation. Consciousness recovered the following morning, limb hypertonia resolved by postoperative day 11, and the patient was discharged on day 14 without neurological deficit.

This case suggests that an occult dural tear during UBE with large-volume irrigation may produce a paradoxical hemodynamic profile of progressive, therapy-resistant hypertension and tachycardia - contrasting with the bradycardia and hypotension classically associated with intracranial hypotension from cerebrospinal fluid leaks. The triad of (i) progressive, treatment-refractory hypertension and tachycardia, (ii) prolonged UBE duration (> 2 h), and (iii) large-volume irrigation (> 20 L) may represent a high-risk pattern warranting immediate intraoperative communication between anesthesia and surgical teams and consideration of intracranial pressure-directed interventions. This observation is hypothesis-generating and requires validation in larger studies.