P028: PARAVERTEBRAL BLOCK: DIAGNOSIS OF RARE ACCIDENTAL SUBDURAL BLOCK
Gianella Russo, MD, Alberto Ardon, MD, Z Deutch, MD; University of Florida-Jacksonville
Case description: A 59 year old male with PMH of HTN, Hep C, GERD, and CKD presented for VATS, 5 days after a robotic left upper lobectomy for early stage lung cancer. He had persistently opacified CXR and marginal respiratory status requiring lavage of hemithorax with removal of clot from left upper lobe.
Intervention: Sedation was provided with 70mg of propofol. Left single-shot PVB at the T6 level was performed using anatomical landmarks technique, a total of 15mL of 0.5% ropivacaine was injected. There was no hemodynamic instability, blood aspirated, nor pain/resistance on injection.
In the OR, the patient only responsive to loud verbal commands. He was hypotensive with a BP of 37/21mmHg and bradycardic with HR in the low 50’s.100 mcg doses of phenylephrine were titrated and an infusion initiated, and 500 mL crystalloid boluses were given. These measures stabilized vital signs, and anesthesia was induced via 100mcg of fentanyl, 120mg of propofol, and 40mg of rocuronium. Intubation with a size 39 left-sided DLT, positioning confirmed via FBO. Anesthesia was maintained via inhaled sevoflurane; the patient received 250mL of 5% albumin and remained on a phenylephrine infusion. NMB was reversed with 3 mg of neostigmine and 0.4 mg of glycopyrrolate. A TOF ratio of 0.7 was present, and clinical assessments indicating adequate muscular function and was extubated.
In the PACU the patient was hypotensive (SBP 50’s) and bradycardic (HR 50’s-60). He was obtunded and had difficulty expiring, however maintaining a SaO2 >99% on 2L nasal cannula. He was positioned in the reverse Trendenlenburg position, administered a second dose of 5% Albumin 250mL, and two 100 mcg boluses of phenylephrine. He was noted to have decreasing motor strength in upper and lower extremities bilaterally, and was not responding to verbal or painful stimuli. 2mg of neostigmine, 0.4 mg of glycopyrrolate, and 0.04 mg of naloxone, were given without improvement. ABG revealed: pH 7.07, CO2 89, O2 160, HCO3 26.4. Therefore the patient was re-intubated. After being mechanically ventilated, ABG normalized, the patient regained normal motor tone, and was extubated.
Discussion: After exclusion of other respiratory insufficiency causes, we theorize that our PVB had a subdural component, resulting in hypotension and bradycardia, with slower-onset diffuse motor weakness, leading to hypoventilation and hypercarbia. The dosage of ropivacaine was insufficient to account for such hypotension, if confined to the paravertebral space. Significant hypotension and slow-onset muscular weakness are not usually seen with PVB. Lubenow et al3 describes diagnosis of a subdural block. Major criteria are negative aspiration and unexpected extensive sensory block. Minor criteria are sensory /motor blockade with delayed onset (greater than 10 minutes), and motor blockade and sympatholysis disproportionate to dosage of local anesthetic. A subdural block should be considered if both major criteria and one minor criteria are met 5, our patient met both major criteria and one minor criterion.
Conclusion: Subdural anesthesia after PVB is a rare complication, but is serious and potentially life-threatening. Prompt recognition and treatment are essential to avoid significant morbidity and mortality.