56-year-old female with continuous intracranial hypotension secondary to nerve root cysts was scheduled for left C5-T1 hemilaminectomy. Patient has history of orthostatic headaches due to CSF leak, status post T7-9 laminectomy, L3-L5 laminectomy, dural reduction surgery, multiple fibrin glue injections, and blood patches, all of which only provided temporary relief. Her headaches were described as bitemporal and sub-occipital associated with neck pain but never revealed any focal near deficits. She also had a history of Ehlers Danlos syndrome, complicated by joint hypermobility and partial detached retina, bicuspid Aortic valve with moderate Aortic regurgitation and a PFO discovered incidentally 2 years earlier during initial workup. Patient denied any other significant medical, surgical or social history and denied any anesthetic complications during prior procedures.
On arrival to the operating room, general anesthesia was induced with propofol 2.5 mg/kg, Succinylcholine 120mg and Fentanyl 50mcg. Patient was intubated with a 7.0 ETT, using a Video MAC and bougie to minimize manipulation of the neck. Patient was intubated without difficulty on the first attempt and the ETT passed through the cords without resistance. An arterial line was placed and the patient was positioned prone on a jackson table, after which all pressure points were checked regularly throughout the case. MEP and SSEP monitoring were obtained during a case and anesthesia was maintained with Desflurane, and fentanyl without neuromuscular blockade. Hemodynamic parameters were stable throughout surgery. The surgery was uneventful and duration of anesthesia was four hours. Extubation was uncomplicated and there were no immediate postoperative complications. On POD1, the patient complained of difficulty in swallowing and slurred speech. Physical examination showed right tongue deviation on protrusion. Gag reflex and taste sensation were normal. To exclude cerebrovascular diseases or internal carotid artery dissection, MRA was performed, confirming isolated right hypoglossal nerve palsy (HNP). Conservative management included speech therapy and regular neuro checks were done. Following discharge, symptoms continued to improve and there was complete recovery at 4 months.
Most reported cases of HNP after airway management suggest involvement of the extra cranial section of the hypoglossal nerve, which exits the skull through the hypoglossal canal and descends caudally, along with internal carotid artery and jugular vein. At the level of the angle of the mandible it becomes superficial, passes just above the greater horn of the hyoid bone, and enters the floor of the mouth. Mechanisms such as hyperextension of the neck during intubation, endotracheal tube cuff pressure, excessive hyperextension, or head lateralization during surgery have been described as causes of this neurological damage. Although the exact mechanism of injury is unclear, the hypothesized etiology in our case was compression of the hypoglossal nerve by the ETT tube at the hyoid bone, which was further exacerbated by continuous MEP monitoring. In conclusion, anesthesiologists should be aware of the possible causes of the HNP and should take extreme care to prevent nerve injuries and other complications.
