BACKGROUND AND IMPORTANCE: Pseudohypoxic brain swelling is a rare event that may occur after uneventful brain surgery when subgaleal vacuum drainage is used. To date, such cases of unexpected postoperative disturbances of consciousness associated with radiological signs of basal ganglia, thalamic, brainstem, and cerebellum damage without any signs of vessel occlusion have not been known to occur after spinal surgery. CLINICAL PRESENTATION: We report for the first time on 2 patients presenting with a clinical and radiological picture of pseudohypoxic brain swelling after spinal surgery. In the first patient, bilateral basal ganglia damage occurred after thoracic spondylodiscitis surgery, manifested by epileptic seizures and coma lasting 1 week postoperatively with subsequent recovery. The second patient suffered basal ganglia and cerebellar and brainstem infarction after lumbar spondylodiscitis surgery, resulting in death. Because intraoperative cerebrospinal fluid leakage and use of postoperative epidural suction drainage with cerebrospinal fluid loss occurred in both cases, they are highly suspected to have potentially caused the complications. CONCLUSION: Pseudohypoxic brain swelling should be considered in patients with unexpected neurological deterioration after spinal surgery. It might be a form of postoperative intracranial hypotension-associated venous congestion, which should be distinguished from common postoperative cerebral ischemic events caused by arterial or venous occlusions.
BACKGROUND AND IMPORTANCE: Pseudohypoxic brain swelling is a rare event that may occur after uneventful brain surgery when subgaleal vacuum drainage is used. To date, such cases of unexpected postoperative disturbances of consciousness associated with radiological signs of basal ganglia, thalamic, brainstem, and cerebellum damage without any signs of vessel occlusion have not been known to occur after spinal surgery. CLINICAL PRESENTATION: We report for the first time on 2 patients presenting with a clinical and radiological picture of pseudohypoxic brain swelling after spinal surgery. In the first patient, bilateral basal ganglia damage occurred after thoracic spondylodiscitis surgery, manifested by epilepticseizures and coma lasting 1 week postoperatively with subsequent recovery. The second patient suffered basal ganglia and cerebellar and brainstem infarction after lumbar spondylodiscitis surgery, resulting in death. Because intraoperative cerebrospinal fluid leakage and use of postoperative epidural suction drainage with cerebrospinal fluid loss occurred in both cases, they are highly suspected to have potentially caused the complications. CONCLUSION:Pseudohypoxic brain swelling should be considered in patients with unexpected neurological deterioration after spinal surgery. It might be a form of postoperative intracranial hypotension-associated venous congestion, which should be distinguished from common postoperative cerebral ischemic events caused by arterial or venous occlusions.