OBJECTIVE: We retrospectively analyzed a series of patients who deteriorated after resection of an intracranial meningioma due to extensive brain edema (EBE) with regard to etiology of the neurological worsening and outcome. METHODS: Out of a series of 376 consecutive patients who underwent resection of an intracranial meningioma, 13 (3.5%) experienced postoperative deterioration due to EBE which necessitated prolonged artificial ventilation, tracheal reintubation, or decompressive craniectomy. Clinical data, radiological findings, operative records and follow-up data of these patients were retrospectively reviewed. RESULTS: The study revealed two different patient groups: Patients in group A (n=7) demonstrated edema due to typical venous infarction (VI). A decompressive craniotomy was performed in all but one patient in this group; nonetheless, an acceptable neurological outcome (Glasgow Outcome Scale (GOS) 4) was achieved in only two cases. Patients in group B (n=6) deteriorated due to an EBE of unknown etiology. Mean tumor volume in this group was higher when compared to group A (75 ml vs. 30 ml). In addition, 83% of patients in group B displayed extensive preoperative peritumoral edema compared to only 14% in group A. Three patients in group B required decompressive surgery; however, neurological outcome was more favorable in this group as 83% achieved a GOS of 4 or 5. CONCLUSION: Extensive brain swelling during or after intracranial meningioma surgery may be due to VI or possibly due to increased postoperative tissue permeability. It is recommended to preserve all venous structures as patients with VI had an unfavorable neurological outcome.
OBJECTIVE: We retrospectively analyzed a series of patients who deteriorated after resection of an intracranial meningioma due to extensive brain edema (EBE) with regard to etiology of the neurological worsening and outcome. METHODS: Out of a series of 376 consecutive patients who underwent resection of an intracranial meningioma, 13 (3.5%) experienced postoperative deterioration due to EBE which necessitated prolonged artificial ventilation, tracheal reintubation, or decompressive craniectomy. Clinical data, radiological findings, operative records and follow-up data of these patients were retrospectively reviewed. RESULTS: The study revealed two different patient groups: Patients in group A (n=7) demonstrated edema due to typical venous infarction (VI). A decompressive craniotomy was performed in all but one patient in this group; nonetheless, an acceptable neurological outcome (Glasgow Outcome Scale (GOS) 4) was achieved in only two cases. Patients in group B (n=6) deteriorated due to an EBE of unknown etiology. Mean tumor volume in this group was higher when compared to group A (75 ml vs. 30 ml). In addition, 83% of patients in group B displayed extensive preoperative peritumoral edema compared to only 14% in group A. Three patients in group B required decompressive surgery; however, neurological outcome was more favorable in this group as 83% achieved a GOS of 4 or 5. CONCLUSION: Extensive brain swelling during or after intracranial meningioma surgery may be due to VI or possibly due to increased postoperative tissue permeability. It is recommended to preserve all venous structures as patients with VI had an unfavorable neurological outcome.