摘要
Objective: To report a patient’s clinical course illustrative of the NPPB mechanism for hyperperfusion-induced injury. Methods: A 65-year-old female presented with a severe headache and was found to have a 6-cm right parietal AVM on imaging. The patient underwent staged, pre-operative embolization and the AVM was surgically resected without intra-operative complication. After the patient emerged from anesthesia she exhibited left hemiplegia and hemispatial neglect. Her systolic blood pressure (SBP) at that time was between 110-120 mmHg. SBP was reduced to 90-100 mmHg and the patient’s symptoms resolved shortly thereafter. The patient’s strict blood pressure goal was relaxed the next morning. However, with her SBP 110-120 mmHg in the ensuing hours, the patient’s left-sided neglect and hemiparesis returned. Her SBP was reduced again to 90-100 mmHg, leading to resolution of her symptoms. Results: This patient’s clinical course supports the NPPB theory of hyperperfusion-induced injury. Despite CT imaging demonstrating no residual AVM following resection, the patient developed neurological deficits in the immediate postoperative period. Aggressive systemic hypotension improved clinical symptoms repeatedly, whereas a brief period of normotension triggered a return of neurological deficits. As a result, there was a direct correlation between fluctuations of neurological status and SBP. This case suggests that the intrinsic autoregulatory capacity was altered in our patient, and that aggressive hypotension was necessary to compensate for diminished autonomic reactivity. Conclusions: This case provides further evidence that NPPB plays a role in hyperperfusion-induced injury following AVM excision and that blood pressure control is vital in managing hyperemic complications following complete resection of cerebral AVMs.
Objective: To report a patient’s clinical course illustrative of the NPPB mechanism for hyperperfusion-induced injury. Methods: A 65-year-old female presented with a severe headache and was found to have a 6-cm right parietal AVM on imaging. The patient underwent staged, pre-operative embolization and the AVM was surgically resected without intra-operative complication. After the patient emerged from anesthesia she exhibited left hemiplegia and hemispatial neglect. Her systolic blood pressure (SBP) at that time was between 110-120 mmHg. SBP was reduced to 90-100 mmHg and the patient’s symptoms resolved shortly thereafter. The patient’s strict blood pressure goal was relaxed the next morning. However, with her SBP 110-120 mmHg in the ensuing hours, the patient’s left-sided neglect and hemiparesis returned. Her SBP was reduced again to 90-100 mmHg, leading to resolution of her symptoms. Results: This patient’s clinical course supports the NPPB theory of hyperperfusion-induced injury. Despite CT imaging demonstrating no residual AVM following resection, the patient developed neurological deficits in the immediate postoperative period. Aggressive systemic hypotension improved clinical symptoms repeatedly, whereas a brief period of normotension triggered a return of neurological deficits. As a result, there was a direct correlation between fluctuations of neurological status and SBP. This case suggests that the intrinsic autoregulatory capacity was altered in our patient, and that aggressive hypotension was necessary to compensate for diminished autonomic reactivity. Conclusions: This case provides further evidence that NPPB plays a role in hyperperfusion-induced injury following AVM excision and that blood pressure control is vital in managing hyperemic complications following complete resection of cerebral AVMs.
