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In this study, we investigated the roles of cerebral blood flow (CBF) and cerebral oxygen delivery (CDO2) in relation to cerebral energy metabolism after aneurysmal subarachnoid hemorrhage (aSAH).Fifty-seven adult aSAH patients treated on the neurointensive care unit at Uppsala, Sweden between 2012 and 2020, with at least 1 xenon-enhanced computed tomography (Xe-CT) scan in the first 14 days after ictus and concurrent microdialysis (MD) monitoring, were included in this retrospective study. CBF was measured globally and focally (around the MD catheter) with Xe-CT, and CDO2 calculated. Cerebral energy metabolites were measured using MD.Focal ischemia (CBF20 mL/100 g/min around the MD catheter was associated with lower median [interquartile range]) MD-glucose (1.2 [0.7 to 2.2] mM vs. 2.3 [1.3 to 3.5] mM; P=0.05) and higher MD-lactate-pyruvate (LPR) ratio (34 [29 to 66] vs. 25 [21 to 32]; P=0.02). A compensated/normal MD pattern (MD-LPR25) was observed in the majority of patients (22/23, 96%) without focal ischemia, whereas 4 of 11 (36%) patients with a MD pattern of poor substrate supply (MD-LPR25, MD-pyruvate120 µM) had focal ischemia as did 5 of 20 (25%) patients with a pattern of mitochondrial dysfunction (MD-LPR25, MD-pyruvate120 µM) (P=0.04). Global CBF and CDO2, and focal CDO2, were not associated with the MD variables.While MD is a feasible tool to study cerebral energy metabolism, its validity is limited to a focal area around the MD catheter. Cerebral energy disturbances were more related to low CBF than to low CDO2. Considering the high rate of mitochondrial dysfunction, treatments that increase CBF but not CDO2, such as hemodilution, may still benefit glucose delivery to drive anaerobic metabolism.

The mechanisms leading to neurological deterioration and the devastating course of delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) are still not well understood. Bedside xenon-enhanced computerized tomography (XeCT) enables measurements of regional cerebral blood flow (rCBF) during neurosurgical intensive care. In the present study, CBF characteristics in the early phase after severe SAH were explored and related to clinical characteristics and early clinical course outcome.Patients diagnosed with SAH and requiring mechanical ventilation were prospectively enrolled in the study. Bedside XeCT was performed within day 0 to 3.Data from 64 patients were obtained. Median global CBF was 34.9 mL/100 g/min (interquartile range [IQR], 26.7 to 41.6). There was a difference in CBF related to age with higher global CBF in the younger patients (30 to 49 y). CBF was also related to the severity of SAH with lower CBF in Fisher grade 4 compared with grade 3. rCBF disturbances and hypoperfusion were common; in 43 of the 64 patients rCBF20 mL/100 g/min was detected in more than 10% of the region-of-interest (ROI) area and in 17 patients such low-flow area exceeded 30%. rCBF was not related to the localization of the aneurysm; there was no difference in rCBF of ipsilateral compared with contralateral vascular territories. In patients who initially were in HuntHess grade I to III, median global CBF day 0 to 3 was significantly lower for patients who were in poor neurological state at discharge compared with patients in good neurological state, 25.5 mL/100 g/min (IQR, 21.3 to 28.3) versus 37.8 mL/100 g/min (IQR, 30.5 to 47.6).CBF disturbances are common in the early phase after SAH. In many patients, CBF was heterogenic and substantial areas with low rCBF were detected. Age and CT Fisher grade were factors influencing global cortical CBF. Bedside XeCT may be a tool to identify patients at risk of deteriorating so they can receive intensified management, but this needs further exploration.

The authors studied the incidence of postoperative intracranial hematoma to improve care after intracranial surgery. Five years (1995-1999) of surgical records were analyzed retrospectively. Patients were included if evacuation of an intracranial postoperative hematoma was reported. A control group was randomly selected. Forty-nine patients (0.8%) had postoperative hematomas requiring evacuation. The amount of intraoperative blood loss was significantly larger in the hematoma group (762 +/-735 mL [median 500 mL]) than in the control group (415 +/-403 mL; median 300 mL) (P = 0.004). Clinical deterioration occurred within the first 24 hours in 80%, within 6 hours in 51%, and within 1 hour in 12% of the patients. Those who deteriorated within 24 hours had a faster and more life-threatening deterioration than those who had a hematoma after 24 hours. A decreased level of consciousness was found in 61% and increased focal neurologic signs were found in 33% of the patients. An elevated intracranial pressure was seen significantly more often in the hematoma group (9/10 patients, 90%) than in the control group (1/8 patients, 12.5%) (P = 0.001). In this study, a large amount of intraoperative blood loss and elevated intracranial pressure were warning signs of postoperative hematoma and should alert the clinician to the increased risk. Most hematomas occurred within 24 hours after surgery, and in this time period the deterioration was more severe compared with the hematomas that occurred later.