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INTRODUCTION: Anesthetic goals in patients undergoing clipping of cerebral aneurysm include maintenance of cerebral blood flow, oxygenation, and metabolism to avoid cerebral ischemia and maintenance of hemodynamic stability. We intend to study the influence of anesthetic agents on the outcome of aneurysmal subarachnoid hemorrhage (SAH). MATERIALS AND METHODS: This is a prospective, randomized, parallel, single-center pilot trial approved by the Institutional Ethics Committee and is prospectively registered with the Clinical Trial Registry of India. Patients with aneurysmal SAH (aSAH) admitted to our institution for surgical clipping, fulfilling the trial inclusion criteria, will be randomized in a 1:1 allocation ratio utilizing a computerized random allocation sequence to receive either total intravenous anesthesia (n = 25) or inhalational anesthesia (n = 25). Our primary objective is to study the effects of these anesthetic techniques on cerebral oxygenation and metabolism in patients with aSAH. Our secondary objective is to evaluate the impact of these anesthetic techniques on the incidence of delayed cerebral ischemia and long-term patient outcomes in patients with aSAH. The Modified Rankin Score and Glasgow Outcome Scale (GOS) at discharge and 3 months following hospital discharge will be evaluated. An observer blinded to the study intervention will assess the outcome measures. DISCUSSION: This study will provide more insight as to which is the ideal anesthetic agent that offers a better neurophysiological profile regarding intraoperative cerebral oxygenation and metabolism, thereby contributing to better postoperative outcomes in aSAH patients.

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BACKGROUND: Intraoperative intracranial pressure (ICP) control continues to be a challenge for anaesthetists during craniotomies. Although many standard brain-dehydrating protocols are available, they may be ineffective in certain surgical situations and may result in harm either to the systemic or cerebral circulation. Sphenopalatine ganglion block (SPGB) can reverse the vasodilatory effects of anaesthesia during craniotomy. METHODS: This prospective randomised study was carried from June 2020 to February 2021. Fifty-two patients were randomly allocated into two groups, the block group (B) and the non-block control group (Non). Twenty-six patients were enrolled in the (B) group and received a bilateral transnasal SPG block with 2% lidocaine using a hallow culture swab prior to anaesthesia induction. Intraoperative monitoring was performed using standard American Society of Anesthesiologists (ASA) monitors in addition to invasive monitoring using intra-arterial cannulas and jugular venous bulb catheters. Subdural ICP monitors were also employed. The arterio-jugular oxygen difference in mmol/l (AjvDO2) was then calculated. Mean flow velocity cm/s (MFV) and pulsatility index (PI) were monitored in both groups using Transcranial Doppler. Haemodynamic data were recorded every 30 min from induction of anaesthesia until the closure of the dura. RESULTS: There was a significant difference in ICP prior to the dural opening between the block group (B), mean ± sd 7.58 ± 1.47, and the non-block group (Non), mean ± sd (11.69 ± 1.72), p-value < 0.001. There was no significant difference in MFV between (B) group, mean ± sd 72.65 ± 2.28 and (Non) group, mean ± sd 71.19 ± 3.09 before intubation (baseline values). While there was a significant difference after intubation between block group, mean ± sd 72.12 ± 1.77 and non-block group, mean ± sd 74.62 ± 5.07, p-value = 0.02. There was an insignificant difference between (B) and (Non) groups before intubation regarding PI values, while PI was significantly higher in (B) group than the (Non) group after intubation where mean ± sd was 1.17 ± 0.05 versus 0.96 ± 0.09, respectively, p-value = 0.001. There was no significant difference regarding cerebral oxygenation between the groups. CONCLUSIONS: SPGB can control factors that increase CBF during anaesthesia by the block of parasympathetic vasodilatory fibres to the arterial system in the anterior cerebral circulation, while neither hindering cerebral venous drainage nor impairing cerebral oxygenation, as it gives no supply to cerebral veins and does not affect basal CBF. Additionally, it does not affect systemic circulation.

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BACKGROUND: We performed a retrospective analysis of our earlier study on cerebral oxygenation monitoring by jugular venous oximetry (SjvO2) in patients of out-of-hospital cardiac arrest (OHCA). The study was focused on high SjvO2 values (≥75%) and their association with neurological outcomes and serum neuron-specific enolase (NSE) concentration. METHOD: Forty OHCA patients were divided into (i) high (Group I), (ii) normal (Group II), and (iii) low (Group III) SjvO2, with the mean SjvO2 ≥ 75%, 55-74% and <55% respectively. The neurological outcome was evaluated using the Cerebral Performance Category scale (CPC) on the 90th day after cardiac arrest (post-CA). NSE concentration was determined after ICU admission and then at 24, 48, and 72 hours (h) post-CA. RESULTS: High mean SjvO2 occurred in 67% of patients, while no patients had low mean SjvO2. The unfavourable outcome was significantly more common in Group I than Group II (74% versus 23%, p < 0.01). Group I patients had significantly higher median NSE than Group II at 48 and 72 h post-CA. A positive correlation was found between SjvO2 and PaCO2. Each 1 kPa increase in CO2 led to an increase of SjvO2 by 2.2 %+/-0.66 (p < 0.01) in group I and by 5.7%+/-1.36 (p < 0.0001) in group II. There was no correlation between SjvO2 and MAP or SjvO2 and PaO2. CONCLUSION: High mean SjvO2 are often associated with unfavourable outcomes and high NSE at 48 and 72 hours post-CA. Not only low but also high SjvO2 values may require therapeutic intervention.

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Accumulating evidence indicates that cerebral desaturation in the perioperative period occurs more frequently than recognized. Combining monitoring modalities that reflect different aspects of cerebral perfusion status, such as near-infrared spectroscopy, jugular bulb saturation, and transcranial Doppler ultrasonography, may provide an extended window for prevention, early detection, and prompt intervention in ongoing hypoxic/ischemic neuronal injury and, thereby, improve neurologic outcome. Such an approach would minimize the impact of limitations of each monitoring modality, while individual components complement each other, enhancing the accuracy of acquired information. Current literature has failed to demonstrate any clear-cut clinical benefit of these modalities on outcome prognosis.

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BACKGROUND: In patients postcardiac arrest, it has been reported that the small value of the difference between mixed venous oxygen saturation (Svo2) and jugular venous oxygen saturation (Sjvo2) is associated with poor neurologic outcome. However, the importance of the difference between mixed venous oxygen saturation and jugular venous oxygen saturation (ΔSo2 [v - jv]) remains unknown in severe traumatic brain injury (TBI). The aim of this study was to examine whether ΔSo2 (v - jv) is associated with neurologic outcome and mortality in patients with severe TBI. METHODS: We conducted post hoc analyses of the Brain Hypothermia Study, a multicenter randomized controlled trial of mild therapeutic hypothermia for the treatment of severe TBI. The value of ΔSo2(v - jv) on day 1 and day 3 was compared between survivors (n = 65) and nonsurvivors (n = 25) or between patients with favorable (n = 47) and unfavorable (n = 43) neurologic outcomes. RESULTS: The reduction in ΔSo2 (v - jv) on day 3 was -2.0% (range, -6.9% to 6.5%) in the nonsurvivor group and 6.3% (range, -2.5% to 16.7%) in the survivor group. The difference was statistically significant (P = 0.03). The same tendencies were observed in the nonsurvivor group on day 1 and in the unfavorable neurologic outcome group on day 1 and day 3, but the difference was not significant. CONCLUSIONS: The reduction in ΔSo2(v - jv) on day 3 was associated with high mortality in patients with severe TBI.

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Regional cerebral oxygen saturation (rSO2) measured using near-infrared spectroscopy has been reported to be significantly lower in hemodialysis (HD) patients than in non-HD ones, but the mechanisms are unknown. The aim of this prospective study was to assess the accuracy of near-infrared spectroscopy to estimate cerebral oxygenation in HD patients undergoing cardiovascular surgery. Our hypothesis was that rSO2 values would underestimate cerebral oxygenation in HD patients. This study included 113 patients (7 HD patients and 106 non-HD ones) undergoing cardiac or major aortic surgery between December 2015 and November 2017. We evaluated the validity of rSO2 by comparing it with ipsilateral jugular venous oxygen saturation (SjvO2). In HD and non-HD patients, rSO2 and SjvO2 showed a weak correlation (R2: 0.46 and 0.28 in HD and non-HD patients, respectively). Bland-Altman analysis revealed that bias (95% limits of agreement) of rSO2 compared to SjvO2 was - 19.2% ( - 41.7-3.3%) in HD patients and - 1.9% (- 19.3-15.5%) in non-HD ones. The large negative bias suggests that the rSO2 values measured using near-infrared spectroscopy substantially underestimate cerebral oxygenation in HD patients.

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OBJECTIVE Few studies have reported on changes in quantitative cerebral blood flow (CBF) after decompressive craniectomy and the impact of these measures on clinical outcome. The aim of the present study was to evaluate global and regional CBF patterns in relation to cerebral hemodynamic parameters in patients after decompressive craniectomy for traumatic brain injury (TBI). METHODS The authors studied clinical and imaging data of patients who underwent xenon-enhanced CT (XeCT) CBF studies after decompressive craniectomy for evacuation of a mass lesion and/or to relieve intractable intracranial hypertension. Cerebral hemodynamic parameters prior to decompressive craniectomy and at the time of the XeCT CBF study were recorded. Global and regional CBF after decompressive craniectomy was measured using XeCT. Regional cortical CBF was measured under the craniectomy defect as well as for each cerebral hemisphere. Associations between CBF, cerebral hemodynamics, and early clinical outcome were assessed. RESULTS Twenty-seven patients were included in this study. The majority of patients (88.9%) had an initial Glasgow Coma Scale score ≤ 8. The median time between injury and decompressive surgery was 9 hours. Primary decompressive surgery (within 24 hours) was performed in the majority of patients (n = 18, 66.7%). Six patients had died by the time of discharge. XeCT CBF studies were performed a median of 51 hours after decompressive surgery. The mean global CBF after decompressive craniectomy was 49.9 ± 21.3 ml/100 g/min. The mean cortical CBF under the craniectomy defect was 46.0 ± 21.7 ml/100 g/min. Patients who were dead at discharge had significantly lower postcraniectomy CBF under the craniectomy defect (30.1 ± 22.9 vs 50.6 ± 19.6 ml/100 g/min; p = 0.039). These patients also had lower global CBF (36.7 ± 23.4 vs 53.7 ± 19.7 ml/100 g/min; p = 0.09), as well as lower CBF for the ipsilateral (33.3 ± 27.2 vs 51.8 ± 19.7 ml/100 g/min; p = 0.07) and contralateral (36.7 ± 19.2 vs 55.2 ± 21.9 ml/100 g/min; p = 0.08) hemispheres, but these differences were not statistically significant. The patients who died also had significantly lower cerebral perfusion pressure (52 ± 17.4 vs 75.3 ± 10.9 mm Hg; p = 0.001). CONCLUSIONS In the presence of global hypoperfusion, regional cerebral hypoperfusion under the craniectomy defect is associated with early mortality in patients with TBI. Further study is needed to determine the value of incorporating CBF studies into clinical decision making for severe traumatic brain injury.

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Objective To investigate the roles of cerebral metabolic rate for oxygen (CMRO2) monitoring in the evaluation of cerebral function after cardiopulmonary resuscitation (CPR) through transcranial doppler (TCD) and SjvO2. Methods In this prospective/retrospective analysis, we included 46 cases admitted to the general intensive care unit (GICU) of the Second Affiliated Hospital of Soochow University from January 2012 to December 2014. Upon admission, TCD and SjvO2 were performed,and the patients' characteristics were recorded. Based on the CPC score upon GICU discharge, the patients were divided into two groups with satisfactory cerebral function and poor cerebral function, respectively. Then the clinical symptoms, cerebral blood flow (CBF), a-vDO2, SjvO2 and CMRO2 were analyzed, followed by investigating their correlation with the prognosis of cerebral function. The measurement data that were normally distributed were presented by mean ± standard deviation. Student's t test was utilized for the inter-group comparison. Correlation analysis was performed. ROC was plotted, followed by evaluating roles of each index in the specificity and sensitivity of nervous prognosis. Results No statistical differences were noted in the gender, age, initial monitoring indicators, ICU duration and initial GCS between the two groups (P>0.05). The CA-ROSC time and APACHE II score in the satisfactory cerebral function group were significantly shorter than those of the poor cerebral function group (P<0.05). The SjvO2 in the satisfactory cerebral function group was significantly lower than that of the poor function group (67.33±10.30 vs. 76.89±13.08, t=-3.579, P<0.05). The Vs and Vd as revealed by TCD in the satisfactory function group were higher than those of the poor function group, together with the CBF. Significant decrease was noted in the PI and RI in the satisfactory function group compared with that of the poor function group (P<0.05). Besides, the CMRO2 and a-vDO2 in the satisfactory function group showed significant increase compared with those of the poor function group (P<0.05). ROC indicated that CMRO2, CBF, a-vDO2 and SjvO2 could be utilized for the evaluation of cerebral function, among which CMRO2 showed the highest accuracy for the cerebral function prognosis. Conclusions CMRO2, CBF, a-vDO2 and SjvO2 were associated with cerebral function prognosis. CMRO2 was the most appropriate parameter to evaluate the oxygen metabolism in brain tissues, which could evaluate the prognosis of cerebral function.

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Acute brain injuries are a major cause of death and disability worldwide. Survivors of life-threatening brain injury often face a lifetime of dependent care, and novel approaches that improve outcome are sorely needed. A delayed cascade of brain damage, termed secondary injury, occurs hours to days and even weeks after the initial insult. This delayed phase of injury provides a crucial window for therapeutic interventions that could limit brain damage and improve outcome. A major barrier in the ability to prevent and treat secondary injury is that physicians are often unable to target therapies to patients' unique cerebral physiological disruptions. Invasive neuromonitoring with multiple complementary physiological monitors can provide useful information to enable this tailored, precision approach to care. However, integrating the multiple streams of time-varying data is challenging and often not possible during routine bedside assessment. The authors review and discuss the principles and evidence underlying several widely used invasive neuromonitors. They also provide a framework for integrating data for clinical decision making and discuss future developments in informatics that may allow new treatment paradigms to be developed.

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BACKGROUND: The beach chair position (BCP) is associated with hypotension that may lead to cerebral ischemia. Arginine vasopressin (AVP), a potent vasoconstrictor, has been shown to prevent hypotension in BCP. It also improves cerebral oxygenation in different animal models. The present study examined the effect of escalating doses of AVP on systemic hemodynamics and cerebral oxygenation during surgery in BCP under general anesthesia. METHODS: Sixty patients undergoing arthroscopic shoulder surgery in BCP under general anesthesia were randomly allocated to receive either saline (control, n = 15) or three different doses of AVP (0.025, 0.05, or 0.075 U/kg; n = 15 each) 2 minutes before BCP. Mean arterial pressure (MAP), heart rate (HR), regional cerebral oxygen saturation (SctO2), and jugular venous oxygen saturation (SjvO2) were measured after induction of anesthesia and before (presitting in supine position) and after BCP. RESULTS: AVP per se given before BCP increased MAP, and decreased SjvO2, SctO2, and HR in all patients (P < 0.05 for all). BCP decreased MAP, the magnitude of which and hence the incidence of hypotension was decreased by AVP in a dose-dependent manner. While in BCP, every dose of AVP reduced the HR and SctO2. Accordingly, it increased the incidence of cerebral desaturation (> 20% SctO2 decrease from the baseline value) with no differences in SjvO2 and the incidence of SjvO2 < 50% or SjvO2 < 40% among the groups. CONCLUSIONS: AVP ameliorates hypotension associated with BCP in a dose-dependent manner in patients undergoing shoulder surgery under general anesthesia. However, AVP may have negative effects on SctO2 before and after BCP and on SjvO2 before BCP.

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BACKGROUND: The effects of total intravenous anaesthesia (TIVA) on cerebral oxygenation in patients undergoing robot-assisted laparoscopic radical prostatectomy (RALP) have not been investigated. We examined the changes in jugular venous oxygen saturation (SjvO2 ) and regional cerebral tissue oxygen saturation (rSO2 ) during RALP under TIVA. Whether rSO2 could reflect SjvO2 was also examined. METHODS: Forty patients (ASA 1-2) undergoing RALP were enrolled. Measurements were obtained at eight time points during the operation. RESULTS: SjvO2 did not decrease at any measurement point, whereas rSO2 fell significantly 120 min after pneumoperitoneum in a steep Trendelenburg position (p <0.01). There was a weak correlation between SjvO2 and rSO2 (Pearson correlation coefficient =0.34; p <0.01). Bland-Altman analysis showed a wide interval for the limit of agreement (47%) between the two measurements. CONCLUSIONS: These findings suggested that TIVA could be safely used for RALP. It was also demonstrated that rSO2 did not accurately reflect SjvO2 during RALP. Copyright © 2014 John Wiley & Sons, Ltd.

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BACKGROUND: The beach chair position (BCP) is associated with hypotension that may lead to cerebral ischemia. Arginine vasopressin (AVP), a potent vasoconstrictor, has been shown to prevent hypotension in BCP. It also improves cerebral oxygenation in different animal models. The present study examined the effect of escalating doses of AVP on systemic hemodynamics and cerebral oxygenation during surgery in BCP under general anesthesia. METHODS: Sixty patients undergoing arthroscopic shoulder surgery in BCP under general anesthesia were randomly allocated to receive either saline (control, n = 15) or three different doses of AVP (0.025, 0.05, or 0.075 U/kg; n = 15 each) 2 minutes before BCP. Mean arterial pressure (MAP), heart rate (HR), regional cerebral oxygen saturation (SctO2), and jugular venous oxygen saturation (SjvO2) were measured after induction of anesthesia and before (presitting in supine position) and after BCP. RESULTS: AVP per se given before BCP increased MAP, and decreased SjvO2, SctO2, and HR in all patients (P 20% SctO2 decrease from the baseline value) with no differences in SjvO2 and the incidence of SjvO2 < 50% or SjvO2 < 40% among the groups. CONCLUSIONS: AVP ameliorates hypotension associated with BCP in a dose-dependent manner in patients undergoing shoulder surgery under general anesthesia. However, AVP may have negative effects on SctO2 before and after BCP and on SjvO2 before BCP.

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Objective To explore the impact of lung-protective mechanical ventilation (low tidal volume and optimal positive end-expiratory pressure (PEEP) on cerebral perfusion pressure (CPP) and cerebral oxygen metabolism.Methods Forty patients with severe cerebral injury along with respiratory failure were randomly assigned into two groups:lung-protective ventilation group A and conventional ventilation group B.Group A was planned to prescribe tidal volume 6 ～ 8 mL/kg,initial FiO240％,PEEP gradually increasing from 2 cmH2O to matched with FiO2 elevation,but the FiO2 was kept at permissive lower level.Group B was formulated with tidal volume 8 ～ 12 mL/kg,PEEP stepwise increasing from 0 2 cmH2O to match with FiO2 elevation,but PEEP was kept at permissive lower pressure.The intracranial pressure (ICP),mean arterial pressure (MAP),CPP,arterial and jugular venous blood gas were monitored.Results PEEP (8.2±3.32 cmH2O),ICP (19.7 ±3.6 mmHg),PaCO2 (54±7.3 mmHg),jugular venous carbon dioxide partial pressure (PjV CO2,56.7 ± 9.6 mmHg) in group A were higher than those (5.7±2.3 cmH2O,16.9±3.8 mmHg,41 ±5.2 mmHg,49.8 ±6.9 mmHg) in group B (P＜ 0.05 or P ＜ 0.01).VT,FiO2 in the group A were lower than those in the group B.There were no differences in PaO2/FiO2,jugular venous oxygen saturation (SjVO2),MAP,and CPP between two groups.PaCO2 were significantly correlated with CPP (r =0.368,P =0.019) while there was no correlation with ICP,PaO2,SjVO2,PjVCO2 (all P ＞0.05).CPP (69.7 ± 12.3 mmHg) was higher in case of PaCO2 (46 ～60mmHg) than those (61.5 ±9.1 mmHg) in case of PaCO2 (35 ～45 mmHg).There was correlation between PEEP and ICP (r =0.436,P =0.005).When PEEP was divided into three groups:≤52 cmH2O,6 ～ 102 cmH2O and ＞ 102 cmH2O,ICPs were different one another among three groups.When PEEP ＞ 102 cmH2O,it had a distinguished negative correlation with CPP (r =-0.395,P =0.017),while PEEP ≤ 102 cmH2O,CPP presented decreasing tendency.SjVO2 correlated with PaO2 (r =0.403,P =0.014) and PjVCO2 (r =-0.502,P =0.001) respectively.There were no significant relationships between SjVO2 and CPP,ICP,MAP,PEEP,respectively.Conclusions Lung-protective mechanical ventilation was relatively safer in patients with severe cerebral injury compared with conventional mechanical ventilation.Mild PaCO2 elevation (46 ～ 60 mmHg) combined with higher PEEP (＜ 102 cmH2O) did not decrease CPP.There was no difference in SjVO2 between the two modes of mechanical ventilation,suggesting no changes in cerebral metabolism occurred.

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Objective To investigate the effect of L-arginine (L-arg) on cerebral oxygen metabolism and ultrastructure during deep hypothermic circulatory arrest (DHCA) in experimental dogs. Methods Fifteen healthy adult mongrel dogs with both sexes, weighing (14.7±2.4)kg, were randomly divided into three groups (n=5): sham treated group, L-arg pretreated group (100mg/kg L-arg was given 60min before circulation arrest), L-arg and 7-Ni combined treated group (100mg/kg L-arg and 25mg/kg 7-Ni were given 60min before circulation arrest). Extracorporeal circulatory was established routinely, and DHCA commenced when the nasopharyngeal temperature was reduced to 18℃, then reperfusion began after 90min of DHCA. SjvO2, NO in plasma were measured 30min before DHCA and 0,45,90min after DHCA commencement and 60min after rewarming. The ultrastructural changes of cortex and hippocampal gyrus were also been observed with transmission electron microscope after the dogs were executed. Results Compared with sham-treated group, L-arg pretreatment combined with 7-Ni or not increased NO content in plasma, SjvO2 during DHCA, improved cerebral oxygen metabolism and reduced brain ultrastructural injury. There was a positive correlation between NO conten in plasma before arrest and SjvO2 after arrest (r=0.679,P=0.005). Conclusion L-arg pretreatment has cerebral protective effects and can improve cerebral oxygen metabolism during DHCA.

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BACKGROUND: Marked changes in systemic hemodynamics during liver transplantation may lead to changes in cerebral hemodynamics and metabolism. Therefore, continuous monitoring of the jugular venous oxygen saturation (SjvO2) may help the anesthetic management of liver transplantation. METHODS: We observed changes in SjvO2 using a double lumen oximetry catheter for continuous monitoring and analyzed the correlation between SjvO2 and hemodynamic measurements in thirty patients undergoing liver transplantation. RESULTS: There were no significant changes in SjvO2 compared to initial SjvO2 during liver transplantation. SjvO2, however, increased from 72.5 to 79.6 % (P < 0.05), before and after reperfusion. There was a weak correlation between changes in SjvO2 and cardiac output (r = 0.38, P < 0.05), whereas no correlation was found among changes in SjvO2 and arterial carbon dioxide tension, mean arterial pressure, central venous pressure, or mixed venous oxygen saturation before and after reperfusion. CONCLUSIONS: SjvO2 that reflects changes in cerebral oxygen demand-supply balance was well maintained during liver transplantation except the reperfusion period. Continuous monitoring of changes in SjvO2 at this period may provide further insight to understand physiology of cerebral oxygenation during liver transplantation and merits further studies.

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BACKGROUND: Fulminant hepatic failure is characterized by rapid progressive liver failure with the onset of encephalopathy within a few weeks of the appearance of jaundice. This illness is frequently complicated by hemodynamic instability, multiple organ dysfunction and intracranial hypertension associated with cerebral edema, which is the most common cause of death in this condition. We reviewed 8 cases of liver transplantation with fulminant hepatic failure with respect to anesthetic management and neurologic monitoring. METHODS: We analyzed anesthetic management, intracranial pressure (ICP), cerebral perfusion pressure (CPP), jugular venous oxygen saturation (SjvO2) and hemodynamics retrospectively during liver transplantation in 8 patients with fulminant hepatic failure. Intracranial hypertension was defined as an ICP >or= 20 mmHg for at least 5 minutes. The goal of management is to keep the CPP above 40 - 50 mmHg and ICP below 30 - 40 mmHg. There were 3 cases of hepatorenal syndrome and continous veno-venous hemodiafiltration (CVVHD) was used in 2 cases. RESULTS: All patients showed characteristic hyperdynamic circulation with severe vasodilation and vasopressive drugs were needed to maintain CPP. The episodes of intracranial hypertension occurred in all patients during transplantation. To decrease ICP, medical therapy with mannitol, furosemide and thiopental infusion were required. Intracranial hemorrhagic complications occurred in 3 cases. SjvO2 decreased transiently below 60% in 3 cases. However, it was improved with an increase of PaCO2 by hypoventilation and maintained above 60 - 80% in all cases. CONCLUSIONS: This data suggests that there is a risk of brain injury secondary to elevated ICP and low CPP during liver transplantation. ICP, CPP and SjvO2 monitoring in patients with fulminant hepatic failure can be useful for the prompt recognition of intracranial hypertension and for guiding therapy. However, correction of the coagulopathy before placement of the ICP tranducer must be performed to prevent hemorragic complications.

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BACKGROUND: There are therapies to lower intracranial pressure (ICP) including head elevation, hyperventilation, diuretics injection, intravenous mannitol, hypothermia, cerebrospinal fluid drainage, and cerebral resection in neurosurgical patients. However in recent reports, hyperventilation followed by mannitol administration may lead to cerebral ischemia. Therefore, we investigated the effect of 0.5-1.0 g/kg mannitol administration on jugular venous oxygen saturation (SjVO2) and cerebral arterial- jugular venous oxygen content difference (AVDO2) at PaCO2 25-30 mmHg and 35-40 mmHg in patients undergoing neurosurgery. METHODS: We studied 17 patients undergoing neurosurgery in the Ajou University Hospital. Anesthesia was induced with fentanyl, midazolam, thiopental, and vecuronium, and maintained with O2-Air-Isoflorane, a continuous infusion of fentanyl, and vecuronium. Patients were divided into two groups. Group 1 (n = 10) which is PaCO2 25-30 mmHg and Group 2 (n = 7) which is PaCO2 35-40 mmHg by controlling ventilator. Measurements of SjVO2 and AVDO2 in following time intervals: I = preinjection of mannitol, II = postinjection 20 minutes of mannitol, III = postinjection 40 minutes of mannitol were obtained for each group. 0.5-1.0 g/kg mannitol was administered intravenously just at duramater opening. RESULTS: Hemodynamics and hematologics were not significantly different among the two groups. SjVO2 of each group are as follows; Group 1; I (70.3+/-8.1%), II (66.3+/-6.9%), III (69.1+/-7.9%) and Group 2; I (78.6+/-7.4%), II (75.1+/-8.1%), III (76.0+/-11.2%). Hyperventilation significantly decreased SjVO2. AVDO2 was not significantly different but SjVO2 in II was significantly decreased compared with I and III in Group 1 (20% patients). CONCLUSIONS: Mannitol produced a change of SjVO2 and AVDO2 during hyperventilation. Therefore, intravenous mannitol during hyperventilation should be given cautiously according to the patients status because it may cause cerebral ischemia in critical patients.

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BACKGROUND: During intracranial brain surgery, numerous factors may alter cerebral blood flow and the oxygen supply-demend balance. Continuous monitoring of the jugular bulb venous oxygen saturation (SjvO2) may help in the anesthetic management of such procedures. METHODS: Fiberoptic SjvO2 was continuously monitored and recorded 1, 3 and 5 min after the skin incision, skull bone craniotomy, dura open and dura closure in 20 patients. RESULTS: The SjvO2 was increased after the skin (scalp) incision at 1, 3 and 5 minutes and also after endotracheal suctioning for removal of secretions. CONCLUSIONS: Although the accuracy of Fibroptic SjvO2 determination is limited, it allows the detection of cerebral blood flow and oxygen supply-demend imbalance during brain surgery. The frequent occurance of SjvO2 elevations is suggestive of reactive hyperemia mechaniams.

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BACKGROUND: Thiopental has a profound impact on the cardiovascular system. The effects of hemody namics after intravenous thiopental on the balance of cerebral metabolism with cerebral blood flow is unknown. The purpose of this study was to monitor hemodynamic change, cerebral arterial-jugular venous oxygen content difference (AVDO2) and jugular venous oxygen saturation (SjVO2) after a thiopental injection for brain protection during cerebral aneurysm surgery. METHODS: Twenty patients received a standard anesthetic consisting of isoflurane, vecuronium and fentanyl with a PaCO2 of 30 35 mmHg. Hemodynamics, arterial and jugular venous blood gases were measured at 3 time points:I; Just before thiopental injection; II; Electroencephalographic (EEG) burst suppression after a 4 5 mg/kg intravenous thiopental injection; and III; EEG recovery. RESULTS: Intravenous thiopental (4 5 mg/kg) induced an EEG burst suppression for 6.5 +/- 1.7 minutes. Hemodynamics and arterial blood gas analysis were not significantly different among the different time points, but mean arterial pressure (68.4 +/- 7.2 mmHg) and systemic vascular resistance (1027.0 +/- 300.9 dynes sec/cm5) in II were significantly (P < 0.05) decreased compared with I (84.3 +/- 9.6, 1169.1 +/- 304.5) and III (89.1 +/- 10.6, 1288.6 +/- 426.1). SjVO2 (71.6 +/- 11.8%) was significantly (p < 0.05) decreased within the normal value compared with I (75.1 +/- 5.6) and III (76.1 +/- 10.1), but AVDO2 was not significantly different among the 3 time points. There was no evidence of cerebral ischemia or infarction in computed tomographic (CT) findings of the 20 patients after surgery. CONCLUSIONS: Hemodynamics after 4 5 mg/kg intravenous thiopental do not modify the balance ofcerebral oxygen metabolism with cerebral blood flow in patients undergoing cerebral aneurysm surgery.

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The continuous measurement of jugular venous oxygen saturation(SjvO2) with a fibroptic catheter is evaluated as a method of detecting cerebral ischemia after head injury. Fifty patients admitted to the hospital who were unconscious after severe head injuries had continuous and simultaneous monitoring of SjvO2, intracranial pressure, arterial oxygen saturation, arterial blood pressure. Whenever SjvO2 dropped to less than 50%, a standardized protocol was followed to confirm the validity of the desaturation and to elucidate its cause. A total of 72 episodes of jugular venous oxygen desaturation occurred in 45 patients, possibly due to intracranial hypertension in 39 episodes, arterial hypoxia in 13, combinations of the above in 9, systemic hypotension in 7, and anemia in 4. Two episodes of hyp-eremia, SjvO2 more than 90%, occurred in 2 patients with carotid-cavernous fistula. The incidence of jugular venous oxygen desaturation found in this study suggests that continuous monitoring of SjvO2 may be of clinical value in patients with head injury.

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