scholarly journals O-161 Cerebral Oxygenation Before And After Neurosurgical Placement Of A Ventricular Reservoir In Neonates With Phvd

2014 ◽  
Vol 99 (Suppl 2) ◽  
pp. A85.2-A85
Author(s):  
AJ Brouwer ◽  
T Alderliesten ◽  
LS de Vries ◽  
PMA Lemmers
1998 ◽  
Vol 23 (2) ◽  
pp. 119-125 ◽  
Author(s):  
Mohamed M. Atallah ◽  
Andreas Hoeft ◽  
Mohamed A. El-Ghorouri ◽  
Golinar E. Hammouda ◽  
Mostafa MA Saied

Background and ObjectivesTransurethral resection of the prostate (TURP) is associated with the unique complication of transurethral resection of prostate syndrome (TURS), which is attributed to the absorption of irrigating fluid. This study was initiated to investigate the effects of spinal anesthesia and TURP on cerebral oxygen balance.MethodsThirty patients scheduled for TURP were included. Jugular bulb oxygen saturation (SjbO2) was measured via retrograde cannulation of jugular venous bulb. Spinal anesthesia was initiated by 3 mL hyperbaric 0.5% bupivacaine injected at L3-L4 in the sitting position, producing a block to the T10 dermatome. Hemodynamic measurements and arterial and jugular bulb blood gasometry were performed before and after spinal anesthesia, throughout surgery, and during the postoperative period.ResultsA significant decrease of cerebral perfusion pressure after spinal anesthesia was accompanied by a significant decrease of SjbO2 below a preoperative value of 61% ± 1. Eight patients developed yawning, irritability, restlessness, and nausea toward the end of surgery, and these were considered to be early signs of TURS. These patients demonstrated SjbO2 below 55% and 50% in 63% and 42% of respective data set points.ConclusionThe neurologic symptoms in patients undergoing TURP during spinal anesthesia might not only be caused by absorption of irrigating fluid but also by impairment of cerebral oxygenation.


Neurosurgery ◽  
2017 ◽  
Vol 80 (6) ◽  
pp. 942-949 ◽  
Author(s):  
Walid Albanna ◽  
Miriam Weiss ◽  
Marguerite Müller ◽  
Marc Alexander Brockmann ◽  
Annette Rieg ◽  
...  

Abstract BACKGROUND: Critical hypoperfusion and metabolic derangement are frequently encountered with refractory vasospasm. Endovascular rescue therapies (ERT) have proven beneficial in selected cases. However, angioplasty (AP) and intraarterial lysis (IAL) are measures of last resort and prospective, quantitative results regarding the efficacy (cerebral oxygenation, metabolism) are largely lacking. OBJECTIVE: To evaluate the efficacy of ERTs for medically refractory vasospasm using multimodal, continuous event neuromonitoring. METHODS: To detect cerebral compromise in a timely fashion, sedated patients with aneurysmal subarachnoid hemorrhage received continuous neuromonitoring (ptiO2 measurement, intraparenchymal microdialysis). ERT (AP and/or IAL) was considered in cases of clinically relevant vasospasm refractory to conservative treatment measures. Oxygen saturation and cerebral and systemic metabolism before and after events of ERT was recorded. RESULTS: We prospectively included 13 consecutive patients and recorded a total of 25 ERT events: AP (n = 10), IAL (n = 11), or both (AP + IAL, n = 4). Average cerebral ptiO2 was 10 ± 11 torr before and 49 ± 22 torr after ERT (P < .001), with a lactate-pyruvate ratio decreasing from 146.6 ± 119.0 to 27.9 ± 10.7 after ERT (P < .001). Comparable improvement was observed for each type of intervention (AP, IAL, or both). No significant alterations in systemic metabolism could be detected after ERT CONCLUSION: Multimodal event neuromonitoring is able to quantify treatment efficacy in subarachnoid hemorrhage-related vasospasm. In our small cohort of highly selected cases, ERT was associated with improvement in cerebral oxygenation and metabolism with reasonable outcome. Event neuromonitoring may facilitate individual and timely optimization of treatment modality according to the individual clinical course.


Neurosurgery ◽  
2006 ◽  
Vol 59 (2) ◽  
pp. 466
Author(s):  
Jeffrey V. Rosenfeld ◽  
Alexios A. Adamides ◽  
D James Cooper ◽  
Naomi Pratt ◽  
Nicholas Tippett ◽  
...  

1988 ◽  
Vol 65 (1) ◽  
pp. 428-433 ◽  
Author(s):  
P. E. Bickler ◽  
L. Litt ◽  
J. W. Severinghaus

Acetazolamide (AZ), a potent carbonic anhydrase inhibitor in human and animal tissues, increases cerebral blood flow (CBF) by acidifying cerebral extracellular fluids. To demonstrate the relationship of increased CBF to brain O2 availability after AZ administration, a compensated fluorometer was used to study changes in the cerebrocortical redox balance in rabbits. Seven rabbits were anesthetized with pentobarbital sodium. Excitation light (366 nm) was conducted to the cerebrocortical surface of each animal by a 4-mm-diam fiberoptic light guide. Fluorescence emissions from cerebrocortical NADH (450 nm) were compared at different inspired O2 (FIO2) tensions. Reflected light (366 nm), which was used to determine a correction to the fluorescence signal, was separately quantitated and interpreted as an index of cerebrocortical blood volume. Reductions in FIO2 from 1.0 to 0.21, 0.14, 0.10, and 0.07 resulted in increases in both tissue blood volume and [NADH]. Intravenous AZ (25 mg/kg) increased cerebrocortical blood volume and reduced the [NADH], even during ventilation with 100% O2. The changes in brain redox balance caused by vasodilation with AZ were compared with those caused by vasodilatation with CO2. The NAD+/NADH redox state was a continuous function of FIO2 at all levels of arterial PCO2 (PaCO2), both before and after AZ administration. The improvement in cerebral O2 delivery caused by AZ-induced vasodilation was comparable to that caused by the vasodilatation that results from a PaCO2 elevation approximately equal to 12-15 Torr above normal. The slope of the relationship between [NADH] and FIO2 was similar at normal, low, and high levels of PaCO2. We conclude that AZ administration and PaCO2 elevation improve cerebral oxygenation by similar mechanisms.


2016 ◽  
Vol 311 (2) ◽  
pp. H453-H464 ◽  
Author(s):  
Michail E. Keramidas ◽  
Roger Kölegård ◽  
Igor B. Mekjavic ◽  
Ola Eiken

The study examined the effects of hypoxia and horizontal bed rest, separately and in combination, on peak oxygen uptake (V̇o2 peak) during upright cycle ergometry. Ten male lowlanders underwent three 21-day confinement periods in a counterbalanced order: 1) normoxic bed rest [NBR; partial pressure of inspired O2(PiO2) = 133.1 ± 0.3 mmHg]; 2) hypoxic bed rest (HBR; PiO2= 90.0 ± 0.4 mmHg), and 3) hypoxic ambulation (HAMB; PiO2= 90.0 ± 0.4 mmHg). Before and after each confinement, subjects performed two incremental-load trials to exhaustion, while inspiring either room air (AIR), or a hypoxic gas (HYPO; PiO2= 90.0 ± 0.4 mmHg). Changes in regional oxygenation of the vastus lateralis muscle and the frontal cerebral cortex were monitored with near-infrared spectroscopy. Cardiac output (CO) was recorded using a bioimpedance method. The AIR V̇o2 peakwas decreased by both HBR (∼13.5%; P ≤ 0.001) and NBR (∼8.6%; P ≤ 0.001), with greater drop after HBR ( P = 0.01). The HYPO V̇o2 peakwas also reduced by HBR (−9.7%; P ≤ 0.001) and NBR (−6.1%; P ≤ 0.001). Peak CO was lower after both bed-rest interventions, and especially after HBR (HBR: ∼13%, NBR: ∼7%; P ≤ 0.05). Exercise-induced alterations in muscle and cerebral oxygenation were blunted in a similar manner after both bed-rest confinements. No changes were observed in HAMB. Hence, the bed-rest-induced decrease in V̇o2 peakwas exaggerated by hypoxia, most likely due to a reduction in convective O2transport, as indicated by the lower peak values of CO.


2020 ◽  
Vol 25 (3) ◽  
pp. 235-241
Author(s):  
Shih-Shan Lang ◽  
Omaditya Khanna ◽  
Natalie J. Atkin ◽  
Judy E. Palma ◽  
Ian Yuan ◽  
...  

OBJECTIVEThe lack of a continuous, noninvasive modality for monitoring intracranial pressure (ICP) is a major obstacle in the care of pediatric patients with hydrocephalus who are at risk for intracranial hypertension. Intracranial hypertension can lead to cerebral ischemia and brain tissue hypoxia. In this study, the authors evaluated the use of near-infrared spectroscopy (NIRS) to measure regional cerebral oxygen saturation (rSO2) in symptomatic pediatric patients with hydrocephalus concerning for elevated ICP.METHODSThe authors evaluated the NIRS rSO2 trends in pediatric patients presenting with acute hydrocephalus and clinical symptoms of intracranial hypertension. NIRS rSO2 values were recorded hourly before and after neurosurgical intervention. To test for significance between preoperative and postoperative values, the authors constructed a linear regression model with the rSO2 values as the outcome and pre- and postsurgery cohorts as the independent variable, adjusted for age and sex, and used the generalized estimating equation method to account for within-subject correlation.RESULTSTwenty-two pediatric patients underwent NIRS rSO2 monitoring before and after CSF diversion surgery. The mean durations of NIRS rSO2 recording pre- and postoperatively were 13.95 and 26.82 hours, respectively. The mean pre- and postoperative rSO2 values were 73.84% and 80.65%, respectively, and the adjusted mean difference estimated from the regression model was 5.98% (adjusted p < 0.0001), suggestive of improved cerebral oxygenation after definitive neurosurgical CSF diversion treatment. Postoperatively, all patients returned to baseline neurological status with no clinical symptoms of elevated ICP.CONCLUSIONSCerebral oxygenation trends measured by NIRS in symptomatic pediatric hydrocephalus patients with intracranial hypertension generally improve after CSF diversion surgery.


PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0253306
Author(s):  
Fiona J. Stenning ◽  
Graeme R. Polglase ◽  
Arjan B. te Pas ◽  
Kelly J. Crossley ◽  
Martin Kluckow ◽  
...  

Background Delayed umbilical cord clamping (UCC) after birth is thought to cause placental to infant blood transfusion, but the mechanisms are unknown. It has been suggested that uterine contractions force blood out of the placenta and into the infant during delayed cord clamping. We have investigated the effect of uterine contractions, induced by maternal oxytocin administration, on umbilical artery (UA) and venous (UV) blood flows before and after ventilation onset to determine whether uterine contractions cause placental transfusion in preterm lambs. Methods and findings At ~128 days of gestation, UA and UV blood flows, pulmonary arterial blood flow (PBF) and carotid arterial (CA) pressures and blood flows were measured in three groups of fetal sheep during delayed UCC; maternal oxytocin following mifepristone, mifepristone alone, and saline controls. Each successive uterine contraction significantly (p<0.05) decreased UV (26.2±6.0 to 14.1±4.5 mL.min-1.kg-1) and UA (41.2±6.3 to 20.7 ± 4.0 mL.min-1.kg-1) flows and increased CA pressure and flow (47.1±3.4 to 52.8±3.5 mmHg and 29.4±2.6 to 37.3±3.4 mL.min-1.kg-1). These flows and pressures were partially restored between contractions, but did not return to pre-oxytocin administration levels. Ventilation onset during DCC increased the effects of uterine contractions on UA and UV flows, with retrograde UA flow (away from the placenta) commonly occurring during diastole. Conclusions We found no evidence that amplification of uterine contractions with oxytocin increase placental transfusion during DCC. Instead they decreased both UA and UV flow and caused a net loss of blood from the lamb. Uterine contractions did, however, have significant cardiovascular effects and reduced systemic and cerebral oxygenation.


PEDIATRICS ◽  
1995 ◽  
Vol 95 (4) ◽  
pp. 555-561
Author(s):  
K. D. Liem ◽  
J. C. W. Hopman ◽  
B. Oeseburg ◽  
A. F. J. de Haan ◽  
C. Festen ◽  
...  

Objective. To investigate cerebral oxygenation and hemodynamics in relation to changes in some relevant physiologic variables during induction of extracorporeal membrane oxygenation (ECMO) in newborn infants. Methods. Twenty-four newborn infants requiring ECMO were studied from cannulation until 60 minutes after starting ECMO. Concentration changes of oxyhemoglobin (cO2Hb), deoxyhemoglobin (cHHb), total hemoglobin (ctHb), and (oxidized-reduced) cytochrome aa3 (cCyt.aa3) in cerebral tissue were measured continuously by near infrared spectrophotometry. Heart rate (HR), transcutaneous partial pressures of oxygen and carbon dioxide (tcPo2 and tcPco2), arterial O2 saturation (saO2), and mean arterial blood pressure (MABP) were measured simultaneously. Intravascular hemoglobin concentration (cHb) was measured before and after starting ECMO. In 18 of the 24 infants, mean blood flow velocity (MBFV) and pulsatility index (PI) in the internal carotid and middle cerebral arteries were also measured before and after starting ECMO using pulsed Doppler ultrasound. Results. After carotid ligation, cO2Hb decreased whereas cHHb increased. After jugular ligation, no changes in cerebral oxygenation were found. At 60 minutes after starting ECMO, the values of cO2Hb, saO2, tcPo2, and MABP were significantly higher than the precannulation values, whereas the value of cHHb was lower. There were no changes in cCyt.aa3, tcPco2, and HR, whereas cHb, decreased. The MBFV was significantly increased in the major cerebral arteries except the right middle cerebral artery, whereas PI was decreased in all measured arteries. Cerebral blood volume, calculated from changes in ctHb and cHb, was increased in 20 of 24 infants after starting ECMO. Using multivariate regression models, a positive correlation of ΔctHb (representative of changes in cerebral blood volume) with ΔMABP and a negative correlation with ΔtcPo2 were found. Conclusions. The alterations in cerebral oxygenation after carotid artery ligation might reflect increased O2 extraction. Despite increase of the cerebral O2 supply after starting ECMO, no changes in intracellular O2 availability were found, probably because of sufficient preservation of intracellular cerebral oxygenation in the pre-ECMO period despite prolonged hypoxemia. The increase in cerebral blood volume and cerebral MBFV may result from the following: (1) reactive hyperperfusion, (2) loss of autoregulation because of prolonged hypoxemia before ECMO and/or decreased arterial pulsatility, or (3) compensation for hemodilution related to the ECMO procedure.


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