Low Cerebral Oxygen Research Articles

Laboratory Variables Associated with Low Near-Infrared Cerebral Oxygen Saturation in Icteric Patients Before Liver Transplantation Surgery

Although regional cerebral oxygen saturation (rSO₂) measurements can detect disturbances in cerebral oxygenation, their usefulness is limited in patients with hyperbilirubinemia. We examined the relationship between rSO₂ and other laboratory variables that may affect interpretation of low rSO₂ in awake patients with end-stage liver disease before liver transplantation surgery. Before induction of general anesthesia, rSO₂ was measured in 164 patients with liver cirrhosis (Child class A/B/C = 19/41/104) and 8 with fulminant hepatic failure. Patients with West Haven hepatic encephalopathy of grade 3 or 4 were excluded. Relationships between rSO₂ and laboratory variables were evaluated by correlation and multivariate regression, and by receiver operating characteristic curve analysis. Univariate analyses showed that rSO₂ (median 58.5%, range 15% to 82%) correlated with serum total bilirubin, hemoglobin (Hb), creatinine, sodium, and magnesium concentrations, and prothrombin time (P < 0.001 each), but not with serum concentrations of glucose, albumin, potassium, and ammonia. Multiple logistic regression analysis showed that only elevated total bilirubin (range 0.4 to 66 mg/dL; odds ratio [OR] = 1.31; 95% confidence interval [CI] = 1.18 to 1.45) and low Hb (range 5.3 to 15.7 g/dL; OR = 0.21; 95% CI = 0.11 to 0.43) were independently related to rSO₂ <50%. The optimum cutoff points for observing an rSO₂ < 50% were total bilirubin >7.2 mg/dL (sensitivity 89%, specificity 90%) and Hb <9.6 g/dL (sensitivity 70%, specificity 82%). High total bilirubin and low Hb concentrations were independently associated with rSO₂ values below 50% in end-stage liver disease patients awaiting liver transplantation. The results of this study identify patients in whom a low rSO₂ may be an artifact rather than cerebral ischemia.

Preoperative regional cerebral oxygen saturation is a predictor of postoperative delirium in on-pump cardiac surgery patients: a prospective observational trial

IntroductionPostoperative delirium is an important problem in patients undergoing major surgery. Cerebral oximetry is a non-invasive method to detect imbalances in the cerebral oxygen supply/demand-ratio. Low preoperative cerebral oxygen saturation (ScO2) levels have been associated with postoperative delirium in non-cardiac surgery patients. The present prospective observational study determines the relationship between pre- and intra-operative ScO2 levels and postoperative delirium in patients undergoing on-pump cardiac surgery.MethodsAfter approval of the local ethical committee and written informed consent, N = 231 patients scheduled for elective/urgent cardiac surgery were enrolled. Delirium was assessed by the confusion-assessment-method for the intensive care unit (CAM-ICU) on the first three days after surgery. ScO2 was obtained on the day before surgery, immediately before surgery and throughout the surgical procedure. Preoperative cognitive function, demographic, surgery related, and intra- and post-operative physiological data were registered.ResultsPatients with delirium had lower pre- and intra-operative ScO2 readings, were older, had lower mini-mental-status-examination(MMSE) scores, higher additive EuroScore and lower preoperative haemoglobin-levels. The binary logistic regression identified older age, lower MMSE, neurological or psychiatric disease and lower preoperative ScO2 as independent predictors of postoperative delirium.ConclusionsThe presented study shows that a low preoperative ScO2 is associated with postoperative delirium after on-pump cardiac surgery.

Cerebral oxygenation in wake and during sleep and its relationship to cognitive function in community-dwelling older adults without sleep disordered breathing.

This descriptive cross-sectional study investigated the relationships between cerebral oxygen reserve and cognitive function in community-dwelling older adults. Participants (72 women and 40 men) underwent standard polysomnography, including regional measures of percent oxyhemoglobin saturation (rcSO(2)) determined by cerebral oximetry. Two variables were used to calculate cerebral oxygen reserve: (a) awake rcSO(2) (mean presleep rcSO(2)) and (b) the change in rcSO(2) from before sleep to the end of the first non-rapid-eye movement cycle. General linear models, adjusted for the effects of education and occupation, tested differences in performance on standard tests of memory, attention, and speed of mental processing. Awake rcSO(2) values were normal (60%-79.9%) in 64 participants, marginal (50%-59.9%) in 41, and low (43%-49.9%) in 7. Participants with normal awake levels had higher cognitive function than those with low levels (p < .05). Changes in rcSO(2) were greatest in participants with marginal awake rcSO(2) values; among whom, those who increased rcSO(2) during sleep (n = 17) had better memory function than the 24 who did not (p < .05). Low awake rcSO(2) values mark individuals with low cerebral oxygen reserves and generally lower cognitive function; marginal awake rcSO(2) values that fall during sleep may indicate loss of cerebral oxygen reserve and an increased risk for cognitive decline. Further studies may clarify the significance of and mechanisms underlying individual differences in awake rcSO(2) and the changes that occur in rcSO(2) while asleep.

Neuroprotection in pediatric cardiac surgery: What is on the horizon?

Neurological injury still occurs in association with pediatric cardiac surgery, despite major progress in reducing mortality. Forty to 50% of 5 year olds who underwent complex open cardiac surgery as neonates and young infants have impaired neurodevelopmental outcomes. In order to apply neuroprotective strategies, it is necessary to develop markers for acute neurological injury, and surrogates that predict later abnormal neurodevelopmental outcomes. Near infrared spectroscopy holds promise as a marker of acute brain injury, with several pediatric cardiac surgery studies indicating a relationship between prolonged low cerebral oxygen saturation and clinical or MRI change. EEG seizures have not been found to have a relationship with acute or longer term neurological injury in recent studies. Brain MRI indicates that approximately 30% of neonates have MRI injury before cardiac surgery, and 40% have new injury postoperatively, predominately white matter injury. Serum or urine biomarkers, such as S100β protein, neuron–specific enolase, or creatine kinase brain band, lack specificity for nervous system injury. Newer biomarkers, such as glial fibrillary acidic protein, ubiquitin C-terminal hydrolase 1, and phosphorylated axonal neurofilament heavy chain, have potential for much greater specificity. Neuroprotective strategies include cardiopulmonary bypass techniques which avoid circulatory arrest and low flows. Certain anesthetic regimens such as halogenated anesthetic agents, ketamine, and dexmedetomidine may be neuroprotective in pediatric cardiac surgery. Therapeutic hypothermia, and remote ischemic preconditioning are two simple techniques that may prove to have neuroprotective properties. Erythropoietin pretreatment, and treatment with neurotrophic factors such as brain-derived neurotrophic factor, glial cell line derived neurotrophic growth factor, vascular endothelial growth factor, and nerve growth factor also have potential to prevent and treat neuronal loss in the perioperative period. Finally, neural stem cells derived from the patient’s own umbilical cord blood could potentially be utilized for neuroprotection in neonates with a prenatal diagnosis of congenital heart disease.

Sex differences in cerebral injury after severe haemorrhage and ventricular fibrillation in pigs

Experimental studies of haemorrhagic shock have documented a superior haemodynamic response and a better outcome in female animals as compared with male controls. Such sexual dimorphism has, nevertheless, not been reported after circulatory arrest that follows exsanguination and shock. We aimed to study differences in cerebral injury markers after exsanguination cardiac arrest in pre-pubertal piglets. The hypothesis was that cerebral injury is less extensive in female animals, and that this difference is independent of sexual hormones or choice of resuscitative fluid. Thirty-two sexually immature piglets (14 males and 18 females) were subjected to 5 min of haemorrhagic shock followed by 2 min of ventricular fibrillation and 8 min of cardiopulmonary resuscitation, using three resuscitation fluid regimens (whole blood, hypertonic saline and dextran, or acetated Ringers' solution plus whole blood and methylene blue). Haemodynamic values, cellular markers of brain injury and brain histology were studied. After successful resuscitation, female piglets had significantly greater cerebral cortical blood flow, tended to have lower S-100beta values and a lower cerebral oxygen extraction ratio. Besides, in female animals, systemic and cerebral venous acidosis were mitigated. Female piglets exhibited a significantly smaller increase in neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) expression in their cerebral cortex, smaller blood-brain-barrier (BBB) disruption and significantly smaller neuronal injury. After resuscitation from haemorrhagic circulatory arrest, cerebral reperfusion is greater, and BBB permeability and neuronal injury is smaller in female piglets. An increased cerebral cortical iNOS and nNOS expression in males implies a mechanistic relationship with post-resuscitation neuronal injury and warrants further investigation.

Brain tissue oxygen monitoring in traumatic brain injury and major trauma: outcome analysis of a brain tissue oxygen–directed therapy

Cerebral ischemia is the leading cause of preventable death in cases of major trauma with severe traumatic brain injury (TBI). Intracranial pressure (ICP) control and cerebral perfusion pressure (CPP) manipulation have significantly reduced the mortality but not the morbidity rate in these patients. In this study, the authors describe their 5-year experience with brain tissue oxygen (PbtO(2)) monitoring, and the effect of a brain tissue oxygen-directed critical care guide (PbtO(2)-CCG) on the 6-month clinical outcome (based on the 6-month Glasgow Outcome Scale score) in patients with TBIs. One hundred thirty-nine patients admitted to Creighton University Medical Center with major traumatic injuries (Injury Severity Scale [ISS] scores >or= 16) and TBI underwent prospective evaluation. All patients were treated with a PbtO(2)-CCG to maintain a brain oxygen level > 20 mm Hg, and control ICP < 20 mm Hg. The role of demographic, clinical, and imaging parameters in the identification of patients at risk for cerebral hypooxygenation and the influence of hypooxygenation on clinical outcome were recorded. Outcomes were compared with those in a historical ICP/CPP patient cohort. Subgroup analysis of severe TBI was performed and compared to data reported in the Traumatic Coma Data Bank. The majority of injuries were sustained in motor vehicle crashes (63%), and diffuse brain injury was the most common abnormality (58%). Mechanism of injury, severity of TBI, pathological entity, neuroimaging results, and trauma indices were not predictive of ischemia. Factors affecting death included gunshot injury, poor trauma indices, subarachnoid hemorrhage, and coma. After standard resuscitation, 65% of patients had an initially low PbtO(2). Data are presented as means +/- SDs. Treatment with the PbtO(2)-CCG resulted in a 44% improvement in mean PbtO(2) (16.21 +/- 12.30 vs 23.65 +/- 14.40 mm Hg; p < 0.001), control of ICP (mean 12.76 +/- 6.42 mm Hg), and the maintenance of CPP (mean 76.13 +/- 15.37 mm Hg). Persistently low cerebral oxygenation was seen in 37% of patients at 2 hours, 31% at 24 hours, and 18% at 48 hours of treatment. Thus elevated ICP and a persistent low PbtO(2) after 2 hours represented increasing odds of death (OR 14.3 at 48 hours). Survivors and patients with good outcomes generally had significantly higher mean daily PbtO(2) and CPP values compared to nonsurvivors. Polytrauma, associated with higher ISS scores, presented an increased risk of vegetative outcome (OR 9.0). Compared to the ICP/CPP cohort, the mean Glasgow Outcome Scale score at 6 months in patients treated with PbtO(2)-CCG was higher (3.55 +/- 1.75 vs 2.71 +/- 1.65, p < 0.01; OR for good outcome 2.09, 95% CI 1.031-4.24) as was the reduction in mortality rate (25.9 vs 41.50%; relative risk reduction 37%), despite higher ISS scores in the PbtO(2) group (31.6 +/- 13.4 vs 27.1 +/- 8.9; p < 0.05). Subgroup analysis of severe closed TBI revealed a significant relative risk reduction in mortality rate of 37-51% compared with the Traumatic Coma Data Bank data, and an increased OR for good outcome especially in patients with diffuse brain injury without mass lesions (OR 4.9, 95% CI 2.9-8.4). The prevention and aggressive treatment of cerebral hypooxygenation and control of ICP with a PbtO(2)-directed protocol reduced the mortality rate after TBI in major trauma, but more importantly, resulted in improved 6-month clinical outcomes over the standard ICP/CPP-directed therapy at the authors' institution.

Comparison between central venous oxygen saturation and tissue oxygenation and perfusion: a case report

Comparison between central venous oxygen saturation and tissue oxygenation and perfusion: a case report

Near-infrared spectra absorbance of blood from sickle cell patients and normal individuals

Limited data are available regarding the physicochemical dynamics of tissue hypoxia in sickle cell disease. Studies using near-infrared spectroscopy (NIRS) have reported that patients with sickle cell disease (SCD) have lower cerebral oxygen saturation values (rSO2) than normal individuals. The reason SCD patients have subnormal rSO2 values is not known. It may be related to the degree of anaemia, sickle haemoglobin, disease complications and the possibility of SCD different NIRS absorbance spectra than normal. This study compared NIRS absorbance spectra of blood with adult haemoglobin AA, sickle haemoglobin SS, and AS. Venous blood was collected from SCD (SS and AS) and non-SCD patients (AA). Whole blood, cell free haemoglobin samples were scanned through the wavelength range of 600–1000 nm. The results showed no different NIRS spectra absorbance between the haemoglobin's AA, SS. It thus appears that lower brain oxygen saturation in sickle cell anaemia patients is related to impaired oxygen carrying capacity or delivery by sickle haemoglobin.

Neonatal cerebral oximetry monitoring during ECMO cannulation

Neonates were monitored with a cerebral oximeter before, during, and after cannulation for ECMO to determine the direct effects of ligation of the right internal jugular vein and right carotid artery on cerebral oxygenation. After obtaining informed consent, we used the FORE-SIGHT Cerebral Oximeter (CAS Medical Systems, Branford, CT, USA) to monitor neonates undergoing surgical preparation for veno-arterial (VA) or veno-venous (VV) extracorporeal membrane oxygenation (ECMO). A total of 17 subjects were monitored pre-ECMO for at least 48 h after cannulation. Of the 17 subjects, 12 experienced low cerebral tissue oxygen saturation (SctO(2)) <60% during pre-ECMO surgery, with most exhibiting the lowest SctO(2) values between cannulation to the onset of ECMO. Two subjects received cardiopulmonary resuscitation (CPR) during surgery and experienced very low SctO(2) (5 and 36%). Pulse oximetry was found to be unreliable during CPR because of diminished pulsatile flow. SctO(2) increased above 60% after the onset of ECMO for all subjects and remained stable. Neonates are vulnerable to SctO(2) during the pre-ECMO surgical period.

Low Cerebral Oxygen Consumption and Blood Flow in Patients With Cirrhosis and an Acute Episode of Hepatic Encephalopathy

It is unclear whether patients with hepatic encephalopathy (HE) have disturbed brain oxygen metabolism and blood flow. We measured cerebral oxygen metabolism rate (CMRO(2)) by using (15)O-oxygen positron emission tomography (PET); and cerebral blood flow (CBF) by using (15)O-water PET in 6 patients with liver cirrhosis and an acute episode of overt HE, 6 cirrhotic patients without HE, and 7 healthy subjects. Neither whole-brain CMRO(2) nor CBF differed significantly between cirrhotic patients without HE and healthy subjects, but were both significantly reduced in cirrhotic patients with HE (P < .01). CMRO(2) was 0.96 +/- 0.07 mumol oxygen/mL brain tissue/min (mean +/- SEM) in cirrhotic patients with HE, 1.34 +/- 0.08 in cirrhotic patients without HE, and 1.35 +/- 0.05 in healthy subjects; and CBF was 0.29 +/- 0.01 mL blood/mL brain tissue/min in patients with HE, 0.47 +/- 0.02 in patients without HE, and 0.49 +/- 0.03 in healthy subjects. CMRO(2) and CBF were correlated, and both variables correlated negatively with arterial ammonia concentration. Analysis of regional values, using individual magnetic resonance co-registrations, showed that the reductions in CMRO(2) and CBF in patients with HE were essentially generalized throughout the brain. The observations imply that reduced cerebral oxygen consumption and blood flow in cirrhotic patients with an acute episode of overt HE are associated with HE and not cirrhosis as such, and that the primary event in the pathogenesis of HE could be inhibition of cerebral energy metabolism by increased blood ammonia.

The effects of normoxia, hypoxia, and hyperoxia on cerebral haemoglobin saturation using near infrared spectroscopy during maximal exercise

At rest, cerebral haemoglobin saturation ( S cO 2), obtained with near infrared spectroscopy (NIRS), tracks the calculated capillary-oxygenation-level-dependent (COLD) signal. However, the relationship between the two variables during maximal exercise is unknown. We evaluated S cO 2 by dual wavelengths NIRS (Somanetics INVOS) and calculated mean cerebral capillary oxygen saturation ( S capO 2) during maximal ergometer rowing in six subjects in normoxia, hypoxia (17% inspired O 2) and hyperoxia (30% O 2). We determined middle cerebral artery blood flow velocity by 2 MHz transcranial ultrasound Doppler, arterial ( S aO 2) and internal jugular venous O 2 saturation ( S vO 2). Maximal rowing reduced S aO 2, S vO 2 and S capO 2 ( P < 0.05) with no significant changes in S cO 2 compared to rest. Hyperoxia prevented, while hypoxia aggravated, the reductions in S aO 2 and S vO 2 ( P < 0.05). Across the range of inspired O 2, S aO 2 varied from 88.6 ± 2.4 to 98.3 ± 0.4% (mean ± SD), S vO 2 from 49.4 ± 8.4 to 64.4 ± 5.6%, and S capO 2 from 68.2 ± 0.5 to 81.1 ± 0.5% while the changes in S capO 2 were tracked by S cO 2 ( r 2 = 0.31; P < 0.01) with values for S cO 2 (63.8 ± 11.7%) being lower than those for S capO 2 (76.7 ± 6.0%; P < 0.05). The present data suggest that during maximal exercise S cO 2, though influenced significantly by venous blood, maintains a tight coupling with the calculated S capO 2. Relevance to industry Personnel working in industrial environments with low ambient oxygen partial pressure or high temperatures may face premature exhaustion from cerebral fatigue caused by low cerebral oxygenation. As cerebral oxygenation can be measured non-invasively during the vigorous movements associated with ergometer rowing, it can also be applied for field studies, e.g. during work in special environments including high altitude and high ambient pressure or temperature.

Continuous monitoring and intervention for cerebral ischemia in tuberculous meningitis

Tuberculous meningitis (TBM) is a massive global problem. The mortality and morbidity associated with the severe form of the disease are exceptionally high. Even when increased intracranial pressure is treated and full conventional therapy is commenced, cerebral ischemia can develop and is associated with a particularly poor prognosis. We sought to evaluate our experience with two patients with severe TBM and cerebral oxygenation monitoring. Case report. Red Cross Children's Hospital, Cape Town. Two comatose patients with TBM. Targeted interventions against low cerebral oxygenation in one patient. Cerebral tissue oxygenation (Ptio2) was measured. In both patients, Ptio2 monitoring demonstrated delayed cerebral ischemia despite the institution of full conventional therapy and the control of intracranial pressure. These data confirm that the vascular involvement in TBM is potentially progressive and that failure to diagnose infarction initially is not merely due to a delay in the radiologic appearance. The first patient developed extensive infarction, consistent with Ptio2 readings, and subsequently died after treatment withdrawal. Intervention in the second patient successfully reversed a precipitous decline of the Ptio2 readings and may have prevented infarction in this patient. The development of delayed cerebral ischemia in TBM despite treatment is confirmed in these two patients. The reversal of a decline in Ptio2 readings suggests a possible benefit for cerebral oxygenation monitoring in selected patients with severe TBM.

Cerebrovascular Effects of Hemodialysis in Chronic Kidney Disease

Patients with end-stage renal disease (ESRD) undergoing hemodialysis are known to suffer cognitive deficits and stroke of unknown etiology. It has been suspected that the treatment itself may contribute to the syndrome by unknown mechanisms, which we investigated in this study. End-stage renal disease patients on hemodialysis (n=19) or peritoneal dialysis (PD, n=5) were compared with 14 healthy controls. Subjects participated in magnetic resonance imaging (MRI) measurements of cerebral atrophy, cerebral blood flow (CBF) arterial spin labeled-MRI (ASL-MRI), quantitative Doppler blood flow through the internal carotid artery, and cerebral oxymetry. The Doppler and oxymetry procedures were also performed at the beginning and end of a single hemodialysis session. End-stage renal disease patients on hemodialysis showed significant cerebral atrophy, associated with longer hemodialysis duration and cognitive deficits, including focal bilateral lesions in the caudate nucleus and midbrain. Cerebral oxygenation was extremely low before dialysis (rSO(2) 41+/-13, compared with 70+/-2 in controls, P<0.02) and improved only slightly after dialysis. Carotid blood flow was also very low at the start of dialysis (115+/-28 mL/sec, versus 193+/-56 in controls, P<0.005) but normalized at the end of the session (181 mL/sec). The PD patients showed intermediate values, between the hemodialysis and controls. Notably, duration of hemodialysis treatment predicted global gray-matter volume (r=-0.74), change of blood flow during dialysis (r=-0.65), and baseline rSO(2) (r=-0.65). The findings suggest that ESRD patients on hemodialysis suffer low CBF during the interdialytic cycle. Coupled with low cerebral oxygenation levels and atherosclerosis, this may contribute significantly to the etiology of the observed cerebral atrophy, cognitive deficits, and high stroke prevalence.

Cerebral oximetry improves detection of sickle cell patients at risk for nocturnal cerebral hypoxia

We previously used cerebral oximetry to identify low cerebral venous oxygen saturation in waking children with sickle cell disease (SCD). Because arterial oxyhemoglobin desaturation is common during sleep in SCD patients, this study compared both waking and sleeping systemic arterial and cerebral venous oxygenation dynamics in children with and without SCD. Seventeen African-American (AA) children with homozygous SCD [8 (4-15) years; 29% male; normal transcranial Doppler velocities] were compared with a control cohort (CON) comprised of six healthy AA children [9 (4-16) years, 33% male]. Standard all-night polysomnographic recordings were performed, including measurement of arterial oxygen saturation by pulse oximetry (SpO(2)). Regional cerebral oxygen saturation (rSO(2)) was measured non-invasively with cerebral oximetry. Intra-cohort comparisons examined the influence of sleep on SpO(2) and rSO(2) in the subjects. Inter-cohort comparisons of SpO(2), rSO(2,) and the rSO(2)/SpO(2) ratio assessed the impact of SCD on systemic and cerebral oxygenation during wakefulness and sleep. Cohort differences in SpO(2) were not statistically significant in either wakefulness or sleep. However, only in the SCD cohort was the magnitude of SpO(2) change statistically significant (P = 0.002). In contrast, both waking and sleep rSO(2) cohort median values did differ significantly [awake: CON 76 (67-86) vs. SCD 62 (58-71), P = 0.01; sleep: CON 65 (60-77) vs. SCD 55 (48-61), P = 0.01)]. The waking rSO(2)/SpO(2) ratio was also significantly lower in the SCD group [CON 0.78 (0.68-0.88) vs. SCD of 0.66 (0.61-0.72); P = 0.015]. During sleep, the ratio was also significantly lower in the SCD group [CON 0.71 (0.66-0.81) vs. SCD 0.59 (0.52-0.65); P = 0.011]. Our findings suggest that SCD patients may be at increased risk of cerebral hypoxia during both wakefulness and sleep.

Cerebral hyperemia and impaired cerebral autoregulation associated with diabetic ketoacidosis in critically ill children*

Cerebral edema associated with diabetic ketoacidosis is an uncommon but severe complication of insulin-dependent diabetes mellitus with unclear pathophysiology. We sought to determine whether cerebral edema in patients with diabetic ketoacidosis was related to changes in cerebral blood flow, autoregulation, regional cerebral saturation, or S100B. Prospective case series. Pediatric intensive care unit of a tertiary children's hospital. Six patients with diabetic ketoacidosis and altered mental status, requiring computed tomographic scan of the head. Study evaluations included: 1) transcranial Doppler evaluations to determine middle cerebral artery flow velocities and cerebral autoregulation, defined by the autoregulatory index, at 6 and 36 hrs; 2) continuous monitoring of regional cerebral oxygenation on the left lateral forehead using near-infrared spectroscopy for the first 24 hrs of admission; 3) serial measurement of S100B as a marker of central nervous system injury; and 4) follow-up head computed tomographic scan. Serial computed tomographic scans showed that four of six patients had changes in brain volume without overt cerebral edema. Initial scans showed narrowing of the third and lateral ventricles when compared with follow-up. There was no difference in middle cerebral artery flow velocities between admission and recovery at 36 hrs, despite Paco2 increasing during treatment. Cerebral flow was normal to increased, despite hypocapnia. Cerebral autoregulation was impaired in five of six patients at 6 hrs and normalized by 36 hrs. Mean regional cerebral oxygenation was measured in five of six patients and decreased linearly with time. Two patients showed maximal regional cerebral oxygenation before returning to baseline. There were no periods of low regional cerebral oxygenation in any patient at any time. No elevation in S100B was found. We found normal to increased cerebral blood flow, elevated regional cerebral oxygenation, impaired autoregulation, and changes in brain volume in clinically ill pediatric patients with diabetic ketoacidosis. We found no evidence of cerebral ischemia. These findings suggest that the pathophysiology of cerebral edema in diabetic ketoacidosis may involve a transient loss of cerebral autoregulation, allowing a paradoxic increase in cerebral blood flow and the development of vasogenic cerebral edema.

Near-infrared spectroscopy to monitor cerebral oxygen saturation in single-ventricle physiology

Near-infrared spectroscopy monitors cerebral oxygen saturation. This parameter parallels jugular venous oxygen saturation and reflects the balance between cerebral oxygen supply and demand. Experience with near-infrared spectroscopy in univentricular physiology is limited. This study explores the relationship between cerebral oxygen saturation, jugular venous oxygen saturation, and other variables of cerebral perfusion in a model of univentricular physiology. Univentricular physiology was created in newborn piglets by means of an aortopulmonary shunt, echocardiography-guided atrial septostomy, tricuspid valve avulsion, and pulmonary artery occlusion. Intra-aortic balloon inflation was used to increase afterload. Cerebral oxygen saturation monitoring (INVOS 5100; Somanetics Corp, Troy, Mich), physiologic recordings, and stable-isotope microsphere determination of cerebral blood flow were performed at baseline and after conversion to univentricular physiology (30 minutes, 120 minutes, and during afterload augmentation). Univentricular physiology resulted in lower cerebral oxygen saturation, arterial oxygen content, jugular venous oxygen saturation, and cerebral oxygen delivery. Afterload augmentation increased cerebral oxygen saturation, arterial oxygen content, and jugular venous oxygen saturation, whereas cerebral oxygen delivery was unaffected because of lower cerebral blood flow. Cerebral oxygen saturation predicted jugular venous oxygen saturation, arterial oxygen saturation, and arterial oxygen content. No association was found with cerebral oxygen delivery, which decreased in parallel with cerebral oxygen saturation when the single-ventricle physiology model was established but failed to increase during afterload augmentation. This study shows that in univentricular physiology cerebral oxygen saturation correlates well with jugular venous oxygen saturation, arterial oxygen saturation, and arterial oxygen content. However, our findings suggest that in singe-ventricle physiology changes in cerebral oxygen saturation need to be interpreted in the context of changes in arterial oxygenation.

421 Preterm Infants on Inotropes Have Lower Cerebral Oxygen Consumption Measured by Near Infrared Spectroscopy

421 Preterm Infants on Inotropes Have Lower Cerebral Oxygen Consumption Measured by Near Infrared Spectroscopy

Effects of hydroxyurea treatment on cerebral oxygenation in adult patients with sickle cell disease: an open-label pilot study

In patients with sickle cell disease (SCD), cerebral oxygen saturation (rSO(2)) has been reported to be below normal and to increase after red blood cell transfusion. This study was designed to determine the effects of long-term and short-term hydroxyurea (HU) treatment on cerebral oxygenation in patients with SCD. This open-label pilot study was conducted at the Department of Anesthesiology and the Center for Sickle Cell Disease, College of Medicine, Howard University, Washington, DC. Adult African American outpatients with SCD and hemoglobin (Hb) genotype HbSS (homozygous sickle Hb) who were receiving long-term (>6 months) HU treatment (15-30 mg/kg . d PO) or who had never received this treatment (control group) were enrolled. Patients in the treated and control groups were matched for age, sex, race, and Hb genotype. Cerebral oximetry (near-infrared spectroscopy) was performed to determine rSO(2) index. In a separate analysis to determine the effects of short-term HU treatment on cerebral oxygenation, hospitalized patients with SCD and vaso-occlusive crisis (VOC)receiving long-term therapy with HU were enrolled. We performed cerebral and pulse (fingernail) oximetry to determine rSO (2)index and arterial oxygen saturation (SpO(2)) after the administration of a single oral dose of HU (500-mg tablet) alone and again after dosing concomitantly with inhaled oxygen. The study enrolled 11 patients in the HU group (6 women, 5 men; mean [SD] age, 37 [8] years) and 20 controls (8 women, 12 men; mean [SD] age, 35 [6] years). Mean (SD) rSO(2) index was significantly increased (but still low) in patients receiving long-term HU treatment compared with controls (46.1% [6.6%] vs 41.2% [7.6%]; P< 0.025). Hb concentration (9.6 [1.4] g/dL vs 8.5 [1.2] g/dL; P< 0.027), hematocrit (28% [3%] vs 24% [4%]; P < 0.028), and mean corpuscular volume (102% [7%] vs 89% [8%]; P < 0.027) also were significantly higher in the HU group compared with controls. In 8 patients with SCD and VOC (6 men, 2 women; mean [SD] age, 28 [5] years), single-dose HU, either alone or in combination with inhaled oxygen, did not significantly affect cerebral oxygenation, and SpO(2) failed to correlate with rSO(2) index in these patients. The results of this open-label pilot study in patients with SCD suggest that the low cerebral oxygenation in these patients is significantly improved but not normalized with long-term HU treatment. A single dose of HU, either alone or in combination with inhaled oxygen, did not appear to influence cerebral oxygenation in patients with VOC.

Postnatal changes in cerebral oxygen extraction in the preterm infant are associated with intraventricular hemorrhage and hemorrhagic parenchymal infarction but not periventricular leukomalacia.

Fluctuations in cerebral hemodynamics have been implicated in the pathogenesis of acquired brain damage in babies born prematurely. This study examined the changes in cerebral fractional oxygen extraction (FOE) over the first 3 d after birth in 25 very-low-birth-weight preterm infants. Twelve infants had no major cerebral injury and 13 had acquired brain injury; cystic periventricular leukomalacia (PVL) was present in 4 and intraventricular hemorrhage (IVH) in 9, of whom 2 also had hemorrhagic parenchymal infarction (HPI). Normal values (median, 5(th)-95(th) centiles) for cerebral FOE in very-low-birth-weight infants with no cerebral injury were 0.38 (0.23-0.53) on d 1, 0.31 (0.18-0.45) on d 2, and 0.28 (0.17-0.38) on d 3. Infants who developed cystic PVL had no significant change in cerebral FOE during the first 3 d after birth. By contrast, cerebral FOE fluctuated in infants with IVH over the 3 d of measurement, decreasing from d 1 to d 2 (p = 0.03) and increasing from d 2 to d 3 (p = 0.02). The highest cerebral FOE values were seen in the two infants with HPI. The different patterns of change in cerebral FOE with HPI and cystic PVL provide additional evidence that the pathogenesis of these two conditions is different. Because high cerebral FOE is likely to be a consequence of low cerebral oxygen delivery, probably because of low cerebral blood flow, our results indicate that fluctuations in cerebral blood flow may occur when there is IVH or HPI.

Cerebral oxygen saturation assessed by near-infrared spectroscopy during coronary artery bypass grafting and early postoperative cognitive function

Background. Cerebral oxygen saturation (ScO 2) can be assessed by near-infrared spectroscopy. We investigated the correlation between early postoperative cognitive performance and intraoperative ScO 2 in a prospective observational setting. Methods. Forty-seven patients undergoing elective coronary artery bypass grafting with cardiopulmonary bypass underwent preoperative and postoperative neuropsychological evaluation. Patients were classified according to the presence or absence of postoperative cognitive dysfunction. Cognitive dysfunction was defined as an individual test score decrease of more than one standard deviation in two or more of the five tests. During operation ScO 2 was continuously measured using an INVOS 4100 device. Cerebral oxygen saturation values were analyzed with reference to two cutoff points, which should reflect low cerebral oxygenation: an ScO 2 less than 40% and a drop of more than 25% from individual baseline values. The duration and extent of ScO 2 values below these two cutoff points was compared between the patients with and without cognitive dysfunction. Results. Sixteen patients (34%) showed postoperative cognitive dysfunction. Cerebral oxygen saturation values less than 40% occurred in 17 patients for a mean (± standard error of the mean) of 17.2 ± 6.5 minutes, whereas a decrease of more than 25% from baseline values occurred in 37 patients for 52.7 ± 7.8 minutes. The duration and extent below the two cutoff ScO 2 values was similar in patients with and without cognitive dysfunction. Conclusions. Intraoperative regional ScO 2 as assessed by near-infrared spectroscopy with the INVOS 4100 device is not predictive for postoperative cognitive performance in patients undergoing coronary artery bypass grafting with cardiopulmonary bypass.