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Validity and Reliability of the Sj[O.sub.2] Catheter in Neurologically Impaired Patients: A Critical Review of the Literature.

Abstract: The purpose of this study was to determine the validity and reliability of the Sj[O.sub.2] catheter in neurologically impaired patients. Cerebral hypoxia and ischemia are two of the most important causes of secondary injury after brain trauma. Early detection and treatment of cerebral ischemia may prevent additional damage to the injured brain. A critical review of literature was conducted by searching the Melvyl database system for the topic of monitor validity and reliability, dating back to 1927. A search of references from current articles also led to more classic studies. Attempts were made to find recent quantitative studies with an emphasis on the incidence of secondary brain ischemia detected by the tool.

At best, the Sj[O.sub.2] catheter measures global cerebral oxygenation and is, therefore, unable to detect regional ischemia. In the literature reviewed, nearly 50% of the Sj[O.sub.2] oximetrix catheters provided an unreliable means for monitoring cerebral oxygenation.

The initial milestones by Myerson et al. and Gibbs et al. have served as the basis for more refined research on cerebral tissue oxygenation and metabolism. The unreliability of the Sj[O.sub.2] catheter demonstrates how little we still know about cerebral physiology. In spite of the many advancements in healthcare technology, limiting secondary brain injury and improving neurologic outcome have remained elusive.

The adverse effects of cerebral hypoxia and ischemia that occur after severe head injury have been well established in laboratory and clinical studies. More recently, ischemic brain damage has been found on neuropathological examination in 88% of head-injured patients.[50] In 1988, Graham et al. performed a histologic study of 71 victims of fatal traumatic brain injury (TBI) who had no premortem evidence of clinical, radiological, or pathological increased intracranial pressure (ICP).[23] Ischemic cell changes were found in 70% of the brains. This study highlighted the need to have a tool that accurately detects brain ischemia. A clinically useful method for detecting cerebral ischemia should be sensitive enough to identify a reduction in cerebral oxygen delivery prior to neurological injury.[7,9,11,12,37,38,42,50]

Measurement of jugular bulb venous oxygen saturation (Sj[O.sub.2]) reflects the overall balance between cerebral oxygen supply and demand.[41] Placing an Sj[O.sub.2] catheter has been suggested as a means of measuring existing or impending cerebral ischemia and the effects of therapeutic interventions.[9,10,37,54] Profound or prolonged episodes of Sj[O.sub.2] desaturation are associated with a poor outcome.[6] Although Sj[O.sub.2] monitoring is currently the most sensitive indicator of cerebral oxygenation,[53] its reported low accuracy rate exemplifies the need for further evaluation before it can be used for clinical decision making.[5,18,54] No catheter to date has yielded consistently reliable and valid, accurate data on cerebral oxygenation and metabolism. Therefore, a critical review of the literature on the validity, reliability, and utility of the Sj[O.sub.2] catheter in assessing neurologically impaired patients was undertaken. This information could be used to guide clinical nurse specialist practice in critical care monitoring and management of patients at risk for suffering secondary brain injury.

More specifically, this article reviews the following concepts:

* Physiology of cerebral venous blood drainage

* Potentiating factors that lead to cerebral ischemia and hypoxia

* Sj[O.sub.2] values

* Current uses and complications of the Sj[O.sub.2] catheter

* Limitations of the catheter

* Effect on outcome

* Review of reliability and validity of the Sj[O.sub.2] catheter.

Clinical studies on the validity and reliability of Sj[O.sub.2] monitoring are reviewed, and the gathered data are evaluated. Nursing implications and strategies are discussed.


Cerebral hypoxia and ischemia are two of the most important causes of secondary injury after trauma and can occur from a variety of both systemic and cerebral causes, including intracranial hypertension, systemic hypotension, and hypoxia.[45] Shackford et al. reported finding secondary brain injury in 66% of patients dying from central nervous system injury. Graham et al. documented a 91% incidence of secondary injury in patients referred to a tertiary neurosurgical unit.[23] Graham's findings were attributed to delays in management and inappropriate prehospital and hospital care (as cited in Shackford, Mackersie, Davis, Wolf, & Hoyt, 1989). Early detection and treatment of cerebral ischemia may prevent additional damage to the injured brain.

Lewis, Myburgh, and Reilly conducted a prospective observational study to assess the reliability of fiberoptic oximetric catheters and identify the incidence and causes of jugular bulb oxygen desaturation in patients with acute closed head injury.[34] They discovered that the majority of jugular bulb oxygen desaturations occurred within the first 48 hours of injury. Schneider et al. had similar findings of desaturations in nonsurvivors of severe head injury.[50] In her study of desaturation episodes after severe head injury and their influence on outcome, Robertson found a strong correlation between the incidence of jugular venous desaturation and poor long-term neurological outcome.[47]

The human brain is highly dependent on aerobic metabolism.[1,4,7,11,26,52] The brain, weighing only approximately 2% of the adult human mass, requires approximately 20% of the total body blood flow under normal physiologic conditions.[9] Studies have suggested that early secondary brain insults such as cerebral hypoxia are deleterious in acute brain trauma.[6,38] Brain injury can be divided into two phases. The primary injury occurs at the scene and consists of direct damage to nerve fiber tracts. Secondary insult occurs within minutes to days whereby cerebral and systemic ischemia, hyperemia, and intracellular calcium accumulation may damage additional neural tissue, resulting in further deficits or death.[36,52] Following neurotrauma, autoregulatory mechanisms for maintaining cerebral perfusion and oxygenation may be compromised, rendering cerebral tissue more vulnerable to secondary ischemic insults.[33] In 1978, Graham, Lawrence, and Adams found that pathology studies showed secondary ischemic brain damage in 92% of fatal head injuries.[23] The same group of investigators reported a similar incidence 10 years later despite improvements in intensive care management.[23] Unfortunately, even with superb advancements in critical care medicine, this number remains morbidly high today.[6]

A primary goal in neurosurgical intensive care is to minimize or prevent secondary brain damage after an acute insult. Use of an oximetric catheter to detect early tissue hypoxia may prevent the spiraling sequelae that ensues in neuronal death. The validity and reliability of the oximetrix measurement is dependent upon technical factors such as the positioning of the catheter and patient, attention to light intensity levels, and calibration of the system.[7,11,47] Bullock et al. found, through meta-analysis, that between 15% and 50% of Sj[O.sub.2] oximetrix readings were unreliable due to these factors.[7]


The review of literature was conducted by using the Melvyl database system to search for the topic of Sj[O.sub.2] monitor reliability and validity, dating back to 1927. This was a logical place to start because the tool's design and placement have historically shown similar traits of unreliability and inaccuracy due to extracerebral contamination, sampling technique, and patient and catheter position. A search of references from current articles also led to more classic studies. Attempts were made to find recent quantitative studies with an emphasis on the incidence of secondary brain ischemia detected by the tool.


Myerson, Halloran, and Hirsch first described percutaneous puncture of the cranial end of the internal jugular vein in 1927.[40] Their studies of this technique were based on the assumption that the blood obtained was cerebral venous blood and free of significant amounts of extracerebral contamination.[32] Since then, this technique, or slight modifications thereof, has been used in numerous studies of circulatory and metabolic functions of the human brain. Cerebral hemometabolism was first investigated in 1942 by Gibbs et al. in a large series of healthy human volunteers, most of whom were medical students.[21] They declared that their measurements of arteriojugular differences of oxygen and glucose (global cerebral extraction) and lactate (global cerebral production) under normocapnic conditions were representative of cerebral metabolism. In 1948 Kety and Schmidt reported another pioneering contribution for quantification of global cerebral blood flow (CBF); it became possible to quantify brain oxygen consumption, or cerebral metabolic rate of oxygen consumption ([CMRO.sub.2]).[9] Kety and Schmidt first used the term gross extracerebral contamination to describe sampling from a vein other than the superior bulb of the internal jugular vein.[29] Gibbs, Lennox, and Gibbs described the importance of using proper technique to insert the needle as cranially as possible in the jugular bulb to reduce the likelihood of extracerebral contamination.[20]

Since ICP monitoring was introduced in humans by Guillaume in 1951, monitoring of cerebral perfusion pressure (CPP) became routine in many centers.[9] However, measurement of ICP and CPP has not reflected clinical practice with cerebral oxygen utilization.[34] Elevations in ICP occurred late or not at all following jugular bulb oxygen desaturation due to cerebral hypoperfusion.[15]


Physiology of Cerebral Blood Drainage

Cerebral blood drains from the intracranial venous sinuses into the sigmoid sinuses before entering the internal jugular veins via the jugular foramina.[22] The bulbous dilatation of the jugular vein just below the base of the skull contains cerebral venous blood.[3] The jugular vein is usually the biggest vein in the neck. The right jugular vein is usually larger than the left and is generally believed to drain most of the blood from the cerebral hemispheres, while blood from the posterior fossa contents drains into the left vein. The jugular vein descends in contact with the lateral side of the internal and common carotid arteries, enclosed with them and the vagus nerve in the carotid sheath. It ends posterior to the medial part of the clavicle by joining the subclavian vein to form the brachiocephalic vein. The following extracranial veins join the internal jugular vein in its passage through the neck; the inferior petrosal sinus, pharyngeal plexus, facial vein, lingual vein, superior thyroid veins, middle thyroid vein, and jugular lymph trunk. Therefore, for monitoring the Sj[O.sub.2] of cerebral blood correctly, the catheter tip must be placed high in the jugular bulb.[3]

The blood in the jugular bulb is a mixture of blood draining from the confluence of the cerebral sinus (CCS) and blood drained directly into the transverse sinus.[31] Great discrepancy in oxygen saturation between the left and right jugular bulb may occur if (a) one transverse sinus receives only a very small proportion of blood from the CCS and (b) blood draining directly into the transverse sinus from one side has a significant difference in oxygen content from the blood in CCS.[31] In the normal brain, measurement of jugular bulb oxygen saturation is similar whether the left or right side is used; 3% of the jugular bulb blood is contaminated by extracerebral sources such as the scalp, meninges, and skull.[20,28,51] It has been recommended that in the abnormal brain the vein ipsilateral to the major pathology be used to obtain readings most representative of cerebral oxygenation of the injured region.[28,46,47] Andrews et al. contended that in global and bilateral injuries, the catheter be placed on the right side, because the right internal jugular vein is usually larger than the left and would, therefore, give the most accurate readings.[3,22] Sj[O.sub.2] values in primary brainstem injuries may not reveal regional ischemia. Sj[O.sub.2] monitoring is contraindicated in local neck trauma, local infection, bleeding diathesis, or any impairment to cerebral venous drainage.[3]

Potentiating Factors That Lead to Cerebral Ischemia

The average CBF is approximately 50-55 ml/100 g of brain tissue per minute.[43] Normally, CBF and metabolism ([CMRO.sub.2]) are coupled, so that the arterio-jugular oxygen saturation difference remains constant. Local CBF is increased or decreased depending on the tissue metabolic requirements.[47] If [CMRO.sub.2] is decreased by anesthesia, for example, then CBF also will decrease, because requirements for metabolic substrates are less. If the [CMRO.sub.2] is increased, for example, by fever, then CBF also will increase.

In the majority of head-injured patients, CBF and metabolic rate are uncoupled due to loss of cerebral autoregulation.[42] With loss of autoregulation, CBF increases or decreases independently of the metabolic rate.[34] Andrews, Dearden, and Miller found that ischemic CBF values (Sj[O.sub.2] [is less than] 55%) were encountered during hyperventilation, after focal severe head injury, after evacuation of intracranial hematoma, and during plateau waves in ICP monitoring.[3] Desaturation was seen during episodes of systemic hypotension and arterial hypoxemia.

Cerebral perfusion pressure (CPP) is the blood pressure gradient across the brain. Its value reflects the difference between the incoming mean arterial pressure (MAP) and the opposing ICP (CPP = MAP - ICP). Numerous studies have shown that CPP must be maintained at 70 mm Hg to provide minimally adequate blood supply to the brain.[1,5,6,14,15,30] However, this value is relatively individualized. Some patients develop cerebral ischemia with borderline CPP. The reason that ICP monitoring and CPP calculations have failed is that changes are seen too late by these values and they are not a measure of cerebral oxygenation. Continued inadequate CPP is incompatible with life and results in neuronal hypoxia and neuronal death.[4,5,6,7,22,23,25] When the MAP equals the ICP, the CPP is zero, and CBF ceases.

Sj[O.sub.2] Values

Jugular bulb oximetry provides information about the balance of brain's oxygen supply and demand.[49] Sj[O.sub.2] values are normally 60%-80%, and values less than 54% are considered desaturations whereby ischemia develops.[6,8,22,27,39,50] In the literature, true jugular desaturations are mostly defined as Sj[O.sub.2] values below 50%.[15,49] However, no clear-cut threshold has been set for this lower margin and studies have shown the presence of cerebral hypoperfusion with Sj[O.sub.2] values below 54%, so the lower margin was set at 55%.[13,39] According to Fick's principle, Sj[O.sub.2] is proportional to CBF if arterial saturation, [CMRO.sub.2], hemoglobin concentration, and hemoglobin dissociation curves are constant.[49] A high Sj[O.sub.2] ([is greater than] 90%), indicative of cerebral hyperemia or high flow states when supply exceeds demand, has been detected in hypertension (CPP [is greater than] 110 mm Hg), increased Pa[CO.sub.2], early sepsis (i.e., increased demand), and brain tissue death.[15,23] Low Sj[O.sub.2] saturation values ([is less than] 54%) indicate ischemia or low flow states when demand exceeds supply.

Bouma et al. confirmed through early invasive monitoring that there is a high incidence of very early cerebral hypoperfusion, underscoring the hypothesis that post-traumatic cerebral hypoperfusion was usually an early event.[5] This illustrates the importance of rapid and adequate hemodynamic and respiratory monitoring and management even in patients suffering from isolated brain injury.[15]

Current Uses and Complications

Sj[O.sub.2] monitoring has been used in the operating room to detect the effects of changes in MAP on Sj[O.sub.2] values during cerebral aneurysm surgery.[39] Moss et al. found that an effective way of increasing Sj[O.sub.2] was to increase Pa[CO.sub.2].[39] They suggested that the increase in Sj[O.sub.2] associated with increasing MAP could be the result of defective autoregulation after subarachnoid hemorrhage (SAH) and was similar to minimal or absent autoregulatory response demonstrated in head injury by Fortune et al.[18,39] Initial Sj[O.sub.2] readings and readings after increases in MAP were found to be poor predictors of initial and long-term outcomes in this patient population.

Chan et al. used the Sj[O.sub.2] catheter as a guide in treating intracranial hypertension after severe head injury.[8] This is currently the primary use of Sj[O.sub.2] monitoring. They evaluated the differences between CPP and pulsatility index (PI) from transcranial doppler velocities (TCDs) on Sj[O.sub.2] values. They found that in states where CPP was above 70 mm Hg, CPP did not significantly correlate with either PI or Sj[O.sub.2]. Their findings contrasted with a recent report by Cruz et al. that distinguished significant increases in Sj[O.sub.2] even when pretreatment CPP exceeded 60 mm Hg.[8,11]

Chan et al. suggested that the Sj[O.sub.2] catheter was useful as a cerebral oxygenation monitoring device and guide to treatment of intracranial hypertension.[8] They did not discuss the tool's reliability but stated that Sj[O.sub.2] monitoring was one tool used in multimodality monitoring for their patient population. They contended that if arterial oxygen saturation, hemoglobin concentration, and the position of the oxygen dissociation curve remain unaltered, the value of the Sj[O.sub.2] might replace arteriovenous oxygen difference ([AVDO.sub.2]; also known as arteriojugular oxygen difference [[AJDO.sub.2]]) as a monitor of the ratio of global cerebral oxygen supply to oxygen consumption. They contended that CPP was the crucial parameter to monitor.

Bell et al. described the use of the Sj[O.sub.2] catheter as a means of monitoring [AJDO.sub.2], which reflects the relationship between the metabolic rate for oxygen and the blood flow of the brain through calculation of [CMRO.sub.2] and CBF.[4] [AJDO.sub.2] is inversely related to CBF. However, CBF ratio parallels Sj[O.sub.2] values. A low [AJDO.sub.2] would suggest that there is relatively more blood flow than is needed to support the metabolic needs of the brain, that is, luxury perfusion (hyperemia).[4] The Sj[O.sub.2] value in this instance would be high. Increased [AJDO.sub.2] indicates relative hypoperfusion in that the metabolic oxygen requirements are higher than the amount of blood flowing through the brain.[4] Sj[O.sub.2] values in this instance would be decreased.

De Vries et al. compared the Sj[O.sub.2] catheter with electroencephalographic (EEG) monitoring and near-infrared spectroscopy.[16] Their aim was to study the effects of induced ventricular fibrillation (VF) and subsequent circulatory arrest on defibrillation threshold testing on the human brain. Thirteen patients undergoing surgery for implantable cardioverter-defibrillator implantation or replacement under general anesthesia were included. They found that Sj[O.sub.2] showed no relevant changes after the induction of VF with a significant drop in blood pressure. It was after successful defibrillation with hemodynamic recovery returning within 3-5 seconds that Sj[O.sub.2] values dropped, followed by an overshoot and a return toward baseline values. They reported that posthypoxic overshoots on the Sj[O.sub.2] were most likely caused by hyperemia and were followed by a slow return toward prearrest values.[53] Notably, the recovery time for Sj[O.sub.2] values were seven times longer than that for EEG.

They concluded that the Sj[O.sub.2] was an unreliable means for monitoring cerebral oxygenation. They declared that catheter positioning, migration, and deviation against the vessel wall, which occurred in all patients and might not be obvious immediately, affected Sj[O.sub.2] catheter reliability. They also proposed that its reliability may have been affected by the backflow of less desaturated blood from large extracranial veins when CBF is low or absent.[53]

Matta et al. examined the feasibility, complications, and potential usefulness of the intraoperative use of jugular bulb catheters in 99 consecutive patients with head injury undergoing neurosurgical procedures.[37] The main thrust of their study was to identify the risk-benefit ratio of Sj[O.sub.2] monitoring. Inadvertent carotid artery puncture on two occasions was the only complication. Mean hematocrit (Hct) and Pa[CO.sub.2] levels of those patients who experienced jugular desaturation were similar to those of patients with no episodes of desaturation. High or low hematocrit and hypocapneic or hypercapneic states would alter Sj[O.sub.2] values and therefore show poor correlation with those patients whose Hct and Pa[CO.sub.2] values were unmatched. Arterial blood pressure, Pa[CO.sub.2], Pa[O.sub.2], and Sj[O.sub.2] were intermittently measured throughout the operation.

They found Sj[O.sub.2] monitoring to be useful in 60 of the 99 patients studied. It was useful for detecting and treating cerebral venous desaturations in 60% of the patients with aneurysms, 72% of patients with intracranial hematomas, 50% of patients with cerebral tumors, and 75% of patients with other intracranial pathology. It proved no benefit in patients with arteriovenous malformations. Overall, cerebral venous desaturations were detected in approximately 50% of the patients studied.[37] This low accuracy rate may have been partly related to the group's choice to monitor Sj[O.sub.2] intermittently instead of continuously, and this method may have caused them to miss important data.

Hantson described the increasing interest in monitoring arteriovenous differences for oxygen and lactate across the brain to assist with the diagnosis of brain death.[25] He contended that this method offered useful data between oxygen delivery and consumption that could be expressed by the oxygen extraction ratio (OER or [CEO.sub.2]). He reported that in patients with severe head trauma with abnormal clinical findings, a dramatic fall in Sj[O.sub.2] values ([is less than] 30%) followed by gradual elevations to very high values approaching arterial saturation suggested the arrest of cerebral metabolism. This was a case report on one 18-year-old boy with head trauma. Electrophysiological studies and EEG confirmed brain death.

Schneider et al. performed a retrospective analysis of 54 comatose patients to determine the context in which cerebral desaturation episodes occurred in survivors and nonsurvivors of severe head injury.[49] Subjects were divided into three groups: severe head injury (SHI), intracranial hemorrhage (ICH), and subarachnoid hemorrhage (SAH). Desaturation episodes were most pronounced in the ICH group followed by the SAH group. Further analysis of data showed that 93% of ICH patients were likely to suffer at least one episode of desaturation following insult, while in 91% of SAH and in 50% of SHI patients at least one desaturation episode was observed.

A clinically relevant finding was that nonsurvivors had a peak incidence of desaturation episodes within the first 48 hours following trauma, while desaturation in surviving patients was highest 4 and 5 days after trauma.[48] Of patients who had Sj[O.sub.2] readings below 50% for at least 15 minutes within the first 24 hours following head injury, 67% of them died. Of patients who had similar readings within the first 48 hours, 93% died. Retrospective analysis of these data also found that 62% of desaturation episodes resulted from the effects of moderate hyperventilation (Pa[CO.sub.2] 28-32 mm Hg), while 38% of the episodes were caused by a CPP [is less than] 60 mm Hg. Conversely, 56% suffering ICH and 80% suffering SAH showed signs of insufficient cerebral oxygenation after lowering MAP from 100 to 82 mm Hg. None of the Sj[O.sub.2] readings fell below 55%. They concluded that continuous Sj[O.sub.2] oximetry enabled the detection and treatment of insufficient cerebral oxygenation in comatose patients and might serve as a guide to make a differential diagnosis of cerebral hypoxia.

Limitations of the Jugular Venous Catheter

The major limitation of jugular bulb oximetry is the relative global nature of the measurement. Focal areas of cerebral oligemia are not detected by this method. In addition, where CBF is low, extracranial contamination may falsely increase the jugular bulb saturation value.[34] Han et al. suggested that a low Sj[O.sub.2] did not equate with cerebral anoxia, but simply indicated an increase in oxygen extraction, which may be an early warning sign of possible ischemia.[24] The brain is inhomogenous both anatomically and physiologically. A normal Sj[O.sub.2] can reflect regional maldistribution of flow consisting of excessive per fusion in some areas and hypoperfusion in others.[24]

Several groups have reported that the technique for oximetric catheter placement may lack general availability and be too awkward for routine clinical practice.[16,36,45,49] Catheters are also expensive, take a longer time to place, require radiographic confirmation, and demonstrate inconsistent and questionable values.[16,37,46,50] It has also been reported that the mean venous oxygen saturation difference between jugular bulbs may be as high as 15% in humans.[13,14,50] Ensuring catheter location in the jugular bulb with dominant venous drainage may be ascertained by computer tomography or a jugular compression test and may reduce this error.[13] Other limitations included the following: poor signal quality related to patient positioning, malposition in the internal jugular vein (coiled or not within the jugular bulb), catheter migration, deviation, and poor design of the catheter itself.[16,37]

Effect on Outcome

Robertson stated the importance of verifying the catheter Sj[O.sub.2] values by measuring oxygen saturation in a blood sample drawn through the catheter before making therapeutic decisions.[45] She performed a prospective randomized study in 116 patients who sustained severe head injury; 76 episodes of jugular desaturation were noted. Only 40% of jugular venous desaturation was detected, although it was not clearly stated how this value was determined. The etiology of the desaturations varied, including both systemic and cerebral causes. Even with a 60% failure rate of the catheter to detect desaturation, Robertson contended that these episodes of desaturation would not have been detected in most patients without continuous monitoring of the Sj[O.sub.2]. Catheter values were verified by measuring the oxygen saturation ([SO.sub.2]) in a blood sample drawn through the catheter before making therapeutic decisions. She concluded that a poor neurological outcome was strongly associated with the occurrence of Sj[O.sub.2] desaturation.

Cruz and Robertson indicated beneficial use of the Sj[O.sub.2] monitor in detecting cerebral ischemia and its beneficial effect on improving outcome.[12,45] DeVries stated that neuromonitoring might help in establishing objective individualized criteria of cerebral recovery after circulatory arrest and thereby enhance safety in defibrillation threshold testing.[16]

Reliability and Validity

In a classic study from 1961, Lassen and Lane analyzed the problem of validity of internal jugular blood for studying CBF and metabolism using a controlled, experimental study of 28 white males separated into three groups by age and mental health.[32] Group 1 comprised normal adults who averaged 25 years of age. Group 2 comprised normal elderly men who averaged 72 years of age. Group 3 comprised aged, demented patients whose average age was 74 years. A series of 67 internal jugular blood studies revealed five markedly deviant observations characterized by a very slow rate of inert gas saturation (very slow blood perfusion) and a narrow arteriovenous oxygen difference. The five samples that demonstrated very slow blood perfusion were analyzed using the krypton-85 modification of the inert gas inhalation method of Kety and Schmidt to measure CBF.[29,32] In all cases, normal and pathologic, the calculated value of CBF continued to decrease slightly throughout the study period.[32] According to the theory of the uptake of inert gas at the tissues, this finding implied that a considerable or complete tapering off of the calculated flow value at 10 minutes might have occurred without necessarily indicating that the true perfusion rate was obtained.[32] The reduced CBF value revealed the underlying heterogeneity of tissue perfusion rates. Lasson and Lane found significant side-to-side differences when they compared bilateral samples of CBF. The difference was accounted for by improper placement of the jugular needle.

Values for CBF and oxygen uptake were significantly lower (p [is less than] .001) in external jugular venous samples and in the CBF study of the aged subjects with mental deterioration. An abnormally rapid rate of decline was found over time and especially at the 10-minute interval when CBF was calculated from minute to minute. There was a steeper rate of decline in the samples obtained from an improperly placed catheter.

In the context of this important study, Lassen and Lane determined that the consistency and statistical significance of the deviations in the five cases analyzed indicated that the abnormal values could not be regarded merely as a group of extreme deviants in the random distribution of a single population. Gross extracerebral contamination occurring from improper needle placement accounted for the deviations observed. They also reported that the hypocapnia of moderate hyperventilation may have been expected to result in a distinct drop in the oxygen saturations of essentially uncontaminated blood. They concluded that the recognition and rejection of grossly contaminated cases would enhance the validity of internal jugular venous blood for the study of cerebral perfusion and metabolism.

This was a study performed on a small group of people without TBI. Therefore, it was likely that autoregulation was intact. The findings were nonetheless significant and established a baseline for determining values in a sample of patients with normal physiology in the noninjured brain. This study emphasized the clinical importance of precise percutaneous puncture of the internal jugular vein at its exit from the cranial cavity. It is unlikely this study could be repeated today because of the risk of placement.

In 1992 Sheinberg et al. performed a prospective quasi-experimental evaluative study of 45 comatose patients with severe head injury who scored less than 8 on the Glasgow Coma Scale (GCS).[50] They purported that a clinically useful method for detecting cerebral ischemia should be sensitive enough to identify a reduction in cerebral oxygen delivery prior to neurologic injury. Sj[O.sub.2] monitoring was performed on all patients as a method for detecting cerebral ischemia. Ninety-one percent of the patients studied were male, with an average age of 31 years (SD = [+ or -] 14 years). On admission to the hospital, 82% of the patients were comatose. Of those studied, 91% had closed head injuries, while the remaining 9% suffered gunshot wounds to the brain.

The reliability of the fiberoptic catheter was investigated during the course of monitoring. Whenever Sj[O.sub.2] values dropped below 50%, a standardized protocol was followed to confirm the validity of the desaturation and to establish its cause. A total of 361 simultaneous measurements of Sj[O.sub.2] by blood sample from the catheter and by co-oximeter were made and then compared by linear regression analysis to determine correlation between the two variables. Co-oximetry is a proven reliable and valid instrument that measures venous oxygen saturation through a pulmonary artery catheter.[17,41]

Linear regression analysis was used to compare the correlation between Sj[O.sub.2] and co-oximeter readings in blood samples. Differences in means were appropriately tested using one-way analysis of variance (ANOVA) to determine how well the catheter values could be used to predict the values obtained by the "gold standard" of cooximetry.[17,41,50] Differences in proportions were tested with chi-square statistic to identify the presence of ischemia.

Sheinberg et al. found that more than half of the catheter readings below 50% were inaccurate due to migration of the catheter against the vessel wall.[50] Although discussion focused on the potential utility of Sj[O.sub.2] measurements, two major limitations in monitoring cerebral ischemia were identified.[50] First, the Sj[O.sub.2] saturation did not usually decrease with intracranial hypertension until after neurological signs of tentorial herniation were already observed. Second, the occurrence of artifacts in the oxygen saturation measurement caused by movement of the catheter within the jugular bulb accounted for nearly 50% of incorrectly read desaturations.

Cruz performed a prospective quasi-experimental study of 69 adults (median age 31 years) with acute severe closed head injury for the period from 1983 to 1992.[10] He tested the validity of the Sj[O.sub.2] catheter by noting correlation between conventional and fiberoptic oximetry values in evaluating the interrelationships of global cerebral hypoxia, intracranial hypertension, and neurologic outcome.

The correlation between conventional and fiberoptic oximetry values was strong (496 values, r = 0.86, p [is less than] 0.00001), but the methods for statistical analysis were not identified. Fisher's exact test was used to test the significance of the difference in proportions between the association of global cerebral hypoxia and neurological deterioration. His documented incidence of unreliable recordings of 8.5% was in sharp contrast to many other study findings. He claimed that the high incidence of false desaturations could have been minimized by "adequate nursing" (p. 231).[10] He concluded that keeping the head and neck in midline position restored reliable recordings. Cruz referred to nine of his own studies in preparing these data.

Dearden and Midgley evaluated 28 40-cm Shaw opticaths and compared them with a new, stiffer 25-cm catheter specially designed for use in the jugular bulb, because the manufacturers had advised that a stiffer catheter might decrease the vessel wall artifact.[14] Correlation regression analysis was used to compare the two different catheters on the congruency of their Sj[O.sub.2] readings. Preinsertion calibration with in vitro measurements was high (r = 0.78). Dearden and Midgley found that the 40-cm catheters overread by 7%, there were wide limits of agreement, and performance was poorer after in vivo calibration in comparison with the stiffer catheters. They suggested that a new catheter specifically designed for the jugular bulb and possibly employing a J loop might be required to improve the reliability and accuracy of continuous jugular venous oximetry.[14]

Several difficulties with the catheters were identified. In addition to the same difficulties found in other studies, Sj[O.sub.2] waves were present whereby rhythmic increases and decreases in Sj[O.sub.2] values occurred with or between rises in ICP. Notably; these waves also were present in the absence of ICP or blood pressure oscillations and were found to be caused by catheter coiling in the internal jugular vein. For unknown reasons, sudden increases in Sj[O.sub.2] saturations up to 100% occurred without changes in light intensity during a period of clinical stability when a ventilated paralyzed patient was left undisturbed. Dearden and Midgley concluded that further work was required to design a more reliable system that would not give false readings.

Fortune et al. conducted a study using Sj[O.sub.2] oximetry to assess the effects of transient changes in arterial pressure on ICP and Sj[O.sub.2], using the Sj[O.sub.2] catheter as a means to detect cerebral ischemia.[18] These data were used to quantify the extent of autoregulation after head injury and to determine the effects of endotracheal suctioning on CBF. This was a quasi-experimental study that included a non-random sampling of 14 patients with a mean age of 22 years who sustained closed head injury with subsequent GCS less than 8. Sj[O.sub.2] monitoring was initiated between 6 and 36 hours after injury. Catheter calibration was checked in vivo every 4-8 hours. The jugular venous blood sampling value was compared to the oximetry reading. If these values differed by more than 6% saturation, the oximetry catheter was recalibrated to the actual oxygen saturation. Fortune et al. found that reliability of Sj[O.sub.2] oximetry varied among patients. Recalibration of the catheter output signal was required 7%-78% of the time, with a mean of 38%.[18] Although a scatterplot demonstrated inconsistency in the stability of the oximetry signal, no consistent error was found. They also found that poor readings were improved when patients were placed with head position strictly perpendicular to the bed.[18,48] Linear regression analysis was used to test the calibrated data correlation between the temporal relationship of Sj[O.sub.2], Sa[O.sub.2], ICP, MAP, and response to endotracheal suctioning. The relationship between CPP and cerebral extraction of oxygen ([CEO.sub.2]) in response to changes in arterial hypertension was measured. Comparisons of Sj[O.sub.2] saturation between patients with normal and hyperemic flow at different points was made by ANOVA, which examined the variation and tested whether the between-group variation was greater than the within-group variation.

Intact autoregulation suggested that no change in [CEO.sub.2] would occur because the CPP was altered. Fortune et al. found a lack of autoregulation in 60% of the observations. Elevations in CPP caused by arterial hypertension resulted in reduction in [CEO.sub.2]. Elevations in CPP resulted in elevations in CBF and elevated Sj[O.sub.2] for short intervals. The temporal relationship between CPP and [CEO.sub.2] in response to elevations of arterial blood pressure showed that hyperemia had no influence on this response. As anticipated, increases in CPP with endotracheal suctioning resulted in decreases in the cerebral extraction of oxygen ([CEO.sub.2]), defined as the difference between Sa[O.sub.2] and Sj[O.sub.2]. These findings could be generalized to state that Sj[O.sub.2] increased with increases in CPP during and after suctioning.[18]

Fortune et al. noted that the fiberoptic catheters currently being used for jugular venous oximetry in this and other studies were primarily developed for neonatal umbilical arteries. The size of the devices (No. 4 French) made them easy to insert retrogradely into the jugular bulb, and the cost (approximately $150) was comparable to that of other specialty medical devices. They concluded that because the catheters were thin-walled, their pliability and position retrograde to blood flow made them especially susceptible to angulation against the wall of the vein with subsequent distortion of the "light-intensity" signal. This was a small but important study that identified the relationship between arterial blood pressure and Sj[O.sub.2] values. Internal threats to the study could have been attributed to the small sample size.

De Deyne et al. performed a retrospective analysis over 24 months of 50 patients 18-70 years of age who were suffering from severe head injury.[15] Severe head injury was defined as GCS score [is less than] 8 on admission. Sj[O.sub.2] monitoring was initiated in all patients within the first 24 hours after injury. Sj[O.sub.2] monitoring was performed for a mean duration of 7.5 days. Reliable abnormal Sj[O.sub.2] values were observed a total of 1,180 hours (13%) out of 9,096 hours. A period with abnormal Sj[O.sub.2] values was defined as more than 30 minutes with Sj[O.sub.2] values below 55% or above 80%. Only data guaranteeing accurate positioning of the catheter tip (i.e., a perfect light intensity signal) were analyzed, and reliability was established when less than 5% oxygen saturation difference between oximetry and co-oximetry control existed.[15,41]

De Deyne et al. found that most of the desaturation periods occurred in the first 2 days of monitoring or within the first 72 hours after trauma. Seventeen percent of the desaturation periods occurred after 5 days of monitoring. Desaturations correlated moderately with CPP [is less than] 70 mm Hg (r = 0.53), Pa[CO.sub.2] [is less than] 32 mm Hg (r = 0.49), and less frequently, elevations in ICE They determined that 40% of the desaturations were caused by CPP insufficiency induced by "blind" hyperventilation. Blind hyperventilation was a method initiated at the scene of an accident whereby the patient was hyperventilated to prevent or treat presumed intracranial hypertension.[6] They discouraged the use of blind hyperventilation except for cases of rapidly progressing intracranial catastrophes such as enlarging pupils, anisocoria, or bilateral mydriasis. Methods of data analysis were not presented; this posed a major threat to the internal validity of the study.

Several major shortcomings were identified that limited the use of the Sj[O.sub.2] catheter in bedside cerebral monitoring. Consistent with other studies, de Deyne et al. found that Sj[O.sub.2] monitoring provided unilateral and global information only. A technical drawback of catheter use was its retrograde insertion in a low-flow venous system, whereby blood flowing toward the fiberoptic tip may have accounted for inaccurate saturations. Reduced reliability necessitated increased maintenance with a routine crosscheck by co-oximetry control. However, the major shortcoming of this report was that the researchers relied on data documented in medical charts with only 30-minute controls. Therefore, they could only analyze periods of abnormal saturation lasting more than 30 minutes, thereby excluding all short-lasting periods of abnormal saturations that might have been detected by continuous data collection.

Sixty percent of the observed jugular desaturations occurred within 72 hours of trauma and 30% occurred at a mean of 4.8 hours after trauma. Sj[O.sub.2] desaturations most closely correlated with a reduced CPP or with a decreased Pa[CO.sub.2] due to hyperventilation. In conclusion, de Deyne et al. emphasized the need for more appropriate systemic monitoring and management in the intensive treatment of severe TBI.

Lam, Chan, and Poon performed a prospective study comparing Sj[O.sub.2] readings from the dominant jugular bulb and the confluence of the cerebral sinuses (Sccs[O.sub.2]) to determine whether Sj[O.sub.2] at the dominant side was representative of the global and cerebral hemispheric venous oxygen saturation.[31] The Sccs[O.sub.2] was compared with the Sj[O.sub.2] by monitoring 13 severely head-injured patients for a mean duration of 58 hours from April 1993 to December 1994. All these patients had cerebral contusions, subdural hematomas, or traumatic subarachnoid injury. Seven of the 13 patients had GCS score of 8 or less during the first 6 hours of admission. The range of Sj[O.sub.2] saturations was 19%-97.8%.

Linear regression was used appropriately to demonstrate the relationship between Sj[O.sub.2] and Sccs[O.sub.2]. In 9 out of 13 cases (70%), Sj[O.sub.2] saturations reflected accurately the venous oxygen saturation at the cerebral hemisphere. In 2 out of 13 cases (15%), the venous oxygen saturation at the cerebral hemisphere was underestimated by 4%-8%. Lam, Chan, and Poon declared this finding clinically insignificant because they set the lower tolerable limit of Sj[O.sub.2] at 55%, which is 5% over the critical level of 50% oxygen saturation set by Gopinath et al.

Of major clinical concern was that in 15% of the cases, the Sj[O.sub.2] underestimated the cerebral hemisphere venous oxygen saturation by up to 40% even when the catheter was properly placed at the "clinically dominant" jugular bulb.[31] Lam, Chan, and Poon found an 85% correlation between Sj[O.sub.2] and Sccs[O.sub.2] saturations. Cannulations of the CCS were found to be less affected by head and neck movement of the patient, but this advantage was outweighed by the need for angiographic guidance for insertion.

Trubiano et al. performed a prospective quasi-experimental study to validate the accuracy of the Sj[O.sub.2] catheter.[54] This included a non-random convenience sample of 20 patients undergoing elective coronary artery bypass graft or valvular replacement surgery. The patients were randomly assigned into one of two groups to determine the potentially confounding influence of temperature on Sj[O.sub.2]. The groups were differentiated by maintaining their assigned nasopharyngeal temperature of either 28 [degrees] C or 32 [degrees] C. All patients were cannulized with Sj[O.sub.2] catheters and co-oximetry.

Trubiano et al. found that Sj[O.sub.2] values coincided with co-oximeter values only 45% of the time. Linear regression analysis showed that Sj[O.sub.2] values obtained via the fiberoptic catheter correlated moderately (r = 0.44), regardless of the temperature at which the patients were maintained during cardiopulmonary bypass surgery. Bland-Altman analysis showed significant disagreement between Sj[O.sub.2] and co-oximetry readings, as most values were distributed diffusely between one or two standard deviations from the mean. The Shrout-Fleiss method was used to determine the correlation between serial measurements of the effect of temperature on Sj[O.sub.2] catheter readings by different examination techniques. This analysis was performed with and without inclusion of the residual of a linear regression of Sj[O.sub.2] against temperature as a dependent variable by comparing Groups A and B. Temperature did not affect the inaccurate and unreliable oxygen saturation values obtained using the fiberoptic catheter.

Trubiano et al. concluded that if co-oximeter values are accepted as the "gold-standard," then the Shrout-Fleiss method established the weaknesses of catheter values as a monitor of Sj[O.sub.2] trend.[54] They suggested that a less flexible catheter might be less sensitive to wall artifact because the catheter tip pointed toward the direction of blood flow instead of downstream.


The articles examined in this literature review collectively make a compelling argument against the Sj[O.sub.2] catheter as a tool for measuring cerebral oxygenation. The Sj[O.sub.2] catheter at best measures global cerebral oxygenation and therefore is unable to detect regional ischemia. The limitations of cerebral oximetry discussed point out how little we know about cerebral physiology.

The initial milestones by Myerson et al. and Gibbs et al. have served as the basis for more refined research on cerebral tissue oxygenation and metabolism.[20,21,40] In spite of the many advancements in healthcare technology, limiting secondary brain injury and improving neurologic outcome have remained elusive.

The need for a reliable tool for monitoring cerebral ischemia is paramount because substantial gain in providing appropriate treatment and improved neurological outcome could result. Substantial gains in providing appropriate treatment and in improving neurological outcome would be the benefits of a respectable monitoring device. The documented poor reliability and validity of the Sj[O.sub.2] catheter have deemed its therapeutic use questionable by many surgeons and anesthesiologists. Researchers continue to experiment and study new techniques that will provide reliable, valid data on regional brain tissue oxygenation after TBI or other problems while exposing patients to minimal risks. A device must be proven valid and reliable to merit use. The norm must be clearly established in a healthy population before further studies can be conducted in the at-risk population.

Despite its described uses, Sj[O.sub.2] monitoring is still not deemed a valid or reliable assessment of cerebral oxygenation. Most recent studies have suggested a change in the design of the Sj[O.sub.2] catheter similar to a J-shape. Theoretically, repositioning the catheter so that blood flow travels away from the fiberoptic tip may reduce catheter inaccuracy. Other recommendations to manufacturers to make the catheter stiffer or more pliable have not yielded improvements in catheter reliability or validity. Research on alternative methods for continuously monitoring regional cerebral oxygenation must continue. Manley et al. have demonstrated reliable monitoring of oxygen concentration (tension) of brain tissue (Pbr[O.sub.2]) in swine by surgical implantation of polarographic microelectrodes into white matter brain tissue.[35]


The battle to reduce, minimize, and prevent secondary ischemia is fought at the bedside. We must develop a method that can be used to monitor current trends and the effects of changes in hemodynamic status, nursing care, and procedures on traumatic brain-injured patients. With the development of such a tool, we can alter practice to influence and create better outcomes for these unfortunate patients who have suffered traumatic brain injury.


[1.] Apuzzo ML (editor): Brain Surgery: Complication Avoidance and Management, Vol. 2. Lippincott, 1993.

[2.] American Psychological Association: Publication Manual of the American Psychological Association, 4th ed. American Psychological Association, 1995.

[3.] Andrews PJ, Dearden NM, Miller JD: Jugular bulb cannulation: Description of a cannulation technique and validation of a new continuous monitor. Brit J Anaesth 1991; 67: 553-558.

[4.] Bell SD, Guyer D, Snyder, MA, Miner M: Cerebral hemodynamics: Monitoring arteriojugular oxygen content differences. J Neurosci Nurs 1994; 26: 270-277.

[5.] Bouma GJ, Muizelaar JP, Choi SC et al: Cerebral circulation and metabolism after severe traumatic brain injury: The elusive role of ischemia. J Neurosurgery 1991; 75: 685-693.

[6.] Brain Trauma Foundation, American Association of Neurological Surgeons, Joint Section on Neurotrauma and Critical Care: Guidelines for the management of severe head injury. J Neurotrauma 1996; 13: 641-734.

[7.] Bullock R, Stewart L, Rafferty C, Teasdale GM: Continuous monitoring of jugular bulb oxygen saturation and the effects of drugs acting on cerebral metabolism. Acta Neurochir 1993; 59(Suppl): 113-118.

[8.] Chan KH, Dearden NM, Miller JD et al: Multimodality monitoring as a guide to treatment of intracranial hypertension after severe brain injury. Neurosurgery 1993; 32: 547-553.

[9.] Cruz J: Jugular-venous oximetry. Acta Neurochir 1993a; 59(Suppl): 86-90.

[10.] Cruz J: On-line monitoring of global cerebral hypoxia in acute brain injury. J Neurosurgery 1993b; 79: 228-233.

[11.] Cruz J, Miner ME, Allen SJ et al: Continuous monitoring of cerebral oxygenation in acute brain injury: Assessment of cerebral hemodynamic reserve. Neurosurgery 1991, 29: 743-749.

[12.] Cruz J, Raps EC, Hoffstead OJ et al: Cerebral oxygenation monitoring. Crit Care Med 1993; 21: 1242-1246.

[13.] Dearden NM: Jugular bulb venous oxygen saturation in the management of severe head injury. Curr Opin Anaesthesiol 1991; 4: 2786-2790.

[14.] Dearden NM, Midgley S: Technical considerations in continuous jugular venous oxygen saturation measurement. Acta Neurochir 1993; 59(Suppl): 91-97.

[15.] De Deyne C, Vandekerckhove T, Decruyenaere J, Colardyn F: Analysis of abnormal jugular bulb oxygen saturation data in patients with severe head injury. Acta Neurochir 1996; 138: 1409-1415.

[16.] DeVries JW, Visser GH, Bakker PF: Neuromonitoring in defibrillation threshold testing. A comparison between EEG, near-infrared spectroscopy and jugular bulb oximetry. J Clin Monitoring 1997; 13: 303-307.

[17.] Enson Y, Briscoe WA, Polanyi ML, Cournand A: In vivo studies with an intravascular and intracardiac reflection oximeter. J Applied Physiol 1961; 17: 552-558.

[18.] Fortune JB, Feustel PJ, Weigle CG, Popp AJ: Continuous measurement of jugular venous oxygen saturation in response to transient elevations of blood pressure in head-injured patients. J Neurosurgery 1991; 80: 461-468.

[19.] Garlick R, Bihari D: The use of intermittent and continuous recordings of jugular venous bulb oxygen saturation in the unconscious patient. Scan J Clin Lab Invest 1987; 47(Suppl 188): 47-52.

[20.] Gibbs EL, Lennox WG, Gibbs FA: Bilateral internal jugular blood. Comparison of A-V differences, oxygen-dextrose ratios and respiratory quotients. Am J Psychiatry 1945; 102(2): 184-190.

[21.] Gibbs EL, Lennox WG, Nims LF, Gibbs FA: Arterial and cerebral blood. Arterial-venous differences in man. J Biol Chem 1942; 144: 325-332.

[22.] Goetting MG, Preston G: Jugular bulb catheterization: Experience with 123 patients. Crit Care Med 1990; 18: 1220-1223.

[23.] Graham D, Lawrence A, Adams J: Brain damage in fatal non-missile head injuries with high intracranial pressure. J Clin Path 1988; 41: 34-37.

[24.] Hans P, Franssen C, Damas F et al: Continuous Measurement of jugular venous bulb oxygen saturation in neurosurgical patients. Acta Anaesthesiol Belgica 1991; 42(4): 213-218.

[25.] Hantson P: Usefulness of cerebral venous monitoring through jugular bulb catheterization in the diagnosis of brain death. Intens Care Med 1992; 18: 59.

[26.] Jakobsen M, Enevoldsen E: Retrograde catheterization of the right internal jugular vein for serial measurements of cerebral venous oxygen content. J Cerebr Blood Flow Metab 1989; 717-720.

[27.] Katayama Y, Tsubokawa T, Hirayama T, Kazuhisa H: Continuous monitoring of jugular bulb oxygen saturation as a measure of the shunt flow of cerebral arteriovenous malformations. J Neurosurg 1994; 80: 826-833.

[28.] Kerr ME, Lovasik D, Darby J: Evaluating cerebral oxygenation using jugular venous oximetry in head injuries. AACN Clin Issues 1995; 6(1): 11-20.

[29.] Kety SS, Schmidt CF: The nitrous oxide method for the quantitative Determination of cerebral blood flow in man: Theory, procedure, and normal Values. J Clin Investi 1948; 27: 484-492.

[30.] Kontos HA, Wei EP, Navari RE et al: Responses of cerebral arteries and arterioles to acute hypotension and hypertension. Am J Physiol 1978; 234: H371-H383.

[31.] Lam JM, Chan MS, Poon WS: Cerebral venous oxygen saturation monitoring: Is dominant jugular bulb cannulation good enough? Brit J Neurosurg 1991; 10(4): 357-364.

[32.] Lassen NA, Lane MH: Validity of internal jugular blood for study of cerebral blood flow and metabolism. J Appl Physiol 1960; 16(2): 313-320.

[33.] Lewelt W, Jenkins L, Miller J: Effects of experimental fluid percussion injury of the brain on cerebrovascular reactivity to hypoxia and to hypercapnia. J Neurosurg 1982; 56: 332-338.

[34.] Lewi, SB, Myburgh JA, Reilly PL: Detection of cerebral venous desaturation by continuous jugular bulb oximetry following acute neurotrauma. Anaesth Intens Care 1995; 23: 307-314.

[35.] Manley GT, Pitts LH, Morabito D et al: Brain tissue oxygenation during hemorrhagic shock, resuscitation, and alterations in ventilation. J Trauma 1999; 46(2): 261-267.

[36.] Marion D, Darby J, Yonas H: Acute regional cerebral blood flow changes caused by severe head injury. J Neurosurg 1991; 74: 407-414.

[37.] Matta BF, Lam AM, Mayberg TS et al: A critique of the intraoperative use of jugular venous bulb catheters during neurosurgical procedures. Anesth Analgesia 1994; 79: 745-750.

[38.] Miller J: Head injury and brain ischemia: Implications for therapy. Brit J Anaesth 1985; 57: 120-129.

[39.] Moss E, Dearden NM, Berridge JC: Effects of changes in mean arterial pressure on Sj[O.sub.2] during cerebral aneursym surgery. Brit J Anaesth 1995; 75: 527-530.

[40.] Myerson A, Halbran RD, Hirsh HL: Technique for obtaining blood from the internal jugular vein and internal carotid artery. Arch Neurol Neurosurg Psychiatry 1927; 17: 807-809.

[41.] Nakajima T, Ohsumi H, Kuro M: Accuracy of continuous jugular bulb venous oximetry during cardiopulmonary bypass. Anesth Analgesia 1993; 77: 1111-1115.

[42.] Obrist WD, Gennarelli TA, Segawa H et al: Relation of cerebral blood flow to neurological status and outcome in head-injured patients. J Neurosurg 1979; 51: 292-300.

[43.] Obrist WD, Langfitt TW, Jaggi JL et al: Cerebral blood flow and metabolism in comatose patients, with acute head injury: Relationship to intracranial hypertension. J Neurosurg 1984; 61: 241-253.

[44.] Polit D, Hungler B: Nursing Research: Principles and Methods, 4th ed. Lippincott, 1991.

[45.] Robertson C: Desaturation episodes after severe head injury: Influences on outcome. Acta Neurochirg 1993; 59(Suppl): 98-101.

[46.] Robertson CS, Contant CF, Gokaslan ZL, Narayan RK, Grossman RG: Cerebral blood flow, arteriovenous oxygen difference, and outcome in head injured patients. J Neurosurg: 1991; 74: 594-603.

[47.] Robertson CS, Narayan RK, Gokaslan ZL et al: Cerebral arteriovenous oxygen difference as an estimate of cerebral blood flow in comatose patients. J Neurosurg 1989; 70: 222-230.

[48.] Schneider GH, Franke R, Lanksch WR, Unterberg A: Influence of body position on jugular venous oxygen saturation, intracranial pressure, and cerebral perfusion pressure. Acta Neurochir 1993; 59(Suppl): 107-112.

[49.] Schneider GH, Helden AV, Lanksch WR, Unterberg A: Continuous monitoring of jugular bulb oxygen saturation in comatose patients: Therapeutic implications. Acta Neurochir 1995; 134: 71-75.

[50.] Sheinberg M, Kanter MJ, Robertson CS et al: Continuous monitoring of jugular venous oxygen saturation in head-injured patients. J Neurosurg 1992; 76: 212-217.

[51.] Shenkin HA, Harmel MH, Kety SS: Dynamic anatomy of the cerebral circulation. Arch Neurol Neurosurg Psychiatry 1948; 60: 240-252.

[52.] Sikes P, Segal J: Jugular bulb oxygen saturation monitoring for evaluating cerebral ischemia. Crit Care Nurs Quart 1994; 17(1): 9-20.

[53.] Smith D, Levy W, Maris M, Chance B: Reperfusion hyperoxia in brain after circulatory arrest in humans. Anesthesiology 1990; 73: 12-19.

[54.] Trubiano P, Heyer EJ, Adams DC et al: Jugular venous bulb oxyhemoglobin saturation during cardiac surgery: Accuracy and reliability using a continuous monitor. Anesth Analgesia 1996; 82: 964-968.

Questions or comments about this article may be directed to: Heidi D. Clay, MS RN CCNS, UCSF Medical Center, Department of Neurological Surgery, 505 Parnassus Avenue, Room M-779, San Francisco, CA 94143. She is a clinical nurse specialist in the Department of Neurological Surgery at the University of California--San Francisco Medical Center, San Francisco, CA.

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Author:Clay, Heidi D.
Publication:Journal of Neuroscience Nursing
Geographic Code:1USA
Date:Aug 1, 2000
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