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Copyright @ 2010 American Association of Neuroscience Nurses. Unauthorized reproduction of this article is prohibited.

Effect of Body Position on CerebralOxygenation and Physiologic Parameters inPatients With Acute Neurological Conditions

Mary B. Ledwith, Stephanie Bloom, Eileen Maloney-Wilensky, Bernadette Coyle,Rosemary C. Polomano, Peter D. Le Roux

ABSTRACTHow body position influences brain tissue oxygen (PbtO2) and intracranial pressure (ICP) in critically illneurosurgical patients remains poorly defined. In a prospective observational repeated measures study, weexamined the effects of 12 different body positions on neurodynamic and hemodynamic outcomes.Thirty-three consecutive patients (mean T SD, age = 48.3 T 16.6 years; 22 men), admitted after traumaticbrain injury, subarachnoid hemorrhage, or craniotomy for tumor, were evaluated in a neurocritical careunit at a level 1 academic trauma center. Patients were eligible if the admission score in the GlasgowComa Scale was e8 and they had a Licox CMP Monitoring System (Integra Neurosciences, Plainsboro, NJ).

Patients were exposed to all 12 positions in random order. Changes from baseline to the 15-minutepostposition assessment mean change scores showed a downward trend for PbtO2 for all positions withstatistically significant decreases observed for supine head of bed (HOB) elevated 30- and 45- ( pG .01)and right and left lateral positioning HOB 30-( pG .05). ICP decreased with supine HOB 45-(pG .01) andknee elevation, HOB 30o and 45- ( pG .05), and increased (pG .05) with right and left lateral HOB 15o.Hemodynamic parameters were similar in the various positions. Positioning practices can positively ornegatively affect PbtO2 and ICP and fluctuate with considerable variability among patients. Nursesmust consider potential effects of turning, evaluate changes with positioning on the basis of monitoringfeedback from multimodality devices, and make independent clinical judgments about optimal positionsto maintain or improve cerebral oxygenation.

Traumatic brain injury (TBI) affects approxi-mately 1.4 million people in the United Statesannually; 235,000 of these cases are serious

enough to require hospital care and intensive care unit(ICU) care. About 50,000 TBI patients die each year

(Langlois, Rutland-Brown, & Thomas, 2004). Virtu-ally, no TBI is without consequence, and it is es-timated that 2% of the U.S. population currently livewith TBI-related disabilities (Thurman, Alverson,Dunn, Guerrero, & Sniezek, 1999). Although lessfrequent, aneurysmal subarachnoid hemorrhage(SAH) can be more devastating with long-lastingneurological impairments. Each year, approximately30,000 people, most between 40 and 60 years of age,suffer aneurysmal SAH in the United States; 60% dieor are disabled. In addition, approximately half thepatients who appear to experience a favorable out-come suffer from significant neuropsychological andcognitive deficits (LeRoux & Winn, 2004).

Not all neuron damage occurs at the time of injuryor aneurysm rupture, and much of the poor outcomesobserved after TBI or SAH are associated with de-layed cerebral injury that develops while the patientreceives ICU care. This concept of secondary neuronalinjury and its prevention is central to modern TBI andSAH critical care management. In particular, second-ary cerebral insults such as hypotension, hypoxia, andincreased intracranial pressure (ICP) or reduced cere-

bral perfusion pressure (CPP) among others have beendemonstrated in multiple studies to adversely affectpatient outcomes (Iacono, 2000; Meixensberger et al.,2003; Phillips, 2003; Rao, 2007; Sullivan, 2000).

Journal of Neuroscience Nursing280

Questions or comments about this article may be directed toMary B. Ledwith, RN, at [email protected]. She is anurse manager in the Neuro Intensive Care Unit, Hospital of theUniversity of Pennsylvania, Philadelphia, PA.

Stephanie Bloom, MSN ACNP, is an ICU nurse practitioner inthe Department of Neurosurgery, University of Pennsylvania,

Philadelphia, PA.

Eileen Maloney-Wilensky, CRNP MSN, is the director of Neu-rosurgery Clinical Research and Midlevel Provider Program inthe Department of Neurosurgery, University of Pennsylvania,Philadelphia, PA.

Bernadette Coyle, RN, is a clinical nurse in the Department ofNursing, Hospital of the University of Pennsylvania, Philadelphia,PA.

Rosemary C. Polomano, PhD RN, is an associate professor for PainPractice at the University of Pennsylvania School of Nursing andan associate professor of Anesthesiology and Critical Care at theUniversity of Pennsylvania, Philadelphia, PA.

Peter D. Le Roux, MD, is an associate professor in the Departmentof Neurosurgery, University of Pennsylvania, Philadelphia, PA.

CopyrightB2010 American Association of Neuroscience Nurses

DOI: 10.1097/JNN.0b013e3181ecafd4


2/8Copyright @ 2010 American Association of Neuroscience Nurses. Unauthorized reproduction of this article is prohibited.

Consequently, the foundation of care in severelybrain-injured patients is to monitor and control ICP,CPP, and mean arterial pressure (MAP) and tomanage fluctuations that may lead to further braininjury. The goal of this care is to maintain adequatecerebral blood flow (CBF) and ultimately delivery ofoxygen and glucose to brain cells (Albano, Comandante,

& Nolan, 2005; Littlejohns & Bader, 2005).Several variables influence ICP, CPP, or MAP af-ter brain injury, among them is body positioning.Multisystem and extracranial pathophysiological pro-cesses that occur after brain injury can render severeSAH and TBI patients vulnerable to random bodyposition changes (Yanko & Mitcho, 2001). However,the exact effects of body position, a critical compo-nent of basic nursing care in the ICU, on intracranialphysiology after brain injury are not well defined.For example, the guidelines for the management ofsevere head injury jointly published by the AmericanAssociation of Neurological Surgeons and the BrainTrauma Foundation (2007) do not include specific rec-ommendations for optimal patient positioning prac-tices after severe brain injury (Bratton et al., 2007).Similarly, guidelines on care of SAH patients are un-clear about optimal patient position (Bederson et al.,2009; Mayberg et al., 1994).

Current positioning practices in neurocritical careunits are largely based on studies that suggest headof bed (HOB) elevation may reduce ICP. However,there is no consensus on the degree of elevation forbest practice. Although 30- of head elevation is be-lieved to be associated with improvements in ICP andCPP (Phillips, 2003; Winkelman, 2000), other studieshave not found the most beneficial backrest positionfor ICP and CPP (March, Mitchell, Grady, & Winn,1990). Other studies show that head rotation andhead and neck flexion may increase ICP, decreasejugular venous outflow, and alter CBF (Albano et al.,2005; Wong, 2000). Turning and repositioning alsomay be associated with transient increases in ICP andsubsequent changes in cerebral and cardiovascular

variables (Price, Collins, & Gallagher, 2003). Thesevarious studies form the basis for current care of thebrain-injured patients, that is, head elevation, avoid-ance of head rotation and head flexion, and cautious

repositioning. In a literature review on positioningfor diverse patient populations, Sullivan (2000) sug-gests that caution should be used with side-lying posi-tions and HOB elevation no greater than 45- shouldbe used for TBI patients.

Several investigators have challenged this tradi-

tional notion of head elevation after SAH or TBI, inlarge part because of potential effects from cerebralautoregulation. The goal of ICP reduction is to im-prove CPP and so CBF. Rosner and Coley (1986), ina study of 18 patients with TBI with intracranial hy-pertension, suggested that ICP reductions duringhead elevation were accompanied by CPP reductions.In a subsequent study of 34 patients with TBI and in-tracranial hypertension, these investigators suggestedthat the head-flat position was associated with reducedmorbidity and mortality (Rosner & Daughton, 1990).

Blissitt (2006) studied 20 patients with aneurismal SAHand examined transcranial doppler velocities when thebed position was moved in sequence 0oY20oY45oY0o

and demonstrated in general that head elevation didnot cause harmful changes in CBF in SAH patients.In 2004, Fan conducted a systematic review to eval-uate existing evidence for the effects of head orbody position on ICP and CPP. Eleven articles werereviewed; 9 concluded that a 30- head elevation de-creased ICP compared with a flat position. A signifi-cant change in CPP was not observed in 5 of these9 studies. However, several of these studies includedfew patients, so Fan was not able to make definitiveconclusions and instead recommended that futureresearch was necessary to investigate the effects ofpatient position to explore the combination of headelevation and lateral side-lying positions in differentneurological and neurosurgical patients.

The goal of ICP and CPP control is to deliveradequate CBF and oxygen to the brain and to avoidcerebral ischemia. Brain tissue oxygen (PbtO2) nowcan be monitored with the devices approved by theFood and Drug Administration. A PbtO2monitor ap-pears to discriminate between normal oxygenation,threatened ischemia, and critical ischemia when ICPand CPP, among other variables, vary (Scheufler,Lehnert, Rohrborn, Nadstawek, & Thees, 2004).Brain oxygen values between 20 and 40 mmHg areregarded as normal, whereas reductions (G15 mmHg)are associated with cerebral ischemia. In addition,poor patient outcome after TBI is associated with thenumber, duration, and intensity of cerebral hypoxicepisodes (PbtO2 G15 mmHg) and any PbtO2 valuesG5 mmHg (Valadka, Gopinath, Contant, Uzura, &

Robertson, 1998; van den Brink et al., 2000). De-creases in PbtO2 also are not benign and are asso-ciated with independent chemical markers of brainischemia (Hlatky, Valadka, & Robertson, 2005),

Random body position change is

one of several variables affecting

ICP, CPP, and MAP following

a brain injury.

Volume 42 & Number 5 & October 2010 281



whereas increases in MAP to elevate CPP can improvePbtO2in ischemic areas of the brain (Stocchetti et al.,1998). A brain oxygen monitor, therefore, may be auseful tool to examine how body position influencesintracranial physiology after brain injury.

Few studies have examined the effects of patient

positioning on PbtO2. Meixensberger et al. (1997)reported that head elevation of 30- produced a de-crease in ICP without risk to the regional cerebralmicrocirculation, as measured by PbtO2 after severebrain injury. Similarly, Ng, Lim, and Wong (2006),who studied 38 patients with severe TBI, found thatroutine nursing care with patient positioning at 30-for head elevation within 24 hours of trauma sig-nificantly decreased ICP. Although there was adownward trend for CPP, this did not adversely af-fect brain oxygenation. We therefore undertook this

study to examine the effects of patient positioning,including a combination of head elevation and sidelying on PbtO2 ICP, CPP, and MAP after severebrain injury. We hypothesized that no single positionis optimal in improving neurodymanic parametersfor all severely brain-injured patients.

Clinical Material and MethodsStudy DesignA quasi-experimental, prospective repeated measuresdesign with control over the intervention was usedto investigate the effects of positioning on PbtO2in severely brain-injured patients. The University ofPennsylvania institutional review board approvedthe study as part of a larger study of the BrainOxygen Monitoring Outcome Study. Waiver of in-formed consent was granted for this study becauseit involved the collection of data in the course ofclinical care and monitoring. All research proce-dures were in accordance and compliance with theHealth Insurance Portability and Accountability Actregulations and the institutions policies and guide-

lines for protection of human subjects.

Patient SamplePatients diagnosed with severe SAH or TBI admittedto the neuro-ICU at the Hospital of the University ofPennsylvania, a university-affiliated level 1 traumacenter, and who underwent PbtO2 monitoring werepart of this study. Severe SAH or TBI was definedby an admission postresuscitation score ofe8 in theGlasgow Coma Scale (GCS) or if they subsequentlydeteriorated to a GCS e8. Each patient underwent

the Licox CMP PbtO2 and ICP monitoring (IntegraNeurosciences, Plainsboro NJ) and hemodynamicmonitoring. At the time of evaluation, all patientswere neurologically and physiologically stable (i.e.,

normal ICP, heart rate, blood pressure, and arterialoxygen saturation [SaO2]).

Body and Head PositionEach subject served as their own control and wasplaced in each of the 12 predetermined body positions

at 2-hour intervals. Random order of assignments tohead and body position was delivered using a randomnumbers table to ensure that the sequence of po-sitioning was different for each subject and to controlfor the potential influences of order of treatment ef-fects. The 12 study positions were supine, supine withknee bent, left lateral position, and right lateralposition, and in each of these positions, the HOBthen was elevated to 15-, 30-, or 45-. To standardizethe degree of head, lateral turns, and knee elevation,commercially available products were used for all of

these positions. Lateral head rotation, neck flexion,and head hyperextension was avoided in each po-sition. The HOB elevation was consistently measuredwith the use of a protractor (Johnson Magnetic An-gle locator no. 700). A commercially available foamwedge (body wedge, model no. 920406; Alimed Inc.,Dedham, MA) was used to consistently measure andmaintain lateral positions. Knee elevation also wasconsistently measured and maintained with a com-mercially available foam wedge (knee elevationmodel no. 9-235; Alimed Inc.). To allow for adequatestabilization of brain and hemodynamic parametersafter turning, subjects remained in each of the studypositions for 15 minutes before postpositioning mea-surements were obtained. No therapeutic interven-tions were initiated during position changes to limitthe confounding influence of treatments.

Intracranial MonitorsICP, brain temperature, and PbtO2were continuouslymonitored before and after each position using com-mercially available products (Licox CMP; IntegraNeuroscience). Cerebral perfusion pressure was cal-culated (CPP = MAP j ICP). Intracranial monitors(ICP, brain temperature, and PbtO2) were inserted atthe bedside in the neuro-ICU through a burr holeinto the frontal lobe and secured with a triple-lumenbolt. The monitors were placed into the white matterthat appeared normal on the head CT scan and on theside of maximal pathology. Follow-up head CTscans were performed in all patients within 24 hoursof insertion to confirm correct placement of the var-ious monitors, for example, not in a contusion orinfarct. Probe function and stability were confirmed

by an appropriate PbtO2 increase after an oxygenchallenge (FiO2 1.0 for 5 minutes). To allow forprobe equilibration, patients were not studied until atleast 6 hours after PbtO2 monitor insertion.




Physiological Measurements andData CollectionThe following systemic parameters were continuous-ly measured before and after each position: (a) heartrate using a 12-lead electrocardiogram of the HewlettPackard Component Monitoring System (Revision C;

Hewlett Packard, Palo Alto, CA); (b) systolic, di-astolic, and mean arterial blood pressure by radialartery catheter connected to an external transducer forstandard fluid-filled column hemodynamic monitor-ing (the transducer was placed at the phlebostatic axis,interface through the parameter module of theHewlett Packard Component Monitoring System,Revision C); and (c) systemic arterial oxygen sat-uration (SaO2) by Plethysmograph Module of theHewlett Packard monitor. Physiologic parametersand data obtained from intracranial monitors were re-

corded using a bedside monitor (Component Moni-toring System M1046-9090C; Hewlett Packard). Inaddition, these physiologic variables and fractionalconcentration of inspired oxygen (FiO2) and centralvenous pressure were recorded every 15 minutes onthe ICU flow sheet. All patients on mechanical venti-lators routinely have daily PaO2measurements. Morefrequent PaO2 readings were obtained if a change ina patients clinical status was observed. In addition,serum hemoglobin and hematocrit levels were mea-sured daily on all patients.

Statistical AnalysisEach position was considered a separate event, andsubjects served as their own controls. Data are ex-pressed as meanTSDor as a median, where the dataare not normally distributed. The differences be-tween preposition (baseline immediately before po-sition change) and postposition (15 minutes afterposition change) measurements for PbtO2, ICP, andCCP were examined using either the Students ttestor the Wilcoxon signed-rank test for paired data de-pending on distribution of the data. Ap value of less

than .05 was considered statistically significant. Allanalyses were performed using the Statistical Packagefor the Social Sciences for Windows (Version 1.5;SPSS Inc., Chicago, IL).

A power analysis performed a priori indicated that33 patients would yield sufficient statistical powerof .80 to detect a treatment effect with body posi-tioning on PbtO2 with sigma = 1, medium treatmenteffect size = .5, and alpha = .05, two-tailed.

ResultsPatient CharacteristicsThirty-three patients, including 11 women and 22men (mean age = 48.3 T 16.6 years), were included

in this study. Of these, eleven patients had SAH,11 had closed head injury, 4 had acute traumaticsubdural hematomas, 2 had gunshot wounds to thehead, 2 had intraparenchymal hemorrhage, and 2were in a coma after craniotomies for tumor. Allpatients had a GCS score e8 before the start of the

study. On admission, 11 patients had a GCS scoreQ8 but deteriorated shortly after that to a GCS scoree8. One subject was eliminated from the studybecause the Licox monitor was found on follow-upCT scan to be incorrectly placed in gray matter,hence causing an artificial increase in PbtO2. Threepatients did not complete all 12 positions. Thirty pa-tients with complete data were included in the fi-nal analysis.

Baseline Values

At the start of the study, mean ICP, CPP, and PbtO2was 10 T 6.15, 90.88 T 16.58, and 37.6 T 13.61, re-spectively, in all patients.

Brain Tissue OxygenTable 1 lists the mean T SDPbtO2 values for all pa-tients at baseline before the position change and 15minutes after each position turn. A significant changewas observed in four positions: (a) supine with HOB30- (decrease), (b) supine with HOB 45- (decrease),(c) left lateral with HOB 30-(decrease), and (d) rightlateral with HOB 30- (decrease).

ICP and Cerebral Perfusion PressureThe ICP and the CPP before and after each positionturn and mean differences are illustrated in Table 2.Four positions led to a significant change in ICP: (a)supine with HOB 45-(decrease), (b) left lateral withHOB 15- (increase), (c) right lateral with HOB 15-

(increase), and (d) knee elevation with HOB (de-crease). Only one position had a significant effect onCPPVleft lateral with HOB 30- (decrease).

DiscussionPatient body and head position may potentially in-fluence intracranial hemodynamics after severe braininjury. Normally, constant CBF is maintained by anintact cerebral autoregulation system, but when thebrain is injured, compensatory mechanisms for sus-taining CBF may be affected. Factors that can overrideor affect these protective mechanisms are elevated ICPin excess of 40 mmHg, mean blood pressures thatexceed 60 to 150 mmHg, local or diffuse injury fromischemia, or inflammation. A critical component of

neurointensive nursing care is identifying the mostoptimal body position that augments adequate CBFwhile controlling ICP, CPP, and PbtO2 (Hickey,2003).




Optimal positions have not been clearly definedfor the severely brain-injured patient. Our results sug-gest that there is no single position that reliablyincreases brain oxygen, decreases ICP, and increasesCPP. This emphasizes the role of multimodalitymonitoring and close observation with any changein position both initially and while patients remain ina particular position. The findings also suggest thatthe lateral position may be the most detrimental toPbtO2, ICP, and CCP, especially when the HOB isnot elevated. With both the right and the left lat-eral positions, trends for adverse effects on ICP, CPP,and brain oxygen were observed, suggesting thatthe lateral position should be used with caution andpatients should be closely monitored when in thisposition.

Body Position and Neurocritical CareThe patient population in critical care units is diverse,and so careful consideration on how body positioninfluences their care is warranted. However, the effect

of body position on patient outcome in brain-injuredpatients is only beginning to be elucidated. For ex-ample, Wojner et al. (2002) observed in 11 patientswith acute ischemic stroke that this patient populationmay benefit from lower HOB positions, specificallya flat position to promote increased blood flow toischemic brain tissue. Studies of TBI patients sug-gest that HOB elevation is preferable (Phillips, 2003;Winkelman, 2000), although a flat position is thoughtby some to improve ICP and CPP (Rosner & Coley1986). These differences may depend on autoregula-tion among other factors. Recommendations for bodyposition and turning of trauma patients includingthose with TBI are summarized (Christie, 2008;Sullivan, 2000). However, there are no universallyaccepted guidelines, and it remains unclear if bodyposition alters outcome. Our data suggest that there

may be no single optimal position. This is consistentwith the heterogeneity of TBI and the concept oftargeted care in which care is individualized to thespecific patient and his or her pathology.

TABLE 1. PbtO2 Before and After a Body Position Change

Body Position PbtO2Before PbtO2After PbtO2Change Percent ChangeDirectionof Change p

1. Supine with

HOB 15-

38.14 T 12.7 37.89 T 13.3 2.523 T 3.4 1.11 T 9.5 , .358

2. Supine withHOB 30-

41.10 T 17.7 37.84 T 12.8 3.25 T 9.0 5.80 T 10.4 , .006

3. Supine with

HOB 45-

36.84 T 13.4 32.89 T 10.1 3.94 T 7.7 9.43 T 16.4 , .004

4. Left lateral

with HOB 15-

36.03 T 12.3 35.23 T 12.9 0.80 T 6.2 1.39 T 18.8 , .71

5. Left lateral

with HOB 30-

41.19 T 12.5 38.31 T 13.1 2.89 T 8.4 5.96 T 17.8 , .046

6. Left lateral

with HOB 45-

33.71 T 14.6 32.46 T 13.2 0.96 T 6.6 j0.8692 T 31.0 , .223

7. Right lateral

with HOB 15-

35.47 T 13.4 35.19 T 14.1 0.49 T 7.0 j4.97 T 31.4 , .753

8. Right lateral

with HOB 30-

37.76 T 12.5 35.86 T13.6 1.91 T 4.1 6.07 T 11.9 , .028

9. Right lateral

with HOB 45-

37.96 T 14.0 37.24 T 14.0 1.30 T 4.8 3.17 T 12.9 , .056

10. Knee elevation

with HOB 15-

37.67 T 15.6 36.34 T 14.2 1.28 T 6.2 1.16 T 14.6 , .313

11. Knee elevation

with HOB 30-

37.67 T 13.5 37.22 T 14.9 0.45 T 4.4 1.98 T 11.8 , .516

12. Knee elevation

with HOB 45-

38.17 T 11.6 36.86 T 11.15 1.31 T 4.9 2.33 T 13.3 , .114

Note. Each subject served as their own control and was placed in random order in each of 12 predetermined body positions at 2-hourintervals. Subjects remained in each of the study positions for 15 minutes before postmeasurements were obtained. Data are expressedas mean T SD. PbtO2= brain tissue oxygen; HOB = head of bed.



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to reduce the risk of pressure sores and receive veryclose attention to pulmonary care and toilette.

Intracranial HemodynamicsSeverely brain-injured patients admitted to an ICUare often complex. Immediately after their initial in-

jury, they may have decreased brain oxygen, hypoxia,hypotension, or increased ICP among other secondarycerebral insults. The primary focus of managementfor these patients is the control of ICP and CPP toprevent secondary injury. Today, multimodality de-vices are used to assist with this management be-cause monitoring ICP and CPP alone does not alwaysreflect brain oxygen or metabolism adequately. Ourdata demonstrate that there was no single position thatconsistently improved ICP, CPP, or brain oxygen. Thissuggests that there may not be a single optimal position

to manage all patients with severe brain injury. Instead,we believe that the use of multimodality devices canbest help determine the optimal position for an in-dividual patient and so help decrease secondary injury.In the absence of monitoring, HOB elevation to 30-augmented with slight knee elevation may be the bestdefault position for ICP and CPP control.

Study LimitationsThe study has several potential limitations. First,although the data showed statistical significance insome positions, the sample size is small. The find-ings therefore should be considered preliminary butcan provide important point estimates to calculatethe adequacy of sample sizes in future studies. Sec-ond, patients with several different pathologies wereexamined. This may introduce bias. However, all pa-tients were in coma at the time of evaluation (i.e.,GCSe 8). Third, all patients in the study were physi-ologically stable before the study and throughout theposition changes. We did not feel it appropriate tosubject unstable patients to random position changes.Nevertheless, we cannot conclude whether the samefindings would apply to patients who were not phy-siologically stable or had increased ICP. Fourth, thestudy and the position changes occurred over a studyperiod often greater than 24 hours. This may influenceour results in two ways: multiple nurses recordedthe data or there was a change in physiologic vari-ables over time. However, because the same team ofICU nurses provided care to the patients in a protocol-driven manner and information and education wereprovided to the bedside nurse during the study, wethink data entry is unlikely to play a significant role.

Moreover, we do not know if changes in CBF thatmay occur over time influenced our results. Fifth,the challenges were administered in a consecutivemanner, and so one position may have influenced the

next. Because the choice of position was random, webelieve that this is unlikely to affect our results. Inaddition, we chose not to examine the prone position.The physiological effects of this position are varied,and although it may improve oxygenation in patientswith acute respiratory distress syndrome (Reinprecht

et al., 2003), it also may increase ICP in some neu-rosurgical patients (Nekludov, Bellander, & Mure,2006). Despite these potential limitations, the data arecompelling and suggest that there is no one optimalposition for all severely brain-injured patients andthat among various positions, the lateral position mayhave the most potential for harm.

ConclusionIn this prospective clinical study, we subjected 30patients to 12 random body and head positions while

they underwent multimodality intracranial monitoring.Our data suggest that there is no single optimal bodyposition and that the lateral position should be usedwith caution.

AcknowledgmentsThis work was supported, in part, by research grantsfrom the Mary Elisabeth Groff Surgical and MedicalResearch Trust (PDLR), the Integra Foundation(PDLR), and the Integra Neuroscience (PDLR). Theauthors thank the Neuro ICU nurses at the University

of Pennsylvania for their support; without their help,the study would not have been possible.

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