Printer Friendly

Effect of backrest position on intracranial pressure and cerebral perfusion pressure in individuals with brain injury: a systematic review.

Abstract: Head elevation is a conventional nursing procedure for brain-injured individuals with intracranial hypertension; it is performed with the intent of reducing intracranial pressure (ICP) by means of a noninvasive physical intervention. However, in certain circumstances, head elevation puts the brain-injured individual at risk for secondary cerebral injury because of impaired arterial blood pressure and compromised cerebral perfusion pressure (CPP). A systematic literature search was conducted to evaluate existing evidence regarding the effect of changing the backrest position on ICP and CPP in brain-injured individuals. Eleven articles were retrieved. In nine articles it was concluded that ICP significantly decreased at 30 degrees of head elevation compared with a fiat position. Five of the nine articles showed no statistical significance in the magnitude of change in CPP from a flat position to 30 degrees of head elevation. Major limitations in the 11 articles were small sample sizes and unclear study protocols, which may have caused a failure to detect the effect of head elevation. In clinical practice, intensive care unit staff members need to cautiously perform head elevation with a thorough understanding of its physiologic effect and potential hazard. Future research should investigate the effects of therapeutic positions on different neurological and neurosurgical populations and explore the combination of head elevation and lateral side-lying positions.

********

Characteristics of the primary injury are not the major determinant of outcome for individuals with brain injury. It is the secondary injury, developing after the acute phase of the primary injury, that plays a crucial role in determining outcome for individuals with brain injury (Chesnut, Marshall, Piek et al., 1993; Cormio, Robertson, & Narayan, 1997; Jones et al., 1994; Narayan, 1995). The causes of secondary injury include both intracranial and extracranial factors. The intracranial factors include the cascade sequence of pathophysiological mechanisms of brain injury, biochemical mechanism, and cellular, metabolic, and chemical events (Dearden, 1998). Extracranial factors, such as hypoxia, pyrexia, and hypotension, also evolve over time (Chesnut, Marshall, Klauber, et al; Chesnut, Marshall, Pieka, et al; Dearden, 1998; Heath & Vink, 1999; Jones et al., 1994; Pietropaoli et al., 1992; Signorini, Andrews, Jones, Wardlaw, & Miller, 1999). More extensive and permanent damage is caused by the secondary injury (Gualtieri, 2002). Many studies have shown that frequent episodes of secondary insults yield poorer outcomes (Boumna, Muizelaar, Choi, Newlon, & Young, 1991; Downard et al., 2000; Jones et al., 1994; Marmarou et al., 1991; Rosner & Daughton, 1990; Rosner, Rosner, & Johnson, 1995).

After brain injury, intracranial hypertension and insufficient cerebral perfusion pressure (CPP), resulting from both primary and secondary injuries, are the major concerns during care of individuals with brain injury (Signorini et al., 1999). Intracranial hematoma, edema, vascular engorgement, and hydrocephalus are common causes of intracranial hypertension after brain injury and occur in 50%-75% of individuals with severe brain injuries (Dearden, 1998; Miller, Deardan, Piper, & Chan, 1992). These consequences are associated with 69%-95% mortality, especially in individuals with increased intracranial pressure (ICP) refractory to treatment (Alberico, Ward, Choi, Marmarou, & Young, 1987; Miller et al., 1977; Saul & Ducker, 1982; Signorini et al., 1999). Representing the pressure gradient between cerebral artery and venous vasculature, CPP is calculated by arriving at the difference between mean arterial blood pressure (MABP) and ICP. CPP is usually maintained above 70 mm Hg to meet the requirement of supplying cerebral metabolism via cerebral autoregulation (Brain Trauma Foundation, 2000b; Rosner & Daughton, 1990). Failure to maintain an adequate CPP worsens the existing ischemic zone and jeopardizes the normally perfused regions (Brain Trauma Foundation, 2000b). Several studies disclosed systemic insults such as unstable hemodynamics, hypoxia, and pyrexia, which have a critical impact on the development of secondary brain injury (Chesnut, Marshall, Klauber et al., 1993; Chesnut, Marshall, Piek, et al., 1993; Dearden, 1998; Heath & Vink, 1999; Jones et al., 1994; Pietropaoli et al., 1992; Signorini et al., 1999). The goals of treating individuals with brain injury are not only to attenuate the impact of the secondary injury through the management of intracranial hypertension but also to preserve adequate CPP and to ensure maintenance of systemic hemodynamic function during the acute stage (Gualtieri, 2002).

In neurosurgical and neurological intensive care units, head elevation is a conventional nursing procedure in the care of brain-injured individuals with intracranial hypertension; it is performed with the intent of reducing ICP by means of a noninvasive physical intervention that promotes intracranial venous return and increases cerebrospinal fluid (CSF) drainage from the head (Kirkness, 1992). Recently, this traditional nursing practice of head elevation has come into question because of its potential to decrease CPP by decreasing the arterial blood pressure (Kirkness, 1992). The purpose of this systematic review is to evaluate the existing evidence regarding the effects of changing the backrest position on ICP and CPP in individuals with brain injury.

Conceptual Basis

Head elevation, a conventional nursing procedure, is performed routinely for brain-injured individuals with intracranial hypertension. The theoretical basis is that the head is above the level of the heart on the vertical axis, and as a result, CSF is redistributed from the cranial to the spinal subarachnoid space (Kenning, Toutant, & Saunders, 1981), and it facilitates cerebral venous return (Magnaes, 1976; Magnaes, 1978; Marmarou, Shulman, & LaMorgese, 1975; Potts & Deonarine, 1973). The redistribution of CSF in response to head elevation occurs immediately after a change in position because of free communication between the cranial and spinal subarachnoid spaces (Magnaes, 1978). The major routes for cerebral venous drainage include the internal jugular veins with the accessory systems of the external jugular veins and the vertebral venous plexi (Kenning et al., 1981). All these venous systems are valveless channels that allow cerebral venous return without interruption after head elevation. The postural impact on the systemic hemodynamics (e.g., when the patient is moved from a supine to an upright position) causes approximately 30% of the blood volume from the upper body to be suddenly displaced into the peripheral vein. In addition to the intravascular pressure in the heart, gravity contributes an additional pressure component to vessels below the heart. That is, standing up causes the compliant veins to distend. This is known as a venous pooling, an effect of hydrostatic pressure. Together these decrease venous return.

For a healthy individual, a sudden shift in blood volume has little effect on systemic arterial blood pressure (SABP) and CPP because various mechanisms maintain adequate cardiac output and cerebral blood flow. Maintaining SABP involves compensatory mechanisms such as baroreceptor reflexes, vasoconstriction, and the pumping effect of the skeleton muscles and the lungs that help facilitate venous return to the heart. However, these mechanisms become less effective when an individual has prolonged bed rest. Cerebral autoregulation is the most important mechanism for maintaining CPP. It maintains a relatively constant cerebral blood flow to the brain across a range of MABP from 50 to 150 mm Hg. This is accomplished by regulation of the diameter of the resistant vessels including the major arteries in the brain parenchyma and the pial arteries (Mchedlishvili, 1980; Rogers & Stump, 1989). Impaired cerebral autoregulation is commonly associated with pathological intracranial conditions such as traumatic brain injury.

Thus, head elevation can produce a particular dilemma for healthcare providers because in certain circumstances elevating the head of the bed does not ensure decreasing ICP. On the contrary, it may put some individuals at risk for increasing ICP and cerebral ischemia due to impaired cerebral autoregulation and unstable arterial blood pressure (Rosner & Coley, 1986; Simmons, 1997). It is therefore critical to evaluate the existing evidence concerning the effects of changing the backrest position on ICP and CPP in brain-injured individuals.

Methods

Sampling and Criteria

Data for this systematic review were retrieved from electronic databases such as MEDLINE, CINAHL, PsycINFO, Health STAR, and Cochrane Library, as well as from dissertation abstracts, a university library catalog, and the bibliographies of relevant studies. Keywords included position, intracranial pressure (ICP), cerebral perfusion pressure (CPP), and head elevation. The search was restricted to works in English published between 1980 and 2003. The following criteria were used to identify appropriate articles: (a) the representation of brain-injured patients including those with traumatic brain injury, subarachnoid hemorrhage (traumatic or aneurysm), stroke, brain tumor, and hydrocephalus; (b) therapeutic positions including supine (flat), head elevation of different degrees with or without knee-gatch, and reverse Trendelenberg; and (c) content including major outcome variables of ICP or CPP. Exclusion criteria were (a) case reports (excluded because they lack statistical inference to validate their scientific significance); and (b) studies with subjects less than 18 months of age (excluded because of the subjects' unfused skulls).

Articles were systematically analyzed and placed into the categories of author(s), year of publication, study title, research design, therapeutic backrest positions, sample size, age range (mean), pathological condition, Glasgow Coma Scale (GCS) score, ICP device, and physiologic parameters (ICP, CPP, MSAP, etc.); see Table 1. Statistical methods, major findings, effect size, strengths, and limitations of studies, and comments on each are presented in Table 2.

Results

The initial search yielded 43 potential references, 15 of which were directly relevant to positioning and ICP or CPP. One was published before 1980 (Shalit & Umansky, 1977); the others were published between 1980 and 2003 and included 13 published articles and 1 unpublished thesis. Three (Hugo, 1992; Jones, 1994; Lee, 1989) were excluded because of the therapeutic positions used, such as head down, head rotation, and turning. Eleven references were analyzed according to the categories described above and are summarized in Tables 1 and 2 (Durward, Amacher, Del Maestro, & Sibbald, 1983; Feldman et al., 1992; Kenning et al., 1981; Kirkness, 1992; March, Mitchell, Grady, & Winn, 1990; Meixensberger, Baunach, Amschler, Dings, & Roosen, 1997; Parsons & Wilson, 1984; Ropper, O'Rourke, & Kennedy, 1982; Rosner & Coley, 1986; Schneider, von Helden, Franke, Lanksch, & Unterberg, 1993; Winkelman, 2000).

Study Characteristics

Five articles (45.5%) were published from 1980 to 1989, and six (54.5%) were published between 1990 and 2003. Two studies (Meixensberger et al., 1997; Schneider et al., 1993) were conducted in Germany, while the other nine were conducted in the United States. A total of 178 participants were enrolled in 11 studies, and the studies' sample sizes ranged from 4 to 25. Three studies did not provide information on the ages of the subjects (Durward et al., 1983; Parsons & Wilson, 1984; Ropper et al., 1982). Subjects in the remaining eight studies ranged in age from 7 to 83 years with a mean age of 37 years. Five studies (45.5%) focused on participants with severe head injury, and six studies (54.5%) reported that more than half of the participants had severe head injury. Ten out of the 11 studies provided the range of GCS scores, from 3 to 15; Ropper et al. (1982) was the exception. GCS scores were lower than 8 for more than half of the participants (69.1%, 124/178), a finding that implied participants had severe brain injury. Most studies reported the range instead of the individual value of GCS scores; only four studies provided each participant's GCS scores, ranging from 3 to 15 with a mean GCS score of 7 (Kenning et al., 1981; Rosner & Coley, 1986; Schneider et al., 1993; Winkelman, 2000).

ICP Device

ICP was measured by an intraventricular catheter, an intraparenchymal or a subarachnoid bolt, or epidural devices, except that four participants were measured by both intraventricular catheter and subarachnoid bolt simultaneously (Ropper et al., 1982). Two studies involving 24.7% of the patients, or 44 out of the 178, did not report what type of device was used for collecting ICP data (Feldman et al., 1992; Meixensberger et al., 1997). Subarachnoid bolt (36.0%, 64/178) was the most commonly used device, in nine studies; other devices used (listed by order of the utilization percentage) were intraventricular catheter (25.8%, 46/178), intraparenchymal device (11.2%, 20/178), and epidural device (2.8%, 5/178).

Design

Two studies (18.2%) used descriptive designs; six (54.5%) used quasi-experimental designs; and three (27.3%) used experimental designs.

Therapeutic Backrest Positions

Flat position. All studies used a flat position as their baseline, which meant that the mattress was horizontal to the bed frame, with the patient lying supine. None of the studies mentioned whether pillows were used.

Elevated head of bed. The bed was adjusted so that the upper part of the bed was elevated to the chosen degree from 10 to 90 degrees. Head elevation of 30 degrees was the most commonly used position in 8 out of 11 studies. Head elevation of 35-90 degrees was used in 3 (18.2%) studies (Kenning et al.,1981; Parsons & Wilson, 1984; Ropper et al., 1982). March et al. (1990) and Kirkness (1992) used a head elevation of 30 degrees, with gatched knee flexion at 20 degrees. The purpose of the "knee-gatch" position was to prevent the patient from sliding down the bed.

Reverse Trendelenberg. The reverse Trendelenberg position requires elevating the head of the bed while simultaneously lowering the foot of the bed, and keeping the mattress frame straight. The beds utilized in studies by March et al. (1990) and Kirkness (1992) allowed a 15-degree angle of elevation in the reverse Trendelenberg position with the patient supine, because the investigators considered that patients in the elevated head position experienced a certain degree of flexion at the hip that might decrease the venous return to the extremities and consequently decrease cardiac output by decreasing preload.

Measurement Parameters

Two studies (Kenning et al., 1981; Ropper et al., 1982) used ICP as the sole outcome measure. The remaining nine used ICP, CPP, and MABP as outcome measurements, and additional outcome variables such as cerebral blood flow (CBF) (Feldman et al., 1992; Kirkness, 1992; March et al., 1990), jugular venous oxygen saturation (Sjv[O.sub.2]; Schneider et al., 1993), and brain tissue oxygenation (ti-P[O.sub.2]; Meixensberger et al., 1997).

Major Findings

ICP Response to Head Elevation and Flat Position

ICP showed a statistically significant decrease with head elevation of 30 degrees in six studies (Durward et al., 1983; Feldman et al., 1992; Meixensberger et al., 1997; Rosner & Coley, 1986; Schneider et al., 1993; Winkelman, 2000), head elevation of 35 degrees in one study (Parsons & Wilson, 1984), head elevation of 45 degrees in one study (Kenning et al., 1981), and head elevation of 60 degrees in one study (Ropper et al., 1982). ICP values were maximal when the patients were placed flat compared with head elevation of different degrees in seven studies (Durward et al., 1983; Feldman et al, 1992; Meixensberger et al., 1997; Parsons & Wilson, 1984; Rosner & Coley, 1986; Schneider et al., 1993; Winkelman, 2000).

CPP Response to Head Elevation and Flat Position

All but two studies (Kenning et al., 1981; Ropper et al., 1982) measured CPP as the main outcome variable. Four studies (Feldman et al., 1992; Kirkness, 1992; March et al., 1990; Schneider et al., 1993), showed no statistically significant changes in CPP from a flat position to 30 degrees of head elevation; one study (Durward et al., 1983) showed no change in CPP; two studies (Meixensberger et al., 1997; Winkelman, 2000) showed increased CPP; and two studies (Parsons & Wilson, 1984; Rosner & Coley, 1986) showed decreased CPP. Two studies (Kirkness, 1992; March et al., 1990) showed no statistically significant difference in CPP between a flat position and head elevation with knee gatched, and between flat and reverse Trendelenberg bed positions. Meixensberger et al. (1997) showed CPP was significantly higher at 30 degrees of backrest elevation (76.5 [+ or -] 13.5 mm Hg) than a flat position (71.5 [+ or -] 13.2 mm Hg). Winkelman (2000) showed a similar result: 84.0 [+ or -] 9.87 mm Hg at 30 degrees of backrest elevation and 79.9 [+ or -] 9.72 mm Hg at a flat position. Parsons and Wilson (1984) showed CPP was significantly lower at 30 degrees of backrest elevation than in the flat position. Rosner and Coley (1986) showed CPP was significantly higher at a flat position (73.0 [+ or -] 3.4 mm Hg) than at 30 degrees of head elevation (67.2 [+ or -] 2.8 mm Hg) resulting from a decrease in SABP from at a flat position (94.8 [+ or -] 3.1 mm Hg) to 30 degrees of head elevation (85.4 [+ or -] 2.4 mm Hg). The ICP was 22.2 [+ or -] 2.3 mm Hg and 17.6 [+ or -] 2.3 mm Hg for the positions of flat and 30-degree head elevation, respectively. The authors also reported that CPP was maximized (73.0 [+ or -] 3.4 mm Hg) with patients lying flat even though ICP was usually highest (22.2 [+ or -] 2.3 mm Hg) at this point. Durward et al. (1983) showed that CPP did not decrease significantly until head elevation reached 60 degrees.

Effect Size

Effect size is defined as the "magnitude of the difference between observations. It answers the question: 'Is the effect large or useful?' rather than the question 'Is there a difference?'" (Winkelman, 2001, p. 216). Effect size also provides information that allows the reader to determine whether the intervention is clinically significant or useful (Winkelman, 2001). One common criterion is based on sociobehavioral research: A small effect size is 0.2, a medium effect size is 0.5, and a large effect size is 0.8 (Cohen, 1988; Winkelman, 2001). Only Winkelman (2000) reported an effect sizes; for decreasing ICP it was 0.55, and for improving CPP it was 0.41, which showed that a head elevation of 30 degrees is a moderately effective intervention for decreasing ICP and has a moderate trend toward improving CPP. According to the available information from each study, effect size for ICP and CPP were calculated retrospectively in four studies (Table 2). The effect size for ICP ranged from 0.74 to 7.68, showing a medium to large effect size, indicating that the head elevation of 30 degrees is beneficial to decreasing ICE The effect size for CPP varied in range from 0.02 to 1.71, indicating that the head elevation of 30 degrees might not improve CPP.

Discussion

Selecting sensitive outcome parameters to measure treatment effect is crucial in an intervention study. Failure to detect a significant effect can be attributed to (a) an inadequate and weak operationalization of the intervention; (b) a sample size too small to verify a statistically significant effect; (c) too much heterogeneity without comparable distribution of data within each stratum of the dependent variables; (d) an ineffective intervention; and (e) the lack of sensitivity of the measure in the outcome variable measurements (Lipsey, 1990; Toseland & Rossiter, 1989). The following section discusses these issues related to integrity of outcome variables, therapeutic positioning, limitations, clinical application, and recommendations for further studies.

Integrity of Outcome Variables

Treatment of individuals with brain injury focuses on prevention or reduction of intracranial hypertension and maintenance of adequate cerebral perfusion to minimize secondary injury (Yanko & Mitcho, 2001). Therefore, therapies to manage intracranial hypertension and maintain CPP should be evaluated on whether they benefit patients or place them at risk (Simmons, 1997).

An extensive body of clinical research demonstrates a correlation between high ICP and a poorer outcome in individuals with severe bran injury (Becker et al., 1977; Marmarou et al., 1991; Miller et al., 1981; Narayan et al., 1981). However, no study to date has clearly shown that lowering ICP will be beneficial for individuals with severe brain injury. If it is accepted that an ICP greater than 20 mm Hg places patients at risk for pathological changes, any therapy that lowers ICP to 20 mm Hg or below and also ensures adequate CPP might be considered beneficial, thus maximizing the likelihood of recovery (Eisenberg et al., 1990; Miller et al., 1981; Narayan et al., 1981). From this point of view, ICP is a very sensitive outcome variable and should be included in each study relevant to brain-injured patients.

Another major goal in the management of severe brain injuries is to prevent or minimize secondary brain damage by maintaining adequate cerebral perfusion. The Brain Trauma Foundation (2000b, 2000c) suggests that maintaining the CPP greater than 70 mm Hg promotes adequate brain perfusion and prevents tissue ischemia.

Many studies considered ICP as the factor to predict patients' outcome but found that it was not enough to measure the cerebral perfusion (Brain Trauma Foundation, 2000a, 2000b; Hilton, 2000; Iacono, 2000). Both ICP and CPP parameters are therefore key determining factors for treatment of brain-injured patients and should be included in each brain injury study. Low CPP (< 60 mm Hg) would cause brain ischemia, especially in brain-injured patients who have had hypotensive episodes (systolic blood pressure < 90 mm Hg) during the first several hours or days after their primary injury (Brain Trauma Foundation, 2000b). Carefully monitoring the MABP is crucial because MABP is a component of CPP (equal to MABP minus ICP), and it also can reflect the adequacy of blood supply to the brain, along with its oxygen substrate (Hilton, 2000; Yanko & Mitcho, 2001).

Some evidence exists that ICP and CPP do not accurately reflect cerebral blood flow (CBF) and autoregulatory capacity (Feldman et al., 1992; Hilton, 2000). CBF was added as an outcome variable in three studies (Feldman et al., 1992; Kirkness, 1992; March et al., 1990). Results showed no statistically significant change between 30 degrees of backrest elevation and a flat position. This may be due to a sample size too small to have relevance for this issue. Jugular venous oxygen saturation (Sjv[O.sub.2]) and brain tissue P[O.sub.2] (ti-P[O.sub.2]) were outcome variables in the studies conducted by Schneider et al. (1993) and Meixensberger et al. (1997). The results demonstrated no significant change in Sjv[O.sub.2] or regional ti-P[O.sub.2] associated with various head positions. Although no evidence was available to validate CBF, Sjv[O.sub.2], and tiP[O.sub.2] as reliable outcome variables, it is highly recommended that studies using these physiologic measures be conducted to clarify their roles in clinical practices.

Therapeutic Positioning

Positioning can influence physiologic variables for brain-injured patients in the critical care setting. Head elevation is a conventional nursing intervention used to control increased ICP in patients with brain injury. Appropriate therapeutic position or optimal level-of-head elevation has been widely investigated. In most studies, head elevation up to 30 degrees, along with fixed head and neck alignment, limited hip flexion, stability of CPP, and other cerebrovascular parameters, decreased ICP. Thus, head elevation up to 30 degrees is highly recommended as a therapeutic position for increased ICP patients.

Limitations

The randomized controlled trial (RCT) is thought to be the scientific gold standard and the most rigorous method for accepting a clinical treatment as the standard of care. Difficulties in conducting an RCT in intensive care units include the unpredictable and debilitating conditions of critically ill individuals. In this report, all studies were crossover designs, with patients as their own control, except two studies (Kenning et al., 1981; Ropper et al., 1982), and only three studies were randomized crossover experimental designs (Kirkness, 1992; March et al., 1990; Winkelman, 2000).

Small sample size is the major limitation in these studies. The sample size in four studies ranged from 4 to 11 (Durward et al., 1983; Kirkness, 1992; March et al., 1990; Winkelman, 2000). Although the remainder were from 18 to 25, Winkelman (2001, p. 216) claimed that "non-significant results do not mean that there is no difference between the positions; rather it means that the researcher cannot rule out the chances or sampling variability as an explanation for the observed difference." Larger sample size and study of specific populations, such as traumatic brain injury or subarachnoid hemorrhage, are highly recommended for future investigations.

The study protocol was not fully described for either the experimental or the control groups. For example, (Feldman et al., 1992; Kenning et al., 1981; Parsons & Wilson, 1984; Rosner & Coley, 1986) did not state how long the subjects stayed in each position before the measurement was taken, so it was not possible to define whether the values reflected an immediate response or an equilibrated response. Only 3 (Durward et al., 1983; Kirkness, 1992; Winkelman, 2000) out of the 11 fully detailed their study protocol. Regarding appropriate time points for measurements, decreased ICP is expected to occur immediately (Winkelman, 2000), but might vary according to different subjects, hemodynamic status, and position manipulation. Multiple time-point measurements are recommended to capture whether the effect of decreasing ICP is transient. This systematic review revealed that all but one (Kenning, 1981) reported collecting the data during the procedure, and the timing in these 10 studies varied. Six measured only at one time point either right after the change in position (Feldman et al., 1992; Parsons & Wilson, 1984; Ropper et al., 1982; Rosner & Coley, 1986) or 10-20 minutes after the change in position (Meixensberger et al., 1997; Schneider et al., 1993). The single time-point measurement could not capture both immediate and equilibrated response; in order to capture these responses, multiple time-point measurements are necessary. In four studies, measurements were taken more than twice: The first measurement was taken at five minutes after the change in position, and 1-3 additional measurements were taken within 60 minutes (Feldman et al., 1992; Kirkness, 1992; March et al., 1990; Winkelman, 2000).

Clinical Applications

Although aimed at providing empirically based guidance on positioning practice with brain-injured patients, all the studies yielded somewhat inconclusive and occasionally conflicting findings, which restricted broader evidence-based clinical applications. On the basis of the studies reviewed, two clinical recommendations for therapeutic positioning can be made: (a) consider using head elevation up to 30 degrees to significantly reduce ICP but without significantly changing CPP, and (b) monitor CPP during head-elevation positioning because head elevation may simultaneously decrease CPP by decreasing MABP.

Recommendations for Future Studies

A comprehensive multisystem physiologic perspective on outcome variables such as cerebral, hemodynamic, and systemic oxygenation is needed (Sullivan, 2000). These variables should be studied with large sample sizes in order to validate statistically and clinically meaningful effects. Future research should examine the effects of therapeutic positions in different neurological and neurosurgical populations such as people with cerebrovascular disorders or brain tumors, the elderly, and children in order to generalize the findings. In clinical practice, most patients with traumatic brain injury have combined multisystem injuries such as lung contusions or multiple bone fractures or underlying diseases such as chronic obstructive pulmonary disease or cardiovascular disease. Therefore, use of supine and head-elevated positions may not be sufficient to address these patients' clinical conditions. Further investigations should evaluate the effect of lateral side-lying positions on ICP and CPP for brain-injured individuals who have multisystem involvement.

Summary

Reviewing current therapeutic positioning research has provided a template of evidence-based data from which preliminary recommendations may guide present nursing practice in the therapeutic positioning of patients with brain injury. A backrest elevation of 30 degrees is a therapeutic intervention for ICP in brain-injured patients. Ongoing and future studies are needed to generate the conclusive, empirically based determination of best practices for positioning critically ill neurology and neurosurgery patients.
Table 1. Study Characteristics

 Research Bedside Care
Reference Title Design Activities

Kenning, Toutant, Upright patient Descriptive Position Change
& Saunders, 1981 positioning in Flat
 the management 45[degrees]
 of intracranial 90[degrees]
 hypertension * Flexed at hip

Ropper, O'Rourke, Head positioning, Descriptive Position Change
& Kennedy, 1982 intracranial Flat
 pressure, and 60[degrees]
 compliance * Flexed at hip

Durward, Amacher, Cerebral and Quasi- Position Change
Del Maestro, & cardiovascular experimental Flat
Sibbald, 1983 responses to design 15[degrees]
 changes in head (pre-post 30[degrees]
 elevation in test) 60[degrees]
 patients with * Flexed at hip
 intracranial
 hypertension

Parsons & Wilson, Cerebrovascular Quasi- Position Change
1984 status of severe experimental Flat
 closed head design 35[degrees]
 injured patients (pre-post * Flexed at hip
 following passive test)
 position changes

Rosner & Coley, Cerebral Quasi- Position Change
1986 perfusion experimental Flat
 pressure, design 10[degrees]
 intracranial (pre-post 20[degrees]
 pressure, and test) 30[degrees]
 head elevation 40[degrees]
 50[degrees]
 * Flexed at hip

March, Mitchell, Effect of Within Position Change
Grady, & Winn, backrest position subjects Flat
1990 on intracranial experimental 30[degrees]
 and cerebral design (Flexed at hip)
 perfusion (pre-post 30[degrees]
 pressures test) with knee
 gatched
 Reverse
 Trendelenberg
 position

Feldman et al., Effect of head Quasi- Position Change
1992 elevation on experimental Flat
 intracranial design (pre- 30[degrees]
 pressure, post test) * Flexed at hip
 cerebral
 perfusion, and
 cerebral blood
 flow in
 head-injured
 patients

Kirkness, 1992 The effect of Experimental Position Change
 head elevation on design (pre- Flat
 cerebral post test) 30[degrees]
 perfusion in (Flexed at hip)
 patients with 30[degrees]
 intracranial with gatched
 pathology knee flexion at
 20[degrees]
 Reverse
 Trendelenberg
 position

Schneider, von Influence of Quasi- Position Change
Helden, Franke, body position on experimental Flat
Lanksch, & jugular venous design (pre- 15[degrees]
Unterberg, 1993 oxygen post test) 30[degrees]
 saturation, 45[degrees]
 intracranial * Flexed at hip
 pressure and
 cerebral
 perfusion
 pressure

Meixensberger, Influence of body Quasi- Position Change
Baunach, position on experimental Flat
Amschler, Dings, tissue-P design (pre- 30[degrees]
& Roosen, 1997 [O.sub.2], post test) * Flexed at hip
 cerebral
 perfusion
 pressure, and
 intracranial
 pressure in
 patients with
 acute brain
 injury

Winkelman, 2000 Effect of Randomized Position Change
 backrest position crossover Flat
 on intracranial experimental 30[degrees]
 and cerebral design (pre- * Flexed at hip
 perfusion post test)
 pressures in
 traumatically
 brain-injured
 adults

 Sample Age Pathological GCS
Reference (N) (Mean) Condition (Mean)

Kenning, Toutant, 24 7-79 (36) 9 with various 3-15 (8.2)
& Saunders, 1981 cranial
 abnormalities,
 15 with severe
 head injury (GCS
 < 8 in 14
 patients)

Ropper, O'Rourke, 19 15-77 13 with head Not
& Kennedy, 1982 injury; 5 with reported
 ICH; 1 with
 stroke

Durward, Amacher, 11 Not 8 with acute GCS < 8
Del Maestro, & reported brain injury; 3
Sibbald, 1983 with anoxic
 brain injury
 related to near
 drowning

Parsons & Wilson, 18 5-67 Severely head- 3T-10T
1984 injured patients

Rosner & Coley, 18 12-83 (36) 8 with severe 3-15 (7.7)
1986 head injury, 3
 with ICH; 3 with
 tumor; 3 with
 hydrocephalus

March, Mitchell, 4 19-30 (23) Traumatic head 4-9
Grady, & Winn, injury 4-8(3
1990 patients)
 9
 patient)

Feldman et al., 22 18-75 (35) Head-injured 3-12
1992 patients 3-5(3
 patients)
 6-8(14
 patients)
 9-12(5
 patients)

Kirkness, 1992 7 19-73 (32) 4 with head 4T-15
 injury; 3 with 4-6T
 cerebrovascular 9T
 pathology 5T
 7T
 15
 patients)

Schneider, von 25 20-79 (48) 17 with severe 4-8(6)
Helden, Franke, head injury; 5
Lanksch, & with
Unterberg, 1993 subarachnoid
 hemorrhage; 3
 with
 intracerebral
 hemorrhage

Meixensberger, 22 17-71 (37) Head-injured 3-5(9
Baunach, patients patients)
Amschler, Dings, 6-8 (8
& Roosen, 1997 patients)
 9-12(5
 patients)

Winkelman, 2000 8 18-45 (28) Traumatic brain GCS < 8
 injury (5)

 Measure
Reference ICP Device Parameter

Kenning, Toutant, Intraventricular ICP
& Saunders, 1981 catheter (7)
 Subarachnoid bolt
 (17)

Ropper, O'Rourke, Subarachnoid bolt ICP
& Kennedy, 1982 (19)
 4 out of 19 also had
 Intraventricular
 catheter (4)

Durward, Amacher, Intraventricular ICP
Del Maestro, & catheter (11) CPP
Sibbald, 1983 MABP at head
 PAP
 PCWP
 CVP
 CO

Parsons & Wilson, Subarachnoid bolt ICP
1984 (18) CPP
 MABP at head
 HR

Rosner & Coley, Intraventricular ICP
1986 catheter (18) CPP
 MABP at heart
 MABP at head
 CVP

March, Mitchell, Subarachnoid bolt ICP
Grady, & Winn, (4) CPP
1990 CBF
 MABP

Feldman et al., Not reported ICP
1992 CPP
 CBF
 Mean carotid
 pressure

Kirkness, 1992 Intraparenchymal ICP
 (7) CPP
 CBF
 MABP at heart
 MABP at head

Schneider, von Intraventricular ICP
Helden, Franke, catheter (7) CPP
Lanksch, & Intraparenchymal MABP at head
Unterberg, 1993 (13) Sjv[O.sub.2]
 Epidural device (5)

Meixensberger, Not reported ICP
Baunach, CPP
Amschler, Dings, MABP
& Roosen, 1997 ti-P[O.sub.2]

Winkelman, 2000 Intraventricular ICP
 catheter (2) CPP
 Subarachnoid bolt MABP at heart
 (6)

Key: GCS = Glasgow Coma Scale; ICP = intracranial pressure;
CPP = cerebral perfusion pressure; OF = cerebral blood flow;
MABP = mean arterial blood pressure; CVP = central venous pressure;
PAP = pulmonary artery pressure; PCWP = pulmonary capillary wedge
pressure, Sjv[O.sub.2] = jugular venous oxygen saturation;
ti-P[O.sub.2] = tissue oxygenation; HR = heart rate; RR = respiratory
rate

Table 2. Statistical Methods, Major Findings, Strengths, Limitations,
and Comments

 Statistic Effective
Reference Methods Major Findings Size

Kenning, Toutant, Descriptive ICP reduced at N/A
& Saunders, 1981 45[degrees] and
 90[degrees] in all 43
 recordings.

Ropper, O'Rourke, Descriptive 10 patients' ICP N/A
& Kennedy, 1982 t-test values were
 significantly reduced
 at 60[degrees]
 (p < .05); 7 patients'
 ICP values did not
 have differences in
 either position; 2
 patients' values were
 lower in flat
 position.

Durward, Amacher, Descriptive ICP was consistently N/A
Del Maestro, & Paired t-test reduced for all
Sibbald, 1983 or ANOVA patients at
 30[degrees] backrest
 position compared
 with flat position.
 Highest ICP at flat
 and 60[degrees].
 CPP did not change
 significantly until it
 decreased
 significantly at
 60[degrees] when
 compared to flat
 (decrease of 7.9
 [+ or -] 9.3 mm Hg).

Parsons & Wilson, Descriptive Elevation of the head N/A
1984 ANOVA from flat to
 35[degrees] produced
 significant decreases
 in MABP & ICP
 (p <.05). Lowering the
 head from 35[degrees]
 to flat yielded
 significant increases
 in MABP, ICP (F & p
 not reported). There
 was a significant
 change in CPP
 (decrease from 73.0
 [+ or -] 3.4 to 67.2
 [+ or -] 2.8) and CPP
 was never less than 50
 mm Hg.

Rosner & Coley, Descriptive Data were analyzed ICP = 2
1986 Linear with linear models and CPP = 1.8
 regression yielded significant
 relationship between
 SABP at head, CPP,
 and CVP.
 This equation
 described the
 relationship between
 ICP and head elevation
 with a statistical
 significance of
 p < .10 to .05.
 Head elevation
 resulted in a decrease
 in SABP at head
 (p < .001) was faster
 than decrease in ICP
 (p < .10) resulting in
 a net decrease in CPP
 (p < .05).
 CPP was maximal with
 patients lying flat
 even though ICP was
 usually highest at
 this point.

Feldman et al., Descriptive Mean ICP value was ICP = 0.74
1992 Paired t-test significantly CPP = 0.02
 ANOVA (p = .0001) lower at
 30[degrees] backrest
 position.
 There was no
 statistically
 significant
 difference in CPP
 (p = .8), CBF
 (p = .657) or any
 other parameter
 measured (cerebral
 metabolic rate of
 oxygen consumption,
 arteriovenous
 difference of lactate,
 or cerebrovascular
 resistance).
 Negative correlation
 between ICP and head
 position (r = -.5890).
 The higher the ICP
 (19.7 [+ or -]
 8.3) in the flat
 position, the greater
 the decrease with head
 elevation.

Kirkness, 1992 Descriptive There were no CPP = 1.12
 Paired t-test statistically
 Wilcoxon significant
 matched-pairs differences in ICP and
 signed-ranks CPP between flat
 test position and head
 elevation.

Schneider, von Descriptive Head elevation ICP = 7.68
Helden, Franke, Friedman test significantly CPP = 0.17
Lanksch, & reduced ICP from 19.8
Unterberg, 1993 [+ or -] 1.3 mm Hg at
 flat to 10.2 [+ or -]
 1.2 mm Hg at
 45[degrees].
 There was no
 statistically
 significant change in
 CPP and Sjv[O.sub.2]
 associated with
 varying head position.

Meixensbenger, Descriptive The mean ICP was ICP = 0.97
Baunach, t-test significantly lower CPP = 0.37
Amschler, Dings, (14.1 [+ or -] 1.3 mm
& Roosen, 1997 Hg) at 30[degrees]
 head elevation than at
 0[degrees] (19.9
 [+ or -] 8.3 mm Hg).
 CPP was slightly
 higher at 30[degrees]
 (76.5 [+ or -] 13.5 mm
 Hg) than at 0[degrees]
 (71.5 [+ or -] 13.2 mm
 Hg).
 MABP was unaffected by
 head elevation.
 Regional ti-P[O.sub.2]
 was unaffected by body
 position.

Winkelman, 2000 Descriptive ICP and CPP changes ICP = 0.55
 Repeated- occurred immediately CPP = 0.41
 measures after elevation of the
 ANOVA head from flat to
 30[degrees] (F(2)
 = 20.21, p = .002).
 During equilibrium,
 ICP was significant
 lower and CPP was
 significantly higher
 for a 30[degrees]-
 backrest elevation
 than for a flat
 position (F(2) =
 8.323, p = .02).

Reference Strengths, Limitations, and Comments

Kenning, Toutant, No level of statistical significance was given for
& Saunders, 1981 the decreases in ICP occurring with head elevation.
 Only considers one aspect of ICP so the reduction
 of ICP that occurred may not have resulted in an
 improvement in CPP.
 It was not stated how long the subjects were in
 each position before the measures were taken, so it
 is not known if the values were reflecting an
 immediate response or an equilibrated response.

Ropper, O'Rourke, Recommend an optimal head position should be
& Kennedy, 1982 established on an individual basis rather than
 routinely placing all patients in a head-raised
 position.
 Examine how positioning affected ICP but did not
 consider the other factors that might affect CPP.

Durward, Amacher, This study incorporated parameters related to
Del Maestro, & cerebral and cardiac function, thus giving a more
Sibbald, 1983 accurate measure of cerebral perfusion.
 In this study, mean pressure readings were used and
 levels of significant change were documented, which
 increase the significance of the result.

Parsons & Wilson, In this study, measurements were only made for 1
1984 minute following the position changes, so further
 changes may occur after this time.

Rosner & Coley, The authors suggested that the compensatory
1986 increase in arterial blood pressure that occurs to
 maintain CPP when the head is elevated could be
 considered to be a result of ischemia or increased
 stress on the injured brain. Thus, head elevation
 would be considered an adverse stimulus that should
 be eliminated.
 It was not stated how long the subjects were in
 each position before the measurements were taken,
 so it is not known it the values were reflecting an
 immediate response or an equilibrated response.
 The authors' conclusions were different than those
 of other investigators due to different analysis.

Feldman et al., The authors suggested that, in general,
1992 head-injured patients with increased in ICP should
 be maintained head elevation to 30[degrees], which
 will result in a decrease in ICP without a
 significant decrease in CBF in the majority of
 patients.
 In this study, t-test score was not reported. It
 was not stated how long the subjects were in each
 position before the measurements were taken, so it
 is not known whether the values were reflecting
 an immediate response or an equilibrated response.

Kirkness, 1992 Fully described study protocol.
 Small sample size (N = 7) is the major limitation.

Schneider, von A moderate head elevation between 15[degrees] and
Helden, Franke, 30[degrees] significantly reduces ICP and, in
Lanksch, & general, does not impair cerebral perfusion.
Unterberg, 1993 Individual responses of CPP to changes in head
 position were quite unpredictable.

Meixensbenger, A moderate head elevation of 30[degrees] reduces
Baunach, ICP without jeopardizing regional cerebral
Amschler, Dings, microcirculation.
& Roosen, 1997

Winkelman, 2000 Fully described study protocol.
 Small sample size (N= 8) is the major limitation;
 therefore, could not generalize about the result.

Key: ICP = intracranial pressure; CPP = cerebral perfusion pressure


References

Alberico, A.M., Ward, J.D., Choi, S.C., Marmarou, A., & Young, H.F. (1987). Outcome after severe head injury: Relationship to mass lesions, diffuse injury, and ICP course in pediatric and adult patients. Journal of Neurosurgery, 67, 648-656.

Becker, D.P., Miller, J.D., Ward, J.D., Greenberg, R.P., Young, H.F., & Sakalas, R. (1977). The outcome from severe head injury with early diagnosis and intensive management. Journal of Neurosurgery, 47, 491-502.

Bouma, G.J., Muizelaar, J.P., Choi, S.C. Newton, P.G., & Young, H.F. (1991). Cerebral circulation and metabolism after severe traumatic brain injury: The elusive role of ischemia. Journal of Neurosurgery, 75, 625-693.

Brain Trauma Foundation, The American Association of Neurological Surgeons, The Joint Section on Neurotrauma and Critical Care. (2000a). Indicators for intracranial pressure monitoring. Journal of Neurotrauma, 17, 479-491.

Brain Trauma Foundation, The American Association of Neurological Surgeons, The Joint Section on Neurotrauma and Critical Care. (2000b). Guidelines for cerebral perfusion pressure. Journal of Neurotrauma, 17, 507-511.

Brain Trauma Foundation, The American Association of Neurological Surgeons, The Joint Section on Neurotrauma and Critical Care. (2000c). Initial management. Journal of Neurotrauma, 17, 463-469.

Chesnut, R.M., Marshall, L.F., Klauber, M.R., Blunt, B.A., Baldwin, N., Eisenberg, H. M., et al. (1993). The role of secondary brain injury in determining outcome from severe head injury. Journal of Trauma. 34, 216-222.

Chesnut, R.M., Marshall, S.B., Piek, J., Blunt, B.A., Klauber, M.R., & Marshall, L.F. (1993). Early and late systemic hypotension as a frequent and fundamental source of cerebral ischemia following severe brain injury in the Traumatic Coma Data Bank. Acta Neurochirurgica Supplement (Wien), 59, 121-125.

Cohen, J. (1988). Statistical power analysis for the behavioral sciences (2nd ed.). Mahwah, NJ: Lawrence Erlbaum Associates.

Cormio, M., Robertson, C.S., & Narayan, R.K. (1997). Secondary insults to the injured brain. Journal of Clinical Neuroscience, 4, 132-148.

Dearden, N.M. (1998). Mechanisms and prevention of secondary brain damage during intensive care. Clinical Neuropathology, 17, 221-228.

Downard, C., Hulka, F., Mullins, R,J., Pialt, J., Chestnut, R., Quint, P. et al. (2000). Relationship of cerebral perfusion pressure and survival in pediatric brain-injured patients. Journal of Trauma, 49, 654-659.

Durward, Q.J., Amacher, A.L., Del Maestro, R.F., & Sibbald, W.J. (1983). Cerebral and cardiovascular responses to changes in head elevation in patients with intracranial hypertension. Journal of Neurosurgery, 59, 938-944.

Eisenberg, H.M., Gary, H.E., Jr., Aldrich, E.F., Saydjari, C., Turner, B., Foulkes, M.A., et al. (1990) Initial CT findings in 753 patients with severe head injury. A report from the NIH Traumatic Coma Data Bank. Journal of Neurosurgery, 73, 688-698.

Feldman, Z., Kanter, M.J., Robertson, C.S., Contant, C.F., Hayes, C., Sheinbers, M.A., et al. (1992). Effects of head elevation on intracranial pressure, cerebral perfusion pressure and cerebral blond flow in head-injured patients. Journal of Neurosurgery, 76, 207-211.

Gualtieri, C.T. (2002). Brain injury and mental retardation: Psychopharmacology and Neuropsychiatry. Philadelphia: Lippincott Williams & Wilkins.

Heath, D.L., & Vink, R. (1999). Secondary mechanisms in traumatic brain injury: A nurse's perspective. Journal of Neuroscience Nursing, 31, 97-105.

Hilton, G. (2000). Cerebral oxygenation in the traumatically brain-injured patient: Are ICP and CPP enough? Journal of Neuroscience Nursing, 32, 278-282.

Hugo, M. (1992). Left or right, up or down: A case for positioning of unconscious head-injured patients. Curationis, 15, 1-7.

Iacono, L.A. (2000). Exploring the guidelines for the management of severe head injury. Journal of Neuroscience Nursing, 32, 54-60.

Jones, B. (1994). The effects of patient repositioning on intracranial pressure. Australian Journal of Advanced Nursing, 12, 32-39.

Jones, P.A., Andrews, P.J., Midgley, S., Anderson, S.I., Piper, I.R., Tocher, J.L., et al. (1994). Measuring the burden of secondary insults in head-injured patients during intensive care. Journal of Neurosurgical Anesthesiology, 6, 4-14.

Kenning, J.A., Toutant, S.M., & Saunders, R.L. (1981). Upright patient positioning in the management of intracranial hypertension. Surgical Neurology, 15, 148-152.

Kirkness, C. (1992). The effect of head elevation on cerebral perfusion in patients with intracranial pathology. Unpublished thesis, University of Washington, Seattle.

Lee, S. (1989). Intracranial pressure changes during positioning of patients with severe head injury. Heart and Lung, 18, 411-414.

Lipsey, M.W. (1990). A scheme for assessing measurement sensitivity in program evaluation and other applied research. Psychological Bulletin, 94, 152-165.

Magnaes, B. (1976). Body position and cerebrospinal fluid pressure. Part 1: Clinical studies on the effect of rapid postural changes. Journal of Neurosurgery, 44, 687-597.

Magnaes, B. (1978). Movement of cerebrospinal fluid within the craniospinal space when sitting up and lying down. Surgical Neurology, 10, 45-49.

March, K., Mitchell, P., Grady, S., & Winn, R. (1990). Effect of backrest position on intracranial and cerebral perfusion pressure. Journal of Neuroscience Nursing, 22, 375-381.

Marmarou, A., Anderson, R.L., Ward, J.D., Choi, S.C., Young, H.F., Eisenberg, H.M., et al. (1991). Impact of ICP instability and hypotension on outcome in patients with severe head trauma. Journal of Neurosurgery, 75, 521-527.

Marmarou, A., Shulman, K., & LaMorgese, J. (1975). Compartmental analysis of compliance and outflow resistance of the cerebrospinal fluid system. Journal of Neurosurgery, 43, 523-534.

Mchedlishvili, G. (1980). Physiological mechanisms controlling cerebral blood flow. Stroke, 11, 240-248.

Meixensberger, J., Baunach, S., Amschler, J., Dings, J., & Roosen, K. (1997). Influence of body position on tissue-P[O.sub.2], cerebral perfusion pressure and intracranial pressure in patients with acute brain injury. Neurology Research, 19, 249-253.

Miller, J.D., Becket, D.P., Ward, J.D., Sullivan, H.G., Adams, W.E., & Rosner, M.J. (1977). Significance of intracranial hypertension in severe head injury. Journal of Neurosurgery, 47, 503-516.

Miller, J.D., Butterworth, J.F., Gudeman, S.K., Faulkner, J.E., Choi, S.C., Selhorst, J.B., et al. (1981). Further experience in the management of severe head injury. Journal of Neurosurgery, 54, 289-299.

Miller, J.D., Dearden, N.M., Piper, I.R., & Chan, K.H. (1992). Control of intracranial pressure in patients with severe head injury. Journal of Neurotrauma, 9 (Suppl. 1), S317-326.

Narayan, R.K. (1995). Development of guidelines for the management of severe head injury. Journal of Neurotrauma, 12, 907-912.

Narayan, R.K., Greenberg, R.P., Miller, J.D., Enas, G.G., Choi, S.C., Kishore, P.R., et al. (1981). Improved confidence of outcome prediction in severe head injury. A comparative analysis of the clinical examination, multimodality evoked potentials, CT scanning, and intracranial pressure. Journal of Neurosurgery, 54, 751-762.

Parsons, L.C., & Wilson, M.M. (1984). Cerebrovascular status of severe closed head injured patients following passive position changes. Nursing Research, 33, 68-75.

Pietropaoli, J.A., Rogers, F.B., Shackford, S.R., Wald, S.L., Schmoker, J.D., & Zhuang, J. (1992). The deleterious effects of intraoperative hypotension on outcome in patients with severe head injuries. Journal of Trauma, 33, 403-407.

Potts, D.G., & Deonarine, V. (1973). Effect of positional changes and jugular vein compression on the pressure gradient across the arachnoid villi and granulations of the dog. Journal of Neurosurgery, 38, 722-728.

Rogers, A.T., & Stump, D.A. (1989). Cerebral physiologic monitoring. Critical Care Clinics, 5, 845-861.

Ropper, A.H., O'Rourke, D., & Kennedy, S. K. (1982). Head position, intracranial pressure, and compliance. Neurology (New York), 32, 1288-1291.

Rosner, M.J., & Coley, I.B. (1986). Cerebral perfusion pressure, intracranial pressure, and head elevation. Journal of Neurosurgery, 65, 636-441.

Rosner, M.J. & Daughton, S. (1990). Cerebral perfusion pressure management in head injury. Journal of Trauma, 30, 933-941.

Rosner, MJ. Rosner, S.D., & Johnson, A.H., (1995). Cerebral perfusion pressure: Management protocol and clinical results. Journal of Neurology. 83, 949-962.

Saul, T.G., & Ducker, T.B. (1982). Effect of intracranial pressure monitoring and aggressive treatment on mortality in severe head injury. Journal of Neurosurgery, 56, 498-503.

Schneider, G.H., von Helden, G.H., Franke, R., Lanksch, W.R., & Unterberg, A. (1993). Influence of body position on jugular venous oxygen saturation, intracranial pressure, and cerebral perfusion pressure. Acta Neurochirurgica Supplement (Wien), 59, 107-112.

Shalit, M.N., & Umansky, F. (1977). Effect of routine bedside procedures on intracranial pressure. Israel Journal of Medical Science, 13, 881-886.

Signorini, D.F., Andrews, P,J., Jones, P.A., Wardlaw, J.M., & Miller, J.D. (1999). Adding insult to injury: The prognostic value of early secondary insults for survival after traumatic brain injury. Journal of Neurology, Neurosurgery, and Psychiatry, 66, 26-31.

Simmons, B.J. (1997). Management of intracranial hemodynamics in the adult: A research analysis of head positioning and recommendations for clinical practice and further research. Journal of Neuroscience Nursing, 29, 44-49.

Sullivan, J. (2000). Position of patients with severe traumatic brain injury: Research-based practice. Journal of Neuroscience Nursing, 32, 204-209.

Toseland, R. W., & Rossiter, C. M. (1989). Group interventions to support family caregivers: A review and analysis. Gerontologist, 29, 438-448.

Winkelman, C. (2000). Effect of backrest position on intracranial and cerebral perfusion pressures in traumatically brain-injured adults. American Journal of Critical Care, 9, 373-380.

Winkelman, C. (2001). Effect size: Utility and application in neuroscience nursing. Journal of Neuroscience Nursing, 33, 216-218.

Yanko, J. R. & Mitcho, K. (2001). Acute care management of severe traumatic brain injuries. Critical Care Nursing, 23, 1-23.

Questions or comments about this article may be directed to Jun-Yu Fan, MSN RN, by phone at 206/543-6227 or by e-mail at jyfan@u.washington.edu. She is a doctoral candidate at the University of Washington School of Nursing, Seattle, WA.
COPYRIGHT 2004 American Association of Neuroscience Nurses
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2004 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Fan, Jun-Yu
Publication:Journal of Neuroscience Nursing
Geographic Code:1USA
Date:Oct 1, 2004
Words:7962
Previous Article:A young onset Parkinson's patient: a case study.
Next Article:Correction.
Topics:


Related Articles
Successful outcome in severe traumatic brain injury: a case study.
Brain tissue oxygen practice guidelines using the LICOX[R] CMP monitoring system.
Administering hypertonic saline to patients with severe traumatic brain injury.
Traumatic brain injury is a common presentation in theatre.

Terms of use | Copyright © 2017 Farlex, Inc. | Feedback | For webmasters