hyper tonic saline in the treatment of intracranial hypertension

8/6/2019 Hyper Tonic Saline in the Treatment of Intracranial Hypertension

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Hypertonic Saline in the Treatment of Intracranial Hypertension

Laura J Griffin MSN, APRN, CCRN, ACNP-BC

Doctor of Nursing Practice Candidate

The University of Texas Health Science Center at Houston School of Nursing

Citation: L. Griffin : Hypertonic Saline in the Treatment of Intracranial Hypertension.

The Internet Journal of Advanced Nursing Practice. 2010 Volume 11 Number 1

Keywords: intracranial hypertension | brain edema | hypertonic saline | osmotic therapy |

brain injury | intracranial pressure

Table of Contents

Background

Intracranial Hypertension

Hypersomolar Therapy Principles

Hypertonic Saline

Findings

Traumatic Brain Injury

Mixed Neurological Insults

Subarachnoid Hemorrhage

Stroke

Patient Outcomes

Limitations

Potential Adverse Effects

Research Implications Conclusions

Correspondence to

Abstract
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Background:Intracranial hypertension is a life threatening complication affecting the

neurological patient. Limited options for treatment can be challenging for healthcare

providers. Current research seems to support the effectiveness of hypertonic saline in

reducing intracranial pressure. Objectives:This article will review the literature to

ascertain the safety and efficacy of hypertonic saline in the treatment of intracranial

hypertension.Method: In order to assess the effect of hypertonic saline administered for

the treatment of intracranial hypertension on intracranial pressure, a search of PubMed,

Ebsco, Scopus, and the Cochrane Library was performed. Search criteria used for this

review included adult human studies using brain edema, neurological injury, intracranial

hypertension, brain injury, stroke, subarachnoid hemorrhage, and hypertonic saline as

search terms yielded 29 studies which were reviewed. Case reports, letters to the editor,

languages other than English, and those which included pediatric participants were

excluded. Also excluded were studies that involved use of hypertonic saline

intraoperatively, studies that focused on the initial resuscitation of traumatic brain injury,

those used for purely elective neurosurgical resuscitation of traumatic brain injury, and

those used for purely elective neurosurgical patients. Elective neurosurgical patients were

excluded since intracranial hypertension is frequently reversed with surgical evacuation

of space occupying lesion and not medical therapy. Of the 29 studies that were obtained,

5 were excluded. Two were case studies. One dealt with the intra-operative use of

hypertonic saline, and two other studies has foci related to variables other than effect on

intracranial hypertension.Results: Whether used as an initial treatment for elevated

intracranial pressure or as a rescue therapy for refractory intracranial hypertension,

hypertonic saline appears to offer an additional means for lowering intracranial pressure

and may provide a bridge to emergent surgical decompression.

Background

Intracranial hypertension (IH) resulting from increased intracranial pressure is a common

complication of neurological injuries. Research has shown that IH is associated with poor

patient outcomes.1 In an effort to improve morbidity and mortality in these patients,

neurologically based research has focused on strategies to reduce IH. Osmotic therapy

has long been recognized as a safe and effective treatment for IH.2 The most researched


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and commonly used osmotic agent, mannitol, has been associated with untoward side

effects. In an effort to find an effective osmotic agent with a safe side effect profile, other

osmotic agents have gained some popularity. This article will review studies performed

using HS as an osmotic agent for the reduction of intracranial pressure in patients with

neurological injury.

Intracranial Hypertension

The cranial vault, or skull, of an average adult has an approximate volume of 1700

milliliters. Eighty-percent of this volume is comprised of brain tissue and the other

twenty percent is comprised of blood and cerebral spinal fluid.3 In a healthy individual,

compensatory mechanisms keep these contents at a constant volume. When a person

suffers from a neurological insult, normal compensatory mechanisms may fail and the

delicate balance is disrupted. The Monro-Kellie doctrine states that the total contents of

the cranial vault must remain at a constant volume in order to maintain equilibrium. If

any one of the contents increases in volume without a corresponding compensatory

decrease in another, the pressure in the cranial vault will increase resulting in intracranial

hypertension. A normal intracranial pressure (ICP) is considered to be 5-10mmHg.1

Intracranial hypertension is defined as an intracranial pressure above normal limits.

Research has shown that values above 20 mmHg are associated with increased morbidity

and mortality.2 Therefore, most institutions including the Brain Trauma Foundation

suggest initiating osmotic treatment for values above 20 mmHg lasting for more than five

minutes.2 The most common cause of IH in patients with neurological insults is related to

increased brain volume either from a space occupying lesion or cerebral edema. Space

occupying lesions, such as tumors, can be treated with surgical evacuation. In contrast,

medical management in the form of osmotic therapy is the cornerstone of treatment for

cerebral edema.

Hypersomolar Therapy Principles


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A traditionally held belief is that hyperosmolar therapy effectiveness is a result of brain

shrinkage caused from the shifting of water out of the brain. Mannitol has been accepted

as treatment for IH, and is considered a safe and effective osmotic diuretic. Considered

the drug of choice for IH in Guidelines for the Management of Severe Brain Injury,

mannitol is not without its drawbacks.2 Mannitol, an osmotic diuretic, has been associated

with volume depletion and hypotension leading to secondary injury to the brain. Injury to

the blood brain barrier (BBB), often found in neurological injuries, can be a confounding

factor in the management of IH. One concern is that solutes may escape from the vascular

system to the brain tissue. In the presence of an injured BBB, mannitol may escape the

intravascular space and accumulate in already edematous tissue, which may lead to an

increase in cerebral edema and intracranial hypertension often referred to as rebound

phenomenon.

In an attempt to find the optimal hyperosmolar agent, the use of other solutions has

been explored. An optimal agent should be nontoxic, simple to administer with minimal

side effects, have a strong osmotic gradient, and would remain in the intravascular space

(reflection coefficient). Reflection coefficient is the measurement of how well a solute

crosses a membrane. In regards to treatment of IH, a reflection coefficient of 1 is given to

a solute that stays in the intravascular space and is impermeable to an intact BBB (See

Table 1).

Table 1. Reflection Coefficients

Research has found other agents such as glycerol and urea, with their low reflectioncoefficients, to be fairly ineffective osmotic agents in the treatment of IH.4 Hypertonic

saline with its low cost, ease of administration, and titratable osmotic gradient (by

adjusting its concentration), and its reflection coefficient of 1 has been recognized as an

effective osmotic agent.


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Hypertonic Saline

The use of hypertonic saline in the treatment of cerebral edema was first proposed in1919 by Weed and McKibben.5 Nearly forgotten, more than sixty years later HS

reemerged as resuscitation agent for patients in shock. Incidentally found through the

resuscitations of patients with multi-organ trauma, use of HS in patients with

neurotrauma alone became a focus of research.6,7 Finding from this early research, in

multi-organ trauma, including brain injury, promoted its use in the treatment of

intracranial hypertension and herniation syndromes as well.

The proposed mechanism of action of HS is similar to that of mannitol. Through osmosis

HS draws water out of the intracellular space, the edematous brain, and back into the

intravascular space. In addition, HS has been shown to be effective in resuscitation of

patients in shock by the same mechanism. Unlike mannitol which promotes diuresis, HS

increases blood volume, decreases viscosity, and increases preload. All of these

characteristics lead to an increase in blood pressure, cardiac output, and cerebral

perfusion pressure (CPP), thereby improving perfusion to the brain and decreasing

secondary injury. Used as a resuscitation agent, HS also has potential to be used as acomponent of triple H therapy (hypervolemia, hemodilution, and hypertension) in the

treatment of patients with subarachnoid hemorrhage (SAH) who are at high risk of severe

vasospasm.

Findings

Traumatic Brain Injury

According the Centers for Disease Control, 1.4 million Americans suffer from traumatic

brain injury (TBI) annually. Of those, more than 200,000 are hospitalized and 50,000 die.

Costs related to TBI, direct and indirect, are figured to be approximately $60 billion. 8 In

an effort to improve morbidity and mortality rates in patients with TBI, research to

combat and treat IH has been on the forefront of neurological research. Most studies


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involving TBI, share similar findings that indicate that HS is consistent with a decrease in

ICP and an increase in CPP (See Table 2). Maintaining a physiologic normal CPP is as

important as decreasing elevated ICP in preventing secondary injury. By increasing blood

volume and preload, HS helps to ensure adequate perfusion and oxygenation to at-risk

brain tissue.

Several studies compared mannitol boluses versus HS boluses.9,10 In one study, Vialet et

al. compared 20% mannitol with 7.5% sodium chloride (NaCl) bolus for the treatment of

ICP above 25mmHg. This study demonstrated that patients given mannitol have two

times more events of elevated ICP compared with HS. In addition, treatment failures

were 7 out of 10 for the mannitol group versus those treated with HS. Shackford et al.

took a unique approach and compared the use of slightly hypertonic solution of 1.6%NaCl with a slightly hypotonic solution of Lactated Ringers in the TBI population.11

Intracerebral pressures decreased in the HS group while the patients receiving Lactated

Ringers showed an upward trend in ICP. While most of the studies used bolus dosing, a

retrospective chart review by Quareshi et al. reviewed the use of HS as a continuous drip

with varying infusion rates with the goal of achieving a serum sodium value between

145-155 meq/dl. The investigators found that patients receiving continuous HS had poor

long-term outcomes as identified by the Glasgow Outcome Scale (GOS).12 The GOS

ranks patients on five levels based on functional recovery with 1 corresponding with

death and 5 corresponding with good recovery. Another unique study design examined

the effects of a bolus of 20% NaCl on not only the ICP but the measurable effect on brain

tissue using computed tomography.13 The results of this study revealed that HS may

lower ICP by decreasing the overall volume of the healthy brain tissue.


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Table 2. Summary of Study Findings for Traumatic Brain Injury

Mixed Neurological Insults

Samples with mixed neurological injuries were examined in six studies (See Table 3).

Battison et al. examined the effect of equiosmolar does of mannitol versus HS. Findings

supported that both agents decreased ICP. Mannitol decreased ICP on average by 7.5

mmHg, whereas, HS decreased by 13.5 mmHg. The investigators also suggested that

patients who received HS appeared to have a longer duration of effect than those who


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received mannitol.14 Francony et al. also compared equiosmolar doses of mannitol with

HS.15 Findings contrasted the research by Battison et al. showing that mannitol decreased

ICP better than HS, though none of the findings were statistically significant. Becoming

more popular as a rescue therapy for malignant IH (i.e., ICPs refractory to traditional

treatments), Koenig et al. reviewed the effect of 23.4 % bolus in patients with signs of

impending herniation syndromes. Concentrated HS was successful at reversing herniation

syndromes in 57 of the 76 events.16

Table 3. Summary of Study Findings for Mixed Neurological Injuries

Subarachnoid Hemorrhage

Only four studies were found that evaluated the use of HS in the SAH population (See

Table 4). Bentsen et al. evaluated the use of 7.5% HS combined with 6% hydroxyethyl

starch 2ml/kg bolus dose in two different studies.17 One study was performed in patients

with elevated ICP. 17 In the other study the same concentration and dose was given to


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Table 4. Summary of Study Findings for Non-Traumatic Injuries

Limitations

All studies reviewed included small sample sizes and a few studies revealed some

selection bias. Often the use of HS was used as a rescue therapy or after the standard of

care had already failed to control intracranial pressure in the most critically ill patients.

Using HS earlier in the course of the patients treatment, instead of as a last resort may

provide better success. Another potential limitation to the studies as a group was that

saline concentrations varied greatly among investigators. Concentrations ranged from 2-

20% sodium chloride. Not all studies that compared mannitol with HS used equiosmolar

dosing (See Table 5).


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Table 5. Comparing Osmolarity of IV Agents

Agents with a stronger osmotic action may affect the ICP values. Therefore, comparing

two agents of unequal osmolar activity may be considered unjust. Varying doses among

the study groups as a whole, as well as in individual studies, occurred throughout many

of the studies. This lack of consistency make findings difficult to generalized the entire

neurological population.

Potential Adverse Effects

Like other osmotic agents, side effects from the administration of HS are potential risks

that must be balanced with the potential benefits of its use. In the studies reviewed, no

significant complications were mentioned. Most studies listed exclusion criteria, to

minimize harm to patients who may be a highest risk for untoward effects. Patients

commonly excluded were those with heart failure, pulmonary edema, and kidney failure

who may be harmed from an increase in intravascular volume. In one study, lung water

was evaluated and unchanged over three hours post HS administration.17 In a


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retrospective chart review, three patients that received HS developed pulmonary edema.

Of the three patients, one of them had underlying cardiomyopathy.12 In a study, that

specifically looked at complication in patients with neurological injury receiving

continuous infusion of HS, the incidence of renal failure was not found to correlate with

HS use.12 Hypernatremia, serum sodium levels greater than 155, did correlate with a

small yet statistically significant increase in BUN and creatinine levels.25

Central pontine myelinolysis (CPM), a demyelination of the pons is a concern during

administration of any concentrated sodium solution. First described in 1958, CPM is

associated with chronically hyponatremic patients who undergo rapid correction

hyponatremia with a concentrated saline solution. No evidence exists to support the fear

of CPM in patients with acute cerebral salt wasting, excessive renal secretion of sodiumin the face of neurological injury, or traumatic brain injury. Since CPM is an irreversible

and devastating condition, practitioners should continue to be cautious when

administrating HS until significant research proves whether or not this population is at

risk.

Electrolyte and acid base imbalances are frequent occurrence in the critical care patient

population. Several studies included potassium levels as dependent variables.23, 26 These

studies collectively revealed a mild decrease in potassium immediately following

administration with a rebound in potassium near baseline levels after a few hours. While

these studies suggest that hypokalemia may not be a concern for patients receiving HS

therapy, it may be wise to monitor potassium levels in patients who are receiving

frequent boluses of HS especially patients who are at risk of arrhythmias.

Hyperchloremic metabolic acidosis may result from continuous or frequent bolus doses

of HS. In the above studies, some institutions alternated sodium chloride concentrations

with sodium acetate concentrations to decrease its incidence.

In hemorrhagic neurological insults, an injured BBB may result in the translocation of

hyperosmolar solutions which have the potential to cause rebound IH. Animal studies

have found mannitol and HS to cross an injured BBB, but no studies have been done in

humans to evaluate post mortem effects of HS in the brain. Impaired platelet aggregation


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and coagulopathy is a concern in hemorrhagic neurologic injuries. Animal studies have

suggested that hypertonic saline may be responsible for increased bleeding. In one human

study, clotting factors diminished when 10% of plasma was replaced with HS versus

normal saline.27 In another study, HS/dextran was similarly mixed with human plasma at

1:5 and 1:10 concentrations, with only minimal increase in PT.28 While none of the above

studies mentioned bleeding complications, no study has specifically looked at bleeding

complications in neurological patients receiving HS. Therefore, the clinician should

consider this possible complication in any patient receiving HS until research in this area

is completed.

Research Implications

The above studies provide a foundation for future research. In order to strengthen the

current foundation, future studies should strive for larger sample size. Noted in the above

studies were the varying concentrations and doses of HS. These variations make

assessment of the overall effectiveness of this solution difficult. Further research is

needed to strengthen the evidence for a standard therapy or to assess the effectiveness of

one concentration compared with another. Research is also needed in the SAH with

vasospasm population, who may benefit from the intravascular volume expansion that HS

offers. At this time, HS has not been shown to improve long-term outcomes, which may

be due to its use in refractory IH. Studies are needed in which HS is used as a treatment

of cerebral edema prior to other treatments. Finally, studies that focus on HS use in other

than severe traumatic brain injury should be considered for future research.

Conclusions

Hypertonic saline offers promise as a treatment for IH. Current research seems to support

its effectiveness in reducing intracranial pressures. Each patients co-morbidities and

expected results before choosing an osmotic therapy is an important consideration.

Whether used as an initial treatment for elevated intracranial pressure or as a rescue

therapy for refractory IH, HS appears to offer an additional means for lowering ICP and

may provide a bridge to surgical decompression.


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Correspondence to

Laura J Griffin, MSN, APRN, CCRN, ACNP-BC

Doctor of Nursing Practice Candidate

The University of Texas Health Science Center at Houston

School of Nursing

Houston, Texas

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http://scholar.google.ca/scholar?q=Vassar%2BMJ%2C%2BFischer%2BRP%2C%2BO%27Brien%2BPE%2C%2BBachulis%2BBL%2C%2BChambers%2BJA%2C%2BHoyt%2BDB%2C%2BHolcroft%2C%2BJ%3A%2BA%2Bmulticenter%2Btrial%2Bfor%2Bresuscitation%2Bof%2Binjured%2Bpatients%2Bwith%2B7.5%25%2Bsodium%2Bchloride.%2BThe%2Beffect%2Bof%2Badded%2Bdextran%2B70.%2BThe%2Bmulticenter%2Bgroup%2Bfor%2Bthe%2Bstudy%2Bof%2Bhypertonic%2Bsaline%2Bin%2Btrauma%2Bpatients.%2BArch%2BSurg%3B%2B1993%3B%2B128(9)%3A%2B1003-1011.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Centers%2Bfor%2BDisease%2BControl.%2BWhat%2Bis%2Btraumatic%2Bbrain%2Binjury%3F%2BRetrieved%2BApril%2B10%2C%2B2009%2Bfrom%2Bhttp%3A%2F%2Fwww.cdc.gov%2Fncipc%2Ftbi%2FTBI.htm.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Oddo%2BM%2C%2BLevine%2BJM%2C%2BFrangos%2BS%2C%2BCarrera%2BE%2C%2BMaloney-Wilensky%2BE%2C%2BPascual%2BJL%2C%2BKofke%2BWA%2C%2BMayer%2BSA%2C%2BLeRoux%2C%2BP%3A%2BEffect%2Bof%2Bmannitol%2Band%2Bhypertonic%2Bsaline%2Bon%2Bcerebral%2Boxygenation%2Bin%2Bpatients%2Bwith%2Bsevere%2Btraumatic%2Bbrain%2Binjury%2Band%2Brefractory%2Bintracranial%2Bhypertension.%2BJ%2BNeurol%2BNeurosurg%2BPsychiatry%3B%2B2009%3B%2B80%2B(8)%3A%2B916-920.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Vialet%2BR%2C%2BAlbanese%2BJ%2C%2BThomachot%2BL%2C%2BAntonini%2BF%2C%2BBourgouin%2BA%2C%2BAlliez%2BB%2C%2BMartin%2C%2BC%3A%2BIsovolume%2Bhypertonic%2Bsolutes%2B(sodium%2Bchloride%2Bor%2Bmannitol)%2Bin%2Bthe%2Btreatment%2Bof%2Brefractory%2Bposttraumatic%2Bintracranial%2Bhypertension%3A%2B2%2BmL%2Fkg%2B7.5%25%2Bsaline%2Bis%2Bmore%2Beffective%2Bthan%2B2%2BmL%2Fkg%2B20%25%2Bmannitol.%2BCrit%2BCare%2BMed%3B%2B2003%3B%2B31(6)%3A%2B1683-1687.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Shackford%2BSR%2C%2BBourguignon%2BPR%2C%2BWald%2BSL%2C%2BRogers%2BFB%2C%2BOsler%2BTM%2C%2BClark%2BDE%3A%2BHypertonic%2Bsaline%2Bresuscitation%2Bof%2Bpatients%2Bwith%2Bhead%2Binjury%3A%2Ba%2Bprospective%2C%2Brandomized%2Bclinical%2Btrial.%2BJ%2BTrauma%3B%2B1998%3B%2B44(1)%3A%2B50-58.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Qureshi%2BAI%2C%2BSuarez%2BJI%2C%2BCastro%2BA%2C%2BBhardwaj%2BA%3A%2BUse%2Bof%2Bhypertonic%2Bsaline%2Facetate%2Binfusion%2Bin%2Btreatment%2Bof%2Bcerebral%2Bedema%2Bin%2Bpatients%2Bwith%2Bhead%2Btrauma%3A%2Bexperience%2Bat%2Ba%2Bsingle%2Bcenter.%2BJ%2BTrauma%3B%2B1999%3B%2B47(4)%3A%2B659-665.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Lescot%2BT%2C%2BDegos%2BV%2C%2BZouaoui%2BA%2C%2BPreteux%2BF%2C%2BCoriat%2BP%2C%2BPuybasset%2BL%3A%2BOpposed%2Beffects%2Bof%2Bhypertonic%2Bsaline%2Bon%2Bcontusions%2Band%2Bnoncontused%2Bbrain%2Btissue%2Bin%2Bpatients%2Bwith%2Bsevere%2Btraumatic%2Bbrain%2Binjury.%2BCrit%2BCare%2BMed%3B%2B2006%3B%2B34(12)%3A%2B3029-3033.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Battison%2BC%2C%2BAndrews%2BPJ%2C%2BGraham%2BC%2C%2BPetty%2BT%3A%2BRandomized%2C%2Bcontrolled%2Btrial%2Bon%2Bthe%2Beffect%2Bof%2Ba%2B20%25%2Bmannitol%2Bsolution%2Band%2Ba%2B7.5%25%2Bsaline%2F6%25%2Bdextran%2Bsolution%2Bon%2Bincreased%2Bintracranial%2Bpressure%2Bafter%2Bbrain%2Binjury.%2BCritical%2BCare%2BMedicine%3B%2B2005%3B%2B33(1)%3A%2B196-202.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Vassar%2BMJ%2C%2BFischer%2BRP%2C%2BO%27Brien%2BPE%2C%2BBachulis%2BBL%2C%2BChambers%2BJA%2C%2BHoyt%2BDB%2C%2BHolcroft%2C%2BJ%3A%2BA%2Bmulticenter%2Btrial%2Bfor%2Bresuscitation%2Bof%2Binjured%2Bpatients%2Bwith%2B7.5%25%2Bsodium%2Bchloride.%2BThe%2Beffect%2Bof%2Badded%2Bdextran%2B70.%2BThe%2Bmulticenter%2Bgroup%2Bfor%2Bthe%2Bstudy%2Bof%2Bhypertonic%2Bsaline%2Bin%2Btrauma%2Bpatients.%2BArch%2BSurg%3B%2B1993%3B%2B128(9)%3A%2B1003-1011.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Centers%2Bfor%2BDisease%2BControl.%2BWhat%2Bis%2Btraumatic%2Bbrain%2Binjury%3F%2BRetrieved%2BApril%2B10%2C%2B2009%2Bfrom%2Bhttp%3A%2F%2Fwww.cdc.gov%2Fncipc%2Ftbi%2FTBI.htm.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Oddo%2BM%2C%2BLevine%2BJM%2C%2BFrangos%2BS%2C%2BCarrera%2BE%2C%2BMaloney-Wilensky%2BE%2C%2BPascual%2BJL%2C%2BKofke%2BWA%2C%2BMayer%2BSA%2C%2BLeRoux%2C%2BP%3A%2BEffect%2Bof%2Bmannitol%2Band%2Bhypertonic%2Bsaline%2Bon%2Bcerebral%2Boxygenation%2Bin%2Bpatients%2Bwith%2Bsevere%2Btraumatic%2Bbrain%2Binjury%2Band%2Brefractory%2Bintracranial%2Bhypertension.%2BJ%2BNeurol%2BNeurosurg%2BPsychiatry%3B%2B2009%3B%2B80%2B(8)%3A%2B916-920.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Vialet%2BR%2C%2BAlbanese%2BJ%2C%2BThomachot%2BL%2C%2BAntonini%2BF%2C%2BBourgouin%2BA%2C%2BAlliez%2BB%2C%2BMartin%2C%2BC%3A%2BIsovolume%2Bhypertonic%2Bsolutes%2B(sodium%2Bchloride%2Bor%2Bmannitol)%2Bin%2Bthe%2Btreatment%2Bof%2Brefractory%2Bposttraumatic%2Bintracranial%2Bhypertension%3A%2B2%2BmL%2Fkg%2B7.5%25%2Bsaline%2Bis%2Bmore%2Beffective%2Bthan%2B2%2BmL%2Fkg%2B20%25%2Bmannitol.%2BCrit%2BCare%2BMed%3B%2B2003%3B%2B31(6)%3A%2B1683-1687.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Shackford%2BSR%2C%2BBourguignon%2BPR%2C%2BWald%2BSL%2C%2BR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hyper tonic saline in the treatment of intracranial hypertension

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