Effects of 23.4% Sodium Chloride Solution in Reducing Intracranial Pressure in Patients with Traumatic Brain Injury: A Preliminary Study

Ware, Marcus L.; Nemani, Venu M.; Meeker, Michele; Lee, Currie; Morabito, Diane; Manley, Geoffrey T.

doi:10.1093/neurosurgery/57.4.727

Cited by 50 publications

(62 citation statements)

References 25 publications

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“…30,45,47 However, hypertonic saline (HTS) has increasing pilot data supporting its efficacy. 1,17,20,21,25,48,51 Recent meta-analyses of observational studies comparing mannitol and HTS in the treatment of raised ICP support HTS as a superior agent for lowering ICP. 24,32 One of the meta-analyses included 5 trials (not restricted to TBI) with a total of 112 patients and found that HTS was overall superior in controlling ICP elevations, with a higher odds ratio favoring ICP control, and a greater reduction in the occurrence and severity of ICP.…”

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confidence: 99%

“…20,37,40,44 Hypertonic saline has a more pronounced and longer-lasting effect on raised ICP than mannitol and does not cause a rebound increase in ICP. 17,25,51 It causes quick and sustained volume expansion and is effective in lowering raised ICP refractory to other therapies. 7,9,17,18,25,51 Single doses of 23.4% HTS can reverse transtentorial herniation and improve cerebral blood flow (CBF), CPP, and cerebral oxygenation.…”

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confidence: 99%

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Hypertonic saline reduces cumulative and daily intracranial pressure burdens after severe traumatic brain injury

Mangat

Chiu²,

Gerber

et al. 2015

JNS

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ObJect Increased intracranial pressure (ICP) in patients with traumatic brain injury (TBI) is associated with a higher mortality rate and poor outcome. Mannitol and hypertonic saline (HTS) have both been used to treat high ICP, but it is unclear which one is more effective. Here, the authors compare the effect of mannitol versus HTS on lowering the cumulative and daily ICP burdens after severe TBI. MetHODS The Brain Trauma Foundation TBI-trac New York State database was used for this retrospective study. Patients with severe TBI and intracranial hypertension who received only 1 type of hyperosmotic agent, mannitol or HTS, were included. Patients in the 2 groups were individually matched for Glasgow Coma Scale score (GCS), pupillary reactivity, craniotomy, occurrence of hypotension on Day 1, and the day of ICP monitor insertion. Patients with missing or erroneous data were excluded. Cumulative and daily ICP burdens were used as primary outcome measures. The cumulative ICP burden was defined as the total number of days with an ICP of > 25 mm Hg, expressed as a percentage of the total number of days of ICP monitoring. The daily ICP burden was calculated as the mean daily duration of an ICP of > 25 mm Hg, expressed as the number of hours per day. The numbers of intensive care unit (ICU) days, numbers of days with ICP monitoring, and 2-week mortality rates were also compared between the groups. A 2-sample t-test or chisquare test was used to compare independent samples. The Wilcoxon signed-rank or Cochran-Mantel-Haenszel test was used for comparing matched samples. reSultS A total of 35 patients who received only HTS and 477 who received only mannitol after severe TBI were identified. Eight patients in the HTS group were excluded because of erroneous or missing data, and 2 other patients did not have matches in the mannitol group. The remaining 25 patients were matched 1:1. Twenty-four patients received 3% HTS, and 1 received 23.4% HTS as bolus therapy. All 25 patients in the mannitol group received 20% mannitol. The mean cumulative ICP burden (15.52% [HTS] vs 36.5% [mannitol]; p = 0.003) and the mean (± SD) daily ICP burden (0.3 ± 0.6 hours/day [HTS] vs 1.3 ± 1.3 hours/day [mannitol]; p = 0.001) were significantly lower in the HTS group. The mean (± SD) number of ICU days was significantly lower in the HTS group than in the mannitol group (8.5 ± 2.1 vs 9.8 ± 0.6, respectively; p = 0.004), whereas there was no difference in the numbers of days of ICP monitoring (p = 0.09). There were no significant differences between the cumulative median doses of HTS and mannitol (p = 0.19). The 2-week mortality rate was lower in the HTS group, but the difference was not statistically significant (p = 0.56). cONcluSiONS HTS given as bolus therapy was more effective than mannitol in lowering the cumulative and daily ICP burdens after severe TBI. Patients in the HTS group had significantly lower number of ICU days. The 2-week mortality rates were not statistically different between the 2 groups.http://thejns.org/doi/abs/10.3171/2014....

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confidence: 99%

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confidence: 99%

Hypertonic saline reduces cumulative and daily intracranial pressure burdens after severe traumatic brain injury

Mangat

Chiu²,

Gerber

et al. 2015

JNS

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“…Also, it reinforces that the cells are dead and that the swelling is not driven by an active cell process. Living brain cells would have responded very differently to hypertonic KCl compared with hypertonic NaCl (Ware et al 2005;Neprasova et al 2007). Water content was also measured following 3 h exposure to hypotonic (200 mOsm), isotonic (control) or hypertonic (2000 mOsm) solutions.…”

Section: Discussionmentioning

confidence: 99%

Fixed negative charge and the Donnan effect: a description of the driving forces associated with brain tissue swelling and oedema

Elkin

Shaik

Morrison

2010

Phil. Trans. R. Soc. A.

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Cerebral oedema or brain tissue swelling is a significant complication following traumatic brain injury or stroke that can increase the intracranial pressure (ICP) and impair blood flow. Here, we have identified a potential driver of oedema: the negatively charged molecules fixed within cells. This fixed charge density (FCD), once exposed, could increase ICP through the Donnan effect. We have shown that metabolic processes and membrane integrity are required for concealing this FCD as slices of rat cortex swelled immediately (within 30 min) following dissection if treated with 2 deoxyglucose + cyanide (2DG+CN) or Triton X-100. Slices given ample oxygen and glucose, however, did not swell significantly. We also found that dead brain tissue swells and shrinks in response to changes in ionic strength of the bathing medium, which suggests that the Donnan effect is capable of pressurizing and swelling brain tissue. As predicted, a non-ionic osmolyte, 1,2 propanediol, elicited no volume change at 2000 × 10 −3 osmoles l −1 (Osm). Swelling data were well described by triphasic mixture theory with the calculated reference state FCD similar to that measured with a 1,9 dimethylmethylene blue assay. Taken together, these data suggest that intracellular fixed charges may contribute to the driving forces responsible for brain swelling.

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“…However, mannitol may lead to systemic hypotension, decreased cerebral perfusion, acute renal failure, and Conducts monovalent cations Absorption of free water in collecting tubule of kidney delayed accumulation within the extravascular compartment that leads to a paradoxical rebound elevation in intracranial pressure [22,23]. Another agent, hypertonic saline, is gaining increasing clinical interest due to its reported efficacy in treating cerebral edema and elevated intracranial pressure [24,25]. Bolus dosing of hypertonic saline was first studied and documented almost 1 century ago by Weed and McKibben [26].…”

Section: Osmotherapymentioning

confidence: 99%

“…Only a few retrospective studies have examined the use of 23.4% hypertonic saline for the treatment of increased intracranial pressure in humans [24,25,37]. They all demonstrated a favorable effect in lowering intracranial pressure.…”

Section: Osmotherapymentioning

confidence: 99%

Novel Treatment Targets for Cerebral Edema

2012

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Cerebral edema is a common finding in a variety of neurological conditions, including ischemic stroke, traumatic brain injury, ruptured cerebral aneurysm, and neoplasia. With the possible exception of neoplasia, most pathological processes leading to edema seem to share similar molecular mechanisms of edema formation. Challenges to brain-cell volume homeostasis can have dramatic consequences, given the fixed volume of the rigid skull and the effect of swelling on secondary neuronal injury. With even small changes in cellular and extracellular volume, cerebral edema can compromise regional or global cerebral blood flow and metabolism or result in compression of vital brain structures. Osmotherapy has been the mainstay of pharmacologic therapy and is typically administered as part of an escalating medical treatment algorithm that can include corticosteroids, diuretics, and pharmacological cerebral metabolic suppression. Novel treatment targets for cerebral edema include the Na(+)-K(+)-2Cl(−) co-transporter (NKCC1) and the SUR1-regulated NC Ca-ATP (SUR1/TRPM4) channel. These two ion channels have been demonstrated to be critical mediators of edema formation in brain-injured states. Their specific inhibitors, bumetanide and glibenclamide, respectively, are well-characterized Food and Drug Administration-approved drugs with excellent safety profiles. Directed inhibition of these ion transporters has the potential to reduce the development of cerebral edema and is currently being investigated in human clinical trials. Another class of treatment agents for cerebral edema is vasopressin receptor antagonists. Euvolemic hyponatremia is present in a myriad of neurological conditions resulting in cerebral edema. A specific antagonist of the vasopressin V1A-and V2-receptor, conivaptan, promotes water excretion while sparing electrolytes through a process known as aquaresis.Keywords Cerebral edema . Hyponatraemia . Osmotherapy . NKCC1 . SUR1/TRPM4 . Vaptan . Glyburide Overview of Perturbations in Brain Fluid HomeostasisCerebral edema in the neurointensive care setting can occur with a heterogenous group of neurological diseases, which typically fall under the categories of metabolic [1, 2], infectious [3], neoplastic [4], cerebrovascular [5][6][7], and traumatic [8,9] brain injury. Irrespective of the inciting process, cerebral edema results in the pathological accumulation of fluid in the brain's intracellular and extracellular spaces. This occurs secondary to alterations in the complex interplay between 4 distinct fluid compartments within the cranium; fluid is present within: 1) the blood in the cerebral blood vessels, 2) the cerebrospinal fluid in the ventricular system and subarachnoid space, 3) the interstitial fluid of the brain parenchyma, and 4) the intracellular fluid of the neurons and glia. These fluid compartments are not isolated, and specific movements of solutes and water from one compartment to another occur under normal conditions. When dysregulation of this normally tightly controlled fluid balance...

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Effects of 23.4% Sodium Chloride Solution in Reducing Intracranial Pressure in Patients with Traumatic Brain Injury: A Preliminary Study

Abstract: This study suggests that 23.4% hypertonic saline is a safe and effective treatment for elevated ICP in patients after traumatic brain injury. These results warrant a rigorous evaluation of its efficacy as compared to mannitol in a prospective randomized controlled trial.

Cited by 50 publications

References 25 publications

Hypertonic saline reduces cumulative and daily intracranial pressure burdens after severe traumatic brain injury

Hypertonic saline reduces cumulative and daily intracranial pressure burdens after severe traumatic brain injury

Fixed negative charge and the Donnan effect: a description of the driving forces associated with brain tissue swelling and oedema

Novel Treatment Targets for Cerebral Edema

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