Hyponatremia in Neurologic Patients: Consequences and Approaches to Treatment

Diringer, Michael N.; Zazulia, Allyson R.

doi:10.1097/01.nrl.0000215741.01699.77

Cited by 70 publications

(58 citation statements)

References 98 publications

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“…Hyponatremia has been implicated in the development of cerebral edema and subsequent increased intracranial pressure [79,80]. In the intensive care setting, control of serum sodium levels and volume status are necessary to optimize outcomes and prevent cerebral edema [81,82].…”

Section: Vasopressin Receptor Antagonistmentioning

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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Section: Vasopressin Receptor Antagonistmentioning

confidence: 99%

Novel Treatment Targets for Cerebral Edema

2012

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“…overall neurological outcome and hospital morbidity & mortality [7][8][9][10]. Hyponatremia is defined as if serum sodium level falls below 135 mmol/L [11].…”

Section: Journal Of Intensive and Critical Care Issn 2471-8505mentioning

confidence: 99%

Effect of Early Correction of Hyponatremia on Neurological Outcome in Traumatic Brain Injury Patients

Ahmad¹,

Alrais²,

Elkholy³

et al. 2017

Intensive & Crit Care

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“…10,11 Post brain injury hyponatremia usually develops due to Syndrome of inappropriate antidiuretic hormone (SIADH) or Cerebral salt wasting (CSW). This drop in sodium (even small drop) has profound impact on the injured brain forming one of the most dreaded complication in brain injury patients.…”

Section: How Is Sodium Homeostasis Maintained In the Body?mentioning

confidence: 99%