Impact of medical complications on outcome after subarachnoid hemorrhage*

Wartenberg, Katja E.; Schmidt, J. Michael; Claassen, Jan; Temes, Richard E.; Frontera, Jennifer A.; Ostapkovich, Noeleen; Parra, Augusto; Connolly, E. Sander; Mayer, Stephan A.

doi:10.1097/01.ccm.0000201903.46435.35

Cited by 460 publications

(312 citation statements)

References 47 publications

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“…This is usually attributed to the syndrome of inappropriate antidiuretic hormone (SIADH) secretion [77,78]. SIADH results in impaired systemic water excretion.…”

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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“…This is usually attributed to the syndrome of inappropriate antidiuretic hormone (SIADH) secretion [77,78]. SIADH results in impaired systemic water excretion.…”

Section: Vasopressin Receptor Antagonistmentioning

confidence: 99%

Novel Treatment Targets for Cerebral Edema

2012

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“…Serum sodium concentration and fluid balance are frequently abnormal in patients after subarachnoid hemorrhage (SAH) [1,2], with dysnatremia causing morbidity in patients with SAH [3][4][5]. Moreover, in other critically ill or emergency patient populations, both severe hyper-and hyponatremia are associated with persistent neurological deficits and high mortality [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Randomized, Double-Blind Trial of the Effect of Fluid Composition on Electrolyte, Acid–Base, and Fluid Homeostasis in Patients Early After Subarachnoid Hemorrhage

et al. 2012

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Background Hyper-and hyponatremia are frequently observed in patients after subarachnoidal hemorrhage, and are potentially related to worse outcome. We hypothesized that the fluid regimen in these patients is associated with distinct changes in serum electrolytes, acid-base disturbances, and fluid balance. Methods Thirty-six consecutive patients with SAH were randomized double-blinded to either normal saline and hydroxyethyl starch dissolved in normal saline (Voluven Ò ; saline) or balanced crystalloid and colloid solutions (Ringerfundin Ò and Tetraspan Ò ; balanced, n = 18, each) for 48 h. Laboratory samples and fluid balance were evaluated at baseline and at 24 and 48 h. Results Age [57 ± 13 years (mean ± SD; saline) vs. Conclusions Treatment with saline-based fluids resulted in a greater number of patients with hyperchloremia, hyperosmolality, and positive fluid balance >1,500 mL early after SAH, while administration of balanced solutions did not cause more frequent hyponatremia or hypo-osmolality. These results should be confirmed in larger studies.

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“…Fever has been associated with worse outcomes [123,124], so that the most recently published guidelines for SAH recommend aggressive treatment of fever to normothermia [125]. No clear evidence exists in using hypothermia after SAH.…”

Section: Subarachnoid Hemorrhagementioning

confidence: 99%

Therapeutic Hypothermia for Acute Neurological Injuries

2012

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Therapeutic hypothermia (TH) is the intentional reduction of core body temperature to 32°C to 35°C, and is increasingly applied by intensivists for a variety of acute neurological injuries to achieve neuroprotection and reduction of elevated intracranial pressure. TH improves outcomes in comatose patients after a cardiac arrest with a shockable rhythm, but other off-label applications exist and are likely to increase in the future. This comprehensive review summarizes the physiology and cellular mechanism of action of TH, as well as different means of TH induction and maintenance with potential side effects. Indications of TH are critically reviewed by disease entity, as reported in the most recent literature, and evidence-based recommendations are provided.

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Impact of medical complications on outcome after subarachnoid hemorrhage*

Abstract: Fever, anemia, and hyperglycemia affect 30% to 54% of patients with SAH and are significantly associated with mortality and poor functional outcome. Critical care strategies directed at maintaining normothermia, normoglycemia, and prevention of anemia may improve outcome after SAH.

Cited by 460 publications

References 47 publications

Novel Treatment Targets for Cerebral Edema

Novel Treatment Targets for Cerebral Edema

Randomized, Double-Blind Trial of the Effect of Fluid Composition on Electrolyte, Acid–Base, and Fluid Homeostasis in Patients Early After Subarachnoid Hemorrhage

Therapeutic Hypothermia for Acute Neurological Injuries

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