Cerebral resuscitation: role of osmotherapy

Harukuni, Izumi; Kirsch, Jeffrey R.; Bhardwaj, Anish

doi:10.1007/s005400200030

Cited by 50 publications

(50 citation statements)

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“…17 This is not surprising because most studies of hypertonic saline solutions did not report safety concerns with sodium values up to 160 mmol/L and osmolality values up to 320 mOsm/kg. 10,18 Thus, based on previous studies and the findings of the present study, continuous infusion of 3% HS with target ranges of sodium of 145 to 155 mmol/L and of osmolality of 310 to 320 mOsm/kg with a maximum daily sodium increase Ͻ10 mmol/L seem to be safe in patients with severe supratentorial ICH.…”

Section: Wagner Et Al Hypertonic Saline Infusion In Ichsupporting

confidence: 66%

“…9 However, optimal dosage and concentration of HS, as well as timing and application schedule, are still unknown. In recent studies, continuous application of HS was investigated in patients with traumatic brain injury 10 or acute liver failure 11 and positive effects on ICP-lowering properties were reported. Furthermore, no major side effects were observed in critically ill patients with severe stroke or traumatic brain injury treated with continuous 3% HS infusion.…”

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confidence: 99%

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Effects of Continuous Hypertonic Saline Infusion on Perihemorrhagic Edema Evolution

Wagner

Hauer

Staykov

et al. 2011

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Background and Purpose-Mass effect of hematoma and the associated perihematomal edema are commonly responsible for neurological deterioration after intracerebral hemorrhage. Efficacy of surgical and medical therapy is limited. We studied the effect of early continuous hypertonic saline infusion on development of perihematomal edema after severe spontaneous supratentorial hemorrhage. Methods-Patients with spontaneous lobar and basal ganglia/thalamic bleeding Ͼ30 mL (nϭ26) were treated with early (Ͻ72 hours) continuous hypertonic saline infusion (3%) to achieve sodium of 145 to 155 mmol/L and osmolality of 310 to 320 mOsmol/kg. Evolution of absolute edema volume and relative edema volume (ratio absolute edema volume/initial hematoma volume) was assessed on repeated cranial CT and compared to historical patients (nϭ64) identified on database with hematoma Ͼ30 mL. Results-In the treatment group, absolute edema volume was significant smaller between day 8 and day 14 (P absolute edema volume ϭ 0.04) and relative edema volume was significant smaller between day 2 and day 14 (P relative edema volume ϭ0.02).Intracranial pressure crisis (Ͼ20 mm Hg for Ͼ20 minutes or new anisocoria) occurred less frequently in the treatment group (12 versus 56; Pϭ0.048). In-hospital mortality was 3 (11.5%) in the hypertonic saline group and 16 (25%) in the control group (Pϭ0.078). Side effects theoretically associated with hypertonic saline including cardiac arrhythmia and acute heart and renal failure occurred in both groups to a similar extent. Conclusions-Early

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Section: Wagner Et Al Hypertonic Saline Infusion In Ichsupporting

confidence: 66%

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confidence: 99%

Effects of Continuous Hypertonic Saline Infusion on Perihemorrhagic Edema Evolution

Wagner

Hauer

Staykov

et al. 2011

Stroke

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“…However, urea has a much lower reflection coefficient (s ϭ 0.59) than mannitol (s ϭ 0.9) or NaCl (s ϭ 1.0), and this may argue for the latter explanation. Urea has been used in osmotherapy after ischemic stroke or traumatic brain injury, but because urea crosses the intact portion of the BBB more readily than NaCl or mannitol and equilibrates more quickly between the brain and intravascular compartment (16), it is more likely to produce a rebound rise in intracranial pressure (20). If urea transporters function in the movement of urea across the BBB in either direction, however, a selective blockade of this move- Fig.…”

Section: Discussionmentioning

confidence: 99%

Differential effects of intravenous hyperosmotic solutes on drinking latency and c-Fos expression in the circumventricular organs and hypothalamus of the rat

Ho¹,

Zierath²,

Savos³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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December 28, 2006; doi:10.1152/ajpregu.00547.2006.-Hyperosmotic intravenous infusions of NaCl are more potent for inducing drinking and vasopressin (AVP) secretion than equally osmotic solutions of glucose or urea. The fact that all three solutes increased cerebrospinal fluid osmolality and sodium concentration led the investigators to conclude that critical sodium receptors or osmoreceptors for stimulating drinking and AVP secretion were outside the blood-brain barrier (BBB) in the circumventricular organs (CVOs). We tested an obvious prediction of this hypothesis: that all three solutes should increase c-Fos-like immunoreactivity (Fos-ir) inside the BBB, but that only NaCl should increase Fos-ir in the CVOs. We gave intravenous infusions of 3.0 Osm/l NaCl, glucose, or urea to rats for 11 or 22 min at 0.14 ml/min and perfused the rats for assay of Fos-ir at 90 min. Controls received isotonic NaCl at the same volume. Drinking latency was measured, but water was then removed. Drinking consistently occurred with short latency during hyperosmotic NaCl infusions only. Fos-ir in the forebrain CVOs, the subfornical organ, and organum vasculosum laminae terminalis was consistently elevated only by hyperosmotic NaCl. However, all three hyperosmotic solutes potently stimulated Fos-ir in the supraoptic and paraventricular nuclei of the hypothalamus inside the BBB. Hyperosmotic NaCl greatly elevated Fos-ir in the area postrema, but even glucose and urea caused moderate elevations that may be related to volume expansion rather than osmolality. The data provide strong support for the conclusion that the osmoreceptors controlling drinking are located in the CVOs. area postrema; c-Fos; drinking; hypernatremia; organum vasculosum laminae terminalis; osmoreceptors; paraventricular nucleus of the hypothalamus; subfornical organ; supraoptic nucleus THE BRAIN AREAS THAT CONTAIN electrophysiologically defined osmoreceptive cells that function in the regulation of fluid and electrolyte balance include the circumventricular organs (CVOs), the median preoptic nucleus (MnPO), the hypothalamic supraoptic and paraventricular nuclei (SON and PVN), and the nucleus of the solitary tract (1,17,18,33,34,40,43). These areas are intricately interconnected by neural pathways into a network subserving fluid balance as originally described by Miselis (29). Candidate mechanisms for osmoreceptors have been identified among aquaporins, the vanilloid family of transient receptor potential channels, and mechanical gating of sodium currents (3,22,44,45). However, electrophysiological studies in single neurons or brain slices do little to differentiate which osmoreceptors are more important for functions such as AVP secretion or drinking.The concept that the critical osmoreceptors for these functions are located in the CVOs and in the peripheral nervous system stems from three influential studies that demonstrated drinking in sheep, dogs, and rats was elicited by intravenous hyperosmotic NaCl or sucrose but not by urea or glucose (8,26,41). The generally...

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“…Death can be caused by 1) compromised regional cerebral blood flow (CBF), which results in irreversible ischemic brain injury from regional or global cerebral ischemia; and 2) generation of intracranial pressure (ICP) gradients, which results in intracranial compartmental shifts and compression of vital structures (cerebral herniation syndromes) that may progress to brain death [2,4,5,7,8•]. Focal or regional cerebral edema may cause lethal intracranial compartmental shifts without causing global increments in ICP [4,5,7]. The over-riding goal of resuscitation from lethal consequences of cerebral edema includes meeting the neuronal metabolic requirements by maintaining adequate regional CBF to prevent cerebral ischemia and the irreversible brain injury that follows [2-5,7,8•].…”

Section: Introductionmentioning

confidence: 99%

Osmotherapy in neurocritical care

Bhardwaj

2007

Curr Neurol Neurosci Rep

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Osmotherapy is the mainstay in the medical management of cerebral edema with or without elevations in intracranial pressure. Several osmotic agents have been utilized in clinical practice over the past five decades in a variety of brain injury paradigms. The over-riding premise for their beneficial effects has been via egress of water from the brain into the vascular compartment. In addition, many of these agents have beneficial extraosmotic properties that portend their use in cerebral resuscitation and treatment of cerebral edema. Although there is a paucity of large, randomized clinical trials that compare various osmotic agents, data are emerging from prospective clinical case series. This article provides a historical perspective of osmotherapy, examines characteristics of osmotic agents, and discusses caveats in their use in the clinical setting. Furthermore, this review highlights the utility of osmotic agents as tools to understand emerging mechanistic concepts in the evolution of brain edema, which are yielding important data of translational significance from laboratory-based research.

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Cerebral resuscitation: role of osmotherapy

Cited by 50 publications

References 55 publications

Effects of Continuous Hypertonic Saline Infusion on Perihemorrhagic Edema Evolution

Effects of Continuous Hypertonic Saline Infusion on Perihemorrhagic Edema Evolution

Differential effects of intravenous hyperosmotic solutes on drinking latency and c-Fos expression in the circumventricular organs and hypothalamus of the rat

Osmotherapy in neurocritical care

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