Successful use of the new high-dose mannitol treatment in patients with Glasgow Coma Scale scores of 3 and bilateral abnormal pupillary widening: a randomized trial

Cruz, Julio; Minoja, Giulio; Okuchi, Kazuo; Facco, Enrico

doi:10.3171/jns.2004.100.3.0376

Cited by 102 publications

(48 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Among the various osmotic agents available for administration to treat cerebral edema, mannitol (administered rapidly in a 1 gm/kg bolus) has been the most commonly selected medication in the neurointensive care setting [21]. 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].…”

Section: Osmotherapymentioning

confidence: 99%

Novel Treatment Targets for Cerebral Edema

2012

View full text Add to dashboard Cite

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...

show abstract

Section: Osmotherapymentioning

confidence: 99%

Novel Treatment Targets for Cerebral Edema

2012

View full text Add to dashboard Cite

show abstract

“…They explained their results as related with young age, initially aggressive treatment and the epidural hematoma (EDH) subgroup, and they emphasized that patients who suffered TBI and presented with a GCS score of 3 should be treated aggressively initially, since a good functional outcome could be obtained in some cases. Cruz et al [8] reported that among patients with SHI and BNDP who were treated with ultra-early high-dose mannitol, 43.5% had a favorable outcome at six months. They also reported that patients with abnormal pupillary widening documented at the scene of the injury did not benefit from ultra-early high-dose mannitol treatment, in contrast to those whose bilateral widened pupils were first seen in the ER.…”

Section: Gcs Score Icp and Cpp Changes And Prognosismentioning

confidence: 99%

“…[6] When the patient demonstrates compression signs of the upper brainstem in the early period of uncal or central transtentorial herniation due to uncontrollable ICP, despite the modern management protocols (intubation, artificial ventilation, ventricular drainage of cerebrospinal fluid (CSF), and osmotherapy with mannitol), DC has been recommended as a last treatment option. [7][8][9][10][11] However, the criteria for the use of DC in such patients with severe traumatic brain injury (STBI) have not been standardized. There are not many reports in the current literature about the necessity of decompressive surgery (DS) in patients with BNDP due to STBI or cerebrovascular accidents (CVA).…”

mentioning

confidence: 99%

Effects of decompressive surgery in patients with severe traumatic brain injury and bilateral non-reactive dilated pupils

Göksu

Uçar²,

Akyuz³

et al. 2012

Ulus Travma Acil Cerrahi Derg

View full text Add to dashboard Cite

AMAÇAğır travmatik beyin yaralanmalı (ATBY) ve bilateral reaktif olmayan pupil dilatasyonu (BRPD) olup, dekompresif cerrahi (DC) uygulanmış hastalarda Glasgow koma skalası (GKS), kafa içi basınç (KİB), serebral perfüzyon basın-cı (SPP) değişiklikleri ve uzun dönem klinik sonuçları değerlendirildi. GEREÇ VE YÖNTEMÇalışma gurubu, bölümümüzde ATBY nedeniyle DC uygulanan 147 hasta içerisinden BRPD'li 28 hastayı (11 kadın, 17 erkek) içerdi. BULGULAROrtalama GKS skoru, başvuruda 4,96±1,20, ameliyat ön-cesi dönemde 4 idi. Ölen hastalarda, DC sonrası ortalama KİB değerleri hayatta kalanlara göre anlamlı ölçüde yük-sekti (p<0,05). Ayrıca, DC sonrası KİB azalması, yaşayan hastalarda yine anlamlı olarak yüksekti (p<0,05). Tümden mortalite oranı %61,02 bulundu. Başvuruda ikinin üzeri GKS motor skoru anlamlı olarak düşük mortalite ile ilişki-li idi (p<0,05). Yaşayan 4 hasta taburcu sonrası birinci yıl-da (%14,28) işlevsel sonuç skoru (Glasgow sonuç skoru 4 ve 5) gösterdi. SONUÇATBY sonrası BRPD'li hastalarda sonuçlar her zaman ölümcül ya da olumsuz olmayabilir. Hızlı DC, özellikle başvuru GKS skoru 6, 7 olan hastalarda işlevsel sağkalım şansını artırabilir.Anahtar Sözcükler: Dekompresif cerrahi; travmatik beyin yaralanması; reaktif olmayan dilate pupil. BACKGROUNDWe investigated Glasgow Coma Scale (GCS) scores, intracranial pressure (ICP) and cerebral perfusion pressure (CPP) changes, and long-term clinical outcomes in patients with severe traumatic brain injury (STBI) associated with bilateral non-reactive dilated pupils (BNDP) who underwent decompressive surgery (DS). METHODSThe study group consisted of 28 patients (11 females, 17 males) with BNDP from among 147 patients who underwent DS due to STBI in our department. RESULTSThe mean GCS score was 4.96±1.20 at admission and 4 preoperatively. Mean ICP in non-surviving patients after DS was higher (p<0.05). ICP decrease after DS was also higher in surviving patients than in non-surviving patients (p<0.05). The overall mortality rate was 61.02%. A GCS motor score >2 at admission was associated with lower mortality (p<0.05). Four of the surviving patients (14.28%) had a functional outcome (Glasgow Outcome Score: 4 and 5) at one year after hospital discharge. CONCLUSIONOutcome in patients with BNDP after STBI may not always be fatal or poor. Rapid DS may increase the chance of functional survival, especially in patients with admission GCS score of 6 or 7.

show abstract

“…En cuanto a la dosis y la forma de administración, los distintos estudios encuentran que es efectivo a dosis de 0,25-1 g/kg peso, pero no hay resultados concluyentes sobre su uso en bolo o en infusión continua, aunque ésta parece que conlleva mayor incidencia de rebote 23,24 . Los estudios de Cruz et al 25,26 sobre la efectividad de altas dosis (1,4 g/kg) en pacientes con lesiones focales y con alteraciones pupilares han sido cuestionados por su metodología.…”

Section: Soluciones Osmolaresunclassified

Actualizaciones en el manejo del traumatismo craneoencefálico grave

2009

View full text Add to dashboard Cite

El traumatismo craneoencefálico (TCE) es una importante causa de morbimortalidad en cualquier lugar del mundo; afecta más a varones jóvenes y genera un problema de salud pública. Desafortunadamente, los avances en los conocimientos fisiopatológicos no han ido seguidos de similar desarrollo en las opciones terapéuticas, y no se dispone en la actualidad de fármacos neuroprotectores contrastados.En este artículo revisamos la epidemiología, la fisiopatología y las medidas terapéuticas utilizadas en el manejo del paciente con TCE grave. Se analizan tanto las medidas generales como las dirigidas al control de la hipertensión intracraneal, el papel de la cirugía y algunas opciones terapéu-ticas más innovadoras actualmente en fase de valoración en estos pacientes. UPDATES OF SEVERE TRAUMATIC BRAIN INJURY MANAGEMENT Traumatic brain injury (TBI)is an important reason of morbidity-mortality all over the world, affecting young males more and generating Public Health problem. Unfortunately, the advances in the pathophysiology knowledge have not followed a similar development in therapeutic options, there currently not being any contrasted neuroprotectants.In this article, we have reviewed the epidemiology, pathophysiology and therapeutic measures used in the management of patient with severe TBI. The general measures as well as those aimed at controlling intracranial hypertension, the role of the surgery and some more innovative therapeutic options currently under evaluation in these patients are analyzed.

show abstract

Successful use of the new high-dose mannitol treatment in patients with Glasgow Coma Scale scores of 3 and bilateral abnormal pupillary widening: a randomized trial

Cited by 102 publications

References 41 publications

Novel Treatment Targets for Cerebral Edema

Novel Treatment Targets for Cerebral Edema

Effects of decompressive surgery in patients with severe traumatic brain injury and bilateral non-reactive dilated pupils

Actualizaciones en el manejo del traumatismo craneoencefálico grave

Contact Info

Product

Resources

About