Central Neurogenic Diabetes Insipidus, Syndrome of Inappropriate Secretion of Antidiuretic Hormone, and Cerebral Salt-Wasting Syndrome in Traumatic Brain Injury

John, Cynthia A.; Day, Michael

doi:10.4037/ccn2012904

Cited by 25 publications

(35 citation statements)

References 8 publications

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“…For example, meningitis and encephalitis are known to cause a syndrome characterised by the inappropriate secretion of antidiuretic hormone secretion. 39 Furthermore, an inflammatory process may be the cause of central neurogenic diabetes insipidus, in an AVP-secretion impairment syndrome characterised by hypernatraemia, which is associated with high mortality in critical care patients. 40 However, some clinical studies demonstrated a long-term AVP secretion impairment following osmotic stimulus in sepsis survivor patients, suggesting that a compensatory mechanism may allow them to survival.…”

Section: Discussionmentioning

confidence: 99%

Alterations in hypothalamic synaptophysin and death markers may be associated with vasopressin impairment in sepsis survivor rats

Santos-Júnior

Catalão

Costa

et al. 2018

J Neuroendocrinology

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The impairment in arginine vasopressin (AVP) secretion during sepsis is described in clinical and experimental studies and has been associated with oxidative stress, apoptosis, and diminished activation of hypothalamic neurons. Few studies have, however, assessed these abnormalities in sepsis survivors. Here we performed two sets of experiments on Wistar rats that had been subjected to sepsis by cecal ligation and puncture (CLP) or nonmanipulated (naive) as control. In the first set, tissues and blood were collected from survivor rats 10 days after CLP to quantify hypothalamic Bcl-2, cleaved caspase- 3 and synaptophysin content, and bacterial load. In the second set, survivor rats were submitted to an acute osmotic stimulus (hypertonic saline), and after 30 minutes the water intake and AVP secretion were analyzed. The sepsis-surviving rats did not show bacterial load in tissues, but their hypothalamic synaptophysin and Bcl-2 levels were decreased, and the cleaved caspase- 3 level was increased when compared with the control group. However, AVP secretion was significantly attenuated in the CLP survivor animals submitted to an acute osmotic stimulus. These results suggest that the persistent AVP impairment in sepsis survivor animals may be due to a hypothalamic dysfunction associated with a synaptic deficit and decreased anti-apoptotic protein expression. This article is protected by copyright. All rights reserved.

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Section: Discussionmentioning

confidence: 99%

Alterations in hypothalamic synaptophysin and death markers may be associated with vasopressin impairment in sepsis survivor rats

Santos-Júnior

Catalão

Costa

et al. 2018

J Neuroendocrinology

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“…Causes include central diabetes insipidus (CDI), cerebral salt wasting (CSW) syndrome and syndrome of inappropriate anti-diuretic hormone (SIADH) secretion. [44] The former condition (CDI) manifests as hypernatremia while later two (CSW, SIADH) present as hyponatremia. [44] The sodium level should be kept between 140 mmol/ml and 150 mmol/ml.…”

Section: Sedation/analgesia/suctioningmentioning

confidence: 99%

“…[44] The former condition (CDI) manifests as hypernatremia while later two (CSW, SIADH) present as hyponatremia. [44] The sodium level should be kept between 140 mmol/ml and 150 mmol/ml. Hypotonic fluids can result in swelling of cerebral cells and increases in ICP.…”

Section: Sedation/analgesia/suctioningmentioning

confidence: 99%

General intensive care for patients with traumatic brain injury: An update

et al. 2014

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Background:Traumatic brain injury (TBI) is a growing epidemic throughout the world and may present as major global burden in 2020. Some intensive care units throughout the world still have no access to specialized monitoring methods, equipments and other technologies related to intensive care management of these patients; therefore, this review is meant for providing generalized supportive measurement to this subgroup of patients so that evidence based management could minimize or prevent the secondary brain injury.Methods:Therefore, we have included the PubMed search for the relevant clinical trials and reviews (from 1 January 2007 to 31 March 2013), which specifically discussed about the topic.Results:General supportive measures are equally important to prevent and minimize the effects of secondary brain injury and therefore, have a substantial impact on the outcome in patients with TBI. The important considerations for general supportive intensive care unit care remain the prompt reorganization and treatment of hypoxemia, hypotension and hypercarbia. Evidences are found to be either against or weak regarding the use of routine hyperventilation therapy, tight control blood sugar regime, use of colloids and late as well as parenteral nutrition therapy in patients with severe TBI.Conclusion:There is also a need to develop some evidence based protocols for the health-care sectors, in which there is still lack of specific management related to monitoring methods, equipments and other technical resources. Optimization of physiological parameters, understanding of basic neurocritical care knowledge as well as incorporation of newer guidelines would certainly improve the outcome of the TBI patients.

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“…Há dois possíveis mecanismos de lesão nesta fase: o impacto direto (por trauma contuso, queda ou ferimento penetrante) e as lesões de impulso, causadas por forças de aceleração e desaceleração. (41,42) A lesão secundária é aquela que acontece segundos, minutos, horas e até dias após o evento traumático, em resposta à injúria inicial ou a suas complicações. (12,42) É um complexo processo, com causas tanto intracranianas quanto sistêmicas.…”

Section: Fisiopatologiaunclassified

“…(41,42) A lesão secundária é aquela que acontece segundos, minutos, horas e até dias após o evento traumático, em resposta à injúria inicial ou a suas complicações. (12,42) É um complexo processo, com causas tanto intracranianas quanto sistêmicas. (41) Entre as causas intracranianas, estão o edema cerebral, o inchaço cerebral, a hipertensão intracraniana, o vasoespasmo, as infecções locais e as convulsões.…”

Section: Fisiopatologiaunclassified

Associação de hipernatremia com o prognóstico e a mortalidade de pacientes com traumatismo cranioencefálico grave em um hospital terciário brasileiro

Carvalho¹

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INTRODUÇÃO: O traumatismo cranioencefálico (TCE) é atualmente uma das maiores causas de incapacidade, custo econômico e morte em todo o mundo. O prognóstico do paciente com TCE depende tanto da lesão encefálica primária, que ocorre no momento do trauma, como da lesão secundária, que ocorre após o evento traumático, em decorrência da evolução da lesão inicial ou de suas complicações intracranianas e sistêmicas. Dentre estas complicações sistêmicas destacam-se os distúrbios hidroeletrolíticos, em especial os distúrbios de sódio, por ser este o principal íon extracelular e o mais importante soluto osmoticamente ativo, estando diretamente ligado à formação de edema cerebral. Estudos recentes têm demonstrado que a hipernatremia é um fator de risco independente para pior prognóstico em pacientes críticos e neurocríticos. Não estão claros, entretanto, a frequência e o impacto clínico da hipernatremia no prognóstico de pacientes com TCE grave em nosso meio. Objetivou-se neste estudo identificar a incidência e os fatores preditivos da hipernatremia na fase aguda em pacientes com TCE grave em uma amostra de pacientes internados em unidade de terapia intensiva (UTI) e verificar se a hipernatremia na fase aguda constitui um fator de risco independente para o óbito intra-hospitalar. MÉTODOS: Estudo observacional, transversal, retrospectivo, unicêntrico, com dados coletados a partir da revisão dos prontuários dos pacientes adultos internados entre 1º de janeiro de 2011 a 17 de maio de 2015 na UTI da UE-HCFMRP com diagnóstico de TCE grave. Foram excluídos pacientes com traumas ocorridos há mais de 5 dias da admissão na UTI ou que tiveram tempo de internação na UTI inferior a 24 horas. Os fatores de risco para hipernatremia (definida como dois ou mais valores de sódio sérico > 145 mEq/L na primeira semana após o trauma), os preditores de óbito intra-hospitalar e de desfecho funcional desfavorável pela Glasgow Outcome Scale na alta hospitalar foram determinados através de análise multivariada por regressão logística linear, Para esta análise, foram também excluídos os pacientes que desenvolveram diabetes insípido e morte encefálica. RESULTADOS: Foram incluídos 254 pacientes, dos quais 89,4% eram do sexo masculino. A média de idade foi 34,11±12,46 anos, sendo os acidentes de trânsito o principal mecanismo de trauma encontrado. A média do valor do sódio sérico na admissão hospitalar foi 136,3±4,6 mEq/L; apenas 5 pacientes já foram admitidos com hipernatremia. A taxa de mortalidade geral foi 26,8%; hipernatremia foi identificada em 40,6% dos casos. Os fatores de risco independentes para a ocorrência de hipernatremia foram a glicemia de

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Central Neurogenic Diabetes Insipidus, Syndrome of Inappropriate Secretion of Antidiuretic Hormone, and Cerebral Salt-Wasting Syndrome in Traumatic Brain Injury

Cited by 25 publications

References 8 publications

Alterations in hypothalamic synaptophysin and death markers may be associated with vasopressin impairment in sepsis survivor rats

Alterations in hypothalamic synaptophysin and death markers may be associated with vasopressin impairment in sepsis survivor rats

General intensive care for patients with traumatic brain injury: An update

Associação de hipernatremia com o prognóstico e a mortalidade de pacientes com traumatismo cranioencefálico grave em um hospital terciário brasileiro

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