RESUMEN
PURPOSE: Hypertonic saline (HTS) is used to control intracranial pressure (ICP) in patients with traumatic brain injury (TBI); however, in prior studies, the resultant hypernatremia has been associated with increased mortality. We aimed to study the effect of HTS on ICP and mortality in patients with severe TBI. METHODS: We performed a retrospective cohort study of 231 patients with severe TBI (Glasgow Coma Scale [GCS] ≤ 8) admitted to two neurotrauma units from 2006-2012. We recorded daily HTS, ICP, and serum sodium (Na) concentration. We used Cox proportional regression modelling for hospital mortality and incorporated the following time-dependent variables: use of HTS, hypernatremia, and desmopressin administration. RESULTS: The mean [standard deviation (SD)] age of patients was 34 (17) and the median (interquartile range [IQR]) GCS was 6 [3-8]. Hypertonic saline was administered as a continuous infusion in 124 of 231 (54%) patients over 788 of 2,968 (27%) patient-days. Hypernatremia (Na > 145 mmol·L(-1)) developed in 151 of 231 (65%) patients over 717 of 2,968 (24%) patients-days. In patients who developed hypernatremia, the median [IQR] Na was 146 [142-147] mmol·L(-1). Overall hospital mortality was 26% (59 of 231 patients). After adjusting for baseline covariates, neither HTS (hazard ratio [HR], 1.07; 95% confidence interval [CI], 0.56 to 2.05; P = 0.84) nor hypernatremia (HR, 1.31; 95% CI, 0.68 to 2.55; P = 0.42) was associated with hospital mortality. There was no effect modification by either HTS or hypernatremia on each another. Patients who received HTS observed a significant decrease in ICP during their ICU stay compared with those who did not receive HTS (4 mmHg; 95% CI, 2 to 6; P < 0.001 vs 2 mmHg; 95% CI, -1 to 5; P = 0.14). CONCLUSIONS: Hypertonic saline and hypernatremia are not associated with hospital mortality in patients with severe TBI.
Asunto(s)
Lesiones Traumáticas del Encéfalo/complicaciones , Lesiones Traumáticas del Encéfalo/mortalidad , Hipernatremia/complicaciones , Hipernatremia/mortalidad , Solución Salina Hipertónica/farmacología , Adulto , Lesiones Traumáticas del Encéfalo/terapia , Estudios de Cohortes , Femenino , Mortalidad Hospitalaria , Humanos , Masculino , Modelos de Riesgos Proporcionales , Estudios Retrospectivos , Solución Salina Hipertónica/administración & dosificación , Resultado del TratamientoRESUMEN
PURPOSE: Increased intracranial pressure (ICP) is associated with worse outcomes following traumatic brain injury (TBI). Studies have confirmed that ICP is correlated with optic nerve sheath diameter (ONSD) on ultrasound. The aim of our study was to assess the independent relationship between ONSD measured using CT and mortality in a population of patients admitted with severe TBI. METHODS: We conducted a retrospective cohort study of patients with a TBI requiring ICP monitoring admitted to the ICU between April 2006 and May 2012 to two neurotrauma centers. ONSD was independently measured by two physicians blinded to patient outcomes. Multivariable logistic regression modeling was used to assess an association between ONSD and hospital mortality. RESULTS: A total of 220 patients were included in the analysis. Overall, the cohort had a mean age of 35 (SD 17) years and 171 of 220 (79 %) were male. The median admission GCS was 6 (IQR 3-8). Intra-class correlation coefficient between raters for ONSD measurements was 0.92 (95 % CI 0.90-0.94, P < 0.0001). On multivariable analysis, each 1 mm increase in ONSD was associated with a twofold increase in hospital mortality (OR 2.0, 95 % CI 1.2-3.2, P = 0.007). Using linear regression, ONSD was independently associated with increased ICP in the first 48 h after admission (ß = 4.4, 95 % CI 2.5-6.3, P < 0.0001). CONCLUSIONS: In patients with TBI, ONSD measured on CT scanning was independently associated with ICP and mortality.
Asunto(s)
Lesiones Encefálicas/mortalidad , Hipertensión Intracraneal/fisiopatología , Nervio Óptico/diagnóstico por imagen , Adulto , Lesiones Encefálicas/diagnóstico por imagen , Femenino , Escala de Coma de Glasgow , Mortalidad Hospitalaria , Humanos , Masculino , Persona de Mediana Edad , Vaina de Mielina/diagnóstico por imagen , RadiografíaAsunto(s)
Amidas/envenenamiento , Anestésicos Locales/envenenamiento , Antídotos/uso terapéutico , Emulsiones Grasas Intravenosas/uso terapéutico , Fosfolípidos/uso terapéutico , Complicaciones Posoperatorias/tratamiento farmacológico , Aceite de Soja/uso terapéutico , Antídotos/administración & dosificación , Sistema Nervioso Central/efectos de los fármacos , Emulsiones/administración & dosificación , Emulsiones/uso terapéutico , Emulsiones Grasas Intravenosas/administración & dosificación , Femenino , Humanos , Persona de Mediana Edad , Contracción Muscular/efectos de los fármacos , Nistagmo Patológico/inducido químicamente , Fosfolípidos/administración & dosificación , Ropivacaína , Aceite de Soja/administración & dosificación , Torniquetes , Resultado del Tratamiento , Inconsciencia/inducido químicamenteRESUMEN
PURPOSE: The aims of this study are to assess adherence to the Brain Trauma Foundation (BTF) cerebral perfusion pressure (CPP) guidelines and to determine if adherence is associated with mortality in patients who have a severe traumatic brain injury. MATERIALS AND METHODS: Retrospective cohort study of 127 patients admitted to one intensive care unit between 2006 and 2012. Adherence to BTF guidelines was measured as the time that the CPP was within 50 to 70 mm Hg divided by the total time of CPP monitoring (CPP time index). RESULTS: The percentage of time that the CPP was within the recommended range was 31.6% (SD, 22.2); CPP was greater than 70 mm Hg for 63.9% (SD, 26.2) of the time and less than 50 mm Hg for 4.5% of the time (SD, 16.3). After adjustment for covariates, CPP time index (between 50 and 70 mm Hg) was not associated with hospital mortality (odds ratio [OR], 1.2; 95% confidence interval [CI], 0.98-1.6; P= .079). The time indices for CPP ≥70 and <50 mm Hg were associated with decreased (OR, 0.66; 95%CI, 0.52-0.82; P< .0001) and increased (OR, 9.9; 95% CI, 1.4-69.6; P= .021) mortality, respectively. CONCLUSION: Cerebral perfusion pressure was greater than 70 mm Hg for most of the time. This level of CPP was associated with decreased hospital mortality.
Asunto(s)
Lesiones Encefálicas/fisiopatología , Circulación Cerebrovascular/fisiología , Adhesión a Directriz , Presión Intracraneal/fisiología , Adulto , Análisis de Varianza , Lesiones Encefálicas/mortalidad , Colombia Británica , Femenino , Mortalidad Hospitalaria , Humanos , Masculino , Persona de Mediana Edad , Monitoreo Fisiológico , Guías de Práctica Clínica como Asunto , Estándares de Referencia , Estudios RetrospectivosRESUMEN
BACKGROUND: Hypernatremia is common following traumatic brain injury (TBI) and occurs from a variety of mechanisms, including hyperosmotic fluids, limitation of free water, or diabetes insipidus. The purpose of this systematic review was to assess the relationship between hypernatremia and mortality in patients with TBI. METHODS: We searched the following databases up to November 2012: MEDLINE, EMBASE, and CENTRAL. Using a combination of MeSH and text terms, we developed search filters for the concepts of hypernatremia and TBI and included studies that met the following criteria: (1) compared hypernatremia to normonatremia, (2) adult patients with TBI, (3) presented adjusted outcomes for mortality or complications. RESULTS: Bibliographic and conference search yielded 1,152 citations and 11 abstracts, respectively. Sixty-five articles were selected for full-text review with 5 being included in our study. All were retrospective cohort studies totaling 5,594 (range 100-4,296) patients. There was marked between-study heterogeneity. The incidence of hypernatremia ranged between 16% and 40%. Use of hyperosmolar therapy was presented in three studies (range 14-85% of patients). Hypernatremia was associated with increased mortality across all four studies that presented this outcome. Only one study considered diabetes insipidus (DI) in their analysis where hypernatremia was associated with increased mortality in patients who did not receive DDAVP. CONCLUSIONS: Although hypernatremia was associated with increased mortality in the included studies, there was marked between-study heterogeneity. DI was a potential confounder in several studies. Considering these limitations, the clinical significance of hypernatremia in TBI is difficult to establish at this stage.