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array:23 [ "pii" => "S2387020623002450" "issn" => "23870206" "doi" => "10.1016/j.medcle.2023.06.005" "estado" => "S300" "fechaPublicacion" => "2023-07-07" "aid" => "6207" "copyright" => "Elsevier España, S.L.U.. All rights reserved" "copyrightAnyo" => "2023" "documento" => "article" "crossmark" => 1 "subdocumento" => "rev" "cita" => "Med Clin. 2023;161:27-32" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "itemSiguiente" => array:19 [ "pii" => "S2387020623002437" "issn" => "23870206" "doi" => "10.1016/j.medcle.2023.04.008" "estado" => "S300" "fechaPublicacion" => "2023-07-07" "aid" => "6246" "copyright" => "Elsevier España, S.L.U." "documento" => "article" "crossmark" => 1 "subdocumento" => "sco" "cita" => "Med Clin. 2023;161:33-6" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "en" => array:10 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Special article</span>" "titulo" => "Legal and medicolegal approach to medical consultation recordings" "tienePdf" => "en" "tieneTextoCompleto" => "en" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "33" "paginaFinal" => "36" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Abordaje jurídico y medicolegal de las grabaciones en la consulta médica" ] ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Josep Arimany-Manso, Umbert Saigí, Marc Roda-Faura, Carles Martin-Fumadó" "autores" => array:4 [ 0 => array:2 [ "nombre" => "Josep" "apellidos" => "Arimany-Manso" ] 1 => array:2 [ "nombre" => "Umbert" "apellidos" => "Saigí" ] 2 => array:2 [ "nombre" => "Marc" "apellidos" => "Roda-Faura" ] 3 => array:2 [ "nombre" => "Carles" "apellidos" => "Martin-Fumadó" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S0025775323001781" "doi" => "10.1016/j.medcli.2023.04.002" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0025775323001781?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020623002437?idApp=UINPBA00004N" "url" => "/23870206/0000016100000001/v2_202311101438/S2387020623002437/v2_202311101438/en/main.assets" ] "itemAnterior" => array:19 [ "pii" => "S2387020623002346" "issn" => "23870206" "doi" => "10.1016/j.medcle.2023.02.007" "estado" => "S300" "fechaPublicacion" => "2023-07-07" "aid" => "6192" "copyright" => "Elsevier España, S.L.U." "documento" => "simple-article" "crossmark" => 1 "subdocumento" => "edi" "cita" => "Med Clin. 2023;161:24-6" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "en" => array:10 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Editorial</span>" "titulo" => "Brown fat" "tienePdf" => "en" "tieneTextoCompleto" => "en" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "24" "paginaFinal" => "26" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Grasa parda" ] ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Moisés Castellá, Francesc Villarroya" "autores" => array:2 [ 0 => array:2 [ "nombre" => "Moisés" "apellidos" => "Castellá" ] 1 => array:2 [ "nombre" => "Francesc" "apellidos" => "Villarroya" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S0025775323000507" "doi" => "10.1016/j.medcli.2023.02.002" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0025775323000507?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020623002346?idApp=UINPBA00004N" "url" => "/23870206/0000016100000001/v2_202311101438/S2387020623002346/v2_202311101438/en/main.assets" ] "en" => array:17 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Review</span>" "titulo" => "Fluid therapy and traumatic brain injury: A narrative review" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "27" "paginaFinal" => "32" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Eduardo Esteban-Zubero, Cristina García-Muro, Moisés Alejandro Alatorre-Jiménez" "autores" => array:3 [ 0 => array:4 [ "nombre" => "Eduardo" "apellidos" => "Esteban-Zubero" "email" => array:1 [ 0 => "eezubero@gmail.com" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "Cristina" "apellidos" => "García-Muro" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 2 => array:3 [ "nombre" => "Moisés Alejandro" "apellidos" => "Alatorre-Jiménez" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "aff0015" ] ] ] ] "afiliaciones" => array:3 [ 0 => array:3 [ "entidad" => "Emergency Department, Hospital San Pedro, Logroño, Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Department of Pediatrics, Hospital San Pedro, Logroño, Spain" "etiqueta" => "b" "identificador" => "aff0010" ] 2 => array:3 [ "entidad" => "Department of Pediatric Gastroenterology, Children's Mercy Hospital, Kansas City, USA" "etiqueta" => "c" "identificador" => "aff0015" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Fluidoterapia y daño cerebral traumático: una revisión narrativa" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Traumatic brain injury (TBI) is a major public health problem and a significant cause of death and disability.<a class="elsevierStyleCrossRef" href="#bib0305"><span class="elsevierStyleSup">1</span></a> The damage may be divided into two phases: (a) a primary acute injury because of the traumatic event; and (b) a secondary injury due to the hypotension and hypoxia generated by the previous lesion, which leads to ischemia and necrosis of neural cells.<a class="elsevierStyleCrossRef" href="#bib0310"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">In middle-aged patients, trauma is the leading cause of death, with TBI responsible for most of these.<a class="elsevierStyleCrossRef" href="#bib0305"><span class="elsevierStyleSup">1</span></a> In the United States, this pathology causes 275,000 hospitalizations and 52,000 deaths per year as a related factor in more than 30% of all injury-related deaths.<a class="elsevierStyleCrossRef" href="#bib0315"><span class="elsevierStyleSup">3</span></a> The relevance of this pathology is also related to the sequelae, generating an economic impact of over $80 billion in the United States. This data is also associated with the clinical stratification of TBI, beginning from 10% (mild TBI), 60% (moderate TBI), and 100% (severe TBI), according to Glasgow Coma Scale Score (GCS).<a class="elsevierStyleCrossRef" href="#bib0320"><span class="elsevierStyleSup">4</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">According to the literature, TBI studies are mainly categorized based on physical examination instead of the underlying cause. This way of stratification catalogs TBI as a neurological condition without a relationship with a pathology. This association is the key to understanding why several clinical trials have not achieved significant results. This situation is not observed in general guidelines, such as “chest pain”. This symptomatology results from different pathologies with well-known management guidelines, such as myocardial infarction, pneumonia, and aortic dissection. Attending to TBI, the underlying pathology may be unclear, without a clear treatment (diffuse swelling, ischemia, blossoming contusion, etc.).</p><p id="par0020" class="elsevierStylePara elsevierViewall">Therefore, the patient evaluation and management of TBI in the Emergency Department and Urgent Cares is critical.<a class="elsevierStyleCrossRef" href="#bib0325"><span class="elsevierStyleSup">5</span></a> The first approach's main goal should be to avoid secondary brain injury. It has been observed that secondary insults such as systolic blood pressure lower<span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>90<span class="elsevierStyleHsp" style=""></span>mmHg or SpO<span class="elsevierStyleInf">2</span><span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>92% in moderate and severe TBI patients increase mortality.<a class="elsevierStyleCrossRef" href="#bib0330"><span class="elsevierStyleSup">6</span></a> Due to the relevance of maintaining correct brain oxygenation, some authors discuss the benefits of delayed patient transfer to a hospital due to complicated intubation. In this line, a study observed that prehospital rapid sequence intubation performed by paramedics in head-injured patients with GCS<span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>9 was associated with an increase in mortality. This result may be related to the transient hypoxia during the prehospital procedures, excessive over-ventilation causing hypocapnia, vasoconstriction, impaired cerebral blood flow (CBF), and longer scene times.<a class="elsevierStyleCrossRef" href="#bib0335"><span class="elsevierStyleSup">7</span></a> This study concludes that rapid transfer and more basic airway strategies to maintain oxygenation in head-injured patients improve the results.</p><p id="par0025" class="elsevierStylePara elsevierViewall">Fluid therapy (FT) also plays an essential role in the early management of TBI. This therapy is required to (a) Normal maintenance; (b) Blood or fluid loss due to wounds, drains, induced diuresis, etc.; (c) Third space losses called fluid sequestration in tissue edema or ileus; and (d) Increased systemic requirements resulting from fever and hypermetabolic state.<a class="elsevierStyleCrossRef" href="#bib0340"><span class="elsevierStyleSup">8</span></a> Consequently, rapid infusion as quickly as possible of large volumes of crystalloids is performed in daily practice, usually an empirical approach due to the lack of studies.<a class="elsevierStyleCrossRefs" href="#bib0340"><span class="elsevierStyleSup">8,9</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">A search for studies on fluid therapy and traumatic brain injury up to October 2022 was performed in the databases PubMed (MEDLINE, Cochrane Library), Web of Science (WoS), and Scopus. A combination of Medical Subjects Headings (MeSH) and free-text terms were used as a search strategy for each database. The searched terms were: (“fluid therapy” [MeSH Terms] AND “traumatic” [MeSH Terms]) AND (“brain injury” [MeSH Terms]). The inclusion criteria were studies with traumatic brain injury patients, with any date or publication language. The exclusion criteria were: (a) articles with a relevant risk of bias, (b) articles without clinical data, and (c) studies with non-usable data.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Pathophysiology of traumatic brain injury</span><p id="par0035" class="elsevierStylePara elsevierViewall">Brain parenchyma (80%), cerebrospinal fluid (CSF) (10%), and cerebral blood volume (CBV) compose the three compartments of the cranium.<a class="elsevierStyleCrossRef" href="#bib0350"><span class="elsevierStyleSup">10</span></a> The main characteristic is the equilibrium among them, regulating the intracranial pressure (ICP) in adults (10<span class="elsevierStyleHsp" style=""></span>mmHg) and children (7<span class="elsevierStyleHsp" style=""></span>mmHg).<a class="elsevierStyleCrossRef" href="#bib0350"><span class="elsevierStyleSup">10</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">As we commented previously, the pathophysiology of TBI involves a complex cascade of events that could be divided into two different phases. The first one is a primary acute injury because of the traumatic event. Secondary damage occurs after the first lesion when alterations in CBF, cerebral oxygen delivery, inflammation, and cellular metabolism lead to ischemia and necrosis of neural cells.<a class="elsevierStyleCrossRef" href="#bib0310"><span class="elsevierStyleSup">2</span></a> An inflammatory response is generated after the acute injury. However, if this situation is maintained, it develops cerebral edema, leak of oxygen delivery, ischemia, and necrosis of cells.<a class="elsevierStyleCrossRef" href="#bib0355"><span class="elsevierStyleSup">11</span></a> Therefore, cerebral edema is a marker of evolving injury in TBI and is the consequence of disrupting the blood-brain barrier (BBB) and lymphatic drainage disruption.<a class="elsevierStyleCrossRef" href="#bib0350"><span class="elsevierStyleSup">10</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">Cytotoxic and vasogenic edema are the main types of edema observed in TBI. The first one promotes the accumulation of intracellular water in cerebral cells, hypoxia, and ischemia.<a class="elsevierStyleCrossRef" href="#bib0360"><span class="elsevierStyleSup">12</span></a> On the other hand, vasogenic edema results from cerebral blood vessels disruption, causing a breakdown of the BBB and increasing leakage into the extravascular interstitial space.<a class="elsevierStyleCrossRefs" href="#bib0350"><span class="elsevierStyleSup">10,12</span></a> As a response to cerebral edema, intracranial volume increases. However, ICP suffers minimal variations due to vasoconstriction and the shunting of CSF (compensatory phase). If edema persists, these regulatory mechanisms fail, promoting intracranial hypertension.<a class="elsevierStyleCrossRef" href="#bib0365"><span class="elsevierStyleSup">13</span></a> This state results from a reduction in CBF of oxygen, glucose, and essential substrates.<a class="elsevierStyleCrossRef" href="#bib0370"><span class="elsevierStyleSup">14</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">TBI is not only defined as the increase of intracranial pressure. In severe TBI, other pathophysiologic states could be observed, including hypovolemia and hypotension. Therefore, it is essential to measure the blood flow gradient, defined as cerebral perfusion pressure (CPP).<a class="elsevierStyleCrossRef" href="#bib0375"><span class="elsevierStyleSup">15</span></a> CPP is defined as the difference between mean arterial pressure (MAP) and ICP (CPP<span class="elsevierStyleHsp" style=""></span>=<span class="elsevierStyleHsp" style=""></span>MAP<span class="elsevierStyleHsp" style=""></span>−<span class="elsevierStyleHsp" style=""></span>ICP). It could be concluded that systemic hypotension implies a decrease of CPP value—hemorrhage, third-space fluid losses, and vasoplegia that can develop hypotension.<a class="elsevierStyleCrossRef" href="#bib0380"><span class="elsevierStyleSup">16</span></a> It is recommended to maintain CPP values<span class="elsevierStyleHsp" style=""></span>><span class="elsevierStyleHsp" style=""></span>70<span class="elsevierStyleHsp" style=""></span>mmHg in adult patients. In contrast, in the pediatric age group, due to the broad age range, it is recommended to aim CPP<span class="elsevierStyleHsp" style=""></span>><span class="elsevierStyleHsp" style=""></span>40–65<span class="elsevierStyleHsp" style=""></span>mmHg as an age-related continuum for the optimal treatment threshold.<a class="elsevierStyleCrossRef" href="#bib0385"><span class="elsevierStyleSup">17</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">Support treatment in TBI aims to enhance CPP, improve cerebral perfusion, and reduce the degree of brain injury. To achieve these results, non-invasive techniques could be performed, including the elevation of the head of the bed with the head in midline position and maintenance of normothermia. If this treatment fails, pain and sedation medications, mechanical ventilation, neuromuscular blockade, and controlled hyperventilation should be initiated. Instead of this, euvolemia is the goal during resuscitation of TBI, being necessary to administrate FT and inotropic medications.<a class="elsevierStyleCrossRef" href="#bib0390"><span class="elsevierStyleSup">18</span></a></p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Fluid therapy and traumatic brain injury</span><p id="par0060" class="elsevierStylePara elsevierViewall">The Brain Trauma Foundation (BTF) and the Lund Concept are the primary organisms that develop guidelines recommendations for TBI treatment.<a class="elsevierStyleCrossRef" href="#bib0395"><span class="elsevierStyleSup">19</span></a> Both documents have in common the lack of a strong recommendation about which FT is recommended to use in TBI.<a class="elsevierStyleCrossRef" href="#bib0400"><span class="elsevierStyleSup">20</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">Prior to the review of the different FT types, it is important to remark the relevance of vigorous resuscitation to achieve the goal of systolic blood pressure between 90 and 110<span class="elsevierStyleHsp" style=""></span>mmHg.<a class="elsevierStyleCrossRef" href="#bib0395"><span class="elsevierStyleSup">19</span></a> The dose-dependent relation between hypotension and irreversible brain damage has been observed.<a class="elsevierStyleCrossRef" href="#bib0405"><span class="elsevierStyleSup">21</span></a> It is known that TBI is usually related to hemorrhage, usually observed after a delay in bleeding control after normotensive resuscitation was not successful.<a class="elsevierStyleCrossRef" href="#bib0410"><span class="elsevierStyleSup">22</span></a> The authors conclude that hypotension is not recommended in TBI patients. However, hemorrhage control usually does not provide the patient's survival, being necessary to explore this field to improve the outcomes.</p><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Crystalloids</span><p id="par0070" class="elsevierStylePara elsevierViewall">This type of FT contains small water-soluble molecules, being easier to cross the semi-permeable membranes. The osmolarity is similar to plasma, and its sodium levels affect the distribution among the body compartments.<a class="elsevierStyleCrossRef" href="#bib0415"><span class="elsevierStyleSup">23</span></a> The extracellular fluid compartment (ECF) contains 75% of interstitial fluid. It implies that 3–4<span class="elsevierStyleHsp" style=""></span>l of crystalloids are required to replace 1<span class="elsevierStyleHsp" style=""></span>l of blood loss.<a class="elsevierStyleCrossRef" href="#bib0420"><span class="elsevierStyleSup">24</span></a> These values are affected by the patient's status (normovolemic or hypovolaemic).<a class="elsevierStyleCrossRef" href="#bib0425"><span class="elsevierStyleSup">25</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">Frequently used in prehospital admission, no benefits in survival outcomes have been observed, including aggressive resuscitation in hemorrhagic patients.<a class="elsevierStyleCrossRef" href="#bib0430"><span class="elsevierStyleSup">26</span></a> As a result, recent studies suggested that transfusion of red blood cells, plasma, and platelets (ratio 1:1:1) is better than crystalloids due to the diminished risk of hemodilution, brain edema, and inflammation secondary to a large volume of fluids.<a class="elsevierStyleCrossRef" href="#bib0435"><span class="elsevierStyleSup">27</span></a> Ko et al.<a class="elsevierStyleCrossRef" href="#bib0440"><span class="elsevierStyleSup">28</span></a> agree with observing an increase in mortality in patients that received ≥2<span class="elsevierStyleHsp" style=""></span>L during resuscitation compared to those who received less.</p><p id="par0080" class="elsevierStylePara elsevierViewall">The osmolarity of crystalloids is possible to divide this solution into isotonic, hypotonic, and hypertonic. Isotonic solutions include normal saline, Ringer's solution, or plasmalyte. These three types of fluids do not affect the brain water content, being distributed easier in the ECF and intracellular fluid compartment (ICF). However, the most frequently used solution (Ringer) has a lower osmolarity (254<span class="elsevierStyleHsp" style=""></span>mOsm/L compared to 300<span class="elsevierStyleHsp" style=""></span>mOsm/L of the gold standard isotonic solution).<a class="elsevierStyleCrossRef" href="#bib0445"><span class="elsevierStyleSup">29</span></a> This difference explains why large volumes of Ringer could generate brain edema due to increased ICP.<a class="elsevierStyleCrossRef" href="#bib0450"><span class="elsevierStyleSup">30</span></a> Consequently, the use of hypotonic solutions does not have sense and must be avoided.<a class="elsevierStyleCrossRef" href="#bib0445"><span class="elsevierStyleSup">29</span></a></p><p id="par0085" class="elsevierStylePara elsevierViewall">A different type of crystalloid fluid is hypertonic saline (HTS). This treatment is primarily used in patients with elevated ICP due to TBI due to its effect in a small volume during resuscitation.<a class="elsevierStyleCrossRefs" href="#bib0450"><span class="elsevierStyleSup">30,31</span></a> It has been suggested that the beneficial effects of HTS are due to its capability to modulate the innate immune response, especially the neutrophil burst activity. Therefore, an improvement in cardiovascular output and cerebral oxygenation is observed, reducing cerebral edema.<a class="elsevierStyleCrossRef" href="#bib0460"><span class="elsevierStyleSup">32</span></a> However, in clinical practice, these theories are not entirely supported in patients affected by TBI or hemorrhagic shock.<a class="elsevierStyleCrossRef" href="#bib0465"><span class="elsevierStyleSup">33</span></a> One of the largest clinical trials evaluating the neurological outcomes after six months of TBI and mortality rate after 28 days of the event did not observe any benefits.<a class="elsevierStyleCrossRef" href="#bib0465"><span class="elsevierStyleSup">33</span></a> These results agree with a later study of the same group, being necessary to stop the study due to an increase of mortality in a subgroup of patients treated with HTS but not blood transfusion in the first 24<span class="elsevierStyleHsp" style=""></span>h.<a class="elsevierStyleCrossRef" href="#bib0470"><span class="elsevierStyleSup">34</span></a> However, in the literature are also observed positive results using hypertonic saline-dextran solution (HSD) in patients presented with hypotension.<a class="elsevierStyleCrossRef" href="#bib0475"><span class="elsevierStyleSup">35</span></a> These authors observed an increase in survival compared to regular treatment. Rockswold et al.<a class="elsevierStyleCrossRef" href="#bib0480"><span class="elsevierStyleSup">36</span></a> also agree with these results, monitoring a decrease of ICP and increase of CPP and brain oxygenation in patients affected by severe TBI, especially those affected with higher baseline ICP and lower CPP levels. In conclusion, HTS is recommended in TBI patients without conferring a survival benefit in a general manner. However, in patients with intracranial hypertension, its benefits are higher than isotonic crystalloid solutions.</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Synthetic colloids</span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Gelatins</span><p id="par0090" class="elsevierStylePara elsevierViewall">This semi-synthetic colloid is not used in daily practice since it has a high risk of anaphylactic reactions, especially in rapid infusions.<a class="elsevierStyleCrossRefs" href="#bib0425"><span class="elsevierStyleSup">25,37</span></a> Gelatin preparations have a low molecular mass range and a mean molecular weight of 30–35<span class="elsevierStyleHsp" style=""></span>kDa. One of their most important characteristics is their rapid renal excretion (80% molecules<span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>20<span class="elsevierStyleHsp" style=""></span>kDa), increasing the risk of dehydration if the adequate crystalloid infusion is not administered. In addition, their intravascular persistence is short (2–3<span class="elsevierStyleHsp" style=""></span>h), especially in the urea-linked gelatins. Due to the negative charges contained in their molecules, chloride concentrations are lower compared to other colloids. Consequently, intracellular edema could be increased if large amounts of fluids are provided due to its hyposmolality.<a class="elsevierStyleCrossRef" href="#bib0485"><span class="elsevierStyleSup">37</span></a></p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Dextranes</span><p id="par0095" class="elsevierStylePara elsevierViewall">Derived from the action of the bacterium Leuconostoc mesenteroides and mediate via the dextran sucrose enzyme, they are neutral, high-molecular-weight glucopolysaccharides based on glucose monomers. Its excretion is mainly via the kidneys (70%). Different molecules are produced in the hydrolysis grade, being the main characteristic of its capacity as a plasma expander.<a class="elsevierStyleCrossRef" href="#bib0345"><span class="elsevierStyleSup">9</span></a> Blood flow improvement results from a reduction in blood viscosity. In addition, dextrans inhibit platelet adhesiveness, enhances fibrinolysis and reduces factor VIII activity.<a class="elsevierStyleCrossRef" href="#bib0345"><span class="elsevierStyleSup">9</span></a></p><p id="par0100" class="elsevierStylePara elsevierViewall">Modern solutions do not affect blood crossmatching or cause rouleaux formation as previously. However, they may generate renal dysfunction via tubular obstruction, especially in renal insufficiency and hypovolaemia patients. As gelatins, severe anaphylactic reactions like immune complex type III can result from prior cross-immunization against bacterial antigens forming dextran reactive antibodies. However, the incidence is low, especially if monovalent hapten pre-treatment is administered (injection of 3<span class="elsevierStyleHsp" style=""></span>g dextran 1).<a class="elsevierStyleCrossRef" href="#bib0425"><span class="elsevierStyleSup">25</span></a></p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Hydroxyethyl-starch (HES)</span><p id="par0105" class="elsevierStylePara elsevierViewall">HES is a semi-synthetic colloid prepared from amylopectin, a glucose polymer derivative. Its viscosity is lower than dextran or gelatin but does not reach the low viscosity of albumin. The mean molecular weight of the different HES preparations ranges from 70 and 670<span class="elsevierStyleHsp" style=""></span>kDa.<a class="elsevierStyleCrossRef" href="#bib0345"><span class="elsevierStyleSup">9</span></a></p><p id="par0110" class="elsevierStylePara elsevierViewall">The kinetics of this degradation is determined by the molar substitution and the C2/C6 ratio representing the quotient of the numbers of glucose residues hydroxyethylated at positions 2 and 6, respectively.<a class="elsevierStyleCrossRef" href="#bib0345"><span class="elsevierStyleSup">9</span></a> Consequently, its intravascular half-life is observed if a high molar substitution and a high C2/C6 ratio are generated, making the HES molecule less susceptible to plasma amylase.<a class="elsevierStyleCrossRef" href="#bib0345"><span class="elsevierStyleSup">9</span></a></p><p id="par0115" class="elsevierStylePara elsevierViewall">HES activity is also characterized by its capacity to decrease plug capillary induced by sepsis and major trauma and restore macrophage function after hemorrhagic shock. Compared with 20% albumin in these patients, 10% HES significantly improves hemodynamic parameters in the systemic and microcirculation.<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">38</span></a></p><p id="par0120" class="elsevierStylePara elsevierViewall">Like previously commented synthetic colloids, the main problem of HES is its increased risk of acute kidney injury. In the literature are few studies of its benefits in TBI. In a single-center retrospective cohort study of 171 people with severe TBI, 78% of patients received 6% HES 200/0.5 during hospitalization. There was no association with mortality, change in serum creatinine, or establishment of renal injury.<a class="elsevierStyleCrossRef" href="#bib0495"><span class="elsevierStyleSup">39</span></a> Another study performed in 7000 patients admitted in the Intensive Care Unit revealed no significant difference in 90-day mortality between patients resuscitated with 6% HES (130/0.4) or saline. However, an increased risk of renal-replacement therapy was observed in patients who received HES treatment.<a class="elsevierStyleCrossRef" href="#bib0500"><span class="elsevierStyleSup">40</span></a></p></span></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Natural colloids</span><p id="par0125" class="elsevierStylePara elsevierViewall">The main characteristic of colloids is their difficulty crossing semi-permeable membranes due to their larger and more insoluble molecules. The molecular weight, shape, ionic charge, and capillary permeability determine their movement out of the intravascular space and their duration of action.<a class="elsevierStyleCrossRef" href="#bib0505"><span class="elsevierStyleSup">41</span></a> Due to its higher osmolality, colloids increase plasma volume in a higher ratio than the volume infused.<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">38</span></a></p><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Albumin</span><p id="par0130" class="elsevierStylePara elsevierViewall">Albumin is one of the most used colloids, being an effective volume expander without allergic-type reactions and no intrinsic effects on clotting.<a class="elsevierStyleCrossRef" href="#bib0510"><span class="elsevierStyleSup">42</span></a> The literature reveals contradictory results comparing albumin with different fluid therapies. A study compared 4% albumin with 0.9% sodium chloride for resuscitation in patients affected by hemorrhagic shock. In the subpopulation of TBI patients, higher mortality was observed in patients treated with albumin.<a class="elsevierStyleCrossRef" href="#bib0390"><span class="elsevierStyleSup">18</span></a> This result can be supported by the increased risk of brain edema.<a class="elsevierStyleCrossRef" href="#bib0515"><span class="elsevierStyleSup">43</span></a> However, these results do not agree with a previous study performed by Tomita et al.<a class="elsevierStyleCrossRef" href="#bib0520"><span class="elsevierStyleSup">44</span></a> Compared to synthetic colloids, increased survival has not been observed, dismissing its use in clinical practice due to its higher costs.<a class="elsevierStyleCrossRef" href="#bib0525"><span class="elsevierStyleSup">45</span></a> The Lund Concept recommendations continue to support the use of 4% albumin<a class="elsevierStyleCrossRef" href="#bib0400"><span class="elsevierStyleSup">20</span></a> in spite of the evidence of harm.<a class="elsevierStyleCrossRefs" href="#bib0510"><span class="elsevierStyleSup">42,43</span></a></p></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Plasma products</span><p id="par0135" class="elsevierStylePara elsevierViewall">It is observed that high ratios of fresh frozen plasma (FFP) added to packed red blood cells results in an increased ratio of survival compared to massive transfusion.<a class="elsevierStyleCrossRef" href="#bib0530"><span class="elsevierStyleSup">46</span></a> It could be due to the complications associated with the large volume of crystalloid required during resuscitation and its protective effect on the endothelium and endothelial glycocalyx layer and BBB.<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">47</span></a> In the literature, there are few studies about the empirical use of FFP in patients affected by severe TBI. However, their results revealed an increased risk of delayed traumatic intracerebral hematoma formation than 0.9% sodium chloride.<a class="elsevierStyleCrossRefs" href="#bib0540"><span class="elsevierStyleSup">48,49</span></a> Regarding mortality, Zhang et al. did not observe significant differences, observing an increased rate in blood transfusions and coagulopathy in patients treated with FFP.<a class="elsevierStyleCrossRef" href="#bib0545"><span class="elsevierStyleSup">49</span></a> However, the study performed by Etemadrezaie et al. revealed contradictory results, observing a decreased ratio of surveillance without differences in coagulopathy in patients treated with FFP.<a class="elsevierStyleCrossRef" href="#bib0540"><span class="elsevierStyleSup">48</span></a></p><p id="par0140" class="elsevierStylePara elsevierViewall">The administration of plasma has also been studied in a ratio of 1:1:1 (FFP: packed red blood cells: platelet) compared to non-ratio.<a class="elsevierStyleCrossRef" href="#bib0550"><span class="elsevierStyleSup">50</span></a> Patients treated with a ratio-based resuscitation had significantly lower mortality than those who did not, and crystalloid administration was associated with increased odds of death. In addition, it was not observed an increased risk of neurosurgical intervention and intracranial hemorrhage.</p><p id="par0145" class="elsevierStylePara elsevierViewall">Chang et al.<a class="elsevierStyleCrossRef" href="#bib0555"><span class="elsevierStyleSup">51</span></a> evaluated the benefits of early plasma transfusion during resuscitation in patients affected by TBI without polytrauma or intracranial hemorrhage. The authors observed that early plasma transfusion increased survival in patients affected by multifocal intracranial hemorrhage. However, this study divided the patients into different subgroups attending the brain lesion, observing significant differences between them, making it difficult to achieve a conclusion.</p><p id="par0150" class="elsevierStylePara elsevierViewall">The benefits of FFP added to standard care have also been observed in patients affected by TBI and transferred by air from the accident scene to the Emergency Department.<a class="elsevierStyleCrossRef" href="#bib0560"><span class="elsevierStyleSup">52</span></a> Their results revealed an improvement of 30-day survival in patients treated with FFP. In addition, these patients received less crystalloid fluid, vasopressors, and packed red blood cells in the first 24<span class="elsevierStyleHsp" style=""></span>h, had lower international normalized ratios, lower 24<span class="elsevierStyleHsp" style=""></span>h mortality, and lower 30-day mortality. These benefits were mainly observed in severe patients. In addition, these results were also increased if the treatment was initiated early, suggesting that minimizing the time from injury to administration may be necessary.</p></span></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Hyperosmolar fluids</span><p id="par0155" class="elsevierStylePara elsevierViewall">The use of hyperosmolar fluids is not discussed in clinical guidelines.<a class="elsevierStyleCrossRef" href="#bib0400"><span class="elsevierStyleSup">20</span></a> This fluids group contains agents such as HTS (a crystalloid solution) and mannitol, used in patients affected by TBI with cerebral edema and raised ICP.<a class="elsevierStyleCrossRef" href="#bib0465"><span class="elsevierStyleSup">33</span></a> Its benefits are mainly based on its activity after administering a small fluid volume during resuscitation.<a class="elsevierStyleCrossRef" href="#bib0460"><span class="elsevierStyleSup">32</span></a> One of the main characteristics of HTS is its capacity to improve cardiovascular output and cerebral oxygenation while reducing cerebral edema. In addition, innate immune-cell functions seem to be modulated by hypertonicity, specifically neutrophil burst activity, probably beneficial for modulation of the inflammatory response to trauma.<a class="elsevierStyleCrossRef" href="#bib0460"><span class="elsevierStyleSup">32</span></a></p><p id="par0160" class="elsevierStylePara elsevierViewall">HTS and/or mannitol could play an essential role in mitigating the pathophysiological consequences observed in the secondary injury of the brain. In the brain, injured areas promote leukocytes congregation, causing vasodilation and peroxidase/protease-mediated cell death. In addition, cell-mediated immunity could be altered, being moderated by HTS.<a class="elsevierStyleCrossRef" href="#bib0565"><span class="elsevierStyleSup">53</span></a></p><p id="par0165" class="elsevierStylePara elsevierViewall">Hypoxemia results in the depletion of ATP, cellular membrane ion pump dysfunction, increased intracellular sodium levels, and endothelial cell swelling. These disturbs promote narrowing of the vascular lumen, hindering the red blood cells passing through vessels, leading to premature apoptosis of neuronal cells. In addition, a decrease of extracellular sodium reversing the direction of the Na-glutamate cotransporter could be observed due to neuronal depolarization induced by brain injury. As a consequence, an increase in extracellular glutamate is observed, increasing the neurotoxicity.<a class="elsevierStyleCrossRef" href="#bib0570"><span class="elsevierStyleSup">54</span></a> The potential benefits of HTS during resuscitation are based due to its capacity to improve alveolar gas exchange by reducing extravascular lung volume, reversing endothelial and red blood cell swelling, improving blood flow and oxygen delivery and restores extracellular sodium and cellular action potential, moderating glutamate toxicity in the brain.<a class="elsevierStyleCrossRef" href="#bib0575"><span class="elsevierStyleSup">55</span></a></p><p id="par0170" class="elsevierStylePara elsevierViewall">During reperfusion of hypoxemic tissue, the production of radical oxygen species can propagate tissue injury. On the other hand, mannitol may limit the secondary oxidative damage in the brain due to its activity as a scavenger of radical oxygen species.<a class="elsevierStyleCrossRef" href="#bib0580"><span class="elsevierStyleSup">56</span></a></p><p id="par0175" class="elsevierStylePara elsevierViewall">Despite these arguments, the literature did not conclude the role of HTS in patients affected by TBI. Cooper et al.<a class="elsevierStyleCrossRef" href="#bib0585"><span class="elsevierStyleSup">57</span></a> did not observe statistical differences in survival outcomes comparing HTS and saline solution. Bulger et al.<a class="elsevierStyleCrossRef" href="#bib0480"><span class="elsevierStyleSup">36</span></a> compared HTS, HTS/dextran, and normal saline in patients affected by TBI, evaluating the neurological outcome at six months after TBI. The study was finished early due to futility, as the interim analysis could not prove neurological status improvement or mortality at six months. However, in patients with increased ICP, HTS and mannitol effectively decreased it.<a class="elsevierStyleCrossRef" href="#bib0580"><span class="elsevierStyleSup">56</span></a></p><p id="par0180" class="elsevierStylePara elsevierViewall">The literature also compared the beneficial effects of HTS and mannitol. Mangat et al.<a class="elsevierStyleCrossRef" href="#bib0590"><span class="elsevierStyleSup">58</span></a> observed that HTS bolus therapy appears to be superior to mannitol in reducing the combined burden of intracranial hypertension and associated hypoperfusion in severe TBI patients. These results agree with two recent meta-analysis.<a class="elsevierStyleCrossRefs" href="#bib0595"><span class="elsevierStyleSup">59,60</span></a></p><p id="par0185" class="elsevierStylePara elsevierViewall">On the other hand, Wade et al.<a class="elsevierStyleCrossRef" href="#bib0475"><span class="elsevierStyleSup">35</span></a> observed that hypertonic saline-dextran solution (HSD) in patients who presented with hypotension increased survival outcomes compared to standard care. Rockswold et al.<a class="elsevierStyleCrossRef" href="#bib0480"><span class="elsevierStyleSup">36</span></a> also agree with these results, observing a decrease of ICP and the increase of CPP and brain oxygenation in patients affected by severe TBI, especially those with higher baseline ICP and lower CPP levels. In conclusion, HTS is recommended in TBI patients without conferring a survival benefit in a general manner. However, in patients with intracranial hypertension, its benefits are higher than isotonic crystalloid solutions.</p></span></span><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Conclusions</span><p id="par0190" class="elsevierStylePara elsevierViewall">The literature does not observe a “gold standard” of fluid therapy on TBI treatment. In addition, the presence of acute hemorrhage or hemorrhagic shock difficult for the outcomes is frequently observed in these patients. Crystalloids and hyperosmolar fluids (especially in patients with increased ICP) could be the most beneficial treatments, being Ringer less desirable than other isotonic crystalloids. In addition, the use of plasma products during resuscitation may convey an improved outcome, especially in the out-of-hospital environment. Future clinical studies should focus on the effect of specific fluid prescriptions and osmotic agents on short- and long-term outcomes.</p></span><span id="sec0070" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Funding</span><p id="par0195" class="elsevierStylePara elsevierViewall">No external funding sources.</p></span><span id="sec0075" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0095">Conflict of interests</span><p id="par0200" class="elsevierStylePara elsevierViewall">The authors have no conflict of interest to declare. The authors declared that this study has received no financial support.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:11 [ 0 => array:3 [ "identificador" => "xres2008324" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec1720694" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres2008325" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec1720693" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Pathophysiology of traumatic brain injury" ] 6 => array:3 [ "identificador" => "sec0015" "titulo" => "Fluid therapy and traumatic brain injury" "secciones" => array:4 [ 0 => array:2 [ "identificador" => "sec0020" "titulo" => "Crystalloids" ] 1 => array:3 [ "identificador" => "sec0025" "titulo" => "Synthetic colloids" "secciones" => array:3 [ 0 => array:2 [ "identificador" => "sec0030" "titulo" => "Gelatins" ] 1 => array:2 [ "identificador" => "sec0035" "titulo" => "Dextranes" ] 2 => array:2 [ "identificador" => "sec0040" "titulo" => "Hydroxyethyl-starch (HES)" ] ] ] 2 => array:3 [ "identificador" => "sec0045" "titulo" => "Natural colloids" "secciones" => array:2 [ 0 => array:2 [ "identificador" => "sec0050" "titulo" => "Albumin" ] 1 => array:2 [ "identificador" => "sec0055" "titulo" => "Plasma products" ] ] ] 3 => array:2 [ "identificador" => "sec0060" "titulo" => "Hyperosmolar fluids" ] ] ] 7 => array:2 [ "identificador" => "sec0065" "titulo" => "Conclusions" ] 8 => array:2 [ "identificador" => "sec0070" "titulo" => "Funding" ] 9 => array:2 [ "identificador" => "sec0075" "titulo" => "Conflict of interests" ] 10 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2023-02-08" "fechaAceptado" => "2023-03-10" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec1720694" "palabras" => array:4 [ 0 => "Traumatic brain injury" 1 => "Fluid therapy" 2 => "Intracranial hypertension" 3 => "Osmotherapy" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec1720693" "palabras" => array:4 [ 0 => "Traumatismo craneoencefálico" 1 => "Fluidoterapia" 2 => "Hipertensión intracraneal" 3 => "Osmoterapia" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Traumatic brain injury (TBI) is an important health and social problem. The mechanism of damage of this entity could be divided into two phases: (1) a primary acute injury because of the traumatic event; and (2) a secondary injury due to the hypotension and hypoxia generated by the previous lesion, which leads to ischemia and necrosis of neural cells. Cerebral edema is one of the most important prognosis markers observed in TBI. In the early stages of TBI, the cerebrospinal fluid compensates the cerebral edema. However, if edema increases, this mechanism fails, increasing intracranial pressure. To avoid this chain effect, several treatments are applied in the clinical practice, including elevation of the head of the bed, maintenance of normothermia, pain and sedation drugs, mechanical ventilation, neuromuscular blockade, controlled hyperventilation, and fluid therapy (FT).</p><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">The goal of FT is to improve the circulatory system to avoid the lack of oxygen to organs. Therefore, rapid and early infusion of large volumes of crystalloids is performed in clinical practice to restore blood volume and blood pressure. Despite the relevance of FT in the early management of TBI, there are few clinical trials regarding which solution is better to apply.</p><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">The aim of this study is to provide a narrative review about the role of the different types of FT used in the daily clinical practice on the management of TBI. To achieve this objective, a physiopathological approach to this entity will be also performed, summarizing why the different types of FT are used.</p></span>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">El traumatismo craneoencefálico (TCE) es un importante problema sanitario y social. El mecanismo de daño de esta entidad se podría dividir en dos fases: 1) una lesión aguda primaria a causa del evento traumático, y 2) una lesión secundaria por la hipotensión e hipoxia generada por la lesión anterior, que conduce a la isquemia y necrosis de las células neurales. El edema cerebral es uno de los marcadores pronósticos más importantes observados en el TCE. En las primeras etapas de TCE, el líquido cefalorraquídeo compensa el edema cerebral. Sin embargo, si aumenta el edema, este mecanismo falla, aumentando la presión intracraneal. Para evitar este efecto en cadena, en la práctica clínica se aplican varios tratamientos, entre ellos la elevación de la cabecera de la cama, el mantenimiento de la normotermia, los fármacos para el dolor y la sedación, la ventilación mecánica, el bloqueo neuromuscular, la hiperventilación controlada y la fluidoterapia (FT).</p><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">El objetivo de la FT es mejorar el sistema circulatorio para evitar la falta de oxígeno a los órganos. Por lo tanto, en la práctica clínica se realiza una infusión rápida y temprana de grandes volúmenes de cristaloides para restablecer el volumen sanguíneo y la presión arterial. A pesar de la relevancia de la FT en el manejo temprano del TCE, existen pocos ensayos clínicos sobre qué solución es mejor aplicar.</p><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">El objetivo de este estudio es proporcionar una revisión narrativa sobre el papel de los diferentes tipos de FT utilizados en la práctica clínica diaria en el manejo del TCE. Para lograr este objetivo, también se realizará un abordaje fisiopatológico de esta entidad, resumiendo por qué se utilizan los diferentes tipos de FT.</p></span>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:60 [ 0 => array:3 [ "identificador" => "bib0305" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "The epidemiology and impact of traumatic brain injury: a brief overview" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "J.A. Langlois" 1 => "W. Rutland-Brown" 2 => "M.M. 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