Ten physiological commandments for severe head injury.

Advances in multiparametric brain monitoring have allowed us to deepen our knowledge of the physiopathology of head injury and how it can be treated using the therapies available today. It is essential to understand and interpret a series of basic physiological and physiopathological principles that, on the one hand, provide an adequate metabolic environment to prevent worsening of the primary brain injury and favour its recovery, and on the other hand, allow therapeutic resources to be individually adapted to the specific needs of the patient. Based on these notions, this article presents a decalogue of the physiological objectives to be achieved in brain injury, together with a series of diagnostic and therapeutic recommendations for achieving these goals. We emphasise the importance of considering and analysing the physiological variables involved in the transport of oxygen to the brain, such as cardiac output and arterial oxygen content, together with their conditioning factors and possible alterations. Special attention is paid to the basic elements of physiological neuroprotection, and we describe the multiple causes of cerebral hypoxia, how to approach them, and how to correct them. We also examine the increase in intracranial pressure as a physiopathological element, focussing on the significance of thoracic and abdominal pressure in the interpretation of intracranial pressure. Treatment of intracranial pressure should be based on a step-wise model, the first stage of which should be based on a physiopathological reflection combined with information on the tomographic lesions rather than on rigid numerical values.

Ten physiological commandments for severe head injury. / Diez mandamientos fisiológicos a lograr durante el traumatismo craneoencefálico grave.

Advances in multiparametric brain monitoring have allowed us to deepen our knowledge of the physiopathology of head injury and how it can be treated using the therapies available today. It is essential to understand and interpret a series of basic physiological and physiopathological principles that, on the one hand, provide an adequate metabolic environment to prevent worsening of the primary brain injury and favour its recovery, and on the other hand, allow therapeutic resources to be individually adapted to the specific needs of the patient. Based on these notions, this article presents a decalogue of the physiological objectives to be achieved in brain injury, together with a series of diagnostic and therapeutic recommendations for achieving these goals. We emphasise the importance of considering and analysing the physiological variables involved in the transport of oxygen to the brain, such as cardiac output and arterial oxygen content, together with their conditioning factors and possible alterations. Special attention is paid to the basic elements of physiological neuroprotection, and we describe the multiple causes of cerebral hypoxia, how to approach them, and how to correct them. We also examine the increase in intracranial pressure as a physiopathological element, focussing on the significance of thoracic and abdominal pressure in the interpretation of intracranial pressure. Treatment of intracranial pressure should be based on a step-wise model, the first stage of which should be based on a physiopathological reflection combined with information on the tomographic lesions rather than on rigid numerical values.

Paroxysmal sympathetic hyperactivity: An entity to keep in mind. / Hiperactividad simpática paroxística: una entidad que no debería pasar desapercibida.

Paroxysmal sympathetic hyperactivity (PSH) is a potentially life-threatening neurological emergency secondary to multiple acute acquired brain injuries. It is clinically characterized by the cyclic and simultaneous appearance of signs and symptoms secondary to exacerbated sympathetic discharge. The diagnosis is based on the clinical findings, and high alert rates are required. No widely available and validated homogeneous diagnostic criteria have been established to date. There have been recent consensus attempts to shed light on this obscure phenomenon. Its physiopathology is complex and has not been fully clarified. However, the excitation-inhibition model is the theory that best explains the different aspects of this condition, including the response to treatment with the available drugs. The key therapeutic references are the early recognition of the disorder, avoiding secondary injuries and the triggering of paroxysms. Once sympathetic crises occur, they must peremptorily aborted and prevented. of the later the syndrome is recognized, the poorer the patient outcome.

Urotensinergic system genes in experimental subarachnoid hemorrhage.

OBJECTIVE: Cerebral vasospasm, one of the main complications of subarachnoid hemorrhage (SAH), is characterized by arterial constriction and mainly occurs from day 4 until the second week after the event. Urotensin-II (U-II) has been described as the most potent vasoconstrictor peptide in mammals. An analysis is made of the serum U-II concentrations and mRNA expression levels of U-II, urotensin related peptide (URP) and urotensin receptor (UT) genes in an experimental murine model of SAH. DESIGN: An experimental study was carried out. SETTING: Experimental operating room of the Biomedicine Institute of Seville (IBiS), Virgen del Rocío University Hospital (Seville, Spain). PARTICIPANTS: 96 Wistar rats: 74 SAH and 22 sham intervention animals. INTERVENTIONS: Day 1: blood sampling, followed by the percutaneous injection of 100µl saline (sham) or blood (SAH) into the subarachnoid space. Day 5: blood sampling, followed by sacrifice of the animals. MAIN VARIABLES OF INTEREST: Weight, early mortality, serum U-II levels, mRNA values for U-II, URP and UT. RESULTS: Serum U-II levels increased in the SAH group from day 1 (0.62pg/mL [IQR 0.36-1.08]) to day 5 (0.74pg/mL [IQR 0.39-1.43]) (p<0.05), though not in the sham group (0.56pg/mL [IQR 0.06-0.83] day 1; 0.37pg/mL [IQR 0.23-0.62] day 5; p=0.959). Between-group differences were found on day 5 (p<0.05). The ROC analysis showed that the day 5 serum U-II levels (AUC=0.691), URP mRNA (AUC=0.706) and UT mRNA (AUC=0.713) could discriminate between sham and SAH rats. The normal serum U-II concentration range in rats was 0.56pg/mL (IQR 0.06-0.83). CONCLUSION: The urotensinergic system is upregulated on day 5 in an experimental model of SAH.

[Usefulness of biomarkers in the prognosis of severe head injuries]. / Utilidad de los biomarcadores en el pronóstico del traumatismo craneoencefálico grave.

Severe head injuries have a great socioeconomic and public health impact. Despite progress in diagnosis and treatment, no sufficiently reliable predictive models have been established for developing clinical trials and promoting effective therapeutic strategies capable of improving the prognosis. In the last decades, several brain damage biomarkers have been studied as potential diagnostic and prognostic tools in traumatic brain injury. However, all of them have limitations that preclude their universalized application. The properties of the known biomarkers -both those traditionally shown to correlate with severity and prognosis, and those recently announced as promising options- should be analyzed. New studies are needed to define their properties, both isolatedly and in combined use.

Severe Supratentorial Intracerebral Hemorrhage: Factors Related to Brain Death Development.

OBJECTIVE: This study sought to identify clinical variables that may contribute to the development of brain death (BD) in patients with severe supratentorial intracerebral hemorrhage (ICH). METHODS: A prospective observational study was carried out from 2012 to 2014 and included patients with severe supratentorial ICH (Glasgow Coma Score ≤ 8). Exclusion criteria included aneurysmal or traumatic hemorrhage origin and hemorrhagic transformation of previous ischemic stroke. The following data were collected: clinical variables (past medical history, clinical severity at admission), head computed tomography scan findings, laboratory data, neurosurgical procedures, and immediate complications. Univariate tests and logistic regression analyses were performed to assess the predictive ability of these variables and identify patients at high risk of progression to BD. RESULTS: A total of 140 patients with severe supratentorial ICH (median age, 60; 68.6% male) were included. Of these 140 cases, 24 progressed to BD. In the multivariate analysis, the following variables were independently associated with BD outcome after supratentorial ICH: a history of arterial hypertension (odds ratio [OR], 11.254; P = .003), anticoagulant therapy (OR, 3.561; P = .050), presence of photomotor impairment at admission (OR, 7.095; P = .001), rebleeding after supratentorial ICH (OR, 5.613; P = .010), and no neurosurgical hematoma evacuation in ICH (OR, 8.314; P = .001). CONCLUSIONS: Certain clinical variables are predictive of an increased risk for BD development after supratentorial ICH. This information would be useful for transplant coordinators, permitting early identification of at-risk patients and increasing the availability of potential donors.

Acute predictors for mortality after severe TBI in Spain: Gender differences and clinical data.

OBJECTIVE: The main objective of this study is to determine whether gender affects global mortality and functional outcome after severe traumatic brain injury (TBI). METHODS: This retrospective cohort study included 629 patients with severe TBI (14.9% female) admitted to the ICU of a university hospital. Patients were split into gender groups to study potential differences in global mortality and functional outcome at ICU discharge and 6 months post-trauma using the GOS. The following variables were analysed: age, intracranial injury, injury mechanism, injury severity, factors contributing to secondary brain injury, monitoring level, treatment, complications, length of stay in the ICU and cause of death. RESULTS: No differences were found between gender groups in neuromonitoring level or surgical procedures. Women had higher APACHE II scores, a higher incidence of pre-hospital hypotension, anaemia and transfusion and higher mortality rates in the ICU (OR = 1.74; 95% CI = 1.09-2.77) and 6 months post-trauma (OR = 1.65; 95% CI = 1.02-2.67). There were no significant differences in functional outcome at ICU discharge or 6 months post-injury. The multivariate analysis did not show gender as an independent predictive factor in mortality after severe TBI. CONCLUSION: In this study, gender was not found to be an independent predictor for poorer outcome after severe TBI.

Predictors of mortality and poor functional outcome in severe spontaneous intracerebral hemorrhage: a prospective observational study.

OBJECTIVE: To analyze mortality and functional outcome in patients with severe spontaneous intracerebral hemorrhage (ICH), and identify the clinical characteristics, radiological findings and therapeutic procedures predictive of mortality in the Intensive Care Unit (ICU) and during hospitalization, as well as of poor functional results at 6 months. DESIGN: A prospective, observational study was carried out. SETTING: Neurocritical Care Unit of a university hospital. PATIENTS: Patients diagnosed with ICH were included over a period of 23 months. VARIABLES OF INTEREST: Demographic characteristics, cardiovascular risk factors, regular medication, laboratory test parameters, cranial CT findings, therapeutic procedures and outcome data. INTERVENTION: None. RESULTS: A total of 186 patients with ICH met the inclusion criteria. Surgery to evacuate ICH was performed in 25.8% of the patients. The mortality rate was 46.7%. The modified Rankin score at 6 months was 5 (RI: 4.6). Multivariate Cox regression analysis showed the presence of diabetes, prior anticoagulation, as well as APACHE II severity and the type of bleeding on the cranial CT scan to be predictors of mortality and poor functional outcomes. On the other hand, neurosurgical procedures and intracranial pressure (ICP) monitoring were associated with better outcomes. CONCLUSION: The presence of comorbidities such as diabetes, or previous anticoagulation, as well as the CT findings were associated to poorer outcomes. In contrast, ICP monitoring and early neurosurgery were predictive of longer survival and better functional outcomes.

[Intracranial pressure monitoring in severe traumatic brain injury: A different perspective of the BestTrip trial]. / Monitorización de la presión intracraneal en el traumatismo craneoencefálico grave: otra visión del Best Trip trial.

The present study outlines a series of questions and reflections upon the recent publication of Chesnut et al., who compared 2 approaches to the treatment of intracranial hypertension (ICH) in severe head injuries: one with and the other without intracranial pressure monitoring (ICP). The authors concluded that no improved outcome was observed in the treatment group guided by ICP monitoring. The main concerns relate to the degree of training of the physicians involved in the monitoring and management of ICH in the ICP group, as well as to the possible inter-observer variability in interpreting the CT scans, the capacity of clinical signs to guide the treatment of ICH, and the suitability of randomization. The analysis of this trial should not be taken to suggest the futility of ICP monitoring but rather the need to correctly use the information afforded by ICP monitoring, with emphasis on the importance of the definition of alternative methods for non-invasive monitoring.