[High-altitude retinopathy]. / Retinopatía de gran altura.

CASE REPORT: This case report presents a 36 year-old male with a sudden loss of vision while taking part in an expedition in the Daulaghiri (8,167 metres high peak located in the Himalayan Mountain Range). DISCUSSION: High altitude retinal haemorrhage is a common condition in those mountaineers who reach altitudes over 5,500m. Depending on its location it may not present any symptoms and the condition improves with no further complications. However, in case of macular involvement the vision decreases dramatically and the consequences are uncertain.

Retinopatía de gran altura / High-altitude retinopathy

Caso Clínico: Varón de 36 años que presenta pérdida súbita de visión central, durante una expedición al Daulaghiri (cordillera del Himalaya), de 8.167 m de altitud. Discusión: Las hemorragias retinianas de la altura son una manifestación frecuente en montañeros que superan los 5.500 m de altitud. Según su localización puede cursar deforma asintomática y suele evolucionar favorablemente. En caso de afectación macular, la visión disminuye de forma drástica y el pronóstico es incierto(AU)

Case report: This case report presents a 36 year-old male with a sudden loss of vision while taking part in an expedition in the Daulaghiri (8,167 metres high peak located in the Himalayan Mountain Range).Discussion: High altitude retinal haemorrhage is a common condition in those mountaineers who reach altitudes over 5,500 m. Depending on its location it may not present any symptoms and the condition improves with no further complications. However, in case of macular involvement the vision decreases dramatically and the consequences are uncertain(AU)

Criterios de respuesta cualitativos en la batería de habilidades interpersonales en personas mayores / No disponible

Fundamentos: El objetivo de este estudio consiste en analizarel papel desempeñado por el género y el lugar deresidencia habitual en el nivel de inteligencia (académicae interpersonal) y satisfacción con la vida en la terceraedad.Método: La muestra que ha participado en el estudioconsta de 100 jubilados con edades comprendidas entre60 y 95 años. Del total de la muestra, el 46% habitandiariamente en una residencia para la tercera edad, mientrasque el 54% restante viven en sus hogares y de vez encuando asisten a centros sociales para personas mayores.Los participantes completaron tres cuestionarios: unopara evaluar el índice de satisfacción con la vida, otropara evaluar el nivel de inteligencia académica y un terceropara medir las habilidades interpersonales en personasmayores.Resultados y discusión: En términos generales, el lugarde residencia habitual desempeña un papel diferencialmayor que el género. Respecto a éste, las mujeres puntúanmás alto que los varones en la toma de perspectivas concomponente emocional negativo, mientras que los varonespuntúan más alto en el pensamiento causal con responsabilidadexterna. En cuanto al lugar de residenciahabitual, los que viven en sus hogares puntúan más altoen el nivel de inteligencia académica y en mássubdimensiones de la batería de habilidades interpersonalesque los que viven en residencias. Por otro lado,las personas que viven en residencias puntúan más altoen el índice de satisfacción con la vida. En la discusión secomentan las implicaciones de este estudio para la investigaciónfutura, intervención y programas de prevenciónque ayuden a mejorar la calidad de vida de nuestrosmayores

Grounds: The aim of this study is to explore the functionof gender and place of residence in the level of intelligence(both academic and interpersonal) and satisfaction withlife in the elders.Methods: A total of 100 retired people, aged 60 to 95,took part in this study. A total of 46% of the participants live in elderly hospitals while the 54% remaining lives intheir homes and occasionally go to leisure social centersfor elderly people. The participants completed threequestionnaires: the first one measured the index ofsatisfaction with life, the second one assessed the level ofacademic intelligence and the last one measured theinterpersonal skills for old age.Results and discussion: The results showed that the placeof residence is more important than the gender. Females,compared with males, scored higher in the take ofperspectives with a negative emotional component,whereas males scored higher in the causal thought withexternal responsibility. However, the place of residenceshowed more principal effects in the subdimensions ofthe battery of interpersonal skills. The participants livingin their houses scored higher in the level of academicintelligence and in more subdimensions of the battery ofinterpersonal skills. While participants living in elderlyhospitals scored higher in the index of satisfaction withlife. In the discussion we remark the implications of thisstudy for the future research that allows to create programsto training our elderly people in these skills to improvetheir quality of live

Coexistence of regional cerebral hypoxia with normal or hyperemic brain detected by global monitoring methods. Analysis of apparently contradictory findings based on the Siggaard-Andersen model of tissue hypoxia.

The aim of our study was to perform and in-depth analysis of several episodes of regional brain hypoxia detected by monitoring brain partial pressure of oxygen (PtiO2) in which simultaneous measurements of cerebral oxygen extraction fraction (O2EF) suggested a normally perfused or even a hyperemic brain. To gain deeper insight into these episodes, we used the model of tissue hypoxia described by Siggaard-Andersen. In 244 simultaneous measurements, 31 episodes (12.7%) of brain hypoxia (PtiO2 < or = 15 mmHg) were detected simultaneously with an O2EF within the normal range or below the lowest normal percentile. Using Siggaard-Andersen methodology, we classified 6 episodes (19%) as high-affinity hypoxia and 25 (81%) as shunt hypoxia or dysperfusion hypoxia. Siggaard-Andersen's comprehensive classification of tissue hypoxia can be used as an integrative model to build coherent algorithms for diagnosing and managing neurocritical patients that are at risk of brain hypoxia due to either intracranial or extracranial conditions.

[First tier measures in the treatment of intracranial hypertension in the patient with severe craniocerebral trauma. Proposal and justification of a protocol]. / Medidas de primer nivel en el tratamiento de la hipertensión intracraneal en el paciente con un traumatismo craneoencefálico grave. Propuesta y justificación de un protocolo.

The management of severe head injuries in general and that of high intracranial pressure (ICP) in particular are among the most challenging tasks in neurocritical care. One of the difficulties still faced by clinicians is that of reducing variability among centers when implementing management protocols. The purpose of this paper is to propose a standardized protocol for the management of high ICP after severe head injury, consistent with recently published clinical practice guidelines and other clinical evidence such as that provided by the systematic reviews of the Cochrane Collaboration. Despite significant advances in neuromonitoring, deeper insight into the physiopathology of severe brain trauma and the many therapeutic options available, standardized protocols are still lacking. Recently published guidelines provide sketchy recommendations without details on how and when to apply different therapies. Consequently, great variability exists in daily clinical practice even though different centers apply the same evidence-based recommendations. In this paper we suggest a structured protocol in which each step is justified and integrated into an overall strategy for the management of severe head injuries. The most recent data from both the preliminary and definitive results of randomized clinical trials as well as from other sources are discussed. The main goal of this article is to provide neurotraumatology intensive care units with a unified protocol that can be easily modified as new evidence becomes available. This will reduce variation among centers when applying the same therapeutic measures. This goal will facilitate comparisons in outcomes among different centers and will also enable the implementation of more consistent clinical practice in centers involved in multicenter clinical trials.

Medidas de primer nivel en el tratamiento de la hipertensión intracraneal en el paciente con un traumatismo craneoencefálico grave. Propuesta y justificación de un protocolo / First tier therapeutic measures in the management of high intracranial pressure after severe head injury. Rationale and proposal for a protocol

El manejo de los traumatismos craneoencefálicos graves en general y de aquéllos que presentan una hipertensión intracraneal en particular, es uno de los desafíos más importantes en el manejo del paciente neurocrítico. Una de las principales dificultades con las que aún se enfrentan los clínicos es la de intentar reducir la variabilidad que todavía existe entre centros en la implementación de protocolos de tratamiento en estos pacientes. El objeto de este artículo es proponer un protocolo estandarizado para el manejo de la hipertensión intracraneal en los traumatismos craneoencefálicos graves (TCEG), que siga las directrices propuestas por las guías de práctica clínica recientemente publicadas y también otra evidencia clínica, como la aportada por las revisiones sistemáticas de la Colaboración Cochrane. A pesar de los avances significativos en la neuromonitorización que han permitido profundizar en la fisiopatología de los TCEG, y de las diversas opciones terapéuticas disponibles, aún no existen protocolos estandarizados para el tratamiento de estos pacientes. Aunque las guías de práctica clínica, recientemente publicadas, ofrecen recomendaciones generales, no aportan detalles explícitos sobre cómo y cuando aplicar estas recomendaciones terapéuticas. Como consecuencia, existe todavía una gran variabilidad en la práctica clínica diaria incluso entre aquellos centros que aplican las mismas medidas terapéuticas. En este artículo se propone un protocolo estructurado, en el que cada paso se justifica e integra dentro de una estrategia global para el manejo de los traumatismos craneoencefálicos graves. Se discuten los datos disponibles más recientes, procedentes de ensayos clínicos controlados tanto preliminares como definitivos, así como de otras fuentes. El principal objetivo de este artículo es dotar a las unidades de neurocríticos de un protocolo unificado que pueda ser fácilmente modificado a medida que se disponga de nueva información basada en evi dencia clase I o II. Esto permite reducir la variabilidad que existe entre centros que aplican las mismas medidas terapéuticas. Por otra parte, este protocolo puede facilitar la comparación de los resultados neurológicos entre diferentes hospitales haciendo más fácil a su vez la implantación de una práctica clínica más uniforme en aquellos centros implicados en estudios clínicos multicéntricos. (AU)

[The use of moderate hypothermia in the treatment of patients with severe craniocerebral trauma]. / Reflexiones sobre el uso de la hipotermia moderada en el tratamiento del paciente con un traumatismo craneoencefálico grave.

Traumatic brain injury initiates several metabolic processes that can increase the primary injury. It is well established that in severe head injuries, posttraumatic secondary insults, such as brain hypoxia, hypotension or anemia, exacerbate neuronal injury and lead to a poorer outcome. Experimental and clinical evidence suggests that moderate hypothermia (32-34 degrees C), may limit some of these deleterious secondary metabolic responses. Recent laboratory studies and prospective controlled clinical trials of induced moderate hypothermia for relatively short periods (24-48 h) in patients with severe head injury, have demonstrated good intracranial pressure control and better outcome when compared with patients maintained in normothermia and given conventional treatment. Despite its proven clinical role in neuroprotection, hypothermia research has been inconstantly followed for various reasons. In this paper we review the mechanisms of neuroprotection in hypothermia, the different preclinical and clinical studies that favor its use as a neuroprotector in severe head injury or in patients in whom high intracranial pressure is refractory to first tier measures. The evidence that favors hypothermia is discussed. We also discuss the negative results of the still unpublished multicentre trial on prophylactic moderate hypothermia developed in the USA. The main problem with moderate hypothermia is the lack of a systematic methodology to induce and maintain it. Also, optimal duration of its use and the methodology and timing for rewarming have not been determined. Consequently, the results of different trials are difficult to analyze and compare. However, most evidence suggests that hypothermia provides remarkable protection against the adverse effects of neuronal damage that is exacerbated by secondary injury. Further prospective controlled trials with clearly defined methodology are needed before this method is implemented in daily clinical practice. The most important task for the years to come may be to focus on refining this procedure, defining the optimal time of cooling and rewarming and to optimize the methods of rapidly inducing and maintaining low temperature. It is also essential to define the most appropriate method and velocity of the rewarming phase, in which many successfully controlled patients deteriorate and die.

Influence of remote substituents on the equatorial/axial selectivity in the monooxygenation of methylene C--H bonds of substituted cyclohexanes.

The reactivity of individual C--H bonds in the methyl(trifluoromethyl)dioxirane TFDO oxygenation of stereogenic methylene groups in conformationally homogeneous monosubstituted cyclohexanes (2) has been determined. The unexpectedly high occurrence of O-atom insertion into C--H(ax) bonds suggests an in plane trajectory attack in the oxygenation while the diastereoselectivity of the reaction is qualitatively interpreted on the basis of the distinct hyperconjugative stabilization by the substituent of diastereomeric transition states due to long-range through bond interactions.

Lesión postraumática de la arteria carótida.Valoración del diagnóstico clinicorradiológico / Posttraumatic lesion of the carotid artery. Evaluation of the clinico-radiological diagnosis

Introducción. Las lesiones vasculares postraumáticas de la arteria carótida (LPAC) son poco frecuentes pero tienen una elevada morbimortalidad por lo cual es importante su diagnóstico y tratamiento precoz. Objetivo. Revisar los hallazgos clínicos y radiológicos de la LPAC con la hipótesis de que existen signos que permiten su diagnóstico precoz. Pacientes y métodos. Estudio retrospectivo de 9 pacientes (p) con LPAC. Resultados. La causa fue un accidente de tráfico (4 p), precipitación (1p) o un movimiento brusco cervical aislado (4 p). La clínica inicial era de dolor cervical (1 p), hipoacusia (1p), síndrome de Claude-Bernard-Horner (4 p) o síntomas de un ataque vascular cerebral (6 p). La TC craneal mostraba un infarto cerebral de arteria cerebral media (6 p), una hemorragia subaracnoidea (1 p) o era normal (3 p). El diagnóstico de la lesión vascular se realizó mediante resonancia magnética (9 p), arteriografía (5 p) y ecografía-Doppler (4 p). Las lesiones vasculares fueron: estenosis grave por trombosis mural (3 p), oclusión por trombosis completa (4 p) y pseudoaneurisma (2p).Conclusiones. La LPAC se debe sospechar tras un traumatismo craneofacial-cervical cuando ha habido un movimiento cervical brusco, cuando existe un síndrome de Claude-Bernard-Horner o cuando se demuestra un infarto cerebral de arteria cerebral media (AU)

[Post-traumatic lesion of the carotid artery. Evaluation of the clinico-radiological diagnosis]. / Lesión postraumática de la arteria carótida. Valoración del diagnóstico clinicorradiológico.

INTRODUCTION: Posttraumatic vascular lesions of the carotid artery (PLCA) are infrequent but have a high morbid-mortality, so early diagnosis and treatment is important. OBJECTIVE: To review the clinical and radiological findings of the PLCA with the hypothesis that there are signs which permit early diagnosis. PATIENTS AND METHODS: A retrospective study of 9 patients (p) with PLCA. RESULTS: The cause was road traffic accident (4p), fall (1p) or a single abrupt cervical movement (4p). The initial clinical feature was cervical pain (1p), deafness (1p), Claude-Bernard-Horner syndrome (4p) or symptoms of a cerebral vascular accident (6p). Cranial CT showed a cerebral infarct in the territory of the middle cerebral artery (6p), subarachnoid hemorrhage (1p) or normal (3p). Diagnosis of the vascular lesion was made using magnetic resonance (9p), arteriography (5p) and echo-Doppler (4p). The vascular lesions were: severe stenosis due to a mural thrombosis (3p), complete obstruction due to thrombosis (4p) and pseudoaneurysm (2p). CONCLUSIONS: PLCA should be suspected following craniofacial-cervical trauma when there was an abrupt neck movement, a Claude-Bernard-Horner syndrome is present or a cerebral infarct in the territory of the middle cerebral artery is shown.

False autoregulation (pseudoautoregulation) in patients with severe head injury. Its importance in CPP management.

False autoregulation has been described as an alteration of autoregulation in which the apparent maintenance of a constant cerebral blood flow (CBF) when increasing cerebral perfusion pressure (CPP) is due to an increase in brain tissue pressure. The objective of our study was to investigate how often false autoregulation occurred in patients with a severe head injury. In forty-six patients with a moderate or severe head injury autoregulation was studied using arteriojugular differences of oxygen (AVDO2) to estimate changes in CBF after inducing arterial hypertension with phenylephrine. Changes in mean arterial blood pressure (MABP), intracranial pressure (ICP), cerebral perfusion pressure (CPP) and AVDO2 were calculated before and after inducing hypertension. Ninety-five episodes of provoked hypertension were studied in 46 patients. In 28 tests (29.5%) a constant or even reduced CBF was detected simultaneously with a median increase in parenchymal ICP of 8.5 mm Hg (false autoregulation). In this group the median of the induced increase in MABP was 20.6 mm Hg with a median increase in CPP of 11.5 mm Hg. From our data we can conclude that false autoregulation is frequently found in patients after a severe head injury. Increasing MABP to obtain a better CPP in these patients is not beneficial because CBF is not modified or may even be reduced.

Evaluation of cerebrovascular CO2-reactivity and autoregulation in patients with post-traumatic diffuse brain swelling (diffuse injury III).

The present study was undertaken to elucidate the status of autoregulation and CO2-reactivity soon after injury in patients with a post-traumatic diffuse bilateral brain swelling. A prospective study was carried out in 31 consecutively admitted patients with a severe head injury and a Diffuse Brain Injury type III, following the definition stated by the Traumatic Coma Data Bank classification. To evaluate CO2-reactivity, AVDO2 was measured before and after ventilator manipulations. Assuming a constant CMRO2 during the test, changes in 1/AVDO2 reflect changes in CBF. Patients with changes in estimated CBF below or equal to 1% were included in the impaired/abolished CO2-reactivity group. To test autoregulation, hypertension was induced using phenylephrine. Arterial and jugular blood samples were taken to calculate AVDO2 before and after a steady state of MABP was obtained. Cerebrovascular response to CO2 was globally preserved in all but two cases (6.5%). In contrast, autoregulation was globally preserved in 10 (32.3%) and impaired/abolished in 21 cases (67.7%). Our data do not support the premise that increasing cerebral perfusion pressure by inducing arterial hypertension is beneficial in those patients with a diffuse brain swelling in whom autoregulation is impaired or abolished. Clinical implications for treatment are discussed.

Cerebral hemodynamic changes during sustained hypocapnia in severe head injury: can hyperventilation cause cerebral ischemia?

Hyperventilation (HV) is routinely used in the management of increased intracranial pressure (ICP) in severe head injury. However, this treatment continues to be controversial because it has been reported that long-lasting reduced cerebral blood flow (CBF) due to profound sustained hypocapnia may contribute to the development or deterioration of ischemic lesions. Our goal in this study was to analyze the effects of sustained hyperventilation on cerebral hemodynamics (CBF, ICP) and metabolism (arterio jugular differences of lactates = AVDL). CO2-reactivity and CBF was estimated using AVDO2 (arteriojugular differences of oxygen content). Global cerebral ischemia and increased anaerobic metabolism were considered according to AVDO2 and AVDL respectively. Thirty-three patients with severe and moderate head injury and increased ICP were included. Within 72 hours after accident, patients were hyperventilated for a period of 4 hours. During this time jugular oxygen saturation (SjO2), arterial oxygen saturation (SaO2), ICP, mean arterial blood pressure (MABP), AVDO2 and AVDL were recorded. In our study, most patients preserved CO2-reactivity (88.2%). In these cases HV was very effective in lowering ICP. Our findings showed that this reduction was due to a CBF decrease. According to basal AVDO2 twenty-five patients (75.7%) were considered as hyperemic and eight (24.2%) as not hyperemic. Global ischemia and increased anaerobic metabolism were detected in one case in the non-hyperemic group. According to AVDO2 and AVDL, no adverse effects were found during four hours of HV in hyperemic patients. Nevertheless, AVDO2 and AVDL are global measurements and might not detect regional ischemia surrounding focal lesions such as contusions and haematomas. We suggest that monitoring of AVDO2 or other haemometabolic variables should be mandatory when sustained HV is used in the management of head injury patients.

Incidence of intracranial hypertension after severe head injury: a prospective study using the Traumatic Coma Data Bank classification.

UNLABELLED: Intracranial hypertension (ICH) is a frequent finding in patients with a severe head injury. High intracranial pressure (ICP) has been associated with certain computerized tomography (CT) abnormalities. The classification proposed by Marshall et al. based on CT scan findings, uses the status of the mesencephalic cisterns, the degree of midline shift, and the presence or absence of focal lesions to categorize the patients into different prognostic groups. Our aim in this study was to analyze the ICP evolution pattern in the different groups of lesions of this classification. PATIENTS AND METHODS: We present the results of a prospective study in 94 patients with severe head injury, in whom ICP was monitored for at least 6 hours. ICP evolution was classified into three different categories: 1) ICP always < 20 mm Hg, 2) Intracranial hypertension at some time during monitoring, but controlled by medical or surgical treatment, 3) Uncontrollable ICP. The ICP pattern was correlated with the final CT diagnostic category. CONCLUSIONS: 3 patients had a normal CT scan, and none of them presented intracranial hypertension. In diffuse injury type II, the ICP evolution may be quite different. Patients with bilateral brain swelling (Diffuse Injury III) have a high risk of increased ICP (63.2%). Although in our study the frequency of Diffuse Injury IV was low, all patients in this category had a refractory ICP. In the category of evacuated mass lesions, two thirds of the patients presented an intracranial hypertension. In one third, ICP was refractory to treatment. 85% of patients with a non-evacuated mass lesion showed an increased ICP.

Arterio-jugular differences of oxygen (AVDO2) for bedside assessment of CO2-reactivity and autoregulation in the acute phase of severe head injury.

Autoregulation and CO2-reactivity can be impaired independently of each other in many brain insults, the so-called 'dissociated vasoparalysis'. The theoretical combination of preserved CO2-reactivity and impaired or abolished autoregulation can have many clinical implications in the daily management of brain injured patients. To optimize their treatment, a bedside assessment of autoregulation and CO2-reactivity is desirable. When cerebral metabolic rate of oxygen is constant, changes in arterio-jugular differences of oxygen (AVDO2) reflect changes in CBF. In these situations relative changes in AVDO2 can be viewed as inverse changes in CBF and used as an evaluation method of CO2-reactivity and autoregulation. In 39 consecutive severe head injury patients with a mean age of 28 +/- 17 years and a diffuse brain injury, cerebrovascular response to changes in pCO2 was tested in the acute phase after injury (18 +/- 8 hours). In 28 of those cases autoregulation was also assessed. A relative CBF value (1/AVDO2) was calculated from baseline AVDO2 and was expressed as 100%. Changes in 1/AVDO2 after inducing pCO2 changes give a good estimate of changes in global CBF. Two different indexes were calculated for CO2-reactivity: 1) absolute CO2-reactivity (CO2RABS) and 2) percentage reactivity (CO2R%). CO2R% was used to separate patients with impaired/abolished CO2-reactivity from those with preserved CO2-reactivity. Patients with CO2R% above 1% were considered in the intact CO2-reactivity group and patients in whom CO2R% was below or equal to 1% were included in the impaired/abolished CO2-reactivity group. Only five cases (12.8%) presented an impaired/abolished CO2-reactivity. AVDO2 response to induced hypertension was studied in a subset of 28 patients. Phenylephrine was used to increase MABP about 25%. All AVDO2 values were corrected for changes in pCO2. Patients with changes in 1/AVDO2 less than or equal to 20% were included in the intact autoregulation group. Patients with estimated CBF changes above 20% were classified as having an impaired autoregulation (impaired/abolished). In 12 patients (43%) autoregulation was intact. In the remaining 16 patients (57%) autoregulation was imparied. Of the 28 cases, CO2-reactivity was impaired in only five cases. All patients with an impaired CO2-reactivity also had an impaired autoregulation. Monitoring relative changes in AVDO2 permits a reliable study of CO2-reactivity and autoregulation at the bedside. Introducing these variables into the day-to-day management should be considered in treatment protocols.