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.

Intracranial hypertension after surgery in patients with Chiari I malformation and normal or moderate increase in ventricular size.

OBJECTIVE: To determine ICP changes in patients with Chiari type I malformation after posterior fossa reconstruction (PFR). PATIENTS AND METHODS: We continuously monitored ICP before and after PFR in 12 patients with Chiari I malformation and with an Evans' Index below or equal to 0.33. Mean ICP (epidural sensor) and percentage of B waves were calculated 24 hours before surgery and during the first 7 days after surgery. RESULTS: Mean ICP and percentage of B waves significantly increased after surgery despite a significant increase in the volume of the posterior fossa. The main finding revealed by control CT scans was compression of the quadrigeminal cistern with a reduction in size of the fourth ventricle. In six patients, a small transitory increase in supratentorial ventricular size was found. CONCLUSIONS: A transitory increase in ICP is common after PFR. This increase could be explained by an initial reperfusion phenomena in the cerebellum that provokes a transitory deterioration in CSF dynamics. The effacement of the quadrigeminal cistern and the reduction in size of the fourth ventricle suggests this hypothesis.

[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.

Neuropsychological outcome in relation to the traumatic coma data bank classification of computed tomography imaging.

The Traumatic Coma Data Bank (TCDB) classification of CT (computed tomography) scan has been related to the general outcome and intracranial pressure evolution. Our aim was to analyse the relationship of this classification with neuropsychological outcome and late indices of ventricular dilatation. Fifty-seven patients with a moderate or severe head injury (mean admission Glasgow Coma Scale Score, 7.7) were studied from 122 consecutive cases. There were 49 males and 8 females (mean age, 27.7 years). Subjects were classified into TCDB categories on the basis of their most serious acute CT scan finding. From the last control CT scan image, performed at a mean of 6.12 months postinjury, several measures of ventricular dilatation were calculated. Neuropsychological assessment at 6-month included tests of verbal and visual memory, visuoconstructive functions, fine motor speed, and frontal lobe functions. Patients with diffuse injury type I showed better neuropsychological outcome than patients with more severe diffuse injuries and those with mass lesions. Within the diffuse injury groups, the degree of diffuse damage was related to measures of verbal memory and attention and cognitive flexibility. Ventricular enlargement was more evident in patients with mass lesions and it decreased in the remaining groups as the severity of diffuse injury diminished. These results show that there is a relationship between acute intracranial lesion diagnosis according to TCDB classification and neuropsychological results and ventricular dilatation indices at 6 months postinjury.

Current aspects of pathophysiology and cell dysfunction after severe head injury.

Traumatic brain injury is a major health problem in all developed countries. The main aim of this review is to provide a short update on the most recent advances in our knowledge of the brains response to mechanical injuries, focusing on metabolic, cellular, subcellular, and molecular events that take place in severe head injuries. Knowledge of these events is essential for a better understanding of new pharmacological avenues and non-pharmacological strategies, such as moderate hypothermia, which are being developed to improve the outcome of this silent epidemic. We will focus on several topics that we consider to be the most significant: diffuse axonal injury, ischemia and the cascades it generates, metabolic derangements, excitotoxicity, oxidative stress, and other phenomena that have been included in the term tertiary injuries. Recent evidence has clearly demonstrated that traumatic brain lesions are highly dynamic and that the different lesions observed after closed head injury are not single events but processes set in motion by the mechanical impact. These processes are not finished until an unpredictable time after injury. We will discuss recent evidence showing that in diffuse axonal injury, primary immediate damage can coexist with axons that, although initially intact, may be evolving towards secondary disconnection. The concept of ischemic penumbra and the more recent concept of traumatic penumbra are discussed, together with recent experimental and clinical data that shed light on the non-ischemic forms of brain hypoxia. The role of excitotoxicity in mechanically-induced cell death and the molecular events that excessive release of glutamate induce, including apoptosis and delayed inflammatory processes, are reviewed. Finally, new knowledge on how central nervous system cells regulate their volume, the new family of channel water molecules known as aquaporins and their possible role in the physiopathology of the swollen brain are discussed. Basic and clinical investigations are still needed to translate the huge amount of pathophysiological knowledge acquired in the last decade into effective treatments for these patients.

Does an increase in cerebral perfusion pressure always mean a better oxygenated brain? A study in head-injured patients.

The adequate management of cerebral perfusion pressure (CPP) continues to be a controversial issue in head-injured patients. The purpose of our study was to test two hypotheses. The first was that in patients with a CPP below 70 mm Hg, oxygen delivery is compromised and that therefore signs of tissue hypoxia would be reflected in low PtiO2 measurements. The second hypothesis was that manipulating mean arterial blood pressure to increase CPP improves oxygen delivery, particularly in patients with a CPP below 70 mm Hg. Twenty-five moderately or severely head-injured patients were included in the study. In all of them PtiO2 was monitored in the non-injured hemisphere using the Licox system (GMS, Kiel-Mielkendorf, Germany). Arterial hypertension was induced with phenylephrine 29 times. To quantify the effect of increasing mean arterial blood pressure (MABP) on oxygen delivery to the brain, the PtiO2-BP index was calculated (PtiO2-BP index = delta PtiO2/delta MABP). In 16 tests (55%) baseline CPP was above or equal to 70 mm Hg and in the remaining 13 (45%) it was below 70 mm Hg. Mean increase in MABP after phenylephrine was 23.7 +/- 10.2 mm Hg. Mean PtiO2 was 29.5 +/- 14.7 mm Hg in patients with a basal CPP of below 70 mm Hg and 28.9 +/- 10.6 mm Hg in patients in the high CPP group. These differences being not statistically significant. The PtiO2-BP index was 0.29 +/- 0.23 in patients with a basal CPP of below 70 mm Hg and in patients with a CPP of above 70 mm Hg this index was 0.16 +/- 0.11 Hg. These differences were not statistically significant (Student's t-test, P = 0.09). In our study a low PtiO2 was not observed in patients with marginally low CPPs (48-70 mm Hg) and readings below 15 mm Hg were observed in cases with both normal or supranormal CPPs. We conclude that episodes of low PtiO2 could not be predicted on the basis of CPP alone. On the other hand, raising CPP did not increase oxygen availability in the majority of cases, even if the CPP was markedly improved.

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.

Horner syndrome as an isolated manifestation of an intrapetrous internal carotid artery dissection.

PURPOSE: To describe the atypical localization and unusual clinical manifestation of an internal carotid artery dissection. METHODS: We examined a 43-year-old woman who had sudden onset of left ptosis and miosis with vague dysesthesia around her eye. RESULTS: Her examination showed an intrapetrous carotid artery dissection. CONCLUSIONS: The intrapetrous segment is an extremely rare localization for an internal carotid artery dissection. The differential diagnosis of acute Horner syndrome should include carotid dissection, which is usually accompanied by other neurologic manifestations.