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N Stocchetti

Publications and source records attributed to N Stocchetti.

At least 19 recordsLinked to original sources
PubMed2003

[Neuro-link, an Italian traumatic coma data bank: what did we learn from the first 1000 patients and how can we do better? ].

To understand the complex physiopathology of post-traumatic brain damage is important to have data on epidemiology, clinical course, monitoring, effect of therapy and outcomes. In 1997 3 neuro-intensive care units in the Milan metropolitan area developed a computer assisted database named Neuro-Link (NL) for collection of information on head injury. All head injured patients requiring intensive care during the first 24 hours post-trauma were eligible. The data collection form was designed for use with a computer interface to cover: 1) general, previous and admission data; 2) secondary insults and complication; 3) CT scan and monitoring data; 4) outcome data. Two different data collections were performed: 1) NL domestic (data from 3 centres from 1997); 2) NL 18 centres (3 month survey of Italian centres with interest in neurotrauma care). An audit of the data was performed. NL domestic included 1 085 patients from 1997 to 2002. NL 18 centres included 282 patients in the 3 month period. Audit is performed on 35 000 data per year.A large number of good quality information on head injury patients is now available. The database is useful for: 1) production of information; 2) base for prospective studies.

Coma↗
PubMed2003

[Brain vulnerability and its modulation].

Clinical and experimental studies revealed that the injured brain is highly vulnerable to a subsequent insult. Surfery of the literature pertinent to clinical and experimental traumatic brain injury (TBI) is made. Increased vulnerability of the traumatically injured brain to an additional sub lethal ischemic, hypoxic, excitotoxic, or mechanical insult has been clearly demonstrated. Compared to traumatic brain injury alone, the double insult paradigm dramatically increases the brain damage. Brain vulnerability following TBI can be explained by a reduced ability to compensate for a reduction of cerebral blood flow (CBF) and oxygen (O(2)) delivery to the brain or inability to meet an increased metabolic demand. In addition, there is a specific increased sensitivity to delayed insults induced by the first injury. Potential mechanisms of the increased sensitivity to a second insult might be related to post-traumatic gene expression alterations leading to changes in neurotransmitters release, density of receptors and reduced thresholds for activation of pathways leading to delayed cell death. The brain is vulnerable to repetitive injuries. Derangements of compensatory mechanisms are responsible, in part, for this vulnerability. Additional work is needed to better understand the molecular pathways leading to secondary damage and to find novel therapeutic strategies to modulate the brain response to TBI.

Brain Chemistry↗
PubMed2003

[How to quantify the severity of brain injury during intensive care after adult head trauma].

Adequate early assessment of brain damage is essential. Location, extension and severity of structural damage affect brain function and ultimately determine the outcome. The extent of functional impairment, and the morphology of intracranial lesions, require specific treatment, often a combination of medical and surgical interventions. Brain damage usually evolves over time, and repeated assessments are necessary. Clinical evaluation is often biased by concomitant sedation and/or anesthesia, but remains necessary. A revision of the literature is presented. Brain damage is assessed combining clinical and instrumental data. Clinical examination is performed assessing the 3 components of the Glasgow Coma Scale. Spontaneous or stimulated (pain stimulus) eye opening, verbal and motor responses are observed after hemodynamic and respiratory stabilisation. Unfortunately a significant proportion of patients can not be properly examined for several reasons: eye opening can be altered by palpebral and facial injuries, verbal response can be impaired by maxillo-facial injuries or by endotracheal intubation, and motor response remains the most consistent parameter. Sedation, analgesia and myorelaxants, however, can profoundly diminish or abolish the motor response to maximal stimulation, so that examination should be performed after clearance of drugs. Often alcohol or other substances can further impair the neurological performances. Pupils diameter and reactivity to light should be observed, excluding pharmacologic effects (as dilation due to catecholamines) and direct ocular or orbital damage. The CT scan is necessary for disclosing surgical masses and for identifying the extent of diffuse damage and the location of focal lesions. These data should be combined with additional functional exploration, as provided by cerebral extraction of oxygen and electrophysiologic data. Early estimation of cerebral damage is complex and prone to mistakes. Accurate, repeated evaluations, based on the combination of clinical observation and imaging, are necessary.

Brain Injuries↗
PubMed2002

Cerebral veno-arterial pCO2 difference as an estimator of uncompensated cerebral hypoperfusion.

The aim of the present study was to assess the veno-arterial difference in pCO2 (delta pCO2) as an indicator of ischemia compared to the arteriovenous O2 difference (AVDO2). Staircase cerebral blood flow (CBF) reductions were obtained in seven domestic pigs by inducing intracranial hypertension: CBF 100%, 50-60% of baseline, 20-30% of baseline. ICP, MAP, CPP and CBF (Laser-Doppler method) were continuously recorded. The superior sagittal sinus was punctured to determine AVDO2 and delta pCO2. AVDO2 was 5.9 (+/- 1.78, range 3.3-7.4), 7.01 (+/- 1.31, range 5-8.9) and 8.17 (+/- 1.51, range 6.0-11.3) ml/100 ml in the three CBF steps (p = 0.001). CBF impairment was accompanied by the following increases in delta pCO2: from 10 (+/- 4, range 4-15) mmHg to 14.5 (+/- 4.11, range 10-27) mmHg, and to 31.2 (+/- 9.0, range 17-39) mmHg (p < 0.001). When CBF declines AVDO2 increases, indicating greater extraction of O2 to satisfy the aerobic metabolism. However, this mechanism can no longer compensate once a critical CBF threshold is reached. delta pCO2 rises slowly during moderate CBF reduction because of defective washout; the rise is impressive during marked CBF impairment when anaerobic metabolism takes place with proton buffering in CO2 and H2O. Therefore, when the brain's ability to compensate for low blood flow is exceeded, CO2 production outweighs O2 extraction.

Animals↗
PubMed2002

Effects of hyperoxia on brain tissue oxygen tension in cerebral focal lesions.

We evaluated the systemic and cerebral effects induced by an increase to 100% of the inspired oxygen fraction (FiO2) on 20 comatose patients with head injury (9 patients) and SAH (11 patients). Brain tissue oxygen tension (PtiO2) was measured through a Clark electrode inserted in penumbra-like areas. We performed 55 hyperoxia tests by increasing FiO2 from 35 +/- 8% to 100% in one second and calculating the PtiO2 index as: PtiO2 variation from baseline at 1 minute/arterial oxygen tension (PaO2) variation from baseline at 1 minute x 100. One hundred percent FiO2 caused an increase of both arterial (from 139 +/- 28 to 396 +/- 77 mmHg) and cerebral (from 22.6 +/- 14 to 65.4 +/- 60 mmHg) oxygenation after 1 minute. The range of the PtiO2 response was not uniform and two groups were identified. The change was small, 0.8 mmHg/min/100 mmHg PaO2 (+/- 0.7; range 0-2) when mean PtiO2 was 19.7 +/- 13.1 mmHg, while a stronger response, 8 mmHg/min/100 mmHg PaO2 (+/- 5; range 3-18) (p < 0.01) was found when mean PtiO2 was 31.7 +/- 14.3 mmHg. Since O2 diffusion should follow the gas diffusion law, the increase in diffusion distance due to a reduction of capillary density in focal lesions may explain this relationship.

Brain↗
PubMed2001

Intensive care management of head-injured patients in Europe: a survey from the European brain injury consortium.

OBJECTIVES: (a) to describe current practice in the monitoring and treatment of moderate and severe head injuries in Europe; (b) to report on intracranial pressure and cerebral perfusion pressure monitoring, occurrence of measured and reported intracranial hypertension, and complications related to this monitoring; (c) to investigate the relationship between the severity of injury, the frequency of monitoring and management, and outcome. METHODS: A three-page questionnaire comprising 60 items of information has been compiled by 67 centres in 12 European countries. Information was collected prospectively regarding all severe and moderate head injuries in adults (> 16 years) admitted to neurosurgery within 24 h of injury. A total of 1005 adult head injury cases were enrolled in the study from 1 February 1995 to 30 April 1995. The Glasgow Outcome Scale was administered at 6 months. RESULTS: Early surgery was performed in 346 cases (35%); arterial pressure was monitored invasively in 631 (68%), ICP in 346 (37%), and jugular bulb saturation in 173 (18%). Artificial ventilation was provided to 736 patients (78%). Intracranial hypertension was noted in 55% of patients in whom ICP was recorded, while it was suspected in only 12% of cases without ICP measurement. There were great differences in the use of ventilation and CPP monitoring among the centres. Mortality at 6 months was 31%. There was an association between an increased frequency of monitoring and intervention and an increased severity of injury; correspondingly, patients who more frequently underwent monitoring and ventilation had a less favourable outcome. CONCLUSIONS: In Europe there are great differences between centres in the frequency of CPP monitoring and ventilatory support applied to head-injured patients. ICP measurement disclosed a high rate of intracranial hypertension, which was not suspected in patients evaluated on a clinical basis alone. ICP monitoring was associated with a low rate of complications. Cases with severe neurological impairment, and with the worse outcome, were treated and monitored more intensively.

Adult↗
PubMed2001

Brain oxygen tension, oxygen supply, and oxygen consumption during arterial hyperoxia in a model of progressive cerebral ischemia.

We investigated the changes in brain oxygen tension (ptiO2) after ventilation with pure O2 in order to (1) clarify the pathophysiology of O2 exchange in the cerebral microcirculation; and (2) investigate the relationship between brain O2 tension, O2 delivery, and consumption in steady-state conditions during stepwise cerebral blood flow (CBF) reductions. A swine model was developed to reduce CBF in three stable steps: (1) baseline (CBF 100%), (2) CBF of 50-60% of baseline, and (3) CBF of <30% of baseline. CBF was reduced by infusing saline into the left lateral ventricle through a catheter connected with an infusion pump. At each step, hyperoxia was tested by increasing the inspired oxygen fraction up to 100%, PtiO2 reflected the CBF reductions, since it was respectively 27.95 (+/-10.15), 14.77 (+/-3.58), and 3.45 (+/-2.89) mm Hg during the three CBF steps. Hyperoxia was followed by an increase in ptiO2, although the increase was significantly lower when hyperoxia was applied during progressive ischemia. O2 supply to the brain did not change during hyperoxia. Arteriovenous oxygen difference (AVDO2) decreased during the phases of intact CBF and moderate impairment, but not during the phase of severe CBF reduction. In conclusion, ptiO2 reductions closely reflect the imbalance between oxygen delivery and demand; this implies a link between low ptiO2 and defective O2 supply due to impaired CBF. However, this relation is not necessarily reciprocal, since manipulating brain oxygen tension does not always influence brain oxygen delivery, as in the case of ventilation with pure oxygen.

Animals↗
PubMed2001

Brain temperature, body core temperature, and intracranial pressure in acute cerebral damage.

OBJECTIVES: To assess the frequency of hyperthermia in a population of acute neurosurgical patients; to assess the relation between brain temperature (ICT) and core temperature (Tc); to investigate the effect of changes in brain temperature on intracranial pressure (ICP). METHODS: The study involved 20 patients (10 severe head injury, eight subarachnoid haemorrhage, two neoplasms) with median Glasgow coma score (GCS) 6. ICP and ICT were monitored by an intraventricular catheter coupled with a thermistor. Internal Tc was measured in the pulmonary artery by a Swan-Ganz catheter. RESULTS: Mean ICT was 38.4 (SD 0.8) and mean Tc 38.1 (SD 0.8) degrees C; 73% of ICT and 57.5% of Tc measurements were > or =38 degrees C. The mean difference between ICT and Tc was 0.3 (SD 0.3) degrees C (range -0.7 to 2.3 degrees C) (p=0. 0001). Only in 12% of patients was Tc higher than ICT. The main reason for the differences between ICT and Tc was body core temperature: the difference between ICT and Tc increased significantly with body core temperature and fell significantly when this was lowered. The mean gradient between ICT and Tc was 0.16 (SD 0.31) degrees C before febrile episodes (ICT being higher than Tc), and 0.41 (SD 0.38) degrees C at the febrile peak (p<0.05). When changes in temperature were considered, ICT had a profound influence on ICP. Increases in ICT were associated with a significant rise in ICP, from 14.9 (SD 7.9) to 22 (SD 10.4) mm Hg (p<0.05). As the fever ebbed there was a significant decrease in ICP, from 17.5 (SD 8.62) to 16 (SD 7.76) mm Hg (p=0.02). CONCLUSIONS: Fever is extremely frequent during acute cerebral damage and ICT is significantly higher than Tc. Moreover, Tc may underestimate ICT during the phases when temperature has the most impact on the intracranial system because of the close association between increases in ICT and ICP.

Adult↗
PubMed2000

Oxygen delivery and oxygen tension in cerebral tissue during global cerebral ischaemia: a swine model.

UNLABELLED: Interest in tissue oxygen (PtiO2) monitoring is increasing. However the exact interactions between ptiO2, systemic and cerebral variables are a matter of debate. Particularly, the relationship between ptiO2, cerebral oxygen supply and consumption needs to be clarified. We designed a model to achieve progressive Cerebral Blood Flow (CBF) reduction through 3 steps: 1. baseline, 2. CBF between 50-60% of the baseline, 3. CBF < 30% of the baseline. In 7 pigs, under general anaesthesia, Cerebral Perfusion Pressure (CPP) and CBF were reduced through the infusion of saline in a lateral ventricle. PtiO2 and CBF were monitored respectively through a Clark electrode (Licox, GMS) and laser doppler (Peri-Flux). Blood from superior sagittal sinus and from an arterial line was simultaneously drawn to calculate the artero-venous difference of oxygen (AVDO2). Brain oxygen supply was calculated by multiplying relative CBF change and arterial oxygen content. PtiO2 reflected CBF reductions, as it was 27.95 (+/- 10.15) mmHg during the first stage of intact CBF, declined to 14.77 (+/- 3.58) mmHg during the first CBF reduction, declined to 3.45 (+/- 2.89) mmHg during the second CBF reduction and finally fell to 0 mmHg when CBF was completely abolished. CBF changes were also followed by a decline in O2 supply and a parallel increase in AVDO2. CONCLUSION: This model allows stable and reproducible steps of progressive CBF reduction in which ptiO2 changes can be studied together with oxygen supply and consumption.

Animals↗
PubMed2000

Brain oxygen tension during hyperoxia in a swine model of cerebral ischaemia.

UNLABELLED: Arterial hyperoxia improves oxygen tension measured into the cerebral tissue (ptiO2). The extent of this improvement in ameliorating O2 delivery to the cerebral tissue, when cerebral blood flow (CBF) is reduced, is still unclear. The present experiment was developed to investigate the effect of arterial hyperoxia at normal or reduced CBF (baseline, CBF = 50-60%, and CBF = 20-30% of the baseline). CBF reduction was achieved in 7 pigs by saline infusion in a lateral ventricle. PtiO2 was measured by Licox equipment. Arterovenous oxygen difference (AVDO2) was calculated as the difference between arterial oxygen content and superior sagittal sinus oxygen content. Hyperoxia was induced by increasing inspired oxygen fraction to 100%. PtiO2 moved respectively from 27.95 (+/- 10.15) to 45.98 (+/- 15.31), from 14.77 (+/- 3.58) to 30.71 (+/- 12.2), and from 3.45 (+/- 2.89) to 11.1 (+/- 12.6) mmHg at normal CBF, after the first reduction and after the second reduction. O2 supply showed only a negligible increase. AVDO2 decreased during the phases of intact and moderate CBF impairment, while it did not change during the phase of severe CBF impairment. IN CONCLUSION: an increase of ptiO2 does not necessarily correspond to an improvement of brain oxygen delivery. The small increase in oxygen delivery due to hyperoxia may cause a slight improvement in the balance between O2 delivery and consumption during mild CBF reduction, but such improvement is negligible when severe CBF reduction occurs.

Animals↗
PubMed2000

Early translaryngeal tracheostomy in patients with severe brain damage.

OBJECTIVES: To describe the effects of early translaryngeal tracheostomy on intracranial pressure (ICP), cerebral perfusion pressure (CPP), and jugular bulb saturation (SjO2); to identify the main mechanisms affecting ICP during tracheostomy; and to evaluate the long-term effects of tracheostomy on tracheal anatomy and function. DESIGN: Prospective, observational, clinical study. SETTING: Neurosurgical intensive care unit in a teaching hospital. PATIENTS: 20 patients admitted to the ICU because of head injury, subarachnoid hemorrhage, or brain tumor with a Glasgow Coma Scale less than 8. INTERVENTIONS: Patients underwent translaryngeal tracheostomy under strict neuromonitoring. MEASUREMENTS AND RESULTS: ICP rose significantly (p < 0.05) at the critical time of cannula placement while all other parameters remained stable. At this time five patients suffered intracranial hypertension (ICP > 20 mmHg). In one of them CPP dropped below 60 mmHg. Arterial CO2 tension (PaCO2) did not rise significantly. No other major complications were recorded during the procedures. Three months after tracheostomy normal findings were detected by tracheoscopy in all cases (11 patients could be examined). CONCLUSIONS: Translaryngeal tracheostomy, performed in selected patients when the risk of intracranial hypertension was reduced to the minimum, was well tolerated in the majority of cases and did not induce persistent intracranial disorders. However, ICP is affected by tracheostomy, and careful monitoring and patient selection is necessary. At follow-up no severe anatomical or functional damage was detected.

Adolescent↗
PubMed2000

Neuro-Link, a computer-assisted database for head injury in intensive care.

Reliable information is vital for clinical trials, so we developed a database, for head trauma victims admitted to neuro-intensive care units (NICU). This database, first step in a sequential project, comprises 176 selected fields mainly focused on the early post-traumatic phase and has a user-friendly computerized interface. The software was tested for a trimester in 18 Italian neuro-intensive care units. The paper describes the main features of the database, the results of a three months' data collection test, its limitations and its potential improvements. A description of the database fields and a brief summary of the 282 patients included so far are also presented.

Adolescent↗
PubMed2000

The value of the "worst" computed tomographic scan in clinical studies of moderate and severe head injury. European Brain Injury Consortium.

OBJECTIVE: Computed tomographic (CT) scanning can reveal the pattern and severity of structural brain damage after head injury. With the proliferation of CT scanners in general hospitals, and with improvements in patient transport, the interval from injury to the first CT scan is decreasing. The potential result is an "admission" scan missing an evolving and potentially operable lesion. Furthermore, the literature is confusing regarding the timing and coding of CT findings. We sought to establish the frequency of deterioration in CT appearance from an admission scan to subsequent scans and the prognostic significance of such deterioration. METHODS: In a survey organized by the European Brain Injury Consortium, data on initial severity, management, and subsequent outcome were gathered prospectively for 1005 patients with moderate or severe head injury admitted to one of 67 European neurosurgical units during a 3-month period in 1995. The findings of the initial and the final ("worst") CT scan were classified according to the Traumatic Coma Data Bank system and were related to outcome as assessed using the Glasgow Outcome Scale 6 months after injury. RESULTS: Data on an initial and a final CT scan were available for 897 patients; of these, 724 patients were assessed using the Glasgow Outcome Scale at 6 months. The initial CT findings were classified as a diffuse injury for 53% of the cohort, with 16% of these diffuse injuries demonstrating deterioration on a subsequent scan. In 56 (74%) of 76 deteriorations, the change was from a diffuse injury to a mass lesion. When the initial CT scan demonstrated a diffuse injury without swelling or shift, evolution to a mass lesion was associated with a statistically significant increase in the risk of an unfavorable outcome (62% versus 38%). When the initial scan demonstrated evidence of swelling or shift, there was a nonsignificant trend in the opposite direction, although the numbers were limited. CONCLUSION: When an admission CT scan demonstrates evidence of a diffuse injury, follow-up scans should be performed, because approximately one in six such patients will demonstrate significant CT evolution. In studies comparing series of head-injured patients, correspondence of timing of CT scans is necessary for valid comparison.

Brain Injuries↗
PubMed2000

Neurophysiological consequences of three tracheostomy techniques: a randomized study in neurosurgical patients.

We describe the effects of different tracheostomy techniques on intracranial pressure (ICP), cerebral perfusion pressure (CPP), and cerebral extraction of oxygen. We attempted to identify the main mechanisms affecting intracranial pressure during tracheostomy. To do so we conducted a prospective, block-randomized, clinical study which took place in a neurosurgical intensive care unit in a teaching hospital. The patients studied consisted of thirty comatose patients admitted to the intensive care unit because of head injury, subarachnoid hemorrhage, or brain tumor. Ten patients per group were submitted to standard surgical tracheostomy, percutaneous dilatational tracheostomy or translaryngeal tracheostomy. In every technique a significant increase of ICP (P < .05) was observed at the time of cannula placement. Intracranial hypertension (ICP > 20 mm Hg) was more frequent in the percutaneous dilatational tracheostomy group (P < .05). Cerebral perfusion pressure dropped below 60 mm Hg in eleven cases, more frequently during surgical tracheostomy. Arterial tension of CO2 significantly increased in all three groups during cannula placement. No other major complications were recorded during the procedures. At follow-up no severe anatomic or functional damage was detected. We conclude that the three tracheostomy techniques, performed in selected patients where the risk of intracranial hypertension was reduced to the minimum, were reasonably tolerated but caused an intracranial pressure rise and cerebral perfusion pressure reduction in some cases.

Adult↗
PubMed2000

Mass volume measurement in severe head injury: accuracy and feasibility of two pragmatic methods.

OBJECTIVE: To assess the clinical feasibility and the accuracy of two pragmatic methods in comparison with a conventional computer based method of measurement of masses from CT. METHODS: Nineteen CT scans of 11 patients with severe head injury, showing 34 traumatic lesions, were examined. The volume of every lesion was digitally measured, then a panel of three examiners independently repeated the measurement using the ellipsoid and the Cavalieri method in random order. RESULTS: All the lesions were identified by all the readers and the mean volume measured by each examiner differed by less than 1.5 ml. The average reading time for each scan was 4 minutes for the ellipsoid and 7 minutes for the Cavalieri method. The average volume of the lesions was 34.2 (SD 35) ml with the digital system, and 38.4 (SD 41) ml and 34.8 (SD 36) ml for the ellipsoid and the Cavalieri readings respectively. The average difference between the applied technique and the digital system was 0.57 (SD 9.99) ml for the Cavalieri direct estimator and 0.20 (SD 15.48) ml for the ellipsoid method. The 95% confidence interval for this difference fell between -2.75 and 3.89 ml for the Cavalieri, and between -4.94 and 5.35 ml for the ellipsoid method. There were 19 lesions >25 ml; the ellipsoid method identified 16 of them, whereas 17 were classified with the Cavalieri method. When considering individual lesions rather than the average volume, discrepancies were detected with both methods. The ellipsoid method was less precise, especially when extracerebral lesions were measured. CONCLUSIONS: Both pragmatic methods are inferior to computer based reading, which is the choice when accurate volume estimation is necessary. However, if a digital volumetric determination of the lesions using a CT computer is not possible, the two pragmatic methods offer an alternative.

Analysis of Variance↗
PubMed2000

Guidelines for the treatment of adults with severe head trauma (part I). Initial assessment; evaluation and pre-hospital treatment; current criteria for hospital admission; systemic and cerebral monitoring.

If pragmatic recommendations for treatment of severely head-injured patients could really be applied, they would probably have a considerable impact in terms of reduction in mortality and disability. Since 1995 a Group of Italian Neurointensivists and Neurosurgeons belonging to the Italian Societies of Neurosurgery (SINch) and Anesthesiology & Intensive Care (SIAARTI) has produced this first part of recommendations that are completed by Medical treatment (Part II) and Surgical treatment criteria (Part III). These recommendations reflect a multidisciplinary consent but are based on scientific evidence, when available, and take origin mainly from expert opinions and the current clinical and organizational situation. For this aspect they differ from other American and European guidelines, which are strictly based on criteria of proven efficacy. These recommendations aim at providing a practical reference for all those dealing with severe head injuries from first-aid to intensive care units, setting out the minimal goals of management to be reached throughout the country. For these reasons they need continual critical review and updating. Main clinical aims are: 1) to prevent secondary cerebral damage by continuous and meticulous maintenance of systemic homeostasis 2) to standardize methods of neurological evaluation and CT scan classification and scheduling; 3) to give simple indications for systemic and cerebral monitoring 4) to pragmatically discuss the organizational scenarios and specify the minimal safe clinical approach when patients are treated in non-specialized settings. Briefly, smooth tracheal intubation and ventilation in all comatose patients, administration of rapidly metabolized sedative and analgesic drugs to permit frequent neurological evaluation, restoration of volemia and systolic blood pressure above 110 mm Hg, oxygen saturation >95% and normocapnia, are all recommended from the very early treatment and transport. Homogeneity of language, reliable and correctly tested Glasgow Coma Score and pupillary reflexes, and a simple CT scan classification are recommended to improve communications and clinical decisions in the multidisciplinary setting of management. In comatose patients, cerebral perfusion pressure, intracranial pressure and oxygen jugular saturation must be monitored according to specific criteria, which are described. Therapy with hyperventilation and mannitol should be used only in case of clinical deterioration and uncal herniation. This therapy could be useful to gain time to reach neurosurgery. The aim of these recommendations is to achieve safer management of severely brain injured patients, immediate diagnosis of clinical deterioration and successful identification and treatment of surgical lesions. The impact of these guidelines requires further verification.

Adult↗