Prone position affects stroke volume variation performance in predicting fluid responsiveness in neurosurgical patients.

BACKGROUND: Stroke volume variation (SVV) during mechanical ventilation predicts preload responsiveness. We hypothesized that the prone position would alter the performance of this dynamic indicator. METHODS: Two parallel groups of ventilated neurosurgical patients with low tidal volume (6-8 ml.kg-1) were studied before surgical incision. SVV was measured at T0, T15 and T30 min during a fluid volume expansion (250 mL hetastarch 6% over 30 min) with patients in either the supine (N.=29; Supine group) or prone position (N.=23; Prone group). Fluid responsiveness was defined as an increase in the stroke volume index (SVI) of ≥20% at T30. Receiver-operating characteristics (ROC) curves were generated for SVV. RESULTS: Prone positioning significantly increased SVV. Volume expansion in the Prone group increased SVI but led to a decline in SVV from 16% (12-22; median, 25-75th percentile) at T0 to 9% (8-13%) at T30. These effects on SVI and SVV were more pronounced compared to those obtained in the Supine group (P ≤0.05). Fluid responsiveness was predicted by SVV >12% at T0 (sensitivity 88%, specificity 62%) in the Supine group. In the Prone group, the area under the ROC curve of SVV (0.53; 95% confidence interval 0.27-0.79) did not allow the determination of a threshold SVV value. CONCLUSION: In ventilated patients with low tidal volume, a prone position may have a direct effect on the heart that alters the performance of SVV in predicting fluid responsiveness. External factor such as prone position renders difficult the interpretation of SVV as a dynamic indicator of cardiac preload.

[Hypernatremia in head-injured patients: friend or foe?]. / Hypernatrémie chez le patient cérébrolésé: utile ou dangereux?

Hypernatremia is defined by a serum sodium concentration of more than 145 mmol/L and reflects a disturbance of the regulation between water and sodium. The high incidence of hypernatremia in patients with severe brain injury is due various causes including poor thirst, diabetes insipidus, iatrogenic sodium administration, and primary hyperaldosteronism. Hypernatremia in the intensive care unit is independently associated with increased mortality and complications rates. Because of the rapid brain adaptation to extracellular hypertonicity, sustained hypernatremia exposes the patient to an exacerbation of brain edema during attempt to normalize natremia. Like serum glucose, serum sodium concentration must be tightly monitored in the intensive care unit.

[Therapeutic hypothermia for severe traumatic brain injury]. / Hypothermie thérapeutique en traumatologie crânienne grave.

Therapeutic hypothermia (TH) is considered a standard of care in the post-resuscitation phase of cardiac arrest. In experimental models of traumatic brain injury (TBI), TH was found to have neuroprotective properties. However, TH failed to demonstrate beneficial effects on neurological outcome in patients with TBI. The absence of benefits of TH uniformly applied in TBI patients should not question the use of TH as a second-tier therapy to treat elevated intracranial pressure. The management of all the practical aspects of TH is a key factor to avoid side effects and to optimize the potential benefit of TH in the treatment of intracranial hypertension. Induction of TH can be achieved with external surface cooling or with intra-vascular devices. The therapeutic target should be set at a 35°C using brain temperature as reference, and should be maintained at least during 48 hours and ideally over the entire period of elevated intracranial pressure. The control of the rewarming phase is crucial to avoid temperature overshooting and should not exceed 1°C/day. Besides its use in the management of intracranial hypertension, therapeutic cooling is also essential to treat hyperthermia in brain-injured patients. In this review, we will discuss the benefit-risk balance and practical aspects of therapeutic temperature management in TBI patients.

[Early rehabilitation for neurologic patients]. / Intérêt d'une rééducation précoce pour les patients neurologiques.

Rehabilitation improves the functional prognosis of patients after a neurologic lesion, and tendency is to begin rehabilitation as soon as possible. This review focuses on the interest and the feasibility of very early rehabilitation, initiated from critical care units. It is necessary to precisely assess patients' impairments and disabilities in order to define rehabilitation objectives. Valid and simple tools must support this evaluation. Rehabilitation will be directed to preventing decubitus complications and active rehabilitation. The sooner rehabilitation is started; the better functional prognosis seems to be.

[Near infrared spectroscopy monitoring in the neurointensive care]. / Monitorage par spectroscopie de proche infrarouge en neuroréanimation.

Near infrared spectroscopy (NIRS) can noninvasively measure cerebral saturation in oxygen, that permits to estimate brain oxygenation and metabolism. This technique could be incorporated into a multimodal monitoring for severely brain-injured patients. This review presents the principles of NIRS, its limits, the main results from clinical studies and its perspectives. More clinical studies are needed before recommending the routine use of NIRS in the ICU.

[Pupillometry in anesthesia and critical care]. / La pupillométrie en anesthésie-réanimation.

Pupil size reflects the balance between sympathetic and parasympathetic systems. Due to technological advances, accurate and repeated pupil size measurements are possible using infrared, video-recorded pupillometers. Two pupil size reflexes are assessed: the pupillary reflex dilation during noxious stimulation, and the pupil light reflex when the pupil is exposed to the light. The pupillary reflex dilation estimates the level of analgesia in response to a painful procedure or to a calibrated noxious stimulus, i.e., tetanic stimulus, in nonverbal patients. This might be of particular interest in optimizing the management of opioids in anaesthetized patients and in assessing pain levels in the intensive care unit. The pupil light reflex measurement is part of the routine monitoring for severely head-injured patients. The impact of pupillometry in this condition remains to be determined.

[Normobaric hyperoxia therapy for patients with traumatic brain injury]. / Hyperoxie normobarique chez le patient traumatisé crânien.

Cerebral ischaemia plays a major role in the outcome of brain-injured patients. Because brain oxygenation can be assessed at bedside using intra-parenchymal devices, there has been a growing interest about whether therapeutic hyperoxia could be beneficial for severely head-injured patients. Normobaric hyperoxia increases brain oxygenation and may improve glucose-lactate metabolism in brain regions at risk for ischaemia. However, benefits of normobaric hyperoxia on neurological outcome are not established yet, that hinders the systematic use of therapeutic hyperoxia in head-injured patients. This therapeutic option might be proposed when brain ischemia persists despite the optimization of cerebral blood flow and arterial oxygen blood content.

[A protocol for the cessation of sedation in brain-injured patients]. / Évaluation d'un protocole d'arrêt de la sédation chez le patient cérébrolésé

OBJECTIVES: The cessation of sedation in brain-injured patients may result in severe agitation and/or acute withdrawal syndrome related to the prolonged administration of large doses of benzodiazepines and/or opioids. The aim of the present study was to assess the clinical efficacy of a written protocol to withdraw sedation for these patients. STUDY DESIGN: Observational prospective study. PATIENTS AND METHODS: After approval by the Institutional Review Board, 40 severely brain-injured patients were included. They had received continuous administration of midazolam and sufentanil or fentanyl for median 15 days. On cessation of midazolam infusion, patients were given clorazepate for 3 days. On cessation of opioid infusion and clorazepate, clinical data were collected for 48 hours: heart rate, systolic blood pressure, respiratory rate, agitation, and pupil diameter. If an opioid withdrawal syndrome occurred, patients received a 48-hour continuous infusion of buprenorphine. RESULTS: Of 40 patients, there were 10 who did not require buprenorphine. An agitation occurred 5 hours (1-21) after cessation of opioid, associated with tachycardia, arterial hypertension, and tachypnea. After 6 hours buprenorphine treatment, these parameters were normalized. No patient needed the reintroduction of the initial sedation. CONCLUSION: The cessation of sedation in severely brain-injured patients can be successfully managed with the use of clorazepate, associated with buprenorphine in the presence of agitation.

[Sedation in neurointensive care unit]. / Neurosédation en réanimation.

The objectives for using sedation in neurointensive care unit (neuroICU) are somewhat different from those used for patients without severe brain injuries. One goal is to clinically reassess the neurological function following the initial brain insult in order to define subsequent strategies for diagnosis and treatment. Another goal is to prevent severely injured brain from additional aggravation of cerebral blood perfusion and intracranial pressure. Depending on these situations is the choice of sedatives and analgesics: short-term agents, e.g., remifentanil, if a timely neurological reassessment is required, long-term agents, e.g., midazolam and sufentanil, as part of the treatment for elevated intracranial pressure. In that situation, a multimodal monitoring is needed to overcome the lack of clinical monitoring, including repeated measurements of intracranial pressure, blood flow velocities (transcranial Doppler), cerebral oxygenation (brain tissue oxygen tension), and brain imaging. The ultimate stop of neurosedation can distinguish between no consciousness and an alteration of arousing in brain-injured patients. During this period, an elevation of intracranial pressure is usual, and should not always result in reintroducing the neurosedation.

[Hazards of therapeutic hypothermia]. / Les dangers de l'hypothermie thérapeutique.

Therapeutic hypothermia (less than 35 degrees C) is a promising strategy to improve neuroprotection after severe brain injury. Except in patients resuscitated from cardiac arrest, its effectiveness has not yet been demonstrated. Therapeutic hypothermia results in various side effects, including cardiovascular, hydroelectrolytic and infectious disorders, which could explain, in part, the lack of conclusive clinical studies. These hazards are associated with practical difficulties to induce and maintain targeted hypothermia and with rewarming management. An improvement in the techniques for achieving targeted hypothermia, more knowledge about side effects and further randomized clinical trials are needed before recommending the use of therapeutic hypothermia for patients with severe traumatic brain injury.

[Can serum protein S100beta predict neurological deterioration after moderate or minor traumatic brain injury?]. / Peut-on prédire l'aggravation neurologique des patients traumatisés crâniens mineurs et modérés par le dosage sanguin de la protéine S-100beta?

INTRODUCTION: Patients with moderate traumatic brain injury (TBI) (Glasgow Coma Scale, GCS, 9-13) or minor TBI (GCS 14-15) are at risk for subsequent neurological deterioration. Serum protein S-100 is believed to reflect brain damage following TBI. In patients with normal or minor CT scan abnormalities on admission, we tested whether the determination of serum protein S-100 beta could predict secondary neurological deterioration. METHODS: Sixty-seven patients with moderate or minor TBI were prospectively studied. Serum samples were collected on admission within 12 hours postinjury to measure serum protein S-100 levels. Neurological outcome was assessed up to seven days after trauma. Secondary neurological deterioration was defined as two points or more decrease from the initial GCS, or any treatment for neurological deterioration. RESULTS: Nine patients had a secondary neurological deterioration after trauma. No differences in serum levels of protein S-100 were found between these patients and those without neurological aggravation (n=58 patients): 0.93 microg/l (0.14-4.85) vs 0.39 microg/l (0.04-6.40), respectively. The proportion of patients with abnormal levels of serum protein S-100 at admission according to two admitted cut-off levels (>0.1 and >0.5 microg/l) was comparable between the two groups of patients. Elevated serum levels of protein S-100 were found in patients with Injury Severity Score (ISS) of more than 16 (n=23 patients): 1.26 microg/l (0.14-6.40) vs 0.22 microg/l (0.04-6.20) in patients with ISS less than 16 (n=44 patients). DISCUSSION: The dosage of serum protein S-100 on admission failed to predict patients at risk for neurological deterioration after minor or moderate TBI. Extracranial injuries can increase serum protein S-100 levels, then limiting the usefulness of this dosage in this clinical setting.

[Contribution of magnetic resonance spectroscopy in predicting severity and outcome in traumatic brain injury]. / Apport de la spectroscopie RMN à l'évaluation du traumatisme crânien.

Nuclear magnetic spectroscopy (MRS) is a useful method for noninvasively studying intracerebral metabolism. Proton MRS can identify markers of the neuronal viability (N-acetyl-aspartate, NAA), of the metabolism of cellular membranes (choline), of the cellular energy metabolism (creatine, lactate). In Phosphorus MRS, the peaks most readily identified are involved in the high-energy cellular metabolism (ATP, phosphocreatine, inorganic phosphate), and intracellular pH (pHi) can be determined using this method. MRS has been used in experimental models of traumatic brain injury (TBI), primarily to study the cellular metabolism and the relation between biochemical and histological changes after trauma. In trauma patients, significant changes in NAA, choline and pHi were found in both grey and white matter comparing with controls, and these alterations correlated with injury severity. Correlations have been reported between these biochemical changes (reduction in NAA, increase in choline) measured at 1 to 6 months after TBI and the clinical outcome of the patients. However, there are methodological issues which still impede to recommend MRS as a tool for predicting neurological outcome in the clinical setting.