Explore the vast range of titles available.

In a trial comparing decompressive craniectomy with medical therapy in patients with traumatic brain injury and raised intracranial pressure refractory to medical therapy, decompressive craniectomy resulted in lower mortality and higher rates of vegetative state and severe disability. After traumatic brain injury (TBI), intracranial pressure can be elevated owing to a mass effect from intracranial hematomas, contusions, diffuse brain swelling, or hydrocephalus. 1 Intracranial hypertension can lead to brain ischemia by reducing the cerebral perfusion pressure. 2 Intracranial hypertension after TBI is associated with an increased risk of death in most studies. 3 , 4 The monitoring of intracranial pressure and the administration of interventions to lower intracranial pressure are routinely used in patients with TBI, despite the lack of level 1 evidence. 5 Decompressive craniectomy is a surgical procedure in which a large section of the skull is removed and the underlying . . .

In this randomized trial involving patients with traumatic brain injury and elevated intracranial pressure, therapeutic hypothermia plus standard care to reduce intracranial pressure did not result in outcomes better than those with standard care alone. In Europe, traumatic brain injury is the most common cause of permanent disability in people younger than 40 years of age, with the annual cost exceeding €33 billion (approximately $37.5 billion in U.S. dollars). 1 , 2 Recent statistics show a 21% increase in the incidence of traumatic brain injury during the past 5 years — three times greater than the increase in population. Despite this, management of traumatic brain injury has been underrepresented in medical research as compared with other health problems. 3 Consequently, there are few data to support the commonly used stage 2 interventions (Figure 1) for the management of . . .

In this randomized trial involving 324 patients with severe traumatic brain injury in Bolivia and Ecuador, guideline-based management with intracranial pressure monitoring was not superior to management based on imaging and clinical assessments. Although the monitoring of intracranial pressure is widely recognized as standard care for patients with severe traumatic brain injury, its use in guiding therapy has incomplete acceptance, even in high-income countries. 1 – 3 Successive editions of the guidelines for the management of severe traumatic brain injury 4 – 7 have documented the inadequate evidence of efficacy, calling for randomized, controlled trials while also noting the ethical issues that would be posed if the control group consisted of patients who did not undergo monitoring. The identification of a group of intensivists in Latin America who routinely managed severe traumatic brain injury without using available . . .

Background Untimely diagnosis of intracranial hypertension may lead to delays in therapy and worsening of outcome. Transcranial Doppler (TCD) detects variations in cerebral blood flow velocity which may correlate with intracranial pressure (ICP). We investigated if intracranial hypertension can be accurately excluded through use of TCD. Method This was a multicenter prospective pilot study in patients with acute brain injury requiring invasive ICP (ICPi) monitoring. ICP estimated with TCD (ICPtcd) was compared with ICPi in three separate time frames: immediately before ICPi placement, immediately after ICPi placement, and 3 hours following ICPi positioning. Sensitivity and specificity, and concordance correlation coefficient between ICPi and ICPtcd were calculated. Receiver operating curve (ROC) and the area under the curve (AUC) analyses were estimated after measurement averaging over time. Results A total of 38 patients were enrolled, and of these 12 (31.6%) had at least one episode of intracranial hypertension. One hundred fourteen paired measurements of ICPi and ICPtcd were gathered for analysis. With dichotomized ICPi (≤20 mmHg vs >20 mmHg), the sensitivity of ICPtcd was 100%; all measurements with high ICPi (>20 mmHg) also had a high ICPtcd values. Bland-Altman plot showed an overestimation of 6.2 mmHg (95% CI 5.08–7.30 mmHg) for ICPtcd compared to ICPi. AUC was 96.0% (95% CI 89.8–100%) and the estimated best threshold was at ICPi of 24.8 mmHg corresponding to a sensitivity 100% and a specificity of 91.2%. Conclusions This study provides preliminary evidence that ICPtcd may accurately exclude intracranial hypertension in patients with acute brain injury. Future studies with adequate power are needed to confirm this result.

Patients with severe traumatic brain injury and refractory intracranial hypertension were randomly assigned to either decompressive craniectomy or standard care. Craniectomy was associated with a significant reduction in intracranial pressure but worse outcomes. Among patients who are hospitalized with severe traumatic brain injury, 60% either die or survive with severe disability. 1 – 3 Of Australia's population of 22 million, 4 approximately 1000 patients annually sustain a severe traumatic brain injury, with associated lifetime costs estimated at $1 billion. 5 In the United States, the annual burden of traumatic brain injury is more than $60 billion. 6 After severe traumatic brain injury, medical and surgical therapies are performed to minimize secondary brain injury. 7 – 9 Increased intracranial pressure, which is typically caused by cerebral edema, is an important secondary insult. 7 , 9 , 10 Although few data regarding the monitoring of . . .

Practices for controlling intracranial pressure (ICP) in traumatic brain injury (TBI) patients admitted to the intensive care unit (ICU) vary considerably between centres. To help understand the rational basis for such variance in care, this study aims to identify the patient-level predictors of changes in ICP management. We extracted all heterogeneous data (2008 pre-ICU and ICU variables) collected from a prospective cohort ( n  = 844, 51 ICUs) of ICP-monitored TBI patients in the Collaborative European NeuroTrauma Effectiveness Research in TBI study. We developed the TILTomorrow modelling strategy, which leverages recurrent neural networks to map a token-embedded time series representation of all variables (including missing values) to an ordinal, dynamic prediction of the following day’s five-category therapy intensity level (TIL (Basic) ) score. With 20 repeats of fivefold cross-validation, we trained TILTomorrow on different variable sets and applied the TimeSHAP (temporal extension of SHapley Additive exPlanations) algorithm to estimate variable contributions towards predictions of next-day changes in TIL (Basic) . Based on Somers’ D xy , the full range of variables explained 68% (95% CI 65–72%) of the ordinal variation in next-day changes in TIL (Basic) on day one and up to 51% (95% CI 45–56%) thereafter, when changes in TIL (Basic) became less frequent. Up to 81% (95% CI 78–85%) of this explanation could be derived from non-treatment variables (i.e., markers of pathophysiology and injury severity), but the prior trajectory of ICU management significantly improved prediction of future de-escalations in ICP-targeted treatment. Whilst there was no significant difference in the predictive discriminability (i.e., area under receiver operating characteristic curve) between next-day escalations (0.80 [95% CI 0.77–0.84]) and de-escalations (0.79 [95% CI 0.76–0.82]) in TIL (Basic) after day two, we found specific predictor effects to be more robust with de-escalations. The most important predictors of day-to-day changes in ICP management included preceding treatments, age, space-occupying lesions, ICP, metabolic derangements, and neurological function. Serial protein biomarkers were also important and may serve a useful role in the clinical armamentarium for assessing therapeutic needs. Approximately half of the ordinal variation in day-to-day changes in TIL (Basic) after day two remained unexplained, underscoring the significant contribution of unmeasured factors or clinicians’ personal preferences in ICP treatment. At the same time, specific dynamic markers of pathophysiology associated strongly with changes in treatment intensity and, upon mechanistic investigation, may improve the timing and personalised targeting of future care.

Purpose Preventive treatments of traumatic intracranial hypertension are not yet established. We aimed to compare the efficiency of half-molar sodium lactate (SL) versus saline serum solutions in preventing episodes of raised intracranial pressure (ICP) in patients with severe traumatic brain injury (TBI). Methods This was a double-blind, randomized controlled trial including 60 patients with severe TBI requiring ICP monitoring. Patients were randomly allocated to receive a 48-h continuous infusion at 0.5 ml/kg/h of either SL (SL group) or isotonic saline solution (control group) within the first 12 h post-trauma. Serial measurements of ICP, as well as fluid, sodium, and chloride balance were performed over the 48-h study period. The primary outcome was the number of raised ICP (≥20 mmHg) requiring a specific treatment. Results Raised ICP episodes were reduced in the SL group as compared to the control group within the 48-h study period: 23 versus 53 episodes, respectively ( p  < 0.05). The proportion of patients presenting raised ICP episodes was smaller in the SL group than in the saline group: 11 (36 %) versus 20 patients (66 %) ( p  < 0.05). Cumulative 48-h fluid and chloride balances were reduced in the SL group compared to the control group (both p  < 0.01). Conclusion A 48-h infusion of SL decreased the occurrence of raised ICP episodes in patients with severe TBI, while reducing fluid and chloride balances. These findings suggest that SL solution could be considered as an alternative treatment to prevent raised ICP following severe TBI.

Intracranial pressure (ICP) monitoring is now viewed as integral to the clinical care of many life-threatening brain insults, such as severe traumatic brain injury, subarachnoid hemorrhage, and malignant stroke. It serves to warn of expanding intracranial mass lesions, to prevent or treat herniation events as well as pressure elevation which impedes nutrient delivery to the brain. It facilitates the calculation of cerebral perfusion pressure (CPP) and the estimation of cerebrovascular autoregulatory status. Despite advancements in our knowledge emanating from a half century of experience with this technology, important controversies remain related even to fundamental aspects of ICP measurements, including indications for monitoring, ICP treatment thresholds, and management of intracranial hypertension. Here, we review the history of ICP monitoring, the underlying pathophysiology as well as current perspectives on why, when and how ICP monitoring is best used. ICP is typically assessed invasively but a number of emerging, non-invasive technologies with inherently lower risk are showing promise. In selected cases, additional neuromonitoring can be used to assist in the interpretation of ICP monitoring information and adapt directed treatment accordingly. Additional efforts to expand the evidence base relevant to ICP monitoring, related technologies and management remain a high priority in neurosurgery and neurocritical care.

This article reviews the methods of monitoring and treating traumatic intracranial hypertension in intensive care settings. An elevation in intracranial pressure can be a medical or surgical emergency. There are many possible conditions that can lead to elevated intracranial pressure on either an acute or a chronic basis (Table 1). In this article, we focus on the increased intracranial pressure that occurs in patients after traumatic brain injury, since this is an area in which there are both physiological and clinical data. Traumatic brain injury is a medical and social problem worldwide, with an estimated 10 million cases leading to hospitalization or death each year. 1 In low- and medium-income countries, in which the use of motor-powered . . .

Purpose of Review Rebound intracranial hypertension (RIH) is a post-procedural treatment complication in patients with spontaneous intracranial hypotension (SIH) characterized by transient high-pressure headache symptoms. This article reviews the epidemiology, clinical features, risk factors, and treatment options for RIH. Recent Findings This article discusses how changes in underlying venous pressure and craniospinal elastance can explain symptoms of RIH, idiopathic intracranial hypertension (IIH), and SIH. Summary The pathophysiology of RIH provides a clue for how high and low intracranial pressure disorders, such as IIH and SIH, are connected on a shared spectrum.