Significant Increase In Intracranial Pressure Research Articles

Dynamics of Intracranial Pressure and Cerebrovascular Reactivity During Intrahospital Transportation of Traumatic Brain Injury Patients in Coma.

Intrahospital transportation (IHT) of patients with traumatic brain injury (TBI) is common and may have adverse consequences, incurring inherent risks. The data on the frequency and severity of clinical complications linked with IHT are contradictory, and there is no agreement on whether it is safe or potentially challenging for neurocritical care unit patients. Continuous intracranial pressure (ICP) monitoring is essential in neurointensive care. The role of ICP monitoring and management of cerebral autoregulation impairments in IHT of patients with severe TBI is underinvestigated. The purpose of this nonrandomized retrospective single-center study was to assess the dynamics of ICP and an improved pressure reactivity index (iPRx) as a measure of autoregulation during IHT. Seventy-seven men and fourteen women with severe TBI admitted in 2012-2022 with a mean age of 33.2 ± 5.2years were studied. ICP and arterial pressure were invasively monitored, and cerebral perfusion pressure and iPRx were calculated from the measured parameters. All patients were subjected to dynamic helical computed tomography angiography using a 64-slice scanner Philips Ingenuity computed tomography scan 1-2days after TBI. Statistical analysis of all results was done using a paired t-test, and p was preset at < 0.05. The logistic regression analysis was performed for cerebral ischemia development dependent on intracranial hypertension and cerebrovascular reactivity. IHT led to an increase in ICP in all the patients, especially during vertical movement in an elevator (maximum 75.2mm Hg). During the horizontal transportation on the floor, ICP remained increased (p < 0.05). The mean ICP during IHT was significantly higher (26.1 ± 13.5mm Hg, p < 0.001) than that before the IHT (19.9 ± 5.3mm Hg). The mean iPRx after and before IHT was 0.52 ± 0.04 and 0.23 ± 0.14, respectively (p < 0.001). Both horizontal and vertical transportation causes a significant increase in ICP and iPRx in patients with severe TBI, potentially leading to the outcome worsening.

TMIC-27. THE ROLE OF AQUAPORIN-4 IN GLIOBLASTOMA-ASSOCIATED VASOGENIC CEREBRAL EDEMA

Abstract Glioblastoma (GBM) is the most common and aggressive primary brain tumor in adults. Vasogenic cerebral edema is a severe complication that occurs in a majority of GBM patients, leading to a significant increase in intracranial pressure, accompanying neurological deficits, and increased mortality rates. Edema in GBM patients is almost exclusively managed by the corticosteroid dexamethasone (DEX), which has recently been found to have several drawbacks, including immunosuppression and interference with radiation therapy. Thus, there is an urgent need to better understand the mechanisms of edema resolution in GBM in order to identify alternative treatment strategies. The water channel aquaporin-4 (AQP4) is a critical player in the brain's water homeostasis, with increased levels in GBM compared to the normal brain. To gain more insight into the role of AQP4 in GBM-associated edema, we used the RCAS/tv-a system to generate de novo GBM with different driver mutations in Aqp4 knockout (KO), heterozygous (HET), and wild-type (WT) mice. Multiplex IF staining combined with RNAScope of tumors showed that AQP4 expression co-localized with GFAP-positive reactive astrocytes in perivascular areas. Our results indicated that tumor-bearing mice in an Aqp4-deficient background had increased edema content and decreased survival, suggesting that AQP4 is important for edema resolution from tumors. Loss of Aqp4 also significantly decreased astrocyte coverage in the tumor core, but not in the tumor periphery. Moreover, anti-VEGFA treatment only improved vessel leakage and reduced edema in WT tumor-bearing mice. Ongoing studies are focused on characterizing the impact of Aqp4 loss on the gene expression profile of tumor core-specific astrocytes using single-cell RNA sequencing and spatial transcriptomics. We are also studying the cellular distribution of AQP4 in GBM and the effect of DEX treatment on AQP4 levels.

Limitations of prone positioning in patients with aneurysmal subarachnoid hemorrhage and concomitant respiratory failure

ObjectiveProne positioning (PP) is an established treatment modality for respiratory failure. After aneurysmal subarachnoid hemorrhage (aSAH), PP is rarely performed considering the risk of intracranial hypertension. The aim of this study was to analyze the effects of PP on intracranial pressure (ICP), cerebral perfusion pressure (CPP) and cerebral oxygenation following aSAH. Patients and methods: Demographic and clinical data of aSAH patients admitted over a 6-year period and treated with PP due to respiratory insufficiency were retrospectively analyzed. ICP, CPP, brain tissue oxygenation (pBrO2), respiratory parameters and ventilator settings were analyzed before and during PP. ResultsThirty patients receiving invasive multimodal neuromonitoring were included. Overall, 97 PP sessions were performed. Mean arterial oxygenation and pBrO2 increased significantly during PP. We found a significant increase in median ICP compared to the baseline level in supine position. No significant changes in CPP were observed. Five PP sessions had to be terminated early due to medically refractory ICP-crisis. The affected patients were younger (p = 0.02) with significantly higher baseline ICP values (p = 0.009). Baseline ICP correlates significantly (p < 0.001) with ICP 1 h (R: 0.57) and 4 h (R: 0.55) after onset of PP. ConclusionPP in aSAH patients with respiratory insufficiency is an effective therapeutic option improving arterial and global cerebral oxygenation without compromising CPP. The significant increase in ICP was moderate in most sessions. However, as some patients experience intolerable ICP crises during PP, continuous ICP-Monitoring is considered mandatory. Patients with elevated baseline ICP and reduced intracranial compliance should not be considered for PP.

REBOA for the Treatment of Blast Polytrauma: Zone 3 Provides Cerebral Perfusion, Attenuates Organ Dysfunction and Reperfusion Coagulopathy Compared to Zone 1 in a Swine Model.

Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a lifesaving therapy for hemorrhagic shock following pelvic/lower extremity injuries in military settings. However, Zone 1 aortic occlusion (AO; above the celiac artery), while providing brain/cardiac perfusion, may induce/worsen visceral ischemia and organ dysfunction. In contrast, AO Zone 3 (below the renal arteries) provides abdominal perfusion potentially minimizing ischemia/reperfusion injury. We hypothesized that, compared with AO Zone 1, AO Zone 3 provides neuro/cardioprotection while minimizing visceral ischemia and reperfusion coagulopathy after severe traumatic hemorrhage due to pelvic/lower extremity injuries. Fifty-kilogram male Yorkshire swine underwent a blast polytrauma injury followed by a resuscitation protocol with randomization to no AO (No AO, n = 6) or AO with REBOA at Zone 1 (AO Zone 1; n = 6) or Zone 3 (AO Zone 3; n = 4). Vital signs and intracranial pressure (ICP) were monitored for 240 minutes. Citrate native and tissue plasminogen activator challenge thrombelastography, prothrombin time, creatinine, lipase, total bilirubin, troponin, and enzyme-linked immunosorbent assays protein levels were measured at set intervals. Both AO groups had significant increases in mean arterial pressure during aortic occlusion. All three groups had significant increases in ICP, but final ICP in the No AO group (26 ± 5.8 mm Hg) was significantly elevated compared with AO Zone 1 (17 ± 5.2 mm Hg) and AO Zone 3 (16 ± 4.2 mm Hg) ( p < 0.01). The final mean troponin in the No AO group (4.10 ± 5.67 ng/mL) was significantly higher than baseline (0.03 ± 0.02 ng/mL, p < 0.05), while the two AO groups had no significant changes ( p > 0.05). AO Zone 1 was the only group associated with hyperfibrinolysis ( p < 0.05) and significantly increased prothrombin time ( p < 0.05). Only AO Zone 1 group had significantly higher markers of organ damage. Compared with AO Zone 1, AO Zone 3 provided similar neuro/cardioprotection but with less organ dysfunction and coagulopathy. This study suggests that Zone 3 REBOA may be preferable over Zone 1 for treating military relevant blast polytrauma with minimal intra-abdominal and chest trauma, but further clinical investigation is warranted.

Cerebrovascular Pressure Reactivity According to Long-Pressure Reactivity Index During Spreading Depolarizations in Aneurysmal Subarachnoid Hemorrhage

BackgroundSpreading depolarization (SD) has been linked to the impairment of neurovascular coupling. However, the association between SD occurrence and cerebrovascular pressure reactivity as a surrogate of cerebral autoregulation (CA) remains unclear. Therefore, we analyzed CA using the long-pressure reactivity index (L-PRx) during SDs in patients with aneurysmal subarachnoid hemorrhage (aSAH).MethodsA retrospective study of patients with aSAH who were recruited at two centers, Heidelberg (HD) and Berlin (BE), was performed. Continuous monitoring of mean arterial pressure (MAP) and intracranial pressure (ICP) was recorded. ICP was measured using an intraparenchymal probe in HD patients and was measure in BE patients through external ventricular drainage. Electrocorticographic (ECoG) activity was continuously recorded between 3 and 13 days after hemorrhage. Autoregulation according to L-PRx was calculated as a moving linear Pearson’s correlation of 20-min averages of MAP and ICP. For every identified SD, 60-min intervals of L-PRx were averaged, plotted, and analyzed depending on SD occurrence. Random L-PRx recording periods without SDs served as the control.ResultsA total of 19 patients (HD n = 14, BE n = 5, mean age 50.4 years, 9 female patients) were monitored for a mean duration of 230.4 h (range 96–360, STD ± 69.6 h), during which ECoG recordings revealed a total number of 277 SDs. Of these, 184 represented a single SD, and 93 SDs presented in clusters. In HD patients, mean L-PRx values were 0.12 (95% confidence interval [CI] 0.11–0.13) during SDs and 0.07 (95% CI 0.06–0.08) during control periods (p < 0.001). Similarly, in BE patients, a higher L-PRx value of 0.11 (95% CI 0.11–0.12) was detected during SDs than that during control periods (0.08, 95% CI 0.07–0.09; p < 0.001). In a more detailed analysis, CA changes registered through an intraparenchymal probe (HD patients) revealed that clustered SD periods were characterized by signs of more severely impaired CA (L-PRx during SD in clusters: 0.23 [95% CI 0.20–0.25]; single SD: 0.09 [95% CI 0.08–0.10]; control periods: 0.07 [95% CI 0.06–0.08]; p < 0.001). This group also showed significant increases in ICP during SDs in clusters compared with single SD and control periods.ConclusionsNeuromonitoring for simultaneous assessment of cerebrovascular pressure reactivity using 20-min averages of MAP and ICP measured by L-PRx during SD events is feasible. SD occurrence was associated with significant increases in L-PRx values indicative of CA disturbances. An impaired CA was found during SD in clusters when using an intraparenchymal probe. This preliminary study validates the use of cerebrovascular reactivity indices to evaluate CA disturbances during SDs. Our results warrant further investigation in larger prospective patient cohorts.

The relationship between myodural bridges, hyperplasia of the suboccipital musculature, and intracranial pressure.

During mammalian evolution, the Myodural Bridges (MDB) have been shown to be highly conserved anatomical structures. However, the putative physiological function of these structures remains unclear. The MDB functionally connects the suboccipital musculature to the cervical spinal dura mater, while passing through the posterior atlanto-occipital and atlanto-axial interspaces. MDB transmits the tensile forces generated by the suboccipital muscles to the cervical dura mater. Moreover, head movements have been shown to be an important contributor to human CSF circulation. In the present study, a 16-week administration of a Myostatin-specific inhibitor, ACE-031, was injected into the suboccipital musculature of rats to establish an experimental animal model of hyperplasia of the suboccipital musculature. Using an optic fiber pressure measurement instrument, the present authors observed a significant increase in intracranial pressure (ICP) while utilizing the hyperplasia model. In contrast, surgically severing the MDB connections resulted in a significant decrease in intracranial pressure. Thus, these results indicated that muscular activation of the MDB may affect CSF circulation, suggesting a potential functional role of the MDB, and providing a new research perspective on CSF dynamics.

Changes In Intracranial Pressure in Patients with External Ventricular Drainage of CSF During Nursing Interventions

Introduction. When managing intracranial pressure (ICP) disorders, that is, deviations from the normal value (5 - 15 mmHg), it helps to understand the variability of cerebral blood volume and cerebrospinal fluid. Aim. To explore from a series of cases the impact of nursing interventions on the increase of intracranial pressure and the possibility of preventive action on possible oscillations of measured pressure values by modifying sedation and analgesia in order to avoid potentially negative effects on brain injury. Methods. The study included six patients, with the average age of 59 years, hospitalized between December 2018 and May 2019, on whom measurements were performed before, immediately after and 30 minutes after the end of a particular intervention using an external drainage and monitoring system. Intracranial pressures of patients in an induced coma were compared with those who were in a natural coma. Results. During morning nursing care and aspiration of secretions, an increase in the mean value of ICP was observed immediately after the intervention, but the t-test for dependent samples showed that it was not statistically significant, while in massaging patients with turning it to the side it was statistically significant. Combining all interventions into one, without categorization, there was also a statistically significant increase in intracranial pressure immediately upon completion of morning nursing care. After 30 minutes, the pressure values in all interventions approach the initial value and remain within the deviation of 1 mmHg. Conclusion. Most nursing interventions are associated with a slight increase in ICP that is not statistically significant. Greater oscillations were observed in patients in an induced coma than in those in a natural coma, which could probably have been avoided by even stricter titration of analgosedation immediately before and during nursing interventions.

The Impact of a Cervical Collar on Intracranial Pressure in Traumatic Brain Injury Patients: A Systematic Review and Meta-Analysis

Purpose: Although the use of a cervical collar in the prehospital setting is recommended to prevent secondary spinal cord injuries and ensure spinal immobilization, it is not known what effects this has on raising intracranial pressure (ICP) in traumatic brain injury (TBI) patients. In the absence of studies measuring ICP in the prehospital setting, the aim of this study was to systematically review the data related to ICP changes measured after presentation at the hospital in patients who had arrived wearing cervical collars. Methods: We searched Medline (PubMed), Embase, CINAHL, and Google Scholar for studies that investigated in-hospital ICP changes in TBI patients arriving at the hospital wearing collars. Titles, abstracts, and full texts were then searched for inclusion in the study. A narrative synthesis, as well as a meta-analysis, was performed. Results: Of the 1006 studies identified, only three met the inclusion/exclusion criteria. The quality of the three included studies was moderate and the risk of bias was low. All three studies used the Laerdal Stifneck collar, but all studies showed an increase in ICP after application of the collar. A further three studies that measured ICP but did not fit the systematic search were also included due to low patient numbers. A meta-analysis of the pooled data confirmed a significant increase in ICP, although between the four studies, only 77 patients were included. The meta-analysis also confirmed that after removal of the collar, there was a significant decrease in ICP. Conclusions: Our study suggests that the use of a cervical collar increases ICP in TBI and head injury patients, which may have detrimental effects. However, due to the extremely low sample size from all six studies, caution must be exercised when interpreting these data. Thus, further high-quality research is necessary to unequivocally clarify whether cervical collars should be used in patients with TBI.

Transient Increases in Intracranial Pressure After Soccer Heading

Objective To evaluate whether intracranial pressure (ICP) continued to stay elevated in trained athletes 24 hours after soccer heading. Methods Eight male subjects (21.7±1.7 years) were recruited from the UCSD soccer team to participate in the study. Baseline ICP and cardiovascular variables were recorded, and measurements were repeated after subjects underwent the heading trial. Acoustical evoked tympanic membrane displacement was used to estimate ICP, where decreasing volume displacement (-Vm) is associated with an increase in ICP. Mean arterial pressure (MAP) and heart rate (HR) were measured through the volume-clamp method. The heading trial consisted of 6 repeated headers of a soccer ball kicked from 32 meters away into a regulation goal. Follow up measurements of ICP, MAP, and HR were recorded 24 hours after heading trial. Measurements were taken in three randomized positions: 15° head-up tilt (HUT), 0° supine, -15° head-down tilt (HDT). Results At 15° HUT, baseline mean Vm was 37.81±133.21 nL, -20.82±158.27 nL immediately after heading trial (P=0.0482, paired t test), and 27.20±140.61 nL at 24 hours post soccer heading (P=0.1738, paired t test), corresponding to a significant increase in ICP immediately after the heading trial that then returns to baseline levels after 24 hours. At 0° supine, baseline mean Vm was -46.19±178.50 nL, -84.27±183.55 nL after heading trial (P=0.0321, paired t test) and -62.90±135.44 nL at 24 hours post soccer heading (P=0.5048, paired t test), corresponding to the same trend observed in the 15° HUT position. At -15° HDT, mean Vm was -148.48±196.07 nL at baseline, -187.02±186.19 nL after heading trial (P=0.1176, paired t test), and -151.10±174.86 nL at 24 hours post soccer heading (P=0.9329), corresponding to no significant increase in ICP at either time point. MAP and HR did not significantly change at any point after soccer heading. Discussions ICP significantly increased after soccer heading at 15° HUT and 0° supine but returned to baseline levels after 24 hours. ICP at -15° HDT, MAP, and HR did not significantly change immediately after soccer heading or 24 hours after soccer heading. While these results demonstrate a mild increase in ICP that subsides after 24 hours, athletes may experience these transient increases in ICP continuously for extended periods of time during their entire athletic careers. These cycles of increased ICP may result in a state of intermittent but persistently altered cerebral blood flow, which may suggest a health risk of participating in head contact sports such as soccer.

Bulk flow of cerebrospinal fluid observed in periarterial spaces is not an artifact of injection

Cerebrospinal fluid (CSF) flowing through periarterial spaces is integral to the brain's mechanism for clearing metabolic waste products. Experiments that track tracer particles injected into the cisterna magna (CM) of mouse brains have shown evidence of pulsatile CSF flow in perivascular spaces surrounding pial arteries, with a bulk flow in the same direction as blood flow. However, the driving mechanism remains elusive. Several studies have suggested that the bulk flow might be an artifact, driven by the injection itself. Here, we address this hypothesis with new in vivo experiments where tracer particles are injected into the CM using a dual-syringe system, with simultaneous injection and withdrawal of equal amounts of fluid. This method produces no net increase in CSF volume and no significant increase in intracranial pressure. Yet, particle-tracking reveals flows that are consistent in all respects with the flows observed in earlier experiments with single-syringe injection.

Intracranial Pressure After Soccer Heading

OBJECTIVETo evaluate the effect of soccer heading on intracranial pressure (ICP) in trained athletes.METHODSEight subjects (all male, 21.7±1.7 years) were recruited from the UC San Diego soccer team. ICP and cardiovascular variables were recorded before and after 6 repeats of heading a soccer ball kicked from 35 yards away, into a goal. ICP was estimated non‐invasively from acoustical evoked tympanic membrane displacement (Vm), where a more negative volume displacement is correlated with higher ICP. Mean arterial pressure (MAP), heart rate (HR; Nexfin, Netherlands), and ICP were recorded in three different postures, 15° head up tilt (HUT), 0° supine, −15° head down tilt (HDT), in a randomized order.RESULTSMean Vm at 15° HUT was 37.81±133.21 nL at baseline and −20.82±158.27 nL immediately post soccer heading (P=0.0482, paired t test), analogous to an increased ICP. At 0° supine, mean Vm was −46.19±178.50 nL at baseline and −84.27±183.55 nL after impact (P=0.0321, paired t test). At −15° HDT, mean Vm was −148.48±196.07 nL at baseline and −187.02±186.19 nL immediately post soccer heading (P=0.1176, paired t test). MAP and HR did not significantly change between the baseline and post soccer heading measurements.DISCUSSIONAfter repeated soccer ball heading, ICP significantly increased at 15° HUT and 0° supine, while ICP at −15° HDT, MAP and HR did not significantly change. The relative increase in ICP associated with HDT is comparable to previously described trends. Although the measurement technique currently employed does not provide an absolute ICP baseline, the technique has been established as useful in evaluating relative changes. Under that interpretation, these results reflect what may be an elevated ICP related to soccer heading impacts. Accordingly, the results of this study suggest a potential health risk of participation in head contact sports.Support or Funding InformationNASA (80NSSC19K0020) and Novo Nordic Foundation (NNF16OC0019196)Soccer Heading Increases Intracranial Pressure at Head Up Tilt and Supine PositionsVolume displacement of tympanic membrane (Vm), measured non‐invasively from acoustical evoked tympanic membrane displacement, indicated an increase in intracranial pressure (ICP) after soccer heading at 15° head up tilt (HUT) and 0° supine (n = 8, paired t test, *P &lt; 0.05). No significant increase in ICP at −15° head down tilt (HDT) was observed after soccer heading.Figure 1

Pulmonary insufficiency in acute stroke: risk factors and mechanisms of development

Various degrees of pulmonary insufficiency (PI) (PaO2 ≤60 mm Hg, SaO2 ≤90%) are diagnosed in most of patients with severe acute stroke (AS). Frequency and severity of PI positively correlates with the severity of AS. PI worsens patient's condition, prolongs the hospitalization period, and increases the probability of fatal outcome. Early clinical signs of PI may be undiagnosed due to the severity of stroke and thus not treated. The initiating pathogenic mechanism of PI is stress-related activation of sympathetic nervous system (SNS) and systemic immunosuppression. In severe stroke with mass effect, the rapid and significant increase in intracranial pressure may additionally activate the SNS. Risk factors of PI include older age, previous pulmonary disease, prolonged supine position, respiratory muscle dysfunction, apnea, and concomitant somatic diseases. Decompensation of somatic diseases leads to multiple stage reactions with facilitation of functional and morphologic changes in the pulmonary system, hypoxemia and hypoxia, promotes infectious complications and multiple organ failure and worsens neurological outcome. Diagnosis and treatment of PI in AS decreases mortality and improves rehabilitation prognosis.

Systemic and CSF Interleukin-1α Expression in a Rabbit Closed Cranium Subarachnoid Hemorrhage Model: An Exploratory Study.

Background: The inflammatory pathway in cerebrospinal fluid (CSF) leads to delayed cerebral vasospasm (DCVS) and delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH). The role of IL-1α has never been evaluated in a rabbit SAH model. The aim of our study is to analyze systemic and CSF changes of IL-1α, and to evaluate potential associations with the onset of DCVS in a rabbit closed cranium SAH model. Methods: 17 New Zealand white rabbits were randomized into two groups, SAH (n = 12) and sham (n = 5). In the first group, SAH was induced by extracranial-intracranial shunting from the subclavian artery into the cerebral cistern of magna under intracranial pressure (ICP) monitoring. The sham group served as a control. The CSF and blood samples for IL-1α measurement were taken at day zero before SAH induction and at day three. Results: There was a significant increase of ICP (p = 0.00009) and a decrease of cerebral perfusion pressure (CPP) (p = 0.00089) during SAH induction. At follow up, there was a significant increase of systemic IL-1α in the SAH as compared with the sham group (p = 0.042). There was no statistically significant difference in the CSF values in both groups. The CSF IL-1α values showed a correlation trend of DCVS. Conclusions: Systemic IL-1α levels are elevated after SAH induction in a rabbit SAH model.

Does Tracheal Lidocaine Instillation Reduce Intracranial Pressure Changes After Tracheal Suctioning in Severe Head Trauma? A Prospective, Randomized Crossover Study.

Tracheal suctioning is a routine procedure in mechanically ventilated children, however, in severe head-injured patients it can result in potential deleterious increase in intracranial pressure. We aimed to assess the effect of tracheal lidocaine administration on intracranial pressure during tracheal suctioning. Prospective randomized controlled crossover study. PICU of a tertiary hospital. Eleven patients with severe head trauma (Glasgow Coma Scale score 4-8) INTERVENTIONS:: Lidocaine (1.5 mg/kg) or saline solution was endotracheally instilled before a standardized tracheal suctioning maneuver. Each patient received both treatments in a crossover design. Cerebral hemodynamic and systemic and ventilatory effects were assessed at four time points: in baseline (T0), within 2 minutes (T1), 5 minutes (T2), and 15 minutes after tracheal instillation (T3). The 2-minute time interval around tracheal suctioning was used to assess each treatment efficacy MEASUREMENTS AND MAIN RESULTS:: The time course of intracranial pressure was different throughout the study in both treatment groups, with a significant increase of intracranial pressure from 14.82 ± 3.48 to 23.27 ± 9.06 with lidocaine (p = 0.003) and from 14.73 ± 2.41 to 30.45 ± 13.14 with saline (p = 0.02). The mean variation in intracranial pressure immediately after tracheal suctioning was smaller with lidocaine instillation than saline (8.45 vs 15.72 mm Hg; p = 0.006). Patients treated with lidocaine returned to baseline intracranial pressure value at 5 minutes after tracheal suctioning whereas those receiving saline solution returned to baseline intracranial pressure value at 15 minutes. Although patients treated with lidocaine had no significant hemodynamic changes, patients receiving saline solution experienced a higher mean value of mean arterial pressure (99.36 vs 81.73 mm Hg; p = 0.004) at T1. This preliminary study showed that tracheal lidocaine instillation can attenuate increase in intracranial pressure induced by tracheal suctioning and favor a faster return to the intracranial pressure baseline levels without significant hemodynamic and ventilatory changes.

The Impact of Intrahospital Transports on Brain Tissue Metabolism in Patients with Acute Brain Injury.

Patients with severe acute brain injury (ABI) often require intrahospital transports (IHTs) for repeated computed tomography (CT) scans. IHTs are associated with serious adverse events (AE) that might pose a risk for secondary brain injury. The goal of this study was to assess IHT-related alterations of cerebral metabolism in ABI patients. We included mechanically ventilated patients with ABI who had continuous multimodality neuromonitoring during an 8-h period before and after routine IHT. Intracranial pressure (ICP), cerebral perfusion pressure (CPP), brain tissue oxygenation (PtiO2) as well as cerebral and subcutaneous microdialysis parameters (lactate, pyruvate, glycerol, and glutamate) were recorded. Values were compared between an 8-h period before (pre-IHT) and after (post-IHT) the IHT. A total of 23 IHT for head CT scans in 18 patients were analyzed. Traumatic brain injury (n = 7) was the leading cause of ABI, followed by subarachnoid hemorrhage (n = 6) and intracerebral hemorrhage (n = 5). The analyzed microdialysis parameters in the brain tissue as in the subcutaneous tissue did not show significant changes between the pre-IHT and post-IHT period. In addition, we observed no significant increase in ICP or decrease in CPP and PtiO2 in the 8-h period after IHT. While the occurrence of AE during IHT is a known risk factor for ABI patients, our results demonstrate that IHTs do not alter the brain tissue chemistry in a significant manner. This fact may help assess the risk for routine IHT more accurately.

The course of intracranial pressure after antipyretic therapy in acute brain injury.

The present study was performed to evaluate intracranial pressure (ICP) variations after antipyretic therapy and their relationship to ICP at baseline (ICPbas) in acute brain injury (ABI) patients. We completed a retrospective analysis on data derived from 2 previously published prospective observational studies. The first study involved 32 ABI patients and was performed to elucidate the cerebral and hemodynamic effects of intravenous (IV) paracetamol. The second study involved 30 ABI patients and was performed to investigate cerebral and hemodynamic effects of intramuscular IM diclofenac sodium (DCF). Overall patient population was divided into 2 groups: 1) group A (G-A) when ICPbas was ≤15 mmHg; and 2) group B (G-B) when ICPbas was >15 mmHg. The main objective was to evaluate if ICPbas affects the time course of ICP after antipyretics administration. Data from 62 ABI patients were analyzed. We failed to observe a significant change in ICP after antipyretic treatment in the overall group of patients (P<inf>1</inf>=0.486). A significant difference, however, was found between the two groups (P<inf>2</inf><0.001). We observed that in the G-A, ICP increased in response to antipyretic administration, whereas in the G-B, ICP decreased. These opposite responses are reflected in the statistically significant interaction (P<inf>3</inf><0.001). Variation in ICP after antipyretic therapy is influenced by ICPbas. Specifically, patients with ICPbas≤15 mmHg showed a significant increase in ICP after antipyretic therapy, while a significant reduction in ICP was observed in patients with ICPbas>15 mmHg.

Possible Spironolactone Induced Intracranial Hypertension in a Patient with Androgenetic Alopecia: A Case Report

Spironolactone is a well-known drug with many indications. In dermatology, it may be used for treating androgenetic alopecia with a high androgen level. A patient with idiopathic papilledema that was inactive for many years experienced a significant increase in intracranial pressure after receiving spironolactone. The symptoms were resolved soon after the medication was discontinued. This report draws physicians’ attention to such rare adverse events that may have unwanted consequences.

Effect of caudal block using different volumes of local anaesthetic on optic nerve sheath diameter in children: a prospective, randomized trial

Background:Caudal block is commonly administered for postoperative analgesia in children. Although caudal block with 1.5 ml kg−1 local anaesthetic has been reported to reduce cerebral oxygenation in infants, the effect of caudal block on intracranial pressure (ICP) in children has not been well investigated. Optic nerve sheath diameter (ONSD) correlates with degree of ICP. This study aimed to estimate the effects of caudal block on ICP according to volume of local anaesthetic using ultrasonographic measurement of ONSD in children. Methods:Eighty patients, 6- to 48-months-old, were randomly allocated to the high-volume (HV) or low-volume (LV) groups for caudal block with ropivacaine 0.15%, 1.5 ml kg−1 or 1.0 ml kg−1, respectively. Measurement of ONSD was performed before (T0), immediately after (T1), and 10 min (T2) and 30 min (T3) after caudal block. Results:The two groups exhibited significant differences in ONSD according to time (PGroup x Time=0.003). The HV group exhibited significantly greater changes in ONSD from T0 to T2 and T3 than the LV group. However, in both groups, ONSDs at T1, T2 and T3 were significantly greater compared with those at T0, with the highest values at T2. Conclusions:Caudal block with a high volume of local anaesthetic can cause a greater increase in ICP than caudal block with a low volume of local anaesthetic. However, caudal block with 1.0 ml kg−1 of local anaesthetic can also result in a significant increase in ICP. Clinical trial registrationNCT02768493.

Effects of Exposure to Blast Overpressure on Intracranial Pressure and Blood-Brain Barrier Permeability in a Rat Model.

Exposure to blast overpressure (BOP) activates a cascade of pathological processes including changes in intracranial pressure (ICP) and blood-brain barrier (BBB) permeability resulting in traumatic brain injury (TBI). In this study the effect of single and multiple exposures at two intensities of BOP on changes in ICP and BBB permeability in Sprague-Dawley rats was evaluated. Animals were exposed to a single or three repetitive (separated by 0.5 h) BOPs at 72 kPa or 110 kPa. ICP was monitored continuously via telemetry for 6 days after exposure to BOP. The alteration in the permeability of BBB was determined by extravasation of Evans Blue (EB) into brain parenchyma. A significant increase in ICP was observed in all groups except the single 72 kPa BOP group. At the same time a marked increase in BBB permeability was also seen in various parts of the brain. The extent of ICP increase as well as BBB permeability change was dependent on intensity and frequency of blast.

Intrahospital Transfer of Patients with Traumatic Brain Injury: Increase in Intracranial Pressure.

To assess the dynamic of intracranial pressure (ICP), cerebral perfusion pressure (CPP), and dynamic pressure reactivity index (PRx) during intrahospital transport. There were 33 comatose patients with severe traumatic brain injury (TBI). The mean age was 36.3 ± 4.8 years (range 19-45 years), and there were 17 men and 16 women. The median Glasgow Coma Scale score at admission was 6.2 ± 0.7. Computed tomography (CT) included native CT, perfusion CT, and CT angiography. The mean CPPs before and after the CT scans were 95.9 ± 10.7 and 81.5 ± 12.5 mmHg respectively. The mean ICP before transport was 19.98 ± 5.3 mmHg (minimum 11.7; maximum 51.7). It was statistically significantly lower (p < 0.001) than during the transfer (26.1 ± 13.5 mmHg). During the period described all patients had increased ICP, especially during vertical movement in an elevator. During horizontal movement on the floor ICP remained higher (p < 0.05). The mean dynamic PRx before and after intrahospital transport was 0.23 ± 0.14 and 0.52 ± 0.04, respectively (p < 0.001). Average duration of the transfer and CT study was 15.3 ± 3.4 min. Intrahospital transport of patients with TBI may lead to a significant increase in ICP, dynamic PRx, and decreased CPP. The results suppose that the decision to perform brain CT in comatose patients with TBI should be carefully considered by clinicians.