Sustained Intracranial Pressure Research Articles

High intracranial pressure following endoscopic third ventriculostomy: illustrative case.

Endoscopic third ventriculostomy (ETV) is an effective procedure for the treatment of triventriculomegaly associated with aqueductal stenosis. However, some patients can develop severe and symptomatic intracranial pressure (ICP) elevations in the immediate postoperative period that can be monitored and treated with external ventricular drain (EVD) placement and controlled cerebrospinal fluid (CSF) diversion until the ICP normalizes and symptoms resolve. The authors describe the case of a 39-year-old male who underwent ETV and intraoperative EVD placement for obstructive hydrocephalus associated with aqueductal stenosis. The patient was noted to have sustained ICP elevations in the immediate perioperative period but ultimately experienced a successful clinical outcome without requiring a ventriculoperitoneal shunt. Significant sustained ICP elevations in the immediate postoperative period following ETV can occur and may indicate a prolonged adjustment period. These elevations can be tolerated if the patient's symptoms and ICP are well controlled, with temporary external CSF diversion if the patient becomes symptomatic, as the ICP will likely normalize with a reassuring clinical outcome. https://thejns.org/doi/10.3171/CASE24478.

869 Early Signs of Elevated Intracranial Pressure (ICP) on Computed Tomography Correlate With Measured ICP in the Intensive Care Unit and Six-month Outcome Following Moderate to Severe TBI

INTRODUCTION: Identifying patients at risk for increased intracranial pressure (ICP) followingTBI via baseline computed tomography (CT) has not previously been validated in a prospective dataset. METHODS: Data were obtained from the Progesterone for Traumatic Brain Injury, Experimental Clinical Treatment (ProTECTIII) multicenter clinical trial. Baseline CT scans for 881 participants were individually reviewed by a blinded central neuroradiologist. Five signs of elevated ICP were measured (sulcal obliteration, lateral ventricle compression, 3rd ventricle compression, midline shift, and herniation). Associations between signs of increased ICP and outcomes (6-month functional outcome and mortality) were assessed. RESULTS: Sulcal obliteration (p = 0.029) and third ventricular compression (p = 0.039) were associated with elevated ICP. Univariate regression analyses indicated that increasing combinations of the five defined signs of elevated ICP were associated with mortality, poor functional outcome, and time to death. There was also an increased likelihood of mortality if patients required craniotomy (OR = 4.318, 95% Confidence Interval [1.330-16.030]) or hemicraniectomy (OR = 2.993 [1.109-8.482]). On multivariate regression analyses, hemorrhage location was associated with mortality (posterior fossa, OR = 3.208 [1.120-9.188] and basal ganglia, OR = 3.079 [1.178-8.077]). Volume of hemorrhage >30cc was also associated with increased mortality, OR = 3.702 [1.575-8.956]). The proportion of patient hours with sustained ICP = 20 mmHg, and maximum ICP = 20 mmHg, were also directly correlated with increased mortality (OR = 64.99 [7.731-635.51]; and OR = 1.025 [1.004-1.047]). Poor functional outcome was predicted by concurrent presence of all five radiographic signs of elevated ICP (OR = 4.44 [1.514-14.183]) and presence of frontal lobe (OR = 2.951 [1.265-7.067]), subarachnoid (OR = 2.231 [1.067-4.717]), or intraventricular (OR = 2.249 [1.159-4.508]) hemorrhage. Time to death was modulated by total patient days of elevated ICP = 20 mmHg (Effect Size = 3.424 [1.500, 5.439]) in the first two weeks of hospitalization. CONCLUSIONS: ICP-related imaging variables can be prognosticate for moderate-severe TBI.

Sustained ICP Elevation Is a Driver of Spatial Memory Deficits After Intraventricular Hemorrhage and Leads to Activation of Distinct Microglial Signaling Pathways.

The mechanisms of cognitive decline after intraventricular hemorrhage (IVH) in some patients continue to be poorly understood. Multiple rodent models of intraventricular or subarachnoid hemorrhage have only shown mild or even no cognitive impairment on subsequent behavioral testing. In this study, we show that intraventricular hemorrhage only leads to a significant spatial memory deficit in the Morris water maze if it occurs in the setting of an elevated intracranial pressure (ICP). Histopathological analysis of these IVH + ICP animals did not show evidence of neuronal degeneration in the hippocampal formation after 2weeks but instead showed significant microglial activation measured by lacunarity and fractal dimensions. RNA sequencing of the hippocampus showed distinct enrichment of genes in the IVH + ICP group but not in IVH alone having activated microglial signaling pathways. The most significantly activated signaling pathway was the classical complement pathway, which is used by microglia to remove synapses, followed by activation of the Fc receptor and DAP12 pathways. Thus, our study lays the groundwork for identifying signaling pathways that could be targeted to ameliorate behavioral deficits after IVH.

Waveform Morphology as a Surrogate for ICP Monitoring: A Comparison Between an Invasive and a Noninvasive Method.

BackgroundAlthough the placement of an intraventricular catheter remains the gold standard technique for measuring intracranial pressure (ICP), the method has several limitations. Therefore, noninvasive alternatives to ICP (ICPni) measurement are of great interest. The main objective of this study was to compare the correlation and agreement of wave morphology between ICP (standard intraventricular ICP monitoring) and a new ICPni monitor in patients admitted with stroke. The second objective was to estimate the discrimination of the noninvasive method to detect intracranial hypertension.MethodsWe prospectively collected data of adults admitted to an intensive care unit with subarachnoid hemorrhage, intracerebral hemorrhage, or ischemic stroke in whom an invasive ICP monitor was placed. Measurements were simultaneously collected from two parameters [time-to-peak (TTP) and the ratio regarding the second and first peak of the ICP wave (P2/P1 ratio)] of ICP and ICPni wave morphology monitors (Brain4care). Intracranial hypertension was defined as an invasively measured sustained ICP > 20 mm Hg for at least 5 min.ResultsWe studied 18 patients (subarachnoid hemorrhage = 14; intracerebral hemorrhage = 3; ischemic stroke = 1) on 60 occasions with a median age of 52 ± 14.3 years. A total of 197,400 waves (2495 min) from both ICP (standard ICP monitoring) and the ICPni monitor were sliced into 1-min-long segments, and we determined TTP and the P2/P1 ratio from the mean pulse. The median invasively measured ICP was 13 (9.8–16.2) mm Hg, and intracranial hypertension was present on 18 occasions (30%). The correlation and agreement between invasive and noninvasive methods for wave morphology were strong for the P2/P1 ratio and moderate for TTP using categoric (κ agreement 88.1% and 71.3%, respectively) and continuous (intraclass correlation coefficient 0.831 and 0.584, respectively) measures. There was a moderate but significant correlation with the mean ICP value (P2/P1 ratio r = 0.427; TTP r = 0.353; p < 0.001 for all) between noninvasive and invasive techniques. The areas under the curve to estimate intracranial hypertension were 0.786 [95% confidence interval (CI) 0.72–0.93] for the P2/P1 ratio and 0.694 (95% CI 0.60–0.74) for TTP.ConclusionsThe new ICPni wave morphology monitor showed a good agreement with the standard invasive method and an acceptable discriminatory power to detect intracranial hypertension.Clinical trial registration Trial registration: NCT05121155.

Intracranial pressure spikes trigger spreading depolarizations.

Spreading depolarizations are highly prevalent and spatiotemporally punctuated events worsening the outcome of brain injury. Trigger factors are poorly understood but may be linked to sudden worsening in supply-demand mismatch in compromised tissue. Sustained or transient elevations in intracranial pressure are also prevalent in the injured brain. Here, using a mouse model of large hemispheric ischaemic stroke, we show that mild and brief intracranial pressure elevations (20 or 30 mmHg for just 3 min) potently trigger spreading depolarizations in ischaemic penumbra (4-fold increase in spreading depolarization occurrence). We also show that 30 mmHg intracranial pressure spikes as brief as 30 s are equally effective. In contrast, sustained intracranial pressure elevations to the same level for 30 min do not significantly increase the spreading depolarization rate, suggesting that an abrupt disturbance in the steady state equilibrium is required to trigger a spreading depolarization. Laser speckle flowmetry consistently showed a reduction in tissue perfusion, and two-photon pO2 microscopy revealed a drop in venous pO2 during the intracranial pressure spikes suggesting increased oxygen extraction fraction, and therefore, worsening supply-demand mismatch. These haemodynamic changes during intracranial pressure spikes were associated with highly reproducible increases in extracellular potassium levels in penumbra. Consistent with the experimental data, a higher rate of intracranial pressure spikes was associated with spreading depolarization clusters in a retrospective series of patients with aneurysmal subarachnoid haemorrhage with strong temporal correspondence. Altogether, our data show that intracranial pressure spikes, even when mild and brief, are capable of triggering spreading depolarizations. Aggressive prevention of intracranial pressure spikes may help reduce spreading depolarization occurrence and improve outcomes after brain injury.

Superior sagittal sinus-to-internal jugular vein bypass shunt with covered stent construct for intractable intracranial hypertension resulting from iatrogenic supratorcular sinus occlusion: technical note.

Acute occlusion of the posterior sagittal sinus may lead to dramatic increase in intracranial pressure (ICP), refractory to standard treatment. Hybrid vascular bypass of cranial venous outflow into the internal jugular vein (IJV) has seldom been described for this in recent neurosurgical literature. To describe creation of a novel vascular bypass shunt from the superior sagittal sinus (SSS) to internal jugular vein (IJV) utilizing a covered stent-Dacron graft construct for control of refractory ICP. We illustrate a patient with refractory ICP increases after acute sinus ligation that was performed to halt torrential bleeding from intraoperative injury. A temporary shunt was created that successfully controlled ICP. From the promising results of the temporary shunt, we utilized a prosthetic hybrid bypass graft to function as a shunt from the sagittal sinus to IJV. Yet the associated anticoagulation led to complications and a poor outcome. Rapid and sustained ICP reduction can be expected after sagittal sinus-to-jugular bypass shunt placement in acute sinus occlusion. Details of the surgical technique are described. Heparin anticoagulation, while imperative, is also associated with worrisome complications. Acute occlusion of posterior third of sagittal sinus carries a very malignant clinical course. Intractable intracranial hypertension from acute sinus occlusion may be effectively treated with a SSS-IJV bypass shunt. A covered stent construct provides an effective vascular bypass conduit. However, the anticoagulation risk can lead to fatal outcomes. The neurosurgeon must always strive for primary repair of an injured sinus.

The Limited Impact of Current Therapeutic Interventions on Cerebrovascular Reactivity in Traumatic Brain Injury: A Narrative Overview

Current intensive care unit (ICU) treatment strategies for traumatic brain injury (TBI) care focus on intracranial pressure (ICP)- and cerebral perfusion pressure (CPP)-directed therapeutics, dictated by guidelines. Impaired cerebrovascular reactivity in moderate/severe TBI is emerging as a major associate with poor outcome and appears to dominate the landscape of physiologic derangement over the course of a patient's ICU stay. Within this article, we review the literature on the known drivers of impaired cerebrovascular reactivity in adult TBI, highlight the current knowledge surrounding the impact of guideline treatment strategies on continuously monitored cerebrovascular reactivity, and discuss current treatment paradigms for impaired reactivity. Finally, we touch on the areas of future research, as we strive to develop specific therapeutics for impaired cerebrovascular reactivity in TBI. There exists limited literature to suggest advanced age, intracranial injury patterns of diffuse injury, and sustained ICP elevations may drive impaired cerebrovascular reactivity. To date, the literature suggests there is a limited impact of such ICP/CPP guideline-based therapies on cerebrovascular reactivity, with large portions of a given patients ICU period spent with impaired cerebrovascular reactivity. Emerging treatment paradigms focus on the targeting individualized CPP and ICP thresholds based on cerebrovascular reactivity, without directly targeting the pathways involved in its dysfunction. Further work involved in uncovering the molecular pathways involved in impaired cerebrovascular reactivity is required, so that we can develop therapeutics directed at its prevention and treatment.

Quantitative pupillometry for the monitoring of intracranial hypertension in patients with severe traumatic brain injury

BackgroundElevated intracranial pressure (ICP) is frequent after traumatic brain injury (TBI) and may cause abnormal pupillary reactivity, which in turn is associated with a worse prognosis. Using automated infrared pupillometry, we examined the relationship between the Neurological Pupil index (NPi) and invasive ICP in patients with severe TBI.MethodsThis was an observational cohort of consecutive subjects with severe TBI (Glasgow Coma Scale [GCS] < 9 with abnormal lesions on head CT) who underwent parenchymal ICP monitoring and repeated NPi assessment with the NPi-200® pupillometer. We examined NPi trends over time (four consecutive measurements over intervals of 6 h) prior to sustained elevated ICP > 20 mmHg. We further analyzed the relationship of cumulative abnormal NPi burden (%NPi values < 3 during total ICP monitoring time) with intracranial hypertension (ICHT)—categorized as refractory (ICHT-r; requiring surgical decompression) vs. non-refractory (ICHT-nr; responsive to medical therapy)—and with the 6-month Glasgow Outcome Score (GOS).ResultsA total of 54 patients were studied (mean age 54 ± 21 years, 74% with focal injuries on CT), of whom 32 (59%) had ICHT. Among subjects with ICHT, episodes of sustained elevated ICP (n = 43, 172 matched ICP-NPi samples; baseline ICP [T− 6 h] 14 ± 5 mmHg vs. ICPmax [T0 h] 30 ± 9 mmHg) were associated with a concomitant decrease of the NPi (baseline 4.2 ± 0.5 vs. 2.8 ± 1.6, p < 0.0001 ANOVA for repeated measures). Abnormal NPi values were more frequent in patients with ICHT-r (n = 17; 38 [3–96]% of monitored time vs. 1 [0–9]% in patients with ICHT-nr [n = 15] and 0.5 [0–10]% in those without ICHT [n = 22]; p = 0.007) and were associated with an unfavorable 6-month outcome (15 [1–80]% in GOS 1–3 vs. 0 [0–7]% in GOS 4–5 patients; p = 0.002).ConclusionsIn a selected cohort of severe TBI patients with abnormal head CT lesions and predominantly focal cerebral injury, elevated ICP episodes correlated with a concomitant decrease of NPi. Sustained abnormal NPi was in turn associated with a more complicated ICP course and worse outcome.

A Comparative Study of Bolus Dose of Hypertonic Saline, Mannitol, and Mannitol Plus Glycerol Combination in Patients with Severe Traumatic Brain Injury

This prospective randomized controlled study compared the efficacy of an equiosmolar and isovolumetric dose of 3% hypertonic saline, 20% mannitol, and 10% mannitol plus 10% glycerol combination in reducing the raised intracranial pressure (ICP) in patients with severe traumatic brain injury (TBI). A total of 120 patients of severe TBI with increased ICP were randomized to receive an equiosmolar and isovolumetric dose of 3% hypertonic saline, 20% mannitol, and 10% mannitol plus 10% glycerol combination at a defined infusion rate, which was stopped when ICP was <15 mm Hg. A total of 120 patients with severe TBI (aged >18 years, Glasgow Coma Scale ≤8, and had sustained elevated ICP of >20 mm Hg for more than 5 minutes) were randomized during the study. All data were presented as mean (minimum-maximum). A one-way analysis of variance test was used to analyze the effect across the treatment group, and Tukey's method was used for multiple comparisons. A paired t-test was employed to analyze the effect of the medication within each group. All 3 drugs decreased ICP below 15 mm Hg (P < 0.0001). The maximum change in ICP occurred after a bolus dose of 3% hypertonic saline followed by 10% mannitol plus 10% glycerol combination and then 20% mannitol (60% vs. 57% vs. 55%, respectively). Mean arterial pressure and cerebral perfusion pressure were increased after the bolus dose of study medications. Maximum changes occurred after infusion of 3% hypertonic saline followed by 10% mannitol plus 10% glycerol combination and 20% mannitol (P < 0.0349 and <0.0013, respectively). There was no statistically significant change in the hematocrit value noted after the bolus dose of any of the study medications. Serum sodium and osmolarity were raised significantly after the bolus dose of study medications. Maximum changes in serum sodium and osmolarity occurred after the bolus dose of 3% hypertonic saline. The mean dose required to reduce ICP below 15 mm Hg for 3% hypertonic saline: 1.4 mL/kg, for 10% mannitol plus 10% glycerine: 1.7 mL/kg, and for 20% mannitol: 2.0 mL/kg. The mean time required to reduce ICP below 15 mm Hg for 3% hypertonic saline: 16 minutes, for 10% mannitol plus 10% glycerine: 19 minutes, and for 20% mannitol: 23 minutes. The maximum change in the Glasgow Coma Scale occurred after the bolus dose of 3% hypertonic saline, followed by 10% mannitol plus 10% glycerol combination and then 20% mannitol. All 3 osmotic compounds exhibit comparable effectiveness in reducing ICP when a similar osmotic load is administrated, but 3% hypertonic saline appeared to be more effective followed by 10% mannitol plus 10% glycerol combination and 20% mannitol. A dose of 1.4 mL/kg can be recommended as an initial bolus dose for 3% hypertonic saline. Hypertonic saline can be recommended to treat patients with pretreatment hypovolemia, hyponatremia, or renal failure. There is no clear benefit compared with 20% mannitol in regard to neurologic outcome, even though there is a minor positive trend for 3% hypertonic saline and 10% mannitol plus 10% glycerol combination.

Characterization of Retinal Ganglion Cell and Optic Nerve Phenotypes Caused by Sustained Intracranial Pressure Elevation in Mice

Elevated intracranial pressure (ICP) can result in multiple neurologic sequelae including vision loss. Inducible models of ICP elevation are lacking in model organisms, which limits our understanding of the mechanism by which increased ICP impacts the visual system. We adapted a mouse model for the sustained elevation of ICP and tested the hypothesis that elevated ICP impacts the optic nerve and retinal ganglion cells (RGCs). ICP was elevated and maintained for 2 weeks, and resulted in multiple anatomic changes that are consistent with human disease including papilledema, loss of physiologic cupping, and engorgement of the optic nerve head. Elevated ICP caused a loss of RGC somas in the retina and RGC axons within the optic nerve, as well as a reduction in both RGC electrical function and contrast sensitivity. Elevated ICP also caused increased hypoxia-inducible factor (HIF)-1 alpha expression in the ganglion cell layer. These experiments confirm that sustained ICP elevation can be achieved in mice and causes phenotypes that preferentially impact RGCs and are similar to those seen in human disease. With this model, it is possible to model human diseases of elevated ICP such as Idiopathic Intracranial Hypertension and Spaceflight Associated Neuro-ocular Syndrome.

Efficacy, Safety, and Timing of 5% Sodium Chloride Compared With 23.4% Sodium Chloride for Osmotic Therapy.

Bolus doses of 23.4% sodium chloride (NaCl) are commonly used for the treatment of intracranial hypertension; however, delays in administration may occur in patients without central intravenous access. At our institution, equiosmolar bolus doses of 5% NaCl have emerged as potential alternatives to 23.4% NaCl because they may be safely administered through peripheral lines. We sought to assess the efficacy in reducing intracranial pressure (ICP), time to administration, and safety of 5% NaCl as compared with 23.4% NaCl for the treatment of intracranial hypertension. Patients admitted from July 2012 to June 2014 who received boluses of 5% NaCl or 23.4% NaCl for a sustained ICP >20 mm Hg were included. Data collected included measurements of ICP, time to administration, and adverse events. A total of 44 patients were identified; 11 received 5% NaCl, and 33 received 23.4% NaCl. The median percentage reductions in ICP at 30, 60, and 120 minutes in patients who received 5% versus 23.4% NaCl were 34% versus 26% ( P = 0.850), 48% versus 40% ( P = 0.700), and 46% versus 30% ( P = 0.064), respectively. The median time to administration was shorter in the 5% NaCl group (7 vs 11 minutes, P = 0.364). Both groups had a 27% rate of adverse events and no infusion site reactions. These data suggest that 5% NaCl may be as effective as 23.4% NaCl at lowering ICP if given at equiosmolar doses, has a shorter time to administration, and has no difference in the prevalence of adverse events.

Management of Intracranial Pressure.

Intracranial pressure (ICP) can be elevated in traumatic brain injury, large artery acute ischemic stroke, intracranial hemorrhage, intracranial neoplasms, and diffuse cerebral disorders such as meningitis, encephalitis, and acute hepatic failure. Raised ICP is also known as intracranial hypertension and is defined as a sustained ICP of greater than 20 mm Hg. ICP must be measured through an invasive brain catheter, typically an external ventricular catheter that can drain CSF and measure ICP, or through an intraparenchymal ICP probe. Proper recognition of the clinical signs of elevated ICP is essential for timely diagnosis and treatment to prevent cerebral hypoperfusion and possible brain death. Clinical signs of elevated ICP include headache, papilledema, nausea, and vomiting in the early phases, followed by stupor and coma, pupillary changes, hemiparesis or quadriparesis, posturing and respiratory abnormalities, and eventually cardiopulmonary arrest. Management of elevated ICP is, in part, dependent on the underlying cause. Medical options for treating elevated ICP include head of bed elevation, IV mannitol, hypertonic saline, transient hyperventilation, barbiturates, and, if ICP remains refractory, sedation, endotracheal intubation, mechanical ventilation, and neuromuscular paralysis. Surgical options include CSF drainage if hydrocephalus is present and decompression of a surgical lesion, such as an intracranial hematoma/large infarct or tumor, if the patient's condition is deemed salvageable. Future research should continue investigating medical and surgical options for the treatment of raised ICP, such as hypothermia, drugs that reduce cerebral edema, and operations aimed at reducing intracranial mass effect.

Effect of Osmotherapy on Optic Nerve Sheath Diameter in Patients with Increased Intracranial Pressure

The measurement of ocular nerve sheath diameter (ONSD) via ocular ultrasound scanning is a recent non-invasive method for intracranial pressure (ICP) assessment. Few clinical studies have assessed ONSD variations during osmotherapy for the treatment of sustained increased ICP episodes. The aim of our study was to determine the rate of ONSD variation after mannitol administration for increased ICP episodes. We consecutively included in a prospective, observational study, the patients who had severe acute brain injury and monitored with an invasive ICP monitor. For each episode of sustained elevated ICP, the ONSD was measured in the right and left eye with a 7.5-MHz echography probe, and the mean value was reported. Simultaneously, ICP and cerebral perfusion pressure (CPP) were recorded. All measurements were performed just before and 20 minutes following a 20% mannitol infusion. Data were expressed as medians and interquartile ranges. Thirteen patients were included and analysed (traumatic brain injury, n=10; subarachnoid haemorrhage, n=3). The median value of the mannitol dose infused was 0.54 g/kg (0.49-0.80 g/kg). In all cases, the ONSD was greater than 5.8 mm before osmotherapy. The ONSD significantly decreased after mannitol infusion from 6.3 (6.1-6.7) to 5. mm (5.5-6.3) (p=0.0007). Concomitantly, the intracranial pressure decreased from 35 (32-41) to 25 (22-29) mmHg (p=0.001) and the CPP increased from 47 (50-60) to 66 (59-69) mmHg (p=0.003). The variations of ONSD appear to be an interesting parameter to evaluate the efficacy of osmotherapy for elevated ICP episodes in patients with acute brain injury.

Effective treatment of refractory intracranial hypertension after traumatic brain injury with repeated boluses of 14.6% hypertonic saline

Normal intracranial pressure (ICP) and cerebral perfusion pressure (CPP) have been identified as favorable prognostic factors in the outcome of patients with traumatic brain injuries (TBIs). Osmotic diuretics and hypertonic saline (HTS) are commonly used to treat elevated ICP in patients with TBI; however, sustained effects of repeated high-concentration HTS boluses for severely refractory ICP elevation have not been studied. The authors' goal in this study was to determine whether repeated 14.6% HTS boluses were efficacious in treating severely refractory intracranial hypertension in patients with TBI. In a prospective cohort study in a neurocritical care unit, adult TBI patients with sustained ICP > 30 mm Hg for more than 30 minutes after exhaustive medical and/or surgical therapy received repeated 15-minute boluses of 14.6% HTS over 12 hours through central venous access. Response to treatment was evaluated in 11 patients. Within 5 minutes of bolus administration, mean ICP decreased from 40 to 33 mm Hg (30% reduction, p < 0.05). Intracranial pressure-lowering effects were sustained for 12 hours (41% reduction, p < 0.05) with multiple boluses (mean number of boluses 7 ± 5.5). The mean CPP increased 22% and 32% from baseline at 15 and 30 minutes, respectively (p < 0.05). The mean serum sodium level (SNa) at baseline was 155 ± 7.1 mEq/L, and after multiple boluses of 14.6% HTS, S(Na) at 12 hours was 154 ± 7.1 mEq/L. The mean heart rate, systolic blood pressure, blood urea nitrogen, and creatinine demonstrated no significant change throughout the study. The subset of TBI patients with intracranial hypertension that is completely refractory to all other medical therapies can be treated effectively and safely with repeated boluses of 14.6% HTS rather than a one-time dose.

Sustained intracranial pressure monitoring for prevention and treatment of kidney injury following craniocerebral trauma

Objective To investigate effect of sustained intracranial pressure (ICP) monitoring in mannitol therapy for kidney function conservation after craniocerebral trauma.Methods A retrospective comparison was conducted on 168 patients with craniocerebral trauma treated between January 2010 and January 2012.The patients were divided into ICP monitoring group (ICP group,77patients) and non-ICP monitoring group (control group,91 patients).Changes of cystatin C,creatinine and urea in plasma were detected dynamically.Data like mannitol dosage,hospital days and GOS score at postoperative 6 months were documented.Results Two groups showed no significant differences regarding in-hospital injury condition,renal function as well as age and gender distribution.Rate of renal failure of control group was 2.2 times more than that of ICP group (P ＜ 0.05).Mannitol dosage of ICP group only accounted for 27.35％ of that of control group,ie,(443 ± 133) g:(1 620 ±412) g (P ＜0.01).Frequency of mannitol use of ICP group was obviously less than that of control group,ie,(4.8 ±3.8) days vs (7.2 ± 2.3) days (P ＜ 0.01).At 6 months postoperatively,GOS score of ICP group was significantly better than that of control group (P ＜ 0.05).Plasma levels of cystatin C and creatinine at days 7,14 and 21 and plasma levels of urea at day 14 were significantly lower of ICP group,when compared with control group (P ＜ 0.05).Conclusion ICP monitoring significantly reduces the dosage and duration of mannitol therapy for craniocerebral trauma and effectually prevents and declines the occurrence of renal failure following craniocrebral trauma. Key words: Craniocerebral trauma; Intracranical pressure ; Mannitol; Kidney function

Chapter 4. Threshold for treatment of intracranial hypertension

Chapter 4. Threshold for treatment of intracranial hypertension

Monitoring and prediction of intracranial hypertension in pediatric traumatic brain injury

Control of intracranial hypertension (ICH) in patients with traumatic brain injury (TBI) is standard care. However, predicting risk for ICH is essential to balance risks and benefits of intracranial pressure (ICP) monitoring. Current recommendations for ICP monitoring in pediatric trauma patients are extrapolated from adult studies. This retrospective study evaluated 299 children admitted to Primary Children's Medical Center with moderate to severe TBI. ICP monitors were used in 120. Demographic, injury, and admission computed tomography (CT) scan characteristics were compared with determine factors associated with monitoring among those with less severe head CT findings. Among all monitored patients, clinical and radiographic features were compared for early ICH defined as any sustained ICP ≥20 mm Hg in the first 24 hours. Factors independently associated with monitoring children with Marshall I or II scores included presence of intraventricular hemorrhage (odds ratio [OR], 21.4; 95% confidence interval [CI], 4.0-114.7) and greater injury severity scores (ISS) (OR, 9.5 [95% CI, 2.9-31.1] for ISS 21 to 29 and OR, 14.3 [95% CI, 4.3-50.5] for ISS >29 compared with ISS <21). Among those with a normal head CT, 9 of 68 had an ICP monitor placed because of the inability to localize pain. Of these, 78% (7 of 9) had early ICH. Among monitored patients radiologic and clinical features of injury severity were not useful to distinguish risk for early ICH. Among children with severe TBI, a normal head CT does not exclude ICH. Need for ICP monitoring should be determined by depth of coma in addition to radiographic imaging.

Der erhöhte intrakranielle Druck – Therapiemaßnahmen

Increased intracranial pressure can be the result of different intracranial pathologies. Sustained intracranial pressure above 20-25 mmHg may cause secondary brain injury by impaired cerebral perfusion or direct pressure with neuronal injury, with in consequence deterioration of neurological outcome. A main cause of critically increased intracranial pressure is traumatic brain injury. Most treatment strategies for increased intracranial pressure were developed and studied on these patients. Most of them were transferred to other pathologies with increased intracranial pressure.Treatment is based on general measures, which can be escalated for medical and surgical options in case of failure to sufficiently decrease intracranial pressure below the established threshold. Despite its enormous medical and socio-economical relevance, the evidence for most treatment strategies of intracranial hypertension, though published in guidelines, is weak.

Forecasting ICP Elevation Based on Prescient Changes of Intracranial Pressure Waveform Morphology

Interventions of intracranial pressure (ICP) elevation in neurocritical care is currently delivered only after healthcare professionals notice sustained and significant mean ICP elevation. This paper uses the morphological clustering and analysis of ICP (MOCAIP) algorithm to derive 24 metrics characterizing morphology of ICP pulses and test the hypothesis that preintracranial hypertension (Pre-IH) segments of ICP can be differentiated, using these morphological metrics, from control segments that were not associated with any ICP elevation or at least 1 h prior to ICP elevation. Furthermore, we investigate whether a global optimization algorithm could effectively find the optimal subset of these morphological metrics to achieve better classification performance as compared to using full set of MOCAIP metrics. The results showed that Pre-IH segments, using the optimal subset of metrics found by the differential evolution algorithm, can be differentiated from control segments at a specificity of 99% and sensitivity of 37% for these Pre-IH segments 5 min prior to the ICP elevation. While the sensitivity decreased to 21% for Pre-IH segments, 20 min prior to ICP elevation, the high specificity of 99% was retained. The performance using the full set of MOCAIP metrics was shown inferior to results achieved using the optimal subset of metrics. This paper demonstrated that advanced ICP pulse analysis combined with machine learning could potentially leads to the forecasting of ICP elevation so that a proactive ICP management could be realized based on these accurate forecasts.

Frequency of Sustained Intracranial Pressure Elevation during Treatment of Severe Intraventricular Hemorrhage

Background: Elevated intracranial pressure (ICP) is an important marker of neurological deterioration. The occurrence and significance of elevated ICP and low cerebral perfusion pressure (CPP) in aggressively treated spontaneous intraventricular hemorrhage (IVH) are not defined. Methods: We performed a secondary longitudinal exploratory data analysis of a randomized multicenter trial of urokinase (UK) versus placebo (Pcb) as a treatment for IVH. Eleven IVH patients who required an external ventricular drain (EVD) were randomized to receive either intraventricular UK or Pcb every 12 h until clinical response permitted EVD removal. ICP and CPP were recorded every 4 or 6 h, as well as before and 1 h after EVD closure for administration of study agent. ICP, CPP and the proportion of ICP readings above 20, 30, 40 and 50 mm Hg were analyzed. Results: Six UK and 5 Pcb patients aged 39–74 years (mean ± standard deviation; 53 ± 11 years) were enrolled. Initial ICP ranged from 0 to 38 mm Hg (10.9 ± 11.0), initial CPP from 65 to 133 mm Hg (100.5 ± 17.7). We recorded 472 ICP readings over the entire monitoring period. Of these 65 (14%) were >20 mm Hg, 23 (5%) >30 mm Hg, 9 (2%) >40 mm Hg and 3 (<1%) >50 mm Hg. Only 2 of 141 intraventricular injections of study agent with EVD closure were not tolerated and required reopening of the EVD. Conclusions: In the intensive care unit, initial ICP measured with an EVD was uncommonly elevated (1/11 patients) in this group of severe IVH patients despite acute obstructive hydrocephalus. Frequent monitoring reveals ICP elevation >20 mm Hg in 14% of observations during use of EVD. ICP elevation, though it can occur, is not routinely associated with EVD closure for thrombolytic treatment with UK.