Dataset Information

A Novel Noninvasive Technique for Intracranial Pressure Waveform Monitoring in Critical Care.

ABSTRACT:

Background

We validated a new noninvasive tool (B4C) to assess intracranial pressure waveform (ICPW) morphology in a set of neurocritical patients, correlating the data with ICPW obtained from invasive catheter monitoring.

Materials and methods

Patients undergoing invasive intracranial pressure (ICP) monitoring were consecutively evaluated using the B4C sensor. Ultrasound-guided manual internal jugular vein (IJV) compression was performed to elevate ICP from the baseline. ICP values, amplitudes, and time intervals (P2/P1 ratio and time-to-peak [TTP]) between the ICP and B4C waveform peaks were analyzed.

Results

Among 41 patients, the main causes for ICP monitoring included traumatic brain injury, subarachnoid hemorrhage, and stroke. Bland-Altman's plot indicated agreement between the ICPW parameters obtained using both techniques. The strongest Pearson's correlation for P2/P1 and TTP was observed among patients with no cranial damage (r = 0.72 and 0.85, respectively) to the detriment of those who have undergone craniotomies or craniectomies. P2/P1 values of 1 were equivalent between the two techniques (area under the receiver operator curve [AUROC], 0.9) whereas B4C cut-off 1.2 was predictive of intracranial hypertension (AUROC 0.9, p < 000.1 for ICP > 20 mmHg).

Conclusion

B4C provided biometric amplitude ratios correlated with ICPW variation morphology and is useful for noninvasive critical care monitoring.

SUBMITTER: Brasil S

PROVIDER: S-EPMC8707681 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature

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Publications

A Novel Noninvasive Technique for Intracranial Pressure Waveform Monitoring in Critical Care.

Brasil Sérgio S Solla Davi Jorge Fontoura DJF Nogueira Ricardo de Carvalho RC Teixeira Manoel Jacobsen MJ Malbouisson Luiz Marcelo Sá LMS Paiva Wellingson da Silva WDS

Journal of personalized medicine 20211205 12

<h4>Background</h4>We validated a new noninvasive tool (B4C) to assess intracranial pressure waveform (ICPW) morphology in a set of neurocritical patients, correlating the data with ICPW obtained from invasive catheter monitoring.<h4>Materials and methods</h4>Patients undergoing invasive intracranial pressure (ICP) monitoring were consecutively evaluated using the B4C sensor. Ultrasound-guided manual internal jugular vein (IJV) compression was performed to elevate ICP from the baseline. ICP valu ...[more]

PMID: 34945774

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Project description:Although the placement of an intraventricular catheter remains the gold standard method for the diagnosis of intracranial hypertension (ICH), the technique has several limitations including but not limited to its invasiveness. Current noninvasive methods, however, still lack robust evidence to support their clinical use. We aimed to estimate, as an exploratory hypothesis generating analysis, the discriminative power of four noninvasive methods to diagnose ICH. We prospectively collected data from adult intensive care unit (ICU) patients with subarachnoid hemorrhage (SAH), intraparenchymal hemorrhage (IPH), and ischemic stroke (IS) in whom invasive intracranial pressure (ICP) monitoring had been placed. Measures were simultaneously collected from the following noninvasive methods: optic nerve sheath diameter (ONSD), pulsatility index (PI) using transcranial Doppler (TCD), a 5-point visual scale designed for brain Computed Tomography (CT), and two parameters (time-to-peak [TTP] and P2/P1 ratio) of a noninvasive ICP wave morphology monitor (Brain4Care[B4c]). ICH was defined as a sustained ICP > 20 mmHg for at least 5 min. We studied 18 patients (SAH = 14; ICH = 3; IS = 1) on 60 occasions with a mean age of 52 ± 14.3 years. All methods were recorded simultaneously, except for the CT, which was performed within 24 h of the other methods. The median ICP was 13 [9.8-16.2] mmHg, and intracranial hypertension was present on 18 occasions (30%). Median values from the noninvasive techniques were ONSD 4.9 [4.40-5.41] mm, PI 1.22 [1.04-1.43], CT scale 3 points [IQR: 3.0], P2/P1 ratio 1.16 [1.09-1.23], and TTP 0.215 [0.193-0.237]. There was a significant statistical correlation between all the noninvasive techniques and invasive ICP (ONSD, r = 0.29; PI, r = 0.62; CT, r = 0.21; P2/P1 ratio, r = 0.35; TTP, r = 0.35, p < 0.001 for all comparisons). The area under the curve (AUC) to estimate intracranial hypertension was 0.69 [CIs = 0.62-0.78] for the ONSD, 0.75 [95% CIs 0.69-0.83] for the PI, 0.64 [95%Cis 0.59-069] for CT, 0.79 [95% CIs 0.72-0.93] for P2/P1 ratio, and 0.69 [95% CIs 0.60-0.74] for TTP. When the various techniques were combined, an AUC of 0.86 [0.76-0.93]) was obtained. The best pair of methods was the TCD and B4cth an AUC of 0.80 (0.72-0.88). Noninvasive technique measurements correlate with ICP and have an acceptable discrimination ability in diagnosing ICH. The multimodal combination of PI (TCD) and wave morphology monitor may improve the ability of the noninvasive methods to diagnose ICH. The observed variability in non-invasive ICP estimations underscores the need for comprehensive investigations to elucidate the optimal method-application alignment across distinct clinical scenarios.

Project description:Morphological alterations in intracranial pressure (ICP) pulse waveform (ICPW) secondary to intracranial hypertension (ICP >20 mmHg) and a reduction in intracranial compliance (ICC) are well known indicators of neurological severity. The exclusive exploration of modifications in ICPW after either the loss of skull integrity or surgical procedures for intracranial hypertension resolution is not a common approach studied. The present study aimed to assess the morphological alterations in ICPW among neurocritical care patients with skull defects and decompressive craniectomy (DC) by comparing the variations in ICPW features according to elevations in mean ICP values. Patients requiring ICP monitoring because of acute brain injury were included. A continuous record of 10 min-length for the beat-by-beat analysis of ICPW was performed, with ICP elevation produced by means of ultrasound-guided manual internal jugular vein compression at the end of the record. ICPW features (peak amplitude ratio (P2/P1), time interval to pulse peak (TTP) and pulse amplitude) were counterweighed between baseline and compression periods. Results were distributed for three groups: intact skull (exclusive burr hole for ICP monitoring), craniotomy/large fractures (group 2) or DC (group 3). 57 patients were analyzed. A total of 21 (36%) presented no skull defects, 21 (36%) belonged to group 2, whereas 15 (26%) had DC. ICP was not significantly different between groups: ±15.11 for intact, 15.33 for group 2 and ±20.81 mmHg for group 3, with ICP-induced elevation also similar between groups (p = 0.56). Significant elevation was observed for the P2/P1 ratio for groups 1 and 2, whereas a reduction was observed in group 3 (elevation of ±0.09 for groups 1 and 2, but a reduction of 0.03 for group 3, p = 0.01), and no significant results were obtained for TTP and pulse amplitudes. In the present study, intracranial pressure pulse waveform analysis indicated that intracranial compliance was significantly more impaired among decompressive craniectomy patients, although ICPW indicated DC to be protective for further influences of ICP elevations over the brain. The analysis of ICPW seems to be an alternative to real-time ICC assessment.

Project description:OBJECTIVES:The lower limit of cerebral blood flow autoregulation is the critical cerebral perfusion pressure at which cerebral blood flow begins to fall. It is important that cerebral perfusion pressure be maintained above this level to ensure adequate cerebral blood flow, especially in patients with high intracranial pressure. However, the critical cerebral perfusion pressure of 50 mm Hg, obtained by decreasing mean arterial pressure, differs from the value of 30 mm Hg, obtained by increasing intracranial pressure, which we previously showed was due to microvascular shunt flow maintenance of a falsely high cerebral blood flow. The present study shows that the critical cerebral perfusion pressure, measured by increasing intracranial pressure to decrease cerebral perfusion pressure, is inaccurate but accurately determined by dopamine-induced dynamic intracranial pressure reactivity and cerebrovascular reactivity. DESIGN:Cerebral perfusion pressure was decreased either by increasing intracranial pressure or decreasing mean arterial pressure and the critical cerebral perfusion pressure by both methods compared. Cortical Doppler flux, intracranial pressure, and mean arterial pressure were monitored throughout the study. At each cerebral perfusion pressure, we measured microvascular RBC flow velocity, blood-brain barrier integrity (transcapillary dye extravasation), and tissue oxygenation (reduced nicotinamide adenine dinucleotide) in the cerebral cortex of rats using in vivo two-photon laser scanning microscopy. SETTING:University laboratory. SUBJECTS:Male Sprague-Dawley rats. INTERVENTIONS:At each cerebral perfusion pressure, dopamine-induced arterial pressure transients (~10 mm Hg, ~45 s duration) were used to measure induced intracranial pressure reactivity (? intracranial pressure/? mean arterial pressure) and induced cerebrovascular reactivity (? cerebral blood flow/? mean arterial pressure). MEASUREMENTS AND MAIN RESULTS:At a normal cerebral perfusion pressure of 70 mm Hg, 10 mm Hg mean arterial pressure pulses had no effect on intracranial pressure or cerebral blood flow (induced intracranial pressure reactivity = -0.03 ± 0.07 and induced cerebrovascular reactivity = -0.02 ± 0.09), reflecting intact autoregulation. Decreasing cerebral perfusion pressure to 50 mm Hg by increasing intracranial pressure increased induced intracranial pressure reactivity and induced cerebrovascular reactivity to 0.24 ± 0.09 and 0.31 ± 0.13, respectively, reflecting impaired autoregulation (p < 0.05). By static cerebral blood flow, the first significant decrease in cerebral blood flow occurred at a cerebral perfusion pressure of 30 mm Hg (0.71 ± 0.08, p < 0.05). CONCLUSIONS:Critical cerebral perfusion pressure of 50 mm Hg was accurately determined by induced intracranial pressure reactivity and induced cerebrovascular reactivity, whereas the static method failed.

Dataset Information

A Novel Noninvasive Technique for Intracranial Pressure Waveform Monitoring in Critical Care.

Background

Materials and methods

Results

Conclusion

Publications

A Novel Noninvasive Technique for Intracranial Pressure Waveform Monitoring in Critical Care.

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