Noninvasive Assessment of Intracranial Pressure: Deformability Index as an Adjunct to Optic Nerve Sheath Diameter to Increase Diagnostic Ability.

BACKGROUND: Today, invasive intracranial pressure (ICP) measurement remains the standard, but its invasiveness limits availability. Here, we evaluate a novel ultrasound-based optic nerve sheath parameter called the deformability index (DI) and its ability to assess ICP noninvasively. Furthermore, we ask whether combining DI with optic nerve sheath diameter (ONSD), a more established parameter, results in increased diagnostic ability, as compared to using ONSD alone. METHODS: We prospectively included adult patients with traumatic brain injury with invasive ICP monitoring, which served as the reference measurement. Ultrasound images and videos of the optic nerve sheath were acquired. ONSD was measured at the bedside, whereas DI was calculated by semiautomated postprocessing of ultrasound videos. Correlations of ONSD and DI to ICP were explored, and a linear regression model combining ONSD and DI was compared to a linear regression model using ONSD alone. Ability of the noninvasive parameters to distinguish dichotomized ICP was evaluated using receiver operating characteristic curves, and a logistic regression model combining ONSD and DI was compared to a logistic regression model using ONSD alone. RESULTS: Forty-four ultrasound examinations were performed in 26 patients. Both DI (R = - 0.28; 95% confidence interval [CI] R < - 0.03; p = 0.03) and ONSD (R = 0.45; 95% CI R > 0.23; p < 0.01) correlated with ICP. When including both parameters in a combined model, the estimated correlation coefficient increased (R = 0.51; 95% CI R > 0.30; p < 0.01), compared to using ONSD alone, but the model improvement did not reach statistical significance (p = 0.09). Both DI (area under the curve [AUC] 0.69, 95% CI 0.53-0.83) and ONSD (AUC 0.72, 95% CI 0.56-0.86) displayed ability to distinguish ICP dichotomized at ICP ≥ 15 mm Hg. When using both parameters in a combined model, AUC increased (0.80, 95% CI 0.63-0.90), and the model improvement was statistically significant (p = 0.02). CONCLUSIONS: Combining ONSD with DI holds the potential of increasing the ability of optic nerve sheath parameters in the noninvasive assessment of ICP, compared to using ONSD alone, and further study of DI is warranted.

Noninvasive intracranial pressure assessment by optic nerve sheath diameter: Automated measurements as an alternative to clinician-performed measurements.

Introduction: Optic nerve sheath diameter (ONSD) has shown promise as a noninvasive parameter for estimating intracranial pressure (ICP). In this study, we evaluated a novel automated method of measuring the ONSD in transorbital ultrasound imaging. Methods: From adult traumatic brain injury (TBI) patients with invasive ICP monitoring, bedside manual ONSD measurements and ultrasound videos of the optic nerve sheath complex were simultaneously acquired. Automatic ONSD measurements were obtained by the processing of the ultrasound videos by a novel software based on a machine learning approach for segmentation of the optic nerve sheath. Agreement between manual and automated measurements, as well as their correlation to invasive ICP, was evaluated. Furthermore, the ability to distinguish dichotomized ICP for manual and automatic measurements of ONSD was compared, both for ICP dichotomized at ≥20 mmHg and at the 50th percentile (≥14 mmHg). Finally, we performed an exploratory subgroup analysis based on the software's judgment of optic nerve axis alignment to elucidate the reasons for variation in the agreement between automatic and manual measurements. Results: A total of 43 ultrasound examinations were performed on 25 adult patients with TBI, resulting in 86 image sequences covering the right and left eyes. The median pairwise difference between automatically and manually measured ONSD was 0.06 mm (IQR -0.44 to 0.38 mm; p = 0.80). The manually measured ONSD showed a positive correlation with ICP, while automatically measured ONSD showed a trend toward, but not a statistically significant correlation with ICP. When examining the ability to distinguish dichotomized ICP, manual and automatic measurements performed with similar accuracy both for an ICP cutoff at 20 mmHg (manual: AUC 0.74, 95% CI 0.58-0.88; automatic: AUC 0.83, 95% CI 0.66-0.93) and for an ICP cutoff at 14 mmHg (manual: AUC 0.70, 95% CI 0.52-0.85; automatic: AUC 0.68, 95% CI 0.48-0.83). In the exploratory subgroup analysis, we found that the agreement between measurements was higher in the subgroup where the automatic software evaluated the optic nerve axis alignment as good as compared to intermediate/poor. Conclusion: The novel automated method of measuring the ONSD on the ultrasound videos using segmentation of the optic nerve sheath showed a reasonable agreement with manual measurements and performed equally well in distinguishing high and low ICP.

Vasospasm Surveillance by a Simplified Transcranial Doppler Protocol in Traumatic Brain Injury.

OBJECTIVE: To detect post-traumatic vasospasm in patients with traumatic brain injury (TBI), we implemented a simplified transcranial Doppler (TCD) surveillance protocol in a neurointensive care setting. In this study, we evaluate the yield of this protocol. METHODS: Adult patients with TBI admitted to the neurointensive care unit were examined with TCD by 2 intensive care nurses trained in TCD examinations. Flow velocities of the middle cerebral arteries were recorded. TCD suspected vasospasm was defined as the mean flow velocity >120 cm/s, and when detected, the protocol recommended a supplementary computed tomography angiography. The rate of detection of TCD suspected vasospasm and the subsequent rate of radiological diagnosis of vasospasm were recorded. In multivariate logistic regression analysis, we evaluated age, initial Glasgow Coma Scale, craniotomy, and decompressive craniectomy as potential predictors of developing increased TCD velocity. RESULTS: A total of 84 patients with TBI with a median initial Glasgow Coma Scale score of 6 were examined by TCD. TCD suspected vasospasm was found in the middle cerebral arteries of 18% of examined patients. Two-thirds of patients with TCD suspected vasospasm were investigated with a subsequent computed tomography angiography, and 80% of these patients received a radiological diagnosis of vasospasm. In logistic regression analysis, decompressive craniectomy was significantly associated with increased risk of developing TCD suspected vasospasm (odds ratio: 11.57, 95% confidence interval: 2.59-51.73, P = 0.001). CONCLUSIONS: The implementation of a simplified TCD surveillance protocol in a neurointensive care setting yielded an 18% detection rate of TCD suspected vasospasm. In our cohort of patients with TBI, decompressive craniectomy was associated with increased risk of developing TCD suspected vasospasm.

Cerebral venous sinus thrombosis in traumatic brain injury: A systematic review of its complications, effect on mortality, diagnostic and therapeutic management, and follow-up.

Objective: Cerebral venous sinus thrombosis (CVST) is increasingly being recognized in the setting of traumatic brain injury (TBI), but its effect on TBI patients and its management remains uncertain. Here, we systematically review the currently available evidence on the complications, effect on mortality and the diagnostic and therapeutic management and follow-up of CVST in the setting of TBI. Methods: Key clinical questions were posed and used to define the scope of the review within the following topics of complications; effect on mortality; diagnostics; therapeutics; recanalization and follow-up of CVST in TBI. We searched relevant databases using a structured search strategy. We screened identified records according to eligibility criteria and for information regarding the posed key clinical questions within the defined topics of the review. Results: From 679 identified records, 21 studies met the eligibility criteria and were included, all of which were observational in nature. Data was deemed insufficiently homogenous to perform meta-analysis and was narratively synthesized. Reported rates of venous infarctions ranged between 7 and 38%. One large registry study reported increased in-hospital mortality in CVSP and TBI compared to a control group with TBI alone in adjusted analyses. Another two studies found midline CVST to be associated with increased risk of mortality in adjusted analyses. Direct data to inform the optimum diagnostic and therapeutic management of the condition was limited, but some data on the safety, and effect of anticoagulation treatment of CVST in TBI was identified. Systematic data on recanalization rates to guide follow-up was also limited, and reported complete recanalization rates ranged between 41 and 86%. In the context of the identified data, we discuss the diagnostic and therapeutic management and follow-up of the condition. Conclusion: Currently, the available evidence is insufficient for evidence-based treatment of CVST in the setting of TBI. However, there are clear indications in the presently available literature that CVST in TBI is associated with complications and increased mortality, and this indicates that management options for the condition must be considered. Further studies are needed to confirm the effects of CVST on TBI patients and to provide evidence to support management decisions. Systematic review registration: https://www.crd.york.ac.uk/prospero/, identifier: PROSPERO [CRD42021247833].

Cerebral venous thrombosis in traumatic brain injury: a cause of secondary insults and added mortality.

OBJECTIVE: Cerebral venous thrombosis (CVT) is increasingly recognized in traumatic brain injury (TBI), but its complications and effect on outcome remain undetermined. In this study, the authors characterize the complications and outcome effect of CVT in TBI patients. METHODS: In a retrospective, case-control study of patients included in the Oslo University Hospital trauma registry and radiology registry from 2008 to 2014, the authors identified TBI patients with CVT (cases) and without CVT (controls). The groups were matched regarding Abbreviated Injury Scale 1990, update 1998 (AIS'98) head region severity score 3-6. Cases were identified by AIS'98 or ICD-10 code for CVT and CT or MR venography findings confirmed to be positive for CVT, whereas controls had no AIS'98 or ICD-10 code for CVT and CT venography or MR venography findings confirmed to be negative for CVT. All images were reviewed by a neuroradiologist. Rates of complications due to CVT were recorded, and mortality was assessed both unadjusted and in a multivariable logistic regression analysis adjusting for initial Glasgow Coma Scale score, Rotterdam CT score, and Injury Severity Score. Complications and mortality were also assessed in prespecified subgroup analysis according to CVT location and degree of occlusion from CVT. Lastly, mortality was assessed in an exploratory subgroup analysis according to the presence of complications from CVT. RESULTS: The CVT group (73 patients) and control group (120 patients) were well matched regarding baseline characteristics. In the CVT group, 18% developed venous infarction, 11% developed intracerebral hemorrhage, and 19% developed edema, all representing complications secondary to CVT. Unadjusted 30-day mortality was 16% in the CVT group and 4% in the no-CVT group (p = 0.004); however, the difference was no longer significant in the adjusted analysis (OR 2.24, 95% CI 0.63-8.03; p = 0.215). Subgroup analysis by CVT location showed an association between CVT location and rate of complications and an unadjusted 30-day mortality of 50% for midline or bilateral CVT and 8% for unilateral CVT compared with 4% for no CVT (p < 0.001). The adjusted analysis showed a significantly higher mortality in the midline/bilateral CVT group than in the no-CVT group (OR 8.41, 95% CI 1.56-45.25; p = 0.032). CONCLUSIONS: There is a significant rate of complications from CVT in TBI patients, leading to secondary brain insults. The rate of complications is dependent on the anatomical location of the CVT, and midline and bilateral CVT is associated with an increased 30-day mortality in TBI patients.