It was believed that the increase of ONSD could quickly and accurately reflect the rise of ICP. Maissan et al. reported that when ICP increased to more than 20 mmHg during tracheotomy in 18 patients with TBI, ONSD rapidly expanded to more than 5 mm. If we consider that the longitudinal measurement of the ONSD width of 5.0 mm is the diagnostic threshold for intracranial hypertension [10, 11], this study found that ICP and ONSD had a strong correlation (r = 0.679, p < 0.001) during seven days post-operation. The correlation was stronger at intracranial hypertension than that at normal ICP level (r = 0.665 vs. r = 0.358, p = 0.039). Rajajee et al. found that ONSD rapidly increased following the increase of ICP. Nevertheless, when ICP returned to normal levels, the ONSD remained to widen. This study also found a strong correlation between ICP and ONSD ≥ 5 mm (r = 0.644, p < 0.001), and no correlation at ONSD < 5 mm (p = 0.137). Hence, the higher the intracranial pressure corresponds to a stronger correlation between ONSD and ICP. When the intracranial pressure is decreased, the tension of dura in the cranial cavity is released, but the nerve sheath may still be in the state of expansion. So when the intracranial pressure is reduced or less than 20 mmHg, ONSD may not allow for the accurate evaluation of the ICP for a weak correlation between them. This conclusion suggested that the therapeutic measures based on the decrease of ONSD width might prolong osmotic drug use or other programs for ICP management.
So far, there are different conclusions about the relationship between PI and invasive ICP. Bellner et al. reported that PI was correlated with ICP, when PI > 2.13 or < 1.2, it was deduced ICP > 22 mmHg or < 12 mmHg respectively. Moreover, Prunet et al. found that TCD-PI could accurately and effectively predict intracranial hypertension in patients with TBI: the area under the curve was 0.901, the optimal threshold was 1.35, the sensitivity was 80%, and the specificity was 90%. On the contrary, de Riva et al.argued that TCD-PI could not accurately predict ICP. It was influenced by cerebral perfusion pressure, heart rate, arterial pressure difference, cerebrovascular resistance, cerebral artery compliance, and cerebral vascular autoregulation function. The formula was put forward:
(a1 is the pressure difference between systolic and diastolic pressure, CPPm mean arterial pressure, Ra vascular resistance, Ca vascular compliance, HR heart rate).
In the present study, we found a moderate correlation between ICP and PI on the whole seven days post-operation (r = 0.458, p < 0.001). When the ICP was stratified, there were no significant differences between these correlation coefficients (r = 0.705 vs. r = 0.716, p = 0.938). Furthermore, the intensity difference of correlation coefficient between invasive ICP and PI no matter at PI < 1.2 or PI ≥ 1.2 was also no significant differences too (r = 0.271 vs. 0.350, p = 0.660). Additionally, the intensity difference of correlation coefficient between ICP and PI at an early stage or a late-stage post-operation was not statistically significant (r = 0.508 vs. r = 0.645, p = 0.433). Therefore, all the findings above mentioned, confirmed that PI should be regarded as a dynamic trend of ICP, rather than an absolute value of ICP. PI is not a pressure indicator, which may be affected by the severity of secondary brain injury, cerebrovascular autoregulation, intracranial pressure, and other factors. So, we should carefully deduce the variation of ICP based on PI parameter in this case, and similarly, it does not mean that the higher intracranial pressure led to the stronger correlation between invasive ICP and PI.
The regression analysis of ONSD and PI evaluation intracranial hypertension was carried out in the present study. It showed that the AUC value of a combination of ONSD ≥ 5 mm and PI ≥ 1.2 for prediction intracranial hypertension was 0.943. Although there was not a statistically significant difference between the AUC value of a combination of ONSD ≥ 5 mm and PI ≥ 1.2 and ONSD ≥ 5 mm alone for predicting intracranial hypertension (p = 0.4119), it was a tendency to enhance the ability to predict intracranial hypertension and helpful for clinicians from qualitative to quantitative assessment of intracranial pressure. Notwithstanding, considering the characteristics of patients and the level of intracranial pressure in this study, we should be comprehensively analysis of the clinical and imaging examination before intervention is taken based on the PI or ONSD.
There are several limitations in the present study that should be pointed out. First, we were not able to overcome the bias of observational research and the small number of patients with TBI included in this study. Second, TCD measurements, including ONSD, were intermittent; invasive parenchymal ICP monitoring was continuous, which may influence the effectiveness of this study. Third, TCD was performed by different physicians, which may lead to variability in performance and differences in data acquisition. Finally, our results showed a different strength correlation between ONSD and TCD-PI with ICP, respectively, which does not suggest that these indicators would replace invasive ICP monitoring in patients with TBI.