Increased intracranial pressure syndrome may emerge due to many different neurological factors. Clinical findings like changes in consciousness level, dilated pupils unresponsive to light, loss of the brainstem reflex, cranial nerve injury, Cushing’s triad, or radiological findings such as shift, effacement in sulci, ventricular collapse, and compression in cisterns may be encountered. Early diagnosis and treatment are important for the prevention of neurologic damage and related mortality. In ICP, the measurement of the intraparenchymal, intraventricular pressures with a special catheter is the gold standard for the determination of the intracranial pressure. However, it is rather uncommon in clinical practice due to complications such as invasive process and infection [1, 2]. Therefore, there is a need for non-invasive methods, which may be used in the monitoring of ICP in pediatric patients.
Ultrasonographic ONSD measurements became increasingly popular as a result of its early detection of increased ICP, non-invasive process, repeatability, and implementation at bedside. There are many studies in the literature focused on the ONSD measurements in patients with increased ICP. Although there are some conflicting results, all studies demonstrated that ONSD increased in patients with increased ICP. Ballantyne et al.  conducted a study of 102 healthy children and found that ONSD was between 2.1–4.0 mm in children under the age of one year and between 2.1–4.3 mm in children over the age of one year. They reported cut-off values of > 4.0 mm and > 4.5 mm in children under and over the age of one year respectively. Malayeri et al.  conducted a study in 78 ill and 78 healthy children; dividing them into two age groups (<four years and > four years), they found that ONSD was 5.5 ± 0.6 mm (<four years) and 5.6 ± 0.7 mm (>four years) in children with the increased ICP, while the same values were 3 ± 0.6 mm (<four years) and 3.6 ± 0.4 mm (>four years) in healthy children. Beare et al.  conducted a study of 21 African children with neurological disease and found that ONSD was 4.3–6.2 mm in children with the clinical and/or cranial CT findings of the increased ICP, while the same value was 2.8–4.4 mm in children with neurological disease and negative clinical and cranial CT results. They reported 4.2 mm as the upper limit for ONSD and stated that ≥4.5 mm should be accepted as the cut-off value for increased ICP. Padayachy et al.  conducted a study of 174 pediatric patients and evaluated invasive ICP and ONSD. They found that in patients with ICP > 20 mmHg, ONSD was 5.6 mm, 5.92 mm and 5.75 mm in the age groups <one year, one to four years and > four years respectively. Rehman Siddiqui et al.  conducted a study of 48 children with increased ICP and determined ONSD values of 4.64 ± 0.48 mm (cut-off> 4 mm) for the age group under one year; 6.44 ± 0.65 mm (cut-off> 4.71 mm) for the one to ten year age group and 6.28 ± 0.62 mm (cut-off> 5.43 mm) for the age group over ten years. In a study conducted in 2019, they evaluated ONSD measurements in children with acute liver failure. 41 children with acute liver failure and 47 healthy children were taken. Those with acute liver failure are also grouped as with and without hepatic encephalopathy (HE). ONSD was 4.2 mm, 4.4 mm and 5.2 mm in controls, ALF without HE and with HE. In children with acute hepatic failure, the presence of ONSD above 5.1 mm is considered significant for hepatic encephalopathy . In a study conducted in 2020, ONSD and ICP measurements were examined in 72 children who underwent neurosurgery operation. They determined that the best ONSD cut-off value for detecting ICP ≥ 15 and ≥ 20 mmHg was 5.28 and 5.57 mm .
However, in the first studies focused on this topic, it was stated that these values were low for increased ICP and higher ONSD values should be considered in children with increased ICP. In our study, six patients were under the age of one year (16.7%), and their mean ONSD value was 4.8 ± 0.7 mm. The mean ONSD values were 6.1 ± 0.6 mm and 5.6 ± 0.7 mm in 14 children (38.9%) in the age group one to ten years and in 16 children (44.4%) in the age group >ten years respectively (Table 2). As in the previous studies, the ONSD values have been increased.
In a study focused on the eight adult patients with cranial trauma and brain injury, the authors determined a significant difference between patients with ICP > 25 mmHg (67 ± 1%) and ICP < 25 mmHg (71 ± 2%) for NIRS values and following the hyperoxia test, a significant increase in NIRS values was determined in the low-ICP group, while no significant increase in NIRS values was noticed in the high-ICP group . Adelson et al.  conducted a study of ten children with serious cranial trauma and reported that an increase in ICP led to an increase in cerebral blood flow, cerebral vasodilation, and oxyhemoglobin. In addition, they warned that the opposite might occur in patients with very high ICP levels. Lewis et al.  conducted a study in ten adult patients with severe cranial trauma and evaluated whether NIRS decreased parallel to the decrease in the jugular bulb venous oxygen saturation (< 55%), and they did not find any significant decrease in NIRS values. In a study conducted in 31 adult patients with serious cranial injury, the changes in NIRS, intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were compared after hyperoxia, hypocapnia, and mannitol administration, and it was found that the changes in NIRS were not significant as in other parameters except for hyperoxia . Zuluaga et al.  conducted a study in 30 children, who had increased ICP and underwent invasive monitoring (ICP), and found that NIRS value was 75.2 ± 10.1% and 70.8 ± 12.5% in patients with ICP < 20 mmHg and ICP > 20 mmHg respectively. They reported that NIRS decreased along with the increase in ICP, but there was no significant correlation between these parameters (p = 0.3). Likewise, we did not find a significant correlation between increased ICP and NIRS in our study.
In a PuBMed based literature search showed us there are just limited number of studies in the literature related to the usage of NIRS in patients with increased ICP, and they reported conflicting results. There is no published study focusing on the concomitant evaluation of both ONSD and NIRS. Our study is the first pediatric study focused on the ultrasonographic ONSD measurements and NIRS values in patients with increased ICP.
The main limitation of our study is the limited number of patients and ONSD values are not yet standardized. Another limitation of our study is that failure to routinely apply invasive ICP monitoring in our PICU due to the lack of an experienced neurosurgery team in our hospital. Therefore, the correlation between the changes seen in ICP with invasive ICP monitoring and the ONSD and NIRS could not be done.