Optic nerve sheath diameter in patients undergoing intracranial tumour resection: Perioperative changes and contributing factors – A prospective observational study

Abstract

Background and Aims:

Ultrasonographic (USG) optic nerve sheath diameter (ONSD) provides a real-time, non-invasive method for assessing intracranial pressure. This study investigates perioperative ONSD variations and contributing factors in patients undergoing elective intracranial tumour resection.

Methods:

A prospective observational study was conducted on 94 adults with intracranial tumours, excluding orbital lesions and sellar/suprasellar tumours. Preoperative symptoms, Glasgow coma scale scores, and radiological findings were noted. USG-ONSD was assessed in the transverse and sagittal plane on each eye, with an average of three readings at the following time-points: pre-induction, post-induction, post-extubation, and 24-hour post-tumour resection. The presence of ventriculo-peritoneal (VP) shunt, duration of surgery/anaesthesia, intraoperative position, use of osmotic agents, and complications during surgery were noted. The data were analysed using linear regression and general linear modelling in R software.

Results:

ONSD increased significantly (P = 0.001) immediately after surgery and decreased 24 hours after surgery (P < 0.001) compared to preoperative values. Although the trend of ONSD changes was similar for both supratentorial and infratentorial tumours, supratentorial tumours consistently showed higher values (P = 0.549). Higher American Society of Anesthesiologists physical status, nausea/vomiting, visual field affection, midline shift, mass effect, and larger tumour size were associated with higher preoperative values. Similarly, large-size tumours (P < 0.001), shorter duration of symptoms (P = 0.001), and lateral intraoperative positioning (P = 0.028) showed significantly higher values and greater changes, whereas the presence of VP shunt, use of osmotherapy, and sitting position for surgery showed a lower trend of ONSD postoperatively.

Conclusion:

USG-ONSD demonstrates dynamic changes in patients undergoing intracranial tumour resection. ONSD is affected by the size of the tumour, duration of symptoms, and intraoperative positioning, though the trend is homogenous among supratentorial and infratentorial tumours.

INTRODUCTION

Intracranial tumours may manifest intracranial hypertension due to direct compression of the brain tissue by the lesion or due to obstructive hydrocephalus.[1] However, accurately predicting the intracranial pressure (ICP) status in the immediate preoperative and postoperative period remains challenging. The usual reliable surrogates are the Glasgow coma scale (GCS) scores and clinical signs and symptoms. However, their constant alignment with the severity of the disease is unequivocal, as significant clinical deterioration occurs until clinical signs (bradycardia/hypertension/pupillary changes) become apparent.[2] Routine imaging techniques, that is, computed tomography and magnetic resonance imaging, are costly, provide only snapshot information, and may be impractical for unstable or mechanically ventilated patients due to the risks associated with transportation to and from imaging facilities, leading to significant morbidity and mortality.[3,4] The most precise ICP measurement methods are invasive, carry risks of infections and haemorrhage, and have limited utility in resource-limited settings due to high cost and need for special equipment and expertise.[5]

The optic nerve sheath is a continuation of the subarachnoid space and distends in response to intracranial hypertension. The changes in ICP reflected by optic nerve sheath diameter (ONSD) guided by ultrasonography (USG) are real-time, non-invasively measured, well correlated with clinical symptoms and radiological signs, and have been extensively studied and validated in traumatic brain injury.[6,7] We hypothesised that perioperative USG-guided ONSD measurements could change dynamically, reflecting ICP status in patients undergoing intracranial tumour resection. The primary objective of this study was to assess the perioperative changes in ONSD in patients with intracranial tumours. The secondary objectives were to discern the differences in ONSD values and their trend in supratentorial versus infratentorial tumours and to find the correlation between ONSD and various patient-related, surgery-related, and tumour-related parameters.

METHODS

After approval from the Institutional Ethics Committee (vide approval number IEC (III)/OUT/288/2023, dated 28/03/2023) and prospective registration in the Clinical Trial Registry-India (vide registration number CTRI/2023/06/053616, accessible at www.ctri.nic.in), this prospective, observational study was conducted according to the principles of Declaration of Helsinki (2013) and Good Clinical Practice guidelines. Written informed consent was obtained from the relatives of all the enroled patients for participation in the study and use of the patient data for research and educational purposes.

This study was conducted over 6 months on 94 patients of either gender over 18 years of age undergoing elective intracranial tumour resection. Pregnant females, patients with hyperthyroidism, cardiac disorder, optic nerve diseases (optic neuritis, optic nerve arachnoid cyst), ocular lesions such as orbital mass, orbital injury, or prior ocular surgery, and patients with sellar/suprasellar lesions were excluded.

Patients’ preoperative symptoms (headache, nausea, vomiting, and visual disturbances) with duration and GCS scores were noted. Preoperative radiological findings were reported, including tumour type, size, location, and signs of raised ICP (e.g., midline shift, cerebral oedema, sulcal effacement, hydrocephalus). General anaesthesia followed institutional protocols with standard American Society of Anesthesiologists (ASA) monitoring. Anaesthesia induction included intravenous (IV) fentanyl (2 µg/kg), propofol (2 mg/kg), and vecuronium (0.2 mg/kg), while maintenance involved IV propofol infusion (50–150 µg/kg/min) and sevoflurane in a 50:50 oxygen-air mix to achieve a minimum alveolar concentration of 0.7–0.8 and bispectral index/entropy values of 40–60. Ventilation settings included a tidal volume of 6–8 mL/kg, positive end-expiratory pressure of 5 cm H₂O, and an adjusted respiratory rate to maintain end-tidal carbon dioxide (EtCO₂) at 32–35 mmHg.

Serial ONSD measurements were done on closed eyelids in the supine position using a high-resolution 7-MHz linear array ultrasound transducer (Sonosite Turbo-M USG machine, FUJIFILM Sonosite, Inc., United States) by two senior neuro-anaesthesiologists, blinded to the study. The power output of the linear ultrasound probe was reduced to a thermal index of 0 and a mechanical index of 0.2 to minimise any thermal injury. The structure of both eyes was visualised such that the optic nerve lies directly opposite the probe kept in the sagittal and transverse plane, and the ONSD width was measured 3 mm behind the optic disc. The measurements were done at T0: preoperative (pre-induction); T1: post-induction, before surgery; T2: postsurgery, before extubation; and T3: 24 hours post-tumour resection. An average of three readings in each plane (transverse and sagittal planes) from each eye were taken for every participant. Values of 3–5 mm were considered normal.[8,9]

GCS assessment was done pre-induction, post-extubation, and 24 hours later. The duration of surgery and anaesthesia, intraoperative position, use of osmotic agents, presence or placement of ventriculo-peritoneal (VP) shunt, and complications during the surgery, if any, were noted. Tracheal extubation was performed at the end of surgery, if the following were present: pulsatile brain post-tumour resection before dura closure, stable haemodynamics, intact airway reflexes, and preserved general neurological status (able to follow simple commands). Otherwise, mechanical ventilation was continued postoperatively.

The primary outcome was the change in ONSD observed from preoperative values at 12 h and 24 h after the surgery. Secondary outcomes were the magnitude of changes in ONSD with respect to the location of the tumour and various patient-related factors [age, gender, ASA class, body mass index (BMI)] or tumour-related factors (GCS, clinical signs and symptoms of raised ICP, radiological signs of raised ICP, location and size of tumour, duration of symptoms) or surgery-related factors (duration of surgery and anaesthesia, intraoperative position, use of osmotic agents or presence of VP shunt).

The sample size was calculated using G Power Software version 3.1.9.7 (Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany) based on a similar study [showing ONSD threshold >5 mm indicative of raised ICP, control group’s (non-neurosurgical) ONSD-standard deviation (SD): 0.28 mm, and cases (intracranial tumour resection) ONSD-SD: 0.63 mm postoperative].[10] Using an ANOVA-repeated measures test, within factors and assuming the power of the study as 95%, level of significance as 5%, and effect size as 0.5, based on a prior study showing MRI ONSD changes after ICP-altering interventions, the sample size calculated was 94. Considering attrition, the sample size was inflated by 15% (n = 108).

The data was analysed using ‘R’ software version 4.1.2 (Bell Laboratories by John Chambers and colleagues, University of Auckland). Descriptive data were presented as mean, SD, median, and interquartile range for continuous variables (ONSD, tumour size, duration) and frequency and proportion for categorical variables (symptoms, radiological signs, ASA, location, position, presence of VP shunt). The continuous data’s normality was checked by the Shapiro-Wilk test, where ONSD and tumour size were normally distributed, whereas GCS, headache, and ASA class were non-normal. The effect of preoperative variables on pre-induction ONSD was calculated using a linear regression model, and the results were represented as regression coefficient, confidence interval, and P value. The change in ONSD over time was analysed using general linear modelling, and the results were represented as regression coefficient, confidence interval, and P value. The effect of pertinent variables on ONSD over the three time-points was analysed using general linear modelling, in which time-effect (effect of surgery) was incorporated as a covariate to account for it. Further post-hoc analysis using Bonferroni adjustment was performed to compare specific time-point differences. A P value of < 0.05 was considered statistically significant.

RESULTS

In total, 108 patients were included in the study; however, the final analysis was conducted on 94 patients [Figure 1]. The demographic details and other characteristics are presented in Table 1.

Figure 1.

Enrolment of patients for the study

Table 1.

Characteristics related to the patients and surgery

Variables	Value
Demographics:
Age (years), mean (SD) (95% CI)	42.54 (14.16) (39.46, 45.66)
Males/Females (n)	49/45
BMI (kg/m2), mean (SD) (95% CI)	23.46 (2.88) (22.74, 24.02)
ASA physical status:
I (n)	53
II (n)	35
III (n)	5
Location of tumour:
Supratentorial (n)	49
Infratentorial (n)	45
Left/right (n)	38/49
Bilateral (n)	1
Midline (posterior fossa) (n)	6
Symptoms of raised ICP:
Headache (n)	90
Nausea/vomiting (n)	26
Visual affection (n)	32
Seizures (n)	28
Radiological findings of raised ICP:
Effacement of sulci (n)	58
Mass effect (n)	62
Midline shift (n)	30
Effacement of basal cistern (n)	38
Obstructive hydrocephalus (n)	32
Tumour type
Schwannoma (n)	20
Meningioma (n)	21
Glioma (n)	35
Epidermoid cyst (n)	7
Arachnoid cyst (n)	3
Metastasis (n)	2
Hemangioblastoma (n)	2
Hemangiopericytoma (n)	1
Cavernoma (n)	1
Papilloma (n)	1
Germinoma (n)	1
Duration of surgery (hours), Mean (SD) (95% CI)	5.53 (1.61) (5.18, 5.88)
Duration of anaesthesia (hours), Mean (SD) (95% CI)	5.8 (1.92) (5.34, 6.23)
Use of an osmotic agent (n)	64
Complications:	10
Massive blood loss (n)	6
Venous air embolism (n)	2
Bradycardia and hypotension (n)	2
Postoperative mechanical ventilation (n)	8

Data expressed as mean (standard deviation) [95% confidence interval] or numbers. ASA=American Society of Anesthesiologists; ICP=intracranial pressure; BMI=body mass index

The difference in the ONSD measurements between the transverse versus sagittal plane in each eye and right eye versus left eye at different time-points was statistically insignificant (P = 0.659), irrespective of the side of the tumour [Table 2]. Therefore, ONSD values were averaged from four readings to a single value at any time-point. No significant change was observed from pre-induction to post-induction ONSD values (P = 0.521); however, statistically significant changes were observed from the preoperative to postoperative period (P < 0.001). The linear regression model with time effect demonstrated a rise of 0.036 mm in the immediate postoperative period and a decline of 0.044 mm 24 hours postsurgery compared to the preoperative measurements [Table 3]. The trend was similar in supratentorial and infratentorial tumours, but the decline was more in infratentorial tumours, although the difference was statistically insignificant (P = 0.101) [Tables 3 and 4] [Figure 2].

Table 2.

Optic nerve sheath diameter values of each eye in transverse and sagittal plane and their changes over time

Mean ONSD values	Preoperative ONSD (pre-induction) (mm)	Preoperative ONSD (post-induction) (mm)	Immediate postoperative ONSD (mm)	24 h postoperative ONSD (mm)	P using ANOVA
Left eye
Transverse	0.553 (0.536, 0.570)	0.552 (0.535, 0.569)	0.594 (0.579, 0.609)	0.506 (0.488, 0.524)	<0.001
Sagittal	0.554 (0.537, 0.571)	0.554 (0.537, 0.571)	0.598 (0.583, 0.613)	0.504 (0.486, 0.522)	<0.001
Right eye
Transverse	0.552 (0.535, 0.569)	0.553 (0.536, 0.570)	0.597 (0.582, 0.612)	0.505 (0.487, 0.523)	<0.001
Sagittal	0.553 (0.536, 0.570)	0.553 (0.536, 0.570)	0.596 (0.581, 0.611)	0.509 (4.917, 5.259)	<0.001
Bilateral eyes
Average values	0.559	0.555	0.593	0.515	<0.001

Data expressed as mean [95% confidence interval]. ONSD=optic nerve sheath diameter

Table 3.

Correlation between optic nerve sheath diameter and variables

Variables	Regression Coefficient [95% CI]	P
Patient Related:
Age	0.171 (−0.935, 1.276)	0.76
Gender male (Ref=female)	22.611 (−7.348, 52.57)	0.137
BMI	2.801 (−2.455, 8.057)	0.293
ASA physical status	25.435 (0.579, 50.29)	0.045
Tumour-Related:
Headache present (Ref=no)	14.875 (−60.159, 89.909)	0.695
Nausea present (Ref=no)	40.192 (7.343, 73.041)	0.017
Visual field affection (Ref=no)	44.501 (13.868, 75.134)	0.005
Duration of symptoms	−0.052 (−0.138, 0.035)	0.023
GCS	13.802 (10.455, 15)	0.392
Supratentorial location (Ref=infratentorial)	9.601 (−22.094, 41.297)	0.549
Volume	0.16 (0.05, 0.27)	0.005
Effacement of sulci present (Ref=no)	12.463 (−18.978, 43.904)	0.433
Effacement of basal cistern present (Ref=no)	7.07 (−23.783, 37.923)	0.65
Midline shift present (Ref=no)	46.368 (15.589, 77.148)	0.004
Mass effect present (Ref=no)	189.382 (46.929, 331.834)	0.01
Hydrocephalus present (Ref=no)	1.606 (−30.15, 33.62)	0.92
Surgery Related: (Time + Variable Effect)
Location Supratentorial (Ref=Infratentorial)	15.029 (−2.866, 32.923)	0.101
Volume	0.166 (0.104, 0.228)	<0.001
Duration of symptoms	−0.983 (−1.701, −0.392)	<0.001
Duration of surgery	0.955 (1.536, 0.374)	<0.001
Duration of anaesthesia	0.963 (1.611, 0.379)	<0.001
Osmotic agent used (Ref=not used)	0.556 (−17.855, 18.968)	0.953
Position: lateral (Ref=supine)	45.848 (−3.156, 94.853)	0.028
Position: prone (Ref=supine)	−14.818 (−53.426, 23.79)	0.453
Position: sitting (Ref=supine)	−10.791 (−29.354, 7.772)	0.256
Change In ONSD: Time Effect
Pre-induction to post-induction	4.59 (−9.395, 18.575)	0.52
Pre-induction to imm. postoperative	36.144 (15.159, 57.129)	<0.001
Immediate postoperative to 24 h postoperative	−57.367 (−42.528, −72.206)	<0.001
Pre-induction to 24 h postoperative	−44.441 (−65.427, −23.456)	<0.001

Data expressed as regression coefficient [95% confidence interval]. BMI=body mass index; ASA=American Society of Anesthesiologists

Table 4.

Correlation between optic nerve sheath diameter and variables in supratentorial and infratentorial tumours

Variables	Supratentorial tumours		Infratentorial tumours
	Regression Coefficient [95% CI]	P	Regression Coefficient [95% CI]	P
Patient-related:
Age	0.221 (−0.488, 0.929)	0.54	−0.007 (−0.798, 0.785)	0.987
Gender- male (Ref=female)	32.208 (12.28, 52.135)	0.002	7.056 (12.817, 26.928)	0.484
BMI	9.114 (4.998, 13.231)	<0.001	−1.885 (−4.683, 0.913)	0.185
ASA physical status	26.802 (9.965, 43.638)	0.002	21.872 (5.918, 37.825)	0.008
Tumour-related:
Headache present (Ref=no)	16.983 (29.841, 63.807)	0.476	11.875 (45.921, 69.671)	0.685
Nausea present (Ref=no)	47.994 (27.545, 68.443)	<0.001	8.821 (18.786, 36.429)	0.528
Visual field affection (Ref=no)	60.339 (40.421, 80.258)	<0.001	15.455 (−5.404, 36.313)	0.145
Duration of symptoms	−0.056 (−0.116, 0.004)	0.068	−0.042 (−0.095, 0.012)	0.127
Volume (cc)	0.34 (0.245, 0.435)	<0.001	0.054 (−0.001, 0.11)	0.055
Effacement of sulci: present (Ref=no)	59.052 (12.779, 105.325)	0.013	−46.855 (−87.6, −6.109)	0.025
Effacement of basal cistern: present (Ref=no)	35.82 (4.343, 67.297)	0.026	46.855 (6.109, 87.6)	0.025
Midline shift: present (Ref=no)	121.623 (83.681, 159.564)	<0.001	72.5 (50.085, 94.915)	<0.001
Mass effect: present (Ref=no)	194.333 (118.399, 270.268)	<0.001	7.07 (23.783, 37.923)	0.65
Hydrocephalus: present (Ref=no)	17.245 (−8.16, −5.649)	0.182	−5.476 (26.063, 15.111)	0.6
VP shunt: present (Ref=no)	−26.583 (53.168, 41.923)	0.512	41.923 (22.983, 60.863)	<0.001
Effect of intraoperative variables on ONSD
Volume (cc)	0.31 (0.263, 0.357)	<0.001	0.077 (0.048, 0.105)	<0.001
Duration of surgery (h)	−0.953 (−1.301, −0.605)	<0.001	−0.667 (−1, −0.334)	<0.001
Osmotic agent	−18.338 (33.816, −2.86)	0.02	−4.505 (15.709, 6.698)	0.431
Position Lateral (ref=supine)	43.735 (20.982, 66.488)	<0.001	45.848 (−3.156, 94.853)	0.028
Position prone (ref=supine)	2.277 (20.477, 25.03)	0.845	2.384 (20.471, 24.98)	0.954
Position sitting (ref=supine)	29.873 (7.561, 48.983)	0.836	27.893 (6.435, 49.351)	0.011
Change in ONSD:
Pre-induction to post-induction	4.59 (−9.395, 18.575)	0.52	4.621 (−9.936, 19.179)	0.534
Pre-induction to immediate postoperative	43.197 (29.212, 57.182)	<0.001	36.212 (21.655, 50.77)	<0.001
Immediate postoperative to 24 h postoperative	−79.795 (93.478, 66.112)	<0.001	−82.045 (97.348, −66.743)	<0.001
Pre-induction to 24 h postoperative	−36.598 (50.583, 22.613)	<0.001	−45.833 (60.391, −31.276)	<0.001

Data expressed as regression coefficient [95% confidence interval]. BMI=body mass index; ASA=American Society of Anesthesiologists, VP = ventriculoperitoneal; BMI = body mass index; ONSD = optic nerve sheath diameter.

Figure 2.

(a) Trend of optic nerve sheath diameter (ONSD) changes in supratentorial and infratentorial tumours; (b) Bland-Altman plot for ONSD variations with duration; (c) Bland-Altman plot for ONSD variations with volume of tumours

The linear regression model for preoperative ONSD and variables demonstrated that a higher ASA physical status was associated with a higher ONSD, while other demographic variables did not affect ONSD [Table 3]. Among the clinical symptoms of raised ICP, ONSD values were higher in patients having nausea/vomiting (P = 0.017) (95% CI: 7.343, 73.041) or visual field affection (P = 0.005) (95% CI: 13.868, 75.134). Among the radiological features, ONSD was found significantly higher in patients with a larger tumour size (calculated as volume = (½ length × width × height)), presence of midline shift, or mass effect. GCS did not show a good correlation with ONSD measurements. The subgroup analysis for supratentorial tumours exhibited that a higher body BMI and effacement of sulci or basal cistern were also associated with higher ONSD. Similarly, for infratentorial tumours, effacement of sulci and basal cistern and midline shift correlated with higher ONSD, while VP shunt was associated with a lower ONSD [Table 4].

The generalised linear model exhibited that the ONSD was higher at all time-points in supratentorial tumours than the infratentorial tumour location, though statistically insignificant (P = 0.101) (95% CI: −2.866, 32.923) [Table 3]. ONSD values showed a significantly greater change in tumours with a large volume (P < 0.001), shorter duration of symptoms (P = 0.020), and longer duration of surgery and anaesthesia (P = 0.001). Regarding the position, ONSD was slightly higher and showed a more significant change in patients with lateral intraoperative positioning (P = 0.028), while it was comparable in supine, prone, and sitting positions at all time-points; however, the trend was similar in all positions. The difference between ONSD values was not statistically significant among cases receiving osmotic agents and those not receiving them (P = 0.932) [Table 3]. Postoperative GCS did not show a good correlation with ONSD (regression coefficient: 12.73, P = 0.467). The subgroup analysis showed similar results where a greater reduction in ONSD was observed in supratentorial tumours if osmotherapy was used and in infratentorial tumours operated in the sitting position [Table 4].

DISCUSSION

Our study showed dynamic perioperative fluctuations in ONSD in patients undergoing intracranial tumour resection, having a transient postoperative rise followed by a 24-hour decline, indicating delayed ICP normalisation post-decompression. Secondary analyses showed no inter-eye or imaging plane differences. Preoperative ONSD correlated with nausea/vomiting, visual disturbances, radiological ICP signs, and larger tumour size, but not with age, gender, or GCS. Infratentorial tumours demonstrated greater postoperative ONSD reduction than supratentorial lesions. Surgical duration and lateral positioning showed higher postoperative ONSD, while osmotherapy and VP shunts showed lower postoperative ONSD.

Many studies have demonstrated an association between raised ICP and ONSD values, advocating the belief that changes in ONSD can indicate shifts in ICP.[11,12] While systematic reviews have established ONSD’s correlation with ICP in TBI,[9,11] similar evidence for intracranial tumours is lacking. Our findings contribute valuable insights and indicate that ONSD can be a useful perioperative monitoring tool, particularly when invasive ICP measurement is not feasible.

Our findings aligned with those of Benhur et al.,[13] who showed an initial rise followed by a decline for 48 hours postoperatively, and Feucht et al.,[14] where ONSD reduced postoperatively until 3 months. Hence, it will be erroneous to assume that ONSD undergoes immediate regression once the ICP reduces post-tumour resection, but a time-lapse exists before it returns to preoperative values or lower. These findings partially support our hypothesis that ONSD reflects ICP changes, though its temporal lag post-decompression warrants cautious interpretation. Additionally, as inter-eye ONSD differences were insignificant, measuring only one eye during ocular ultrasound is sufficient for routine use, saving time and reducing patient discomfort.

A higher ONSD in patients with elevated ASA grades or BMI suggests that uncontrolled comorbidities may manifest higher ICP. While research on ONSD in such patients is lacking, plausible mechanisms include microvascular changes affecting cerebral, retinal, and optic nerve blood flow. Conditions such as obesity and chronic kidney disease may also raise ICP due to hypertension and fluid retention. Symptoms (nausea/vomiting and visual disturbances) and radiological signs of intracranial hypertension (sulcal/basal cistern effacement, midline shift, and mass effect) correlated with higher preoperative ONSD, while headache was a vague symptom. It corroborated with the findings of Othman et al.[15] A shorter tumour duration linked to higher ONSD suggests that an acute presentation manifests significant intracranial hypertension due to less compensatory time. Larger tumours correlated with higher preoperative ONSD but a steeper postoperative decline, indicating significant decompression effects.

Our study showed comparable ONSD trends in supratentorial and infratentorial tumours, though infratentorial lesions had a greater postoperative decline. While Zhang et al.[16] reported higher ICP in supratentorial tumours, Mehrotra et al.[17] found significantly elevated ICP in posterior fossa lesions in children. These conflicting results highlight the complexity of tumour location and ICP dynamics, warranting further research. Prolonged anaesthesia and surgical duration showed higher postoperative ONSD, while supratentorial lesions showed lower ONSD after osmotherapy, which resonated with Robba et al.’s findings in TBI patients.[18]

Notably, intraoperative lateral position showed higher ONSD than supine, prone, or sitting positions, possibly due to extreme neck rotation/flexion, to gain tumour access, raising jugular flow resistance and impairing cerebral venous drainage. Uğraş et al.[19] observed similar findings. GCS did not correlate with ONSD, which can be ascribed to the localised involvement and preservation of the general neurological status. In our study, most patients had a preserved preoperative GCS and were extubated immediately postsurgery.

The key strengths of this study include its prospective design, comprehensive evaluation of confounding variables, and a novel comparison of ONSD dynamics between supratentorial and infratentorial tumours. However, there are certain limitations. While ethically justified, the lack of direct invasive ICP correlation represents a significant constraint. The heterogeneous tumour population (meningioma/glioma/schwannoma) and exclusion of patients with low GCS scores may limit the generalisation of our findings.

Future research should focus on addressing these knowledge gaps. Multicentre studies incorporating invasive ICP monitoring and studies focusing on specific tumour types to identify histology-specific patterns, and to understand the delayed ONSD normalisation observed post-resection, would be helpful. Interventional trials examining whether ONSD-guided ICP management can improve patient outcomes can be valuable.

CONCLUSION

Ultrasonography-guided ONSD measurements undergo a dynamic change in patients undergoing intracranial tumour resection. The trend is similar in supratentorial and infratentorial tumours, and it is affected by the size of the tumour, duration of presentation, and intraoperative positioning. We recommend it as a bedside tool to assess sudden neurological deterioration or suspected intracranial hypertension in postoperative patients in conjunction with traditional radiological scans to aid management.

Author contribution

AS: Concept, design, definition of intellectual content, literature search, data acquisition, manuscript preparation, editing and review. SO: Concept, design, definition of intellectual content, manuscript review. KD: Literature search, manuscript preparation, manuscript editing. SS: Data acquisition, data analysis. CM: Data acquisition, data analysis. AS: Literature search, data analysis, statistical analysis.

Study data availability

De-identified data may be requested with reasonable justification from the authors (email to the corresponding author) and shall be shared after approval as per the authors’ Institution policy.

Disclosure of use of artificial intelligence (AI)-assistive or generative tools

The AI tools or language models (LLM) have not been utilised in the manuscript, except that software has been used for grammar corrections and references.

Declaration of use of permitted tools

Nil.

Presentation at conferences/CMEs and abstract publication

None.

Conflicts of interest

The authors declare that they have no conflicts of interest.

Funding Statement

None.