Trauma continues to be a leading global health challenge, often referred to as the “silent epidemic,” particularly due to its high mortality rate among young adults. Among traumatic injuries, neurotrauma contributes substantially to this burden. An estimated 10 million individuals experience traumatic brain injuries (TBI) each year worldwide [1]. In the United States, TBI affects around two million people annually, with nearly half a million requiring hospitalization. In India, over 100,000 deaths and more than a million serious cases of TBI occur each year, making it one of the countries with the highest TBI prevalence [2].

TBI represents a critical public health issue, contributing significantly to both mortality and long-term disability. Among those who survive a head injury, about 10% suffer fatal outcomes, while many others endure varying levels of neurological impairment. Approximately 5–10% of survivors face serious, irreversible deficits, and another 20–40% experience moderate disability [3]. Many more are affected by subtle neurological disturbances often categorized as “minimal brain trauma”.

There is a direct correlation between the severity of brain injury and low Glasgow Coma Scale (GCS) scores on admission, which generally indicates a poorer prognosis [4]. In India, the absence of adequate medical intervention during the “golden hour” following injury contributes to poor outcomes, with nearly 50% of TBI-related deaths occurring within the first two hours post-trauma. This is often due to ischemic injury to neurons, frequently triggered by elevated intracranial pressure (ICP) [5].

An ICP level exceeding 20 mmHg is commonly associated with adverse outcomes in TBI cases, particularly during the early post-traumatic period⁵. Prompt identification and management of raised ICP are vital to prevent secondary ischemic brain injury and to maintain sufficient cerebral perfusion. Therefore, timely and precise monitoring of ICP is critical for optimizing outcomes [6].

While invasive techniques like intracranial catheter placement remain the gold standard for direct ICP measurement, these methods are not without risk, including infection, hemorrhage, and other procedural complications. Cross-sectional imaging, particularly non-contrast CT (NCCT), plays a pivotal role in the acute evaluation of TBI and is the most widely used diagnostic modality in tertiary level hospital settings [7-8].

A prospective observational study was conducted on 100 adult TBI patients over 12 months at a tertiary care hospital. ONSD was measured 3 mm posterior to the globe using a high-frequency linear transducer (Fig No. 1).

The procedure was explained to the patients/attendants. Informed written consent was obtained from all patients or their attendants. Each patient was examined in supine position and quiet state with high-frequency (7–13 MHz) linear array transducer portable ultrasound system after using adequate amount of transmitting media gel and the probe was gently placed on the closed upper eyelid space (Fig No. 1).

CT brain was performed and evaluated for signs of raised ICP. Data were statistically analyzed, including ROC curve for optimal ONSD cut-off, and correlation with Glasgow Coma Scale (GCS) and Glasgow Outcome Scale (GOS).

Inclusion criteria –

All adult patients (age >18 years) admitted to emergency / ICU with traumatic brain injury.

Fig No. 1: (a) Proper transducer placement for ONSD measurement; (b) Ultrasonographic view showing optic nerve sheath measurement 3 mm behind the globe.

Table No. 1: ONSD values with CT findings

Values are mean ± SD. Statistical significance assessed using independent t-test; p < 0.05 considered significant.

Table No. 2: Area under the Curve

AUC: Area under ROC curve; CI: Confidence Interval.

Fig No. 2: Distribution bar chart (cut-off 5.75 mm)

Subjects grouped by diagnostic threshold of 5.75 mm (ONSD).

Table No. 3: Diagnostic Performance.

PPV: Positive Predictive Value; NPV: Negative Predictive Value; CI: Confidence Interval.

Table No. 4: Comparison of ONSD among subjects with different GCS score.

One-way ANOVA applied; p < 0.05 considered significant.

Fig No. 3: ONSD among subjects with different GCS score.

Box plot shows increasing ONSD with worsening GCS severity.

Table No. 5: Association between ONSD and Glassgow Outcome Scale

Chi-square test used; p < 0.05 considered significant.

This study demonstrates the utility of ultrasonographic measurement of optic nerve sheath diameter (ONSD) as a non-invasive and reliable surrogate marker for detecting raised intracranial pressure (ICP) in patients with traumatic brain injury (TBI). ONSD and Glasgow Coma Scale (GCS) assessments were performed at emergency presentation, prior to CT imaging. Functional outcome was later evaluated at follow-up using the Glasgow Outcome Scale (GOS) [9].

Traumatic brain injury (TBI) predominantly affects young adults and continues to impose a major global health burden. In our study cohort of 100 patients, the mean age was 38.09 ± 14.23 years, with a male preponderance (79%), and road traffic accidents (59%) were the most common mechanism of injury—consistent with epidemiological trends reported in developing countries [1–4].

Clinically, the majority of patients presented with symptoms indicative of raised ICP, including headache (95%), loss of consciousness (86%), and vomiting (43%). Most cases were categorized as moderate TBI (GCS 9–12; 69%), with lesser proportions having mild (17%) or severe (14%) head injury.

The central objective of this study was to evaluate the utility of ONSD measured by ultrasonography as a non-invasive marker for raised ICP in TBI. Our results robustly support this role. The mean ONSD in patients with CT-proven raised ICP was significantly higher (Right: 6.08 ± 0.31 mm; Left: 6.07 ± 0.34 mm) compared to those with normal ICP (Right: 5.38 ± 0.40 mm; Left: 5.34 ± 0.37 mm), with p < 0.001 for both eyes (Table 1). These findings are consistent with prior studies suggesting that ONSD >5.7 mm correlates with intracranial hypertension [7–9].

Diagnostic performance of ONSD was excellent, with ROC AUC values of 0.915 and 0.927 for right and left eyes, respectively (Table 2). A cut-off value of 5.75 mm yielded high sensitivity (87%), specificity (80–83%), and overall accuracy (83%) (Table 3), indicating that ONSD is a reliable discriminator of raised ICP in acute settings. Figure 2 visually demonstrates the proportion of subjects with ONSD above and below the diagnostic threshold.

A graded rise in ONSD was observed with worsening GCS scores, with the highest values recorded in severe TBI. This suggests a direct correlation between the severity of neurological impairment and raised ICP. Post-hoc analysis confirmed statistically significant differences in ONSD between mild and moderate, and mild and severe GCS groups (p < 0.001) (Table 4). This trend is also illustrated in Fig No. 3, showing the distribution of ONSD values across GCS strata.

Furthermore, ONSD >5.75 mm was significantly associated with poor clinical outcomes, as measured by the GOS. Among patients with elevated ONSD, 64% experienced poor outcomes (GOS 1–3), compared to only 24.5% in those with normal ONSD (Table 5). This underscores the prognostic value of ONSD, making it a valuable tool not just for detection but also for risk stratification in TBI.

Additional sonographic findings, such as papilledema (17%) and altered perineural echogenicity (23%), were observed but were less consistently present than elevated ONSD, reinforcing the latter’s reliability. Fig No. 1 demonstrates correct transducer positioning.

Our findings are consistent with those of Rajajee et al. and Soldatos et al. [14,15], who also reported similar ONSD thresholds and correlations with raised ICP and clinical outcomes. The practical advantages of ONSD measurement—its non-invasive nature, rapid acquisition, and bedside availability—make it an especially valuable tool in emergency and intensive care settings, particularly where CT access or invasive monitoring is limited [6,12]

Limitations

This single-center study did not include direct invasive ICP measurements for validation. Additionally, although scanning technique was standardized, inter-observer variability was not formally assessed.

The strong inverse correlation between ONSD values and Glasgow Coma Scale (GCS) scores, along with a statistically significant association with Glasgow Outcome Scale (GOS) scores, validates the role of ONSD as both a diagnostic and prognostic marker. The study’s cutoff value of 5.75 mm demonstrated high sensitivity and specificity, with an AUROC exceeding 0.9, which is comparable to or exceeds diagnostic accuracy reported in recent international literature. These metrics highlight its potential for early risk stratification, allowing for timely therapeutic intervention and improved outcomes. Our findings are consistent with a growing body of literature emphasizing the diagnostic accuracy and clinical relevance of ONSD measurements across diverse patient populations and healthcare environments.

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