Active distension of ventricular system due to mismatch between CSF production and absorption is called as hydrocephalus (7). Hydrocephalus can cause excessive buildup of CSF leading to increased ICP. Raised ICP can occur in conditions such as traumatic brain injury, meningitis, stroke, post resuscitation syndrome and intracranial tumors(8). Poor intracranial compliance can lead to catastrophic results such as hydrocephalus , uncal, central, transtentorial, or foramen magnum herniation (6). Early detection and intervention of raised ICP results in reduction of morbidity and mortality rates (6). The Brain Trauma Foundation recommends monitoring of raised ICP among patients with Glasgow Coma Scale of 3 to 8 and an abnormal computed tomography scan (6) (9). Patients had poor outcome when ICP exceeded 22 mm of Hg and better outcome when it was lesser than 15 mm of Hg. Serial change in ventricular size alone is not a very good indicator of raised ICP as normal ventricular size or small ventricle can have raised ICP (7).
Invasive methods of monitoring ICP are intraventricular catheter, extraventricular drains, extraparenchymal probes and subarachnoid bolts (6). The noninvasive methods of measuring raised ICP are transcranial Doppler usg, transcranical ultrasound propagation, ONSD, MRI, CT , measurement of dielectric property of cranium , magnetic angiography (6). ONSD is a well-accepted measure for early detection of raised ICP correctly. In recent days it is gaining popularity and is in practice at multiple centers.
Optic nerve sheath is continuation of dura and beneath it subarachnoid space continues along with optic nerve. Therefore when there is a rise in ICP it gets transmitted to optic nerve sheath eventually resulting in swelling of optic disc and papilledema (4) . ONSD as an extension of dura matter enclosing optic nerve was an established fact as early as 1780’s by Zinn and Wisberg (6). Optic nerve a part of central nervous system is covered by a leptomeningeal sheath is an expandable structure present at anterior segment behind the eye globe (6). With the rise in ICP CSF is pushed towards the tiny rim of subarachnoid space between the sheath and nerve causing expansion of dural covering. Previous studies have demonstrated that increase in ICP results in retrobulbar ONSD enlargement within seconds (10) (11). Expansion of sheath is more marked at anterior part of sheath behind the globe (6). The greatest degree of distension occurs 3 mm behind the globe (12). ONSD is usually measured by 3 radiological techniques: ultrasound, CT and MRI.
ONSD measurement by CT scan:
Traditionally, detection of raised ICP was performed during signs such as significant midline shift, effacement of basal cisterns, sulcal effacement, ventricular compression, and cerebral herniation as previously mentioned by Rajajee et al (4). Measurement of ONSD by CT to accurately diagnose raised ICP has been proved by previous studies (6) (13).
A retrospective observational study was conducted by Luyt et al. (8) on 56 patients to study relationship between ONSD measured on CT and raised ICP. Opening pressure manometry was measured during LP for detecting raised ICP (8). 14 patients had elevated ICP > 20 mm Hg and 42 had normal opening pressure. They showed that ONSD cutoff of 4.8mm by CT measurement had sensitivity and specificity of 92.9 % and 97.6%, respectively to detect the raised ICP. Furthermore, authors of this study mentioned that increasing the cut off value to more than 5mm decreased the sensitivity to 85%.
A retrospective cohort study was conducted by Sekhon et al. (13) on 57 TBI patients by measuring ONSD in CT scan and by invasive ICP. They found ONSD as better predictor of raised ICP than other parameters of CT scan such as cisternal effacement, sulcal effacement, ventricular compression and cerebral herniation. Linear and logistic regressions were used in study to see correlation between ONSD and invasive ICP values. Strong correlation between ICP and ONSD r = 0.74 p 7.3mm to be independently associated with ICU mortality rate among TBI patients. Authors of the article suggest ONSD to be included with initial management of TBI patients along with other clinical, radiological and laboratory parameters (11). However they also point out higher ONSD does not necessarily rule out good outcome.
ONSD measurement by MRI:
Kang et al. (1) conducted a study to look for relationship between ONSD in brain MRI and elevated ICP. This study showed that patients with raised ICP have significantly greater diameter of ONSD compared to normal group. Out of 31 patients in the study, 13 patients with mass effect had average ONSD of right and left to be 5.06mm and 5.13mm, respectively. Similarly, patients without features of mass effect had ONSD of 4.545mm (Rt) and 4.35mm (Lt). Kang et al. cited hemodynamic instability and time as a restrictive factor for radiological examinations (1). Kang et al. concluded ONSD measurement by MRI as an efficient tool to predict increased ICP in an unconscious patient.
A study conducted by Geeraerts et al. (10) showed ONSD as an excellent predictor of raised ICP. 38 patients with TBI had undergone MRI in which ONSD was measured and ICP monitoring was done via parenchymal sensor. Results of the study showed ONSD to be 6.31mm +/- 0.5mm among patients with ICP > 20mm of Hg and ONSD of 5.29mm +/- 0.48mm among patients with ICP below 20mm of Hg. Authors say ONSD