LAUSR

performed which revealed infarction of size 3 cm 2 cm in left temporoparietal region of the brain but there was no midline shift (Fig. 1B). Conservative management consisting of mannitol, furosemide, aspirin, and low– molecular-weight heparin was given. The ONSD remained persistently high during subsequent days. The patient developed septicemia and succumbed to multiple organ failure and expired on fifth postoperative day. The true neurological status of the patient on ventilator remains unclear, as it may be masked by desirable or necessary sedation rendering neurological evaluation difficult or impossible.3 In our case, elevated ONSD raised the suspicion of traumatic brain injury that must have occurred during road traffic accident. CT scan was, however, suggestive of ischemic infarct involving left middle cerebral artery. The exact timing and mechanism of stroke remains unclear. We speculate that the most likely etiology was atherothrombosis as the patient had several risk factors such as age, hypertension, obesity, and obstructive sleep apnea.4 Animal studies have shown that ONSD increases within an hour after increase in ICP. The rate of increase was 0.0034mm for an increase of 1mm Hg of ICP.5 Our patient had significant increase in ONSD, but CT scan did not reveal any midline shift probably due to the fact that increase in ONSD is an early indicator of raised ICP. To conclude, our case highlights the utility of ONSD measurement using ocular ultrasound as an important diagnostic tool to detect raised ICP. We, therefore, suggest its routine use in the ICU where clinical signs of raised ICP are nonspecific and difficult to interpret.