How Ultrasonographic Measurement of Optic Nerve Sheath Diameter (ONSD) Aids in Diagnosis of Cerebrovascular Accident in a Patient on Ventilator?

    loading  Checking for direct PDF access through Ovid

Excerpt

To JNA Readers:
A wide range of noninvasive methods have been proposed and utilized to measure intracranial pressure (ICP): ultrasonographic measurement of optic nerve sheath diameter (ONSD) being one of them.1 It has high sensitivity and specificity in predicting raised ICP, and hence recently, ONSD has been increasingly used in emergency departments and intensive care units (ICU).2 A 55-year-old female patient with BMI of 31 presented to emergency department with blunt abdominal trauma sustained due to road traffic accident. There were several episodes of vomiting but there was no history of unconsciousness, ENT bleed, or seizures. Past history revealed that she was a known case of hypertension (on amlodipine), chronic obstructive pulmonary disease, and obstructive sleep apnea. Emergency laparotomy was performed following which successful extubation was performed. However, after 4 hours, she became tachypneic, and developed respiratory distress and hypotension. Ionotropes (dopamine and noradrenaline) were started and she was shifted to ICU. Initially, noninvasive ventilation was performed but gradually she became drowsy and disoriented owing to hypoxia, and thus, invasive ventilation was started. Oxygen saturation was maintained on FiO2 0.4 and ionotropes were tapered off over a period of 12 hours. Her neurological status was E4VTM6, moving all 4 limbs, and pupils were normal in size but sluggishly reacting to light. As a routine, ONSD was measured using Sonosite M-Turbo (Sonosite Inc., Bothell, WA) ultrasound machine with a 6 to 13 MHz linear-array probe on first postoperative day. The diameter was found to be increased in both the eyes. It was 0.80 and 0.82 cm in the left and the right eye, respectively (Fig. 1A). A CT scan of the head was 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 0.0034 mm for an increase of 1 mm 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.2
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.

Related Topics

    loading  Loading Related Articles