Response [to: Optic nerve sheath diameter as ICP marker]

We thank Ravishankar S. Goel and Pooja Goel for their comments on our paper. We also believe that ultrasonographic measurement of ONSD has the potential to be a useful tool, especially in prehospital settings and at the emergency department, where invasive ICP monitoring is often impossible. We compared 2 tests to determine ICP: the noninvasive sonographic measurement and the invasive gold standard, use of an ICP probe. Furthermore, we were interested in a tool to be used in the prehospital setting to assess instantaneous changes in ICP more than static ICP measurements. In our prospectively designed study we found a strong correlation between ICP changes and ONSD changes. ONSD was measured 3 mm behind the retina in a transverse axis. We used the international definition of ONSD as the distance inside the hyperechoic dura mater.
All patients who suffered severe brain injury were treated according to our hospital protocol “raised ICP after traumatic brain injury.” This includes elevated head position (20°–30°), heavy sedation and analgesia, and mannitol administration 6–12 times a day, depending on baseline ICP. Mean arterial pressure was titrated to 80–100 mm Hg in patients with a baseline ICP < 20 mm Hg to guarantee cerebral perfusion pressure of at least 60 mm Hg. If baseline ICP exceeded 20 mm Hg, the treatment was intensified. No additional sedatives or muscle relaxants were administered prior to suctioning the endotracheal tube. All study measurements were done during daytime shifts (8:00 am to 6:00 pm; Amsterdam time, i.e., Greenwich Mean Time + 1 hour).
Our results are in contradiction with the suggestions made by Rajajee et al. in their retrospective analysis of their data.1 They observed a rapid response of ONSD to ICP increase but a delayed return to normal ONSD after ICP had already lowered to baseline levels. However, they included patients with raised ICP due to causes other than brain injury. Furthermore, the delayed return may be the result of brain edema in their patients, and this may explain the difference in results. In our study, we focused on the value of ONSD in brain-injured patients as a tool in the prehospital setting. We do realize that our population was rather specific and small but believe our study should be interpreted as a proof of principle. We fully agree that more studies should be done in larger groups and in different circumstances to assess the efficacy and the place of this noninvasive technique.