We would like to thank you for the opportunity of responding to the letter by Drs. Khandelwal and Kumar about our recent paper . We appreciate the interest of the authors in our article. Below, we respond to their concerns.
First, the evaluation of aphasia in intubated patients may be challenging but it is feasible. Intubation is a barrier to evaluate spontaneous language, fluency, naming and repetition, but comprehension to spoken or written commands can be easily assessed. Moreover, writing can be used as a surrogate measure of verbal output. For instance, the instructive of the National Institutes of Health stroke scale clearly states “intubated patients should be asked to write” (https://www.stroke.nih.gov/resources/scale.htm). Our patient did not follow either spoken or written commands and was unable to write. We made the diagnosis of aphasia based on these findings, along with the presence of a hematoma within the lenticular nucleus of the dominant cerebral hemisphere. Additionally, the patient was mute and unable to follow commands following extubation, confirming our initial diagnosis.
Second, our patient clearly had vasospasm. We suggested that hyperemia also played a role because the mean blood flow velocity (MBFV) of the extracranial internal carotid artery was above normal limits (30 ± 9 cm/s) , yet we acknowledge it can be inaccurate. We also recognize that Lindergaard was misspelled and apologize for the typographical error.
Third, the MBFV was high on post-operative day (POD) 6, but the uptrend stopped on POD5. Indeed, on POD6 the MBFV as well as the Lindegaard ratio (LR) had decreased compared with POD5 (MBFV on the right middle cerebral artery 187 vs. 156 cm/s, MBFV on the left middle cerebral artery [LMCA] 269 vs. 161 cm/s, LR on the LMCA 6.1 vs. 4.3). In other words, the rising course of MBFV and LR had an inflexion point in POD5 right after the initiation of intravenous milrinone.
Fourth, the pulsatility index (PI) is usually regarded as a measure of downstream vascular resistance. Besides intracranial pressure (ICP), several variables influence the PI. While it is difficult to point with certainty the main determinant of increased PI in our patient despite hemicraniectomy, we believe that a combination of the following factors may have played a role. (1) After hemicraniectomy, ICP values improve, but not always normalize . In fact, at the moment of transcranial doppler (TCD) evaluation (POD6), the ICP of our patient was 18 mm Hg with the head of the bed elevated 30° (normal values in a supine healthy adult range between 7 and 15 mm Hg) . (2) The mean arterial blood pressure at the time of TCD measurement (POD6) was 100 mm Hg (cerebral perfusion pressure [CPP] = 82 mm Hg). This is relevant because the PI increases with CPP > 70 mm Hg . (3) The biologic behavior of perihematomal edema (PHE) increases for 2–3 weeks after intracranial hemorrhage . Furthermore, PHE is heightened after hemicraniectomy [7, 8]. PHE may compress distal vessels, increasing the resistance of the distal vascular bed. (4) PI decreases in patients with large-vessel vasospasm with a preserved autoregulatory response. Once vasospasm improves, as in our patient, the PI is expected to increase .
Lastly, not only the abnormal TCD values on POD1, but also their uptrend despite appropriate medical treatment prompted us to start milrinone. We highlight the unfavorable clinical evolution because the vasospasm on POD1 was mild and expected in the context of Reversible Cerebral Vasoconstriction Syndrome. Available data on this therapeutic approach may help to guide decisions on special circumstances, but do not allow for routine recommendation of its early use in all patients.