Dilated Pupil as a Diagnostic Component of Brain DeathDoes it Really Matter? To JNA Readers: We encountered a 50-year-old woman with severe traumatic brain injury who further deteriorated during the course of treatment to a point where brain death was suspected. After estab- lishing the prerequisites, we decided to proceed to the conrmation of brain death. Although the patients both pupils were unreactive, their diameters were 3.0 and 3.2 mm in the right and left eyes, respectively (conrmed by ultrasound). As the pupil sizes were within a normal range, there was a dilemma about whether to proceed with the brain death assessment. However, on careful exami- nation, all brainstem reexes, including direct and indirect pupillary responses to light bilaterally, were absent; the apnea test conrmed the absence of sponta- neous respiration. Repeat assessment 6 hours later conrmed the diagnosis of brain death. Of note, the pupil sizes re- mained unchanged (midsize at 3.0 and 3.2 mm) at the time of the second ex- amination. Nonetheless, sedative medi- cation or other drug effects that are known to affect pupillary diameter were ruled out before commencement of the brain death examination. One of the criteria for the diagnosis of brain death in Japan, Australia, and New Zealand is bilaterally unreactive pupils with diameter > 4 mm. 1,2 Although Canadian and United States guidance note that pupils are usually midsize or dilated after brain death, there is no requirement for pupil diameter to be > 4 mm. 3,4 The UK guidance also does not require that pupils be > 4 mm for the diagnosis of brain death, only that they are xed and do not respond to changes in the intensity of incident light. 5 In most jurisdictions, therefore, it is the absence of pupillary responses rather than pupil size that is the essential factor for the diagnosis of brain death. The stipulation of a minimum pupil diameter for the diagnosis of brain death in the few countries that continue to do so should be reconsidered given the multiple inuences on pupillary size. Al- though the exact mechanism of mydriasis in anoxia and brain ischemia is unknown, postulated mechanisms include para- sympathetic inhibition and loss of tone of the third cranial nerve. The exact in- cidence of pupil size > 4 mm after brain death also remains unknown. In the process of establishing the Japanese brain death criteria, it was found that ~20% of patients in whom brain death was sus- pected had pupil diameters <4 mm. 1 Further, pupil size need not always re- main constant. In a retrospective study, Sagishima and Kinoshita 6 observed that pupillary sizes were not identical at the rst and second brain death assessments, with average ( ± SD) diameters of 6.1 ( ± 1.1) mm during the initial examination and 6.4 mm ( ± 1.1) ~6 hours later. Although a minimum pupil size is not a prerequisite for the diagnosis of brain death in most jurisdictions including India, this is often unknown or misunderstood by clinicians. Ankur Khandelwal, MD, DNB Rajeeb K. Mishra, MD Sneha Singh, MD Shalendra Singh, MD, DNB, DM Girija P. Rath, MD, DM Department of Neuroanaesthesiology and Critical Care, All India Institute of Medical Sciences (AIIMS) New Delhi, Delhi, India REFERENCES 1. Takeuchi K, Takeshita H, Takakura K, et al. Evolution of criteria for determination of brain death in Japan. Acta Neurochir (Wien). 1987;87:9398. 2. Australian and New Zealand Intensive Care Society. The ANZICS Statement on Death and Organ Donation (Edition 32). Melbourne: ANZICS; 2013. 3. Shemie SD, Doig C, Dickens B, et al. Severe brain injury to neurological determination of death: Canadian forum recommendations. CMAJ. 2006;174:S1S30. 4. Wijdicks EF, Varelas PN, Gronseth GS, et al. Evidence-based guideline update: de- termining brain death in adults: report of the quality standards subcommittee of the Amer- ican Academy of Neurology. Neurology. 2010;74:19111918. 5. Academy of the Medical Royal Colleges. A Code of Practice for the Diagnosis and Confirmation of Death. London: Academy of the Medical Royal Colleges; 2008. 6. Sagishima K, Kinoshita Y. Pupil diameter for confirmation of brain death in adult organ donors in Japan. Acute Med Surg. 2016;4:1924. Scalp Block for Management of Subarachnoid Hemorrhage (SAH)-induced Headache To JNA Readers: SAH-induced headache, often described as the worst headache of ones life,has been undertreated be- cause of a variety of reasons. 1 Cur- rently, no newer treatment modalities are being explored, so we propose using an existing technique, the scalp block, as an adjunct to the manage- ment of SAH-induced headache. Scalp block has previously been suc- cessfully used during awake neuro- surgical procedures and in chronic pain management to prevent and treat headaches of various etiologies. 2,3 The 2 most commonly accepted mechanisms of headache after SAH are meningeal irritation secondary to inammation caused by hemoglobin breakdown products, and hyper- algesia caused by central sensitization by NMDA receptors. 4,5 Irrespective of the etiology of the SAH or mecha- nism of the pain, the afferent pathway is through the meningeal branches of the various branches of the trigeminal nerve and roots of C2 and C3 nerves. Hence, scalp block has the potential to block any nociceptive stimulus from the meninges. Our standard analgesic regimen after SAH consists of a combination of systemic analgesics and, if these fail to control the headache, a trial of scalp block. The systemic analgesics include intravenous acetaminophen, tramadol, keterolac, and transdermal fentanyl at appropriate doses. Scalp block is ad- ministered if the patients Visual Analog Scale (VAS) for pain is > 7 (out of 10), The authors have no funding or conicts of interest to disclose. DOI: 10.1097/ANA.0000000000000521 The authors have no funding or conicts of interest to disclose. DOI: 10.1097/ANA.0000000000000523 Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved. Correspondence J Neurosurg Anesthesiol Volume 31, Number 3, July 2019 356 | www.jnsa.com Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.