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these happen all the time and in many places.2 This is not the first time that the description of an attack with a discussion on possible causes is criticized, and we thank Dr Brunnschweiler for doing precisely that. Discussing these aspects, however, may well lead to more caution and common sense when dealing with these types of animals. That will certainly improve human-wildlife relations, reduce conflicts, and certainly diminish high degrees of intolerance toward wildlife3—and that will ultimately be of great help in protecting precisely these animals, including sharks. In conclusion, we would like to add that, apparently, Dr Brunnschweiler expressed his legitimate concern for the industry of shark diving. We express our deep concern on behalf of the welfare of both humans and sharks. João Pedro Barreiros Centre for Ecology, Evolution and Environmental Changes / Azorean Biodiversity Group and Universidade dos Açores - Departamento de Ciências Agrárias, Angra do Heroísmo Azores, Portugal Otto B.F. Gadig Elasmobranch Research Laboratory São Paulo State University São Vicente, Brazil

Vidal Haddad Jr. Botucatu Medical School São Paulo State University São Paulo, Brazil References 1. Brunnschweiler J. Shark Attacks and Shark Diving. Wilderness Environ Med. 2015;26:276–277. 2. Conover MR. Why are so many people attacked by predators? Human–Wildlife Interactions. 2008;2:139–140. Accessed 14 November 2014. 3. Treves A, Bruskotter J. Tolerance for predatory wildlife. Science. 2014;344:476–477.

High Altitude Cerebral Edema—Serial MRI Findings To the Editor: High altitude cerebral edema (HACE) is a unique and life-threatening condition seen in a select group of individuals, such as mountaineers, soldiers, and trekkers, who are exposed to very high altitudes. The incidence of HACE is from 0.5% to 4%1 and varies with altitude. There are very few case reports of HACE serial magnetic resonance imaging (MRI) findings.2 We wish to report such a case here. A 23-year-old patient was brought in an unconscious state of 8 hours’ duration with a history of ascent to 3650

Figure 1. (A) Chest radiograph anteroposterior view on day 1 showing patchy alveolar opacities in right middle, lower, and left upper zone with normal cardiac silhouette. (B) Follow-up chest radiograph after 7 days, showing complete resolution.

Letters to the Editor m over 3 days. On admission, he had decreased responsiveness with cold clammy extremities. No oxygen saturation tracing could be obtained. He had marked tachycardia of 140 beats per minute, blood pressure of 140/76 mm Hg, and respiratory rate of 46 breaths per minutes. His breathing was labored, and accessory muscles of respiration were used. He was comatose, only localizing to pain. His pupils were normal in size and in reaction to light, and fundus examination was normal without focal deficit. There were bilateral coarse crackles in the chest extending up to the clavicles. The remainder of the clinical examination was normal. After initiation of basic supportive therapy and stabilization of the patient, a chest radiograph (Figure 1) revealed patchy alveolar infiltrates in the

279 right middle and lower zones and left upper zone consistent with pulmonary edema. An MRI scan of the brain (Figure 2) revealed mild hyperintensity on T2 and fluid-attenuated inversion recovery (FLAIR) sequences involving the corpus callosum, especially in the splenium. On diffusion-weighted imaging (DWI), restricted diffusion was noted in bilateral centrum semiovale, corona radiata, corpus callosum, and posterior limb of bilateral internal capsules. That was seen as bright signals on b1000 images and dark on apparent diffusion coefficient (ADC) maps. No other signal abnormality was seen in the other MRI sequences. Supportive treatment, including ventilatory support and intravenous dexamethasone, was initiated. The patient made a gradual recovery over 48 hours and was

Figure 2. (A) Fluid-attenuated inversion recovery axial scan on day 1 shows mild hyperintensity, in the splenium of the corpus callosum. (B) On diffusion-weighted imaging, b1000 shows bright signal in the posterior limb of internal capsule, splenium of the corpus callosum, deep white matter, and (C) dark signals on the apparent diffusion coefficient map. On follow-up magnetic resonance imaging after 6 days, (D) fluid-attenuated inversion recovery axial scan shows hyperintensity in the splenium of the corpus callosum, genu, and posterior limb of internal capsule. (E) On diffusion-weighted imaging, b1000 shows mildly bright signals in the splenium of the corpus callosum, normal appearance in the posterior limb of the internal capsule and deep white matter. (F) The apparent diffusion coefficient map shows near normal appearance.

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extubated. The patient recovered completely by the seventh day. Follow-up brain MRI was done on the seventh day and revealed moderate T2 and FLAIR hyperintensity in deep white matter, corpus callosum, and posterior limb of the internal capsule. Relatively increased diffusibility was noted on DWI, with near normal appearance in centrum semiovale and reduced restriction in corona radiata and corpus callosum. The patient was discharged on the eighth day, with advice to avoid further induction into high altitude. The most common MRI finding in HACE is that of increased T2 and FLAIR signal in the splenium of the corpus callosum2 with restricted diffusion, which is completely reversible on recovery.3,4 The predominant involvement of white matter without significant gray matter involvement suggests the presence of vasogenic edema. In our case, there was improvement in restricted diffusion, but FLAIR and T2 signal changes were noted to increase and became more prominent in the follow-up scan. Thus, T2 and FLAIR sequences can be used for diagnosis even after clinical recovery, as the vasogenic edema appears to take time to normalize.2 The diffusion studies and ADC maps in the previous reports show curious findings. In some cases, they are seen to be reversible, and in others they are not. The latter cases often have gliotic changes over time. That suggests the coexistence of both vasogenic and cytotoxic edema in the pathophysiology of the disease process.5 Our patient had findings of restricted diffusion in the initial scan that normalized in the follow-up scan, suggesting reversal of cytotoxic edema before progression to irreversibility. The vasogenic edema as seen in the FLAIR images persisted, and even resolved in the follow-up study. This finding raises the possibility that DWI and ADC maps can be used as key indicators of response to treatment as well as prognostic markers for future gliotic change. HACE is a life-threatening condition requiring aggressive management, and MRI scans of the brain may provide an understanding of the pathophysiology of the disease process. Involvement of the splenium of the corpus callosum is characteristic. The T2, FLAIR, DWI, and ADC maps are the essential sequences in the study: FLAIR can be used to confirm diagnosis even after clinical normalization of the patient, and DWI and ADC maps may be useful in prognostication of the cases. Ivaturi Venkata Nagesh, MD Department of Medicine Military Hospital Secunderabad Secunderabad, Telangana Pin, India

Gopinath Manoj, MD Madan Gurdarshdeep, MD Department Of Radiodiagnosis Military Hospital Secunderabad Secunderabad, Telangana Pin, India References 1. Anuj C. High altitude medicine. In: Munjal YP, Sharma SK, Agarwal AK, eds. API Textbook of Medicine. 9th ed. Mumbai, India: Jaypee Brothers Medical Publishers; 2012. 2. Hackett PH, Roach RC. High altitude cerebral edema. High Alt Med Biol. 2004;5:136–146. 3. Hartig GS, Hackett PH. Cerebral spinal fluid pressure and cerebral blood velocity in acute mountain sickness. In: Sutton JR, Coates G, Houston CS, eds. Hypoxia and Mountain Medicine. Burlington, VT: Queen City Press; 1992:260–265. 4. Hackett PH, Yarnell PR, Hill R, Reynard K, Heit J, McCormick J. High-altitude cerebral edema evaluated with magnetic resonance imaging: clinical correlation and pathophysiology. JAMA. 1998;280:1920–1925. 5. Wong SH, Turner N, Birchall D, Walls TJ, English P, Schmid ML. Reversible abnormalities of DWI in highaltitude cerebral edema. Neurology. 2004;62:335–336.

Improvised Method for Increasing the Temperature of an i-STAT Analyzer and Cartridge in Cold Environments To the Editor: The i-STAT point-of-care analyzers (Abbott, East Windsor, NJ, USA) have become increasingly common for clinical care and research in ultramarathons.1 However, there are implicit limitations when one attempts to implement a high-technology diagnostic tool in the low-technology wilderness settings where these events are commonly held, as there is a narrow temperature operating range of 161 to 301C (611 to 861F). Like hot weather,2 cold conditions can adversely affect the performance of the i-STAT analyzer and introduce unique challenges with not only the analyzer but also the cartridges and subject from whom blood is drawn. During a recent ultraendurance research study in September at Bear Valley, CA (18.41 N, 1201 W; 2018 m [6621 feet]), the nighttime temperature dropped to 21C (351F) from 2:00 to 4:30 AM. When we attempted to collect blood samples, the analyzer displayed a message that indicated the i-STAT was recording an ambient temperature outside its operating range. To warm the

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