To the Editor: In the Images in Clinical Medicine entitled "FatalCerebral Hypoxemia after Cardiac Arrest" (Feb. 27 issue),1 theterm "hypoxemia" is misused.2 How can hypoxemia be cerebral,when the term refers to oxygen levels in the blood? More important,hypoxemia is a distinct insult from ischemia,3,4 and controlledexperiments in animal models have shown that pure hypoxemiawithout heart stoppage does not cause brain necrosis.5,6 A bettertitle for the image would have been "Widespread Brain Necrosisafter Cardiac Arrest." This title would not have perpetuatedthe myth that hypoxemia by itself causes necrotizing brain damage.
Roland N. Auer, M.D., Ph.D. University of Calgary Calgary, AB T2N 4N1, Canada rauer{at}ucalgary.ca
References
Kelsen J, Obel A. Fatal cerebral hypoxemia after cardiac arrest. N Engl J Med 2003;348:817-817. [Free Full Text]
Auer RN, Sutherland GR. Hypoxia and related conditions. In: Graham DI, Lantos PL, eds. Greenfield's neuropathology. 7th ed. Vol. 1. London: Edward Arnold, 2002:233-80.
Auer RN, Siesjö BK. Biological differences between ischemia, hypoglycemia, and epilepsy. Ann Neurol 1988;24:699-707. [CrossRef][Web of Science][Medline]
Simon RP. Hypoxia versus ischemia. Neurology 1999;52:7-8. [Free Full Text]
Pearigen P, Gwinn R, Simon RP. The effects of in vivo hypoxia on brain injury. Brain Res 1996;725:184-191. [Medline]
Miyamoto O, Auer RN. Hypoxia, hyperoxia, ischemia, and brain necrosis. Neurology 2000;54:362-371. [Free Full Text]
Dr. Kelsen replies: I thank Dr. Auer for his interest in theimages and his comment on the inappropriate use of the term"hypoxemia" in the title. On the basis of research by Dr. Auerand others, a clear distinction has been established betweenthe terms "hypoxia" and "ischemia" and between their respectiveroles in cerebral infarction.1,2 I understand that the titlecould lead to the misinterpretation that hypoxemia caused thereported brain damage. This patient obviously had primary cerebralischemia — as opposed to primary cerebral hypoxia —due to cardiac and circulatory arrest. The proposed title byDr. Auer refers to a morphologic description of the cerebralinjury. However, the dramatic changes seen on three consecutivecomputed tomographic (CT) scans represented developing edemaand infarction but did not reflect widespread brain necrosis.Panel A of our image shows a CT scan obtained one hour afterpresentation, and Panel B shows a scan obtained four hours later— not eight hours later, as stated in the legend. Thescan obtained at eight hours is shown in Figure 1. An alternativetitle that summarizes the underlying pathophysiological featuresof the case could be "Evolving Diffuse Cerebral Infarction afterCardiac Arrest."
Figure 1. Computed Tomographic Scan of the Brain, Obtained Eight Hours after Cardiac Arrest, Showing Severe Edema and Infarction in the Anterior and Posterior Circulation of Both Hemispheres.
Jesper Kelsen, M.D. University Hospital of Aarhus DK-8000 Aarhus C, Denmark jesper.kelsen{at}iekf.au.dk
References
Miyamoto O, Auer RN. Hypoxia, hyperoxia, ischemia, and brain necrosis. Neurology 2000;54:362-371. [Free Full Text]
Simon RP. Hypoxia versus ischemia. Neurology 1999;52:7-8. [Free Full Text]
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