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Excerpt
This letter is in regard to a recently published paper by Dr. Lewis and colleagues [1], addressing the fact that near-infrared spectroscopy monitoring is not clinically useful in brain-injured patients. The authors [1] presented a well-organized data analysis on a large number of observations, and their findings and conclusions are very important.
I would like to remind Dr. Lewis and colleagues and the readership that: a) what is being called "regional" monitoring by near-infrared spectroscopy is, in fact, just a focal (not at all regional) measurement; b) according to the largest known series of healthy volunteers [2], the upper normal value for jugular oxyhemoglobin saturation is 69%, not 75%, as presented by Dr. Lewis and colleagues [1]; c) one of the main goals of neuromonitoring is not only to detect and prevent secondary hypoxic-ischemic insults [3], but also to detect the reciprocal of hypoxic-ischemic insults, namely, relative cerebral hyperperfusion [4]. The latter is a most frequent, sustained problem in patients with brain swelling and acute intracranial hypertension, and once identified, usually responds to treatment [4,5].
Relative cerebral hyperperfusion has been found to be a sustained, repetitive finding, even in studies that emphasize cerebral ischemia [6]. In the earliest hours post injury, there is evidence of no ischemia but normal coupling between reduced cerebral oxygen consumption and cerebral blood flow, as reflected by normal mean values for arteriojugular oxygen content difference in the range of 7.1 vol% (Table 1 in the study by Bouma et al. [6]). Sequentially, abnormally low arteriojugular oxygen content differences (<5.1 vol% [2]) are a general rule as early as 12 to 18 hrs post injury [6]. These changes are usually associated with jugular oxyhemoglobin saturation values of >69% [4], not values >75%.
If one waits for jugular oxyhemoglobin saturation of >or=to75% to start treating relative cerebral hyperperfusion with optimized hyperventilation [4,5], many patients will have developed pronounced intracranial hypertension, and may no longer respond to treatment. Conversely, by carefully tracking the gradual increases in jugular oxyhemoglobin saturation and therapeutically offsetting those changes with optimized hyperventilation, excellent outcome figures may be expected [4,5].
Finally, it is about time for this "too good to be true" [7] monitoring with near-infrared spectroscopy to be carefully reconsidered, because according to technical features, it is only "reliable" in the normal brain, where monitoring is usually not necessary.
