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219126_NCS_Currents_March_2_eMag

EDITOR’S MEMORANDUM Coming Up in Neurocritical Care Eelco Wijdicks, MD, PhD, FNCS, Editor-in-chief The brain connects with virtually every organ system and, therefore, the acutely injured brain may refl ect itself in impaired vital organ function. The heart, lung, and gut are all quickly affected. Both the brain and kidney maintain homeostasis with changes in sodium and water balance. The kidney is equally important because the brain regulates renal blood fl ow, glomerular fi ltration rate, and renal sodium handling. Acute kidney injury is not commonly observed in the Neuro ICU, but there are often risky circumstances with triggers such as hypovolemia and hypernatremia, use of iodinated contrast for CTs and cerebral angiography, and also drug toxicity and rhabdomyolysis, all leading to additional acute kidney injury in patients with acute brain injury. Little is known about how the kidney is acutely affected and how kidney injury may affect the brain. In the April issue of Neurocritical Care, the reader will fi nd original articles on this brain-kidney connection. Three articles, accompanied by an editorial by Freeman and Wadei, describe problems when patients with acute kidney injury need renal replacement therapy. Kumar and colleagues from Barnes-Jewish Hospital in St. Louis describe a case series of dialysis-induced worsening of cerebral edema. All patients had elevation of ICP within the fi rst hour of hemodialysis. Mechanisms continue to be debated and could relate to paroxysmal brain acidosis. The authors provide potential options such as using gradual urea removal with continuous renal replacement. Higher composition of sodium in the dialysate or preemptive use of mannitol to maintain higher plasma tonicity are also suggested as possible preemptive measures. In addition, Osgood and coworkers from the Department of Neurology at the University of Massachusetts Medical School also raise awareness for the potential for rapid brain edema and herniation with acute brain-injured patients who are undergoing continuous venovenous hemofi ltration. These articles clearly point out that some guidelines for renal replacement therapy in neurocritical care patients are needed. Recommendations may look at use of high sodium dialysate and continuous monitoring of blood pressure and oxygenation in these patients. Dias and colleagues present a cohort of 18 consecutive patients with severe traumatic brain injury and report multiple measurements of creatinine clearance. They found that kidney hyperfi ltration is a frequent fi nding, and they found a strong correlation between the cerebral vascular reactivity pressure index and creatinine clearance. The paper suggests there might be a “brain-kidney crosstalk and a possible biochemical interplay between brain and kidney.” They conclude that better cerebral autoregulation is signifi cantly correlated with augmented renal clearance in trauma patients and also is associated with a better outcome. They speculate that the brain and the kidney with their “small-resistance vascular beds” present a unique way to react to fl uctuations in blood pressure and fl ow. Such a similarity may mean that information about microvascular damage in one organ may provide information about damage in the other organ. A great research opportunity. These three articles bring an interesting topic in neurocritical care to the attention of the readership and provide some new insights into the brain-kidney connection. It is undisputed that in our daily ICU practice better study of the risks of global brain edema after dialysis is needed. This is another example of how the brain and other organs are connected and how changes in organ function and its subsequent treatment may affect outcome. 19


219126_NCS_Currents_March_2_eMag
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