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Department of Anesthesiology, AI DuPont Hospital for Children, Wilmington, DE Department of Anesthesiology, Wake Forest University School of Medicine, Winston-Salem, NC
To the Editor:
We read with interest the article by Schwartz et al. (1) on patients with pyloric stenosis presenting with hyperkalemia instead of the classic laboratory finding of hypokalemia.
The authors speculate about the possible contracted intravascular volume status and its relationship to acid-base status, but there is no mention of the volume status of these patients. What was the range of time and intravascular volume resuscitation provided, and when were the blood chemistry panels obtained during the resuscitation? It could be assumed the patients who were normo- to hyperkalemia in this study might have been intravascular volume-deficient to the point of developing acidosis with a concomitant shift of potassium from intra- to extracellular spaces. The authors report the majority of the patients were not acidotic; however, they may have been relatively acidotic in the face of being initially alkalotic.
Despite the reduction in preoperative laboratory investigations in most patients, infants with a limited renal maturity and a disorder involving active fluid and electrolyte loss should be monitored closely for improvement from resuscitation rather than taken quickly to the operating room. Would we be comfortable taking adult patients with a potassium value above 5.3 or 5.5 mEq/L to the operating room with a planned rapid sequence induction utilizing succinylcholine? We are concerned that preoperative hyperkalemia should not go unheeded and requires a more conservative and slower approach to the administration of anesthesia.
To paraphrase the last sentence of the article, what do you do with a child who presents to the operating room with presumed pyloric stenosis and hyperkalemia? We would suggest consider the diagnosis of congenital adrenal hyperplasia! Children with the salt-losing variant of this disorder present like the child with pyloric stenosis at a similar age with vomiting, hyponatremia, and similar to patients described in this article, hyperkalemia. Hydration with normal saline is also important in the child with congenital adrenal hyperplasia; however, they also require glucocorticoid and possibly mineralocorticoid replacement. Induction of anesthesia in these patients could be potentially lethal without this replacement.
Reference
Baystate Medical Center, Tufts University School of Medicine, Boston, MA
In Response:
We thank Drs. McCloskey and Tobin for their interest in our recent publication. We did not measure the intravascular volume during resuscitation. Nor did we determine the time from hospital admission to the exact time when blood chemistries were obtained. However, we can state with a good deal of certainty that all of our infants with the presumptive diagnosis of pyloric stenosis get their admission (and for most, their only) set of electrolytes during the first 4 h following admission.
We agree that preoperative hyperkalemia should not go unheeded. There is a tendency to dismiss a lab value that runs counter to physiologic principles as "probably not real," but in this instance, especially given the practice of using succinylcholine, we felt uncomfortable inducing so many pyloric stenosis infants with hyperkalemia (over 36%); this was our rationale for studying it. When we originally submitted our article for publication, we also presented potassium data on nonsurgical pediatric patients 2 wk to 6 mo of age admitted over the same time period with medical diagnoses not known to be associated with electrolyte abnormalities; this information was removed during the editing process. In the nonpyloric stenosis group, a surprising 45% (60 of 133 patients) had potassium values characterized as hyperkalemia. Our results call into question the clinical usefulness of high potassium levels in children, at least in our hospital’s laboratory.
Finally, all of the infants at our hospital with presumed pyloric stenosis have the diagnosis confirmed with ultrasound. We agree that congenital adrenal hyperplasia should be considered when there is hyperkalemia in the face of a negative ultrasound.
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