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Anesth Analg 2003;97:355-357 © 2003 International Anesthesia Research Society
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Abstract |
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Children presenting with pyloric stenosis have hypochloremic metabolic alkalosis and their serum potassium levels are thought to be low or normal. We reviewed potassium levels in infants with pyloric stenosis. Thirty-six percent of patients with pyloric stenosis had increased serum potassium levels. We conclude that hyperkalemia may be more common in children with pyloric stenosis than previously thought.
IMPLICATIONS: A significant number of infants with pyloric stenosis have a serum potassium value above the normal limit.
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Introduction |
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Pyloric stenosis is a relatively common condition that presents in infants 1–2 mo of age and usually requires surgical intervention (pyloromyotomy). Surgery is usually not performed until after adequate hydration has been achieved. The classic presenting electrolyte profile of these patients is hypochloremic metabolic alkalosis (1). Potassium levels are generally low to normal (1).
Our clinical impression over several years was that an unusually large number of infants with pyloric stenosis presented with hyperkalemia. We decided to retrospectively examine the potassium levels of infants with pyloric stenosis presenting to our institution. In addition, we examined whether the preoperative potassium value had any bearing on the choice of muscle relaxant used for anesthetic induction.
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Methods |
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After obtaining IRB approval, we reviewed the charts of infants who were diagnosed with pyloric stenosis and who underwent pyloromyotomy at our hospital over a 6-yr period (1995–2000). Preoperative potassium values on each of these infants were obtained. The upper limit of normal for serum potassium at our hospital’s laboratory is 5.3 mEq/L. If an infant had more than one set of electrolytes drawn before surgery, the larger value (nonhemolyzed) of the two was used. In addition, the muscle relaxant (succinylcholine, a nondepolarizing drug, or no muscle relaxant if awake intubation was performed) used for the induction of anesthesia was determined by looking at the anesthetic records. The usual method of blood sampling at our institution is by means of venipuncture.
Statistical analysis involved contingency testing (
2 analysis). A P value < 0.05 was considered significant.
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Results |
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A total of 143 charts were reviewed; 3 were discounted because the potassium sample was reported as hemolyzed. The age of the patients (in weeks) was 7.3 ± 4.3. Approximately 36% of preoperative potassium samples exceeded 5.3 mEq/L (51of 140). Of the hyperkalemic patients, the mean potassium was 5.7 ± 0.5 mEq/L. There were 63 patients who had succinylcholine administered, 46 patients who had a nondepolarizing muscle relaxant administered, and 31 patients who underwent awake intubation. The mean potassium value in the patients who received succinylcholine was 5.0 ± 1.0 mEq/L, the mean value in the nondepolarizing group was 5.0 ± 0.7 mEq/L, and the mean value in the awake intubation group was 4.8 ± 0.8 mEq/L. The incidence of awake intubations decreased on a yearly basis (approximately 41% in the first 2 yr compared with approximately 6% in the last 2 yr), whereas the incidence of rapid sequence inductions following NDMRs remained relatively constant (Table 1). There was no correlation between use of succinylcholine and potassium value. There were no electrocardiogram changes noted, and no episodes of dysrhythmia suggestive of acute hyperkalemia after succinylcholine use were reported.
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The percentages of patients with potassium levels exceeding various "upper normal limits" for potassium are as follows:
5.3 = 36%, >5.3 = 30%, >5.5 = 19%, >5.7 = 9%, >6.1 = 7%. Using our laboratory’s definition of hypokalemia (<3.6 mEq/L), there were 11 patients (8%) with hypokalemia. The potassium values, when categorized by CO2 level, are shown in Table 2.
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Discussion |
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Our clinical impression—that hyperkalemia was prevalent in our pyloric stenosis population—proved to be correct. Almost one-third of these infants had a preoperative serum potassium value exceeding the upper limit of normal. There is no reasonable physiologic explanation for hyperkalemia in this population. These infants are generally normokalemic or hypokalemic, as a result of the concomitant hypochloremic metabolic alkalosis, caused by the pyloric stenosis and accompanying vomiting, dehydration, and renal compensatory mechanisms (1). Our findings support this to the extent that patients with alkalosis (CO2 >30 mmol/L) tended to have a smaller potassium level. However, only 10% of our patients were hypokalemic.
Although acidosis can cause a shift of potassium extracellularly, pyloric stenosis patients are usually thought to be alkalotic (2). Consistent with a previous report finding approximately 12% of pyloric patients being acidotic (2), we found 18% of pyloric patients who were acidotic. However, most of the patients who were hyperkalemic were not acidotic. Although a small incidence of alkalemia can explain the small incidence of hypokalemia, and acidemia can explain a small number of the hyperkalemic patients, the relatively frequent incidence of hyperkalemia cannot solely be explained by acid-base changes.
Possible causes of pseudohyperkalemia include: excessive squeezing at the site of skin puncture (up to 0.44 mEq/L in infants) (2), fist clenching with or without tourniquet use (up to 1.4 mEq/L) (3,4), hemolysis from traumatic venipuncture using a small-gauge needle, or delayed transportation and processing in the laboratory (significant increases) (5,6), and the icing of samples during transport (increases up to 0.1 mEq/L) (7). Infants in our hospital and elsewhere typically have their blood drawn either by venipuncture or by the heel-stick method. This process can be difficult, but the laboratory routinely inspects samples and comments on cases of mild, moderate, or gross hemolysis. Our hospital further uses rapid pneumatic tube for transportation of hospitalized inpatient specimens; thus, delays in transportation and processing are rare. Electrolyte and chemistry specimens are also transported at room temperature. Thus, the common causes of pseudohyperkalemia do not occur at our hospital.
The value of serum potassium that actually constitutes the upper level of "normal" may be open to debate but is very relevant to this discussion. The 1987 Merck Manual states >5.0 mEq/L whereas the 1999 edition revises it to >5.5 mEq/L (8,9). Our hospital’s upper limit of "normal" potassium is >5.3 mEq/L. If we re-do our calculations using >5.5 mEq/L, then 19% of our patients were hyperkalemic; this would still constitute a significant unexpected incidence of hyperkalemia. The upper limit of "normal" potassium varies by the patient age (10–13). For the pyloric age group, this value has been reported as 5.3 (12), 5.6 (13), and 5.8 mEq/L (10). Even using the very conservative value of 5.8, >10% of the children with pyloric stenosis in our report would remain classified as "hyperkalemic." There is a lack of consensus as to what ranges are appropriate. Part of the variability arises because different instruments are used at different institutions, and collecting a sufficient number of "normal" infants to develop a statistically significant age-specific range is difficult.
Federal and state guidelines require laboratories to validate their own reference ranges before clinical use. Laboratories frequently use volunteers’ blood (e.g., blood bank) to verify the manufacturer’s recommended ranges. These samples do not usually include infants’ blood. Despite a laboratory wishing to establish an age-appropriate electrolyte range, most hospitals do not have enough samples on healthy children to adequately define the reference range.
Infants with pyloric stenosis have full stomachs, and standard anesthetic practice dictates rapid sequence induction if the children are to be intubated asleep (1); this is to prevent aspiration from occurring during a mask induction (1). Despite the frequent incidence of reported hyperkalemia in our pyloric stenosis infants, we were not able to discern that anesthesiologists avoided succinylcholine for induction of anesthesia. We found no correlation between potassium level and the use of succinylcholine. Of interest, the number of awake intubations has dramatically decreased at our institution. This reduction coincides with literature that supports rapid sequence inductions, as opposed to awake intubations, in children presenting for pylorotomy (14).
In conclusion, we have demonstrated that a significant number of children with pyloric stenosis can be classified as being hyperkalemic. These results raise the clinical question of what to do in a child with pyloric stenosis presenting to the operating room with an increased potassium level.
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Acknowledgments |
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We thank our pediatric surgical colleagues, Drs. Courtney, Konefal, Moriarty, and Sachs, for help in data acquisition, and Ms. Lynda Paglia for help in manuscript preparation.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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- Bissonnette B, Sullivan PJ. Pyloric stenosis. Can J Anaesth 1991; 38: 668–76.[Web of Science][Medline]
- Meites S, Lin SS, Thompson C. Studies on the quality of specimens obtained by skin puncture of children. 1. Tendency to hemolysis and hemoglobin and tissue fluids as contaminants. Clin Chem 1981; 27: 875–8.
[Abstract/Free Full Text] - Don BR, Sebastian A, Cheitlin M, et al. Pseudohyperkalemia caused by fist clenching during phlebotomy. N Engl J Med 1990; 322: 1290–2.[Web of Science][Medline]
- Henry RJ. Clinical chemistry: principles and technics. New York: Harper and Row Hoeber Division, 1964.
- Wilding P, Zilva JF, Wilde CE. Transport of specimens for clinical chemistry analysis. Ann Clin Biochem 1977; 14: 301–6.[Web of Science][Medline]
- Pearce CJ, Bosomworth MP. Storage of heparinized blood. Ann Clin Biochem 1991; 28: 112.
- Muller-Plathe O, Heyduck S. Stability of blood gases, electrolytes and haemoglobin in heparinized whole blood samples: influence of the type of syringe. Eur J Clin Chem Clin Biochem 1992; 30: 249–355.
- Berkow R, ed. The Merck manual. 15th ed. Rahway, NJ: Merck, Sharp, and Dohme Research Laboratories, 1987.
- Beers MH, Berkow R, eds. The Merck manual of diagnosis and therapy. 17th ed. Rahway, NJ: The Merck Publishing Group, 1999.
- Heil W, Koberstein R, Zawta B. Reference ranges for adults and children: pre-analytical considerations. 6th ed. Mannheim, Germany: Roche Diagnostics GmbH, 1999.
- Burritt MF, Slockbower JM, Forsman RW, et al. Pediatric reference intervals for 19 biologic variables in healthy children. Mayo Clin Proc 1990; 65: 329–36.[Web of Science][Medline]
- Burtis CA, Ashwood ER. Tietz textbook of clinical chemistry. 3rd ed. Philadelphia: WB Saunders, 1999.
- Soldin SJ, Brugnara C, Gunter KC, Hicks JM. Pediatric reference ranges. 2nd ed. Washington, DC: AACC Press, 1997.
- Cook-Sather SD, Tulloch HV, Cnaan A, et al. A comparison of awake versus paralyzed tracheal intubation for infants with pyloric stenosis. Anesth Analg 1998; 86: 945–51.[Abstract]
This article has been cited by other articles:
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  J. J. McCloskey, J. R. Tobin, D. Schwartz, and N. R. Connelly Pyloric Stenosis, Hyperkalemia, and Anesthesia Practice * Response Anesth. Analg., February 1, 2004; 98(2): 558 - 558. [Full Text] [PDF]
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