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Polycythemia, Prognostication, and Plausibility After the Norwood Operation.

Intensivists caring for newborns undergoing stage 1 palliative surgery (S1P) for hypoplastic left heart syndrome (HLHS) and its anatomic variants continue to search for markers of illness severity that could serve to guide treatment early in a patient’s course (1). Systemic inflammation after pediatric cardiac surgery contributes to cardiovascular instability, oxygen debt, organ injury, and fluid retention (2–5). All of these pathophysiologic processes place patients at risk of mortality and both shortand long-term morbidity (6, 7). Unfortunately, few reliable biomarkers of clinically important systemic inflammation exist, and none are regularly used in standard care of these patients. Is it possible that a routine laboratory test collected multiple times in every ICU that treats infants after S1P provides insight into the degree of systemic inflammation and predicts clinical outcome? In this issue of Pediatric Critical Care Medicine, Siehr et al (8) present an analysis suggesting that relative polycythemia early after S1P associates with prolonged ICU and hospital length of stay. The investigators defined polycythemia as a mean hematocrit of 49% in the first 72 postoperative hours after analyzing more than 6,700 hematocrit values in a 32-patient cohort of neonates with HLHS undergoing S1P from their institution. Patients at or above this level had greater median total ICU (30 vs 14 d) and hospital (45 vs 30 d) lengths of stay (p < 0.05 for both). The investigators accounted for measurable patient risk factors and markers of illness severity in their analysis and appropriately controlled for total RBC transfusion volumes. Polycythemic patients had less urine output and greater net fluid retention over 72 hours than those without polycythemia. Based on the sum of their findings, the authors inferred that higher hematocrit values reflect hemoconcentration resulting from underlying systemic inflammation and that this pathophysiology explains the differences in clinical outcomes. The difference in the lengths of stay between the two groups is striking. A closer look at the Kaplan-Meier curve for hospital discharge presented in the article reveals that the two exposure groups separate early on, further suggesting that the observed difference is not simply driven by a few outliers at the extreme high end of length of stay; small study cohorts are particularly susceptible to this phenomenon. The authors’ findings and hypotheses match those from studies of other patient populations with critical illness (9, 10). However, other aspects of the analysis—both the methods and the results—give a reader reasons to pause before accepting the conclusions. First, although there are no statistically significant differences in patients or disease-severity factors, patients in the polycythemia group had higher point estimates for average vasoactive-inotropic score and lower estimates for Pao 2 / Fio 2 ratio. The p values were greater than 0.05, but in this small cohort, very large differences would be necessary to conclude a difference based on significance testing. Thus, the groups may have been inherently different in the immediate postoperative period, or these could be further surrogates for systemic inflammation. Second, there was no difference in mortality between groups; it is reasonable to believe that greater systemic inflammation would also confer greater risk of death. Exclusion of two patients who died in the first 72 hours complicates this assessment slightly but was appropriate for the planned analysis using a primary exposure variable collected over that time period. The authors report that their institution does not routinely use ultrafiltration, but other intraoperative fluid management practices are not described, raising the question of generalizability of the hematocrit cutoff across centers; indeed, many would consider a mean population hematocrit of 49% to be in excess of commonly observed values in this patient population. Finally, and perhaps most importantly, there are many potential confounding clinical factors present in the first 72 hours and beyond that could profoundly impact ICU and hospital lengths of stay, completely unrelated to systemic inflammation, that were not either measured or analyzed. These include reinterventions, residual cardiac lesions, and respiratory complications (e.g., diaphragm paralysis), among others. Perhaps the greatest limitation of this study remains the plausibility of the authors’ conclusion that polycythemia represents hemoconcentration resulting from systemic inflammation and that this exposure results in such a large difference in length of stay between the two groups. It is certainly possible to envision a pathway by which inflammation begets fluid retention that impairs weaning from cardiopulmonary support and leads to *See also p. 216.