Applying an Equity Lens to Clinical Practice Guidelines: Getting Out of the Gate

Abstract

In theory, clinical practice guidelines (CPGs) are designed to reduce cognitive load, standardize care delivery, improve clinical outcomes, and mitigate disparities through equitable practice.1However, pediatric CPGs have recently come under scrutiny for being outdated and methodologically challenged in keeping up with emerging evidence.2 In addition, a systematic review found that, although there were some positive effects of the use of race or ethnicity in pediatric CPGs, there was a potential for negative effect almost half of the time.3In this issue of Pediatrics, Kemper et al offer a revision of the CPG on Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation.4 Initially published in 2004 and updated with clarifications and modifications in 2009,5,6 this CPG has been among the most frequently cited of the American Academy of Pediatrics’ practice guidelines, as well as, a highly referenced resource by practitioners commensurate with the almost universal incidence of jaundice in the newborn period. This CPG is the first published, following the American Academy of Pediatrics’ concerted commitment to applying an equity lens in developing its policy statements, practice guidelines, and clinical and technical reports as outlined in the Eliminating Race-Based Medicine policy statement.7 The policy statement defines race-based medicine as the inappropriate use of race or ethnicity as an independent or dichotomizing risk-adjusting variable in clinical algorithms, practice guidelines, or policy statements. This new policy is relevant to the revised Management of Hyperbilirubinemia CPG in that the 2004 version of the practice guideline identified race and ethnicity assignment of the newborn as a risk-adjusting variable in clinical decision-making. Specifically, an infant race-assigned as Black received a downgraded quantitative score for risk of severe hyperbilirubinemia, thus obviating the urgency for aggressive diagnostic work-up. However, a more recent and nuanced analysis of the incidence of hazardous hyperbilirubinemia, ie, the risk for encephalopathy and neurotoxicity, reveals that Black babies are disproportionately represented in kernicterus databases at 25% as compared with their 14% representation in the overall population of newborns.8 Missed or delayed recognition of the acute hemolysis associated with glucose- 6-phosphate dehydrogenase (G6PD) deficiency has been implicated among the root causes of this irreversible condition. Persistence of this dangerous disparity potentially related to algorithmic minimization of risk for Black infants warranted attention and reconciliation. The authors have addressed this in the revision by: (1) striking the race and ethnicity terms from among the independent variables included in assessing risk for severe hyperbilirubinemia, and (2) emphasizing the critical importance of probing ancestry as a critical component of the decision-making process in the assessment of jaundice. As an x-linked recessive enzymopathy that renders children with G6PD deficiency highly susceptible to rapid onset hemolysis in the setting of oxidative stress, pediatricians need to understand the underlying biology of G6PD deficiency and its relevance to geographic distribution around the world.The linkage of race, ancestry, and genetics is inextricable, particularly in the face of conditions that result from a defined polymorphism.9 However, race assignment is a social construct and should not necessarily be conflated with genetic ancestry. For instance, in the case of the 2004 Management of Hyperbilirubinemia CPG, the decision-making risk assessment was predicated on the mother’s assignment of the newborn’s race. This approach is problematic, particularly with increasing genetic admixture worldwide and families who may identify themselves as mixed-race or defer racial definitions altogether. Determination of care delivery based on capricious, subjective stratification as judged by the phenotypic physical characteristic of skin color is fraught with uncertainty. Whereas we must surely be cognizant of the significance of assigned race along the causal pathway of disease or condition manifestation, we cannot independently substitute race alone as a proxy for underlying biologic mechanisms. Therefore, we must be conscious of the role that race plays as a driver of systemic inequities and disparate outcomes, especially as relates to the influences of the social determinants of health.10 However, we cannot be dependent on race as a substitute for contributory factors either known and not measured, or unknown and in need of discovery. An excellent example of progress in this area is the Urinary Tract Infection (UTI) Risk Calculator,11 which was recently revised by incorporating 2 new clinical factors and dropping race as a risk-adjusting variable. The UTI Calc version 3.0 with race now removed and the clinical variables, history of prior UTI, and fever for ≥48 hours, added performs comparably to prior versions.12 The observed epidemiologic difference initially identified by the investigators that prompted the inclusion of race as a dichotomizing variable remains unexplained. Still, the decision-making pathway is clinically efficient and no longer race-based.13From an epidemiologic perspective, we cannot completely ignore race, especially in the context of biomedical research given the sustained impacts of bias and discrimination in healthcare and society over time.14 However, we must responsibly incorporate it into the complex milieu of interdisciplinary factors that constitute adversity, define differential lived experiences, and ultimately confer resilience to our patients and their families, especially those from historically vulnerable and minoritized communities.

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