Dr. Saunders (he/him) is a Clinical Associate Professor of Pediatrics, and the medical director of the Pediatric Hospitalist Program at SHC Tri-Valley. His academic interests include diversity, equity, and inclusion in medicine; LGBTQIA+ health; ethics in technology; global health; medical education; public health; and physician wellness.

Clinical Focus

  • Pediatric Hospital Medicine
  • Medical Director, Pediatric Hospitalist Program at Stanford Health Care ValleyCare

Academic Appointments

Boards, Advisory Committees, Professional Organizations

  • Member, American Medical Association (2008 - Present)
  • Fellow, American Academy of Pediatrics (2008 - Present)

Professional Education

  • Fellowship: UCSF Benioff Children's Hospital Pediatric Hospital Medicine Fellowship (2014) CA
  • Residency: UCSF Pediatric Residency (2012) CA
  • Board Certification: American Board of Pediatrics, Pediatrics (2011)
  • Medical Education: Dartmouth Medical School (2008)

All Publications

  • Incidence of Pediatric Urinary Tract Infections Before and During the COVID-19 Pandemic. JAMA network open Liang, D., Wang, M. E., Dahlen, A., Liao, Y., Saunders, A. C., Coon, E. R., Schroeder, A. R. 2024; 7 (1): e2350061


    Urinary tract infection (UTI) is common in children, but the population incidence is largely unknown. Controversy surrounds the optimal diagnostic criteria and how to balance the risks of undertreatment and overtreatment. Changes in health care use during the COVID-19 pandemic created a natural experiment to examine health care use and UTI diagnosis and outcomes.To examine the population incidence of UTI in children and assess the changes of the COVID-19 pandemic regarding UTI diagnoses and measures of UTI severity.This retrospective observational cohort study used US commercial claims data from privately insured patients aged 0 to 17 years from January 1, 2016, to December 31, 2021.Time periods included prepandemic (January 1, 2016, to February 29, 2020), early pandemic (April 1 to June 30, 2020), and midpandemic (July 1, 2020, to December 31, 2021).The primary outcome was the incidence of UTI, defined as having a UTI diagnosis code with an accompanying antibiotic prescription. Balancing measures included measures of UTI severity, including hospitalizations and intensive care unit admissions. Trends were evaluated using an interrupted time-series analysis.The cohort included 13 221 117 enrollees aged 0 to 17 years, with males representing 6 744 250 (51.0%) of the population. The mean incidence of UTI diagnoses was 1.300 (95% CI, 1.296-1.304) UTIs per 100 patient-years. The UTI incidence was 0.86 per 100 patient-years at age 0 to 1 year, 1.58 per 100 patient-years at 2 to 5 years, 1.24 per 100 patient-years at 6 to 11 years, and 1.37 per 100 patient-years at 12 to 17 years, and was higher in females vs males (2.48 [95% CI, 2.46-2.50] vs 0.180 [95% CI, 0.178-0.182] per 100 patient-years). Compared with prepandemic trends, UTIs decreased in the early pandemic: -33.1% (95% CI, -39.4% to -26.1%) for all children and -52.1% (95% CI, -62.1% to -39.5%) in a subgroup of infants aged 60 days or younger. However, all measures of UTI severity decreased or were not significantly different. The UTI incidence returned to near prepandemic rates (-4.3%; 95% CI, -32.0% to 34.6% for all children) after the first 3 months of the pandemic.In this cohort study, UTI diagnosis decreased during the early pandemic period without an increase in measures of disease severity, suggesting that reduced overdiagnosis and/or reduced misdiagnosis may be an explanatory factor.

    View details for DOI 10.1001/jamanetworkopen.2023.50061

    View details for PubMedID 38170521

    View details for PubMedCentralID PMC10765266

  • Diagnosis and Treatment of Tuberculosis Among Children at an HIV Care Program in Dar es Salaam, Tanzania PEDIATRIC INFECTIOUS DISEASE JOURNAL Adams, L. V., McQuillan, T., Naburi, H. E., Lyatuu, G., Ippolito, M. M., Saunders, A., Kiravu, A., Palumbo, P., von Reyn, C. F. 2014; 33 (12): 1234-1236


    Diagnosis and treatment of tuberculosis is challenging in children with human immunodeficiency virus (HIV) infection. We describe the clinical features, diagnostic testing results, tuberculosis and HIV treatment and clinical outcomes of 57 HIV-infected children diagnosed with tuberculosis at the DarDar Pediatric Program in Dar es Salaam, Tanzania. In this cohort, tuberculosis was common, microbiologic studies were frequently negative and mortality was high.

    View details for DOI 10.1097/INF.0000000000000452

    View details for Web of Science ID 000345454300009

    View details for PubMedID 24945878

    View details for PubMedCentralID PMC4229430

  • Impaired intestinal iron absorption in Crohn's disease correlates with disease activity and markers of inflammation. Inflammatory bowel diseases Semrin, G., Fishman, D. S., Bousvaros, A., Zholudev, A., Saunders, A. C., Correia, C. E., Nemeth, E., Grand, R. J., Weinstein, D. A. 2006; 12 (12): 1101-6


    Anemia in patients with Crohn's disease (CD) is a common problem of multifactorial origin, including blood loss, malabsorption of iron, and anemia of inflammation. Anemia of inflammation is caused by the effects of inflammatory cytokines [predominantly interleukin-6 (IL-6)] on iron transport in enterocytes and macrophages. We sought to elucidate alterations in iron absorption in pediatric patients with active and inactive CD.Nineteen subjects with CD (8 female, 11 male patients) were recruited between April 2003 and June 2004. After an overnight fast, serum iron and hemoglobin levels, serum markers of inflammation [IL-6, C-reactive protein (CRP), and erythrocyte sedimentation rate], and a urine sample for hepcidin assay were obtained at 8 am. Ferrous sulfate (1 mg/kg) was administered orally, followed by determination of serum iron concentrations hourly for 4 hours after the ingestion of iron. An area under the curve for iron absorption was calculated for each patient data set.There was a strong inverse correlation between the area under the curve and IL-6 (P = 0.002) and area under the curve and CRP levels (P = 0.04). Similarly, the difference between baseline and 2-hour serum iron level (Delta[Fe]2hr) correlated with IL-6 (P = 0.008) and CRP (P = 0.045). When cutoff values for IL-6 (>5 pg/mL) and CRP (>1.0 mg/dL) were used, urine hepcidin levels also positively correlated with IL-6 and CRP levels (P = 0.003 and 0.007, respectively).Subjects with active CD have impaired oral iron absorption and elevated IL-6 levels compared with subjects with inactive disease. These findings suggest that oral iron may be of limited benefit to these patients. Future study is needed to define the molecular basis for impaired iron absorption.

    View details for DOI 10.1097/01.mib.0000235097.86360.04

    View details for PubMedID 17119383

    View details for PubMedCentralID PMC2788427

  • Hepatic glycogen synthase deficiency: an infrequently recognized cause of ketotic hypoglycemia. Molecular genetics and metabolism Weinstein, D. A., Correia, C. E., Saunders, A. C., Wolfsdorf, J. I. 2006; 87 (4): 284-8


    The glycogen storage diseases comprise several inherited diseases caused by abnormalities of enzymes that regulate the synthesis or degradation of glycogen. In contrast to the classic hepatic glycogen storage diseases that are characterized by fasting hypoglycemia and hepatomegaly, the liver is not enlarged in GSD0. Patients with GSD0 typically have fasting ketotic hypoglycemia without prominent muscle symptoms. Most children are cognitively and developmentally normal. Short stature and osteopenia are common features, but other long-term complications, common in other types of GSD, have not been reported in GSD0. Until recently, the definitive diagnosis of GSD0 depended on the demonstration of decreased hepatic glycogen on a liver biopsy. The need for an invasive procedure may be one reason that this condition has been infrequently diagnosed. Mutation analysis of the GYS2 gene (12p12.2) is a non-invasive method for making this diagnosis in patients suspected to have this disorder. This mini-review discusses the pathophysiology of this disorder, use of mutation analysis to diagnose GSD0, and the clinical characteristics of all reported cases of GSD0.

    View details for DOI 10.1016/j.ymgme.2005.10.006

    View details for PubMedID 16337419

    View details for PubMedCentralID PMC1474809

  • Clinical evaluation of a portable lactate meter in type I glycogen storage disease JOURNAL OF INHERITED METABOLIC DISEASE Saunders, A. C., Feldman, H. A., Correia, C. E., Weinstein, D. A. 2005; 28 (5): 695-701


    High lactate concentrations occur in type I glycogen storage disease (GSD) whenever glycogenolysis occurs. Not only does hyperlactataemia cause acute clinical deterioration, but chronic lactate elevations have also been associated with many of the long-term complications in GSD. A portable finger-stick blood lactate meter has recently been marketed as a training tool for high-performance athletes, but it has not been tested as a clinical diagnostic tool. This study was performed to assess the accuracy of the portable lactate meter in subjects with GSD I who are predisposed to high lactate concentrations. A total of 166 intravenous and 39 capillary samples from 13 subjects were tested concomitantly on three different lactate meters. The meter readings were compared with the lactate concentration determined by the laboratory gold-standard enzymatic colorimetric assay. Almost no inter-meter variability was found. The lactate meter values had outstanding correlation with the laboratory lactate determination, although the meters were found to run 0.5 mmol/L higher than the laboratory assay. The meter deviation was independent of lactate concentration. More variability was noted with finger-stick capillary lactate determinations, but monitoring of trends with capillary samples should prove valuable as a method for determining long-term control or acute deterioration. The portable lactate meter is a highly accurate tool for monitoring lactate concentrations, and should prove valuable for monitoring metabolic control in patients with GSD type I and other disorders associated with hyperlactataemia.

    View details for DOI 10.1007/s10545-005-0090-1

    View details for Web of Science ID 000231759900009

    View details for PubMedID 16151900