Bio

Bio


Dr. Lindsay Sceats is a general surgery resident at Stanford Hospital. Research interests include colorectal surgery, inflammatory bowel disease, and health care cost containment. She is supported by a Stanford Spectrum KL2 Training Grant.

Clinical Focus


  • Residency
  • General Surgery Resident

Honors & Awards


  • Arnold P Gold Award for Humanism and Excellence in Teaching, Stanford School of Medicine (May 2017)

Professional Education


  • Bachelor of Arts, Mount Holyoke College, Biochemistry (2011)
  • Doctor of Medicine, Stanford University, MED-MD (2015)
  • MS, Stanford University, Health Services Research Masters Student
  • Internship, Stanford Hospital and Clinics, General Surgery (2016)
  • MD, Stanford School of Medicine, Doctor of Medicine (2015)
  • BA, Mount Holyoke College, Biochemistry, English (2011)

Research & Scholarship

Current Clinical Interests


  • General Surgery
  • Colorectal Surgery
  • Inflammatory Bowel Disease
  • Immunology

Lab Affiliations


Teaching

Graduate and Fellowship Programs


Publications

All Publications


  • Lost in translation: Informed consent in the medical mission setting. Surgery Sceats, L. A., Morris, A. M., Narayan, R. R., Mezynski, A., Woo, R. K., Yang, G. P. 2018

    Abstract

    BACKGROUND: Informed consent is a fundamental tenet of ethical care, but even under favorable conditions, patient comprehension of consent conversations may be limited. Little is known about providing informed consent in more uncertain situations such as medical missions. We sought to examine the informed consent process in the medical mission setting.METHODS: We studied informed consent for adult patients undergoing inguinal herniorrhaphy during a medical mission to Guatemala using a convergent mixed-methods design. We audiotaped informed consents during preoperative visits and immediately conducted separate surveys to elicit comprehension of risks. Informed consent conversations and survey responses were translated and transcribed. We used descriptive statistics to examine informed consent content, including information provided by surgeon, the translation of information, and patient comprehension, and used thematic analysis to examine the consent process.RESULTS: Thirteen adult patients (median age 53 years, 69% male) participated. Surgeons conveyed 4 standard risks in 10 out of 13 encounters (77%); all 4 risks were translated to patients in 10 out of 13 encounters (77%). No patient could recall all 4 risks. Qualitative themes regarding the informed consent process included limited physician language skills, verbal domination by physicians and interpreters, and mistranslation of risks. Patients relied on faith and prior or vicarious experiences to qualify surgical risks instead of consent conversations. Many patients restated surgical instructions when asked about risks.CONCLUSION: Despite physicians' attempts to provide informed consent, medical mission patients did not comprehend surgical risks. Our data reveal a critical need to develop more effective methods for communicating surgical risks during medical missions.

    View details for DOI 10.1016/j.surg.2018.06.010

    View details for PubMedID 30061041

  • Association of Opioid Abuse and Peripheral Arterial Disease Itoga, N. K., Sceats, L. A., Stern, J. R., Mell, M. W. MOSBY-ELSEVIER. 2018: E87
  • Risk of post-operative surgical site infections after vedolizumab vs anti-tumour necrosis factor therapy: a propensity score matching analysis in inflammatory bowel disease. Alimentary pharmacology & therapeutics Park, K. T., Sceats, L., Dehghan, M., Trickey, A. W., Wren, A., Wong, J. J., Bensen, R., Limketkai, B. N., Keyashian, K., Kin, C. 2018

    Abstract

    Perioperative vedolizumab (VDZ) and anti-tumour necrosis factor (TNFi) therapies are implicated in causing post-operative complications in inflammatory bowel disease (IBD).To compare the risk of surgical site infections (SSIs) between VDZ- and TNFi-treated IBD patients in propensity-matched cohorts.The Optum Research Database was used to identify IBD patients who received VDZ or TNFi within 30 days prior to abdominal surgery between January 2015 and December 2016. The date of IBD-related abdominal surgery was defined as the index date. SSIs were determined by ICD-9/10 and CPT codes related to superficial wound infections or deep organ space infections after surgery. Propensity score 1:1 matching established comparable cohorts based on VDZ or TNFi exposure before surgery based on evidence-based risk modifiers.The propensity-matched sample included 186 patients who received pre-operative biologic therapy (VDZ, n = 94; TNFi, n = 92). VDZ and TNFi cohorts were similar based on age, gender, IBD type, concomitant immunomodulator exposure, chronic opioid or corticosteroid therapy, Charlson Comorbidity Index and malnutrition. VDZ patients were more likely to undergo an open bowel resection with ostomy. After propensity score matching, there was no significant difference in post-operative SSIs (TNFi 12.0% vs VDZ 14.9%, P = 0.56). Multivariable analysis indicated that malnutrition was the sole risk factor for developing SSI (OR 3.1, 95% CI 1.11-8.71) regardless of the type of biologic exposure.In the largest, risk-adjusted cohort analysis to date, perioperative exposure to VDZ therapy was not associated with a significantly higher risk of developing an SSI compared to TNFi therapy.

    View details for DOI 10.1111/apt.14842

    View details for PubMedID 29876995

  • Frequency and Timing of Short-Term Complications Following Abdominoperineal Resection Journal of Surgical Research Tooley, J. E., Sceats, L. A., Bohl, D. D., Read, B., Kin, C. 2018; 231: 69-76
  • Starting Young: Trends in Opioid Therapy Among US Adolescents and Young Adults With Inflammatory Bowel Disease in the Truven MarketScan Database Between 2007 and 2015. Inflammatory bowel diseases Wren, A. A., Bensen, R., Sceats, L., Dehghan, M., Yu, H., Wong, J. J., MacIsaac, D., Sellers, Z. M., Kin, C., Park, K. T. 2018

    Abstract

    Opioids are commonly prescribed for relief in inflammatory bowel disease (IBD). Emerging evidence suggests that adolescents and young adults are a vulnerable population at particular risk of becoming chronic opioid users and experiencing adverse effects.This study evaluates trends in the prevalence and persistence of chronic opioid therapy in adolescents and young adults with IBD in the United States.A longitudinal retrospective cohort analysis was conducted with the Truven MarketScan Database from 2007 to 2015. Study subjects were 15-29 years old with ≥2 IBD diagnoses (Crohn's: 555/K50; ulcerative colitis: 556/K51). Opioid therapy was identified with prescription claims within the Truven therapeutic class 60: opioid agonists. Persistence of opioid use was evaluated by survival analysis for patients who remained in the database for at least 3 years following index chronic opioid therapy use.In a cohort containing 93,668 patients, 18.2% received chronic opioid therapy. The annual prevalence of chronic opioid therapy increased from 9.3% in 2007 to 10.8% in 2015 (P < 0.01), peaking at 12.2% in 2011. Opioid prescriptions per patient per year were stable (approximately 5). Post hoc Poisson regression analyses demonstrated that the number of opioid pills dispensed per year increased with age and was higher among males. Among the 2503 patients receiving chronic opioid therapy and followed longitudinally, 30.5% were maintained on chronic opioid therapy for 2 years, and 5.3% for all 4 years.Sustained chronic opioid use in adolescents and young adults with IBD is increasingly common, underscoring the need for screening and intervention for this vulnerable population.

    View details for DOI 10.1093/ibd/izy222

    View details for PubMedID 29986015

  • Association between Latent Proviral Characteristics and Immune Activation in Antiretrovirus-Treated Human Immunodeficiency Virus Type 1-Infected Adults. Journal of virology Liang, E. C., Sceats, L., Bayless, N. L., Strauss-Albee, D. M., Kubo, J., Grant, P. M., Furman, D., Desai, M., Katzenstein, D. A., Davis, M. M., Zolopa, A. R., Blish, C. A. 2014; 88 (15): 8629-8639

    Abstract

    Generalized immune activation during HIV infection is associated with an increased risk of cardiovascular disease, neurocognitive disease, osteoporosis, metabolic disorders, and physical frailty. The mechanisms driving this immune activation are poorly understood, particularly for individuals effectively treated with antiretroviral medications. We hypothesized that viral characteristics such as sequence diversity may play a role in driving HIV-associated immune activation. We therefore sequenced proviral DNA isolated from peripheral blood mononuclear cells from HIV-infected individuals on fully suppressive antiretroviral therapy. We performed phylogenetic analyses, calculated viral diversity and divergence in the env and pol genes, and determined coreceptor tropism and the frequency of drug resistance mutations. Comprehensive immune profiling included quantification of immune cell subsets, plasma cytokine levels, and intracellular signaling responses in T cells, B cells, and monocytes. These antiretroviral therapy-treated HIV-infected individuals exhibited a wide range of diversity and divergence in both env and pol genes. However, proviral diversity and divergence in env and pol, coreceptor tropism, and the level of drug resistance did not significantly correlate with markers of immune activation. A clinical history of virologic failure was also not significantly associated with levels of immune activation, indicating that a history of virologic failure does not inexorably lead to increased immune activation as long as suppressive antiretroviral medications are provided. Overall, this study demonstrates that latent viral diversity is unlikely to be a major driver of persistent HIV-associated immune activation.Chronic immune activation, which is associated with cardiovascular disease, neurologic disease, and early aging, is likely to be a major driver of morbidity and mortality in HIV-infected individuals. Although treatment of HIV with antiretroviral medications decreases the level of immune activation, levels do not return to normal. The factors driving this persistent immune activation, particularly during effective treatment, are poorly understood. In this study, we investigated whether characteristics of the latent, integrated HIV provirus that persists during treatment are associated with immune activation. We found no relationship between latent viral characteristics and immune activation in treated individuals, indicating that qualities of the provirus are unlikely to be a major driver of persistent inflammation. We also found that individuals who had previously failed treatment but were currently effectively treated did not have significantly increased levels of immune activation, providing hope that past treatment failures do not have a lifelong "legacy" impact.

    View details for DOI 10.1128/JVI.01257-14

    View details for PubMedID 24850730

    View details for PubMedCentralID PMC4135944

  • Podoplanin-Rich Stromal Networks Induce Dendritic Cell Motility via Activation of the C-type Lectin Receptor CLEC-2 IMMUNITY Acton, S. E., Astarita, J. L., Malhotra, D., Lukacs-Kornek, V., Franz, B., Hess, P. R., Jakus, Z., Kuligowski, M., Fletcher, A. L., Elpek, K. G., Bellemare-Pelletier, A., Sceats, L., Reynoso, E. D., Gonzalez, S. F., Graham, D. B., Chang, J., Peters, A., Woodruff, M., Kim, Y., Swat, W., Morita, T., Kuchroo, V., Carroll, M. C., Kahn, M. L., Wucherpfennig, K. W., Turley, S. J. 2012; 37 (2): 276-289

    Abstract

    To initiate adaptive immunity, dendritic cells (DCs) move from parenchymal tissues to lymphoid organs by migrating along stromal scaffolds that display the glycoprotein podoplanin (PDPN). PDPN is expressed by lymphatic endothelial and fibroblastic reticular cells and promotes blood-lymph separation during development by activating the C-type lectin receptor, CLEC-2, on platelets. Here, we describe a role for CLEC-2 in the morphodynamic behavior and motility of DCs. CLEC-2 deficiency in DCs impaired their entry into lymphatics and trafficking to and within lymph nodes, thereby reducing T cell priming. CLEC-2 engagement of PDPN was necessary for DCs to spread and migrate along stromal surfaces and sufficient to induce membrane protrusions. CLEC-2 activation triggered cell spreading via downregulation of RhoA activity and myosin light-chain phosphorylation and triggered F-actin-rich protrusions via Vav signaling and Rac1 activation. Thus, activation of CLEC-2 by PDPN rearranges the actin cytoskeleton in DCs to promote efficient motility along stromal surfaces.

    View details for DOI 10.1016/j.immuni.2012.05.022

    View details for Web of Science ID 000308261800012

    View details for PubMedID 22884313

    View details for PubMedCentralID PMC3556784