Bio

Clinical Focus


  • Sports Medicine

Academic Appointments


Administrative Appointments


  • Team Physician, Golden State Warriors (2016 - Present)
  • Team Physician, Stanford Athletics (2016 - Present)
  • Assistant Fellowship Director, Primary Care Sports Medicine Fellowship (2016 - Present)

Boards, Advisory Committees, Professional Organizations


  • Member, American Medical Society for Sports Medicine (2016 - Present)
  • Fellow, American Academy of Emergency Medicine (2014 - Present)
  • Member, American Academy of Emergency Medicine (2011 - Present)
  • Member, American College of Emergency Physicians (2011 - Present)

Professional Education


  • Board Certification: Sports Medicine, American Board of Emergency Medicine (2015)
  • Board Certification: Emergency Medicine, American Board of Emergency Medicine (2015)
  • Fellowship:Stanford Hospital and Clinics - Dept of Orthopaedics (2015) CA
  • Residency:Stanford University - Emergency Medicine (2014) CA
  • MD, Case Western Reserve University School of Medicine (2011)
  • BS, Stanford University, Biological Sciences with Honors (2007)

Teaching

2018-19 Courses


Graduate and Fellowship Programs


  • Sports Medicine (Fellowship Program)

Publications

All Publications


  • Calculated Decisions: Ottawa Knee Rule Pediatric emergency medicine practice Hwang, C. 2018; 14 (Suppl 9): 3–5

    Abstract

    The Ottawa Knee Rule describes criteria for knee trauma patients who are at low risk for clinically significant fracture and do not warrant knee imaging.

    View details for PubMedID 30183241

  • Calculated Decisions: Ottawa Ankle Rule Pediatric emergency medicine practice Hwang, C. 2018; 14 (Suppl 9): 1–3

    Abstract

    The Ottawa Ankle Rule shows the areas of tenderness to be evaluated in ankle trauma patients to determine the need for imaging.

    View details for PubMedID 30183240

  • Calculated decisions: LRINEC Score for necrotizing soft-tissue infection Emergency medicine practice Hwang, C. 2017: 5–6

    View details for PubMedID 29068632

  • Current Concepts in Concussion: A Review. Journal of the California Dental Association Ray, J. W., Hwang, C., Baine, J., Fredericson, M., Keane, G. P. 2017; 45 (6): 285–89

    View details for PubMedID 29016093

  • Improved insulin sensitivity after exercise training is linked to reduced plasma C14:0 ceramide in obesity and type 2 diabetes OBESITY Kasumov, T., Solomon, T. P., Hwang, C., Huang, H., Haus, J. M., Zhang, R., Kirwan, J. P. 2015; 23 (7): 1414-1421

    Abstract

    To assess the effect of exercise training on insulin sensitivity and plasma ceramides in obesity and type 2 diabetes (T2D).Twenty-four adults with obesity and normal glucose tolerance (NGT, n = 14) or diabetes (n = 10) were studied before and after a 12-week supervised exercise-training program (5 days/week, 1 h/day, 80-85% of maximum heart rate). Changes in body composition were assessed using hydrostatic weighing and computed tomography. Peripheral tissue insulin sensitivity was assessed by a 40 mU/m(2) /min hyperinsulinemic euglycemic clamp. Plasma ceramides (C14:0, C16:0, C18:0, C18:1, C20:0, C24:0, and C24:1) were quantified using electrospray ionization tandem mass spectrometry after separation with HPLC.Plasma ceramides were similar for the subjects with obesity and NGT and the subjects with diabetes, despite differences in glucose tolerance. Exercise significantly reduced body weight and adiposity and increased peripheral insulin sensitivity in both groups (P < 0.05). In addition, plasma C14:0, C16:0, C18:1, and C24:0 ceramide levels were reduced in all subjects following the intervention (P < 0.05). Decreases in total (r = -0.51, P = 0.02) and C14:0 (r = -0.56, P = 0.009) ceramide were negatively correlated with the increase in insulin sensitivity.Ceramides are linked to exercise training-induced improvements in insulin sensitivity, and plasma C14:0 ceramide may provide a specific target for investigating lipid-related insulin resistance in obesity and T2D.

    View details for DOI 10.1002/oby.21117

    View details for Web of Science ID 000356893400014

    View details for PubMedID 25966363

    View details for PubMedCentralID PMC4482773

  • Effect of an emergency department fast track on press-ganey patient satisfaction scores. The western journal of emergency medicine Hwang, C. E., Lipman, G. S., Kane, M. 2015; 16 (1): 34-38

    Abstract

    Mandated patient surveys have become an integral part of Medicare remuneration, putting hundreds of millions of dollars in funding at risk. The Centers for Medicare & Medicaid Services (CMS) recently announced a patient experience survey for the emergency department (ED). Development of an ED Fast Track, where lower acuity patients are rapidly seen, has been shown to improve many of the metrics that CMS examines. This is the first study examining if ED Fast Track implementation affects Press-Ganey scores of patient satisfaction.We analyzed returned Press-Ganey questionnaires from all ESI 4 and 5 patients seen 11AM - 1PM, August-December 2011 (pre-fast track), and during the identical hours of fast track, August-December 2012. Raw ordinal scores were converted to continuous scores for paired student t-test analysis. We calculated an odds ratio with 100% satisfaction considered a positive response.An academic ED with 52,000 annual visits had 140 pre-fast track and 85 fast track respondents. Implementation of a fast track significantly increased patient satisfaction with the following: wait times (68% satisfaction to 88%, OR 4.13, 95% CI [2.32-7.33]), doctor courtesy (90% to 95%, OR 1.97, 95% CI [1.04-3.73]), nurse courtesy (87% to 95%, OR 2.75, 95% CI [1.46-5.15]), pain control (79% to 87%, OR 2.13, 95% CI [1.16-3.92]), likelihood to recommend (81% to 90%, OR 2.62, 95% CI [1.42-4.83]), staff caring (82% to 91%, OR 2.82, 95% CI [1.54-5.19]), and staying informed about delays (66% to 83%, OR 3.00, 95% CI [1.65-5.44]).Implementation of an ED Fast Track more than doubled the odds of significant improvements in Press-Ganey patient satisfaction metrics and may play an important role in improving ED performance on CMS benchmarks.

    View details for DOI 10.5811/westjem.2014.11.21768

    View details for PubMedID 25671005

  • ECG diagnosis: ST-elevation myocardial infarction. The Permanente journal Hwang, C., Levis, J. T. 2014; 18 (2)

    View details for DOI 10.7812/TPP/13-127

    View details for PubMedID 24867559

  • Hippocampal-dependent learning requires a functional circadian system PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Ruby, N. F., Hwang, C. E., Wessells, C., Fernandez, F., Zhang, P., Sapolsky, R., Heller, H. C. 2008; 105 (40): 15593-15598

    Abstract

    Decades of studies have shown that eliminating circadian rhythms of mammals does not compromise their health or longevity in the laboratory in any obvious way. These observations have raised questions about the functional significance of the mammalian circadian system, but have been difficult to address for lack of an appropriate animal model. Surgical ablation of the suprachiasmatic nucleus (SCN) and clock gene knockouts eliminate rhythms, but also damage adjacent brain regions or cause developmental effects that may impair cognitive or other physiological functions. We developed a method that avoids these problems and eliminates rhythms by noninvasive means in Siberian hamsters (Phodopus sungorus). The present study evaluated cognitive function in arrhythmic animals by using a hippocampal-dependent learning task. Control hamsters exhibited normal circadian modulation of performance in a delayed novel-object recognition task. By contrast, arrhythmic animals could not discriminate a novel object from a familiar one only 20 or 60 min after training. Memory performance was not related to prior sleep history as sleep manipulations had no effect on performance. The GABA antagonist pentylenetetrazol restored learning without restoring circadian rhythms. We conclude that the circadian system is involved in memory function in a manner that is independent of sleep. Circadian influence on learning may be exerted via cyclic GABA output from the SCN to target sites involved in learning. Arrhythmic hamsters may have failed to perform this task because of chronic inhibitory signaling from the SCN that interfered with the plastic mechanisms that encode learning in the hippocampus.

    View details for DOI 10.1073/pnas.0808259105

    View details for Web of Science ID 000260360500068

    View details for PubMedID 18832172

    View details for PubMedCentralID PMC2563080

  • blue cheese mutations define a novel, conserved gene involved in progressive neural degeneration JOURNAL OF NEUROSCIENCE Finley, K. D., Edeen, P. T., Cumming, R. C., Mardahl-Dumesnil, M. D., Taylor, B. J., RODRIGUEZ, M. H., Hwang, C. E., Benedetti, M., McKeown, M. 2003; 23 (4): 1254-1264

    Abstract

    A common feature of many human neurodegenerative diseases is the accumulation of insoluble ubiquitin-containing protein aggregates in the CNS. Although Drosophila has been helpful in understanding several human neurodegenerative disorders, a loss-of-function mutation has not been identified that leads to insoluble CNS protein aggregates. The study of Drosophila mutations may identify unique components that are associated with human degenerative diseases. The Drosophila blue cheese (bchs) gene defines such a novel degenerative pathway. bchs mutants have a reduced adult life span with the age-dependent formation of protein aggregates throughout the neuropil of the CNS. These inclusions contain insoluble ubiquitinated proteins and amyloid precursor-like protein. Progressive loss of CNS size and morphology along with extensive neuronal apoptosis occurs in aged bchs mutants. BCHS protein is widely expressed in the cytoplasm of CNS neurons and is present over the entire length of axonal projections. BCHS is nearly 3500 amino acids in size, with the last 1000 amino acids consisting of three functional protein motifs implicated in vesicle transport and protein processing. This region along with previously unidentified proteins encoded in the human, mouse, and nematode genomes shows striking homology along the full length of the BCHS protein. The high degree of conservation between Drosophila and human bchs suggests that study of the functional pathway of BCHS and associated mutant phenotype may provide useful insights into human neurodegenerative disorders.

    View details for Web of Science ID 000181094300020

    View details for PubMedID 12598614

    View details for PubMedCentralID PMC1975817