Dr. Cooke is a clinical assistant professor in the Department of Orthopaedic Surgery at Stanford University School of Medicine. She has a strong clinical interest in hand, wrist, and elbow surgery for adult and pediatric patients. She is dual fellowship trained in Hand & Upper Extremity Surgery and Pediatric & Congenital Hand Surgery.
As an orthopaedic surgeon, Dr. Cooke’s goal is to alleviate pain and improve hand, wrist, and elbow function so that her patients can return to the activities they enjoy. Her primary clinical interests are nerve compression (carpal tunnel), nerve injuries (traumatic/lacerations), joint instability/arthritis (degenerative conditions of the hand wrist and elbow), sports/athletic injuries, fracture care, and pediatric & congenital conditions of the hand and upper extremity.
Dr. Cooke utilizes a multi-disciplinary approach in order to provide comprehensive care for each patient. She works closely with colleagues from oncology, radiology, physical therapy, and other specialties. Her team includes certified hand therapists, cast technicians, medical assistants, and patient care coordinators. Together, Dr. Cooke and her team are committed to providing the best possible care for patients.
She invites patient referrals as early as possible when an upper extremity problem is suspected. She ensures a trusting relationship with referring physicians (whether primary care providers or specialists) by staying in communication so they understand and are comfortable with her recommendations.
In addition to patient care, Dr. Cooke has enjoyed contributing to her field through research. Among Dr. Cooke’s clinical research interests is fracture healing, including gene expression following administration of medication to stimulate bone repair. She has authored articles on topics like infection prediction and pain management after surgical repair of fractures. Her work has appeared in the Journal of Orthopaedic Trauma, Journal of Orthopaedic Research, Osteoarthritis & Cartilage, Spine, and Transplantation. She also co-wrote the chapter “The History of Carpal Tunnel” for the textbook Carpal Tunnel Syndrome and Related Median Neuropathies.
Dr. Cooke’s honors include a Howard Hughes Research Fellowship, an Outstanding Chief Resident Research Award, and recognition for authoring one of the top ten Foot & Ankle research papers at the 2016 American Academy of Orthopaedic Surgeons conference.
In addition to her practice in the U.S., Dr. Cooke has traveled abroad as a physician volunteer to provide surgical services in underserved areas where there is no access to hand surgery specialists. In partnership with the surgeon-founded nonprofit organization Touching Hands, she has performed hand surgeries on adult and pediatric patients in Honduras. Dr. Cooke also has traveled with Shriners Hospital to treat children in Davao, Philippines.
- Congenital Hand Surgery
- Hand, Elbow and Wrist Surgery
- Orthopaedic Surgery
Clinical Assistant Professor, Orthopaedic Surgery
Honors & Awards
Outstanding Chief Resident Research Award, Boston University Medical Center (2018)
Third Place Research Award, OREF Northeast Resident Research Symposium (2017)
Top 10 Foot & Ankle Papers: Paper 746, AAOS (2016)
AAOS Resident Delegate, AAOS (2015)
Howard Hughes Research Fellowship Award, Howard Hughes Medical Institute (2010)
PACCTR Quarterly Research Fellowship, UCSF Medical School (2010)
UCSF Dean's Prize in Outstanding Medical Student Research, UCSF Medical School (2010)
Certificate Program in Biomedical Sciences, UCSF Medical School (2009-2011)
M.D. with Thesis, UCSF Medical School (2009-2011)
Dean's Quarterly Research Fellowship, UCSF Medical School (2009)
Medical Student Curriculum Ambassador Grant, UCSF Medical School (2007)
American Heart Association Undergraduate Research Grant, American Heart Association (2004)
Board Certification: American Board of Orthopaedic Surgery, Orthopaedic Surgery (2022)
Fellowship: Shriners Hospitals for Children Orthopaedic Surgery (2020) CA
Fellowship: Hospital for Special Surgery Orthopaedic Surgery Residency (2019) NY
Residency: Boston University Medical Ctr Orthopaedic Surgery (2018) MA
Medical Education: University of California at San Francisco School of Medicine (2012) CA
Open Ankle Fractures: What Predicts Infection? A multi-center study.
Journal of orthopaedic trauma
OBJECTIVE: To identify the patient, injury and treatment factors associated with an acute infection during the treatment of open ankle fractures in a large multi-center retrospective review. To evaluate the effect of infectious complications on the rates of nonunion, malunion, and loss of reduction.DESIGN: Multi-center Retrospective Review.SETTING: Sixteen Trauma Centers.PATIENTS: One thousand and three consecutive skeletally mature patients (514 men and 489 women) with open ankle fractures.MAIN OUTCOME MEASURES: Fracture-related infection (FRI) in open ankle fractures.RESULTS: The charts of 1,003 consecutive patients were reviewed and 712 patients (357 women and 355 men) had at least 12 weeks of clinical follow-up. Their average age was 50 years (range 16-96), and average BMI was 31; they sustained OTA/AO types 44A (12%), 44B (58%), and 44C (30%) open ankle fractures. The rate FRI rate was 15%. A multivariable regression analysis identified male sex, diabetes, smoking, immunosuppressant use, time to wound closure, and wound location as independent risk factors for infection. There were 77 cases of malunion, nonunion, loss of reduction and/or implant failure; FRI was associated with higher rates of these complications (p=0.01).CONCLUSION: Several patient, injury and surgical factors were associated with fracture-related infection in the treatment of open ankle fractures.LEVEL OF EVIDENCE: Prognostic Level IV. See Instructions for Authors for a complete description of levels of evidence.
View details for DOI 10.1097/BOT.0000000000002293
View details for PubMedID 34711768
Are Continuous Femoral Nerve Catheters Beneficial for Pain Management After Operative Fixation of Tibial Plateau Fractures? A Randomized Controlled Trial
JOURNAL OF ORTHOPAEDIC TRAUMA
2019; 33 (12): E447–E451
To determine whether a continuous femoral nerve block after open reduction internal fixation of tibial plateau fractures would diminish Visual Analog Scale (VAS) scores and/or systemic narcotic intake.Randomized controlled trial.Level 1 academic trauma center.Forty-two consecutive patients with operatively treated tibial plateau fractures.Continuous femoral nerve catheter for postoperative pain management was performed in the experimental group.Both the VAS scores for pain and narcotic intake were assessed at 4, 8, 12, 24, 36, 48, and 72 hours postoperatively.Forty-two patients were enrolled in this study. There were 21 women and 21 men 21-70 years of age (avg 49) with operatively treated tibial plateau fractures. Twenty-one patients were randomized to receive a femoral nerve block with 5 crossovers for technical reasons. Accordingly, we analyzed 16 patients with femoral nerve blocks and 26 with standard care. There were no significant differences between the study groups regarding age, sex, or fracture type. There was no significant difference in VAS scores between the control and experimental group at any time point. The total systemic morphine equivalent for the femoral nerve block group and the control group was 375 and 397 respectively (P = 0.76). Across groups, patients with bicondylar fractures tended to have higher VAS than those with unicondylar fractures and to use more narcotics, although neither was statistically significant.Femoral nerve blocks for postoperative pain management in tibial plateau fractures did not demonstrate an improvement in pain relief or narcotic use.Therapeutic Level I. See Instructions for Authors for a complete description of levels of evidence.
View details for DOI 10.1097/BOT.0000000000001594
View details for Web of Science ID 000510647700001
View details for PubMedID 31361682
Serum proteomic assessment of the progression of fracture healing
JOURNAL OF ORTHOPAEDIC RESEARCH
2018; 36 (4): 1153–63
A targeted proteomic analysis of murine serum over a 35-day course of fracture healing was carried out to determine if serum proteomic changes could be used to monitor the biological progression of fracture healing. Transverse, closed femoral fractures where generated and stabilized with intramedullary fixation. A single stranded DNA aptamer-based multiplexed proteomic approach was used to assay 1,310 proteins. The transcriptomic profiles for genes matching the 1,310 proteins were obtained by microarray analysis of callus mRNA. Of the 1,310 proteins analyzed, 850 proteins showed significant differences among the time points (p-value <0.05). Ontology assessment associated these proteins with osteoblasts, monocyte/macrophage lineages, mesenchymal stem cell lines, hepatic tissues, and lymphocytes. Temporal clustering of these data identified proteins associated with inflammation, cartilage formation and bone remodeling stages of healing. VEGF, Wnt, and TGF-βsignaling pathways were restricted to the period of cartilage formation. Comparison of the proteomic and transcriptomic profiles showed that 87.5% of proteins in serum had concordant expression to their mRNA expression in the callus, while 12.5% of the protein and mRNA expression patterns were discordant. The discordant proteins that were elevated in the serum but down regulated in callus mRNA expression were related to clotting functions, allograft rejection, and complement function. While proteins down regulated in the serum and elevated in callus mRNA were associated with osteoblast function, NF-ĸb, and activin signaling. These data show the serum proteome may be used to monitor the different biological stages of fracture healing and have translational potential in assessing human fracture healing. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:1153-1163, 2018.
View details for DOI 10.1002/jor.23754
View details for Web of Science ID 000430787200014
View details for PubMedID 28971515
View details for PubMedCentralID PMC5880751
Correlation between RUST assessments of fracture healing to structural and biomechanical properties
JOURNAL OF ORTHOPAEDIC RESEARCH
2018; 36 (3): 945–53
Radiographic Union Score for Tibia (RUST) and modified RUST (mRUST) are radiographic tools for quantitatively evaluating fracture healing using a cortical scoring system. This tool has high intra-class correlation coefficients (ICCs); however, little evidence has evaluated the scores against the physical properties of bone healing. Closed, stabilized fractures were made in the femora of C3H/HeJ male mice (8-12 week-old) of two dietary groups: A control and a phosphate restricted diet group. Micro-computed tomography (µCT) and torsion testing were carried out at post-operative days (POD) 14, 21, 35, and 42 (n = 10-16) per group time-point. Anteroposterior and lateral radiographic views were constructed from the µCT scans and scored by five raters. The raters also indicated if the fracture were healed. ICCs were 0.71 (mRUST) and 0.63 (RUST). Both RUST scores were positively correlated with callus bone mineral density (BMD) (r = 0.85 and 0.80, p < 0.001) and bone volume fraction (BV/TV) (r = 0.86 and 0.80, p < 0.001). Both RUST scores positively correlated with callus strength (r = 0.35 and 0.26, p < 0.012) and rigidity (r = 0.50 and 0.39, p < 0.001). Radiographically healed calluses had a mRUST ≥13 and a RUST ≥10 and had excellent relationship to structural and biomechanical metrics. Effect of delayed healing due to phosphate dietary restrictions was found at later time points with all mechanical properties (p < 0.011), however no differences found in the RUST scores (p > 0.318). Clinical relevance of this study is both RUST scores showed high correlation to physical properties of healing and generally distinguished healed vs. non-healed fractures. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:945-953, 2018.
View details for DOI 10.1002/jor.23710
View details for Web of Science ID 000429324600017
View details for PubMedID 28833572
View details for PubMedCentralID PMC5823715
- The History of Carpal Tunnel Carpal Tunnel Syndrome and Related Median Neuropathies Springer. 2017: 7–12
ECM stiffness primes the TGF beta pathway to promote chondrocyte differentiation
MOLECULAR BIOLOGY OF THE CELL
2012; 23 (18): 3731–42
Cells encounter physical cues such as extracellular matrix (ECM) stiffness in a microenvironment replete with biochemical cues. However, the mechanisms by which cells integrate physical and biochemical cues to guide cellular decision making are not well defined. Here we investigate mechanisms by which chondrocytes generate an integrated response to ECM stiffness and transforming growth factor β (TGFβ), a potent agonist of chondrocyte differentiation. Primary murine chondrocytes and ATDC5 cells grown on 0.5-MPa substrates deposit more proteoglycan and express more Sox9, Col2α1, and aggrecan mRNA relative to cells exposed to substrates of any other stiffness. The chondroinductive effect of this discrete stiffness, which falls within the range reported for articular cartilage, requires the stiffness-sensitive induction of TGFβ1. Smad3 phosphorylation, nuclear localization, and transcriptional activity are specifically increased in cells grown on 0.5-MPa substrates. ECM stiffness also primes cells for a synergistic response, such that the combination of ECM stiffness and exogenous TGFβ induces chondrocyte gene expression more robustly than either cue alone through a p38 mitogen-activated protein kinase-dependent mechanism. In this way, the ECM stiffness primes the TGFβ pathway to efficiently promote chondrocyte differentiation. This work reveals novel mechanisms by which cells integrate physical and biochemical cues to exert a coordinated response to their unique cellular microenvironment.
View details for DOI 10.1091/mbc.E12-03-0172
View details for Web of Science ID 000312222200021
View details for PubMedID 22833566
View details for PubMedCentralID PMC3442419
Structured three-dimensional co-culture of mesenchymal stem cells with chondrocytes promotes chondrogenic differentiation without hypertrophy
OSTEOARTHRITIS AND CARTILAGE
2011; 19 (10): 1210–18
This study investigated a novel approach to induce chondrogenic differentiation of human mesenchymal stem cells (hMSC). We hypothesized that a structured three-dimensional co-culture using hMSC and chondrocytes would provide chondroinductive cues to hMSC without inducing hypertrophy.In an effort to promote optimal chondrogenic differentiation of hMSC, we created bilaminar cell pellets (BCPs), which consist of a spherical population of hMSC encased within a layer of juvenile chondrocytes (JC). In addition to histologic analyses, we examined proteoglycan content and expression of chondrogenic and hypertrophic genes in BCPs, JC pellets, and hMSC pellets grown in the presence or absence of transforming growth factor-β (TGFβ) following 21 days of culture in either growth or chondrogenic media.In either growth or chondrogenic media, we observed that BCPs and JC pellets produced more proteoglycan than hMSC pellets treated with TGFβ. BCPs and JC pellets also exhibited higher expression of the chondrogenic genes Sox9, aggrecan, and collagen 2A1, and lower expression of the hypertrophic genes matrix metalloproteinase-13, Runx2, collagen 1A1, and collagen 10A1 than hMSC pellets. Histologic analyses suggest that JC promote chondrogenic differentiation of cells in BCPs without hypertrophy. Furthermore, when cultured in hypoxic and inflammatory conditions intended to mimic the injured joint microenvironment, BCPs produced significantly more proteoglycan than either JC pellets or hMSC pellets.The BCP co-culture promotes a chondrogenic phenotype without hypertrophy and, relative to pellet cultures of hMSCs or JCs alone, is more resistant to the adverse conditions anticipated at the site of articular cartilage repair.
View details for DOI 10.1016/j.joca.2011.07.005
View details for Web of Science ID 000295770300006
View details for PubMedID 21816228
View details for PubMedCentralID PMC3188316
Transfusion-Related Acute Lung Injury After Transfusion of Maternal Blood A Case-Control Study
2010; 35 (23): E1322–E1327
This is a single-center retrospective case-control study of 7 transfusion-related acute lung injury (TRALI) cases and 28 controls in the pediatric spinal surgery population.To determine the association between maternal transfusion and risk of TRALI in pediatric spinal surgery patients.Previous studies support a "2-hit" model for the pathogenesis of TRALI-activation and sequestration of neutrophils in the pulmonary vasculature followed by transfusion of a biologic response modifier such as antileukocyte antibodies. Maternal donation of blood products is a potential risk factor for TRALI because of the development of antileukocyte antibodies during pregnancy. Until now there have been no studies specifically addressing the risk of TRALI following maternal transfusions.This is a retrospective case-control study of 7 TRALI cases with 4 controls per case, matched by strata for volume of plasma transfused. All cases identified by the Transfusion Biology and Medicine Specialized Center of Clinically Oriented Research with a TRALI diagnosis were eligible for inclusion. Electronic medical records and operative notes were reviewed to obtain demographic data, diagnosis, surgical approach, and number of spine levels for each operation.An increased prevalence of maternal blood transfusion was found among the TRALI cases compared with the control cases: 43% (3 of 7) versus 7% (2 of 28), P = 0.044. There were otherwise no statistical differences between the groups, including age, gender, surgical approach, number of spinal levels, or type of blood product transfused.Pediatric patients undergoing spinal surgery may be at increased risk for the development of TRALI following the transfusion of maternal blood products. Accordingly, we recommend that directed donation of maternal blood products should be avoided in this population. This study also found that TRALI may be underrecognized and underreported to the transfusion service.
View details for DOI 10.1097/BRS.0b013e3181e3dad2
View details for Web of Science ID 000283490100011
View details for PubMedID 20938390
View details for PubMedCentralID PMC2964398
Peripheral blood leukocyte counts in cytomegalovirus infected heart transplant patients: Impact of acute disease versus subclinical infection
2006; 82 (11): 1419-1424
Cytomegalovirus (CMV)-associated leucopenia in heart transplant patients is poorly characterized.We conducted a retrospective analysis of timing, degree, and type of leukopenia in four groups of patients: cases (n=20); controls (n=20); subclinical early infection (n=21), and subclinical late infection (n=22). In the cases, white blood cells (WBC) count at diagnosis was compared to prediagnosis; and cases were compared to controls. Subclinical cases (early and late) were identified by measurement of CMV DNA in peripheral blood mononucleocytes, and WBC was compared to those of the cases and controls.First, in human heart transplant recipients the total leukocyte count decreased prior to the time of diagnosis of CMV disease: cases: 5.4+/-2.1 x 10/microL vs. 3.7+/-2.1x10/muL (P<0.01); subclinical early: 8.1+/-4.1 x 10/microL vs. 6.9+/-1.6 x 10/microL (P<0.01). Second, the leukocyte populations most reduced during CMV disease are the neutrophils: 4.4 x 10/microL (78%) to 2.5 x 10/microL (69%) (P<0.05), and monocytes 0.6 x 10/microL (11%) to 0.3 x 10/microL (7.5%) (P<0.05). Third, the reduction in leukocyte count that occurs during CMV disease appears to be independent of immunosuppressive therapy (using cyclosporine A, mycophenolate mofetil, or azathioprine and prednisone). Finally, subclinical CMV infection in stable long-term heart transplant patients without disease is unassociated with a reduction in the leukocyte count.Aside from implications for early diagnosis, CMV-associated decrease in monocytes is important because viral infections like Epstein-Barr virus cause monocytosis. The absence of leucopenia in subclinical late infections is a new important finding.
View details for DOI 10.1097/01.tp.0000242139.13197.7f
View details for Web of Science ID 000242948600009
View details for PubMedID 17164711