Bio

Dr. Kristen MacKenzie is a Clinical Assistant Professor in the Department of Anesthesiology, Perioperative, and Pain Medicine. Dr. MacKenzie graduated AOA from medical school at UCSF and then completed her anesthesia residency and pain medicine fellowships at Stanford. She works at the Stanford Pain Management Center with specialty interests in chronic pelvic and abdominal pain, as well as peripartum pain. She is part of the Stanford Pelvic Health Center for interdisciplinary, multimodal care.

She also teaches in the Stanford Medical School as the pain team lead for clinical rotations and serves a Clinical Continuity Clerkship Instructor. Additionally, Dr. MacKenzie completed the Clinical Teaching Seminar Series (CTSS) Honors Scholars Program focusing on education of non-anesthesia trained pain medicine fellows on inpatient pain management curriculum, which was a project supported by the Anesthesia Teaching Awards Scholar Program. She enjoys being able to spend time with learners and participates in the Women in Medicine mentoring program annually.

Most recently, she completed a Stanford Faculty Medical Humanities Fellowship, focusing on the role of communication and the arts in modern medicine. She serves as the co-director for the Women's Sexual Dysfunction Case Conference as well as the Pain Division representative to the Stanford Anesthesia Communications Council.

Outside of work, she enjoys being outdoors in the Bay Area, trail running, and spending time with her husband and two boys.

Clinical focus:

Pelvic pain, due to multiple causes including:
Dyspareunia
Painful Bladder Syndrome/ Interstitial cystitis/ Dysuria
Endometriosis
Fibroids
Pelvis Congestion Syndrome
Pelvic Floor Dysfunction
Pudendal Nerve Pain
Rectal/Anal Pain
Vulvar Pain/ Vulvodynia/ Vaginismus

Nerve entrapment syndromes, including hernia nerve entrapment

Post-partum and Peri-partum pain
Abdominal pain
Musculoskeletal pain

She focuses treatment plans around ultrasound and fluoroscopy procedures, non-opioid pain medications, non-drug treatments such as pain psychology, acupuncture, massage, movement therapy and physical therapy.

For new patients: (650)723-6238 (telephone) and (650)320-9443 (fax)
For existing patients: (650)723-6238 (telephone)

Clinical Focus

  • Pain Medicine

Academic Appointments

  • Clinical Assistant Professor, Anesthesiology, Perioperative and Pain Medicine

Honors & Awards

  • Faculty Fellowship in Medical Humanities, Stanford University (2024)
  • Anesthesia Teaching Scholars Program, Stanford Department of Anesthesia (2022-2023)
  • Clinical Teaching Seminar Series (CTSS) Honors Scholars Program, Medical Education Program (2022-2023)
  • Chief Fellow, Stanford Pain Medicine Fellowship (2022)

Boards, Advisory Committees, Professional Organizations

  • Pain Medicine Board Certified, American Society of Anesthesiologists (2023 - Present)
  • Anesthesiology Board Certified, American Society of Anesthesiologists (2022 - Present)

Professional Education

  • Board Certification: American Board of Anesthesiology, Pain Medicine (2023)
  • Board Certification: American Board of Anesthesiology, Anesthesia (2022)
  • Fellowship, Stanford University, Pain Medicine (2022)
  • Residency, Stanford University, Anesthesiology (2021)
  • Internship, Kaiser Permanente Santa Clara, Internal Medicine (2018)
  • MD, University of California, San Francisco (2017)
  • Post- Baccalaureate, Johns Hopkins University, Pre-Medical (2011)
  • BA, Dartmouth College, Neuroscience (2010)

Contact

  • Academic
    University - Academic staff Department: Anesthesia - Adult Pain (Designated) Position: Clinical Assistant Professor
  • Clinical (Primary)  San Jose Medical Group Good Samaritan 2585 Samaritan Dr Ste 300 San Jose, CA 95124 (650) 725-8544 (fax)

Additional Clinical Info

Links

2024-25 Courses

All Publications

  • Processed Electroencephalogram Monitoring and Postoperative Delirium: A Systematic Review and Meta-analysis. Anesthesiology MacKenzie, K. K., Britt-Spells, A. M., Sands, L. P., Leung, J. M. 2018; 129 (3): 417-427

    Abstract

    WHAT THIS ARTICLE TELLS US THAT IS NEW: BACKGROUND:: Postoperative delirium complicates approximately 15 to 20% of major operations in patients at least 65 yr old and is associated with adverse outcomes and increased resource utilization. Furthermore, patients with postoperative delirium might also be at risk of developing long-term postoperative cognitive dysfunction. One potentially modifiable variable is use of intraoperative processed electroencephalogram to guide anesthesia. This systematic review and meta-analysis examines the relationship between processed electroencephalogram monitoring and postoperative delirium and cognitive dysfunction.A systematic search for randomized controlled trials was conducted using Ovid MEDLINE, PubMed, EMBASE, Cochrane Library, and Google search using the keywords processed electroencephalogram, Bispectral Index, postoperative delirium, postoperative cognitive dysfunction. Screening and data extraction were conducted by two independent reviewers, and risk of bias was assessed. Postoperative delirium combined-effect estimates calculated with a fixed-effects model were expressed as odds ratios with 95% CIs.Thirteen of 369 search results met inclusion criteria. Postoperative cognitive dysfunction data were excluded in meta-analysis because of heterogeneity of outcome measurements; results were discussed descriptively. Five studies were included in the quantitative postoperative delirium analysis, with data pooled from 2,654 patients. The risk of bias was low in three studies and unclear for the other two. The use of processed electroencephalogram-guided anesthesia was associated with a 38% reduction in odds for developing postoperative delirium (odds ratio = 0.62; P < 0.001; 95% CI, 0.51 to 0.76).Processed electroencephalogram-guided anesthesia was associated with a decrease in postoperative delirium. The mechanism explaining this association, however, is yet to be determined. The data are insufficient to assess the relationship between processed electroencephalogram monitoring and postoperative cognitive dysfunction.

    View details for DOI 10.1097/ALN.0000000000002323

    View details for PubMedID 29912008

    View details for PubMedCentralID PMC6092196

  • Cerebrospinal fluid neurofilament concentration reflects disease severity in frontotemporal degeneration. Annals of neurology Scherling, C. S., Hall, T., Berisha, F., Klepac, K., Karydas, A., Coppola, G., Kramer, J. H., Rabinovici, G., Ahlijanian, M., Miller, B. L., Seeley, W., Grinberg, L. T., Rosen, H., Meredith, J., Boxer, A. L. 2014; 75 (1): 116-26

    Abstract

    Cerebrospinal fluid (CSF) neurofilament light chain (NfL) concentration is elevated in neurological disorders, including frontotemporal degeneration (FTD). We investigated the clinical correlates of elevated CSF NfL levels in FTD.CSF NfL, amyloid-β1-42 (Aβ42), tau, and phosphorylated tau concentrations were compared in 47 normal controls (NC), 8 asymptomatic gene carriers (NC2) of FTD-causing mutations, and 79 FTD (45 behavioral variant frontotemporal dementia [bvFTD], 18 progressive nonfluent aphasia [PNFA], 16 semantic dementia [SD]), 22 progressive supranuclear palsy, 50 Alzheimer disease, 6 Parkinson disease, and 17 corticobasal syndrome patients. Correlations between CSF analyte levels were performed with neuropsychological measures and the Clinical Dementia Rating scale sum of boxes (CDRsb). Voxel-based morphometry of structural magnetic resonance images determined the relationship between brain volume and CSF NfL.Mean CSF NfL concentrations were higher in bvFTD, SD, and PNFA than other groups. NfL in NC2 was similar to NC. CSF NfL, but not other CSF measures, correlated with CDRsb and neuropsychological measures in FTD, but not in other diagnostic groups. Analyses in 2 independent FTD cohorts and a group of autopsy-verified or biomarker-enriched cases confirmed the larger group analysis. In FTD, gray and white matter volume negatively correlated with CSF NfL concentration, such that individuals with the highest NfL levels exhibited the most atrophy.CSF NfL is elevated in symptomatic FTD and correlates with disease severity. This measurement may be a useful surrogate endpoint of disease severity in FTD clinical trials. Longitudinal studies of CSF NfL in FTD are warranted.

    View details for DOI 10.1002/ana.24052

    View details for PubMedID 24242746

    View details for PubMedCentralID PMC4020786

  • Too good to be true: rhesus monkeys react negatively to better-than-expected offers. PloS one Knight, E. J., Klepac, K. M., Kralik, J. D. 2013; 8 (10): e75768

    Abstract

    To succeed in a dynamically changing world, animals need to predict their environments. Humans, in fact, exhibit such a strong desire for consistency that one of the most well-established findings in social psychology is the effort people make to maintain consistency among their beliefs, attitudes, and behavior. However, displeasure with unpredictability leads to a potential paradox, because a positive outcome that exceeds one's expectations often leads to increased subjective value and positive affect, not the opposite. We tested the hypothesis that two evolutionarily-conserved evaluation processes underlie goal-directed behavior: (1) consistency, concerned with prediction errors, and (2) valuation, concerned with outcome utility. Rhesus monkeys (Macaca mulatta) viewed a food item and then were offered an identical, better, or worse food, which they could accept or reject. The monkeys ultimately accepted all offers, attesting to the influence of the valuation process. However, they were slower to accept the unexpected offers, and they exhibited aversive reactions, especially to the better-than-expected offers, repeatedly turning their heads and looking away before accepting the food item. Our findings (a) provide evidence for two separable evaluation processes in primates, consistency and value assessment, (b) reveal a direct relationship between consistency assessment and emotional processes, and (c) show that our wariness with events that are much better than expected is shared with other social primates.

    View details for DOI 10.1371/journal.pone.0075768

    View details for PubMedID 24130742

    View details for PubMedCentralID PMC3794042

  • Memantine in patients with frontotemporal lobar degeneration: a multicentre, randomised, double-blind, placebo-controlled trial. The Lancet. Neurology Boxer, A. L., Knopman, D. S., Kaufer, D. I., Grossman, M., Onyike, C., Graf-Radford, N., Mendez, M., Kerwin, D., Lerner, A., Wu, C. K., Koestler, M., Shapira, J., Sullivan, K., Klepac, K., Lipowski, K., Ullah, J., Fields, S., Kramer, J. H., Merrilees, J., Neuhaus, J., Mesulam, M. M., Miller, B. L. 2013; 12 (2): 149-56

    Abstract

    Memantine has been used off-label to treat frontotemporal lobar degeneration (FTD). A previous 26-week open-label study suggested a transient, modest benefit on neuropsychiatric symptoms as measured by the neuropsychiatric inventory (NPI). We aimed to determine whether memantine is an effective treatment for FTD.We did a randomised, parallel group, double-blind, placebo-controlled trial of 20 mg memantine taken orally daily for 26 weeks in patients with FTD. Participants met Neary criteria for behavioural variant FTD (bvFTD) or semantic dementia and had characteristic brain atrophy. Use of acetylcholinesterase inhibitors was prohibited. Individuals were randomly assigned to receive either memantine or matched placebo tablets (1:1) in blocks of two and four patients. All patients and study personnel were masked to treatment assignment. Primary endpoints were the change in total NPI score and clinical global impression of change (CGIC) score after 26 weeks and were analysed by intention to treat. This study is registered with Clinicaltrials.gov, number NCT00545974.Of 100 patients screened, 81 were randomly assigned to receive memantine (39 patients) or placebo (42 patients). Five (6%) patients discontinued, and 76 completed the 26-week treatment. Enrolment numbers were lower than planned because of many patients' preference to take memantine or cholinesterase inhibitors off-label rather than participate in a clinical trial. Memantine treatment had no effect on either the NPI (mean difference 2·2, 95% CI -3·9 to 8·3, p=0·47) or CGIC (mean difference 0·0, -0·4 to 0·4, p=0·90) after 26 weeks of treatment. Memantine was generally well tolerated; however, patients in the memantine group had more frequent cognitive adverse events (six patients) than those in the placebo group (one).Memantine treatment showed no benefit in patients with FTD. These data do not support memantine use in FTD.Forest Research Institute.

    View details for DOI 10.1016/S1474-4422(12)70320-4

    View details for PubMedID 23290598

    View details for PubMedCentralID PMC3756890