Dr. Sarita Khemani is a Clinical Associate Professor of Medicine and a Neurosurgery Hospital Medicine physician. Her clinical focus is preventing and managing medical complications in hospitalized neurosurgical patients in the postoperative setting. Her interests include the intersection of medicine and technology to optimize a healthy lifespan.

Dr. Khemani is passionate about education and has served as Director of perioperative medicine rotations for Stanford medicine residents, medical students, and physician assistant students. She is the recipient of Department of Medicine Excellence in Teaching Award. Dr. Khemani is also the founder and co-director of Stanford Medicine Clinical Summer Internship, a globally recognized program for premed students. The program provides numerous scholarships to minority/underrepresented students to empower future leaders in medicine.

Dr. Khemani has been an invited speaker at various medical conferences and meetings. In addition, she was invited to speak at the Stanford Neurosurgery Grand Rounds and give the keynote speech at the Stanford Physician Assistant student graduation ceremony. She has appeared as a guest on various media outlets in the US and on international television.

Dr. Khemani is a member of the American College of Physicians and currently serves on the Stanford Hospital Pharmacy and Therapeutics Committee and Hospital Medicine Wellness Committee.

Clinical Focus

  • Internal Medicine
  • Neurosurgery Hospitalist
  • Perioperative Medicine

Academic Appointments

  • Clinical Associate Professor, Medicine

Administrative Appointments

  • Head, Stanford Lifestyle Medicine Stress Neuroscience, Stanford University (2022 - Present)
  • Director, Medical Student Perioperative Medicine Rotation (IM), Stanford School of Medicine (2018 - Present)
  • Co-Director, Stanford Medicine Clinical Summer Internship, Department of Medicine (2015 - Present)
  • Director, Resident Peri-operative Medicine Rotation (IM), Department of Medicine (2015 - 2022)
  • Director, PA student inpatient rotation (IM), Surgical Co-management Hospitalist (2012 - 2018)
  • Preceptor, Practice of Medicine course, Stanford School of Medicine (2012 - 2018)

Honors & Awards

  • Awardee: Division of Hospital Medicine Excellence in Teaching Award, Stanford School of Medicine, Department of Medicine (2016)
  • Nominee: Division of Hospital Medicine Excellence in Teaching Award, Stanford University School of Medicine, Department of Medicine (2015)
  • Malinda S. Mitchell Quality Award for development of Perioperative Medicine Program (Co-Recipient), Stanford Hospital and Clinics (2013)

Professional Education

  • Board Certification: American Board of Internal Medicine, Internal Medicine (1997)
  • Internship: UCSF-Internal Medicine (1995) CA
  • Residency: UCSF-Internal Medicine (1997) CA
  • Medical Education: Indira Gandhi Medical College (1992) India

All Publications



    The in vivo and in vitro effects of M-CSF on bronchoalveolar macrophages (BAM) activity against the intracellular fungal pathogen Histoplasma capsulatum (Hc) were studied. Three days after a single subcutaneous (s.c.) dose of M-CSF (2.5 mg/kg), enhanced ex vivo antifungal activity of BAM was measured. BAM from M-CSF-treated CD-1 mice significantly (P < 0.01) inhibited the intracellular multiplication of Hc yeast cells in 20 h assays compared to BAM from control mice. This effect was not observed at days 1, 7, 11 or 21 post-treatment. A dose of 5 mg/kg s.c., but not 1 mg/kg, induced similar antifungal activity in BAM by day 3. Peritoneal macrophages (PM) from M-CSF-treated mice did not have enhanced antifungal activity at days and doses tested. BAM could also be activated for antihistoplasmal activity by M-CSF in vitro. M-CSF at 10,000 U/ml for 24 h or 5000 U/ml for 48 h induced significant (P < 0.01) inhibition of intracellular multiplication of Hc. Interferon-gamma (IFN) plus lipopolysaccharide (LPS) activated BAM and PM in vitro to inhibit intracellular multiplication of Hc (P < 0.001); the antihistoplasmal activity was completely inhibited by NG-monomethyl L-arginine (N-MMA), indicating that an L-arginine-dependent nitric oxide-producing mechanism was operative. N-MMA could not inhibit the antihistoplasmal activity of BAM or PM activated by M-CSF in vitro. The mechanism by which M-CSF-activated macrophages inhibit intracellular multiplication of Hc remains to be determined.

    View details for Web of Science ID A1995QN91500006

    View details for PubMedID 7782153