Bio

Bio


Subhro K. Sen, MD, Clinical Assistant Professor in the Division of Plastic and Reconstructive Surgery, graduated from Northwestern University with a degree in biomedical engineering. He went on to receive his medical degree from the Northwestern University Feinberg School of Medicine. After medical school, he completed a yearlong peripheral nerve research fellowship under Dr. Susan Mackinnon at the Washington University School of Medicine in St. Louis. He received his postgraduate training in general surgery at Indiana University, followed by plastic and reconstructive surgery at Johns Hopkins University. He completed his training with a hand and upper extremity surgery fellowship at Stanford University.

Dr. Sen’s general clinical interests are in reconstructive surgery, microvascular surgery, and hand and upper extremity surgery. His practice includes: post-traumatic extremity reconstruction; post-oncologic reconstruction of the head and neck, trunk and extremities; perforator flap surgery; and melanoma surgery. He is also leading the effort to develop a comprehensive Wound and Limb Salvage Center at Stanford. As a hand surgeon in the Robert A. Chase Hand and Upper Limb Center, he has interests in hand trauma, degenerative conditions, peripheral nerve injuries, and congenital hand differences.

In addition to his clinical practice, Dr. Sen is involved in research, publication, and teaching. His peer-reviewed research includes studies on peripheral nerve regeneration, and he has authored a number of book chapters on a variety of hand surgery topics. He currently reviews manuscripts submitted for publication in Plastic and Reconstructive Surgery and Annals of Plastic Surgery. Dr. Sen is double board certified by the American Board of Plastic Surgery and the American Board of Surgery. He is a member of the American Society of Plastic Surgeons and the American Society for Reconstructive Microsurgery, and is a candidate member of the American Society for Surgery of the Hand, and the American Association for Hand Surgery.

Clinical Focus


  • Upper and Lower Extremity Reconstruction
  • Hand and Upper Extremity Surgery
  • Wound Healing
  • Microvascular Surgery
  • Plastic and Reconstructive Surgery
  • Peripheral Nerve Surgery
  • Head & Neck Reconstruction

Academic Appointments


Administrative Appointments


  • Medical Co-Director, Stanford Wound Center (2014 - Present)

Professional Education


  • Residency:Indiana University Medical Center (2006) IN
  • Fellowship:Stanford University Plastic Surgery Program (2009) CA
  • Board Certification: Plastic and Reconstructive Surgery, American Board of Plastic Surgery (2010)
  • Board Certification: General Surgery, American Board of Surgery (2008)
  • Residency:Johns Hopkins University (2008) MD
  • Residency:Johns Hopkins University (2004) MD
  • Medical Education:Northwestern University Feinberg School of Medicine (2000) IL

Publications

Journal Articles


  • Assessment of the immune response to dose of nerve allografts PLASTIC AND RECONSTRUCTIVE SURGERY Sen, S. Y., Lowe, J. B., Brenner, M. J., Hunter, D. A., Mackinnon, S. E. 2005; 115 (3): 823-830

    Abstract

    Nerve allotransplantation provides a limitless source of nerve graft material for the reconstruction of large neural defects. It does require systemic immunosuppression or induction of immune unresponsiveness to prevent allograft rejection. It is unknown whether a greater volume of nerve graft material will increase the risk of rejection or the need for more intensive immunosuppression. This study assessed the relationship between the quantity of nerve tissue transplanted and the magnitude of the resulting immune response. Forty female (BALB/c) mice were randomly assigned to two groups that received either nerve isografts (BALB/c) or nerve allografts (C57BL/6). Each group was then subdivided into two groups that received either one or 10 sciatic nerve graft inlays. Histological and immunological assessments were performed at 10 days after engraftment. Histologic analysis demonstrated greater cellular infiltration in the allograft than the isograft groups but no appreciable difference in infiltration related to quantity of transplanted nerve tissue. In vitro assessments of the immune response using mixed lymphocyte assays and limiting dilution analysis similarly demonstrated a robust immune response to allografts but no effect on quantity of transplanted nerve tissue. These data suggest that larger peripheral nerve allografts may not be subject to increased risk for rejection.

    View details for DOI 10.1097/01.PRS.0000153032.68405.DA

    View details for Web of Science ID 000227432100021

    View details for PubMedID 15731684

  • Dose-dependent effects of FK506 on neuroregeneration in a rat model PLASTIC AND RECONSTRUCTIVE SURGERY Yang, R. K., Lowe, J. B., Sobol, J. B., Sen, S. K., Hunter, D. A., Mackinnon, S. E. 2003; 112 (7): 1832-1840

    Abstract

    This study explored the effects of different doses of FK506 on peripheral nerve regeneration, to determine whether neuroregeneration could be enhanced without the toxicity of systemic immunosuppression. In the first part of the study, subimmunosuppressive doses of FK506 were determined by examining skin allograft survival in a rat model. Full-thickness skin grafts (2 cm2) from Wistar rats were grafted to recipient Lewis rats. The procedure was performed for six groups (n = 6). The control group received no FK506, and the other five groups received daily doses of FK506 of 0.125, 0.25, 0.5, 1.0, or 2.0 mg/kg. Animals that received 2.0 mg/kg FK506 per day exhibited complete skin graft take, whereas all other groups demonstrated complete rejection. After determination of the immunosuppressive dose of FK506, the neuroregenerative effects of different doses of FK506 were explored by assessing nerve regeneration in 80 rats after tibial nerve transection and repair. The control group received no FK506, whereas the other four groups were given daily doses of FK506 of 0.25, 0.5, 1.0, or 2.0 mg/kg. Rats were euthanized at three time points (25, 30, and 35 days), to fully investigate the effects of different FK506 dosing regimens on neuroregeneration. Histomorphometric analyses performed on postoperative days 30 and 35 demonstrated statistically significant improvements in neuroregeneration with subimmunosuppressive FK506 doses of 0.5 and 1.0 mg/kg per day. Therefore, the study demonstrated that neuroregeneration was enhanced at low doses of FK506 that were not sufficient to prevent skin allograft rejection.

    View details for DOI 10.1097/01.PRS.0000091167.27303.18

    View details for Web of Science ID 000220063000012

    View details for PubMedID 14663227

  • Effects of delaying FK506 administration on neuroregeneration in a rodent model JOURNAL OF RECONSTRUCTIVE MICROSURGERY Sobol, J. B., Lowe, J. B., Yang, R. K., Sen, S. K., Hunter, D. A., Mackinnon, S. E. 2003; 19 (2): 113-118

    Abstract

    FK506 is an immunosuppressant drug that has been shown experimentally to stimulate nerve growth and speed functional recovery, when administered immediately after peripheral nerve injury. However, the clinical scenario of a peripheral nerve injury is often associated with either a delayed diagnosis or reconstruction. The purpose of this study was to determine the efficacy of FK506 on neuroregeneration with delayed administration. Thirty-two Lewis rats underwent tibial nerve transection with immediate repair. Animals were left untreated, or were treated with daily injections of FK506 (2 mg/kg), started on the day of surgery, postoperative day 3, or postoperative day 5. Animals underwent walking track analysis to assess functional nerve recovery. Nerves were harvested for histomorphometric analysis on postoperative days 21, 28, and 42. Histomorphometry demonstrated that all treatment groups, regardless of the time of drug initiation, demonstrated evidence of enhanced neuroregeneration, compared to the untreated group. Histomorphometric data from groups harvested on day 21 demonstrated a statistically significant improvement in neuroregeneration in the immediate and 3-day delay groups. Therefore, the beneficial effects of FK506 on neuroregeneration are not restricted to immediate administration, but these effects significantly diminish when FK506 is administered 3 days after nerve injury.

    View details for Web of Science ID 000181327800011

    View details for PubMedID 12632311

  • Current approach to radial nerve paralysis PLASTIC AND RECONSTRUCTIVE SURGERY Lowe, J. B., Sen, S. Y., Mackinnon, S. E. 2002; 110 (4): 1099-1112

    Abstract

    After studying this article, the participant should be able to: 1. Identify all potential points of radial nerve compression and other likely causes of radial nerve injury. 2. Accurately diagnose both surgical and nonsurgical causes of radial nerve paralysis. 3. Define a safe and effective approach to the surgical release and reconstruction of the radial nerve. Radial nerve paralysis, which can result from a complex humerus fracture, direct nerve trauma, compressive neuropathies, neuritis, or (rarely) from malignant tumor formation, has been reported throughout the literature, with some controversy regarding its diagnosis and management. The appropriate management of any radial nerve palsy depends primarily on an accurate determination of its cause, severity, duration, and level of involvement. The radial nerve can be injured as proximally as the brachial plexus or as distally as the posterior interosseous or radial sensory nerve. This article reviews the etiology, prognosis, and various treatments available for radial nerve paralysis. It also provides a new classification system and treatment algorithm to assist in the management of patients with radial nerve palsies, and it offers a simple, five-step approach to radial nerve release in the forearm.

    View details for DOI 10.1097/01.PRS.0000020996.11823.3F

    View details for Web of Science ID 000177643200016

    View details for PubMedID 12198425

  • The effects of rapamycin in murine peripheral nerve isografts and allografts PLASTIC AND RECONSTRUCTIVE SURGERY Myckatyn, T. M., Ellis, R. A., Grand, A. G., Sen, S. K., Lowe, J. B., Hunter, D. A., Mackinnon, S. E. 2002; 109 (7): 2405-2417

    Abstract

    The FKBP-12-binding ligand FK506 has been successfully used to stimulate nerve regeneration and prevent the rejection of peripheral nerve allografts. The immunosuppressant rapamycin, another FKBP-12-binding ligand, stimulates axonal regeneration in vitro, but its influence on nerve regeneration in peripheral nerve isografts or allografts has not been studied. Sixty female inbred BALB/cJ mice were randomized into six tibial nerve transplant groups, including three isograft and three allograft (C57BL/6J) groups. Grafts were left untreated (groups I and II), treated with FK506 (groups III and IV), or treated with rapamycin (groups V and VI). Nerve regeneration was quantified in terms of histomorphometry and functional recovery, and immunosuppression was confirmed with mixed lymphocyte reactivity assays. Animals treated with FK506 and rapamycin were immunosuppressed and demonstrated significantly less immune cell proliferation relative to untreated recipient animals. Although every animal demonstrated some functional recovery during the study, animals receiving an untreated peripheral nerve allograft were slowest to recover. Isografts treated with FK506 but not rapamycin demonstrated significantly increased nerve regeneration. Nerve allografts in animals treated with FK506, and to a lesser extent rapamycin, however, both demonstrated significantly more nerve regeneration and increased nerve fiber widths relative to untreated controls. The authors suggest that rapamycin can facilitate regeneration through peripheral nerve allografts, but it is not a neuroregenerative agent in this in vivo model. Nerve regeneration in FK506-treated peripheral nerve isografts and allografts was superior to that found in rapamycin-treated animals. Rapamycin may have a role in the treatment of peripheral nerve allografts when used in combination with other medications, or in the setting of renal failure that often precludes the use of calcineurin inhibitors such as FK506.

    View details for Web of Science ID 000175761500035

    View details for PubMedID 12045568

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