Doctor of Medicine, Stanford University, MED-MD (2009)
Bachelor of Science, Florida Atlantic University, UG Other not listed (2003)
John Sunwoo, Postdoctoral Research Mentor
OBJECTIVES:: Uvulopalatopharyngoplasty (UPPP) is a commonly performed surgical intervention used to treat obstructive sleep apnea (OSA) syndrome. Continuous peripheral nerve blocks have been shown to reduce postoperative pain and opioid requirements for other surgical procedures but have not been described previously for palate surgery. We present the use of a continuous lesser palatine nerve block catheter as a part of the multimodal postoperative pain management for UPPP. CASE REPORT:: Three patients were scheduled to undergo elective UPPP and tonsillectomy for OSA with scheduled postoperative hospital admission. Each patient gave written consent to share the details of his or her case. Upon completion of the surgical procedure, but before emergence from general anesthesia, a 20-G multiorifice epidural catheter was inserted into the left nasal passage, passed into the oropharynx, and either tunneled posteriorly within the anterior portion of the soft palate with the aid of a 16-G angiocatheter or placed submucosally within the soft palate by the surgeon. Each catheter was secured using clear adhesive dressings along the cheek and anchored to the ipsilateral shoulder. A continuous infusion of ropivacaine 0.2% at 2 mL/h was delivered using a disposable infusion device postoperatively, in addition to the prescribed oral and intravenous opioids. No immediate or long-term complications due to catheter placement were identified during the patient follow-up. DISCUSSION:: Continuous lesser palatine nerve block may be a useful regional anesthetic technique in the multimodal postoperative pain management of opioid-sensitive OSA patients undergoing UPPP and deserves further study.
View details for DOI 10.1097/AJP.0b013e3182971887
View details for PubMedID 23669453
Animal study.Development of an animal model for the study of biochemical changes that occur in the epidural space after intervertebral disc herniation.Although strong evidence for an inflammatory component exists, the biochemical processes underlying pain after disc herniation remain unknown.Epidural lavage was performed in 48 rats after L5 dorsal root ganglion exposure at baseline and 3, 6, or 24 hours after placement of autologous nucleus pulposus (NP) (N = 15), saline (N = 15), or NP + an interferon-? antibody (anti-IFN-?; N = 18) directly onto the dorsal root ganglion. Multiplex assays quantifying interleukin (IL)-1?, IL-1?, IL-2, IL-4, IL-6, IL-10, tumor necrosis factor ? (TNF-?), IFN-?, and granulocyte-macrophage colony-stimulating factor (GM-CSF) were performed. NP (N = 7) was also analyzed for these cytokines by placing NP into saline and measuring the relative concentration.Cytokines measured low at baseline (0-100 pg/mL) in all groups. Compared with saline, NP application caused IL-6 elevation, peaking at T = 3 hours, that was prevented by anti-IFN-?. NP induced elevation of TNF-?, peaking at T = 24 hours and was prevented by anti-IFN-?. IFN-? was elevated after NP at T = 3 hours and T = 24 hours. IL-1? was similar after saline versus NP. The concentrations of IL-1? and IL-10 were elevated at T = 3 hours, 6 hours, and 24 hours in all groups without between-groups difference. The level of IL-4 peaked at T = 3 hours in the NP group and was different than saline and NP + anti-IFN-? groups, but the time effect was insignificant. There was no change for GM-CSF. The concentration of cytokines measured in normal NP was less than 2 pg/mL for all cytokines except TNF-?.In this model of acute noncompressive disc herniation, NP caused the elevation of epidural IL-6, TNF-?, and IFN-?--all attenuated by IFN-? blockade. IL-1? and IL-10 were both significantly elevated by saline alone and their response was not prevented by IFN-? blockade. This model may prove useful for the study of the biochemical processes by which NP induces inflammation-induced nerve root irritation and radiculopathic pain.
View details for DOI 10.1097/BRS.0b013e3182604baa
View details for Web of Science ID 000312946800014
View details for PubMedID 22648034