ABSTRACT
BACKGROUND: While it is assumed that neuraxial analgesia and pain management may beneficially influence perioperative hemodynamics, few studies provided data quantifying such effects and none have assessed the potential contribution of the addition of a nerve block. QUESTIONS/PURPOSES: This clinical trial compared the visual analog scale (VAS) scores and measurement of arterial tone using augmentation index of patients who received combined spinal-epidural (CSE) only to patients who received both CSE and lumbar plexus block. METHODS: After obtaining written consent, 92 patients undergoing total hip arthroplasty were randomized to receive either CSE or CSE with lumbar plexus block (LPB). Perioperative pain and arterial tone were measured using VAS scores and augmentation index (AI) respectively, at baseline and at various times postoperatively. RESULTS: After the exclusion of 2 patients, 44 patients received CSE alone and 46 patients received CSE and LPB. Patient demographics and perioperative characteristics were similar in both groups. AI continuously decreased after placement of a CSE with or without LBP, beyond full resolution of neuraxial and peripheral blockade. Although the LPB group demonstrated a statistically significant reduction of VAS pain scores in the postanesthesia care unit (PACU; P < 0.05), overall, the addition of a LPB did not significantly reduce the AI when compared to the control group. CONCLUSION: The addition of a LPB provided better pain control in the PACU but did not reduce the AI, compared to the control group. We conclude that the addition of a LPB may have limited ability to affect arterial tone in the presence of a continuous infusion of epidural analgesics. In summary, the addition of a LPB in patients undergoing total hip arthroplasty is clinically effective and provided better pain control, especially in the immediate postoperative period. The continuous decrease on the AI in both groups beyond the full resolution of the neuroaxial and LPB will require further studies.
Subject(s)
Diabetes Mellitus, Type 1/therapy , Diabetic Nephropathies/surgery , Islets of Langerhans Transplantation/methods , Kidney Failure, Chronic/surgery , Kidney Transplantation/methods , Antilymphocyte Serum/therapeutic use , Azathioprine/therapeutic use , C-Peptide/blood , Cells, Cultured , Cyclosporine/therapeutic use , Humans , Immunosuppression Therapy/methods , Islets of Langerhans , Islets of Langerhans Transplantation/immunology , Islets of Langerhans Transplantation/physiology , Kidney Transplantation/immunology , Kidney Transplantation/physiology , Muromonab-CD3/therapeutic use , Postoperative Complications , Prednisone/therapeutic use , Tissue Preservation , Transplantation, Heterotopic , Transplantation, HomologousSubject(s)
C-Peptide/metabolism , Cryopreservation , Insulin/metabolism , Islets of Langerhans , Organ Preservation Solutions , Adenosine , Allopurinol , Cell Separation/methods , Culture Techniques/methods , Glutathione , Humans , Hypertonic Solutions , Insulin Secretion , Islets of Langerhans/cytology , Islets of Langerhans/metabolism , Raffinose , Time FactorsABSTRACT
Human islets were macroencapsulated in permselective hollow fiber membrane devices and successfully allotransplanted subcutaneously with > 90% viability after 2 weeks in situ. Recipients were patients with type I or type II diabetes and normal control subjects; none was immunosuppressed. Between 150 and 200 islet equivalents were implanted in each of the nine patients. No adverse patient complications were observed. Biocompatibility of devices was excellent. Insulin-positive beta-cells were confirmed in encapsulated islets recovered from the implanted devices in all patient populations including the type I diabetic patients. Glucose-stimulated insulin release could be demonstrated in vitro from recovered islets. These data demonstrate that macroencapsulated human islets can survive at the subcutaneous site and that permselective membranes can be designed to protect against both allogeneic immune responses as well as the autoimmune component of type I diabetes.
