Anesthesia and analgesia
-
Anesthesia and analgesia · Dec 2011
Review Case ReportsApparent dexmedetomidine-induced polyuric syndrome in an achondroplastic patient undergoing posterior spinal fusion.
A 40-year-old achondroplastic patient underwent posterior spinal fusion under general endotracheal anesthesia. Anesthesia was maintained with isoflurane, and sufentanil, dexmedetomidine, and lidocaine infusions. Urine output increased from 150 mL/hr to 950 mL/hr the fourth hour. ⋯ Within 2 hours of discontinuing the dexmedetomidine infusion urine output greatly decreased. Within 24 hours all signs of the polyuric syndrome resolved spontaneously. Alpha(2) agonists block arginine-vasopressin release and action; however, a polyuric syndrome has not been reported in the human literature.
-
Anesthesia and analgesia · Dec 2011
ReviewShortage of perioperative drugs: implications for anesthesia practice and patient safety.
Several medications used in clinical perioperative medicine are currently cited on the national shortage list. Medication shortages may be attributed to lack of raw materials, manufacturing issues, and discontinuation of production. Medication shortage has a substantial impact on patient care, and is responsible for creating an environment conducive to an increase in medication errors. Anesthesiologists should be taking an active role with the pharmacy and hospital management to alert caregivers and help to prevent adverse effects on patient care and safety.
-
Anesthesia and analgesia · Dec 2011
Comparative StudyMorphine-induced epidermal growth factor pathway activation in non-small cell lung cancer.
Epidermal growth factor receptor (EGFR) is coactivated by the μ-opioid receptor (MOR), expressed on non-small cell lung cancer (NSCLC) cells and human lung cancer. We hypothesized that clinically used opioid analgesics that are MOR agonists coactivate EGFR, resulting in growth- and survival-promoting signaling. ⋯ Morphine-induced phosphorylation of EGFR occurs via ORs, leading to downstream MAPK/ERK, Akt phosphorylation, cell proliferation, and increased invasion. Notably, ORs are also associated with EGF-induced phosphorylation of EGFR. Increased coexpression of MOR and EGFR in human lung cancer suggests that morphine may have a growth-promoting effect in lung cancer.
-
Anesthesia and analgesia · Dec 2011
Comparative Study2-Deoxy-D-glucose attenuates isoflurane-induced cytotoxicity in an in vitro cell culture model of H4 human neuroglioma cells.
β-Amyloid protein (Aβ) accumulation and caspase activation have been shown to contribute to Alzheimer disease neuropathogenesis. Aβ is produced from amyloid precursor protein through proteolytic processing by aspartyl protease β-site amyloid precursor protein-cleaving enzyme (BACE). The inhaled anesthetic isoflurane has been shown to induce caspase activation and increase levels of BACE and Aβ. However, the underlying mechanisms and interventions of the isoflurane-induced neurotoxicity remain largely to be determined. The glucose analog 2-deoxy-d-glucose (2-DG) has neuroprotective effects. Therefore, we sought to determine whether 2-DG can reduce caspase-3 activation and the increase in the levels of BACE and reactive oxygen species (ROS) induced by isoflurane. ⋯ These results suggest that 2-DG may decrease oxidative stress and increase cytosolic calcium levels, thus attenuating isoflurane-induced neurotoxicity.
-
Anesthesia and analgesia · Dec 2011
ReviewActivation of the hemostatic system during cardiopulmonary bypass.
Cardiopulmonary bypass (CPB) is a unique clinical scenario that results in widespread activation of the hemostatic system. However, surgery also results in normal increases in coagulation activation, platelet activation, and fibrinolysis that are associated with normal wound hemostasis. Conventional CPB interferes with normal hemostasis by diluting hemostatic cells and proteins, through reinfusion of shed blood, and through activation on the bypass circuit surface of multiple systems including platelets, the kallikrein-kinin system, and fibrinolysis. ⋯ Additionally, strategies used to reduce this activation are discussed, including limiting cardiotomy suction, increasing circuit biocompatibility, antithrombin supplementation, and antifibrinolytic use. Determining which patients will most benefit from specific therapies will ultimately require investigation into genetic phenotypes of coagulation protein expression. Until that time, however, a combination of approaches to reduce the hemostatic activation from CPB seems warranted.