Readmission after orthognathic surgery.

OBJECTIVE: To evaluate the readmission rate after orthognathic surgery and identify associated risk factors. STUDY DESIGN: Retrospective analysis of patients who underwent orthognathic surgery and had an unexpected hospital admission, with or without return to the operating room (OR), within the first postoperative year. Study variables included sex, age, American Society of Anesthesiologists (ASA) status, type of surgery, concomitant third molar extraction, concomitant genioplasty, duration of surgery, first assistant experience, and duration of hospitalization. Bivariate associations were calculated between variables and readmission status. Chi-square and Fisher's Exact tests were used to compare categorical variables, and a 2-sample t test was used to compare continuous variables. RESULTS: There were 701 patients included in the study. The readmission rate was 9.70%. Twelve patients were managed non-surgically, and 56 patients required an OR procedure. The most common reason for readmission without return to the OR was an infection, and for reoperation was hardware removal. Age, sex, type of surgery, third molar extraction, genioplasty, duration of surgery, and experience of first assistant were not found to be predictors for readmission. CONCLUSIONS: Only ASA classification and duration of initial hospitalization were significant risk factors for readmission of patients within the first postoperative year after orthognathic surgery.

Impact of depth of invasion on local recurrence in R0 resected node-negative oral tongue squamous cell carcinoma.

BACKGROUND: This study evaluates the impact of depth of invasion (DOI) on local recurrence (LR) in node-negative oral tongue squamous cell carcinoma (SCC). METHODS: Fifty-one patients were retrospectively reviewed from an institutional database. Patients were evaluated for local control (LC). Cox-proportional hazards modeling was used to calculate hazard ratios. RESULTS: There were 84.3% T1/2 and 15.7% T3/4 classification tumors. The 3-year overall survival rate was 97.9%. Local failure rate was 5.7% with a 3-year LC of 93.6%. On Univariate analysis, increased hazard of LR was noted with each unit increase in DOI (HR 1.40, 95% CI 1.07-1.83, p = 0.014). Age, sex, T classification, margins ≥5 mm, lymphovascular invasion (LVI) and perineural invasion (PNI), and adjuvant treatment were not associated with LR. On Multivariate analysis, adjusting for age and adjuvant treatment, results for DOI remained significant (aHR 1.46, 95% CI 1.08-1.98, p = 0.013). CONCLUSION: On evaluation of our institutional dataset increasing DOI was associated with increased hazard of local recurrence with oral tongue SCC.

Calcium sensitization involved in dexmedetomidine-induced contraction of isolated rat aorta.

Dexmedetomidine, a full agonist of the α2B-adrenoceptor that is mainly involved in vascular smooth muscle contraction, is primarily used for analgesia and sedation in intensive care units. High-dose dexmedetomidine produces hypertension in children and adults. The goal of this in vitro study was to investigate the role of the calcium (Ca(2+)) sensitization mechanism involving Rho-kinase, protein kinase C (PKC), and phosphoinositide 3-kinase (PI3-K) in mediating contraction of isolated rat aortic smooth muscle in response to dexmedetomidine. The effect of dexmedetomidine on the intracellular Ca(2+) level ([Ca(2+)]i) and tension was measured simultaneously. Dexmedetomidine concentration-response curves were generated in the presence or absence of the following antagonists: rauwolscine, Y 27632, LY 294002, GF 109203X, and verapamil. Dexmedetomidine-induced phosphorylation of PKC and membrane translocation of Rho-kinase were detected with Western blotting. Rauwolscine, Y 27632, GF 109203X, LY 294002, and verapamil attenuated dexmedetomidine-induced contraction. The slope of the [Ca(2+)]i-tension curve for dexmedetomidine was higher than that for KCl. Dexmedetomidine induced phosphorylation of PKC and membrane translocation of Rho-kinase. These results suggest that dexmedetomidine-induced contraction involves a Ca(2+) sensitization mechanism mediated by Rho-kinase, PKC, and PI3-K that is secondary to α2-adrenoceptor stimulation in rat aortic smooth muscle.

Levobupivacaine-induced contraction of isolated rat aorta is calcium dependent.

Levobupivacaine is a long-acting local anesthetic that intrinsically produces vasoconstriction in isolated vessels. The goals of this study were to investigate the calcium-dependent mechanism underlying levobupivacaine-induced contraction of isolated rat aorta in vitro and to elucidate the pathway responsible for the endothelium-dependent attenuation of levobupivacaine-induced contraction. Isolated rat aortic rings were suspended to record isometric tension. Cumulative levobupivacaine concentration-response curves were generated in either the presence or absence of the antagonists verapamil, nifedipine, SKF-96365, 2-aminoethoxydiphenylborate, Gd(3+), N(W)-nitro-l-arginine methyl ester (L-NAME), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), and methylene blue, either alone or in combination. Verapamil, nifedipine, SKF-96365, 2-aminoethoxydiphenylborate, low calcium concentrations, and calcium-free Krebs solution attenuated levobupivacaine-induced contraction. Gd(3+) had no effect on levobupivacaine-induced contraction. Levobupivacaine increased intracellular calcium levels in vascular smooth muscle cells. L-NAME, ODQ, and methylene blue increased levobupivacaine-induced contraction in endothelium-intact aorta. SKF-96365 attenuated calcium-induced contraction in a previously calcium-free isotonic depolarizing solution containing 100 mmol/L KCl. Levobupivacaine-induced contraction of rat aortic smooth muscle is mediated primarily by calcium influx from the extracellular space mainly via voltage-operated calcium channels and, in part, by inositol 1,4,5-trisphosphate receptor-mediated release of calcium from the sarcoplasmic reticulum. The nitric oxide - cyclic guanosine monophosphate pathway is involved in the endothelium-dependent attenuation of levobupivacaine-induced contraction.

c-Jun NH2-terminal kinase contributes to dexmedetomidine-induced contraction in isolated rat aortic smooth muscle.

PURPOSE: Dexmedetomidine, a full agonist of α2B-adrenoceptors, is used for analgesia and sedation in the intensive care units. Dexmedetomidine produces an initial transient hypertension due to the activation of post-junctional α2B-adrenoceptors on vascular smooth muscle cells (SMCs). The aims of this in vitro study were to identify mitogen-activated protein kinase (MAPK) isoforms that are primarily involved in full, α2B-adrenoceptor agonist, dexmedetomidine-induced contraction of isolated rat aortic SMCs. MATERIALS AND METHODS: Rat thoracic aortic rings without endothelium were isolated and suspended for isometric tension recording. Cumulative dexmedetomidine (10⁻9 to 10⁻6 M) dose-response curves were generated in the presence or absence of extracellular signal-regulated kinase (ERK) inhibitor PD 98059, p38 MAPK inhibitor SB 203580, c-Jun NH2-terminal kinase (JNK) inhibitor SP 600125, L-type calcium channel blocker (verapamil and nifedipine), and α2-adrenoceptor inhibitor atipamezole. Dexmedetomidine-induced phosphorylation of ERK, JNK, and p38 MAPK in rat aortic SMCs was detected using Western blotting. RESULTS: SP 600125 (10⁻6 to 10⁻5 M) attenuated dexmedetomidine-evoked contraction in a concentration- dependent manner, whereas PD 98059 had no effect on dexmedetomidine- induced contraction. SB 203580 (10⁻5 M) attenuated dexmedetomidine-induced contraction. Dexmedetomidine-evoked contractions were both abolished by atipamezole and attenuated by verapamil and nifedipine. Dexmedetomidine induced phosphorylation of JNK and p38 MAPK in rat aortic SMCs, but did not induce phosphorylation of ERK. CONCLUSION: Dexmedetomidine-induced contraction involves a JNK- and p38 MAPK-mediated pathway downstream of α2-adrenoceptor stimulation in rat aortic SMCs. In addition, dexmedetomidine-induced contractions are primarily dependent on calcium influx via L-type calcium channels.

Lipid emulsion reverses Levobupivacaine-induced responses in isolated rat aortic vessels.

BACKGROUND: The goal of this in vitro study was to investigate the effects of lipid emulsion (LE) on local anesthetic levobupivacaine-induced responses in isolated rat aorta and to determine whether the effect of LE is related to the lipid solubility of local anesthetics. METHODS: Isolated rat aortic rings were suspended for isometric tension recording. The effects of LE were determined during levobupivacaine-, ropivacaine-, and mepivacaine-induced responses. Endothelial nitric oxide synthase and caveolin-1 phosphorylation was measured in human umbilical vein endothelial cells treated with levobupivacaine alone and with the addition of LE. RESULTS: Levobupivacaine produced vasoconstriction at lower, and vasodilation at higher, concentrations, and both were significantly reversed by treatment with LE. Levobupivacaine and ropivacaine inhibited the high potassium chloride-mediated contraction, which was restored by LE. The magnitude of LE-mediated reversal was greater with levobupivacaine treatment than with ropivacaine, whereas this reversal was not observed in mepivacaine-induced responses. In LE-pretreated rings, low-dose levobupivacaine- and ropivacaine-induced contraction was attenuated, whereas low-dose mepivacaine-induced contraction was not significantly altered. Treatment with LE also inhibited the phosphorylation of endothelial nitric oxide synthase induced by levobupivacaine in human umbilical vein endothelial cells. CONCLUSIONS: These results indicate that reversal of levobupivacaine-induced vasodilation by LE is mediated mainly through the attenuation of levobupivacaine-mediated inhibition of L-type calcium channel-dependent contraction and, in part, by inhibition of levobupivacaine-induced nitric oxide release. LE-mediated reversal of responses induced by local anesthetics may be related to their lipid solubility.

Acute respiratory alkalosis occurring after endoscopic third ventriculostomy -A case report-.

An endoscopic third ventriculostomy was performed in a 55-year-old man with an obstructive hydrocephalus due to aqueductal stenosis. The vital signs and laboratory studies upon admission were within the normal limits. Anesthesia was maintained with nitrous oxide in oxygen and 6% desflurane. The patient received irrigation with approximately 3,000 ml normal saline during the procedure. Anesthesia and operation were uneventful. However, he developed postoperative hyperventilation in the recovery room, and arterial blood gas analysis revealed acute respiratory alkalosis. We report a rare respiratory alkalosis that occurred after an endoscopic third ventriculostomy.