Thoracoscopic Vertebral Body Tethering for Adolescent Idiopathic Scoliosis: Follow-up Curve Behavior According to Sanders Skeletal Maturity Staging.

STUDY DESIGN: Retrospective analysis of prospectively collected data. OBJECTIVE: To report the follow-up curve behaviors in different Sanders staging groups. SUMMARY OF BACKGROUND DATA: Vertebral body tethering (VBT) is a growth modulation technique that allows gradual spontaneous follow-up curve correction as the patient grows. There is a lack of scientific evidence regarding appropriate patient selection and timing of implantation. METHODS: Patients were grouped into five as: Sanders 1, 2, 3, 4-5, and 6-7. Data were collected preoperatively, at the day before discharge, and at each follow-up. Outcome measures were pulmonary and mechanical complications, readmission, and reoperation rates. Demographic, perioperative, clinical, radiographic, and complication data were compared using Fisher-Freeman-Halton exact tests for categorical variables and Kruskal-Wallis tests for the continuous variables. RESULTS: Thirty-one (29 F, 2 M) consecutive patients with a minimum of 12 months of follow-up were included. The mean age at surgery was 12.1 (10-14). The mean follow-up was 27.1 (12-62) months. The mean preoperative main thoracic curve magnitude was 47°â€Š±â€Š7.6°. For all curves, preoperative and first erect curve magnitudes, bending flexibility, and operative correction percentages were similar between groups (for all comparisons, P > 0.05). The median height gained during follow-up was different between groups (P < 0.001), which was reflected into median curve correction during follow-up. Total curve correction percentage was different between groups (P = 0.009). Four (12.9%) patients had pulmonary and six (19.4%) had mechanical complications. One (3.2%) patient required readmission and two (6.5%) required reoperation. Occurrence of pulmonary complications was similar in Sanders groups (P = 0.804), while mechanical complications and overcorrection was significantly higher in Sanders 2 patients (P = 0.002 and P = 0.018). CONCLUSION: Follow-up curve behavior after VBT is different in patients having different Sanders stages. Sanders 2 patients experienced more overcorrection, thus timing and/or correction should be adjusted, since Sanders 3, 4, and 5 patients displayed a lesser risk of mechanical complications. LEVEL OF EVIDENCE: 3.

Ischemia modified albumin: does it change during pneumoperitoneum in robotic prostatectomies?

BACKGROUND: The unique positioning of the patient at steep Trendelenburg with prolonged and increased intra-abdominal pressure (IAP) during robotic radical prostatectomy may increase the risk of splanchnic ischemia. We aimed to investigate the acute effects of IAP and steep Trendelenburg position on the level of ischemia modified albumin (IMA) and to test if serum IMA levels might be used as a surrogate marker for possible covert ischemia during robotic radical prostatectomies. PATIENTS AND METHODS: Fifty ASA I-II patients scheduled for elective robotic radical prostatectomy were included in this investigation. EXCLUSION CRITERIA: The patients were excluded from the study when an arterial cannulation could not be accomplished, if the case had to be converted to open surgery or if the calculated intraoperative bleeding exceeded 300ml. All the patients were placed in steep (45 degrees) Trendelenburg position following trocar placement. Throughout the operation the IAP was maintained between 11-14mmHg. Mean arterial blood pressure (MAP), cardiac output (CO) were continuously monitored before the induction and throughout the surgery. Blood gases, electrolytes, urea, creatinine, alanine transferase (ALT), aspartate transferase (AST) were recorded. Additionally, IMA levels were measured before, during and after surgery. RESULTS: (1) MAP, CO, lactate and hemoglobin (Hb) did not significantly change in any period of surgery (p>0.05); (2) sodium (p<0.01), potassium (p<0.05) and urea (p<0.05) levels decreased at postoperative period, and no significant changes at creatinine, AST, ALT levels were observed in these patients; (3) At the end of surgery (180 min) pCO2, pO2, HCO3 and BE did not change compared to after induction values (p>0.05) but mild acidosis was present in these patients (p<0.01 vs. after induction); (4) IMA levels were found to be comparable before induction (0.34±0.04), after induction (0.31±0.06) and at the end of surgery (0.29±0.05) as well. CONCLUSION: We did not demonstrate any significant mesenteric-splanchnic ischemia which could be detected by serum IMA levels during robotic radical prostatectomies performed under steep Trendelenburg position and when IAP is maintained in between 11-14 mmHg.

Ischemia modified albumin: does it change during pneumoperitoneum in robotic prostatectomies?

ABSTRACT Background The unique positioning of the patient at steep Trendelenburg with prolonged and increased intra-abdominal pressure (IAP) during robotic radical prostatectomy may increase the risk of splanchnic ischemia. We aimed to investigate the acute effects of IAP and steep Trendelenburg position on the level of ischemia modified albumin (IMA) and to test if serum IMA levels might be used as a surrogate marker for possible covert ischemia during robotic radical prostatectomies. Patients and Methods Fifty ASA I-II patients scheduled for elective robotic radical prostatectomy were included in this investigation. Exclusion criteria The patients were excluded from the study when an arterial cannulation could not be accomplished, if the case had to be converted to open surgery or if the calculated intraoperative bleeding exceeded 300ml. All the patients were placed in steep (45 degrees) Trendelenburg position following trocar placement. Throughout the operation the IAP was maintained between 11-14mmHg. Mean arterial blood pressure (MAP), cardiac output (CO) were continuously monitored before the induction and throughout the surgery. Blood gases, electrolytes, urea, creatinine, alanine transferase (ALT), aspartate transferase (AST) were recorded. Additionally, IMA levels were measured before, during and after surgery. Results (1) MAP, CO, lactate and hemoglobin (Hb) did not significantly change in any period of surgery (p>0.05); (2) sodium (p<0.01), potassium (p<0.05) and urea (p<0.05) levels decreased at postoperative period, and no significant changes at creatinine, AST, ALT levels were observed in these patients; (3) At the end of surgery (180 min) pCO2, pO2, HCO3 and BE did not change compared to after induction values (p>0.05) but mild acidosis was present in these patients (p<0.01 vs. after induction); (4) IMA levels were found to be comparable before induction (0.34±0.04), after induction (0.31±0.06) ...

Comparative study of intravenous opioid consumption in the postoperative period.

BACKGROUND: Intravenous patient-controlled analgesia (IV PCA) using opiods is an accepted method for delivering postoperative analgesia. The aim of this study was to compare fentanyl and tramadol with IV PCA after spinal anesthesia (SA) and general anesthesia (GA) following cesarean section (C/S). METHODS: Ninety women were randomly assigned to three groups (n=30). Group 1 was treated with IV fentanyl PCA after SA. Groups 2 and 3 were treated with IV fentanyl PCA and IV tramadol PCA after GA. Outcome measures were recorded for the first 24 h post-anesthesia. RESULTS: PCA use was significantly lower after SA (P<0.05). Eighteen patients in the SA Group and 27 patients and 24 patients from the GA groups required additional opioid. Opioid consumption and patient satisfaction were similar for groups after GA (P>0.05). 638.4 ± 179.1 µg fentanyl was consumed by patients of Group 2, 356.3 ± 87.0 µg fentanyl and 559.5 ± 207.0 mg tramadol was consumed by Group 1 and Group 3 respectively. There was no significant difference in the overall severity and incidence of nausea, drowsiness or pruritus. CONCLUSION: Our study shows that analgesic consumption and post-operative pain scores after SA in C/S decreased, without increase in adverse reactions.

Esophageal balloon dilation in children: prospective analysis of hemodynamic changes and complications during general anesthesia.

STUDY OBJECTIVE: To investigate hemodynamic changes and complications in children during balloon dilation of esophageal strictures. DESIGN: Prospective, controlled study. SETTING: University teaching hospital. PATIENTS: 5 ASA physical status I and II pediatric patients with benign esophageal stricture related to ingestion of caustic substances. INTERVENTIONS: Anesthesia was induced with intravenous propofol two mg/kg and cisatracurium 0.2 mg/kg and maintained with 66% nitrous oxide and one minimum alveolar concentration of sevoflurane in oxygen. In each session, balloon size was increased until the stricture was opened. MEASUREMENTS AND RESULTS: A total of 18 sessions and 99 dilations in 5 children performed over a one-year period were included in the study. In 8 of 18 sessions, esophageal stricture was located in the middle one third of the esophagus; and in the others, in the upper one third. Four cases experienced bleeding; two cases, inability to ventilate due to obstruction of the endotracheal tube tip by the inflated balloon; and two cases, postextubation bronchospasm. In 95 of the 99 dilations, while the balloon was inflated, heart rate was faster and blood pressure increased significantly. CONCLUSION: Anesthesiologists should keep in mind the possibility of hemodynamic instability and possible endotracheal tube tip obstruction by the inflated balloon and safeguard the airway against bleeding, secretions, and radio-opaque fluid during esophageal balloon dilation.

Store-operated Ca2+ influx in airway smooth muscle: Interactions between volatile anesthetic and cyclic nucleotide effects.

BACKGROUND: Volatile anesthetics produce bronchodilation in part by depleting sarcoplasmic reticulum Ca stores in airway smooth muscle (ASM). Other bronchodilatory drugs are known to act via cyclic nucleotides (cyclic adenosine 3',5'-cyclic monophosphate, cyclic guanosine 3',5'-cyclic monophosphate). Intracellular Ca regulation in ASM involves plasma membrane Ca influx, including that triggered by sarcoplasmic reticulum Ca depletion (store-operated Ca entry [SOCE]). The authors hypothesized that anesthetics and bronchodilatory agents interact in inhibiting SOCE, thus enhancing ASM relaxation. METHODS: In enzymatically dissociated porcine ASM cells imaged using fluorescence microscopy, sarcoplasmic reticulum Ca was depleted by 1 microm cyclopiazonic acid in 0 extracellular Ca, nifedipine, and potassium chloride (preventing Ca influx through L-type channels and SOCE). Extracellular Ca was rapidly reintroduced to selectively activate SOCE in the presence or absence of 1 minimum alveolar concentration (MAC) halothane, isoflurane, or sevoflurane. Anesthetic interference with SOCE regulation by cyclic nucleotides was examined by activating SOCE in the presence of (1) 1 microm acetylcholine, (2) 100 microm dibutryl cyclic adenosine 3',5'-cyclic monophosphate, or (3) 100 microm 8-bromo-cyclic guanosine 3',5'-cyclic monophosphate. RESULTS: SOCE was enhanced by acetylcholine, whereas volatile anesthetics and both cyclic nucleotides partially inhibited Ca influx. Preexposure to 1 or 2 MAC anesthetic (halothane > isoflurane > sevoflurane) inhibited SOCE. Only halothane and isoflurane inhibited acetylcholine-induced augmentation of Ca influx, and significantly potentiated cyclic nucleotide inhibition such that no influx was observed in the presence of anesthetics and cyclic nucleotides. CONCLUSIONS: These data indicate that volatile anesthetics prevent sarcoplasmic reticulum refilling by inhibiting SOCE and enhancing cyclic nucleotide blunting of Ca influx in ASM. Such interactions likely result in substantial airway relaxation in the presence of both anesthetics and bronchodilatory agents such as beta agonists or nitric oxide.

Neurotrophin effects on intracellular Ca2+ and force in airway smooth muscle.

Neurotrophins [e.g., brain-derived neurotrophic factor (BDNF), neurotrophin 4 (NT4)], known to affect neuronal structure and function, are expressed in nonneuronal tissues including the airway. However, their function is unclear. We examined the effect of acute vs. prolonged neurotrophin exposure on regulation of airway smooth muscle (ASM) intracellular Ca(2+) concentration ([Ca(2+)](i)): sarcoplasmic reticulum (SR) Ca(2+) release and Ca(2+) influx (specifically store-operated Ca(2+) entry, SOCE). Human ASM cells were incubated for 30 min in medium (control) or 1 or 10 nM BDNF, NT3, or NT4 (acute exposure) or overnight in 1 nM BDNF, NT3, or NT4 (prolonged exposure) and imaged after loading with the Ca(2+) indicator fura-2 AM. [Ca(2+)](i) responses to ACh, histamine, bradykinin, and caffeine and SOCE following SR Ca(2+) depletion were compared across cell groups. Force measurements were performed in human bronchial strips exposed to neurotrophins. Basal [Ca(2+)](i), peak responses to all agonists, SOCE, and force responses to ACh and histamine were all significantly enhanced by both acute and prolonged BDNF exposure (smaller effect of NT4) but decreased by NT3. Inhibition of the BDNF/NT4 receptor trkB by K252a prevented enhancement of [Ca(2+)](i) responses. ASM cells showed positive immunostaining for BDNF, NT3, NT4, trkB, and trkC (NT3 receptor). These novel data demonstrate that neurotrophins influence ASM [Ca(2+)](i) and force regulation and suggest a potential role for neurotrophins in airway diseases.

Cyclic nucleotide regulation of store-operated Ca2+ influx in airway smooth muscle.

Sarcoplasmic reticulum (SR) Ca2+ release and plasma membrane Ca2+ influx are key to intracellular Ca2+ ([Ca2+]i) regulation in airway smooth muscle (ASM). SR Ca2+ depletion triggers influx via store-operated Ca2+ channels (SOCC) for SR replenishment. Several clinically relevant bronchodilators mediate their effect via cyclic nucleotides (cAMP, cGMP). We examined the effect of cyclic nucleotides on SOCC-mediated Ca2+ influx in enzymatically dissociated porcine ASM cells. SR Ca2+ was depleted by 1 microM cyclopiazonic acid in 0 extracellular Ca2+ ([Ca2+]o), nifedipine, and KCl (preventing Ca2+ influx through L-type and SOCC channels). SOCC was then activated by reintroduction of [Ca2+]o and characterized by several techniques. We examined cAMP effects on SOCC by activating SOCC in the presence of 1 microM isoproterenol or 100 microM dibutryl cAMP (cell-permeant cAMP analog), whereas we examined cGMP effects using 1 microM (Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA-NO nitric oxide donor) or 100 microM 8-bromoguanosine 3',5'-cyclic monophosphate (cell-permeant cGMP analog). The role of protein kinases A and G was examined by preexposure to 100 nM KT-5720 and 500 nM KT-5823, respectively. SOCC-mediated Ca2+ influx was dependent on the extent of SR Ca2+ depletion, sensitive to Ni2+ and La3+, but not inhibitors of voltage-gated influx channels. cAMP as well as cGMP potently inhibited Ca2+ influx, predominantly via their respective protein kinases. Additionally, cAMP cross-activation of protein kinase G contributed to SOCC inhibition. These data demonstrate that a Ni2+/La3+-sensitive Ca2+ influx in ASM triggered by SR Ca2+ depletion is inhibited by cAMP and cGMP via a protein kinase mechanism. Such inhibition may play a role in the bronchodilatory response of ASM to clinically relevant drugs (e.g., beta-agonists vs. nitric oxide).

Differential inhibition of neuronal Na+-Ca2+ exchange versus store-operated Ca2+ channels by volatile anesthetics in pheochromocytoma (PC12) cells.

BACKGROUND: Ca2+ influx is a key component of neuronal intracellular Ca2+ ([Ca2+]i) regulation. The authors hypothesized that volatile anesthetic inhibition of neuronal activity is mediated by inhibition of Ca2+ influx via two major mechanisms: plasma membrane Na+-Ca2+ exchange (NCX) and the novel mechanism of Ca2+ influx triggered by endoplasmic reticulum Ca2+ depletion (store-operated Ca2+ channels [SOCCs]). METHODS: Differentiated rat pheochromocytoma cells loaded with the Ca2+ indicator fura-2 were Na+-loaded with 0 Ca2+, 145 mm Na+ Tyrode's and 5 microm cyclopiazonic acid plus 10 microm ryanodine (functionally isolating plasma membrane). Influx-mode NCX was rapidly reactivated by 0 Na+ and 2.5 mm Ca2+. The protocol was repeated in the presence of volatile anesthetics (0.5-1.5 minimum alveolar concentration [MAC] halothane, isoflurane, or sevoflurane) or other drugs to characterize NCX. To examine SOCCs, endoplasmic reticulum Ca2+ was depleted by cyclopiazonic acid in 0 extracellular Ca2+, and Ca2+ influx was triggered by rapid reintroduction of extracellular Ca2+. The protocol was repeated in the presence of anesthetics or other drugs to characterize SOCCs. RESULTS: Influx via NCX was not inhibited by voltage-gated Ca2+ channel blockers but was sensitive to NCX inhibitors. Halothane and isoflurane (0.5-1.5 MAC) significantly inhibited NCX (P < 0.05; paired comparisons), whereas sevoflurane at less than 1.5 MAC did not inhibit NCX. SOCC-mediated Ca2+ influx was insensitive to a variety of Ca2+ channel blockers but was inhibited by Ni2+. Such influx was sensitive only to halothane at greater than 1 MAC but not isoflurane or sevoflurane. CONCLUSIONS: These data indicate that volatile anesthetics, especially halothane and isoflurane, interfere with neuronal [Ca2+]i regulation by inhibiting NCX but not SOCC-mediated Ca2+ influx (except high concentrations of halothane).

Effects of volatile anesthetics on store-operated Ca(2+) influx in airway smooth muscle.

BACKGROUND: In airway smooth muscle (ASM), volatile anesthetics deplete sarcoplasmic reticulum (SR) Ca(2+) stores by increasing Ca(2+) "leak." Accordingly, SR replenishment becomes dependent on Ca(2+) influx. Depletion of SR Ca(2+) stores triggers Ca(2+) influx via specific plasma membrane channels, store-operated Ca(2+) channels (SOCC). We hypothesized that anesthetics inhibit SOCC triggered by increased SR Ca(2+) "leak," preventing SR replenishment and enhancing ASM relaxation. METHODS: In porcine ASM cells, SR Ca was depleted by cyclopiazonic acid or caffeine in 0 extracellular Ca(2+), nifedipine and KCl (preventing Ca(2+) influx through L-type and SOCC channels). Extracellular Ca(2+) was rapidly introduced to selectively activate SOCC. After SOCC activation, SR was replenished and the protocol repeated in the presence of 1 or 2 minimum alveolar concentration halothane, isoflurane, or sevoflurane. In other cells, characteristics of SOCC and interactions between acetylcholine (Ach) and volatile anesthetics were examined. RESULTS: Cyclopiazonic acid produced slow SR leak, whereas the caffeine response was transient in ASM cells. Reintroduction of extracellular Ca(2+) rapidly increased [Ca(2+)]i. This influx was insensitive to nifedipine, SKF-96365, and KBR-7943, inhibited by Ni and blockade of inositol 1,4,5-triphosphate-induced SR Ca(2+) release, and enhanced by ACh. Preexposure to 1 or 2 minimum alveolar concentration halothane completely inhibited Ca(2+) influx when extracellular Ca(2+) was reintroduced, whereas isoflurane and sevoflurane produced less inhibition. Only halothane and isoflurane inhibited ACh-induced augmentation of Ca(2+) influx. CONCLUSION: Volatile anesthetics inhibit a Ni/La-sensitive store-operated Ca(2+) influx mechanism in porcine ASM cells, which likely helps maintain anesthetic-induced bronchodilation.

Pyloromyotomy in a patient with paramyotonia congenita.

UNLABELLED: A 2-mo-old infant with paramyotonia congenita was scheduled for pyloromyotomy and repair of inguinal hernia. Diagnosis of paramyotonia congenita was done with positive family history, myotonia at eyelids, provocation by cold, and electromyogram analysis. Anesthesia was induced via face mask with sevoflurane at 4 minimum alveolar anesthetic concentration in oxygen. Tracheal intubation was attempted without a neuromuscular relaxant. Anesthesia was maintained with sevoflurane at 0.5 minimum alveolar anesthetic concentration in oxygen and remifentanil infusion at a rate of 0.2 micro g. kg(-1). min(-1). After discontinuation of sevoflurane and remifentanil, the patient was awake and had full recovery of muscle activity. IMPLICATIONS: The literature concerning general anesthesia in paramyotonic patients is limited. We report a case of paramyotonia congenita in a 2-mo-old male infant undergoing surgery for pyloric stenosis and inguinal hernia after an uneventful anesthesia.

Store-operated Ca2+ entry in porcine airway smooth muscle.

Ca(2+) influx triggered by depletion of sarcoplasmic reticulum (SR) Ca(2+) stores [mediated via store-operated Ca(2+) channels (SOCC)] was characterized in enzymatically dissociated porcine airway smooth muscle (ASM) cells. When SR Ca(2+) was depleted by either 5 microM cyclopiazonic acid or 5 mM caffeine in the absence of extracellular Ca(2+), subsequent introduction of extracellular Ca(2+) further elevated [Ca(2+)](i). SOCC was insensitive to 1 microM nifedipine- or KCl-induced changes in membrane potential. However, preexposure of cells to 100 nM-1 mM La(3+) or Ni(2+) inhibited SOCC. Exposure to ACh increased Ca(2+) influx both in the presence and absence of a depleted SR. Inhibition of inositol 1,4,5-trisphosphate (IP)-induced SR Ca(2+) release by 20 microM xestospongin D inhibited SOCC, whereas ACh-induced IP(3) production by 5 microM U-73122 had no effect. Inhibition of Ca(2+) release through ryanodine receptors (RyR) by 100 microM ryanodine also prevented Ca(2+) influx via SOCC. Qualitatively similar characteristics of SOCC-mediated Ca(2+) influx were observed with cyclopiazonic acid- vs. caffeine-induced SR Ca(2+) depletion. These data demonstrate that a Ni(2+)/La(3+)-sensitive Ca(2+) influx via SOCC in porcine ASM cells involves SR Ca(2+) release through both IP(3) and RyR channels. Additional regulation of Ca(2+) influx by agonist may be related to a receptor-operated, noncapacitative mechanism.

QT dispersion increases during intubation in patients with coronary artery disease.

Anesthetic drugs have been shown to increase QT interval, however data regarding their effects on QT dispersion (QTd) are scarce, especially in patients with coronary artery disease (CAD). We tested whether induction of Anesthesia with thiopental and etomidate would increase QTd in patients with CAD. Thirty American Society of Anesthesiologists (ASA) physical status I-II patients without CAD were randomly allocated to groups I (n = 15) and II (n = 15) and 30 ASA physical status III patients with CAD were randomly allocated to groups III (n = 15) and IV (n=15). Anesthesia was induced with thiopental 5-7 mg/kg IV in groups I and III and with etomidate 0.2-0.3 mg/kg IV in groups II and IV. Endotracheal intubation was facilitated with vecuronium bromide 0.1 mg/kg IV. Twelve-lead electrocardiogram (ECG) was recorded in all patients at baseline (ECG(1)), 1 min after the induction agent (ECG(2)), 1 min (ECG(3)) and 5 min (ECG(4)) after intubation. Anesthesia was maintained with isoflurane and nitrous oxide in 34 % oxygen after ECG(2) recording. QTd and corrected QT dispersion (QTcd) were calculated. In patients with CAD induced with thiopental, QT dispersion increased significantly during the intubation period compared with baseline (from 43.0 +/- 25.6 ms to 69.2 +/- 25.3 ms; P <.01). Likewise, QT dispersion also increased during intubation in patients with CAD induced with etomidate (from 41.5 +/- 17.2 ms to 80.0 +/- 33.6 ms; P <.001). There was no increase in QT dispersion in patients without known CAD. QT dispersion seems to be increased during the intubation period in patients with CAD regardless of the induction agents used.