Antinausea Protocol Reduces Hospital Length of Stay for Laparoscopic Nissen Fundoplication.

OBJECTIVE: The perioperative course of patients undergoing laparoscopic Nissen fundoplication (LNF) was reviewed to determine whether the use of a new treatment protocol consisting of total intravenous anesthesia (TIVA) plus triple antiemetic therapy was associated with shorter hospital length of stay (HLOS). DESIGN: Retrospective cohort. SETTING: Single academic center. PARTICIPANTS: The study comprised 448 patients. Fifty-four patients undergoing LNF who received TIVA were compared with 394 who received standard inhalational anesthesia (non-TIVA) between January 2010 and June 2017. INTERVENTIONS: Patients who received TIVA were compared with those who received non-TIVA. MEASUREMENTS AND MAIN RESULTS: In multivariate analysis, TIVA was significantly associated with reduced HLOS (odds ratio 2.91, 95% confidence interval 1.47-5.78) and a 7.8% reduction in cost of care (p < 0.01). Female sex, length of surgery, and older age all were negatively associated with length of stay. The association between the use of TIVA and reduced HLOS and institutional cost was compared using univariate and multivariate analyses. CONCLUSIONS: The use of TIVA in patients undergoing uncomplicated LNF shortens HLOS and is associated with reduced cost of care. This study illustrates that communication among surgeons and anesthesiologists results in improved patient care.

Introduction of Microwave Ablation Into a Renal Ablation Practice: Valuable Lessons Learned.

OBJECTIVE: The purpose of this study was to evaluate the early outcomes of percutaneous microwave ablation (MWA) for clinical stage T1 (cT1) renal masses when performed within a high-volume ablation practice with critical emphasis on procedural safety. MATERIALS AND METHODS: A retrospective review of a percutaneous renal ablation registry identified 26 patients with a total of 27 cT1 renal masses treated with MWA between 2011 and 2017. Mean patient age was 63.8 years and 16 (61.5%) patients were male. Mean renal mass size ± SD was 2.3 ± 0.8 cm (range, 1.1-4.7 cm). The main outcome parameters investigated were technical success, local tumor progression, survival rates, and complications. Complications were categorized using the Clavien-Dindo classification system. Rates of local progression-free and cancer-specific survival (PFS and CSS, respectively) were estimated using the Kaplan-Meier method. RESULTS: Technical success was 100% on contrast-enhanced CT or MRI performed immediately after renal MWA. Twenty-four patients (92%) with 25 tumors had follow-up imaging for 3 months or longer (mean, 20.6 ± 11.6 months), with no local tumor recurrences identified. Estimated 3-year local PFS and CSS were 96% and 94%, respectively. The overall complication rate was 19.2%; two patients (7.7%) experienced minor complications (grade I or II) and three patients (11.5%) experienced major bleeding or urinary-related complications (grade III or higher), including one death. CONCLUSION: This study suggests that percutaneous MWA is a promising minimally invasive treatment option for cT1 renal masses. Nonetheless, major bleeding and urinary-related complications can occur, and further studies are needed to determine optimal patient and tumor selection for renal MWA.

Comprehensive assessment of renal tumour complexity in a large percutaneous cryoablation cohort.

OBJECTIVE: To evaluate the association between renal tumour complexity and outcomes in a large cohort of patients undergoing percutaneous cryoablation (PCA). PATIENTS AND METHODS: Patients with renal tumours treated with PCA were identified using our prospectively maintained ablation registry (2003-2015). Salvage procedures and inherited tumour syndromes were excluded. The associations between R.E.N.A.L. nephrometry score (NS) and risk of complications, renal function impairment, local failure and cancer-specific mortality (CSM) were evaluated using univariate and multivariable logistic, linear and Cox regression models. RESULTS: The cohort included 618 tumours treated during 580 procedures in 565 patients. The median (interquartile range [IQR]) follow-up was 34 (14.66) months. Complications (any grade) during a procedure (n[total] = 87, 15%) were more frequent with higher NS (NS 4-6: 10%; NS 7-9: 14%; NS 10-12: 36%; P < 0.001). Higher NS was independently associated with risk of complications (odds ratio [OR; per 1 point] = 1.3; 95% confidence interval [CI] 1.2-1.5; P < 0.001). Of all the NS components, tumour size was the most strongly associated with complication risk (OR 3.4; 95% CI 2.2-5.2; P < 0.001). The median (IQR) decline in glomerular filtration rate (GFR) from baseline was 9% (0, 22) at last follow-up. Each additional point in NS was associated with a 1.3% (95% CI 0.4-2.1; P = 0.005) greater GFR decline from baseline. NS was not significantly associated with local failure (n [total] = 14, 2%; NS 4-6: 2%; NS 7-9: 3%; NS 10-12: 5%; P = 0.32) or CSM (n [total] = 8, 2%; NS 4-6: 2%; NS 7-9: 3%; NS 10-12: 2%; P = 0.88). CONCLUSION: In high-complexity tumours PCA was associated with a tumour size-driven increased risk of post-procedural complications. Higher NS was associated with a small, clinically minor additional decline in renal function. Risks for local failure and CSM were low, regardless of tumour complexity.

Time to extubation during propofol anesthesia for spine surgery with sufentanil compared with fentanyl: a retrospective cohort study.

STUDY DESIGN: Retrospective cohort study. OBJECTIVE: This study compares time to extubation between major spine surgery patients anesthetized with fentanyl versus sufentanil infusions in combination with propofol. SUMMARY OF BACKGROUND DATA: In patients undergoing spinal fusion with intraoperative electrophysiological monitoring of the spinal cord, total intravenous anesthesia with a propofol/opioid combination results in better electrophysiological signals compared with volatile anesthetics. Pharmacokinetic data suggest that total intravenous anesthesia with sufentanil should lead to more rapid emergence from anesthesia than with fentanyl. However, this has never been tested in the spine surgery patient population. METHODS: With institutional review board approval, all major spine patients receiving a propofol-based total intravenous anesthesia with fentanyl were compared with those receiving sufentanil. Time to extubation, defined as the time from surgical closure to tracheal extubation, was the study outcome. Relevant demographic, anthropomorphic, anesthetic, and surgical data were collected. Association between type of opioid and time to extubation was tested for statistical significance. Multiple linear regression analysis was used to control for confounders. RESULTS: A total of 167 patients met inclusion criteria (fentanyl = 72, sufentanil = 95). There was no statistically significant difference between the 2 groups in terms of baseline characteristics. Time from surgical closure to extubation in the fentanyl versus sufentanil groups was not statistically different (mean [SD]: 40.2 [26.7] min vs. 45.0 [36.9] min; P = 0.36). On multivariate analysis, total dose of propofol and male sex were associated with increased time to extubation. CONCLUSION: The use of sufentanil may not reduce time to extubation compared with fentanyl despite its favorable pharmacokinetic profile. Higher doses of propofol and male sex were associated with longer time to extubation and seem to play a greater role than choice of opioid. LEVEL OF EVIDENCE: 3.

Intraoperative adrenal insufficiency in a patient with prader-willi syndrome.

Prader-Willi syndrome (PW) is a rare genetic disorder with multi-organ system involvement. These patients present many perioperative challenges including sleep-related breathing disorders, morbid obesity, thick salivary secretions, mental retardation, and difficult intravenous access. PW has been suggested to be associated with central adrenal insufficiency. We report a novel case of persistent severe hypotension from previously undiagnosed and asymptomatic adrenal insufficiency in a pediatric patient with Prader-Willi syndrome during spine surgery that resolved upon treatment with hydrocortisone.

Ca2+: is there something new for the cardiovascular anesthesiologist?

PURPOSE OF REVIEW: Anesthesiologists are frequently called upon to treat abnormalities of heart rhythm or pumping ability. Intracellular Ca is crucial for normal excitation-contraction coupling in the heart and plays a major role in the sequence of events that starts with an electrical signal generated in the atria and ends with myocardial contraction. RECENT FINDINGS: From controlled diffusion within the cell to a potential role as a biological clock, intracellular Ca is receiving a great deal of attention. For example, the pacemaking electrical signal is known to originate in the sinoatrial node myocyte, but exactly what role Ca plays is controversial despite the fact that the sinoatrial node was discovered over 100 years ago. Basic mechanisms involved in disease processes such as atrial fibrillation and new interventions for heart rate control are beginning to emerge. New discoveries in ventricular myocytes are also stimulating the development of promising therapeutic interventions to safely increase the pumping ability of the heart. SUMMARY: As our understanding of cardiac physiology and pharmacology progresses at the subcellular and molecular levels, new therapies will continue to emerge and the practice of anesthesia will benefit greatly.

The effect of isoflurane during reoxygenation on the sarcoplasmic reticulum and cellular injury in isolated ventricular myocytes.

In contrast to pretreatment with isoflurane its benefit when applied during reperfusion in rat hearts was only modest. As cellular injury during reoxygenation is greatly determined by sarcoplasmic reticulum (SR) calcium [Ca2+] handling we investigated the effect of isoflurane after simulated ischemia in rat ventricular myocytes. Hypoxic metabolic inhibition was induced by exposure to an acidic medium (pH: 6.3) containing deoxyglucose. Ambient pO2 was reduced to <15 mm Hg. After 30 min, cells were reoxygenated for 30 min with a glucose containing medium (pH: 7.4) in air (Air) or in the presence of isoflurane (Iso), or two SR blockers, i.e. either 3 microM ryanodine (Rya) or 10 microM of cyclopiazonic acid (CPA). During inhibition, diastolic cytosolic calcium ([Ca2+]i) increased and systolic cell shortening decreased. [Ca2+]i further increased in all groups towards the end of reoxygenation. However, [Ca2+]i in the Iso and the Rya group climbed twice as high as in the Air and the CPA group (P < 0.05). Hypercontracture occurred in 23% and 18% in the Iso and the Rya and in 10% and 9% in the Air and the CPA group, respectively (P < 0.05). Cell relengthening and shortening was impaired in Iso, Rya, and CPA treated cells (P < 0.05 vs. Air). Isoflurane given solely during reoxygenation appears to augment cellular injury. Its action seems to be blockade of SR Ca2+ release and Ca2+ efflux. SR Ca2+ overload induces spontaneous Ca2+ oscillations that cause hypercontracture. However, [Ca2+]i does not independently govern cellular systolic and diastolic dysfunction.

Dynamics of crossbridge-mediated activation in the heart.

Both intracellular calcium and strongly bound crossbridges contribute to thin filament activation in the heart, but the magnitude and the duration of the effects due to crossbridges are not well characterized. In this study, crossbridge attachment was altered in tetanized ferret papillary muscles and changes in the rate constant for the recovery of force (k (TR)) and unloaded shortening velocity (V (U)) were measured to track thin filament activation. k (TR) decreased as the time the muscles spent at low levels of crossbridge attachment (shortening deactivation) increased (0.02 s=17.9+/-2.3 s(-1), 0.32 s=3.3+/-0.4 s(-1); half-time=0.052 s; P<0.05). Furthermore, the deactivation was reversible and k (TR) recovered when muscles were allowed to regenerate force isometrically during the same tetanus. V (U) also decreased when the preceding load was lower (isometric load, V (U)=1.93+/-0.26 muscle lengths/s (ML/s); zero load, V (U)=0.93+/-0.14 ML/s, P<0.05) and as the length of time the muscle spent unloaded increased (>60% decline after 0.3 s). In addition, V (U) recovered when the muscle was allowed to regenerate force isometrically. These results indicate that crossbridge attachment increases thin filament activation as reflected in measurements of V (U) and k (TR). This 'extra' activation by crossbridges appears to be a dynamic process that decays during unloaded shortening and redevelops during isometric contraction.

Increased tolerance to hypoxic metabolic inhibition and reoxygenation of cardiomyocytes from apolipoprotein E-deficient mice.

Although hypercholesterolemia is a strong risk factor for cardiovascular disease, it has in some instances paradoxically been associated with reduced infarct size and preserved contractile function in isolated hearts after ischemia and reperfusion. To elucidate potential cellular protective mechanisms, myocytes of hypercholesterolemic apolipoprotein E-deficient (ApoE-/-) and wild-type mice were subjected to hypoxic metabolic inhibition (I) with subsequent reoxygenation (R). Intracellular Ca2+ concentration ([Ca2+]i) and pH (pHi) were monitored as well as cell length and arrhythmic events. Force measurements in papillary muscles were also recorded, and myocardial expression of Na+/H+ exchanger 1 (NHE1) and three Ca2+ handling proteins [sarco(endo)plasmic reticulum Ca2+-ATPase, Na+/Ca2+ exchanger, and plasma membrane Ca2+-ATPase] was quantified. After 30 min of I and 35 min of R, Ca2+ overload was more pronounced in wild-type cells (P < 0.05). In these myocytes, pHi also dropped faster and remained below those values determined in ApoE-/- cells (P < 0.05). Furthermore, more wild-type myocytes remained in a contracted state (P < 0.05). This group also showed a higher incidence of arrhythmic events during R (P < 0.05). No group difference was found in the expression of the Ca2+ handling proteins. However, NHE1 protein was downregulated in hearts of ApoE-/- mice (P < 0.05). Histological results depict hyperplasia in ApoE-/- hearts without atherosclerosis of the coronaries. Contractile dysfunction was not observed in papillary muscles from ApoE-/- hearts. Our results suggest that downregulated myocardial NHE1 expression in hypercholesterolemic ApoE-/- mice could have contributed to increased tolerance to I/R. It remains to be elucidated whether NHE1 downregulation is a unique feature of these genetically altered animals.

The impact of isoflurane during simulated ischemia/reoxygenation on intracellular calcium, contractile function, and arrhythmia in ventricular myocytes.

Some of isoflurane's cellular actions, such as interference with intracellular Ca(2+) handling, inhibition of the respiratory chain, and the capability to produce oxygen radicals, could result in impaired cellular function during ischemia/reoxygenation (I/R). We investigated the effects of isoflurane applied during I/R on intracellular Ca(2+), oxygen radical formation, arrhythmic events, and contractile function in rat cardiomyocytes. Single ventricular myocytes were subjected to 30 min of simulated ischemia followed by 30 min of reoxygenation. After baseline measurements, isoflurane-treated cells were exposed to 1 minimum alveolar concentration of isoflurane in air, whereas control cells were exposed to air only. Cytosolic Ca(2+) overload was observed in the isoflurane group (P < 0.05). During ischemia, systolic cell shortening decreased in both groups. In the isoflurane group, arrhythmic events and hypercontracture occurred more often during I/R, and the recovery of contractility during reoxygenation was less marked (P < 0.05). Furthermore, increased oxygen radical generation was detected in isoflurane-treated myocytes during reoxygenation (P < 0.05). Isoflurane given during I/R in this study induced intracellular Ca(2+) accumulation and impaired cell function. These potentially harmful effects were associated with a diminished Ca(2+) clearance and an accelerated oxygen radical production.

Effects of isoflurane and sevoflurane on intracellular calcium and contractility in pressure-overload hypertrophy.

BACKGROUND: Depression of myocardial contractility as a result of isoflurane appears to be greater in myocardial hypertrophy, and the cellular basis for this difference in susceptibility is not clear. In this study we examined the effects of isoflurane and sevoflurane on contractility and intracellular calcium in an animal model of pressure-overload hypertrophy. METHODS: Pressure-overload hypertrophy was established in young male ferrets by banding the main pulmonary artery for 1 month and the effects of isoflurane and sevoflurane on contractility and intracellular calcium ([Ca]i) were examined in isolated right ventricular papillary muscles, trabeculae, and myocytes. Intracellular calcium was measured with the bioluminescent photoprotein aequorin in isolated papillary muscles, and also with the fluorescent indicator fluo-3 in isolated ventricular myocytes. In addition, Ca sensitivity was assessed in isolated trabeculae after disruption of the surface membrane with a nonionic detergent (skinned fibers). RESULTS: In the presence of isoflurane and sevoflurane, papillary muscles from banded animals exhibited a greater depression of contractility and isolated ventricular myocytes showed a greater decrease in peak [Ca]i. Furthermore, baseline calcium sensitivity was decreased and the slope of the relationship between [Ca] and force was increased in skinned trabeculae from banded animals. Isoflurane decreased calcium sensitivity in trabeculae from both normal and banded animals. CONCLUSIONS: These results suggest that changes in [Ca]i and altered calcium sensitivity are both responsible for the exaggerated effects of some volatile anesthetics on contractility in pressure-overload hypertrophy.

Isotonic force modulates force redevelopment rate of intact frog muscle fibres: evidence for cross-bridge induced thin filament activation.

We tested the hypothesis that force-velocity history modulates thin filament activation, as assessed by the rate of force redevelopment after shortening (+dF/dt(R)). The influence of isotonic force on +dF/dt(R) was assessed by imposing uniform amplitude (2.55 to 2.15 microm sarcomere(-1)) but different speed releases to intact frog muscle fibres during fused tetani. Each release consisted of a contiguous ramp- and step-change in length. Ramp speed was changed from release to release to vary fibre shortening speed from 1.00 (2.76 +/- 0.11 microm half-sarcomere(-1) s(-1)) to 0.30 of maximum unloaded shortening velocity (V(u)), thereby modulating isotonic force from 0 to 0.34 F(o), respectively. The step zeroed force and allowed the fibre to shorten unloaded for a brief period of time prior to force redevelopment. Although peak force redevelopment after different releases was similar, +dF/dt(R) increased by 81 +/- 6 % (P < 0.05) as fibre shortening speed was reduced from 1.00 V(u). The +dF/dt(R) after different releases was strongly correlated with the preceding isotonic force (r = 0.99, P < 0.001). Results from additional experiments showed that the slope of slack test plots produced by systematically increasing the step size that followed each ramp were similar. Thus, isotonic force did not influence V(u) (mean: 2.84 +/- 0.10 microm half-sarcomere(-1) s(-1), P < 0.05). We conclude that isotonic force modulates +dF/dt(R) independent of change in V(u), an outcome consistent with a cooperative influence of attached cross-bridges on thin filament activation that increases cross-bridge attachment rate without alteration to cross-bridge detachment rate.

Effects of volatile anesthetics on sarcolemmal calcium transport and sarcoplasmic reticulum calcium content in isolated myocytes.

BACKGROUND: The surface membrane Ca(2+)-adenosine triphosphatase and Na(+)-Ca(2+) exchanger transport Ca(2+) out of the ventricular myocyte, competing for cytosolic Ca(2+) with the Ca(2+)-adenosine triphosphatase located in the sarcoplasmic reticulum. In this study the authors examined the effects of halothane, isoflurane, and sevoflurane on Ca(2+) extrusion from the cell and sarcoplasmic reticulum Ca(2+) content. METHODS: Single myocytes from the right ventricular free wall of adult male ferret hearts were isolated, loaded with the acetoxymethyl ester of the fluorescent Ca(2+) indicator fluo-3, and electrically stimulated at 0.25 Hz to reach a steady state level of intracellular Ca(2+) stores. The effects of halothane, isoflurane, and sevoflurane (1 minimum alveolar concentration) on the peak and rate of decline of the Ca(2+) transient induced by 10 mm caffeine were examined. The peak was used as an index of sarcoplasmic reticulum Ca(2+) content, and the rate of decline was used to monitor Ca(2+) extrusion from the cell. RESULTS: During control conditions, halothane reduced the Ca(2+) content of the sarcoplasmic reticulum, isoflurane maintained it, and sevoflurane caused it to increase. Halothane did not affect Ca(2+) extrusion from the cell, but both isoflurane and sevoflurane inhibited it. When Na(+)-Ca(2+) exchange was inhibited by ionic substitution, isoflurane and sevoflurane still reduced the rate of Ca(2+) efflux from the cell. However, when the sarcolemmal Ca(2+)-adenosine triphosphatase was inhibited by carboxyeosin, isoflurane and sevoflurane had no effect on Ca(2+) efflux. CONCLUSIONS: These results suggest that isoflurane and sevoflurane inhibit Ca(2+) transport from the cell via the sarcolemmal Ca(2+)-adenosine triphosphatase. This effect seems to counteract the decrease in Ca(2+) influx through sarcolemmal L-type Ca(2+) channels and maintains sarcoplasmic reticulum Ca(2+) stores.