[ANESTHESIOLOGY AND CRITICAL CARE, PERIOPERATIVE MEDICINE, PAIN MANAGEMENT, EMERGENCY MEDICINE AND RESUSCITATION].

INTRODUCTION: Anesthesia and intensive care, perioperative medicine and pain management, emergency medicine and resuscitation, all together constitute the field of action of the anesthesiologist. The definition of "anesthesiologist" underestimates the profession, and the lack of anesthesiologists seems understandable when we examine the scope of their activities throughout the hospital. There is little awareness among the public of the extent of the anesthesiologist's activity. The anesthesia segment itself, with all its importance, occupies a unique, yet modest part. The main activity of the anesthesiologist during surgery is reanimation, maintaining the patient in good shape while under anesthesia, and coping with hemodynamic changes that occur at every moment. The advantage of the anesthesiologist is that he is a "hospitalist," both the internal medical and surgical doctor. He must be profoundly skilled in all areas of medicine, CPR, pediatrics, women's medicine, general surgery, heart surgery, brain and orthopedic surgery, blood vessels, and many other fields. An important goal is to maintain our patients almost painless. Thus, early at the patient interview, the anesthesiologist will determine the course of the multi-modal analgesic management during hospitalization. Preemptive analgesic medication prior to surgical incision will reduce the pain that the patient will suffer after surgery. Whenever possible, the patient will receive a nerve blockage, or minute doses of opioids added to regional anesthetics. Pain management in the recovery room will be intensified by patient-controlled analgesia via infusion pumps, or by a wide variety of therapies, minimizing the use of oral opioid medications, thus avoiding addictive-prone behavior. This special issue of "Harefuah" is dedicated to anesthesia, pain management, and intensive care. The articles published in the current issue deal with key topics, such as fundamental changes occurring in resident education, emphasizing competent judgement and technical skills, and personal and caring approaches to the patient. The possibility that anesthesia may be associated with cognitive changes in infancy and in older age became a major concern and an active research field. Anesthetic complications can rapidly deteriorate and endanger the life of the patient, may leave him confused, and incapacitated. Larger and complicated modern surgeries are now possible thanks to the special skills and capabilities of the modern anesthesiologist to keep the patient alive and well, even in the presence of major surgery.

Sevoflurane postconditioning is not mediated by ferritin accumulation and cannot be rescued by simvastatin in isolated streptozotocin-induced diabetic rat hearts.

Sevoflurane postconditioning (sevo postC) is an attractive and amenable approach that can protect the myocardium against ischemia/reperfusion (I/R)-injury. Unlike ischemic preconditioning (IPC), sevo postC does not require additional induced ischemic periods to a heart that is already at risk. IPC was previously shown to generate myocardial protection against I/R-injury through regulation of iron homeostasis and de novo ferritin synthesis, a process found to be impaired in the diabetic state. The current study investigated whether alterations in iron homeostasis and ferritin mRNA and protein accumulation are also involved in the cardioprotective effects generated by sevo postC. It was also investigated whether the protective effects of sevo postC in the diabetic state can be salvaged by simvastatin, through inducing nitric oxide (NO) bioavailability/activity, in isolated streptozotocin (STZ)-induced diabetic hearts (DH). Isolated rat hearts from healthy Controls and diabetic animals were retrogradely perfused using the Langendorff configuration and subjected to prolonged ischemia and reperfusion, with and without (2.4 and 3.6%) sevo postC and/or pre-treatment with simvastatin (0.5 mg/kg). Sevo postC significantly reduced infarct size and improved myocardial function in healthy Controls but not in isolated DH. The sevo postC mediated myocardial protection against I/R-injury was not associated with de novo ferrtin synthesis. Furthermore, simvastatin aggravated myocardial injury after sevo postC in STZ-induced DHs, likely due to increasing NO levels. Despite the known mechanistic overlaps between PC and postC stimuli, distinct differences underlie the cardioprotective interventions against myocardial I/R-injury and are impaired in the DH. Sevo postC mediated cardioprotection, unlike IPC, does not involve de novo ferritin accumulation and cannot be rescued by simvastatin in STZ-induced DHs.

Minocycline Before Aortic Occlusion Reduces Hindlimb Motor Impairment, Attenuates Spinal Cord Damage and Spinal Astrocytosis, and Preserve Neuronal Cytoarchitecture in the Rat.

OBJECTIVES: Spinal cord ischemia secondary to trauma or a vascular occlusive event is a threatening phenomenon. The neuroprotective properties of minocycline have been shown in several models of central nervous system diseases and after spinal cord ischemia; however, the benefit of using the drug requires additional confirmation in different animal models. Astrocytes are essential as regulators of neuronal functions and for providing nutrients. The authors hypothesized that astrocytes in the spinal cord may be an important target for minocycline action after ischemia and thus in the prevention of secondary spreading damage. DESIGN: A prospective, randomized animal study. SETTING: University research laboratory, single institution. PARTICIPANTS: Adult male Sprague Dawley rats, weighing between 400 and 450 g. INTERVENTIONS: A model of spinal cord ischemia in the rat was used for this study to determine whether a single, high-dose (10 mg/kg) of minocycline protects against damage to the neuronal cytoskeleton, both in the white and gray matter, and whether it reduces glial fibrillary acidic protein levels, which is an index for prevention of astrocyte activation during ischemia. Thirty minutes before thoracic aorta occlusion, minocycline was administered for 18 minutes using a 2 F Fogarty catheter. MEASUREMENTS AND MAIN RESULTS: Minocycline given prophylactically significantly mitigated severe hindlimb motor impairment and reduced glial fibrillary acidic protein plus astrocytosis in both the white and gray matter of the spinal cord, caudal to the occlusion. Neuronal histologic cytoarchitecture, which was severely and significantly compromised in control animals, was preserved in the minocycline-treated animals. CONCLUSIONS: This study's data imply that minocycline may attenuate reactive astrocytosis in response to injury with better neurologic outcome in a model of spinal cord ischemia in rats. The data suggest that future use of minocycline, clinically, might be advantageous in surgeries with a potential risk for paraplegia due to spinal cord ischemia.

Protection by Nitric Oxide Donors of Isolated Rat Hearts Is Associated with Activation of Redox Metabolism and Ferritin Accumulation.

Preconditioning (PC) procedures (ischemic or pharmacological) are powerful procedures used for attaining protection against prolonged ischemia and reperfusion (I/R) injury, in a variety of organs, including the heart. The detailed molecular mechanisms underlying the protection by PC are however, complex and only partially understood. Recently, an 'iron-based mechanism' (IBM), that includes de novo ferritin synthesis and accumulation, was proposed to explain the specific steps in cardioprotection generated by IPC. The current study investigated whether nitric oxide (NO), generated by exogenous NO-donors, could play a role in the observed IBM of cardioprotection by IPC. Therefore, three distinct NO-donors were investigated at different concentrations (1-10 µM): sodium nitroprusside (SNP), 3-morpholinosydnonimine (SIN-1) and S-nitroso-N-acetylpenicillamine (SNAP). Isolated rat hearts were retrogradely perfused using the Langendorff configuration and subjected to prolonged ischemia and reperfusion with or without pretreatment by NO-donors. Hemodynamic parameters, infarct sizes and proteins of the methionine-centered redox cycle (MCRC) were analyzed, as well as cytosolic aconitase (CA) activity and ferritin protein levels. All NO-donors had significant effects on proteins involved in the MCRC system. Nonetheless, pretreatment with 10 µM SNAP was found to evoke the strongest effects on Msr activity, thioredoxin and thioredoxin reductase protein levels. These effects were accompanied with a significant reduction in infarct size, increased CA activity, and ferritin accumulation. Conversely, pretreatment with 2 µM SIN-1 increased infarct size and was associated with slightly lower ferritin protein levels. In conclusion, the abovementioned findings indicate that NO, depending on its bio-active redox form, can regulate iron metabolism and plays a role in the IBM of cardioprotection against reperfusion injury.

Minocycline Effectively Protects the Rabbit's Spinal Cord From Aortic Occlusion-Related Ischemia.

OBJECTIVES: To identify the minocycline anti-inflammatory and antiapoptotic mechanisms through which it is believed to exert spinal cord protection during aortic occlusion in the rabbit model. DESIGN: An animal model of aortic occlusion-related spinal cord ischemia. Randomized study with a control group and pre-ischemia and post-ischemia escalating doses of minocycline to high-dose minocycline in the presence of either hyperglycemia, a pro-apoptotic maneuver, or wortmannin, a specific phosphatidylinositol 3-kinase antagonist. SETTING: Tertiary medical center and school of medicine laboratory. PARTICIPANTS: Laboratory animals-rabbits. INTERVENTIONS: Balloon obstruction of infrarenal aorta introduced via femoral artery incision. RESULTS: Severe hindlimb paralysis (mean Tarlov score 0.36±0.81 out of 3) was observed in all the control group animals (9 of 11 with paraplegia and 2 of 11 with paraparesis) compared with 11 of 12 neurologically intact animals (mean Tarlov score 2.58±0.90 [p = 0.001 compared with control]) in the high-dose minocycline group. This protective effect was observed partially during a state of hyperglycemia and was completely abrogated by wortmannin. Minocycline administration resulted in higher neurologic scores (p = 0.003) and a shift to viable neurons and more apoptotic-stained nuclei resulting from reduced necrosis (p = 0.001). CONCLUSIONS: In a rabbit model of infrarenal aortic occlusion, minocycline effectively reduced paraplegia by increasing the number of viable neurons in a dose-dependent manner. Its action was completely abrogated by inhibiting the phosphatidylinositol 3-kinase pathway and was inhibited partially by the pro-apoptotic hyperglycemia maneuver, indicating that the activation of cell salvage pathways and mitochondrial sites are possible targets of minocycline action in an ischemic spinal cord.

Novel approaches to spinal cord protection during thoracoabdominal aortic interventions.

PURPOSE OF REVIEW: Spinal cord ischemia after thoracoabdominal aortic interventions is a devastating complication because it significantly worsens the perioperative morbidity and mortality. Long-term outcome is also affected because of medical complications which are directly related to the neural deficits. Paraplegia has significant medical, social, and financial aspects. Limited mobility, the need for assistance in activities of daily living, makes paraplegia an important target for prevention. An understanding of spinal cord blood supply, risk factors for spinal ischemia, and strategies for spinal cord rescue in this setting can help minimize the negative outcome effects of this important complication. RECENT FINDINGS: The vascular supply of the spinal cord is via an extensive collateral arterial network with multiple auxiliary arterial supplies. Risk factors for spinal cord ischemia include extensive aortic repair, prior aortic repair, spinal cord malperfusion on clinical presentation, systemic hypotension, acute anemia, prolonged aortic clamping, and vascular steal. Spinal rescue strategies include systemic hypothermia, endovascular aortic repair, permissive systemic hypertension, cerebrospinal fluid drainage, pharmacologic neuroprotection, and intensive neuromonitoring. SUMMARY: The progression of spinal cord ischemia after thoracoabdominal aortic interventions can frequently be arrested before irreversible infarction results. This spinal cord rescue depends on the early detection and immediate multimodal intervention to maximize spinal cord oxygen supply. The devastating outcomes associated with spinal infarction in this setting offset the risks and knowledge gaps currently associated with contemporary interventions.

Patterns of use of perioperative angiotensin-converting enzyme inhibitors in coronary artery bypass graft surgery with cardiopulmonary bypass: effects on in-hospital morbidity and mortality.

BACKGROUND: Despite proven benefit in ambulatory patients with ischemic heart disease, the pattern of use of angiotensin-converting enzyme inhibitors (ACEIs) in coronary artery bypass graft surgery has been erratic and controversial. METHODS AND RESULTS: This is a prospective observational study of 4224 patients undergoing coronary artery bypass graft surgery. The cohort included 1838 patients receiving ACEI therapy before surgery and 2386 (56.5%) without ACEI exposure. Postoperatively, the pattern of ACEI use yielded 4 groups: continuation, 915 (21.7%); withdrawal, 923 (21.8%); addition, 343 (8.1%); and no ACEI, 2043 (48.4%). Continuous treatment with ACEI versus no ACEI was associated with substantive reductions of risk of nonfatal events (adjusted odds ratio for the composite outcome, 0.69; 95% confidence interval, 0.52-0.91; P=0.009) and a cardiovascular event (odds ratio, 0.64; 95% confidence interval, 0.46-0.88; P=0.006). Addition of ACEI de novo postoperatively compared with no ACEI therapy was also associated with a significant reduction of risk of composite outcome (odds ratio, 0.56; 95% confidence interval, 0.38-0.84; P=0.004) and a cardiovascular event (odds ratio, 0.63; 95% confidence interval, 0.40-0.97; P=0.04). On the other hand, continuous treatment of ACEI versus withdrawal of ACEI was associated with decreased risk of the composite outcome (odds ratio, 0.50; 95% confidence interval, 0.38-0.66; P<0.001), as well as a decrease in cardiac and renal events (P<0.001 and P=0.005, respectively). No differences in in-hospital mortality and cerebral events were noted. CONCLUSIONS: Our study suggests that withdrawal of ACEI treatment after coronary artery bypass graft surgery is associated with nonfatal in-hospital ischemic events. Furthermore, continuation of ACEI or de novo ACEI therapy early after cardiac surgery is associated with improved in-hospital outcomes.

Diabetes blockade of sevoflurane postconditioning is not restored by insulin in the rat heart: phosphorylated signal transducer and activator of transcription 3- and phosphatidylinositol 3-kinase-mediated inhibition.

BACKGROUND: The possibility of restoring sevoflurane postconditioning (sevo-postC) cardioprotection in diabetic animals is uncertain. We hypothesized that attenuation of myocardial injury by sevo-postC might be hindered by inhibition of signal transducer and activator of transcription (STAT) 3-regulated activity of phosphatidylinositol 3-kinase (PI3K) in diabetic animals. To determine whether postC cardioprotection can be restored by normoglycemia, we treated rats with insulin. METHODS: Diabetic or nondiabetic rats were randomly subjected to 30-min ischemia/reperfusion, with ischemic postC or sevo-postC, with and without mitochondrial adenosine triphosphate-dependent potassium channel blocker 5-hydroxy decanoate sodium and PI3K antagonist wortmannin. The infarct area, phosphorylated STAT3, and apoptosis were examined. Studies were repeated after insulin treatment. RESULTS: Ischemic postC and sevo-postC significantly reduced infarct size by 50% in the nondiabetic rats (P < 0.002), a phenomenon completely reversed by 5-hydroxy decanoate sodium and wortmannin. Diabetes mellitus blocked the protective effect of postC, and insulin treatment to achieve normoglycemia did not restore cardioprotection. Phosphorylated STAT3 nuclear retention was significantly increased after ischemia-reperfusion and was further enhanced in response to ischemic postC (P < 0.05) but was significantly reduced in diabetic rats (by 43%; P < 0.01). CONCLUSIONS: The effective reduction in infarct size and apoptosis in the nondiabetic rat heart by postC was completely abrogated in diabetic rats. This inhibition is not relieved by insulin-induced normoglycemia. The PI3K pathway and mitochondrial adenosine triphosphate-dependent potassium channel activation are involved in the mechanism of postC. In diabetic rats, STAT3 activation was strongly reduced, as was postC cardioprotection, suggesting that the inability of insulin to restore postC may be attributed to diabetes-induced STAT3-mediated inhibition of PI3K signaling.

Pulse pressure and risk of adverse outcome in coronary bypass surgery.

BACKGROUND: Among ambulatory patients, an increase in pulse pressure (PP) is a well-established determinant of vascular risk. The relationship of PP and acute perioperative vascular outcome among patients having coronary artery bypass graft (CABG) surgery is less well known. METHODS: We conducted a prospective observational study involving 5436 patients having elective CABG surgery requiring cardiopulmonary bypass. Of these, 4801 met final inclusion criteria. Comprehensive data were captured for medical history, intraoperative and postoperative physiologic and laboratory measures, diagnostic testing, and clinical events. The relationship between preoperative hypertension (systolic, diastolic, PP) and ischemic cardiac and cerebral outcomes and death was assessed using multivariable logistic regression; P<0.05 was considered significant. RESULTS: Nine hundred and seventeen patients (19.1%) had fatal and nonfatal vascular complications, including 146 patients (3.0%) with cerebral and 715 patients (14.9%) with cardiac events. In-hospital mortality occurred in 147 patients (3.1%). Among all blood pressure variables measured preoperatively, PP was most strongly associated with an increased risk of postoperative complications. PP increments of 10 mm Hg (above a threshold of 40 mm Hg) were associated with an increased risk of cerebral events (adjusted odds ratio: 1.12; 95% CI [1.002-1.28]; P=0.026). The incidence of a cerebral event and/or death from neurologic complications nearly doubled for patients with PP>80 mm Hg versus

Myocardial metabolism altered by ischemic preconditioning and enflurane in off-pump coronary artery surgery.

OBJECTIVE: During off-pump coronary artery bypass (OPCAB) surgery, the heart is subjected to ischemia and reperfusion. The authors hypothesized that the volatile anesthetics are as effective as ischemic preconditioning (IPC) in preserving myocardial function during off-pump cardiac surgery, and this effect is because of multiple mechanisms of action. Therefore, the effects of enflurane with its calcium inhibition and antioxidative properties were compared with mechanical IPC in preserving myocardial cellular markers. DESIGN: A prospective, randomized, controlled, and partly blinded study. SETTING: A tertiary care university hospital. PARTICIPANTS: Twenty-five patients undergoing elective single-graft OPCAB surgery. INTERVENTIONS: Patients were randomized into 3 groups: (1) control (n = 8), (2) a single 5-minute ischemia/reperfusion interval of IPC before coronary occlusion (n = 9), and (3) 1.6% enflurane anesthesia 15 minutes before and during graft attachment (n = 8). Arterial and coronary sinus venous blood were analyzed for biochemical indices of ischemia and hydroxyl radical generation. MEASUREMENTS AND MAIN RESULTS: Although the hemodynamic changes were small, myocardial lactate production in the control group increased by 120%, whereas in the enflurane group it decreased significantly (p < 0.01) compared with the control and IPC groups. Oxygen utilization in the control group was 44% higher (p < 0.03), and there was also a larger release of the hydroxyl radical-dependent adduct 2,3-dihydroxybenzoic acid (225% increase, p < 0.05) compared with both study groups. During reperfusion, initial anterior wall hypokinesis by TEE was observed, with slow recovery during reperfusion compared with early recovery in both study groups. CONCLUSIONS: Coronary occlusion during OPCAB surgery results in increased production of ischemia-related metabolic products. The application of methods such as IPC or volatile anesthesia appears to reduce the metabolic deficit, free-radical production, and physiologic changes.

Flumazenil mimics whereas midazolam abolishes ischemic preconditioning in a rabbit heart model of ischemia-reperfusion.

BACKGROUND: The goal of the current study was to assess the effects of flumazenil, a benzodiazepine receptor antagonist, in limiting infarct size and in reducing hydroxyl free radical production. METHODS: After intravenous salicylate (100 mg/kg) administration, rabbits were subjected to 40 min of regional myocardial ischemia and 2 h of reperfusion. In one group, flumazenil (0.05 mg/kg) and, in another, midazolam (0.05 mg/kg) was administered 15 min before 40 min of ischemia. Ischemic preconditioning (IP) was elicited by 5 min of ischemia followed by 10 min of reperfusion (before the 40-min ischemia period). In two other groups, midazolam was added to flumazenil and IP. Infarct size was determined using triphenyl tetrazolium chloride staining. The authors quantified the hydroxyl-mediated conversion of salicylate to its 2,3- and 2,5-dihydroxybenzoate derivatives during reperfusion by high-performance liquid chromatography coupled with electrochemical detection. Results are expressed as mean +/- SEM. RESULTS: Flumazenil, like IP, significantly decreased infarct size (23 +/- 4 and 22 +/- 5%, respectively, vs. 57 +/- 6% in control group; P < 0.01). Midazolam inhibited the effects of flumazenil and IP. Flumazenil and IP significantly limited the increase in the normalized concentrations of 2,3- and 2,5-dihydroxybenzoic acids. With midazolam, however, the increase was comparable to that of the control group. 5-Hydroxydecanoate, a selective mitochondrial adenosine triphosphate-sensitive K channel blocker, given with flumazenil, abolished the protection obtained with the latter. CONCLUSIONS: Flumazenil mimics preconditioning to decrease infarct size and hydroxyl radical production during reperfusion. Midazolam, however, abolishes these effects. Blockade of benzodiazepine receptors is upstream to the mitochondrial adenosine triphosphate-sensitive K channels in the preconditioning cascade.

Ischemic preconditioning decreases the reperfusion-related formation of hydroxyl radicals in a rabbit model of regional myocardial ischemia and reperfusion: the role of K(ATP) channels.

The objective of this study was to assess the effects of ischemic preconditioning (IP) on hydroxyl free radical production in an in vivo rabbit model of regional ischemia and reperfusion. Another goal was to determine whether K(ATP) channels are involved in these effects. The hearts of anesthetized and mechanically ventilated New Zealand White rabbits were exposed through a left thoracotomy. After i.v. salicylate (100 mg/kg) administration, all animals underwent a 30-min stabilization period followed by 40 min of regional ischemia and 2 h of reperfusion. In the IP group, IP was elicited by 5 min of ischemia followed by 10 min of reperfusion (prior to the 40-min ischemia period). Glibenclamide, a K(ATP) channel blocker, was administered prior to the preconditioning stimulus. Infarct size was measured by 2,3,5-triphenyl tetrazolium chloride (TTC) staining. We quantified the hydroxyl-mediated conversion of salicylate to its 2,3 and 2,5-dihydroxybenzoate derivatives during reperfusion by high performance liquid chromatography coupled with electro-chemical detection.IP was evidenced by reduced infarct size compared to control animals: 22% vs. 58%, respectively. Glibenclamide inhibited this cardioprotective effect and infarct size was 53%. IP limited the increase in 2,3 and 2,5-dihydroxybenzoic acid to 24.3 and 23.8% above baseline, respectively. Glibenclamide abrogated this effect and the increase in 2,3 and 2,5-dihydroxybenzoic acid was 94.3 and 85% above baseline levels, respectively, similar to the increase in the control group. We demonstrated that IP decreased the formation of hydroxyl radicals during reperfusion. The fact that glibenclamide inhibited this effect, indicates that K(ATP) channels play a key role in this cardioprotective effect of IP.

Epidural clonidine, bupivacaine and methadone as the sole analgesic agent after thoracotomy for lung resection.

Thoracic epidural analgesia can effectively relieve post-thoracotomy pain but may also adversely affect pulmonary function. This randomised, prospective study compared the effects on pulmonary function of three different epidural analgesics (clonidine, bupivacaine and methadone). Forty-seven patients undergoing thoracotomy were treated postoperatively for 72 h with one of the study drugs. Doses were titrated to maintain visual analogue pain scale values below 4 out of 10. Throughout the postoperative period, reductions of up to 70% of the pre-operative value were observed in forced expiratory volume in 1 s, forced vital capacity and peak expiratory flow rate. Patients who received clonidine showed significantly faster recovery rates of forced expiratory variables compared to other patients, and by the third postoperative day significantly higher spirometry values (10-15%) were recorded in this group. As clonidine was the most effective drug in terms of preservation of pre-operative lung function, it may be clinically advantageous in post-thoracotomy patients.

A pediatric sedation/anesthesia program with dedicated care by anesthesiologists and nurses for procedures outside the operating room.

OBJECTIVE: To examine the performance of a pediatric sedation team working according to a specific protocol and to assess parental satisfaction with the service. STUDY DESIGN: A descriptive observational study of all procedures performed by the sedation team (comprising sedation-trained pediatric intensive care nurses and dedicated anesthesiologists) in a university hospital over 6 years. Data collected included demographics, procedure and location, sedation staff present, sedation failure, drugs used, requirements for escalation of sedation, complications, and parental satisfaction. RESULTS: Sedation was provided for 8760 procedures in 5554 children. The sedation nurse started 1769 (20%) procedures using triclofos sodium and required the assistance of the anesthesiologist in 115 (6.5%) cases. The remaining 6991 (80%) cases were performed by the anesthesiologist, predominantly using propofol (in 72.5% of cases). No cases were deferred as a result of insufficient sedation. Adverse events were recorded in 153 (1.7%) children. Of these, 132 (86%) were mild decreases in oxygen saturation. Three children were not discharged as a result of oversedation. Feedback indicated that 95% of parents were very satisfied with the sedation service. CONCLUSION: A dedicated sedation team using a written protocol provides a service with minimal case cancellation, zero sedation failure, very good safety, and excellent parental satisfaction.

Peripheral nerve block for ambulatory surgery and postoperative analgesia.

PURPOSE OF REVIEW: With this article we intend to increase the awareness of the efficiency and efficacy of peripheral nerve block as a treatment option for outpatient surgical anesthesia and postoperative home-based analgesia. RECENT FINDINGS: Current investigations have demonstrated that peripheral nerve block is associated with a superior outcome (reduced pain, nausea and vomiting) and more efficient patient turnover than general anesthesia. Continuous peripheral nerve block and patient controlled peripheral nerve block lead to further improvement in postoperative analgesia and patient satisfaction. SUMMARY: The recent advances and techniques described indicate that peripheral nerve block is both a valid and frequently a preferred option for ambulatory surgery.