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Although much has been learned about cerebral physiology during CPB in the past decade, the role of alterations in CBF and CMRO2 during CPB and the unfortunately common occurrence of neuropsychologic injury still is understood incompletely. It is apparent that during CPB temperature, anesthetic depth, CMRO2, and PaCO2 are the major factors that effect CBF. The systemic pressure, pump flow, and flow character (pulsatile versus nonpulsatile) have little influence on CBF within the bounds of usual clinical practice. Although cerebral autoregulation is characteristically preserved during CPB, untreated hypertension, profound hypothermia, pH-stat blood gas management, diabetes, and certain neurologic disorders may impair this important link between cerebral blood flow nutrient supply and metabolic demand (Figure 5). During stable moderate hypothermic CPB with alpha-stat management of arterial blood gases, hypothermia is the most important factor altering cerebral metabolic parameters. Autoregulation is intact and CBF follows cerebral metabolism. Despite wide variations in perfusion flow and systemic arterial pressure, CBF is unchanged. Populations of patients have been identified with altered cerebral autoregulation. To what degree the impairment of cerebral autoregulation contributes to postoperative neuropsychologic dysfunction is unknown. It must be emphasized that not the absolute level of CBF, but the appropriateness of oxygen delivery to demand is paramount. However, the assumption that the control of cerebral oxygen and nutrient supply and demand will prevent neurologic injury during CPB is simplistic. A better understanding of CBF, CMRO2, autoregulation and mechanism(s) of cerebral injury during CPB has lead to a scientific basis for many of the decisions made regarding extracorporeal perfusion.

The flipped classroom approach to didactic education resulted in a small improvement in knowledge retention and was preferred by anesthesiology residents.

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Residency programs are charged with teaching, assessing, and documenting resident competency for a multitude of skills throughout the course of residency training. An innovative, competition-based objective structured clinical examination event was designed in our department to objectively assess the skill level of anesthesiology residents. After conducting the identical event for 2 years in postgraduate year 1 (PGY1) and postgraduate year 2 (PGY2) residents, we tested the hypothesis that the event can provide adequate standardization to appropriately document progression in technical and nontechnical skills. Twenty-one residents participated in both events during their PGY1 and PGY2 years: n = 10, 2012/2013, n = 11, 2013/2014. The PGY1 participants in 2012 were retested in 2013 (as PGY2 residents) during an identical event, and their performance was compared as a group and on an individual level. The PGY1 residents in 2013 did the same in 2014. Four workstations were analyzed to determine whether improvement in performance occurred between the PGY1 and the PGY2 years: (1) preoperative assessment, (2) operating room anesthesia station checkout, (3) peripheral IV and endotracheal tube placement, and (4) transfer of care in the postanesthesia care unit. The performances of PGY1 and PGY2 residents were compared. The assessments were performed by anesthesiology faculty using checklists, time to complete task, and Likert scale ratings. Data analysis showed improved technical anesthesia skills (operating room setup, peripheral IV, and endotracheal tube placement) and more complete anesthesia-related information management in the preoperative assessment and postoperative transition of care in the postanesthesia care unit in PGY2 residents compared with the PGY1 performance of the same residents. The described event is a valuable tool for objective assessment of multiple anesthesia skills and possible milestones during residency.

ABSTRACT:The effect of hemodilution, with a-oc cross-linked hemoglobin (DCLHb), on brain injury and edema was assessed after temporary middle cerebral artery occlusion in rats. Injury was analyzed with 2,3,5-triphenyltetrazolium chloride (TTC) stain and edema by microgravimety. Part A: DCLHb was given to maintain one of the following hematocrits (Hct) and normotension: 1) 45/Hct, 2) 30/Hct, 3) 16/Hct, or 4) 9/Hct. Brain injury (% of ischemic hemisphere, mean ± SD) was less in the 30/Hct group (31 ± 4 ) versus the 45/Hct group (42 ± 5); and in the 16/Hct (20 ± 3) and 9/Hct (19 ± 4) groups versus the 45/Hct and 30/Hct groups. Edema was less in the hemodiluted groups versus the 45/Hct group. Part B: DCLHb was given to maintain one of the following hematocrits and hyper (HTN) -or normotension (Norm): 1) 45/Norm, 2) 30/Norm, 3) 30/HTN, 4) 16/Norm, or 5) 16/HTN. In hematocrit matched groups hypertension decreased brain injury (30/HTN -24 ± 2 < 30/Norm -34 ± 4; and 16/HTN -17 ± 3 < 16/Norm -24 ± 4). Edema was not effected by hypertension. These results suggest that hemodilution with DCLHb decreases focal ischemic injury, and is most effective when given in a manner that induces hypertension.

In 1907, the technique of continuous spinal anaesthesia (CSA) was introduced using intermittent injections of amylocaine via a needle which remained in the spinal canal. 1 This technique was refined in 1944 by threading a ureteral catheter into the lumbar subarachnoid space,2 and subsequently has been performed with standard epidural equipment. In an attempt to decrease the complication of post-dural puncture headache following CSA with standard epidural equipment, a microcatheter technique has been developed. 3,4 Neurological deficits following spinal anaesthesia are rare. 5 However, cauda equina syndrome following CSA has been reported recently. 6 We report two cases of persistent sacral nerve root deficits following transurethral resection of the prostate (TURP) for benign prostatic hypertrophy. A neurologist was involved in the postoperative care to validate the deficits. In each case, CSA was performed with hyperbaric lidocaine through a lumbar microcatheter.Case #1 A 67-yr-old male with normal coagulation studies and neurological examination was prepared (10% povidoneiodine solution (Kendall Healthcare)), and a 22-gauge spinal needle was introduced easily into the subarachnoid space (L3-4). A 28-gauge CSA catheter (CoSpan~, Kendall Healthcare; Mansfield, MA) was inserted (4 cm) without difficulty and its position was verified by the aspiration of cerebrospinal fluid. In the supine position, 0.7 ml, 5% lidocaine in 7.5% dextrose (without epinephfine) was given, and followed by four incremental injections. The total dose before incision was 3.2 ml over 20 min. There was no pain or paraesthesia with needle placement, catheter insertion, or local anaesthetic injection. After surgical incision, another 2.5 ml (three injections) of 5% lidocaine were administered over ten minutes with the patient in the lithotomy position. Though