An Introductory Point-of-Care Ultrasound Curriculum for an Anesthesiology Residency Program.

Introduction: The use of point-of-care ultrasound (POCUS) is a growing trend in the field of anesthesiology. However, formal POCUS curriculums are still not widely implemented in residency programs. As the Accreditation Council for Graduate Medical Education and the American Board of Anesthesiology have both incorporated POCUS into their educational aims and expectations for graduates, we recognized the need for a formal POCUS curriculum for our residency program. We developed and implemented a comprehensive 3-week POCUS curriculum for our first-year anesthesiology residents (CA1s) in the latter half of their academic year. Methods: Twenty CA1s participated in this educational activity. The POCUS curriculum spanned seven topics and was given in weekly 2-hour sessions over the course of 3 weeks. Each session was designed with the first hour consisting of a traditional lecture-based presentation followed by live hands-on practice. A pretest on POCUS knowledge was given to every resident before the curriculum, and a posttest and survey were administered afterwards. Results: Every CA1 showed an improvement in their posttest scores. The median scores of the pretest and posttest were 49% and 75%, respectively. Survey results were positive, with all of the CA1s agreeing that the POCUS educational materials were appropriate to their level of training and that their POCUS knowledge and technical skills improved after the curriculum. Discussion: We have shown that our formal POCUS curriculum improved anesthesiology residents' knowledge as well as resulting in positive views on the implementation of this intervention.

Advances in Anesthesia Monitoring.

During surgery, one of the primary functions of the anesthesiologist is to monitor the patient and ensure safe and effective conduct of anesthesia to provide the optimum operating conditions. Standard guidelines for perioperative monitoring have been firmly established by the American Society of Anesthesiologists. However, in recent years, new advances in technology has led to the development of many new monitoring modalities, especially involving the neurologic and cardiovascular systems. This article presents a targeted review to discuss the functions and limitations of these new monitors and how they are applied in the modern operating room setting.

Management of Acute Unilateral Nondisplaced Subaxial Cervical Facet Fractures.

BACKGROUND: Few studies have focused on the management of patients with nondisplaced cervical facet fractures. OBJECTIVE: To determine the rate of successful nonoperative management and risk factors for instability in patients with acute traumatic, unilateral, nondisplaced cervical facet fractures. METHODS: We reviewed patients with single or multilevel unilateral nondisplaced or minimally displaced subaxial cervical facet fractures between 2008 and 2014. Facet fractures were classified as type A1 fractures: superior facet fracture of caudal vertebra; type A2: inferior facet fracture of rostral vertebral; and type A3: floating lateral mass (fracture of pedicle and vertical laminar fracture). All patients were given a trial of nonoperative management with external immobilization using a hard cervical collar. Follow-up clinical data and cervical spine radiographs were analyzed to determine factors associated with instability. RESULTS: Thirty-five patients (34 males, mean age 40.2 ± 2.4 yr) were reviewed. The mean follow-up duration was 2.7 ± 0.4 mo. The distribution of fracture types was type A1 (n = 15), type A2 (n = 4), type A3 (n = 5), type A1 and A2 fractures (n = 10), and type A1 and A3 fractures (n = 1). Nonoperative management was successful in 29 patients (82.9%), and 6 patients developed instability requiring surgery. All patients who failed nonoperative management had associated injuries suggesting a more severe mechanism of injury. No significant association was found between the type of facet fracture and outcome (Fisher's exact test, P = .18). CONCLUSION: In our series, more than 80% of the patients with unilateral, nondisplaced cervical facet fractures underwent successful nonoperative management in the short term.

Erythropoietin neuroprotection with traumatic brain injury.

Numerous experimental studies in recent years have suggested that erythropoietin (EPO) is an endogenous mediator of neuroprotection in various central nervous system disorders, including TBI. Many characteristics of EPO neuroprotection that have been defined in TBI experimental models suggest that it is an attractive candidate for a new treatment of TBI. EPO targets multiple mechanisms known to cause secondary injury after TBI, including anti-excitotoxic, antioxidant, anti-edematous, and anti-inflammatory mechanisms. EPO crosses the blood-brain barrier. EPO has a known dose response and time window for neuroprotection and neurorestoration that would be practical in the clinical setting. However, EPO also stimulates erythropoiesis, which can result in thromboembolic complications. Derivatives of EPO which do not bind to the classical EPO receptor (carbamylated EPO) or that have such a brief half-life in the circulation that they do not stimulate erythropoiesis (asialo EPO and neuro EPO) have the neuroprotective activities of EPO without these potential thromboembolic adverse effects associated with EPO administration. Likewise, a peptide based on the structure of the Helix B segment of the EPO molecule that does not bind to the EPO receptor (pyroglutamate Helix B surface peptide) has promise as another alternative to EPO that may provide neuroprotection without stimulating erythropoiesis.

Brain stimulation for the treatment of epilepsy.

The treatment of patients with refractory epilepsy has always been challenging. Despite the availability of multiple antiepileptic medications and surgical procedures with which to resect seizure foci, there is a subset of epilepsy patients for whom little can be done. Currently available treatment options for these unfortunate patients include vagus nerve stimulation, the ketogenic diet, and electric stimulation, both direct and indirect, of brain nuclei thought to be involved in epileptogenesis. Studies of electrical stimulation of the brain in epilepsy treatment date back to the early 20th century, beginning with research on cerebellar stimulation. The number of potential targets has increased over the years to include the hippocampus, subthalamic nucleus, caudate nucleus, centromedian nucleus, and anterior nucleus of the thalamus (ANT). Recently the results of a large randomized controlled trial, the electrical Stimulation of the Anterior Nucleus of Thalamus for Epilepsy (SANTE) trial, were published, demonstrating a significant reduction in mean seizure frequency with ANT stimulation. Soon after, in 2011, the results of a second randomized, controlled trial-the NeuroPace RNS trial-were published. The RNS trial examined closed-loop, responsive cortical stimulation of seizure foci in patients with refractory partial epilepsy, again finding significant reduction in seizure frequency. In the present review, the authors examine the modern history of electrical stimulation of the brain for the treatment of epilepsy and discuss the results of 2 important, recently published trials, the SANTE and RNS trials.

Neuroprotection with an erythropoietin mimetic peptide (pHBSP) in a model of mild traumatic brain injury complicated by hemorrhagic shock.

Pyroglutamate helix B surface peptide (pHBSP) is an 11 amino acid peptide, designed to interact with a novel cell surface receptor, composed of the classical erythropoietin (EPO) receptor disulfide linked to the beta common receptor. pHBSP has the cytoprotective effects of EPO without stimulating erythropoiesis. Effects on early cerebral hemodynamics and neurological outcome at 2 weeks post-injury were compared in a rat model of mild cortical impact injury (3m/sec, 2.5 mm deformation) followed by 50 min of hemorrhagic hypotension (MAP 40 mm Hg for 50 min). Rats were randomly assigned to receive 5000 U/kg of EPO, 30 µg/kg of pHBSP, or an inactive substance every 12 h for 3 days, starting at the end of resuscitation from the hemorrhagic hypotension, which was 110 min post-injury. Both treatments reduced contusion volume at 2 weeks post-injury, from 20.8±2.8 mm(3) in the control groups to 7.7±2.0 mm(3) in the EPO-treated group and 5.9±1.5 mm(3) in the pHBSP-treated group (p=0.001). Both agents improved recovery of cerebral blood flow in the injured brain following resuscitation, and resulted in more rapid recovery of performance on beam balancing and beam walking tests. These studies suggest that pHBSP has neuroprotective effects similar to EPO in this model of combined brain injury and hypotension. pHBSP may be more useful in the clinical situation because there is less risk of thrombotic adverse effects.

Histopathological and behavioral effects of immediate and delayed hemorrhagic shock after mild traumatic brain injury in rats.

The purpose of this study was to investigate the increased susceptibility of the brain, after a controlled mild cortical impact injury, to a secondary ischemic insult. The effects of the duration and the timing of the secondary insult after the initial cortical injury were studied. Rats anesthetized with isoflurane underwent a 3 m/sec, 2.5-mm deformation cortical impact injury followed by hypotension to 40 mm Hg induced by withdrawing blood from a femoral vein. The duration of hypotension was varied from 40 to 60 min. The timing of 60 min of hypotension was varied from immediately post-injury to 7 days after the injury. Outcome was assessed by behavioral tasks and histological examination at 2 weeks post-injury. A separate group of animals underwent measurement of the acute physiology including mean blood pressure (MAP), intracranial pressure (ICP), and cerebral blood flow (CBF) using a laser Doppler technique. Increasing durations of hypotension resulted in marked expansion of the contusion, from 6.5±1.8 mm³ with sham hypotension to 27.1±3.9 mm³ with 60 min of hypotension. This worsening of the contusion was found only when then hypotension occurred immediately after injury or at 1 h after injury. CA3 neuron loss followed a similar pattern, but the injury group differences were not significant. Motor tasks, including beam balance and beam walking, were significantly worse following 50 and 60 min of hypotension. Performance on the Morris water maze task was also significantly related to the injury group. Studies of the acute cerebral hemodynamics demonstrated that CBF was significantly more impaired during hypotension in the animals that underwent the mild TBI compared to those that underwent sham TBI. The perfusion deficit was worst at the impact site, but also significant in the pericontusional brain. With 50 and 60 min of hypotension, CBF did not recover following resuscitation at the impact site, and recovered only transiently in the pericontusional brain. These results demonstrate that mild TBI, like more severe levels of TBI, can impair the brain's ability to maintain CBF during a period of hypotension, and result in a worse outcome.