Transesophageal Echocardiography Performed by Intensivist and Emergency Physicians-A 5-Year, Single-Center Experience.

Purpose: Data on the use of transesophageal echocardiography (TEE) by intensivist physicians (IP) and emergency physicians (EP) are limited. This study aims to characterize the use of TEE by IPs and EPs in critically ill patients at a single center in the United States. Materials and Methods: Retrospective chart review of all critical care TEEs performed from January 1, 2016 to January 31, 2021. The personnel performing the exams, location of the exams, characteristics of exams, complications, and outcome of the patients were reviewed. Results: A total of 396 examinations was reviewed. TEE was performed by IPs (92%) and EPs (9%). The location of TEE included: intensive care unit (87%), emergency department (11%), and prehospital (2%) settings. The most common indications for TEE were: hemodynamic instability/shock (44%), cardiac arrest (23%), and extracorporeal membrane oxygenation (ECMO) facilitation, adjustment, or weaning (21%). The most common diagnosis based on TEE were: normal TEE (25%), left ventricular dysfunction (19%), and vasodilatory shock (15%). A management change resulted from 89% of exams performed. Complications occurred in 2% of critical care TEEs. Conclusion: TEE can be successfully performed by IPs and EPs on critically ill patients in multiple clinical settings. TEE frequently informed management changes with few complications.

Venoarterial extracorporeal membrane oxygenation is an effective management strategy for massive pulmonary embolism patients.

OBJECTIVE: Treatment of massive pulmonary embolism (MPE) is controversial, with mortality rates ranging from 25% to 65%. Patients commonly present with profound shock or cardiac arrest. Venoarterial extracorporeal membrane oxygenation (VA-ECMO) is increasingly being used as a form of acute cardiopulmonary support in critically ill patients. We reviewed our institution's pulmonary embolism response team experience using VA-ECMO for patients presenting with advanced shock and/or cardiac arrest from MPE. METHODS: From March 2017 to July 2019 we retrospectively reviewed 17 consecutive patients at our institution with MPE who were placed on VA-ECMO for initial hemodynamic stabilization. RESULTS: The mean patient age and body mass index was 55.8 years and 31.8, respectively. Ten of 17 patients (59%) required cardiopulmonary resuscitation before or during VA-ECMO cannulation. All patients had evidence of profound shock with a mean initial lactate of 8.95 mmol/L, a mean pH of 7.10, and a mean serum creatinine of 1.78 mg/dL. Seventeen of 17 cannulations (100%) were performed percutaneously, with 41% (n = 7) of patients placed on VA-ECMO while awake and using local analgesia. Five of 17 patients (29%) required reperfusion cannulas, with 0% incidence of limb loss. Overall survival was 13 of 17 patients (76%), with causes of death resulting from anoxic brain injury (n = 2), septic shock (n = 1), and cardiopulmonary resuscitation-induced hemorrhage from liver laceration (n = 1). In survivors, 12 of 13 patients (92%) were discharged without evidence of neurologic insult. The median duration of the VA-ECMO run for survivors was 86 hours (range, 45-218 hours). In survivors, the median length of time from ECMO cannulation to lactate clearance (<2.0 mmol/L) was 10 hours and the median length of time from ECMO cannulation to freedom from vasopressors was 6 hours. Three of 13 patients (23%) required concomitant percutaneous thrombectomy and catheter-directed thrombolysis to address persistent right heart dysfunction, with the remaining survivors (77%) receiving VA-ECMO and anticoagulation alone as definitive therapy for their MPE. The median intensive care and hospital length of stay for survivors was 9 and 13 days, respectively. CONCLUSIONS: VA-ECMO was effective at salvaging highly unstable patients with MPE. Survivors had rapid reversal of multiple organ failure with ECMO as their primary therapy. The majority of survivors required ECMO and anticoagulation alone for definitive therapy of their MPE.

Atypical echocardiographic findings in traumatic aortic transection.

Aortic rupture and transection are constituents of the acute aortic syndrome. Injury to the thoracic aorta during motor vehicle crashes is associated with blunt chest trauma and rapid deceleration mechanisms. Type A dissections and/or rupture of the aorta at the level of the aortic isthmus are the more common presentations of aortic injuries associated with motor vehicle crashes. We present the case of atypical echocardiographic findings of a nearly complete circumferential transection of the proximal ascending aorta injury after a motorcycle crash.

Family presence during brain death evaluation: a randomized controlled trial*.

OBJECTIVE: To evaluate if a family presence educational intervention during brain death evaluation improves understanding of brain death without affecting psychological distress. DESIGN: Randomized controlled trial. SETTING: Four ICUs at an academic tertiary care center. SUBJECTS: Immediate family members of patients suspected to have suffered brain death. INTERVENTIONS: Subjects were group randomized to presence or absence at bedside throughout the brain death evaluation with a trained chaperone. All randomized subjects were administered a validated "understanding brain death" survey before and after the intervention. Subjects were assessed for psychological well-being between 30 and 90 days after the intervention. MEASUREMENTS AND MAIN RESULTS: Follow-up assessment of psychological well-being was performed using the Impact of Event Scale and General Health Questionnaire. Brain death understanding, Impact of Event Scale, and General Health Questionnaire scores were analyzed using Wilcoxon nonparametric tests. Analyses were adjusted for within family correlation. Fifty-eight family members of 17 patients undergoing brain death evaluation were enrolled: 38 family members were present for 11 brain death evaluations and 20 family members were absent for six brain death evaluations. Baseline understanding scores were similar between groups (median 3.0 [presence group] vs 2.5 [control], p = 0.482). Scores increased by a median of 2 (interquartile range, 1-2) if present versus 0 (interquartile range, 0-0) if absent (p < 0.001). Sixty-six percent of those in the intervention group achieved perfect postintervention "understanding" scores, compared with 20% of subjects who were not present (p = 0.02). Median Impact of Event Scale and General Health Questionnaire scores were similar between groups at follow-up (Impact of Event Scale: present = 20.5, absent = 23.5, p = 0.211; General Health Questionnaire: present = 13.5, absent = 13.0, p = 0.250). CONCLUSIONS: Family presence during brain death evaluation improves understanding of brain death with no apparent adverse impact on psychological well-being. Family presence during brain death evaluation is feasible and safe.

Treatment of rats with antipsychotic drugs: lack of an effect on brain N-acetyl aspartate levels.

BACKGROUND: Proton magnetic resonance spectroscopy (1H-MRS) studies of schizophrenia suggest an effect of the disease or of antipsychotic medications on brain N-acetyl aspartate (NAA), a marker of neuronal viability. We studied in the rat the effect of antipsychotic drugs on NAA in several brain regions where NAA reductions have been reported in chronically medicated patients with schizophrenia. METHODS: Three groups of nine rats each were treated with haloperidol (6 mg/kg/day), clozapine (70 mg/kg/day) and vehicle for 6 weeks and were sacrificed. Concentrations of NAA were determined by high-performance liquid chromatography (HPLC) from the following brain regions: cortex, striatum, thalamus, hippocampus and cerebellum. RESULTS: Mixed-factorial ANOVA of NAA concentrations revealed no significant effect of drug group [F(2, 24) = 0.034; p = 0.966] or a group by brain region interaction [F(8, 44) = 0.841; p = 0.572]. There was a significant main effect of region [F(4, 21) = 6.104; p = 0.002] with higher NAA in the cortex. CONCLUSIONS: These results are consistent with the only other study of the effect of typical and atypical antipsychotic drugs on NAA in the rat brain. The well-documented lower NAA in chronically treated schizophrenia patients is probably not a simple effect of antipsychotic medications.

Chronic prenatal ethanol exposure alters ionotropic glutamate receptor subunit protein levels in the adult guinea pig cerebral cortex.

BACKGROUND: The superfamily of glutamate-gated ion channels mediates fast excitatory synaptic transmission in the central nervous system and is composed of the NMDA, AMPA, and kainate receptors. Binding studies have shown that chronic prenatal and/or neonatal ethanol exposure produces persistent effects on the numbers of some of these channels. However, whether or not this chronic ethanol exposure produces long-lasting effects on the expression of specific ionotropic receptor subunits remains an open question. METHODS: Timed pregnant Dunkin-Hartley strain guinea pigs received oral administration of one of the following regimens between gestational days 2 and 67: (1) 4 g of ethanol per kilogram of maternal body weight per day with ad libitum access to pellet food and water (ethanol group), (2) isocaloric sucrose- and pair-feeding with ad libitum access to water (sucrose group), or (3) isovolumetric water with ad libitum access to food and water (water group). The maternal blood ethanol concentration produced by the ethanol regimen was 71 +/- 12 mM. Adult offspring were killed on postnatal day 61, and cerebral cortical tissue was analyzed for ionotropic glutamate receptor subunit expression by Western immunoblotting. RESULTS: There was a statistically significant decrease in NR2B subunit protein expression and an increase in GluR2/3 subunit protein expression in the ethanol group. Expression of NR1, NR2A, NR2C, GluR1, GluR6/7, and KA2 subunit proteins was not affected. CONCLUSIONS: These results demonstrate that chronic prenatal ethanol exposure produces long-lasting effects on the subunit composition of NMDA and AMPA receptors in the cerebral cortex of the adult guinea pig.

Ethanol withdrawal upregulates kainate receptors in cultured rat hippocampal neurons.

We have previously demonstrated that kainate receptors (KA-Rs) are acutely inhibited by ethanol (EtOH). Here we show that KA-Rs are also affected by long-term EtOH exposure. Whole-cell recordings of pharmacologically isolated KA-R-mediated currents in cultured hippocampal neurons revealed that exposure to 80 mM EtOH for 3 days followed by a 24 h withdrawal period increased KA-R current densities. Quantitative confocal microscopy showed that expression of GluR6/7 subunits increases after ethanol withdrawal in these neurons. Since KA-Rs control hippocampal excitability and seizure generation, we postulate that upregulation of these receptors may have a role in the pathophysiology of alcohol withdrawal syndrome.