Data and debriefing observations on healthcare simulation to prepare for the COVID-19 pandemic.

We report on data and debriefing observations in the context of an immersive simulation conducted to (a) train clinicians and (b) test new protocols and kits, developed in table-top exercises without prior clinical experience to fit anticipated clinical encounters in the setting of the rapidly expanding COVID-19 pandemic. We simulated scenarios with particular relevance for anesthesiology, perioperative and critical care, including (1) cardiac arrest, (2) emergency airway management, (3) tele-instruction for remote guidance and supervision, and (4) transporting an intubated patient. Using a grounded theory approach, three authors (MHA, DLR, EHS) developed emergent themes. First alone and then together, we sought consensus in uncovering overarching themes and constructs from the debriefings. We thus performed an informal qualitative thematic analysis based in a critical realist epistemological position - the understanding that our findings, while real, are affected by situational variables and the observer's perspective[1,2]. We compared data from videos and triangulated the data by member checking. All participants and course instructors volunteered to participate in this educational project and contributed as co-authors to this manuscript. During debriefing, we applied crisis resource management concepts including situation awareness, prioritization of tasks, and clear communication practices, conducting the debriefing with emphasis on current TeamStepps 2.0 terminology and concepts. [3,4] In addition, we re-evaluated formerly familiar processes, as shortcomings of protocols, kits, and interdisciplinary cooperation became apparent. The data provide detailed observations on how immersive simulation and debriefing among peers mitigated the unfamiliarity of individual clinicians and the organization at large with the demands of an unprecedented healthcare crisis. We also observed and report on the anxiety caused by resource constraints, risk to clinicians in the face of limited personal equipment, and the overall uncertainty surrounding COVID-19. We began to summarize, interpret, critique, and discuss our data and debriefing observations in a rapid co-publication in the Journal of Clinical Anesthesia. [Healthcare Simulation to Prepare for the COVID-19 Pandemic][5].

Transcranial Doppler ultrasonography with induction of anesthesia and neuromuscular blockade in surgical patients.

STUDY OBJECTIVES: To evaluate the cerebral vascular effects of cis-atracurium and rocuronium given after thiopental induction of anesthesia. DESIGN: Randomized, single-blinded study. SETTING: University-affiliated hospital. PATIENTS: 39 adult ASA physical status I and II patients undergoing nonintracranial procedures. INTERVENTIONS: Patients received intravenously (IV), either saline placebo, cis-atracurium, or rocuronium after induction of general anesthesia with thiopental sodium. MEASUREMENTS: The right middle cerebral artery was insonated using a pulsed-wave range-gated transcranial Doppler, and data were recorded at preinduction, immediately postinduction, at injection of the study drug, and at 15-second intervals for 3 minutes thereafter. The variables recorded for each subject included the systolic, diastolic, and mean flow velocity, as well as pulsality index, systolic, diastolic, and mean arterial blood pressure (MAP), and end-tidal carbon dioxide concentration. MAIN RESULTS: No significant differences between the groups were present in the postanesthetic induction maximal or minimal mean flow velocity. CONCLUSIONS: cis-Atracurium and rocuronium, administered after thiopental, do not produce clinically relevant changes in cerebral blood flow velocity.

Basic and advanced life support, acute resuscitation, and cardiac resuscitation.

The global approach to resuscitation has changed dramatically in the past year. The groundwork for these changes began a decade ago with the development of the Utstein guidelines for uniform reporting of critical events. Consistency in data collection was necessary to enable evidence-based review and comparison of current practice. Resuscitation protocols have been significantly altered based upon these data. Basic life support (BLS) protocols have been simplified. Early access to electrical cardioversion is the key to survival. Mobilization of AED technology in the community is essential. Several issues were identified as crucial to future improvement of resuscitation statistics. Prevention strategies should be developed for high-risk patients. There is a need to identify cases in which resuscitation should not be started. Enhancement of educational methods to improve performance and retention of skills is key. Finally, the roadblocks for performance of ethical prospective research must be minimized.

Phenytoin, midazolam, and naloxone protect against fentanyl-induced brain damage in rats.

UNLABELLED: In previous studies, large-dose fentanyl produced electrographic seizure activity and histologically evident brain damage. We assessed whether fentanyl-induced brain damage is attenuated by using anticonvulsant drugs. Using halothane/nitrous oxide anesthesia, 40 Sprague-Dawley rats underwent tracheal intubation, arterial and venous cannulation, and insertion of biparietal electroencephalogram electrodes and a rectal temperature probe. Halothane was discontinued. The dose of IV fentanyl shown previously to cause maximal brain damage was given to all animals and N(2)O was discontinued. Control rats were given fentanyl only. Rats in the three study groups also received midazolam, phenytoin, or N(2)O/naloxone. After characteristic seizure activity began with fentanyl loading the study drug was started. After a 2-h infusion, wounds were closed, and animals recovered overnight and underwent cerebral perfusion-fixation. Neuropathologic alterations were ranked on a scale of 0-5 for both neuronal death (0 = normal, 5 = more than 75% neuronal death) and for malacia. Significantly fewer rats in the N(2)O/Naloxone, Phenytoin, and Midazolam Groups sustained any brain damage compared with controls. Protection against opioid neurotoxicity is achieved with midazolam, naloxone, and phenytoin. If opioid neurotoxicity is clinically relevant, a small change in anesthetic practice might reduce any potential neurologic morbidity. IMPLICATIONS: Narcotics in large doses can cause brain damage in rats. This brain damage is attenuated by a narcotic antagonist, a sedative, and an antiepileptic drug.

Inducible nitric oxide synthase is an endogenous neuroprotectant after traumatic brain injury in rats and mice.

Nitric oxide (NO) derived from the inducible isoform of NO synthase (iNOS) is an inflammatory product implicated both in secondary damage and in recovery from brain injury. To address the role of iNOS in experimental traumatic brain injury (TBI), we used 2 paradigms in 2 species. In a model of controlled cortical impact (CCI) with secondary hypoxemia, rats were treated with vehicle or with 1 of 2 iNOS inhibitors (aminoguanidine and L-N-iminoethyl-lysine), administered by Alzet pump for 5 days and 1. 5 days after injury, respectively. In a model of CCI, knockout mice lacking the iNOS gene (iNOS(-/-)) were compared with wild-type (iNOS(+/+)) mice. Functional outcome (motor and cognitive) during the first 20 days after injury, and histopathology at 21 days, were assessed in both studies. Treatment of rats with either of the iNOS inhibitors after TBI significantly exacerbated deficits in cognitive performance, as assessed by Morris water maze (MWM) and increased neuron loss in vulnerable regions (CA3 and CA1) of hippocampus. Uninjured iNOS(+/+) and iNOS(-/-) mice performed equally well in both motor and cognitive tasks. However, after TBI, iNOS(-/-) mice showed markedly worse performance in the MWM task than iNOS(+/+) mice. A beneficial role for iNOS in TBI is supported.

Quinolinic acid in the cerebrospinal fluid of children after traumatic brain injury.

OBJECTIVE: To measure quinolinic acid, a macrophage-derived neurotoxin, in the cerebrospinal fluid (CSF) of children after traumatic brain injury (TBI) and to correlate CSF quinolinic acid concentrations to clinically important variables. DESIGN: A prospective, observational study. SETTING: The pediatric intensive care unit in Children's Hospital of Pittsburgh, a tertiary care, university-based children's hospital. PATIENTS: Seventeen critically ill children following severe TBI (Glasgow Coma Scale score <8) whose care required the placement of an intraventricular catheter for continuous drainage of CSF. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Patients ranged in age from 2 mos to 16 yrs (mean 6.0 yrs). CSF was collected immediately on placement of the ventricular catheter and daily thereafter. Quinolinic acid concentration was measured by gas chromatography/mass spectroscopy in 69 samples (4.0 +/- 0.4 [SEM] samples per patient). CSF quinolinic acid concentration progressively increased after injury (p = .034, multivariate analysis) and was increased in nonsurvivors vs. survivors (p = .002, multivariate analysis). CSF quinolinic acid concentration was not associated with age. Although overall CSF quinolinic acid concentration was not associated with shaken injury (p = .16, multivariate analysis), infants suffering with shaken infant syndrome had increased admission CSF quinolinic acid concentrations compared with children with accidental mechanisms of injury (p = .027, Mann-Whitney Rank Sum test). CONCLUSIONS: A large and progressive increase in the macrophage-derived neurotoxin quinolinic acid is seen following severe TBI in children. The increase is strongly associated with increased mortality. Increased CSF quinolinic acid concentration on admission in children with shaken infant syndrome could reflect a delay in presentation to medical attention or age-related differences in quinolinic acid production. These findings raise the possibility that quinolinic acid may play a role in secondary injury after TBI in children and suggest an interaction between inflammatory and excitotoxic mechanisms of injury following TBI.

Quinolinic acid is increased in CSF and associated with mortality after traumatic brain injury in humans.

We tested the hypothesis that quinolinic acid, a tryptophan-derived N-methyl-D-aspartate agonist produced by macrophages and microglia, would be increased in CSF after severe traumatic brain injury (TBI) in humans, and that this increase would be associated with outcome. We also sought to determine whether therapeutic hypothermia reduced CSF quinolinic acid after injury. Samples of CSF (n = 230) were collected from ventricular catheters in 39 patients (16 to 73 years old) during the first week after TBI, (Glasgow Coma Scale [GCS] < 8). As part of an ongoing study, patients were randomized within 6 hours after injury to either hypothermia (32 degrees C) or normothermia (37 degrees C) treatments for 24 hours. Otherwise, patients received standard neurointensive care. Quinolinic acid was measured by mass spectrometry. Univariate and multivariate analyses were used to compare CSF quinolinic acid concentrations with age, gender, GCS, time after injury, mortality, and treatment (hypothermia versus normothermia). Quinolinic acid concentration in CSF increased maximally to 463 +/- 128 nmol/L (mean +/- SEM) at 72 to 83 hours after TBI. Normal values for quinolinic acid concentration in CSF are less than 50 nmol/L. Quinolinic acid concentration was increased 5- to 50-fold in many patients. There was a powerful association between time after TBI and increased quinolinic acid (P < 0.00001), and quinolinic acid was higher in patients who died than in survivors (P = 0.003). Age, gender, GCS, and treatment (32 degrees C versus 37 degrees C) did not correlate with CSF quinolinic acid. These data reveal a large increase in quinolinic acid concentration in CSF after TBI in humans and raise the possibility that this macrophage-derived excitotoxin may contribute to secondary damage.

Trial of nurse practitioners in intensive care.

As public concern for quality control of medical care at the beginning of this century forced regulations on medical licensing of physicians, the forces of change in health care are again substantial, this time driven by concerns for cost and access. Our experience at the University of Pittsburgh Medical Center leads us to believe that well-trained physician extenders will play a valuable role in improving efficiency and effectiveness in the care of critically ill patients. We have developed a method for training and supervision. Graded practice supervision, with physician-led professional review, is considered a reasonable goal. We propose that the appropriate degree of supervision in any given area can be determined by: a) careful development of training programs; b) careful assessment of the individual's practice with the target patient population; and c) application of a review process that is sensitive in that population. Issues surrounding the independent practice and reimbursement of acute care nurse practitioners (ACNPs) are not resolved. These issues should be addressed by joint position statements that are based on objective documentation of the safe, effective performance of ACNPs, and on the incorporation of routine performance measurements with continued medical or joint evaluation of the quality review system. Guidelines regarding the evolving roles of ACNPs should be established by professional associations and state or national boards of both nursing and medical practice. Critical care physician and nursing leaders should lead such initiatives.