Hospital-wide cardiac arrest in situ simulation to identify and mitigate latent safety threats.

BACKGROUND: Cardiac arrest resuscitation requires well-executed teamwork to produce optimal outcomes. Frequency of cardiac arrest events differs by hospital location, which presents unique challenges in care due to variations in responding team composition and comfort levels and familiarity with obtaining and utilizing arrest equipment. The objective of this initiative is to utilize unannounced, in situ, cardiac arrest simulations hospital wide to educate, evaluate, and maximize cardiac arrest teams outside the traditional simulation lab by systematically assessing and capturing areas of opportunity for improvement, latent safety threats (LSTs), and key challenges by hospital location. METHODS: Unannounced in situ simulations were performed at a city hospital with multidisciplinary cardiac arrest teams responding to a presumed real cardiac arrest. Participants and facilitators identified LSTs during standardized postsimulation debriefings that were classified into equipment, medication, resource/system, or technical skill categories. A hazard matrix was used by multiplying occurrence frequency of LST in simulation and real clinical events (based on expert opinion) and severity of the LST based on agreement between two evaluators. RESULTS: Seventy-four in situ cardiac arrest simulations were conducted hospital wide. Hundreds of safety threats were identified, analyzed, and categorized yielding 106 unique latent safety threats: 21 in the equipment category, 8 in the medication category, 41 in the resource/system category, and 36 in the technical skill category. The team worked to mitigate all LSTs with priority mitigation to imminent risk level threats, then high risk threats, followed by non-imminent risk LSTs. Four LSTs were deemed imminent, requiring immediate remediation post debriefing. Fifteen LSTs had a hazard ratio greater than 8 which were deemed high risk for remediation. Depending on the category of threat, a combination of mitigating steps including the immediate fixing of an identified problem, leadership escalation, and programmatic intervention recommendations occurred resulting in mitigation of all identified threats. CONCLUSIONS: Hospital-wide in situ cardiac arrest team simulation offers an effective way to both identify and mitigate LSTs. Safety during cardiac arrest care is improved through the use of a system in which LSTs are escalated urgently, mitigated, and conveyed back to participants to provide closed loop debriefing. Lastly, this hospital-wide, multidisciplinary initiative additionally served as an educational needs assessment allowing for informed, iterative education and systems improvement initiatives targeted to areas of LSTs and areas of opportunity.

Prone during pandemic: development and implementation of a quality-based protocol for proning severe COVID-19 hypoxic lung failure patients in situationally or historically low resource hospitals.

BACKGROUND: Intermittent Prone Positioning (IPP) for Acute Respiratory Distress Syndrome (ARDS) decreases mortality. We present a program for IPP using expedient materials for settings of significant limitations in both overwhelmed established ICUs and particularly in low- and middle-income countries (LMICs) treating ARDS due to COVID-19 caused by SARS CoV-2. METHODS: The proning program evolved based on the principles of High Reliability Organizations (HROs) and Crew Resource Management (CRM). Patients with severe ARDS [PaO2:FiO2 ratio (PFr) ≤ 150 on FiO2 ≥ 0.6 and PEEP ≥ 5 cm H2O] received IPP. Patients were placed prone 16 h each day. When PFr was ≥ 200 for > 8 h supine IPP ceased. IPP used available materials without requiring additional work from the bedside team. Changes in PFr, PaCO2, and the SaO2:FiO2 ratio (SaFr) positionally were evaluated using t-statistics and ANOVA with Bonferroni correction (p < 0.017). RESULTS: Between 14APR2020 and 09MAY2020, at the peak of deaths in New York, there were 202 IPPs in 29 patients. Patients were 58.5 ± 1.7 years of age (37, 73), 76% male and had a body mass index (BMI) of 27.8 ± 0.8 (21, 38). Pressor agents were used in 76% and 17% received dialysis. The PFr prior to IPP was 107.5 ± 5.6 and 1 h after IPP was 155.7 ± 11.2 (p < 0.001 compared to pre-prone). PFr after the patients were placed supine was 131.5 ± 9.1 (p = 0.02). Pre-prone PaCO2 was 60.0 ± 2.5 and the 1-h post-prone PaCO2 was 67.2 ± 3.1 (p = 0.02). Supine PaCO2 after IPP was 60.4 ± 3.4 (p = 0.90). The SaFr prior to IPP was 121.3 ± 4.2 and the SaFr 1 h after positioning was 131.5 ± 5.1 (p = 0.03). The post-IPP supine SaFr was 139.7 ± 5.9 (p < 0.001). With ANOVA and Bonferroni correction there were statistically significant changes in PFr (p < 0.001) and SaFr (p < 0.001) and no significant changes in PaCO2 over the four time points measured. Using regression coefficients, the SaFrs predicted by PFrs of 150 and 200 at baseline are 133.2 and 147.3, respectively. CONCLUSIONS: An IPP program for patients with COVID-19 ARDS can be instituted rapidly, safely, and effectively during an overwhelming mass casualty scenario. This approach may be equally applicable in both traditionally austere environments in LMICs and in otherwise capable centers facing situational resource limitations.

Rebound metabolic acidosis following intentional amygdalin supplement overdose.

Introduction: Amygdalin, marketed misleadingly as supplement "Vitamin B17," is a cyanogenic glycoside. When swallowed, it is hydrolyzed into cyanide in the small intestine, which causes histotoxic hypoxia via inhibition of cytochrome c oxidase. It remains available for purchase online despite a ban from the US Food and Drug Administration. We report a case of massive intentional amygdalin overdose resulting in recurrent cyanide toxicity after initial successful antidotal therapy.Case summary: A 33-year-old woman intentionally ingested 20 g of "apricot POWER B17 Amygdalin" supplements. She presented five hours post-ingestion with vital signs: P 127 bpm, BP 112/65 mmHg, RR 25/min, temperature 98.1 °F, and SpO2 98% RA. She was in agitated delirium, diaphoretic, and mydriatic. Her VBG was notable for a pH of 7.27 (rr 7.32-7.42) and lactate 14.1 mmol/L (rr 0.5-2.2), with ECG demonstrating QTc 538 ms (normal <440 ms). She was empirically treated with hydroxocobalamin and supportive care, but worsened clinically, requiring intubation and additional hydroxocobalamin and sodium thiosulfate, which resolved her toxicity. Twelve hours later, she developed recurrent hypotension, acidemia, and QTc prolongation that resolved with repeat hydroxocobalamin and sodium thiosulfate dosing.Discussion: Our case demonstrates rebound metabolic acidosis after massive amygdalin overdose. Toxicity was associated with prolonged QTc, which warrants further investigation into clinical significance. Redosing of combination antidotal therapy suggested efficacy without adverse effects.