Rapid deployment of an emergency department-intensive care unit for the COVID-19 pandemic.

The coronavirus disease 2019 (COVID-19) pandemic mandated rapid, flexible solutions to meet the anticipated surge in both patient acuity and volume. This paper describes one institution's emergency department (ED) innovation at the center of the COVID-19 crisis, including the creation of a temporary ED-intensive care unit (ICU) and development of interdisciplinary COVID-19-specific care delivery models to care for critically ill patients. Mount Sinai Hospital, an urban quaternary academic medical center, had an existing five-bed resuscitation area insufficiently rescue due to its size and lack of negative pressure rooms. Within 1 week, the ED-based observation unit, which has four negative pressure rooms, was quickly converted into a COVID-19-specific unit, split between a 14-bed stepdown unit and a 13-bed ED-ICU unit. An increase in staffing for physicians, physician assistants, nurses, respiratory therapists, and medical technicians, as well as training in critical care protocols and procedures, was needed to ensure appropriate patient care. The transition of the ED to a COVID-19-specific unit with the inclusion of a temporary expanded ED-ICU at the beginning of the COVID-19 pandemic was a proactive solution to the growing challenges of surging patients, complexity, and extended boarding of critically ill patients in the ED. This pandemic underscores the importance of ED design innovation with flexible spacing, interdisciplinary collaborations on structure and services, and NP ventilation systems which will remain important moving forward.

A 37-year-old Woman with Altered Mental Status and Urinary Frequency.

We present a case report of a patient who initially presented with altered mental status and significant urinary frequency. Over the course of her emergency department stay, she then developed tachycardia out of proportion to a new fever along with a respiratory alkalosis. Although each objective finding has a broad differential diagnosis, thyroid storm was the only unifying diagnosis when all findings were present.

Use of a ß-hCG discriminatory zone with bedside pelvic ultrasonography.

STUDY OBJECTIVE: We seek to assess the performance of the ß human chorionic gonadotropin (ß-hCG) "discriminatory zone" when using bedside pelvic ultrasonography in the evaluation of symptomatic pregnant emergency department (ED) patients. METHODS: This was a cross-sectional study of bedside pelvic ultrasonography performed on consecutive pregnant patients in the first trimester who presented to the ED with abdominal pain or vaginal bleeding. Patients received pelvic ultrasonography, serum ß-hCG testing, and blinded formal radiologic ultrasonography. All patients were followed for 8 weeks to determine outcomes. The sensitivity and specificity of a discriminatory ß-hCG level of 3,000 mIU/mL for the diagnosis of ectopic pregnancy were calculated for patients without an intrauterine pregnancy visualized by bedside ultrasonography. RESULTS: Thirty-six faculty physicians performed bedside pelvic ultrasonography on 256 patients. There were 161 cases with a confirmed visualizable intrauterine pregnancy and 29 ectopic pregnancies. Bedside ultrasonography identified 115 intrauterine pregnancies. The range of ß-hCG for cases of confirmed visualizable intrauterine pregnancy with a nondiagnostic bedside ultrasonography was 15 mIU/mL to 123,368 mIU/mL (median 6,633; interquartile range 1,551 to 32,699). For patients with nondiagnostic bedside ultrasonography, using a discriminatory ß-hCG level of 3,000 mIU/mL to further assess for ectopic pregnancy showed sensitivity of 35% (95% confidence interval [CI] 18% to 54%) and specificity of 58% (95% CI 48% to 67%). Finally, the overall sensitivity of bedside pelvic ultrasonography for the detection of intrauterine pregnancy was 71% (95% CI 63% to 78%), and the specificity was 99% (95% CI 94% to 100%). CONCLUSION: When bedside pelvic ultrasonography does not demonstrate an intrauterine pregnancy, serum ß-hCG level is not helpful in differentiating intrauterine from ectopic pregnancy in symptomatic ED patients.

Do California counties with lower socioeconomic levels have less access to emergency department care?

OBJECTIVES: The study objective was to examine the relationship between number of emergency departments (EDs) per capita in California counties and measures of socioeconomic status, to determine whether individuals living in areas with lower socioeconomic levels have decreased access to emergency care. METHODS: The authors linked 2005 data from the American Hospital Association (AHA) Annual Survey of Hospitals with the Area Resource Files from the United States Department of Health and Human Services and performed Poisson regression analyses of the association between EDs per capita in individual California counties using the Federal Information Processing Standard (FIPS) county codes and three measures of socioeconomic status: median household income, percentage uninsured, and years of education for individuals over 25 years of age. Multivariate analyses using Poisson regression were also performed to determine if any of these measures of socioeconomic status were independently associated with access to EDs. RESULTS: Median household income is inversely related to the number of EDs per capita (rate ratio = 0.83; 95% confidence interval [CI] = 0.71 to 0.96). Controlling for income in the multivariate analysis demonstrates that there are more EDs per 100,000 population in FIPS codes with more insured residents when compared with areas having less insured residents with the same levels of household income. Similarly, FIPS codes whose residents have more education have more EDs per 100,000 compared with areas with the same income level whose residents have less education. CONCLUSIONS: Counties whose residents are poorer have more EDs per 100,000 residents than those with higher median household incomes. However, for the same income level, counties with more insured and more highly educated residents have a greater number of EDs per capita than those with less insured and less educated residents. These findings warrant in-depth studies on disparities in access to care as they relate to socioeconomic status.

Overexpression of Myostatin2 in zebrafish reduces the expression of dystrophin associated protein complex (DAPC) which leads to muscle dystrophy.

Myostatin, a member of the TGF-beta superfamily, is a potent negative regulator of skeletal muscle and growth. Previously, we reported Mstn1 from zebrafish and studied its influence on muscle development. In this study, we identified another form of Myostatin protein which is referred to as Mstn2. The size of Mstn2 cDNA is 1342 bp with 109 and 132 bp of 5' and 3'-untranslated regions (UTRs), respectively. The coding region is 1101 bp encoding 367 amino acids. The identity between zebrafish Mstn1 and 2 is 66%. The phylogenetic tree revealed that the Mstn2 is an ancestral form of Mstn1. To study the functional aspects, we overexpressed mstn2 and noticed that embryos became less active and the juveniles with bent and curved phenotypes when compared to the control. The RT-PCR and in situ hybridization showed concurrent reduction of dystrophin associated protein complex (DAPC). In cryosection and in situ hybridization, we observed the disintegration of somites, lack of transverse myoseptum and loss of muscle integrity due to the failure of muscle attachment in mstn2 overexpressed embryos. Immunohistochemistry and western blot showed that there was a reduction of dystrophin, dystroglycan and sarcoglycan at translational level in overexpressed embryos. Taken together, these results indicate the suitability of zebrafish as an excellent animal model and our data provide the first in vivo evidence of muscle attachment failure by the overexpression of mstn2 and it leads to muscle loss which results in muscle dystrophy that may contribute to Duchenne syndrome and other muscle related diseases.

Thioacetamide accelerates steatohepatitis, cirrhosis and HCC by expressing HCV core protein in transgenic zebrafish Danio rerio.

Hepatocellular carcinoma (HCC) is one of the common cancers worldwide, caused by Hepatitis C virus (HCV) and hepatotoxins. Here we report the development of HCC in wild type as well as HCV core protein (HCP)-transgenic zebrafish upon treatment with a hepatotoxin, thioacetamide (TAA). Two-fold accelerated HCC development could be achieved in the TAA-treated transgenic fish, that is, the progression of the disease in TAA-treated wild type zebrafish developed HCC in 12 weeks whereas that of HCP-transgenic zebrafish shortened the HCC progression to 6 weeks. Histopathological observation showed the specific pathological features of HCC. The HCC progression was confirmed through RT-PCR that revealed an up and down regulation of different marker genes at various stages of HCC progression such as, steatohepatitis, fibrosis and HCC. Moreover, HCV core protein expressed in the HCP-transgenic zebrafish and TAA synergistically accelerate the HCC development. It must be mentioned that, this is the first report revealing HCV core protein along with TAA to induce HCC in zebrafish, particularly, in a short period of time comparing to mice model. As zebrafish has already been considered as a good human disease model and in this context, this HCC-zebrafish model may serve as a powerful preclinical platform to study the molecular events in hepatocarcinogenesis, therapeutic strategies and for evaluating chemoprevention strategies in HCC.

Thioacetamide induced liver damage in zebrafish embryo as a disease model for steatohepatitis.

Steatohepatitis has recently been increasing as a cofactor influencing the progression of fibrosis, cirrhosis, adenoma and carcinoma in liver; however, the mechanisms by which it contributes to liver injury remain uncertain. We induced steatohepatitis in zebrafish embryos using thioacetamide (TAA). TUNEL assay revealed significant increasing of apoptosis in liver after 5 days post fertilization and the increasing of apoptosis was observed to be associated with the up-regulation of apoptotic genes such as, bad, bax, P-38a, caspase-3 and 8, and JNK-1. Histological sections by oil red O stain showed the accumulation of fatty droplets which causes the pushing of the nucleus towards one side. Up-regulation of steatosis markers such as, ACC, adiponectin, PTL, CEBP- alpha and beta, SREBP-1 was also observed. Furthermore, the elevation of glutathione peroxidase in TAA treated embryos indicated that TAA induces lipid peroxidation which leads to causes liver damage. Zebrafish has already been considered as a good human disease model and in this context; TAA-treated zebrafish may serve as a good animal model to study the molecular pathogenesis of steatohepatitis. Moreover, non-availability of specific drugs to prevent steatohepatitis, this animal model may serve as a powerful preclinical platform to study the therapeutic strategies and for evaluating chemoprevention strategies for this disease.