IntroductionTransesophageal echocardiography (TEE) is a well-established method of evaluating cardiac pathology. It has many advantages over transthoracic echocardiography (TTE), including the ability to image the heart during active cardiopulmonary resuscitation. This prospective simulation study aims to evaluate the ability of emergency medicine (EM) residents to learn TEE image acquisition techniques and demonstrate those techniques to identify common pathologic causes of cardiac arrest.MethodsThis was a prospective educational cohort study with 40 EM residents from two participating academic medical centers who underwent an educational model and testing protocol. All participants were tested across six cases, including two normals, pericardial tamponade, acute myocardial infarction (MI), ventricular fibrillation (VF), and asystole presented in random order. Primary endpoints were correct identification of the cardiac pathology, if any, and time to sonographic diagnosis. Calculated endpoints included sensitivity, specificity, and positive and negative predictive values for emergency physician (EP)-performed TEE. We calculated a kappa statistic to determine the degree of inter-rater reliability.ResultsForty EM residents completed both the educational module and testing protocol. This resulted in a total of 80 normal TEE studies and 160 pathologic TEE studies. Our calculations for the ability to diagnose life-threatening cardiac pathology by EPs in a high-fidelity TEE simulation resulted in a sensitivity of 98%, specificity of 99%, positive likelihood ratio of 78.0, and negative likelihood ratio of 0.025. The average time to diagnose each objective structured clinical examination case was as follows: normal A in 35 seconds, normal B in 31 seconds, asystole in 13 seconds, tamponade in 14 seconds, acute MI in 22 seconds, and VF in 12 seconds. Inter-rater reliability between participants was extremely high, resulting in a kappa coefficient across all cases of 0.95.ConclusionEM residents can rapidly perform TEE studies in a simulated cardiac arrest environment with a high degree of precision and accuracy. Performance of TEE studies on human patients in cardiac arrest is the next logical step to determine if our simulation data hold true in clinical practice.

Background The COVID-19 pandemic has drastically affected everyone in a hit or miss manner. Since it began, evidence of the neuro-invasive potential of the virus has been intensifying significantly. Several pathways have been hypothesized to elucidate the neurotropic nature of SARS-CoV2. It is the need of the hour to collect vital information. Objective To evaluate and correlate the neuro-radiological and neurological manifestations in patients diagnosed with SARS-CoV2. To identify neuro-invasive pathways of COVID infection. Methods Relevant studies were identified through four databases—the Cochrane Library, PubMed, Science Direct, and Web of Science. These were searched using relevant keywords—“COVID-19,” “SARS-CoV2,” “neurological manifestations,” “neuroimaging,” “CT,” and “MRI.” Relevant articles were screened according to a pre-defined inclusion and exclusion criteria from December 2019 to August 2020. Results Our review included a total of 63 full text publications with 584 patients, composed mainly of observational studies, case reports, and case series. The most common neurological manifestations associated with COVID-19 were altered mental status, stroke, and paralysis. About 17.85% patients who underwent neuroimaging were found to be having ischemic changes suggestive of a stroke. This was followed by hemorrhagic changes as the second most common finding. The most commonly involved vessel was the Middle Cerebral Artery. Besides stroke, we found that SARS-CoV2 could be the cause for new-onset seizures, Guillain-Barre Syndrome, encephalitis, and many other severe neurological diseases. Conclusion The information that we have obtained so far will prove dynamic to healthcare providers working against the COVID-19 pandemic. It is necessary to be aware of these atypical neurological findings for the early diagnosis and treatment of COVID-19 infected patients. However, to completely understand the connection between SARS-CoV2 and the nervous system, further research is necessary.

The treatment of myocardial infarction (MI) in coronavirus disease 2019 (COVID-19)-positive patients is both controversial and challenging, particularly in a healthcare setup unable to fulfill COVID-19 protocols. In this report, we describe a case of a COVID-19-positive patient admitted with COVID-19 pneumonia treated symptomatically with a non-rebreathing mask, dexamethasone, remdesivir, and low-molecularweight heparin (LMWH). On day two of the hospital stay, the patient developed inferolateral wall myocardial infarction (MI) without hemodynamic instability. He was treated successfully with thrombolytic (streptokinase) with no severe complications. However, his hospital stay was further complicated by decreasing oxygen saturation and rising inflammatory markers including procalcitonin and IL-6, suggesting superimposed bacterial infection. Thereafter, he was placed on BiPAP oxygen, and aggressive antibiotic therapy including tigecycline along with clindamycin and moxifloxacin was initiated. He showed gradual daily improvements and was discharged after a prolonged hospital stay. To decrease the exposure and spread of COVID-19 infection among the healthcare workers, when there is a deficiency in medical staff, and no negative-pressure catheterization laboratory, thrombolytic can be used for treatment in low-risk, hemodynamically stable MI during this pandemic. However, this needs further research.

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