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Background: Multisystem inflammatory syndrome in children (MIS-C) is a dangerous pediatric complication of COVID-19., Objective: The purpose of this review article is to provide a summary of the diagnosis and management of MIS-C with a focus on management in the acute care setting., Discussion: MIS-C is an inflammatory syndrome which can affect nearly any organ system. The most common symptoms are fever and gastrointestinal symptoms, though neurologic and dermatologic findings are also well-described. The diagnosis includes a combination of clinical and laboratory testing. Patients with MIS-C will often have elevated inflammatory markers and may have an abnormal electrocardiogram or echocardiogram. Initial treatment involves resuscitation with careful assessment for cardiac versus vasodilatory shock using point-of-care ultrasound. Treatment should include intravenous immunoglobulin, anticoagulation, and consideration of corticosteroids. Interleukin-1 and/or interleukin-6 blockade may be considered for refractory cases. Aspirin is recommended if there is thrombocytosis or Kawasaki disease-like features on echocardiogram. Patients will generally require admission to an intensive care unit., Conclusion: MIS-C is a condition associated with morbidity and mortality that is increasingly recognized as a potential complication in pediatric patients with COVID-19. It is important for emergency clinicians to know how to diagnose and treat this disorder., Competing Interests: Declaration of competing interest We have neither conflicts of interest nor financial support to disclose., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: Current vaccines for the Coronavirus Disease of 2019 (COVID-19) have demonstrated efficacy with low risk of adverse events. However, recent reports of thrombosis with thrombocytopenia syndrome (TTS) associated with adenovirus vector vaccines have raised concern., Objective: This narrative review summarizes the current background, evaluation, and management of TTS for emergency clinicians., Discussion: TTS, also known as vaccine-induced immune thrombotic thrombocytopenia, is a reaction associated with exposure to the ChAdOx1 nCoV-19 (Oxford-AstraZeneca) and AD26.COV2·S (Johnson & Johnson) vaccine, which may result in thrombocytopenia and thrombotic events. There are several case series of patients diagnosed with TTS, but the overall incidence is rare. TTS is characterized by exposure to one of the aforementioned vaccines 4-30 days prior to presentation, followed by thrombosis, mild-to-severe thrombocytopenia, and a positive platelet factor-4 (PF4)-heparin enzyme-linked immunosorbent assay (ELISA). Thrombosis typically involves atypical locations, including cerebral venous thrombosis and splanchnic vein thrombosis. Evaluation should include complete blood count, peripheral smear, D-dimer, fibrinogen, coagulation panel, renal and liver function, and electrolytes, as well as PF4-heparin ELISA if available. Consultation with hematology is recommended if suspected or confirmed. Treatment may include intravenous immunoglobulin and anticoagulation, while avoiding heparin-based agents and platelet transfusion., Conclusions: With increasing vaccine distribution, it is essential for emergency clinicians to be aware of the evaluation and management of this condition., (Published by Elsevier Inc.)

Background: Myocarditis is a potentially fatal condition that can be misdiagnosed in the emergency department (ED) setting., Objective: The purpose of this narrative review article is to provide a summary of the background, pathophysiology, diagnosis, and management of myocarditis, with a focus on emergency clinicians., Discussion: Myocarditis occurs when inflammation of the heart musculature causes cardiac dysfunction. Symptoms may range from mild to severe and are often preceded by a viral prodrome. Laboratory assessment and an electrocardiogram can be helpful for the diagnosis, but echocardiography is the ideal test in the ED setting. Some patients may also require advanced imaging, though this will often occur during hospitalization or follow-up. Treatment is primarily focused on respiratory and hemodynamic support. Initial hemodynamic management includes vasopressors and inotropes, whereas more severe cases may require an intra-aortic balloon pump, extracorporeal membrane oxygenation, or a ventricular assist device. Nonsteroidal anti-inflammatory drugs should be avoided while intravenous immunoglobulin is controversial., Conclusion: Myocarditis is a serious condition with the potential for significant morbidity and mortality. It is important for clinicians to be aware of the current evidence regarding the diagnosis, management, and disposition of these patients., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening hematologic disorder resulting from an ineffective and pathologic activation of the immune response system that may mimic common emergency department presentations, including sepsis, acute liver failure, disseminated intravascular coagulation, and flu-like illnesses such as coronavirus disease 2019 (COVID-19)., Objective: This narrative review provides a summary of the disease and recommendations for the recognition and diagnostic evaluation of HLH with a focus on the emergency clinician., Discussion: Though the condition is rare, mortality rates are high, ranging from 20% to 80% and increasing with delays in treatment. Importantly, HLH has been recognized as a severe variation of the cytokine storm associated with COVID-19. Common features include a history of infection or malignancy, fever, splenomegaly or hepatomegaly, hyperferritinemia, cytopenias, coagulopathies, abnormal liver enzymes, and hypertriglyceridemia. Using specific features of the history, physical examination, laboratory studies, and tools such as the HScore, HLH-2004/2009, and hyperferritinemia thresholds, the emergency clinician can risk-stratify patients and admit for definitive testing. Once diagnosed, disease specific treatment can be initiated., Conclusion: This review describes the relevant pathophysiology, common presentation findings, and a framework for risk stratification in the emergency department., (Published by Elsevier Inc.)

Background: Ludwig's angina is a potentially deadly condition that must not be missed in the emergency department (ED)., Objective: The purpose of this narrative review article is to provide a summary of the epidemiology, pathophysiology, diagnosis, and management of Ludwig's angina with a focus on emergency clinicians., Discussion: Ludwig's angina is a rapidly spreading infection that involves the floor of the mouth. It occurs more commonly in those with poor dentition or immunosuppression. Patients may have a woody or indurated floor of the mouth with submandibular swelling. Trismus is a late finding. Computed tomography of the neck soft tissue with contrast is preferred if the patient is able to safely leave the ED and can tolerate lying supine. Point-of-care ultrasound can be a useful adjunct, particularly in those who cannot tolerate lying supine. Due to the threat of rapid airway compromise, emergent consultation to anesthesia and otolaryngology, if available, may be helpful if a definitive airway is required. The first line approach for airway intervention in the ED is flexible intubating endoscopy with preparation for a surgical airway. Broad spectrum antibiotics and surgical source control are keys in treating the infection. These patients should then be admitted to the intensive care unit for close airway observation., Conclusion: Ludwig's angina is a life-threatening condition that all emergency clinicians need to consider. It is important for clinicians to be aware of the current evidence regarding the diagnosis, management, and disposition of these patients., Competing Interests: Declaration of Competing Interest None., (Published by Elsevier Inc.)

Background: Much of the focus regarding the global pandemic of coronavirus disease of 2019 (COVID-19) has been on the cardiovascular, pulmonary, and hematologic complications. However, neurologic complications have arisen as an increasingly recognized area of morbidity and mortality., Objective: This brief report summarizes the neurologic complications associated with COVID-19 with an emphasis on the emergency medicine clinician., Discussion: COVID-19 has infected over 3.5 million people and killed over 240,000 people worldwide. While pulmonary complications are profound, the neurologic system is also significantly impacted, with complications including acute cerebrovascular events, encephalitis, Guillain-Barré syndrome, acute necrotizing hemorrhagic encephalopathy, and hemophagocytic lymphohistiocytosis. Additionally, patients on immunosuppressive medications for pre-existing neurologic issues are at an increased risk for complications with COVID-19 infection, and many of the currently proposed COVID-19 therapies can interact with these medications., Conclusions: When caring for COVID-19 patients, emergency medicine clinicians should be aware of the neurologic complications from COVID-19., (Published by Elsevier Inc.)

This study examined the fate of axon terminals of one of the major sources of hypoglossal afferents, the spinal V nucleus, after XIIth nerve resection in adult Sprague-Dawley rats. In order to anterogradely label trigemino-hypoglossal projections, small quantities of horse radish peroxidase were pressure-injected into the ipsilateral dorsal (mandibular) portion of the spinal V nucleus two days before the animals were killed. Survival periods ranged from 5 to 33 days after nerve injury (dpo). Axonal injury produced relative changes in the association of labelled axon terminals to structures in the hypoglossal nucleus on the injured side. The proportion of horse radish peroxidase-labelled spinal V nucleus terminals with spherical vesicles (S-terminals) that were unapposed to hypoglossal somata or dendrites increased rapidly and reached maximal levels by 11 dpo. By contrast, the isolation of labelled terminals with pleomorphic/flattened vesicles (P/F-terminals) from postsynaptic structures began later, advanced at a slower rate and did not attain maximal levels until 20 dpo. S-terminals not apposed to neuronal cell parts increased at a rate of 2.2 times greater than unapposed P/F-terminals. In addition, at peak levels, the proportion of labelled S-terminals that were detached from somata and dendrites was significantly greater than unapposed, labelled P/F-terminals. Axotomy did not alter the caliber of the labelled axon terminals. However, by 29 days after axotomy, the average diameter of dendrites remaining in contact with SPVN terminals was 1/3 the diameter of dendrites of uninjured neurons apposed to labelled axon terminals. These findings provide the morphological correlate for physiological and pharmacological evidence that the effectiveness of excitatory and inhibitory synapses are down-regulated in a coordinated manner after hypoglossal nerve injury.