Background. There have been an increasing number of reports of myocarditis and pericarditis in adolescents and young adults after coronavirus disease 19 vaccinations. The pathophysiology of myocarditis after this vaccination is indeterminate currently. The problem is a relatively new phenomenon, and so there are no current guidelines on how to manage these cases of myopericarditis. We intend to describe our management in these two cases so that it can help guide pediatricians, intensivists, and cardiologists taking care of similar cases. Case Summaries. The first case is a young adolescent who presented with chest pain after receiving his second dose of coronavirus disease 19 vaccination with no other symptoms. His troponin was found to be 40 ng/mL. He had a normal echocardiogram and chest CT angiogram. His troponins trended down with symptomatic pain management after 3 days. The second case is another adolescent who presented with fever, fatigue, headache, and chest pain 3 days after receiving his second dose of coronavirus vaccine. His troponin was elevated to 5 ng/mL, electrocardiogram with ST segment elevations, and mildly decreased systolic function on echocardiogram. His troponins and electrocardiogram were normalized in 3 days at the time of his discharge. Conclusion. The clinical course of vaccine-associated myocarditis appears favorable as both our patients have responded well to medications and rest with prompt improvement in symptoms with full recovery. The experience remains limited at this time regarding the investigations, management, and follow-up of this novel clinical entity. It is vital for all the health care providers taking care of adolescents to have knowledge about this phenomenon and make correct diagnosis in those presenting with chest pain after COVID-19 vaccine and in preventing unnecessary invasive procedures such as coronary angiogram to rule out acute coronary syndromes.
There has been a worldwide increase in cases of diabetic ketoacidosis in both adults and children with diabetes during the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic. This can be multifactorial: delayed care due to reduced medical services, fear of approaching hospitals, or SARS-CoV-2 infection itself. It is well-known that infection is an important trigger for diabetic ketoacidosis in children with type 1 or type 2 diabetes mellitus, but little is known whether SARS-CoV-2 infection can trigger diabetic ketoacidosis and new-onset diabetes mellitus in a child with no previous history of diabetes mellitus. The association of SARS-CoV-2 as a trigger for new-onset diabetes requires further investigation, as the incidence of diabetes is steadily rising in the pediatric population during the pandemic. This case report explores two cases where children present in diabetic ketoacidosis with concurrent SARS-CoV-2 infection and no known history of type 1 diabetes mellitus.
Methaemoglobinaemia is a potentially life-threatening condition characterised by hypoxaemia, cyanosis, pallor, fatigue, metabolic acidosis, headache and in severe cases, coma or death. Topical anaesthetics have been reported to cause methaemoglobinaemia. Topical benzocaine was specifically implicated in roughly 66% of anesthetic-induced methaemoglobinaemia cases in a large systematic review in adults. This complication has occurred often in adult patients with pre-existing comorbidities resulting in diminished use in children overall with only few paediatric cases reported worldwide. Additionally, there is growing evidence of a link between sepsis and methaemoglobinaemia due to increased circulating nitrous oxide from infectious pathogen metabolism. In this report, we discuss a case of a 16-year-old young boy, being evaluated for suspected endocarditis, presenting with acute methaemoglobinaemia after use of topical benzocaine spray for transesophageal echocardiogram. This case exemplifies the importance of blood gas with co-oximetry testing in all cases of refractory hypoxemia who have had procedures requiring topical anaesthetics.
Background. We report two pediatric cases of anticholinergic toxidrome, including the youngest reported to date, in which standard therapeutic strategies were either contraindicated or ineffective, while treatment with dexmedetomidine was rapidly efficacious with no adverse effects. Moreover, with the recent shortage of physostigmine, we highlight an alternative treatment in this clinical setting. Case Summaries. In case 1, a two-year-old had an overdose presenting with an anticholinergic toxidrome. However, his hypopnea precluded the use of benzodiazepines due to the high likelihood of intubation. In case 2, a 14-year-old had a polypharmacy overdose inducing agitated delirium that was refractory to high-dose benzodiazepines. Due to the unknown ingestion, physostigmine was avoided. In both cases, dexmedetomidine helped the patient remain calm and metabolize the ingestions. Conclusion. Our experience suggests that dexmedetomidine may be a useful adjunct in anticholinergic presentations in the setting of polypharmacy, when standard therapy is proven ineffective, contraindicated, or unavailable.
Myasthenia gravis, an autoimmune disorder of neuromuscular transmission, can lead to varying degrees of weakness and fatigability of the skeletal musculature. Juvenile myasthenia gravis accounts for 10–15% of all cases of myasthenia gravis. The clinical presentation of juvenile myasthenia gravis varies tremendously, which presents itself as a diagnostic challenge for clinicians. We report a case of a 15-year-old female with mild intermittent asthma presenting with shortness of breath. Acute onset of dyspnea is a common chief complaint amongst the pediatric population with a broad differential diagnosis. Our patient was presumptively treated for status asthmaticus and required invasive mechanical ventilation. After extubating, the patient showed persistent ptosis, which led to the eventual work-up of myasthenia gravis. Upon further review, this patient had months of intermittent symptoms including ptosis and fatigue which went previously undiagnosed. This case demonstrates that dyspnea in an asthmatic can occur from nonairway processes and, if missed, may result in overtreatment of asthma or delayed diagnosis of an important neuromuscular process.
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