Ludwig’s angina is a diffuse cellulitis in the submandibular, sublingual, and submental spaces, characterized by its propensity to spread rapidly to the surrounding tissues. Early recognition and treatment for Ludwig’s angina are of paramount importance due to the myriad of complications that can occur in association with Ludwig’s angina. Known complications of Ludwig’s angina include carotid arterial rupture or sheath abscess, thrombophlebitis of the internal jugular vein, mediastinitis, empyema, pericardial effusion, osteomyelitis of the mandible, subphrenic abscess, aspiration pneumonia, and pleural effusion. By reporting a case of Ludwig’s angina, we hope to raise the awareness in our medical community for this rare clinical entity.This case describes a 54-year-old woman with Ludwig’s angina that evolved from a chronic odontogenic infection. She presented with perioral swelling with the involvement of bilateral submandibular and sublingual areas, accompanied by excruciating pain, chills, fever, and vomiting. She was treated with clindamycin and cefoxitin for infection and vigorously hydrated.This case is exemplary for the successful management of this potentially lethal clinical condition. Our early recognition and aggressive treatment helped to prevent complications from Ludwig’s angina.

Background SARS-CoV-2 has been found to be exquisitely adept at triggering autoimmunity and multiple new onset autoimmune diseases have been described as a post-infectious complication of COVID-19 infection in the adult population. Less has been described in the pediatric population, as infections are more likely to be asymptomatic and less severe. This case reports a previously healthy adolescent patient with new onset antineutrophil cytoplasmic autoantibody-associated vasculitis (AAV) diagnosed in the setting of acute COVID-19 infection. Case presentation A previously healthy adolescent male was diagnosed with COVID-19 pneumonia after presenting with infectious symptoms of fever, cough, congestion, and shortness of breath. After worsening of disease, he was found to have pulmonary nodules, atypical for COVID-19. Further imaging and laboratory workup showed elevated inflammatory markers, negative infectious testing, and positive antineutrophil cytoplasmic antibodies (ANCA) diagnostic for AAV. He was treated with pulse dose steroids followed by a prolonged taper and rituximab. Symptoms resolved and laboratory abnormalities improved over time. At six-month follow-up, lesions were much improved, laboratory markers were within normal limits, and patient remained asymptomatic off medications. Conclusions This case is one of the first in the pediatric population to describe new onset AAV presenting with an acute, symptomatic COVID-19 infection. There is increasing evidence for COVID-19 induced autoimmunity in the pediatric population and pediatric care providers should be on high alert for new onset autoimmune disease in children afflicted by COVID-19.

Summary:The purpose of the present study was to analyze the prevalence of asymptomatic (silent) myocardial ischemia during exercise testing among patients with effort-induced angina pectoris, and further, to compare the pain threshold of patients with symptomatic and asymptomatic myocardial ischemia. A group of 26 patients comprised the study. In half of the patients myocardial ischemia during the exercise testing was silent and in one half it was symptomatic. Asymptomatic myocardial ischemia was defined as an asymptomatic ST-segment depression 20.1 mV, lasting longer than 60 s during an exercise test. In patients with asymptomatic ischemia the pain thresholds both on toe and finger were significantly higher than in patients with symptomatic ischemia: mean values were 10.1 versus 4.9 mA on the toes, p<0.025, and 8.4 versus 2.5 mA on the fingers, p < 0.01. We conclude that asymptomatic myocardial ischemia during exercise test is seen often in patients with angina pectoris and that this may be due to an increased pain threshold.

Although rare, usually asymptomatic, and without concurrent disease, dual left anterior descending arteries (LAD) poses great challenges. We describe a 55-year-old male with no history of coronary disease, who presented with worsening substernal chest pain with exertion, and was ruled out for myocardial infarction. On left heart catheterization and subsequent computed tomography angiogram, he was determined to have a dual LAD with a long LAD emerging from the right coronary artery. Moreover, this long LAD gave collaterals to a native long diagonal that ran parallel to this vessel from the left system and was chronically occluded. The long LAD, consistent with type IV classification, traveled in the anterior intraventricular groove to supply left ventricular myocardium; the chronically occluded long left native diagonal supplying lateral walls and apex is a unique variant. It is important to be aware of these anomalies to establish correct diagnoses and determine treatment options.

This report illustrates a case of a 42-year-old male with a history of intravenous drug abuse who presented with septic shock. Diagnostic studies, including a transthoracic echocardiogram, chest computed tomography angiography, transesophageal echocardiogram, and blood cultures ultimately revealed Serratia marcescens pulmonic valve infective endocarditis that was treated with intravenous antibiotics. In addition to the rare form of endocarditis and bacterium involved, this case brings into awareness the dynamic nature of the hospital course that requires vigilance in responding to hypotensive episodes for consideration of pulmonary embolism. Surgical valve replacement was opted for due to such a complication in addition to the large size of the vegetation, 2.5 cm.