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Systemic inflammation-related sinus bradycardia in COVID-19 infection has not been well described yet. This six-patient case series excludes common causes of bradycardia. As bradycardia may be a sequela of COVID-19 infection, we recommend closely monitoring hemodynamics and stopping medications that can exacerbate bradycardia in these patients.

Neurological manifestations, such as encephalopathy, intracranial neuropathy, headache, and cognitive decline, are often presented in patients with COVID-19 infection. Since the onset of the pandemic, acute ischemic stroke associated with a hypercoagulable state caused by COVID-19 is increasingly being reported. Hemorrhagic stroke is also reported via poorly understood mechanisms. We report one of the first-ever cases of intraparenchymal hemorrhage, subarachnoid hemorrhage secondary to reversible cerebral vasoconstriction syndrome in a patient with COVID-19 infection.

Moyamoya syndrome is a chronic and progressive narrowing of the arteries in the brain caused by different mechanisms than the genetic mutation that leads to moyamoya disease. It is characterized by the narrowing and/or closing of the carotid artery with a collateral circulation development around the blocked vessels to compensate for the ischemia. In this report, we present a unique case of moyamoya syndrome that developed over the course of a few months in a patient with new-onset strokes and seizures in the setting of late diagnosis of neurosyphilis and acquired immunodeficiency syndrome (AIDS). To our knowledge, moyamoya syndrome secondary to coinfection with AIDS and meningovascular neurosyphilis has only been reported once in the literature.

In this case report, we present a patient who suffered ceftaroline-associated encephalopathy, while receiving ceftaroline for acute bacterial skin and skin structure infections (aBSSSIs) that resolved after cessation of the suspected agent. We recommend close monitoring for encephalopathy in patients with creatinine clearance (CrCl) of

Flood syndrome is caused by spontaneous rupture of an umbilical hernia in a patient with tense, long-standing ascites. It is a rare complication of hepatic cirrhosis and has a high mortality rate. Flood syndrome is so named because a rush of ascitic fluid often follows the spontaneous umbilical hernia rupture. We present a case of a 39-year-old male patient with a history of alcoholic liver cirrhosis and recurrent ascites who underwent multiple abdominal paracentesis prior to developing an umbilical hernia that eventually ruptured, causing flood syndrome. The authors would like to discuss flood syndrome with a focus on management options. J Med Cases. 2019;10(10):309-311 doi: https://doi.org/10.14740/jmc3375

Introduction: Respiratory, kidney and gastrointestinal are some of the systems affected by COVID-19. Although COVID-19 has been studied as a lung pathogen, endocrine system involvement has rarely been studied. In this case report, we present a case of diabetic ketoacidosis (DKA) and acute pancreatitis in the setting of COVID-19. Case Description: A 52-year-old female with a PMH of type 1 diabetes mellitus and hypothyroidism, presented to the ED with nausea, vomiting, fatigue and diffuse abdominal pain. She reports cosmetic surgery a few weeks prior and she started feeling these symptoms at the beginning of admission day of admission. On admission, WBC was 34.9, blood glucose was 496, lactic acid of 3.1. Arterial blood gas revealed pH of 6.96, PCO2 of 17 mEq/L, PO2 of 143, HCO3 of 5 and anion gap of 23. DKA protocol was initiated and was upgraded to ICU. She was found to be RT-PCR positive for SARS-CoV-2. She denied other symptoms, including melena, jaundice, hematochezia, hematemesis, cough, SOB or diarrhea. She also denied use of alcohol, tobacco or illicit drugs, prior hospitalizations, or family history of pancreatitis. The physical exam was significant for tenderness to palpation in epigastric region without guarding or rebound. Laboratory studies revealed lipase: > 4000U/L, AST: 64 U/L, ALT: 57 U/L, ALKPHOS: 152 U/L, and total bilirubin: 1.1 mg/dL. Serum triglycerides and calcium levels were within normal limits. CT abdomen showed a severe peripancreatic inflammation and edema, moderate non-organized fluid surrounds pancreas. An abdominal ultrasound showed no calcified gallstone or gallbladder wall thickening. The common bile duct was 3 mm, normal size. Over the course of 24 hours, anion gap was 7, pH was 7.28, blood glucose was 158. For sepsis, lactic acid was 0.7 after initiation of azithromycin. For acute pancreatitis, she was treated conservatively with intravenous fluids, bowel rest and analgesia. Patient denied any upper respiratory symptoms and did not require oxygen so steroids were not started for COVID PNA. Her symptoms improved and she was discharged home. Discussion: Here we report a case of a patient who presented with DKA, found to have severe acute pancreatitis as well as SARS-CoV2 PCR positive. Few case reports have reported an association of DKA and acute pancreatitis. Although the exact mechanism by which SARS-CoV-2 is evolving, it is thought to be mediated by the Angiotensin-Converting Enzyme-2 which is present in intestine, and on islet cells of the pancreas. This injury may be due to cytopathic effect of viral replication or indirectly caused by the inflammatory response induced by the virus. Further studies are needed to better understand the pathophysiology behind AP in the setting of COVID-19. Conclusion: This case highlights DKA and AP as a possible initiating presenting manifestation of COVID-19 infection

TOPIC: Cardiovascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Viral Myocarditis is generally a self-limiting condition. Patients usually recover from viral myocarditis within a few weeks to months. Some patients can develop hemodynamic instability and may require critical care management. We present a unique case of acute systolic heart failure secondary to Coxsackievirus myocarditis which recovered within a few days. CASE PRESENTATION: A 19-year-old male came to ER for vomiting and abdominal pain for five days. Initial vitals were Temperature of 98 F, BP of 80/47 mm Hg HR of 124/min, and oxygen saturation of 93% on room air. EKG showed sinus tachycardia without ischemic changes. Initial labs were creatinine-2.6 mg/dl, troponin-2.15 ng/ml. CT of abdomen was unremarkable. CT of chest showed bilateral pulmonary edema and pleural effusion. Lung perfusion scan showed no perfusion defect. He did not respond to intravenous(IV) fluid. Initially it required IV vasopressor support- norepinephrine, phenylephrine, and dobutamine. Echocardiogram showed ejection fraction(EF) of 20-24% with severe global hypokinesis. COVID-19 PCR was negative. The pleural fluid study revealed transudative in nature. On day 3, he was weaned off from vasopressors. Acute kidney injury also resolved. Cytomegalovirus, HIV, autoimmune panel, and respiratory virus panel were negative. Coxsackievirus antibody came back positive. It was consistent with viral myocarditis. Patient showed clinical improvement, and we decided to repeat echocardiogram before discharge. On day 6, repeat echocardiogram showed significant improvement of EF to 54%. The patient was discharged on low dose carvedilol and lisinopril. Clinic follow up showed the patient's significant clinical recovery within a few weeks. DISCUSSION: In case of severe cardiomyopathy secondary to viral myocarditis, patient generally recovers within a few weeks to months. However, in our case, the patient developed acute systolic heart failure from Coxsackievirus myocarditis recovered within a few days after aggressive hemodynamic support. Repeat echocardiogram on the same admission also showed significant improvement in ejection fraction from 24% to 54%. It is a rapid recovery as per our knowledge and published data. CONCLUSIONS: Our case highlights that viral myocarditis has the potency to recover quickly, even from severe systolic dysfunction. This case also emphasizes the importance of repeating an echocardiogram on the same admission rather than waiting for a couple of months to ensure cardiac function recovery, particularly with very low ejection fraction on presentation. REFERENCE #1: Tschope, C., Cooper, L., Torre-Amione, G., & Van Linthout, S. (2019). Management of Myocarditis-Related Cardiomyopathy in Adults. Circulation Research, 124(11), 1568-1583. https://doi.org/10.1161/circresaha.118.313578 REFERENCE #2: 3. Schultz J, Hilliard A, Cooper L, Rihal C. Diagnosis and Treatment of Viral Myocarditis. Mayo Clin Proc. 2009;84(11):1001-1009. doi:10.4065/84.11.1001 DISCLOSURES: No relevant relationships by Gnananandh Jayaraman, source=Web Response No relevant relationships by Ramesh Babu Kesavan, source=Web Response No relevant relationships by Tusharkumar Pansuriya, source=Web Response No relevant relationships by Hytham Rashid, source=Web Response No relevant relationships by Sivatej Sarva, source=Web Response No relevant relationships by Aswin Srinivasan, source=Web Response No relevant relationships by BRANDEN WILSON, source=Web Response