Background SARS-CoV2, also known as COVID-19, is a specific strain of coronavirus that is responsible for an ongoing global pandemic. COVID-19 primarily targets the respiratory system via droplet transmission, causing symptoms similar to influenza, including fever, cough, and shortness of breath. It is now known to impact other organ systems, causing significant cardiovascular and gastrointestinal illness, among others. Case summary We describe two cases of COVID-19 induced myocarditis presenting with cardiogenic shock. These cases highlight the importance of understanding the lethal cardiac complications of COVID-19 infection, as well as its presentation, diagnosis, pathophysiology, and potential treatment options. These two cases involve patients without underlying cardiovascular disease risk factors who experienced prolonged symptoms of COVID-19 infection. Both patients presented with cardiogenic shock more than one week after symptom onset and diagnosis. These cases demonstrate the late presentation of myocarditis and cardiogenic shock, treated with corticosteroids and inotropes, with subsequent recovery of cardiac function. Discussion The cases highlight the importance of recognizing late presentation viral myocarditis secondary to COVID-19 infection, even in patients without underlying cardiac disease.
Hydroxychloroquine has gained popularity as a potential preventative and treatment of COVID-19 pneumonia due to its in vitro activity against the virus. These three cases of COVID-19 pneumonia of varying severities occurred in the setting of chronic hydroxychloroquine use. These cases argue against the use of hydroxychloroquine as a preventative or therapeutic option for COVID-19 pneumonia.
We present a case of a 47-year-old female with a history of anxiety, depression, and alcohol dependence with history of alcohol withdrawal seizures, who presented after a witnessed seizure episode. She admitted to drinking only copious amounts of black tea 1 week prior to presentation in an attempt to quit alcohol. She was subsequently found to be severely hyponatremic with a serum sodium level of 112 mEq/L and was admitted to the intensive care unit. Approximately 48 h after admission, she experienced sudden-onset of dizziness, diaphoresis, and nausea, with a heart rate of 42 beats/min and blood pressure of 70/40 mm Hg. STAT EKG revealed new T-wave inversions in the lateral and precordial leads and troponin was elevated to 5.99 ng/ mL. Treatment was initiated for NSTEMI with continuous heparin infusion, aspirin, clopidogrel, carvedilol, and lisinopril. Transthoracic echocardiogram revealed apical and mid ventricular dyskinesia with hyperkinesis of the basal walls, with an estimated left ventricular ejection fraction of 35%. Cardiac catheterization revealed no significant coronary disease with ejection fraction 30-35% and similar areas of hypo and hyperkinesis, classic for apical ballooning syndrome. This case not only illustrates the rare phenomenon of hyponatremiainduced Takotsubo cardiomyopathy, but is one of the only incidents caused by primary polydipsia.
Signet ring cell carcinoma of the colon is an extremely rare subtype of mucinous adenocarcinoma, comprising of less than one percent of all tumors of the colon and rectum. Because of its rare and aggressive nature, its presentation is usually late its course. CASE PRESENTATION: We present the case of a 62-year-old male with a history of colon cancer treated with surgical resection and chemotherapy one year prior to presentation. He had no radiographic evidence of disease during follow up with his oncologist four months prior to presentation. He presented to the hospital with complaints of shortness of breath and cough. CT angiogram of the chest revealed diffuse patchy consolidative airspace disease with bilateral adenopathy, suspicious for multifocal pneumonia (Figure 1). The patient was started on broad spectrum antibiotics and underwent diagnostic bronchoscopy, with no significant luminal abnormalities reported. The cell count from the bronchoalveolar lavage (BAL) and cytology were both unremarkable, along with all infectious, inflammatory, and rheumatologic workups. Given lack of improvement, the patient was treated with high dose systemic corticosteroids and completed a 7-day course of broad-spectrum antibiotics. Despite therapy, his respiratory status continued to decline, necessitating high flow nasal cannula and intermittent noninvasive ventilation. A subsequent CT of the abdomen showed new retroperitoneal adenopathy. He then underwent Endobronchial Ultrasound and bronchoscopy with biopsies of two new endobronchial lesions and areas of abnormal appearing mucosa. Lymph node sampling was completed at stations 11L, 7, and 11R, along with BAL of the right middle lobe. Following this procedure, our patient was started on pulse dose steroids. On the third day of this therapy, his respiratory status further declined, requiring intubation and mechanical ventilation. He demonstrated severely reduced compliance and was difficult to ventilate despite multiple modes of mechanical ventilation. He clinically deteriorated with progressive respiratory acidosis and vasopressor refractory shock. He subsequently arrested and expired shortly thereafter on hospital day 24.
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