Coronavirus disease 2019 (COVID-19) has rapidly evolved into a global pandemic, with affecting to-date over 23 million people and causing over 800,000 deaths around the globe. The major pathogenetic mechanisms include inflammation, vasoconstriction and thrombogenesis. Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) typically manifests as fever, cough, shortness of breath, and exhibits radiographic evidence of bilateral pneumonic infiltrates. Recent meta-analyses have shown that myocardial injury, including viral myocarditis, is prevalent among infected patients, especially in patients requiring ICU level care. Diagnosis of viral myocarditis is multifactorial and involves detection of elevated cardiac biomarkers and echocardiographic evidence of cardiomyopathy, in the absence of diseased coronary arteries. Endomyocardial biopsy with histopathologic examination provides definitive confirmation. We present a case of a previously healthy 52-year-old male who presented clinically with suspected myocarditis with new-onset dilated cardiomyopathy (DCM) and systolic dysfunction as a sequela of infection with SARS-CoV-2. In this report we highlight the clinical presentation of echocardiographic findings and proposed pathogenetic mechanisms of myocarditis associated with COVID-19 which has a varied presentation, ranging from clinically silent to life-threatening arrhythmias with hemodynamic compromise.
A common treatment and management of BPH is transurethral resection of the prostate (TURP) with at least 150,000 TURPs performed per year in the United States. Rates of bacteremia following TURP can be as low as 1% when antimicrobial prophylaxis is given. Patients can develop many common sequelae as a result of bacteremia secondary to TURP including bacteriuria and urinary tract infection; however, more serious complications such as endocarditis are quite rare (~1 in 4200 cases). Here we present a case of a 67 year-old-male with BPH who underwent two TURP procedures; both with appropriate antibiotic prophylaxis who was subsequently diagnosed with endocarditis
INTRODUCTION: The association of Streptococcus milleri group with pyogenic liver abscess is well recognized. Streptococcus gordonii, however, is a bacterium not of the milleri group and is included among the colonizers of the periodontal environment as it has a high affinity for molecules in the salivary pellicle on tooth surfaces. Here, we describe a case where Streptococcus gordonii was isolated from a pyogenic liver abscess in a retired dentist with hepatic metastasis of colon carcinoma. The clinical features, work up, management, and significance are described. CASE DESCRIPTION/METHODS: An 85-year-old male with colon carcinoma status post hemicolectomy complicated by metastasis to the liver status post chemotherapy and resection presented to the ED with intermittent abdominal discomfort for 2 weeks. Laboratory values were significant for WBC count of 16,000 with a predominance of granulocytes at 85%. CT of the abdomen and pelvis demonstrated a large, 7.6 cm by 5.3 cm, collection in the liver, likely an abscess. Infectious Diseases was consulted and recommended initiation of Meropenem and Daptomycin, in addition to drainage of the collection. The suspected abscess was drained by IR and Streptococcus gordonii sensitive to Linezolid was isolated on bacterial culture. The patient was transitioned to IV Linezolid and Metronidazole given susceptibilities. The patient's WBC count then began trending upwards. CT of the chest exhibited a 1.2 cm by 0.7 cm loculated pleural effusion on the right side. The pleural fluid collection was drained and a chest tube was placed. Studies of the drainage revealed an exudative process, although gram stain and culture were negative. Repeat CT imaging one week later revealed reduction in the size of the liver abscess. The WBC count normalized to less than 10,000 and the patient was discharged with a two-week course of oral Linezolid and Metronidazole with close outpatient follow-up with Infectious Diseases and Oncology. DISCUSSION: Pyogenic liver abscesses are generally associated with enteric gram-negative bacilli, Streptococcus milleri group, Streptococcus pyogenes, and Staphylococcus aureus. Hepatic abscesses secondary to periodontal flora have not been demonstrated in the literature without direct trauma to the GI tract involving foreign bodies contaminated with these organisms. We propose a possible hematogenous route of infection likely associated with possible risk factors related to the patient’s occupation as a dentist and history of dental manipulation.
INTRODUCTION: Pyogenic liver abscess (PLA) is due to leakage of intra-abdominal contents with hepatic spread via the portal circulation. The incidence of PLA is estimated to be 2.3 cases per 100,000 people with higher rates among men than women [1]. We present a case of a 58-year-old male with no abdominal tenderness, risk factors, or recent travel history, who was found to have a 3 cm liver abscess growing Klebsiella Pneumoniae (K.pneumoniae). CASE DESCRIPTION/METHODS: The patient is a 58-year-old African American man with a medical history of HTN and HLD who presented with 3-day history of muscle aches, subjective fevers, and chills. Initially the patient was suspected to have a flu and was treated with fluids and antipyretics. He was noted to have transaminitis (AST/ALT: 202/139), however denied nausea or abdominal pain. An ultrasound demonstrated a complex cystic mass in the right lobe of the liver, and a CT Abd/Pelvis showed a 3.2 × 3.1 × 2.3 cm heterogeneous hypodense mass in segment V. The patient remained febrile with a Tmax of 102 and began to develop severe RUQ on day two of admission. The patient was maintained on Zosyn 3.375g q6h and initial blood cultures grew gram negative rods. Patient tolerated IR drainage of liver abscess yielding 10cc pustular fluid with subsequent resolution of fever. Both blood and liver cultures grew pan-sensitive K.pneumoniae. DISCUSSION: PLA commonly develops as a complication of biliary tract disease in 40% of cases [2]. In the United States, K. pneumoniae is the predominant pathogen causing PLA; isolated in greater than 60% of monomicrobial and polymicrobial PLA [3]. Groups who are susceptible to infection with K. pneumoniae include patients of Asian ethnicity, diabetics, and those with antibiotic use [2]. Our patient did not have any risk factors for PLA; he had minimal medical history and only took amlodipine on presentation. Common symptoms of PLA include fever, right upper quadrant abdominal pain, and rarely jaundice [1]. Our patients' initial presentation was consistent with a flu like prodrome; however, his transaminitis suggested an underlying hepatic process. While a PLA was unlikely on admission, worsening sepsis and new abdominal pain elucidated the diagnosis. K. pneumoniae PLA can lead to disseminated infections including meningitis; the identification and drainage of an abscess early in the hospital course can alter a patients' mortality. While PLA is rare, it should still remain on the differential diagnosis for septic patients.
INTRODUCTION: Gastrointestinal stromal tumors (GISTs) are a common mesenchymal tumor of the GI tract. Here we present a case of a 60-year-old male with a 33.5 × 27 cm GIST arising from the greater stomach curvature, increased in size from 18.1 × 13.4 cm in five months; an alarming growth rate for a tumor known to grow slowly. CASE DESCRIPTION/METHODS: 60-year-old male with history of GIST and HTN presented to the hospital with abdominal pain and shortness of breath. Physical exam revealed decreased bowel sounds and diffuse tenderness to palpation in the right and left lower quadrants. Patient had previously been diagnosed with a 18.1 × 13.4 cm GIST 5 months prior, and was positive for CKIT (CD117) and DOG1, with 6 mitotic figures/21 HPFs (Figure 1). The patient was lost to follow up and never started on Imatinib. Over a span of five months, the necrotic mass had doubled in size with a repeat CT scan on admission showing a 33.5 × 27 cm GIST (Figures 2 and 3) arising from the greater stomach curvature, invading the left hepatic lobe and compressing the inferior vena cava (IVC). During this admission, he was also found to have bilateral pulmonary embolism, with large clot burden and right heart strain. An IVC filter would have been ideal for prevention of further clot migration, however the compression of the IVC by enlarging GIST prevented intervention. Patient was treated with heparin and started on Imatinib as an outpatient, patient is doing well and following with oncology. DISCUSSION: GISTs can be found in any part of the gastrointestinal tract, with predominance in the stomach. GISTs are often asymptomatic and diagnosed incidentally or they may present with nonspecific symptoms such as early satiety, abdominal pain, anemia, GI bleed or gastric outlet obstruction. Treatment options are dictated by risk of progression which is determined by size (≥3 cm), location, and mitotic count. [1] While the exact rate of tumor growth is unknown, studies have shown a range of 1.2 to 50.7% per annum [2]. On representation to the hospital five months after initial diagnosis, our patients’ mass had increased in size by 54% which surpasses documented growth rates. His mass also created significant compression and prevented integral placement of an IVC filter. While GIST tumors are traditionally thought to be slow growing tumors our case highlights the importance of earlier intervention in high-risk patients; metastatic and compressive complications could have been avoided for this patient had he returned for initial follow-up.
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