Recurrent Hydropneumothorax After COVID-19.

A 60-year-old male with a past medical history of heart failure with reduced ejection fraction, obstructive sleep apnea, atrial flutter, and hypertension initially presented to the emergency department with a chief complaint of shortness of breath. He was diagnosed with COVID-19-induced acute hypoxic respiratory failure. Before his presentation to the emergency department, he was treated with a brief course of hydroxychloroquine, azithromycin, and prednisone. His initial hospitalization was relatively uncomplicated. He then presented back to the emergency department approximately five months later with chief complaints of continued dyspnea and increased work of breathing. On this presentation, he was noted to have a right-sided pneumothorax with a moderate right-sided pleural effusion. The effusion was drained through CT (computed tomography)-guided catheter insertion. Pleural fluid culture and sensitivity were negative, and a cartridge-based nucleic acid amplification test (CBNAAT) was not performed. He was discharged a few days later to home. Over the next several weeks, the patient had recurrent admissions and chest tube placements for unresolving hydropneumothorax. He eventually had a right-sided posterolateral thoracotomy performed. The tissue sample from the thoracotomy was noted to have positive gram staining for fungal hyphae consistent with aspergillosis. This was initially considered a contaminant and not treated with antifungal medication. Unfortunately, after the thoracotomy, the patient continued to have complications including subcutaneous emphysema and recurring hydropneumothoraces. He was taken for another procedure after a repeat CT showed intercostal herniation of the pleura between the fifth and sixth ribs. The herniation was excised, and the pleura was repaired. This pleural tissue was then sent to pathology and noted to have non-caseating granulomas consistent with aspergillosis. At this time, the patient was started on voriconazole. After initiating this medication, the patient's last chest x-ray showed stable findings of his chronic disease process with no new or worsening hydropneumothorax.

Bemoan My Collarbone: A Case of Costocondral Junction Syndrome Complicated by Methicillin Sensitive Staphylococcus aureus Sternoclavicular Osteomyelitis and Septic Arthritis.

A 35-year-old female with a past medical history of untreated Hepatitis-C, and a history of intravenous (IV) drug use initially presented to the emergency department with chief complaints of gradual worsening sharp, constant left-sided chest pain with no radiation starting three weeks before presentation. In the emergency department (ED), she was afebrile, normotensive, and tachycardia with 99% oxygen saturation on room air. A physical exam revealed a well-developed Caucasian female, alert and oriented with moderate distress. Respiratory exam with symmetrical bilateral excursions without wheezes, crackles, or rhonchi. On cardiovascular exam, she was tachycardic with a regular rhythm without murmurs, rubs, or gallops. There was a 2 x 2 cm tender erythematous swelling on the left sternal border inferior to the clavicle. The neck was supple and negative for Jugular Venous Distension (JVD). Neurologically grossly intact. Abnormal laboratory findings included leukocytosis with neutrophilic predominance. The patient received intravenous (IV) antibiotics with broad-spectrum vancomycin, cefepime, and azithromycin and underwent computed tomography angiography (CTA) chest, revealing a 26.8 mm x 26.5 mm left anterior subapical pleural-based pulmonary mass-like lesion with central hypoattenuation in surrounding ground-glass changes. Biopsy of the left subapical pulmonary lesion results showed chronic inflammatory infiltrate. Unfortunately, the patient left the hospital against medical advice after supportive care and pain control. Our patient's history of intravenous drug use and active Hepatitis-C infection were typical risk factors associated with invasive infections. In the clinical context, leukocytosis with hypo-attenuated pulmonary lesion should raise suspicion for septic emboli, localized abscess pocket, infection by atypical organisms, infective endocarditis, and malignancy which was considered upon initial assessment.

Group B Streptococcus Bacteremia and Endocarditis in a Middle-Aged Male.

Group B Streptococcus (GBS) is a rare but increasingly recognized cause of invasive disease in nonpregnant adults, particularly in the United States. Invasive GBS can take on many forms and may involve virtually any organ system. This case report describes the presentation, diagnosis, and management of a middle-aged male with GBS bacteremia and endocarditis. A 59-year-old Caucasian male with a history of a heart murmur presented to the emergency department (ED) with two weeks of intermittent fevers, chills, rigors, and back pain. He had also become increasingly agitated and confused over this time. His heart murmur was discovered years prior during a work physical examination but was not investigated further. On arrival, he was afebrile but hypotensive and tachycardic. Physical examination revealed petechiae at the bilateral inferior palpebral conjunctivae as well as a grade 2 holosystolic murmur heard best at the apex. Abnormal laboratory findings included leukocytosis, transaminitis, elevated ferritin, and elevated D-dimer. Blood cultures were positive for Streptococcus agalactiae, and echocardiography demonstrated large mitral valve vegetations. The patient received intravenous (IV) antibiotics and eventually underwent a successful mitral valve replacement with a 31-mm pericardial tissue valve. No source of infection was identified in this patient despite an extensive workup. The incidence of invasive GBS among nonpregnant adults has increased significantly in recent decades. The majority of affected patients are elderly and with significant underlying medical conditions. GBS bacteremia and endocarditis carry a very high mortality rate despite appropriate antimicrobial therapy. Combined medical-surgical therapy confers better outcomes in cases of endocarditis. Our patient's history of a heart murmur could have represented previously undiagnosed mitral valve pathology, placing him at higher risk of endocarditis. Apart from that, however, he lacked most of the typical risk factors associated with invasive GBS infections. Otherwise healthy patients with invasive GBS should undergo a comprehensive workup for potential underlying chronic illnesses. In the proper clinical context, conjunctival petechiae should elicit concern for infective endocarditis as they are present at a rate similar to that of Janeway lesions, splinter hemorrhages, and Roth spots.

Weak Knees: A Case of Atorvastatin-induced Dermatomyositis.

HMG-CoA reductase inhibitors (statins) are one of the most widely used medications in the primary care setting, and like any medications they have many side effects. The common ones include myalgias and rare ones include dermatomyositis. Here we present the case of atorvastatin-induced dermatomyositis with an unfortunate progression. This mandates a low threshold for first contact doctors to screen their patients for new-onset muscle weakness and rash after starting a statin recently, like our patient who had started atorvastatin several months before. This case adds to the previously reported cases and provides further evidence for statins being triggers of immune-mediated disease. The appropriate management of this condition requires a collaborative effort involving clinical judgment, laboratory testing, and imaging.

A Rare Case of Plummer-Vinson Syndrome.

Plummer-Vinson syndrome (PVS) is characterized by a triad of symptoms comprising microcytic hypochromic anemia, esophageal webs, and dysphagia. PVS is commonly found in women of middle age especially in the fourth and fifth decade of life and is rarely reported in males. We report a case of a 39-year-old female patient who had a classic presentation of PVS. PVS is precancerous with high malignant potential; early diagnosis is of utmost importance for better prognosis and surveillance endoscopy is recommended. Iron repletion oftentimes improves the dysphagia; seldom esophageal dilatation is used to provide symptomatic relief.