The success of a vaccination program is dependent on vaccine efficacy and the number of people vaccinated. Healthcare workers are the first to receive the COVID-19 vaccine based on CDC phase 1a recommendations and are a point of contact for information for patients, so they must be well-educated on common misconceptions about the vaccine. ObjectiveTo identify acceptance/refusal rates of COVID-19 vaccine, reasons for refusal, and to understand the impact of demographics, work environment, and comorbidities on vaccine acceptance. Methods

We present the case of a 56-year-old woman who was diagnosed with severe coronavirus disease 2019 (COVID-19) pneumonia complicated by severe acute respiratory distress syndrome who was intubated for 19 days. She recovered from COVID-19 after a month. A computed tomography (CT) scan of the chest, after a month, showed improved infiltrates with a small residual cavity within the lingula. A CT angiogram showed a more confluent density in the lingular portion on follow-up 2 months later. She developed intermittent hemoptysis after 3 months in December 2020, which persisted for almost 6 months, and CT of the chest showed the lingular nodular with resolution of the cavitation. She underwent bronchoscopy with bronchoalveolar lavage, confirming Aspergillus fumigatus by galactomannan assay and histology showing branching hyphae. Once she started treatment with itraconazole, her hemoptysis resolved. The follow-up CT of the chest after 2 months of treatment did not show a cavity or a nodule in the lingula. Our patient developed invasive pulmonary aspergillosis (IPA) as a sequela of severe COVID-19 infection. COVID-19-associated invasive pulmonary aspergillosis (CAPA) is an underrecognized complication that needs to be investigated on whether prophylactic treatment is required. Our case also demonstrates that the diagnosis of IPA needs to be considered months after COVID-19 infection when a superimposed fungal infection can occur after a viral infection if the patient continues to have persistent symptoms.

We report a rare case of a 32-year-old male who ingested 32.4 to 54 mg of colchicine and presented after 44 hours. He developed progressive multiple organ failure with shock, acute kidney failure, troponemia, pancytopenia, absolute neutropenia, disseminated intravascular coagulation, acute liver failure, rhabdomyolysis, and lactic acidosis. He also developed electrolyte abnormalities and refractory hypoglycemia. Initial treatment consisted of activated charcoal, fluids, and broad-spectrum antibiotics with supportive treatment of mechanical ventilation, hemodialysis, vasopressors, N-acetylcysteine, colony-stimulating factors, and blood products. Literature shows potential benefit of colchicine-specific Fab fragments for acute toxicity with limited studies and is not currently available in the United States. Further research for N-acetylcysteine protocol for acute liver failure in colchicine toxicity and potential use of colchicine-specific Fab fragments is needed. Our case demonstrates the importance of early use of activated charcoal for ingestion overdose with the incorporation of poison control into multidisciplinary team for coordinated patient care.

The cytokine storm associated with coronavirus disease 2019 (COVID-19) triggers a hypercoagulable state leading to venous and arterial thromboembolism. Lab findings associated with this phenomenon are elevated D-dimer, fibrinogen, C-reactive protein (CRP), ferritin, and procalcitonin. We present the case of a 66-year-old male with dyslipidemia who was diagnosed with COVID-19 with worsening shortness of breath, myalgia, and loss of taste. Physical examination was remarkable for crackles with diminished lung sounds and use of his accessory muscles. Labs showed normal white blood cell count, D-dimer of 1.42 mg/L, ferritin of 961 ng/mL, lactate dehydrogenase (LDH) of 621 U/L, and CRP of 2.1 mg/dL. Chest X-ray showed atypical pneumonitis with patchy abnormalities. He required oxygen supplementation with fraction of inspired oxygen of 100% proning as tolerated. He received remdesivir, ceftriaxone, azithromycin, dexamethasone, prophylactic enoxaparin, and a unit of plasma therapy. His D-dimer had increased from 1.65 to 3.51 mg/L with worsening dyspnea. At this time, computed tomography angiogram (CTA) of the chest showed extensive ground-glass opacities and a 2.4 × 1.9 × 1.3 cm distal thoracic aortic intraluminal thrombus. He was started on a heparin drip. A follow-up CTA of the aorta showed thrombus or hypoattenuation within the splenic artery and wedge-shaped areas extending from the hilum with possible infarction and a 6 mm thrombus in the infrarenal abdominal aorta. He was transitioned to enoxaparin 1 mg/kg twice daily. He remained asymptomatic from his splenic infarction. This case adds more insight to splenic infarction associated with COVID-19 in addition to the 32 reported cases documented thus far. Management of thromboembolism includes a therapeutic dose of anticoagulation. To prevent thromboembolism, prophylactic anticoagulation is recommended for those hospitalized with COVID-19.

Chylothorax is a pleural effusion of >110 mg/dL of triglycerides with a milky appearance with transudative being rare. In this article, we present a case of transudative chylothorax with concurrent chylous ascites that is secondary to congestive heart failure (CHF). A 70-year-old male with CHF with ejection fraction of 10%, coronary artery disease status post coronary artery bypass graft, sleep apnea, chronic kidney disease stage 3, and chronic obstructive pulmonary disease presented with worsening abdominal distention, shortness of breath, and increased lower extremities edema. He denied any cough or fever but had orthopnea and paroxysmal nocturnal dyspnea. He requires monthly paracentesis with drainage of 5 to 9 L each time. On physical examination, he had crackles bilaterally with no wheezes or jugular venous distension. His cardiac examination was unremarkable. He did have abdominal distension with dullness to percussion and a positive fluid wave. There was +2 bilateral pitting edema of lower extremities. He had a diagnostic paracentesis where 9.2 L of cloudy milky fluid was drained and therapeutic thoracentesis where 1.1 L of milky fluid was drained. Pleural fluid for triglycerides was 280. His peritoneal fluid had triglycerides of 671 confirming chylous ascites. CHF can lead to chylous ascites due to the increased lymph production in the abdomen, which flows to the thoracic duct. Due to the stiffness at the lymphatic junction, there is high pressure for less flow. The diaphragm plays a role allowing the chylous ascites to be absorb into the thorax.