RESUMO
Patients infected with coronavirus disease 2019 (COVID-19) on invasive mechanical ventilation were found to have high rates of barotrauma. Herein, we present five patients admitted to the intensive care unit between March and April 2020, who developed barotrauma as a complication of COVID-19 pneumonia. This series includes four males and one female with a mean age of 54 years, most without significant chronic comorbidities or former tobacco use. All were intubated for hypoxic respiratory failure due to the COVID-19 infection. The diagnosis of barotrauma was confirmed via radiography showing the presence of pneumothorax, pneumomediastinum, or subcutaneous emphysema on radiographic imaging. At the time, they were evaluated for convalescent plasma infusion, remdesivir, and interleukin-6 inhibitor. Each of the five patient's hospital courses were documented. The average number of days between intubation and subsequent barotrauma was 6.8 days with the mean length of hospital stay being 49 days. Three of the five patients passed away due to complications related to COVID-19. Due to the unknown nature of the virus, our findings add to the growing evidence that those infected, even without significant comorbidities, are at high risk for pulmonary complications and in-hospital mortality.
RESUMO
Mycotic aneurysms account for less than 5% of all aneurysms of the aorta, with most cases linked to infection with either Staphylococcus or Salmonella species. Emphysematous aortitis is a rare consequence of mycotic aneurysms and is associated with high morbidity and mortality. It typically occurs from infection superimposed on already damaged endothelium, which is commonly seen in conditions such as atherosclerosis. This report discusses the presentation and relevant imaging findings of a unique case of emphysematous aortitis from Clostridial infection of the thoracic aorta. The patient was a 66-year-old male with a past medical history of end-stage renal disease, arteriovenous fistula for dialysis, hypertension, and diabetes, who presented with tachycardia and tachypnea. Computed tomography of the chest showed inflammatory changes of the thoracic aorta with gas bubbles along the aortic wall, and post-mortem aortic tissue cultures were positive for Clostridium innocuum. Although emphysematous aortitis is rare, the radiographic findings are strikingly characteristic and should prompt immediate and aggressive management.
RESUMO
Lung cancer metastases to the pancreas are rare but potentially life-threatening. Oftentimes, the presence of symptoms is indicative of extensive disease burden. This report describes a case of primary lung adenocarcinoma metastasizing to the head of the pancreas presenting as obstructive jaundice. The patient was a 61-year-old female veteran who presented with a chronic dyspnea, weight loss, and 3-weeks of nausea and vomiting found to have jaundice, elevated alkaline phosphatase levels, hyperbilirubinemia, and transaminitis. Imaging of her chest revealed large pulmonary parenchymal nodules throughout both lungs with a large left lower lobe mass and consolidation. Abdominal imaging showed a large heterogeneous mass in the pancreatic head, a grossly dilated common bile duct, and enlarged retroperitoneal lymph nodes contiguous with the mass. Pancreatic head biopsies revealed metastatic cancer cells from her lung adenocarcinoma which was confirmed via cytology and the presence of thyroid transcription factor - 1 and cytokeritin-7 expression and the absence of tumor protein 63 staining. Lung adenocarcinomas commonly metastasize to the bones, liver, and central nervous system but very rarely to the pancreas. There have been only a few reported cases of pancreatic tumors that manifested clinically as a result of primary lung cancer metastases however, even though uncommon, hematogenous spread of cancerous tissue should be considered on the differential as a cause for obstructive jaundice in the setting of lung adenocarcinoma.
RESUMO
Pulmonary large cell neuroendocrine carcinoma (LCNEC) is an uncommon type of non-small cell lung cancer (NSCLC) with an incidence of approximately 3% of all lung cancer diagnoses. The patient was a 60-year-old male with a 90-pack year smoking history who presented with dyspnea on exertion and productive cough for five weeks. Decreased breath sounds without respiratory distress and generalized cachexia were noted on the initial physical exam. Laboratory results were unremarkable except for chronic microcytic anemia. Computed tomography revealed extensive lymphadenopathy of the paratracheal, paraaortic, hilar, and nodes surrounding the left pulmonary arteries. Additionally, there were areas of necrosis in the left upper lobe, lingula, and left lower lobe with extensive pleural thickening extending to the abdomen and subcutaneous tissue of the anterior chest wall. Biopsy and staining showed disorganized tight cell clusters with irregular and prominent nuclei and numerous lymphocytes consistent with LCNEC. Immunohistochemistry was positive for neural cell adhesion molecule CD56 and synaptophysin, which was indicative of neuroendocrine origin. It was also positive for pan-cytokeratin antibody AE1 and AE3 and cytokeratin (CAM) 5.2, which arise from epithelial origin consistent with NSCLCs. Lastly, the patient's tissue was positive for thyroid transcription factor-1, which confirmed the tumor's primary lung origin. This combination of neuroendocrine and primary lung tumor markers, in conjunction with the histology, confirmed the patient's diagnosis of LCNEC.