Small Bilateral Pleural Effusions Research Articles

Abstract 15913: Takotsubo Cardiomyopathy, is It Preventable?

Introduction: Takotsubo cardiomyopathy (TCM) is a reversible type of heart failure that occurs mostly in postmenopausal women. There are no definitive preventive measures in literature for this condition. Case: A 75-year-old female with a past medical history of hypertension presented with a new intermittent pressure-like chest pain and dyspnea right after a 1000-miles road trip. she reported that she had been feeling sad after her best friend died. Physical exam showed bilateral lower lung lobes crepitation and hypoxia. Lab work up revealed troponin of 1522 ng/L trending up to 2400 ng/L on serial measurements and elevated BNP. EKG showed ST changes and inverted T wave. Chest x-ray showed pulmonary vascular congestion and small bilateral pleural effusion. TTE showed LVEF 25-30% and mid and apical LV hypokinesis. Chest CT angiography was normal. Left heart catheter showed nonoccluded coronary arteries. LV angiogram portrayed mid and apical hypokinesis. Serology and PCR of EBV, Coxsackie B virus, CMV, HSV, influenza A and B, adenovirus and parvo virus were negative. She was started on a diuretic, a Beta blocker and an ACE inhibitor. Her symptoms improved. A follow up echocardiogram after 1 month showed improved ejection fraction and resolution of LV mid and apical hypokinesis. Recent combined emotional and physical stress of driving a long distance were thought to be the cause of stress cardiomyopathy. Discussion: Approximately 1-2% of patients presenting with symptoms of MI meet the criteria for TCM. A recent systematic review by Nyman et al on triggers of TCM found that physical factors are more common than emotional factors. However, some cases had both emotional and physical stressors. This patient had combined psychological and physical stressors, which may have precipitated TCM. postmenopausal women with recent emotional stressors should be advised to avoid physical stress until emotional issues have been resolved.

13-Year-Old Female With New Onset Multifocal Pulmonary Ground-Glass Opacities.

A 13-year-old female who recently emigrated from Honduras presented to an emergency department in Texas with a 2-month history of weight loss, fatigue, cough, and progressive shortness of breath. Her symptoms started with a nonproductive cough, and she later developed dyspnea on exertion and orthopnea. On physical examination, she was tachycardic and tachypneic. She had a thin, emaciated body habitus. She was visibly in respiratory distress with nasal flaring, tracheal tugging, and intercostal and subcostal retractions. She had diminished breath sounds at the bases and bibasilar crackles. A computed tomography scan of the chest revealed multifocal ground-glass opacities throughout all lobes of both lungs with small bilateral pleural effusions and prominent bilateral hilar lymph nodes. We will discuss the approach to the initial evaluation and subsequent diagnosis.

P15 JAKi of all trades

P15 JAKi of all trades

CARDIAC TAMPONADE SECONDARY TO COVID-19 INFECTION

CARDIAC TAMPONADE SECONDARY TO COVID-19 INFECTION

A NOVEL CASE OF LYMPHANGIOLEIOMYOMATOSIS AND PULMONARY LIGHT CHAIN DEPOSITION DISEASE

A NOVEL CASE OF LYMPHANGIOLEIOMYOMATOSIS AND PULMONARY LIGHT CHAIN DEPOSITION DISEASE

EOSINOPHILIC GRANULOMATOSIS WITH POLYANGIITIS WITHOUT ANY PERIPHERAL EOSINOPHILIA

EOSINOPHILIC GRANULOMATOSIS WITH POLYANGIITIS WITHOUT ANY PERIPHERAL EOSINOPHILIA

A RARE CAUSE OF MULTIFOCAL PNEUMONIA AND CONSTRICTIVE PERICARDITIS: COXSACKIEVIRUS A

A RARE CAUSE OF MULTIFOCAL PNEUMONIA AND CONSTRICTIVE PERICARDITIS: COXSACKIEVIRUS A

A Nonimmune Hydrops Case.

A Nonimmune Hydrops Case.

Diffuse and Nodular Pericardial Metastases From Esophageal Carcinoma

A 62-year-old man was admitted to Hwa Mei Hospital (Ningbo, China) with a 1-week history of swallowing discomfort. He was given a diagnosis of esophageal squamous cell carcinoma by endoscopic biopsy. Thoracic computed tomography (CT) showed a large pericardial effusion and a small bilateral pleural effusion. Pericardiocentesis with ultrasound guidance was performed, and 500 mL of hemorrhagic pericardial effusion fluid was drained. A 18fluorodeoxyglucose (18F-FDG) positron emission tomography (PET)–CT scan showed thickening of the upper thoracic esophageal wall (Figure 1A, arrowhead), with intense uptake of 18F-FDG.

COVID-19 VARIANTS AMONG US? PATIENT WITH COVID-19 CLINICAL PHENOTYPE, NEGATIVE RT-PCR TESTING, BUT POSITIVE IGM ANTIBODIES

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: As the COVID-19 pandemic progresses, genetic variants have been identified globally, including the UK, South Africa, and Brazil strains. These variants exhibit genetic mutations in spike proteins and open reading frame regions. Rising cases of COVID-19 strains call to question the accuracy of current polymerase chain reaction (PCR) testing in detecting genetic variants. CASE PRESENTATION: A 76-year-old male nursing home resident was brought to the emergency department (ED) by ambulance due to progressively worsening dyspnea. His past medical history was remarkable for COPD and diabetes mellitus type II. On initial presentation, his respiratory rate was 30 breaths per minute, heart rate was 128 beats per minute, blood pressure was 135/64 mmHg, and oxygen saturation was 92% on supplemental oxygen via bilevel positive airway pressure (BIPAP). Physical exam was remarkable for bilateral rhonchi with accessory muscle use. Labs were remarkable for a white blood cell count of 16.5 109/L with lymphopenia, lactic acid of 2.2 mmol/L, and a d-dimer of 5250 ng/mL. Chest CT showed bilateral patchy ground glass infiltrates, fibrotic changes, and small bilateral pleural effusions (Image 1). He tested negative for influenza A and B, Mycoplasma pneumoniae, Streptococcus pneumonia, and Legionella. Sputum cultures showed no growth. The patient tested negative for COVID-19 twice by RT-PCR analysis (Abbott Laboratory, Chicago, IL). He was treated with intravenous steroids and broad-spectrum antibiotics. He was unable to be weaned from BIPAP to a lower level of supplemental oxygen. Eight days after hospital admission, the patient tested positive for COVID-19 IgM and IgG antibodies. After 12 days of treatment, the patient suffered a fatal cardiac arrest. DISCUSSION: We present an elderly man with a clinical symptoms and imaging findings highly suggestive of COVID-19, despite multiple negative RT-PCR tests. The patient did not improve despite treatment with broad spectrum antibiotic and intravenous corticosteroids. Patients had positive COVID-19 IgM antibodies, despite no known recent prior infection. Although the lab utilized for COVID-19 RT-PCR analysis asserts that testing is not impacted by genetic variants, these cases challenge the true sensitivity of this testing in detecting emerging strains. CONCLUSIONS: There are potentially many patients in the community hospitals presenting with COVID-19 variants that are not detected by existing RT-PCR testing. The genetic diversity of COVID-19 may diminish the sensitivity of RT-PCR testing, as labs across the country utilize different primers and probes with variable sensitivities in detecting variants. Clinicians should maintain a high suspicion for COVID-19, despite negative PCR testing. REFERENCE #1: Wang R, Hozumi Y, Yin C, Wei G-W. Mutations on COVID-19 diagnostic targets. Genomics. 2020;112(6):5204-5213. REFERENCE #2: Sapoval N, Mahmoud M, Jochum MD, et al. SARS-CoV-2 genomic diversity and the implications for qRT-PCR diagnostics and transmission. Genome Res. 2021;31(4):635-644. DISCLOSURES: No relevant relationships by Gustavo Avila, source=Web Response No relevant relationships by Jessica Baek, source=Web Response No relevant relationships by Renuka Reddy, source=Web Response No relevant relationships by Claudia Tejera Quesada, source=Web Response no disclosure on file for Adam Wellikoff;

AB0739 MULTISYSTEM INFLAMMATORY SYNDROME ASSOCIATED WITH SARS-COV-2 INFECTION AND E.COLI SEPSIS: THE POTENTIAL ROLE OF PROCALCITONINE AS A RAPID DIAGNOSTIC BIOMARKER TO DISTINGUISH TWO DIFFERENT PHASES OF SYSTEMIC INFLAMMATORY RESPONSE SYNDROME

Background:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is typically very mild and often asymptomatic in children. A complication is the rare multisystem inflammatory syndrome in children (MIS-C) associated with COVID-19, presenting 4-6 weeks after infection as high fever, organ dysfunction, and strongly elevated markers of inflammation. The pathogenesis is unclear but has overlapping features with Kawasaki disease suggestive of vasculitis and a likely autoimmune etiology.Objectives:We report a case of multisystem inflammatory syndrome in children (MIS-C) in patient with SARS-CoV-2 infection and Enteropathogenic Escherichia coli (EPEC) sepsis due to acute enteritis, observed at end of December 2020 to a tertiary-care center (San Carlo Hospital), in Basilicata region (Italy).Methods:This healthy 12-year- old male patient was tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Clinical presentations was characterized by fever, abdominal pain, gastrointestinal complaints and evanescent rash. Laboratory values were remarkable for high levels of procalcitonin, C-reactive protein (CRP), D-dimers, B-type natriuretic peptide (BNP), and troponin. He also had low albumin levels. Autoantibodies tests were negative. Chest tomography showed ground-glass opacities in less than 25% of the lungs, small bilateral pleural effusion and increased cardiac area; abdominal tomography showed enlargement of the lymphnodes and ascites. Evaluation for other infectious etiologies showed molecular test positivity on fecal samples for EPEC E. coli. He received broad spectrum intravenous antibiotics (macrolids and quinolones and then carbapenems). On the seventh day the enteritis resolved and procalcitonin normalized, however he continued to have lymphopenia, thrombocytopenia, hypoalbuminemia, elevated levels of CRP, D-dimers, ferritin, troponin, and increased BNP. On the ninth day he was feverish again and developed severe cardiac and respiratory failure requiring advanced respiratory support and admission to the intensive care unit. He received IVIG (intravenous immunoglobulin at 2 g/Kg, glucocorticoids (Methylprednisolone 1mg/kg) and enoxaparin.Results:The patient was discharged asymptomatic at home after 28 days of hospital stay.Conclusion:We observed multisystem inflammatory syndrome in children (MIS-C) in a previously healthy patient with SARS-CoV-2 infection and E.coli sepsis, who became critically ill with multisystem involvement. In this case viral and bacterial infections could be considered as a double hit for the etiopathogenesis of MIS-C. The trend of procalcitonin was better than C-reactive protein for differentiating bacterial from non-bacterial phase of systemic inflammatory response syndrome (SIRS) in this critically ill child. Although the accuracy of both tests is moderate. Diagnostic accuracy could be enhanced by combining these tests with bedside clinical judgment.

STREPTOCOCCUS AGALACTIAE ENDOCARDITIS: AN UNUSUAL COMPLICATION OF GOOD'S SYNDROME

SESSION TITLE: Medical Student/Resident Disorders of the Mediastinum Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Good's Syndrome is a rare disorder characterized by thymoma associated with hypogammaglobulinemia resulting in combined B and T cell immunodeficiency in adults. We present a case of Good’s syndrome manifesting as infective endocarditis. CASE PRESENTATION: A 66-year-old female without significant medical history presented with a 14-day history of fevers, malaise, myalgias, anorexia, night sweats, and weight loss. She denied chest pain, cough, and dyspnea, syncope or orthopnea. On arrival, vitals were stable. She appeared cachectic without any other significant physical exam findings. Initial blood work was unremarkable. Further testing revealed low immunoglobulin levels IgA <5, IgM <5 and IgG <37. Blood cultures remained negative. Chest CT showed an anterior mediastinal mass and small bilateral pleural effusions. Transesophageal echocardiogram showed aortic valve vegetation (1.5x0.5 cm2) with moderate aortic regurgitation. She was empirically started on broad-spectrum antibiotics. She underwent aortic valve replacement and mediastinal mass removal with pathology confirmed as thymoma on biopsy. Valve tissue PCR was positive for Streptococcus Agalactiae. Flow cytometry of CD45+ lymphoid gate showed normal T cells with an absent B cell population. She was given a dose of intravenous immunoglobulins (IVIG) resulting in the normalization of IgG levels. She was discharged with close clinic follow-up for IVIG infusions. Her repeat IgG levels after 6 months remained in a normal range. DISCUSSION: Hypogammaglobinemia seen in Good's syndrome leads to increased susceptibility to opportunistic infections with predominance for encapsulated bacteria, viruses and fungi. Diagnosis is often challenging as the initial presentation can vary. As noted in our case, It should be suspected after an incidental finding of thoracic mass is seen on imaging in an appropriate clinical context. It can also present with symptoms due to local compressive effects of thymoma including cough, chest pain, hoarseness of voice, Horner syndrome, Superior vena cava syndrome, and dysphagia. When Good Syndrome is suspected, further investigation with measurement of T-cell subsets, B-cell and immunoglobulin levels is warranted. Treatment requires surgical resection of thymoma and immunoglobulin replacement in addition to the treatment of opportunistic infections. It is associated with worse outcomes as compared to X-linked agammaglobulinemia and combined variable immunodeficiency. It is reported that survival at 5-years following diagnosis is around 70%. CONCLUSIONS: Good’s syndrome should be considered in adults with thymoma with unexplained hypogammaglobulinemia. Its diagnosis is often challenging due to variable symptomatology and lack of awareness of this condition. However, due to high mortality and morbidity associated with it, early recognition and timely intervention are essential to improve prognosis. Reference #1: Kelleher P, Misbah SA. Review: What is Good's syndrome? Immunological abnormalities in patients with thymoma. J Clin Pathol Jan. 2003;56(1):12–16. Reference #2: Kelesidis T, Yang O. Review: Good's syndrome remains a mystery after 55 years: A systematic review of the scientific evidence. Clinical Immunology Jun. 2010;135(3):347–363 Reference #3: Ohuchi M, Inoune S, Igarashi T, et al. Good Syndrome Coexisting With Leukopenia. Ann Thorac Surg. 2007;84:2095–2097 DISCLOSURES: No relevant relationships by Shahrukh Arif, source=Web Response No relevant relationships by Firas Jafri, source=Web Response

A Curious Case of Confusion in a Patient With Cirrhosis

A Curious Case of Confusion in a Patient With Cirrhosis

2027 Upper GI Bleeding With Black Esophagus: Case Report of Acute Esophageal Necrosis

INTRODUCTION: Acute esophageal necrosis, a very rare cause of upper GI bleeding, is seen mainly in elderly men. We report a new case in an elderly woman. CASE DESCRIPTION/METHODS: A 90-year-old woman with a history of DM, HTN, and CHF presented with SOB and abdominal pain of 2-day duration. She didn’t vomit. Confusion, pallor, and large melanotic bowel movement were noted. Temperature was 36.1°C, BP 86/68 mmHg, HR 104 bpm, and RR 22 br/min. She had bilateral shallow coarse breath sounds and otherwise unremarkable abdominal and neurological exams. Urine ketones was negative, plasma glucose 98 mg/dL, WBC 40.8 K/mcL, hemoglobin 9.3 g/dL, platelet 437 K/mcL, GFR 18 mL/min/1.73 m2, lactate 15.5 mmol/L, and procalcitonin 1.49 ng/mL. Blood culture was negative. Chest CT showed small bilateral pleural effusions and ground glass opacities. Abdominal CT showed fecal impaction. Working diagnoses included septic/hypovolemic shock, pneumonia, encephalopathy, acute upper GI bleed, and acute hypoxic respiratory failure. Volume resuscitation, vasopressors (norepinephrine, phenylephrine, and vasopressin), mechanical ventilation, broad spectrum antibiotics (vancomycin, cefepime, and azithromycin), total parenteral nutrition, and proton pump inhibitor were started. EGD revealed friable, black, circumferential esophageal mucosal changes starting 25-30 cm from incisors and extending to GE junction without gastric outlet obstruction (Figure 1). Follow up EGD one week later showed slow healing with black and thin tissue, starting 4 cm proximal to GE junction without stricture (Figure 2). She continued to be encephalopathic, requiring mechanical ventilation and vasopressor support. She died upon intensive care withdrawal at family request. DISCUSSION: Our patient had endoscopic diagnosis of acute ischemic esophagitis, which was likely due to compromised esophageal perfusion secondary to septic/hypovolemic shock in the setting of chronic vascular compromise. Biopsy to differentiate ischemic esophageal necrosis from other etiologies, such as infection and malignancy, carries a high risk for perforation and was not performed. As seen in our patient, acute esophageal necrosis typically affects the relatively hypovascular distal esophagus down to GE junction and quickly resolves when blood flow is restored. Nevertheless, mortality remains high due to the underlying conditions. Unlike our case, acute esophageal necrosis affects mainly men, with a men/women ratio of 4/1.

3205 A Rare Case of Salmonella Gastroenteritis Presenting as Aspiration Pneumonia With Pleural Empyema in Immunocompetent Patient

INTRODUCTION: Salmonellae are gram negative rods belongs to Enterobacteriaceae. They commonly cause enterocolitis, enteric fever, endovascular infection and bacteremia with localized infection which can occur at any site. Pulmonary involvement especially empyema is very rare and usually reported in immunosuppressed patients secondary to co-morbidities such as HIV,malignancy,diabetes and iatrogenic (steroids/chemotherapy). CASE DESCRIPTION/METHODS: 76-year-old male with past medical history of Ischemic cardiomyopathy with 35% EF status post AICD, CKD stage 3, dementia and stroke presented to ER for generalized weakness, fever, coughing, right sided lower chest pain, abdominal pain, non-bloody watery diarrhea and vomiting for 3 days. Physical examination revealed new oxygen requirement with respiratory rate 24/min, blood pressure 110/75 mmgh, heart rate 70/min and temperature 100.9 F. He was ill appearing, lethargic with +1 pedal edema. Abdomen was soft but with epigastric/right upper quadrant tenderness. Decreased breath sounds were present at bases. Initial laboratory results showed leukocytosis of 12000 K/ul, normal AST/ALT, elevated bilirubin 2.1 mg/dl, Alkaline phosphatase 324 u/l, BUN 37 mg/dl and Creatinine of 1.8 (at baseline). Chest x-ray showed right greater than left small bilateral pleural effusions and bibasilar atelectasis/infiltrates. Ultrasound RUQ negative for acute cholecystitis. Patient was started on intravenous lasix was started given concern for volume overload and IV antibiotics for possible aspiration pneumonia. Low grade fevers persisted for next 24-36 hrs along with worsening breathing. Repeat chest x-ray showed worsening right pleural effusion. CT chest revealed large loculated left pleural effusion with infiltrates, small right effusion with nearby atelectasis and distended esophagus. Chest tube was placed along with injecting tPA/DNase to help break up loculations. Patient passed swallow evaluation and further testing was negative like blood/sputum cultures and stool studies. Pleural fluid was exudative and grew few non-typhoid salmonella species without reporting of exact identification by laboratory. Patient was discharged in stable condition on 4 weeks of Amoxicillin/clavulanic acid after consultation with Infectious disease specialist. DISCUSSION: Non-typhi salmonella causing pneumonia and empyema is very rare. Most common presentation is gastroenteritis. Patients presenting with gastroenteritis and pulmonary involvement, clinicians should keep salmonella as a differential diagnosis.

A Chest X-Ray causing confusion

The Chest X-Ray (Figure 1) shows right unilateral pulmonary oedema with small bilateral pleural effusions. Unilateral pulmonary oedema can easily be mistaken for other pathologies such as pneumonia or pulmonary haemorrhage or even malignancy.

A CASE OF ACUTE INTERSTITIAL PNEUMONIA

SESSION TITLE: Lung Pathology 1 SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Acute interstitial pneumonia (AIP) is a rare and life-threatening condition resulting in acute respiratory failure. Early recognition is paramount as patients often deteriorate rapidly. The pathogenesis is not well understood. Computed tomography (CT) imaging may show a pattern similar to that observed in acute respiratory distress syndrome (ARDS) (1) and the histopathologic pattern is characterized by diffuse alveolar damage (DAD). CASE PRESENTATION: We present a 56 year-old male with a history of tobacco use and type-2 diabetes mellitus who presented with new symptomatic anemia (hemoglobin 7.3 mg/dL), fever (39.4 degrees Celsius), tachycardia, and a non-productive cough. Physical examination was unremarkable except for skin and conjunctival pallor. Laboratory values revealed neutropenia (absolute neutrophil count of 0.33 K/uL) and 33 percent blast cells on the differential. CT chest demonstrated bilateral ground glass opacities and small bilateral pleural effusions. A bone marrow biopsy and peripheral flow cytometry findings were consistent with acute myeloid leukemia (AML). Broad-spectrum antibiotics were initiated for neutropenic fever. The patient underwent bronchoscopy with bronchoalveolar lavage (BAL) and transbronchial biopsies to evaluate for infection prior to initiation of chemotherapy. Infectious work up and cytology findings were negative. Pathology from the biopsy demonstrated a mild inflammatory infiltrate with fibrin exudate and hyaline membranes consistent with DAD, a non-specific finding consistent with acute lung injury. The patient proceeded to develop acute hypoxic respiratory failure with rapidly rising oxygen requirements. Following a negative rheumatologic work up, a diagnosis of AIP was made. Pulse-dose steroids were initiated and over the next several days his respiratory status significantly improved. Steroids were tapered over the course of several months and he was able to tolerate initiation of chemotherapy. A follow up CT chest after one month showed improvement of the ground glass opacities noted on the initial scan. DISCUSSION: DAD in a non-specific histological finding that may result from various types of lung injury. When there is no known trigger, it is called AIP or Hamman-Rich Syndrome. The exact mechanism of AIP is not well understood. Treatment consists primarily of supportive measures, which may include mechanical ventilation and extracorporeal membrane oxygenation (ECMO) (2). Management of early stages of AIP has had some success with high dose steroids (3). Evidence for the role of non-steroid immunosuppressive agents is limited. CONCLUSIONS: Prompt recognition of AIP is critical. Despite treatment, it carries a poor prognosis. The mainstay of therapy consists of supportive measures and the use of steroids. AIP is a diagnosis of exclusion and one must consider other known causes of DAD, including infection, medications, and autoimmune processes. Reference #1: Avnon LS, Pikovsky O, Sion-Vardy N, Almog Y. Acute Interstitial Pneumonia–Hamman-Rich Syndrome: Clinical Characteristics and Diagnostic and Therapeutic Considerations. Anesthesia & Analgesia. 2009 Jan 1;108(1):232-7. Reference #2: Newmarch W, Puopolo A, Weiler M, Casserly B. Hamman-Rich syndrome: a forgotten entity. Monaldi Archives for Chest Disease. 2017 May 18;87(1). Reference #3: Suh GY, Kang EH, Chung MP, Lee KS, Han J, Kitaichi M, Kwon OJ. Early intervention can improve clinical outcome of acute interstitial pneumonia. CHEST Journal. 2006 Mar 1;129(3):753-61. DISCLOSURES: No relevant relationships by Michael Esposito, source=Web Response No relevant relationships by Craig Fryman, source=Web Response No relevant relationships by Becky Lou, source=Web Response No relevant relationships by Gulrukh Zaidi, source=Web Response

Metastatic Gastric Adenocarcinoma Mimicking Pulmonary Tuberculosis

Gastric Cancer is a leading cause of morbidity and mortality worldwide, which makes timely and accurate detection critical. The rare presentation of Gastric Adenocarcinoma (GA) with miliary pulmonary metastases, known as Bard's Syndrome, can be easily mistaken for more common primary pulmonary diseases, such as tuberculosis. We present a case of a 43 year old El Salvadorian male with persistent pleuritic chest pain and fevers despite treatment for disseminated infiltrates suggestive of TB. Diagnostic biopsies obtained after failed treatment confirmed GA which prompted initiation of palliative chemotherapy. A 43-year-old male from El Salvador with no significant PMH, presented with a two day history of fevers, chills and pleuritic chest pain. Chest imaging (Figures 1 and 2) revealed bilateral miliary infiltrates suggestive of TB as well as PE, which prompted initiation of RIPE therapy and anticoagulation. He returned two weeks later with worsening symptoms and repeat imaging of the chest raised suspicion for pneumonia. He improved and was discharged home on antibiotics. One week later, he developed severe abdominal pain and was found to have abdominal ascites. CT Abdomen revealed extensive clot formation throughout iliac venous system and omental caking, initially worrisome for TB peritonitis versus carcinomatosis. TB therapy was discontinued as prior AFB cultures came back negative. Omental biopsy was consistent with CK7 positive adenocarcinoma. Linitis plastica was observed on EGD (Figure 3) and EUS biopsy later confirmed malignant cells from primary gastric adenocarcinoma. The patient was initiated on palliative chemotherapy with Epirubicin, Oxaliplatin, Capecitabine (EOX). Given our patient's demographics, symptoms and radiographic imaging, a diagnosis of TB was initially made with differentials focused on primary pulmonary pathology. However, this limited differential caused an unintentional delay in detection and treatment of gastric adenocarcinoma, a disease of remarkable morbidity and mortality. Gastric carcinoma is the fourth leading cause of cancer worldwide, the second leading cause of cancer related death, and carries a significant cancer burden. GA has a 2:1 male predominance, and while incidence in North America has decreased there is a higher incidence in Hispanic populations. By adding Bard's Syndrome to the differential of miliary pulmonary infiltrates, the burden of this destructive and deadly disease can be decreased.2676_A Figure 1. Diffuse miliary pulmonary nodular opacities.2676_B Figure 2. Innumerable small bilateral pulmonary nodules with small bilateral pleural effusions.2676_C Figure 3. Linitis Plastica noted on Esophagogastroduodenoscopy

A Rare Case of Undifferentiated High-Grade Sarcoma Masquerading as Thrombus Resulting in Acute Budd-Chiari Syndrome

We present a rare case of Budd-Chiari Syndrome (BCS) from a high-grade undifferentiated sarcoma that invaded and obstructed the inferior vena cava (IVC), hepatic veins and right atrium. There are just 6 cases of venous undifferentiated intimal sarcomas reported in the literature. A 56-year-old Caucasian female with hypertension presented to her primary doctor with 2 weeks of abdominal bloating, abdominal pain, 10-pound weight gain and lower extremity swelling. On exam she had mild ascites, tender hepatomegaly and lower extremity edema. Liver tests were unremarkable, but abdominal ultrasound revealed both mild ascites and both IVC and hepatic vein thrombosis. She was referred to the hospital and a CT revealed extensive thrombus within the entire IVC extending into the right atrium showing a separate 5.0 cm right atrial mass, as well as thrombus extending into the right gonadal vein and the renal veins bilaterally. Imaging showed moderate ascites as well as heterogeneous liver appearance presumably related to passive congestion. A 2-D echocardiogram revealed an ejection fraction of 50-55% with IVC thrombus extending into the right atrium creating a functional tricuspid stenosis from inflow obstruction. The patient was started on a heparin drip to prevent further clot burden and transferred to a tertiary care facility for further intervention. During open heart surgery the right atrial portion of the 5.0cm mass was excised and freed from the tricuspid valve. The portion of the mass coming from the IVC was adherent to the wall of the vessel and right atrium and unresectable. Frozen section immunostains of the tumor cells revealed negative epithelial differentiation (pancytokeratin), endothelial cell markers (CD34, CD117), nerve sheath differentiation (S100), and smooth muscle actin (SMA). Additional stains were negative for actin (HHF), desmin, CD99, EMA and CAM 5.2. The histology showed that there was cell neoplasm with pleomorphism - bizarre, enlarged nuclei, high nuclear-cytoplasmic ratio and abundant mitoses indicative of undifferentiated high-grade sarcoma. The patient was referred to an oncology center for chemotherapy and the patient is doing well. Without surgical intervention this could have been misdiagnosed and treated with long term anticoagulation. This unique BCS case stresses the importance of using different image modalities such as ultrasound and CT imaging to promptly diagnosis and assess the surgical approach.2429_A Figure 1. High-grade undifferentiated sarcoma extension into the inferior vena cava (IVC) and the right atrium showing a separate 5.0 cm right atrial mass, which caused a functional tricuspid stenosis from inflow obstruction.2429_B Figure 2. CT imaging shows a massive high-grade sarcoma tumor continuously present within the dilated inferior vena cava and tumor occupation extending into the right atrium. Thrombus extends into the right gonadal vein and the renal veins bilaterally. Moderate ascites and subcutaneous edema with small bilateral pleural effusions and heterogeneous appearance to the liver presumably related to passive congestion.2429_C Figure 3. Frozen section immunostains of the tumor cells revealed negative epithelial differentiation (pancytokeratin), endothelial cell markers (CD34, CD117), nerve sheath differentiation (S100), and smooth muscle actin (SMA). Additional stains were negative for actin (HHF), desmin, CD99, EMA and CAM 5.2. The histology showed that there was cell neoplasm with pleomorphism - bizarre, enlarged nuclei, high nuclear-cytoplasmic ratio and abundant mitoses indicative of undifferentiated high-grade sarcoma.

Dysphagia: The Primary Indicator of Esophageal Compression by a Pericardial Effusion

Introduction: Dysphagia is a relatively common symptom seen in late adulthood and can be classified as oropharyngeal or esophageal. Esophageal dysphagia typically presents due to scarring from acid reflux, strictures within the lumen, a tumor causing obstruction or an infection causing inflammation. A rare occurrence of dysphagia is reported here as an outcome of extrinsic compression of the esophagus by a large pericardial effusion. Case: A 61-year-old male with a history of DM, epilepsy, schizophrenia, vertigo and hyperlipidemia presented with an episode of hemoptysis and dysphagia for 3 weeks duration. Although this was the first account of hemoptysis, he admitted to a dry cough for a few months. He noted his dysphagia was predominantly to solids and unless he ate slowly, he would regurgitate. He denied any fever, shortness of breath, chest pain, weight loss or night sweats. On initial examination the patient was an obese male with stable vitals except for a slightly low oxygen saturation of 94%. Inspection of the neck revealed no masses. On auscultation, heart sounds were difficult to appreciate. Labs initially revealed an elevated WBC of 15.3, platelet count of 110, a blood sugar of 222 and the remaining results were within normal limits. Chest X-Ray showed infra-hilar infiltrates suggesting pneumonia and cardiomegaly. Modified barium swallow was negative. An esophagogastroduodenoscopy revealed mild extrinsic compression in the mid-esophagus but no strictures. CT of the chest showed a large pericardial effusion of 3.3 cm compressing the esophagus and chronic atelectasis with small bilateral pleural effusions. An echocardiogram confirmed a worsening pericardial effusion from 1 year previous and a dropping left ventricular ejection fraction (40-45% to 20-25%). Initial option for treatment was a pericardial window, but a cardiac catheterization revealed 2-vessel CAD with left main involvement. The patient ended up having a CABG and having his pericardial effusion drained. Follow up echocardiogram one month later revealed no pericardial effusion and a complete resolve of his dysphagia. Discussion: While there are documented cases of pericardial effusion resulting in compression of the esophagus, it is a rare occurrence. This case emphasizes that while dysphagia is often an esophageal complaint, the origin of the symptom may be non-GI and communication between GI and cardiac specialists is essential.