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SESSION TITLE: Etiologies of Cardiovascular Disease Case Report Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Troponin level (Tnl) is usually used as confirmation of acute myocardial infarction (AMI) and is a sensitive marker. It is usually increased within 2-3 hours after AMI. In most cases, increased in Tnl is associated with symptomatic chest pain, cardiac ischemia, chronic coronary syndromes, etc. It can also be elevated in other conditions without cardiac injuries, like critical illness: COVID infection, septic shock, acute stroke and burns. CASE PRESENTATION: A 72 y/o man with history of b/l internal carotid artery (ICA) stenosis (70% in R-ICA and 80-90% in L-ICA) underwent elective left trans-carotid artery revascularization (TCAR). He was transferred to ICU after an uneventful procedure, for monitoring. His history was significant for HTN, HLD, Meniere's disease, gout, prior CVA of L-frontal lacunar and R-PICA (posterior inferior cerebellar artery). Postop vitals: BP 114/60 mmHg, HR 65, RR 16, O2 sat 98%. Tnl increased to 1.95 and then declined (normal 0 - 0.4 ng/ml). He was AAOx4, and asymptomatic. Post-op serial EKGs: normal sinus rhythm with no ST/T wave changes. Echo: EF 60%, normal biventricular size and function. LDL <70, A1C 5.9, normal TSH, no CPK elevation. Other labs: normal, No new neurological deficits. He was continued on ASA, clopidogrel, metoprolol, amlodipine and lisinopril. His hospital stay was uneventful, and he was discharged on post-op day 3. DISCUSSION: Cardiac troponin complex has its distinct subunits according to their functions: highly conserved Ca2+ binding subunit (cTnC);actomyosin ATPase inhibitory subunit and tropomyosin binding subunit. They play the pivotal role in regulating myocardial muscle contraction and relaxation and demonstrate as sensitive biomarkers for the myocardial injuries. Interestingly, there are many other causes that lead to increased cardiac troponin level without remarkable myocardial injuries or ischemia. Elevated Tnl after TCAR procedure can also be due to its surgical complication of a chance of hypoperfusion during the procedure. Our patient's surgery was uneventful. In one randomized controlled trial, it is stated that the risk of having CVA and AMI is higher in carotid endarterectomy compared to revascularization in patients with carotid artery stenosis. Our patient did not have any post-op complication, and only had an idiopathic elevation of troponin. CONCLUSIONS: The role of Tnl plays an important role in confirmation of myocardial infarction or ischemia but it can be idiopathic. Unpublished data from our institution revealed no increase in troponin s/p TCAR after uneventful procedures. This is the first reported case presenting with elevated troponin level without any pertinent positive findings (EKG changes/symptoms). Maybe in uneventful TCAR procedure troponin should not be ordered? Reference #1: Defilippi, C.R., Tocchi, M., Parmar, R.J., Rosanio, S., Abreo, G., Potter, M.A., Runge, M.S., & Uretsky, B.F. (2000). Cardiac troponin T in chest pain unit patients without ischemic electrocardiographic changes: angiographic correlates and long-term clinical outcomes. Journal of the American College of Cardiology, 35 7, 1827-34. Reference #2: Gordon AM, Homsher E, Regnier M. Regulation of contraction in striated muscle. Physiol Rev. 2000 Apr;80(2):853-924. doi: 10.1152/physrev.2000.80.2.853. PMID: 10747208. Reference #3: Brott, T.G., Hobson, R.W., Howard, G., Roubin, G.S., Clark, W.M., Brooks, W., Mackey, A., Hill, M.D., Leimgruber, P.P., Sheffet, A.J., Howard, V.J., Moore, W.S., Voeks, J., Hopkins, L.N., Cutlip, D.E., Cohen, D.J., Popma, J.J., Ferguson, R.D., Cohen, S.N., Blackshear, J.L., Silver, F.L., Mohr, J.P., Lal, B.K., & Meschia, J.F. (2010). Stenting versus endarterectomy for treatment of carotid-artery stenosis. The New England journal of medicine, 363 1, 11-23. DISCLOSURES: No relevant relationships by Moses Bachan No relevant relationships by Zin Min Htet No relevant relationships by Z nobia Khan No relevant relationships by Zin Oo
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SESSION TITLE: Drug-Induced Lung Injury Pathology Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Acute eosinophilic pneumonia (AEP) is an atypical cause of acute hypoxic respiratory failure in adults, however if not identified can prove to be fatal. It can all be a COVID19 mimic during the pandemic. AEP has several causes, such as inhalational drugs, infections and various pharmaceuticals. Often, patients will have an acute respiratory syndrome for less than one-month, pulmonary infiltrates on chest computed tomography (CT) or radiography (CXR), in addition to bronchoalveolar lavage (BAL) with more than 25% of eosinophils. CASE PRESENTATION: A 79 y/o man underwent an elective total knee replacement complicated by acute lower limb ischemia from an occluded bypass graft. He developed methicillin-resistant Staphylococcus aureus (MRSA) and Vancomycin-resistant Enterococcus (VRE) joint and soft tissue infection of the lower extremity. He was prescribed a 6-week course of Daptomycin. He presented about 3 weeks into treatment with shortness of breath. He was initially diagnosed with acute on chronic congestive heart failure (CHF) exacerbation and COVID negative. He was initially treated with diuretics. He developed acute renal failure requiring dialysis and acute hypoxic respiratory failure requiring intubation. CXR revealed bilateral lung infiltrates with BAL having 80% eosinophils, eosinophilia and urinalysis positive for eosinophils. Daptomycin was discontinued and he was started on systemic steroids for a two-week course. He was successfully extubated 5 days after diagnosis of AEP and was subsequently discharged to a rehabilitation facility on lifelong Doxycycline for MRSA prosthetic joint infection prophylaxis. DISCUSSION: AEP related to Daptomycin was first reported in 2007, in a patient that developed the condition after receiving treatment for endocarditis. Daptomycin caused an inflammatory reaction within the lungs, due to an accumulation of the drug within the pulmonary surfactant. Our case report patient met all components for AEP diagnosis, in addition to symptom onset being approximately 3 weeks into treatment. The ultimate treatment for AEP is to stop the reversible cause, if identifiable, along with glucocorticoids and symptomatic support. Prognosis for patients with AEP is excellent when diagnosis is prompt, and usually infiltrates are resolved within 1 month without long term adverse pulmonary effects. Our patient was discharged to an acute rehab facility without supplemental oxygen therapy and continues to improve from functional standpoint. This case a definite cause of AEP from Daptomycin presented as COVID19 pneumonia mimic. It highlights the importance of rapid diagnosis to prevent morbidity and mortality. CONCLUSIONS: The differential in a patient with acute hypoxic respiratory failure is numerous, especially during the COVID19 pandemic. During these challenging times, it is important to think of atypical causes, such as AEP to improve the patient's clinical status. Reference #1: Allen JN, Pacht ER, Gadek JE, Davis WB. Acute Eosinophilic Pneumonia as a Reversible Cause of Noninfectious Respiratory Failure. N Engl J Med. 1989;321:569-574 Reference #2: Hayes Jr. D, Anstead MI, Kuhn RJ. Eosinophilic pneumonia induced by daptomycin. J Infect. 2007;54(4):e211-213. Reference #3: Rachid M, Ahmad K, Saunders-Kurban M, Fatima A, Shah A, Nahhas A. Daptomycin-Induced Acute Eosinophilic Pneumonia: Late Onset and Quick Recovery. Case Reports in Pulmonology. 2017. DISCLOSURES: No relevant relationships by Moses Bachan No relevant relationships by Zinobia Khan No relevant relationships by Kaitlyn Mehern
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SESSION TITLE: Critical Renal and Endocrine Disorders Case Report Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: About 7% of acute pancreatitis (AP) cases are caused by hypertriglyceridemia (HTG). In such cases bowel rest, IV fluids, symptomatic therapy, and triglyceride (TG) lowering interventions are initiated. Plasmapheresis is one of the treatment options, but it has specific indications. We present a case of severe hypertriglyceridemia-induced pancreatitis that required plasmapheresis. CASE PRESENTATION: A 30 y/o man with type 2 diabetes, hyperlipidemia, multiple previous admissions for HTG-AP, presented with severe abdominal pain, nausea, and vomiting x 1 day. On admission, he was tachycardic, hypotensive, afebrile, SpO2 > 96% on RA. Labs: Glu 491 mg/dL, TG > 1000 mg/dL, Cholesterol 509 mg/dL, Lipase 987 U/L, Cr/BUN 2.4 mg/dL /20 mg/dL, VBG pH 7.25/PCO2 36.2 mmHg/PO2 19.4 mmHg/Ca 0.8/lactate 5.6;WBC 13.07 K/cm;COVID PCR positive. CXR: diffuse patchy opacities. CTAP with contrast was deferred because of AKI. He was admitted to the ICU and started on insulin drip with no improvement over 24hrs. He was still acidotic, Ca persistently low, TG still >1000, and kidney function worsened. Plasmapheresis was initiated. After one session his TG lowered to 700. He was restarted on insulin drip and in the next 24hr TG decreased to < 500 and metabolic acidosis resolved. Once AKI resolved, CT abdomen/pelvis with contrast confirmed acute pancreatitis, with focal hypodensities within the uncinate process and the proximal body, concerning infarcts as well as large phlegmon surrounding the pancreas, but no evidence of necrotizing or hemorrhagic pancreatitis. His hospital course was complicated with sepsis and DVT, which resolved with therapy. He was discharged home with TG lowering agents, Apixaban, and his previous T2DM regimen. DISCUSSION: Plasmapheresis is indicated in patients with severe HTG (>1000- 2000 mg/dl), severe HTG-AP, and when standard treatment options are inadequate. It lowers the lipid levels and removes proinflammatory markers and cytokines stopping further inflammation and damage to the pancreas and other organs faster compared to conservative therapy. Most patients need only one session which lowers TG level by 50-80%, as seen in our patient. CONCLUSIONS: Plasmapheresis should be considered in cases of HTGP with worrisome features such as lactic acidosis, hypocalcemia, worsening inflammation, and multi organ failure. Reference #1: Rajat Garg, Tarun Rustagi, "Management of Hypertriglyceridemia Induced Acute Pancreatitis", BioMed Research International, vol. 2018, Article ID 4721357, 12 pages, 2018. https://doi.org/10.1155/2018/4721357 Reference #2: Pothoulakis I, Paragomi P, Tuft M, Lahooti A, Archibugi L, Capurso G, Papachristou GI. Association of Serum Triglyceride Levels with Severity in Acute Pancreatitis: Results from an International, Multicenter Cohort Study. Digestion. 2021;102(5):809-813. doi: 10.1159/000512682. Epub 2021 Jan 21. PMID: 33477149. Reference #3: Gavva C, Sarode R, Agrawal D, Burner J. Therapeutic plasma exchange for hypertriglyceridemia induced pancreatitis: A rapid and practical approach. Transfus Apher Sci. 2016 Feb;54(1):99-102. doi: 10.1016/j.transci.2016.02.001. Epub 2016 Feb 20. PMID: 26947356. DISCLOSURES: No relevant relationships by Adam Adam No relevant relationships by Moses Bachan No relevant relationships by Chen Chao No relevant relationships by Vaishali Geedigunta No relevant relationships by Zinobia Khan No relevant relationships by Jelena Stojsavljevic
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SESSION TITLE: Critical Care Presentations of TB SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: TNFα plays a pivotal role in inflammation and maintenance of immune response against tuberculosis. The use of TNF inhibitors (TNFi) is associated with a significant increase in the incidence of tuberculosis (TB). TNFi may cause drug-induced lupus (ATIL) presenting as constitutional symptoms, rashes, pericardial and pleural effusions with positive autoantibodies. We present a case of pleural TB masquerading as drug-induced lupus. CASE PRESENTATION: A 68y/o woman with a history of ulcerative colitis (on infliximab, mesalamine), hypertension, T2DM, CAD, complained of low-grade fever, rashes, left-sided chest pain, dyspnea, and arthralgias for two weeks. Chest pain- worse with inspiration and cough. She emigrated from India to the USA 40 years ago. Six months before infliximab therapy, Quantiferon gold was negative. Exam: faint hyperpigmentation over shins, minimal swelling of MCPs and ankles, dullness to percussion over the left chest with decreased breath sounds. Labs: CRP 101 mg/dL, Hb 10.8 iron deficient, rheumatoid factor and anti-CCP negative, ANA 1:40, dsDNA 1:640, a reminder of ENA negative, anti-histone negative, C3/C4 normal, UA bland, protein/Cr 0.4 mg/gm, negative blood cultures, SPEP and LDH normal. CXR: opacification of the left lung up to midfield. CT chest: moderate left and small right pleural effusions, enlarged mediastinal lymph nodes. COVID and Quantiferon: negative. Thoracentesis: 850 ml of exudative fluid (2 out of 3 Light's criteria), lymphocytic predominance (76% of 4148 nucleated cells), adenosine deaminase (ADA) 42 U/L, gram stain, culture, acid-fast and MTB PCR negative, cytology negative. Thoracoscopy with biopsy of the parietal pleura: necrotizing granulomatous pleuritis with acid-fast bacilli. Sensitivity: pan-sensitive M. tuberculosis. Sputum: negative for TB. She was discharged on RIPE treatment for reactivation of TB. DISCUSSION: The incidence of infliximab-induced lupus is approximately 0.19% and confirming the diagnosis is challenging. The immunogenicity of infliximab is high, 66% of patients develop positive ANA. Anti-histone antibodies are less commonly associated with ATIL as opposed to classic drug-induced lupus and dsDNA is positive in up to 90% of cases of ATIL. Renal involvement is rare. The diagnostic usefulness of ADA (over 40 U/L) in lymphocytic pleural effusions for the diagnosis of tuberculosis in an immunosuppressed individual is demonstrated here. In countries with low TB burden, such as the USA, the positive predictive value of ADA in pleural fluid declines but the negative predictive value remains high. CONCLUSIONS: Tuberculous pleuritis is not always easily diagnosed since AFB smears and sputum may remain negative. When ADA level in lymphocytic pleural fluid is not low thorough search for TB with thoracoscopy and biopsy is justified. Reference #1: Shovman O, Tamar S, Amital H, Watad A, Shoenfeld Y. Diverse patterns of anti-TNF-α-induced lupus: case series and review of the literature. Clin Rheumatol. 2018 Feb;37(2):563-568. Reference #2: Benucci, M., Gobbi, F. L., Fossi, F., Manfredi, M. & Del Rosso, A. (2005). Drug-Induced Lupus After Treatment With Infliximab in Rheumatoid Arthritis. JCR: Journal of Clinical Rheumatology, 11 (1), 47-49. Reference #3: Valdés L, San José ME, Pose A, Gude F, González-Barcala FJ, Alvarez-Dobaño JM, Sahn SA. Diagnosing tuberculous pleural effusion using clinical data and pleural fluid analysis A study of patients less than 40 years-old in an area with a high incidence of tuberculosis. Respir Med. 2010 Aug;104(8):1211-7. DISCLOSURES: No relevant relationships by Adam Adam No relevant relationships by Moses Bachan No relevant relationships by Chen Chao No relevant relationships by Zinobia Khan No relevant relationships by Milena Vukelic
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INTRODUCTION: Covid- 19 has been associated with various fungal infections in immunocompetent/immunocompromised patients. We report the second case of PCP pneumonia coinfection in a HIV- uninfected man with COVID-19. CASE: A 52 y/o man with PMH of hyperlipidemia, gout, viral myocarditis and no prior immunodeficient conditions was admitted to hospital for COVID-19 SARS (Severe Acute Respiratory Syndrome) CoV- 2 Pneumonia. He was initially treated with Dexamethasone 6mg/day, Remdesivir and Tocilizumab x 2doses and oxygen therapy. On day 4, he was transferred to ICU for acute hypoxemic respiratory failure requiring NIV eventually requiring intubation with Fio2-60-90%. His course was complicated by AKI, septic shock requiring pressor for BP support. He received empiric ceftriaxone and Hydrocortisone for suspected adrenal insufficiency. Despite antibiotics, labs showed increasing WBC count with decreasing procalcitonin. Blood/urine cultures: no growth. Tracheal cultures: Ceftriaxone-sensitive E.coli therefore was continued on ceftriaxone. On ICU day3, he was still febrile so was started on prophylactic Bactrim for PCP suspecting immunosuppression although he was never treated with long term high dose steroids. Fungal cultures, Aspergillus, HIV, Beta-D glucan - negative. He was afebrile after 7days of antibiotics and PCP testing was done to discontinue Bactrim. Tracheal aspirate culture reported positive for PCP diagnosed with IFA stain. LDH - 471 but is an unreliable marker in the setting of covid pneumonia. HRCT was not attained due to unstable hemodynamics. Prophylactic Bactrim was then switched to therapeutic dose and also started on Prednisone 40mg twice daily on tapered dose. DISCUSSION: PCP is an infection commonly seen in immunocompromised individuals but may colonize healthy individuals remaining asymptomatic and serving as a reservoir to transmit and affect immunocompromised hosts with immunodeficiency syndromes/malignancy/organ transplant. Diagnosis is made via identification of organism via staining/PCR. Based on previous case series reported by Mayo Clinic amongst HIV- uninfected individuals, an average dose of steroids was 30mg/ day (minimum-16mg/ day) for an average duration of 12 weeks (minimum-8weeks) to acquire PCP infection. Our subject was treated with Hydrocortisone dose equivalent to a prednisone dose ∼ 75mg/day x 1 week which may have induced immunosuppression or due to COVID-19 infection itself making him susceptible for PCP infection. First case of PCP pneumonia coinfection in COVID-19 (recovered) was reported in March 2021. CONCLUSION: Our case report is unique for two reasons, PCP diagnosis via tracheal aspirate and two, detected in COVID-19 infected patient post prophylaxis. PCP coinfection with COVID-19 should be identified and treated.
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INTRODUCTION: Dietary and herbal supplements can contain clinically significant amounts of exogenous thyroid stimulants and hormones, including T3 and T4, thus placing consumers at increased risk of thyrotoxicosis and other metabolic-related adverse effects. We present a case of thyrotoxicosis in a young man with no history of thyroid disease, who was found to be consuming an extensive variety of supplements. DESCRIPTION: A 31 year old man with hypertension presented with 1 week of intermittent palpitations. He was in his usual state of health until 1 week prior to admission, when he noticed intermittent, self-resolving episodes of tachycardia as high as the 160s on his smart watch, associated with palpitations, dyspnea, low grade fevers, and intermittent dry cough. He came to the ED for persistence of symptoms. In the ED: T 98.8 F, HR 129, BP 152/77, RR 18, SpO2 98% on RA. CBC, BMP, UA, UTox, blood alcohol content, troponin and COVID tests were unremarkable. TSH was < .007 [0.358-3.740 ulU/mL], with a free thyroxine of 0.54 [0.70-1.48 ng/dL];other thyroid studies later returned with TSI < 0.10 [0.00-0.55 IU/L], free T3 32.50 [1.80-4.60 pg/mL], and an unremarkable thyroid ultrasound. CXR showed no acute infiltrates. EKG revealed sinus tachycardia, no Wolff-Parkinson-White syndrome, and no Brugada waveforms. He was given 2L NS, ceftriaxone 1g IV, aspirin 81mg PO, and tylenol 650mg PO, and admitted to the telemetry unit. Exam revealed an anxious appearing man with tachycardia. On ROS, patient admitted to drinking 6-8 cups of coffee daily, and to taking at least a dozen different supplements. He was started on propranolol 30 mg every 6 hours with improvement in his heart rate, and was counseled to stop the supplements and wean his caffeine intake. He was discharged the following day with plan for endocrinology and primary care follow-up. DISCUSSION: Thyrotoxicosis in this young patient with no history of thyroid disease posed a diagnostic quandary. This prompted further investigation into a more detailed social history, which revealed the extensive variety of supplements he was taking, consistent with thyrotoxicosis factitia. In patients presenting with newonset tachycardia, our case highlights the importance of collecting a thorough social history and maintaining early suspicion for thyroid disease and thyrotoxicosis.
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TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Hypertriglyceridemia (TGL) is the abnormal concentration of triglycerides in the blood associated with atherosclerosis. It is known to cause skin lesions when the blood levels are more than 3000 mg/dl. It is also associated with 1 to 10 percent cases of acute pancreatitis and 10 to 20 percent when levels are higher than 2000 mg/dl. CASE PRESENTATION: A 36-year old morbidly obese man with medication non-compliance was evaluated by a dermatologist via a video tele visit due to COVID19 Pandemic. He has a history of uncontrolled IDDM, hypertriglyceridemia status post plasmapheresis a year ago associated with pancreatitis. He has no family history of hypertriglyceridemia. He reported rashes on his forearms and thighs for 3 weeks and was advised to go to the Emergency Department to rule out cutaneous manifestation of his underlying conditions. He initially reported epigastric pain radiating to his back, but his lipase and CT abdomen were negative for pancreatitis. He was vitally stable, and his exam was significant for yellowish papules on his forearms, legs bilaterally with erythematous borders. Labs: TGL 1618, total cholesterol 647, Glucose 223, A1c 12.6%, no Anion Gap.Imaging: Splenomegaly with Hepatic Steatosis likely due to TGL deposition.Patient was placed on Insulin drip to prevent pancreatitis and was started on fenofibrate, fish oil and rosuvastatin. Kept NPO initially with dextrose infusion to increase insulin drip & metabolize the triglycerides. Triglycerides gradually improved, and insulin drip was d/c. Shave Biopsy confirmed Eruptive Xanthoma. DISCUSSION: Eruptive xanthomas are characterized by an eruption of yellowish skin papules, encircled by an erythematous halo, most commonly arising over the extensor surfaces of the extremities, buttocks and shoulders in the setting of high triglyceride levels secondary to diabetes, diet or familial causes. The lipid deposits in these xanthomas are derived from circulating plasma lipoproteins. CONCLUSIONS: This case was unique as our patient developed eruptive xanthomas even at TGL level under 2000 mg/dl which is rarely seen. Clinically diagnosing Xanthomas are extremely important in order to treat hypertriglyceridemia in order to prevent pancreatitis, which has a grim prognosis. It is also important for reducing CAD risk. Xanthomas should be evaluated to prevent pancreatitis and long-term cardiac events rather than the lipid deposit itself. They can also be the only signs of underlying metabolic diseases like diabetes. Management should include pharmacological agents, counseling for compliance, nutrition & lifestyle modifications. All these patients with high TGLs will benefit from E3/E4 genotype testing as it is associated with higher cardiac disease and low response to statins. REFERENCE #1: Severe hypertriglyceridemia presenting as eruptive xanthomatosisSameera S Vangara, Kyle D Klingbeil, Raymond M Fertig, Jason L RadickDepartment of Internal Medicine, University of Miami Miller School of Medicine, Florida, USA REFERENCE #2: Eruptive Xanthomas as a cutaneous Manifestation of HypertriglyceridemiaA Case ReportMichael Digby, Md, Robert Belli, MS, Timothy McGraw, and Abigail Lee, MD DISCLOSURES: no disclosure on file for Moses Bachan;no disclosure on file for Zinobia Khan;No relevant relationships by Robert Siegel, source=Web Response No relevant relationships by Goutham Talluri, source=Web Response
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TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: It is well known now that COVID-19 cause lymphopenia. In the retrospective study the number of total T cells, CD4+ and CD8+ T cells were dramatically reduced in COVID-19 patients, especially in patients requiring Intensive Care Unit (ICU) care. (1) Lymphopenia and drastic reduction of CD4+ T cell counts in COVID-19 patients have been linked with poor clinical outcome too. (2) We present a case of a patient with well controlled HIV infection with stable absolute CD4 count but significant drop during COVID infection CASE PRESENTATION: A 67 year-old-man with history of HIV on ARV therapy with undetectable viral load, panhypopituitarism with central hypothyroidism, adrenal insufficiency and hypogonadism, recurrent DVT/PE on AC therapy, BPH, overactive bladder, stable angina presented with 3 days of fever, chills, diarrhea and malaise to ER. He received first dose of Moderna vaccine 2 weeks before admission. VS -saturation 79% on RA, and 96% on NRB mask, HR 122 beats/min, BP 159/87 mmHg, RR 18/min, T 101. PE unremarkable. Labs: Covid PCR +, WBC 15.3 K/cmm, ferritin 585.8 ng/ml, LDH 489 U/LAST 122 U/l, ALT 100U/L, CRP quant 321 mg/L, D dimer 1287 D-DU ng/ml, HIV RNA quant undetectable, CD4 67 cell/Ul, previous CD4 568 cmm 2 weeks prior admission. CXR:b/l patchy infiltrates. He was treated with dexamethasone, therapeutic Lovenox and received 1 U of convalescent plasma. His oxygen saturation improved, overall course was uneventful and patient was discharged home. CD4 count improved to 523 cmm 2 months later. DISCUSSION: It is shown that HIV infection does not increase the occurrence of COVID-19 and there is no increase in morbidity and mortality (2). The exact influence of COVID-19 on absolute T4 cells subset in HIV and their significance is presently unknown. Our patient had stable absolute CD4 count for years. He was compliant with ART and HIV viral load was undetectable. However, there was a drastic decline in his CD4 count that occurred during an acute COVID infection although he was on the same medications. CD4 recovered to baseline after COVID infection resolved. CONCLUSIONS: This is a unique case with such a dramatic drop of absolute CD4 count in acute COVID infection and further investigation on CD4 cells and it effects on HIV infection will need to be studied. REFERENCE #1: Diao B, Wang C, Tan Y, et al. Reduction and Functional Exhaustion of T Cells in Patients With Coronavirus Disease 2019 (COVID-19). Front Immunol. 2020;11:827. Published 2020 May 1. doi:10.3389/fimmu.2020.00827 REFERENCE #2: Peng Xiaorong, Ouyang Jing, Isnard Stéphane, Lin John, Fombuena Brandon, Zhu Biao, Routy Jean-Pierre, Sharing CD4+ T Cell Loss: When COVID-19 and HIV Collide on Immune System, JOURNAL=Frontiers in Immunology VOLUME=11, YEAR=2020, PAGES=3307, URL=https://www.frontiersin.org/article/10.3389/fimmu.2020.596631 DOI=10.3389/fimmu.2020.596631, ISSN=1664-3224 DISCLOSURES: no disclosure on file for Moses Bachan;no disclosure on file for Zinobia Khan;No relevant relationships by Mirjana Petrovic Elbaz, source=Web Response No relevant relationships by Robert Siegel, source=Web Response
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TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: COVID infection can present with diverse manifestations. We present an interesting case of very high troponin elevation in patient with COVID infection without obvious reason for troponin elevation. CASE PRESENTATION: A 66-year-old man with history of HTN, DM2, CAD (CABG in 2009, percutaneous vascularization of RCA with multiple DES in 2018), NSTEMI- 1 year ago, PVD, status post left BKA, ESRD on HD presented with 1 week of watery diarrhea after being tested positive for COVID. He denied chest pain, had minimal SOB. He received first dose of COVID vaccine 2 weeks prior. Vital signs: afebrile, BP 145/68 mmhg, HR 75 beats/min, RR 20/min, oxygen saturation 90% on RA and 96% on 3L of O2 via NC. PE: R- IJ permanent catheter, L- BKA, lungs clear. Labs: COVID PCR assay (+), D dimer 359 D-DU ng/ml, LDH 330 U/l, ferritin 3207 ng/ml, CRP quant 87 ml/l, SARS-CoV-2 Ig G (RBD) 1.14 S/CO, SARS-COV-2 IgM (Beckman) 2.56. troponin (AccuTnI) 13.46 ng/ml, CPK normal, Cr 7.5 (at the baseline), EKG - sinus rhythm, left axis deviation, negative T waves in lateral leads and ST depression up to 1 m in anterior leads, no changes from old EKG, CXR - Increased b/l pulmonary opacities compatible with atypical/viral pneumonia. The most recent ECHO 1 year ago – mild LV dysfunction with thin and akinetic inferior and basal posterior walls, LVEF 50%. Patient was already on aspirin, plavix, statin and that treatment was continued during hospital course. COVID pneumonia was treated with dexamethasone and convalescent plasma versus placebo (VA Cures- 1 Trial). His hospital stay was uneventful, he remained hemodynamically stable and asymptomatic and was discharged home DISCUSSION: Our patient has known history of CAD and ESRD which are well known cause for elevated troponin. However his Cr level was at his baseline and his previous troponin levels were never this high even when he had NSTEMI, it was only 1.44 ng/ml. During this admission with Covid infection his troponin level was as high as 13.46 ng/ml and trended down to 4.15 ng/ml on discharge, his baseline level of troponin is 0.03-0.88 ng/ml. Reasons for such a high level of troponin can be due to Type II MI or myocarditis. In the settings of COVID infection it has been suggested that troponemia can be due to microvascular damage occurring in the heart with perfusion defects, vessel hyperpermeability, vasospasm and high cytokine levels may represent the key player of myocardial injury (1). Our patient did not have a very severe form of COVID pneumonia that required intubation in fact, he was saturating well on minimal oxygen requirements. He remained asymptomatic with no new interval EKG changes or any other signs of acute coronary syndrome (ACS). CONCLUSIONS: Serum Troponin can be significantly elevated in the setting of COVID infection and in the absence of ACS. REFERENCE #1: Reference #1: Tersalvi G, Vicenzi M, Calabretta D, Biasco L, Pedrazzini G, Winterton D. Elevated Troponin in Patients With Coronavirus Disease 2019: Possible Mechanisms. J Card Fail. 2020;26(6):470-475. doi:10.1016/j.cardfail.2020.04.009 DISCLOSURES: no disclosure on file for Moses Bachan;no disclosure on file for Zinobia Khan;No relevant relationships by Dileep Kumar, source=Web Response No relevant relationships by Mirjana Petrovic Elbaz, source=Web Response
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Introduction: COVID-19 was declared a global pandemic by the WHO in March 2020. The gold standard for diagnosis relies heavily on clinical suspicion along with PCR based assays of respiratory swabs. This nucleic acid study is highly sensitive and specific, however, there are faults, especially during the incubation period, during which the virus is hard to detect. Here we present a case of a patient, presenting with signs and symptoms of pneumonia, with serial negative viral swabs spaced out over time, who was ultimately diagnosed with COVID-19 infection via more invasive means. Case: A 49-year-old female with no significant past medical history presented to the emergency department with cough and shortness of breath for 2 days which developed when she returned to New York from Florida. Her personal history was significant for her occupation as an ER nurse and a history of vaping for 5-6 years.After arrival to the emergency department, the patient was febrile to 103.3 F, tachycardic, and hypoxic, saturating 89% on room air. Her laboratory work was significant for a mildly elevated D-dimer level, elevated CRP (11.23), normal procalcitonin level, and two negative COVID-19 swabs over 2 days. Her initial chest X ray showed multifocal pneumonia and a CT chest showed ground glass opacities amid dense consolidation. The patient was empirically treated for community-acquired bacterial pneumonia with antibiotics. The patient's respiratory and hemodynamic status started to decline, despite treatment. Ultimately, the patient required further investigation - a bronchoalveolar lavage was ultimately found to be positive for the COVID-19 virus, and the patient was immediately started on Remdesivir. Discussion: In this day and age, countries are increasingly utilizing the COVID-19 reverse-transcriptase PCR and are pushing for widespread testing for case detection, but how sensitive and specific is this test, really? Serial testing with swabs performed at intervals should be the answer as the viral load of the COVID RNA steadily rises and peaks over 0-9 days after onset of symptoms. However, this may not be the case in a majority of patients and more invasive testing using bronchoscopy and bronchoalveolar lavage may be the only way to truly diagnose COVID-19 pneumonia. The delay in confirmation, however, could prove to be truly fatal, subjecting patients to painful measures like intubation. This case brings to light the realization that nasopharyngeal/oropharyngeal swabs may not be sufficient to detect the virus with full certainty.
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SESSION TITLE: Medical Student/Resident Lung Pathology SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Coronavirus disease 2019 (Covid-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a devastating ongoing global pandemic. Its disease severity ranges from asymptomatic, mild to severe disease, which can be complicated by developing hypoxemic respiratory failure and acute respiratory distress syndrome (ARDS). Pulmonary fibrosis is condition that occurs due to scarring of lung tissue. Most common cause being idiopathic occurring over a long period of time but it can also occur several days after severe bacterial pneumonias due to activation of fibroblasts. Our case shows that Covid-19 infection can acutely cause pulmonary fibrosis. CASE PRESENTATION: A 76-year old woman, life time non-smoker, with a history of well controlled intermittent asthma (rescue inhaler only) never hospitalized for any exacerbations. She was transferred to our facility due to persistent oxygen requirements after diagnosed with Covid-19 pneumonia. She presented to an outside hospital 3 months prior with fever and shortness of breath. Her course was complicated with hypoxemia requiring oxygen via non-rebreather mask, bilateral lower extremity deep vein thrombosis requiring apixaban. Her oxygen requirement slowly improved to 2 liters via nasal cannula. Despite clinically improvement she became oxygen dependent. She failed weaning off oxygen multiple times. CT of her chest even showed predominant upper lobe scarring. She was discharged home with oxygen 5 months after her Covid-19 pneumonia diagnosis. DISCUSSION: Pulmonary fibrosis leads to lung scarring. Fibrotic tissue is dead tissue, no gas exchange happens and there is a restrictive pattern on Pulmonary function tests (PFTs). There are many different conditions that can lead to pulmonary fibrosis but it is not common to develop post viral infections. Classic Covid-19 pneumonia causes diffuse bilateral infiltrates causing severe inflammatory response leading to macrophage activation, cytokine release with activation and proliferation of fibroblasts causing tissue destruction and scarring. Except for well controlled intermittent asthma our patient did not have any underlying lung etiologies that could make her oxygen dependent. She is a life time non-smoker, no occupational exposure to any chemicals, pollutants, toxic fumes etc., no history of autoimmune diseases or connective tissue diseases, no radiation exposure, no usage of any pulmonary toxic medications like amiodarone, bleomycin. Review of old medical records and imaging did not show any evidence of pulmonary fibrosis. Unfortunately, there were no post Covid-19 PFTs available for comparison. CONCLUSIONS: Covid-19 pneumonia with diffuse bilateral infiltrates can rapidly progress into pulmonary fibrosis due to severe inflammatory response/cytokine storm (post-COVID fibrotic ARDS), which made our patient oxygen dependent with significant reduction in her quality of life. Reference #1: Belloli EA, Beckford R, Hadley R, Flaherty KR. Idiopathic non-specific interstitial pneumonia. Respirology. 2016 FEb.21(2): 259-68 Reference #2: Zhu N Zhang D Wang W et al.A novel coronavirus from patients with pneumonia in China, 2019.N Engl J Med. 2020;382: 727-733 DISCLOSURES: No relevant relationships by Moses Bachan, source=Web Response No relevant relationships by Zinobia Khan, source=Web Response No relevant relationships by swetha Nadella, source=Web Response No relevant relationships by Robert Siegel, source=Web Response No relevant relationships by Vijaya Vudathaneni, source=Web Response
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SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: COVID-19 disease usually presents as a respiratory infection which can progress to pneumonia, acute respiratory distress syndrome (ARDS) and multi organ dysfunction. The more severe cases occur in older adults, with chronic conditions such as cardiovascular and cerebrovascular diseases and diabetes[1,2]. We present a case of COVID-19 infection complicated by central diabetes insipidus (DI). CASE PRESENTATION: A 68 y/o man with history of HTN, HLD, DM- 2, A flutter presented with fever, headache, diarrhea and productive cough for 10 days. In the ED he was hypoxemic with O2 sat of 70% on room air and had diffuse wheezing throughout the lung fields. Covid PCR was positive. He was started on Lopinavir/Ritonavir x 2 days, which was aborted due to transaminitis. He was then started on Hydroxychloroquine and steroids. His hypoxemia worsened and on hospital day #15 he was intubated. On day #23 his mentation changed, he became nonresponsive to noxious stimuli, gag reflex was absent and he was polyuric. Over 24 hours his urine output increased to 7 L, serum Na increased from 136 to 153 mEq/L, urine osm was 152, specific gravity 1.005, urine specific gravity Na 43, MRI of the head showed no acute infarction, intracranial hemorrhage or mass, no abnormal intracranial enhancement. He was diagnosed with Central Diabetes Insipidus (DI) He was given DDAVP which lead to decreased urine output, increased urine Na, increased urine osm and specific gravity. His mentation returned to baseline, with a good gag reflex. He subsequently required tracheotomy, had a prolonged ICU course, and died due to worsening hypoxic respiratory failure. DISCUSSION: Multiple electrolyte derangements were described in the COVID positive patients;hyponatremia was the most frequent sodium abnormality[2]. Our patient demonstrated rapid and adequate response to DDAVP administration. Central DI can be produced by many entities like idiopathic, autoimmune, trauma or malignancy. He did not have a history of head trauma, cancer or brain surgery. The patient was briefly placed on Ketamine for sedation which was described as a cause of the central DI in some cases[3]. However,Ketamine's half life is 160 min. Patient was placed on Ketamine during the subsequent hospital stay without repeated electrolyte derangements. Hypothalamus and hypophysis infarct was less likely given negative imaging results and continuous AC. No other infectious causes were identified at that time. CONCLUSIONS: Critically ill patients with COVID pneumonia may develop central DI. We assume possible mechanism of central DI can be hypoxic encephalopathy which can occur in the setting of severe ARDS, or some more specific mechanism like autoimmune dysregulation leading to autonomic and neuroendocrine derangements. It can also be a sign of poor prognosis. We believe further studies and data analysis regarding this novel and complex viral infection will give more answers. Reference #1: Harapan H, Itoh N, Yufika A, et al. Coronavirus disease 2019 (COVID-19): A literature review. J Infect Public Health. 2020;13(5):667-673. Reference #2: Zhang X, Cai H, Hu J, et al. Epidemiological, clinical characteristics of cases of SARS-CoV-2 infection with abnormal imaging findings. Int J Infect Dis. 2020;94:81-87. Reference #3: Gaffar S, Eskander JP, Beakley BD, McClure BP, Amenta P, Pierre N. A case of central diabetes insipidus after ketamine infusion during an external to internal carotid artery bypass. J Clin Anesth. 2017;36:72-75. DISCLOSURES: No relevant relationships by Moses Bachan, source=Web Response No relevant relationships by Zinobia Khan, source=Web Response No relevant relationships by Hana Rajevac, source=Web Response
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SESSION TITLE: Medical Student/Resident Lung Pathology SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: COVID-19 is caused by SARSCoV-2 virus which affects many organs, but mostly the respiratory system. We report a case of COVID-19 disease associated with acute moderate pericardial effusion. CASE PRESENTATION: 53 year old man with history of OSA, DM type 2, HTN, obesity and HLD had fever, chills and cough for which he was treated with Azithromicin for 5 days as an outpatient. However, on day 6 he presented to the hospital with diarrhea, fever, chills and a productive cough. He denied chest pain, palpitations, PND, orthopnea, previous cardiac issues. In the ED, his vitals were: T 102 F, HR 87/min, BP 181/94 mmHg, O2 Sat 96% on RA. On chest auscultation he had scattered bi-basilar rhonchi, and muffled heart sounds, no JVD. Laboratory: WBC 3.4 K/cmm, Hgb 12.1 g/dl, Plt 166 K/cmm, Na 131, K 5.5, Cr 2.3, BUN:33, pro BNP 187;troponin negative. COVID PCR assay (+), EKG: low voltage QRS, no ischemic changes. Chest CT scan showed moderate size pericardial effusion, small scattered low attenuation patchy areas throughout both lungs. He was started on Azithromycin/Hydroxychloroquine and given a dose of Tocilizumab. Previous transthoracic ECHO 5 years ago was normal. On hospital day 3 he developed worsening of hypoxic respiratory failure and was intubated. He subsequently developed severe ARDS.Repeated EKG with low voltage QRS, no cardiac ischemia, troponin level peaked up to 0.13, and trended down to 0.04, CPK 586 U/L. The patient developed worsening renal failure, remained intermittently hypotensive requiring vasopressors, and hypoxemic to 70s despite maximal ventilator settings. On day 8 he became bradycardic, developed PEA and passed away. DISCUSSION: COVID-19 is caused by SARS COV 2 RNA beta coronavirus. Fever, cough, dyspnea are most common symptoms. Troponemia has been described as a cardiac manifestation of COVID-19 [1]. Most common radiological findings are ground glass opacities (88.0%), bilateral involvement (87.5%), and multilobarity (78.8%)[2]. Pericardial effusion can be acute or chronic. Most common causes are viruses, bacteria, rheumatological diseases, malignancy, trauma and idiopathic. Changes like pericardial effusion are very rarely described in COVID infected patients, mentioned with disease progression[2,3]. Our case had a moderately sized pericardial effusion on initial presentation before he developed worsening of hypoxic respiratory failure. Upon review of the old EKGs and CXR patient did not have any signs of pericardial effusion. Radiological finding of pericardial effusion may also be a poor prognostic sign of COVID-19, which may be explained by escalation of the severe systemic inflammatory response. Limitations of this case are no ECHO or pericardiocentesis were done due Infection control recommendations for COVID -19 at the time. CONCLUSIONS: Pericardial effusion can be associated with COVID-19 infection, and may be an indicator of more severe disease. Reference #1: Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19).Inciardi RM1, Lupi L1, Zaccone G1, Italia L1, Raffo M1, Tomasoni D1, Cani DS1, Cerini M1, Farina D2, Gavazzi E2, Maroldi R2, Adamo M1, Ammirati E3, Sinagra G4, Lombardi CM1, Metra M1. Reference #2: Coronavirus Disease 2019 (COVID-19): A Systematic Review of Imaging Findings in 919 Patients.Salehi S1, Abedi A1, Balakrishnan S1, Gholamrezanezhad A1 Reference #3: Imaging and clinical features of patients with 2019 novel coronavirus SARS-CoV-2Xi Xu,#1 Chengcheng Yu,#2 Jing Qu,2 Lieguang Zhang,2 Songfeng Jiang,2 Deyang Huang,2 Bihua Chen,2 Zhiping Zhang,2 Wanhua Guan,2 Zhoukun Ling,2 Rui Jiang,2 Tianli Hu,2 Yan Ding,2 Lin Lin,2 Qingxin Gan,2 Liangping Luo,corresponding author1 Xiaoping Tang,corresponding author2 and Jinxin Liucorresponding author2 DISCLOSURES: No relevant relationships by Moses Bachan, source=Web Response No relevant relationships by Nikola Djurdjevic, source=Web Response No relevant relationships by Zino ia Khan, source=Web Response No relevant relationships by Hana Rajevac, source=Web Response