ABSTRACT
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