Managing Severe Acute Asthma Exacerbation in Pregnancy during the COVID-19 Pandemic: A Case Report from a Resource-limited Setting

BACKGROUND: One-third of pregnant women will experience worsening asthma requiring emergency hospitalization. However, no report comprehensively discussed the management of asthma attacks in pregnant women in impoverished settings. We attempt to illuminate what general practitioners can do to stabilize and improve the outcome of severe acute asthma exacerbations in primary care with resource limitations. CASE REPORT: A nulliparous 29-year-old woman in her 21st week of pregnancy presented severe acute asthma exacerbation in moderate persistent asthma with uncontrolled asthma status along with gestational hypertension, uncompensated metabolic acidosis with a high anion gap, anemia, respiratory infection, and asymptomatic bacteriuria, all of which influenced her exacerbations. This patient was admitted to our resource-limited subdistrict hospital in Indonesia during the COVID-19 pandemic for optimal stabilization. Crystalloid infusions, oxygen supplementation, nebulized beta-agonist with anticholinergic agents, inhaled corticosteroids, intravenous methylprednisolone, broad-spectrum antibiotics, subcutaneous terbutaline, mucolytics, magnesium sulphate, oral antihypertensives, and continuous positive airway pressure were used to treat her life-threatening asthma. After she was stabilized, we referred the patient to a higher-level hospital with more advanced pulmonary management under the supervision of a multidisciplinary team to anticipate the worst scenario of pregnancy termination. CONCLUSION(S): Limitations in primary care, including the lack of sophisticated intensive care units and laboratory panels, may complicate challenges in managing severe acute asthma exacerbation during pregnancy. To enhance maternal-fetal outcomes, all multidisciplinary team members should be well-informed about key asthma management strategies during pregnancy using evidence-based guidelines regarding the drug, rationale, and safety profile.Copyright © 2023 Muhammad Habiburrahman, Triya Damayanti, Mohammad Adya Firmansha Dilmy, Hariyono Winarto.

Association between Type 2 Diabetes Mellitus and Covid-19 Severity: A Literature Review

We conducted a review and evaluated the already documents reports for the relationship among diabetes and COVID-19. The review outcome shows that the COVID-19 severity seems to be greater among patients with diabetes as comorbidity. So, strict glycemic control is imperative in patients infected with COVID-19. Thus, world-wide diabetes burden and COVID-19 pandemic must be deliberated as diabetes increases the COVID-19 severity. Established on this, it is precise significant to follow specific treatment protocols and clinical management in COVID-19 patients affected with diabetes to prevent morbidity and mortality.Copyright © 2023 The Authors.

Resurgence of Shoshin beriberi during the COVID-19 pandemic.

This report describes two patients who presented with severe type B lactic acidosis and shock, initially thought to be due to bowel ischaemia/myocardial infarction and pulmonary sepsis, respectively. This led to a delay in the diagnosis of thiamine deficiency. In both cases there was a dramatic response to intravenous thiamine, confirming the diagnosis of Shoshin beriberi. Both patients admitted to drinking home-brewed alcohol during the time of COVID-19 restrictions on alcohol consumption. These cases highlight the need for early diagnosis and immediate empirical treatment with intravenous thiamine in patients presenting with unexplained severe metabolic acidosis and circulatory shock.

The use of alanine, free carnitine and IGFBP-1 as potential biomarkers for glycogen storage disease type I

Background: Glycogen Storage Disease Ia (GSDIa) and Ib (GSDIb) are inborn errors of carbohydrate metabolism due to a deficiency of glucose-6-phosphatase (G6Pase) or glucose-6-phosphate translocase (G6PT), respectively. Consuming prescribed amounts of uncooked cornstarch (UCCS) to prevent hypoglycemia is the standard of care for GSDIa and GSDIb. Patients followed in our GSD Program are admitted to the hospital annually for evaluation of their metabolic control by measuring glucose and lactate levels and revising treatment regimens accordingly. Lack of bed space due to the COVID-19 pandemic has created a need for alternate markers of metabolic control as lactate measurements are unreliable in the outpatient setting. This research aims to identify alternative biomarkers to show degree of metabolic control in individuals with GSDI. Method(s): A retrospective chart review was conducted on 45 adults and children with GSDI using data from January 1, 2014 toMay 6, 2021. Plasma alanine and free carnitine levels were compared with laboratory reference ranges. Results from the three tests were not available on every subject. Plasma alanine was evaluated on 24 subjects (16-GSDIa, 8-GSDIb) and free carnitine was evaluated on 25 subjects (17-GSDIa, 8-GSDIb). Result(s): Alanine levels in subjects with GSDIa ranged from 378 to 786 umol/L, while alanine levels in subjects with GSDIb ranged from 254 to 506 umol/L (reference range = 103-528 umol/L). Free carnitine levels ranged from26 to 72 umol/L in subjects with GSDIa and from 44 to 90 umol/L in subjects with GSDIb (reference range = 19-55 umol/L). Conclusion(s): Our analysis showed that plasma alanine and free carnitine have potential to be used as biomarkers of metabolic control. For plasma alanine, there seemed to be differences between subjects with GSDIa and GSDIb, as the majority of subjects with GSDIa had elevations in plasma alanine, while subjects with GSDIb did not. Elevated plasma alanine levels indicate lactic acidosis. For GSDIb, we hypothesize that there may be some type of G6Pase enzyme activity that occurs outside of the endoplasmic reticulum. When looking at both groups, free carnitine levels were mostly elevated. This indicates that there could be inhibition of fatty acid oxidation.Copyright © 2022 Elsevier Inc. All rights reserved.

Atypical Presentation of Burkitt Lymphoma With Isolated Peritoneal Involvement and Association With Refractory Type B Lactic Acidosis and Hypoglycemia Secondary to the Warburg Effect.

Lactic acidosis is considered to be one of the most common causes of high anion gap metabolic acidosis in hospitalized patients. Warburg effect can present with type B lactic acidosis and is considered to be a rare but well-known complication of hematological malignancies. Here, we present the case of a 39-year-old male who had type B lactic acidosis and recurrent hypoglycemia secondary to newly diagnosed Burkitt lymphoma. This case highlights the importance of considering malignancy workup in any case of unexplained type B lactic acidosis with vague clinical presentation, which can aid in early diagnosis and management.

Not all shortness of breath and throat pain is COVID

Case Report: A previously, healthy 18-year-old female presents to a Pediatric Emergency Medicine Department with shortness of breath, fever, and worsening throat and abdominal pain for 3 days. She had a sick contact, a teacher that tested positive for COVID-19 2 weeks prior to presentation. She denies runny/stuffy nose, cough, loss of taste/smell, or rashes/lesions. She denies any significant past medical history including allergies, as well as any history of smoking or any illicit drug use. Upon arrival to the ED, the patient was noted to be tachycardic, hypotensive and febrile. There were no desaturations. Initial physical examination revealed a generally uncomfortable female that was alert and oriented, with noted tenderness over the right anterior neck region, diffuse cervical lymphadenopathy, and painful neck range of motion. Her pharynx was noted to be erythematous without exudates or any unilateral tonsillar swelling. In the ED patient received IV fluid resuscitation and was started on norepinephrine drip, broad spectrum antibiotics. Initial lab workup revealed an anion gap metabolic acidosis, likely secondary to uremia or lactic acidosis from poor perfusion in setting of sepsis and hypovolemia. BUN and creatinine were elevated, likely due to an acute kidney injury (AKI) secondary to hypovolemia. The patient was also found to have an elevated LDH, fibrinogen, and mild elevation of AST. D-Dimer was elevated at 29 000. Covid PCR, Rapid Strep, and respiratory PCR panel were negative. Her chest X-ray (CXR) was negative and ECG showed sinus tachycardia. Given the patient's history of throat and neck pain with shortness of breath, in the setting of a septic picture, a CT scan of neck, chest, abdomen was ordered prior to transferring the patient to the PICU. CT scan of the chest revealed small patches of consolidation with ground glass opacities in the right lung apex, as well as an nearly occlusive, acute thrombosis of the anterior right facial vein. The patient's initial blood cultures grew gram negative bacilli which later were revealed to be Fusobacterium necrophorum. These findings are consistent with Lemierre's syndrome. The patient was treated in the PICU on vasopressors, heparin anticoagulation, and antibiotics for 6 days and discharged with a course of Augmentin. Lemierre's syndrome is an infectious thrombophlebitis of the internal jugular vein. First described by Andre Lemierre in 1936, it begins as a bacterial pharyngitis, generally developing into a peritonsillar abscess or other deep space neck infection with progressive erosion into the internal jugular vein. Diagnostic criteria for Lemierre's syndrome includes radiographically evidence of thrombophlebitis of the internal vein and positive blood cultures. CT and MRI can help make the diagnosis, but are not always required. Treatment is prompt intravenous antibiotics with beta-lactamase penicillins, metronidazole, clindamycin, and third generation cephalosporins. [Figure presented] Copyright © 2023 Southern Society for Clinical Investigation.

GATA2 deficiency presenting as fever and rash

Case Report: Our patient is an 8-year-old Caucasian female with a history of choanal atresia, first degree heart block, recurrent urinary tract infections, and recent COVID-19 infection, who initially presented with an episode of syncope and vomiting. By history, she had two weeks of daily fever and an intermittent nonspecific rash. She was diagnosed with a UTI 5 days prior to presentation but had not defervesced despite treatment. Shewas initially found to be in shock with tachycardia and poor perfusion and was treated with fluid resuscitation, antipyretics, and empiric antibiotics. Labs were significant for leukopenia, elevated inflammatory markers, lactic acidosis, coagulopathy, and mildly elevated troponin. Chest x-ray showed abnormal but non-specific widespread infiltrates. She was initially treated with IVIG and pulse steroids for a working diagnosis of MIS-C, however she did not improve and a more extensive infectious, oncologic, and rheumatologic work-up was performed. Her workup revealed a disseminated Mycobacterium abscessus infection. Bone marrow biopsy revealed myelodysplasia with monosomy 7. Her buccal swab testing revealed a heterozygous germline mutation in the GATA2 gene, a variant that is predicted to cause loss of normal protein function. She is presently on multidrug regimen for her mycobacterial infection. Her myelodysplasia evolved into an acute leukemia, and she is undergoing chemotherapy for that at this time. Discussion(s): GATA2 deficiency, first identified in 2011, is a rare immune disorder resulting in a wide variety of clinical presentations. It is caused by a germline mutation of the GATA2 gene that disrupts blood cell differentiation, resulting in decreased or absent monocytes, B cells, NK cells, and dendritic cells1. This case presented multiple challenges due to the broad range of differential diagnoses. This patient was ultimately diagnosed with myelodysplastic syndrome associated with monosomy 7 and GATA2 deficiency, confirmed by FISH testing. Due to the presentation and lab derangements this patient had, there was a delay in targeted treatment while managing her cytopenias and presumed pulmonary infection. GATA2 deficiency carries a high risk of progression from myelodysplastic syndrome to acute myelogenous leukemia. The best long-term treatment for GATA2 deficiency is hematopoietic stem cell transplant, which is the ultimate goal for our patient. Copyright © 2023 Southern Society for Clinical Investigation.

Toxicokinetics of metformin overdose treated with CVVHDF

Background: Metformin is the most commonly used diabetes medication and at supratherapeutic levels can result in a severe type-A metabolic lactic acidosis known as metformin-associated lactic acidosis (MALA). Treatment of MALA includes aggressive fluid resuscitation, supporting blood pressure and correcting acidosis. Renal replacement therapy (RRT), usually hemodialysis (HD) is recommended in severe cases with refractory acidosis (with elevated lactate), altered mental status, or shock. To our knowledge, this is the second report of metformin half-life during treatment with continuous veno-venous hemodiafiltration (CVVHDF). Case report: A 53-year-old man died following a reported acute on chronic ingestion of 80 g of his metformin tablets resulting in severe, refractory shock and MALA. His peak serum metformin concentration was 53mcg/mL (therapeutic range 1-2mcg/mL), peak lactic acid concentration was 49.7 mmol/L, and arterial pH nadir was 7.06. Serial serum metformin concentrations were obtained while on RRT;both HD and CVVHDF. The switch from HD to CVVHDF was done due to staffing shortages during the COVID-19 pandemic. The patient died despite aggressive therapy with renal replacement therapy and multiple vasopressors on hospital day five. Serial metformin concentrations during CVVHDF suggested a half-life of 33-h. Discussion(s): Hemodialysis has been reported to clear metformin at a rate greater than 200mL/min and continuous venous-venous hemofiltration (CVVH) at greater than 50mL/min. In this case, metformin levels appear to follow first-order elimination kinetics during CVVHDF with an estimated half-life of 33 h. Comparatively, metformin has a half-life of 4.7-5.5 h during HD. To our knowledge, this is the second report of estimated metformin half-life while using the CVVHDF form of continuous renal replacement. The previous case report measured a half-life of 16.5 h on CVVHDF. This case report shows CVVHDF decreases half-life of metformin and provides first order elimination in the setting of overdose. Conclusion(s): The early initiation of HD appears warranted but prognostic indicators have not been well established. In the absence of HD availability, other forms of RRT (e.g., CCVHDF) can be used and may provide first-order elimination of metformin.

PATHOPHYSIOLOGY OF LACTIC ACIDOSIS IN PATIENTS WITH ASTHMA

SESSION TITLE: Challenges in Asthma SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 10:15 am - 11:10 am INTRODUCTION: Asthma is a chronic illness affecting 334 million people worldwide[1]. Asthma affects the respiratory gas exchange, which plays a significant role in acid-base balance. Acid-base disorders in asthma involve respiratory alkalosis, respiratory acidosis, and AG acidosis[2]. CASE PRESENTATION: A 37 years old Hispanic male with a PMH of intermittent asthma presents with progressive dyspnea for three days, worse with activity and decreases with rest. He reported no [cough, fever, rhinorrhea, chest pain]. No orthopnea. He is vaccinated for COVID ( 2 Pfizer doses), has no sickness exposure, and works as a driver. The patient is not a smoker. Physical Exam: Blood pressure 124/72 mmHg. Heart Rate 100 PPM. Temperature 97.1 F.Respiratory Rate 21BPM.SPO2 90% General appearance: acute distress with nasal flaring. Heart: Normal S1, S2. RRR. Lung: Poor air entry with diffuse wheeze bilaterally. He was placed on a 6 LPM NC. CBC and differential were unremarkable. He was started on methylprednisone, Ceftriaxone, and azithromycin. The patient was started on inhaled Salbutamol and Budesonide. Chest X-ray was unremarkable, Chemistry was unremarkable except for elevated Lactic acid 4.7, There was no concern for reduced tissue perfusion or hypoxia, with no evidence of an infectious process because both viral and bacterial causes for pneumonia were excluded, and antibiotics were stopped. A serial lactic acid level trend was 4.5/4.3/ 4.1/ 4 on the first day, while on the next day, it was 3.1/ 2.9/ 2.7/ 2.5/ 3.5, we stopped trending his lactic acid level. He improved and was discharged on an oral taper steroid and inhaled steroids with a B2 agonist. DISCUSSION: There are two types of Lactic acidosis in patients with asthma: 1- Type-A results from impaired oxygen delivery to tissues and reduced tissue perfusion in severe acute asthma may be accompanied by reduced cardiac output. 2- Type B where oxygen delivery is normal, but the cellular function is impaired due to increased norepinephrine in plasma, increasing metabolic rate and lactate production, drugs like beta-agonists increase glycogenolysis leading to an increased pyruvate concentration;pyruvate is converted to lactic acid. B2 agonist increases lipolysis and increases Acetyl CoA, this increase in Acetyl CoA inhibits the conversion of pyruvate to Acetyl CoA, increasing pyruvate which will be converted to lactic acid[2], Theophylline is a non-selective 5'-phosphodiesterase inhibitor and potentiates the activity of ß-adrenergic agents by increasing the intracellular concentration of cAMP, Glucocorticoids are also known to increase the ß-receptor's sensitivity to ß-adrenergic agonists. CONCLUSIONS: Providers are increasingly challenged by hyperlactatemia,it is not harmful but elevated Lactic acid levels and clearance rate is used for prognostication,hyperlactatemia might be misleading,and all possible causes of elevated lactic acid levels must be explored. Reference #1: 10.5334/aogh.2412 Reference #2: https://doi.org/10.3390/jcm8040563 Reference #3: Edwin B. Liem, Stephen C. Mnookin, Michael E. Mahla;Albuterol-induced Lactic Acidosis. Anesthesiology 2003;99:505–506 doi: https://doi.org/10.1097/00000542-200308000-00036 DISCLOSURES: No relevant relationships by Vasudev Malik Daliparty No relevant relationships by Abdallah Khashan No relevant relationships by Samer Talib No relevant relationships by MATTHEW YOTSUYA

ELEVATED ANION GAP AS A MARKER OF SEVERE SARS-COV-2 INFECTION IN PREGNANT PATIENTS WITHOUT DIABETES: A CASE SERIES

SESSION TITLE: Biological Markers in Patients with COVID-19 Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/18/2022 01:30 pm - 02:30 pm PURPOSE: In December 2019, a disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) resulted in a global pandemic. The literature has been slowly growing in the subgroup of pregnant women but the metabolic derangements of pregnancy and SARS-CoV-2 have not been well described. METHODS: In this case series, we review 9 patients with severe SARS-CoV-2 infections admitted to the medical ICU at a single institution between 2020-2022, during the delta variant wave. RESULTS: Of the nine critically ill patients, the mean age was 32 ± 6.4 years with fetal age on admission of 27 ±2.81 weeks and 29 ±2.91 weeks at delivery. Average CRP of 114 ± 25 mg/L. In eight of 9 patients (89%), there was an anion gap metabolic acidosis (AGMA) on admission. The average albumin-corrected anion gap was 18±1.93. 75% of patients had mild ketonuria based on urinalysis. However, 50% had documented symptoms of nausea, vomiting, or diarrhea. While betahydroxybutyrate was checked in 2 patients, neither were abnormal. One had lactic acidosis, but none required vasopressors at time of identification. No renal failure or diabetes was noted and only two had abnormal glucose tolerance tests. At delivery, average PEEP was 10± 4 cmH2O with an average respiratory rate of 28 ± 4 breaths per minute. All patients with AGMA delivered early resulting in preterm delivery. 75% of the fetuses showed signs of distress at the time of delivery, which was the primary indication for delivery in 37.5% of deliveries. 37.5% of deliveries were due to significant maternal hypoxia. The only patient without AGMA did not deliver early. CONCLUSIONS: After excluding renal failure, toxin ingestion, and lactic acidosis, only ketosis can weakly explain the AGMA. There have been several studies that highlighted the association between COVID and ketone production. In pregnancy, placental production of glucagon and human placental lactogen and subsequent insulin resistance increases susceptibility to ketosis. A recent study posited that COVID could cause placental abnormalities. Therefore, pregnant women may be more susceptible to significant ketosis because of COVID infection. In one of our cases, the combination of hypoxia and acidosis could not be managed safely by the ventilator and resulted in early delivery. CLINICAL IMPLICATIONS: Ketosis and an elevated anion gap could be a marker for more severe outcomes in pregnant patients with COVID. This case series highlights the challenges of managing the metabolic demands of critically ill pregnant patients infected with SARS-CoV-2. DISCLOSURES: No relevant relationships by Calli Bertschy no disclosure on file for Joey Carlin;No relevant relationships by Jessica Ehrig No relevant relationships by Shekhar Ghamande no disclosure on file for Jordan Gray;No relevant relationships by Abirami Subramanian

MULTISYSTEM INFLAMMATORY SYNDROME OF ADULTS: A RARE COMPLICATION AFTER COVID-19 INFECTION

SESSION TITLE: Unique Inflammatory and Autoimmune Complications of COVID-19 Infections SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Multisystem inflammatory syndrome in adults (MIS-A) is a rare but clinically significant complication of COVID-19 infection characterized by severe illness with extrapulmonary organ dysfunction, markedly elevated inflammatory markers in the absence of severe respiratory illness or other obvious source of infection (1). We present a case of a 37-year-old male, with negative infectious evaluation and marked clinical improvement after administration of IVIG. CASE PRESENTATION: We present a 37-year-old black male with a past medical history of type 2 diabetes who was admitted to the hospital with shock and organ failure;prior to his presentation, he was diagnosed with COVID-19 pneumonia requiring outpatient therapy. On presentation, he was tachycardic, febrile, hypotensive with significant renal failure and lactic acidosis;inflammatory markers were elevated (CRP 640, ESR 108). Imaging was significant for mediastinal and hilar lymphadenopathy, with clear parenchyma (Figure 1). Broad coverage antibiotics, vasopressors, and stress dose steroids were initiated. Infectious evaluation was unrevealing with negative blood, urine, and sputum cultures;Echocardiogram revealed LVEF of 40% with mild RV dysfunction. His renal failure worsened, requiring CRRT. Vasculitis evaluation with ANA, ANCA, MPO, PR3, GBM, HIV, C3-C4 and cryoglobulins returned normal. Eventually, the patient was weaned from vasopressor support on hospital day four. Trials of weaning steroids resulted in recurrence of fevers and increasing vasopressor support. Given continued fevers without obvious infection there were concerns for MIS-A occurring shortly after COVID-19 infection. Antibiotics were discontinued and he received 2g/kg of IVIG with marked clinical improvement and was rapidly weaned from vasopressor support. We initiated methylprednisolone 1 mg/kg twice daily with steroid taper. He had improvement in inflammatory markers after IVIG and high dose steroids (CRP-6.7, ESR-49 prior to discharge). DISCUSSION: MIS-A is a rare disease that occurs after COVID-19 infection, with few reported cases in literature. Presentation is variable, but symptoms include high fever, dyspnea, lethargy, myalgias, and a diffuse maculopapular rash. Notably, hypoxia is not a prominent feature, a significant distinction from classic COVID-19 infection. Patel et al noted a predominance in young adults, males, and non-Hispanic black or Hispanic persons (2). The proposed mechanism stems from dysregulated immune response, with abnormal interferon production which drives macrophage activation and organ damage (3). There are no treatment guidelines available, and treatment of MIS-A is extrapolated from MIS-C and includes immunomodulatory therapies with IV IG, IL-1 receptor antagonist, and methylprednisolone. CONCLUSIONS: Prompt recognition of MIS-A critical given its potential for significant multi-organ dysfunction. Reference #1: Centers for Disease Control and Prevention. Multisystem Inflammatory Syndrome in Adults (MIS-A) Case Definition Information for Healthcare Providers. Available at Multisystem Inflammatory Syndrome in Adults (MIS-A) Case Definition Information for Healthcare Providers (cdc.gov). Accessed 3/19/2022 Reference #2: Patel, P., Decuir, J., Abrams, J., Campbell, A. P., Godfred-Cato, S., & Belay, E. D. (2021). Clinical Characteristics of Multisystem Inflammatory Syndrome in Adults: A Systematic Review. In JAMA Network Open (Vol. 4, Issue 9). https://doi.org/10.1001/jamanetworkopen.2021.26456 Reference #3: Weatherhead, J. E., Clark, E., Vogel, T. P., Atmar, R. L., & Kulkarni, P. A. (2020). Inflammatory syndromes associated with SARS-cov-2 infection: Dysregulation of the immune response across the age spectrum. Journal of Clinical Investigation, 130(12). https://doi.org/10.1172/JCI145301 DISCLOSURES: No relevant relationships by Mohammed Al-Charakh No relevant relationships by John Pare t no disclosure on file for Maximiliano Tamae Kakazu;

PLASMAPHERESIS FOR HYPERTRIGLYCERIDEMIA-INDUCED PANCREATITIS

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

THE PANDEMIC'S FUNGAL REVENGE: COVID-19 ASSOCIATED PULMONARY ASPERGILLOSIS (CAPA)

SESSION TITLE: Pathologies of the Post-COVID-19 World SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 10:15 am - 11:10 am INTRODUCTION: Since the start of the COVID-19 pandemic, COVID-19 Associated Pulmonary Aspergillosis (CAPA) has been on the rise. This superinfection, if not properly identified and treated, has shown to increase mortality up to 67% in COVID-19 patients. We are presenting a late presentation of CAPA after 4-month of COVID-19 infection and treated successfully. CASE PRESENTATION: A 57-year-old female patient with past medical history type 2 diabetes mellitus, hypertension and cardiomyopathy in addition to COVID-19 pneumonia treated for months ago with azithromycin, Bamlanivimab/Etesevimab, and Dexamethasone who presents to the hospital with massive hemoptysis and shortness of breath requiring intubation and mechanical ventilation. There was no reported history of recent travel, smoking, alcohol, or illicit drug use. Physical exam showed diminished lung sounds at the right lower lobe. Her labs showed mild leukocytosis, lactic acidosis and negative COVID-19 PCR. CT scan showed dense consolidation on right lower lobe consistent with lobar pneumonia and centrilobular ground glass opacities in the right upper lobe. Bronchoscopy showed complete obstruction of right bronchus intermedius and minimal blood clots in LLL. BAL respiratory culture, fungal smear, acid fast bacilli were non-diagnostic and negative for malignancy. Patient continued to have hemoptysis and bronchoscopy was repeated with negative cytology and cultures. The patient continued to have hemoptysis and she was transferred to tertiary center were bronchoscopy was repeated and confirmed right bronchus intermedius stenosis, blood clots, and suspicious right mainstem nodules with mucosal lesion. Biopsy results from bronchoscopy came back positive for the morphologic features of Aspergillus species. The patient was started on voriconazole with significant improvement in her symptoms. DISCUSSION: The recent literature of COVID-19 suggest association between COVID infection and invasive pulmonary Aspergillosis. COVID-19 virus causes damage in the airway epithelium and enable aspergillus to invade the pulmonary tract leading to serious infections with Aspergillus. It has also been known that Aspergillus infections are associated with diabetes mellitus and immune suppression which can be precipitated by steroid use and other treatments for COVID-19 infection like IL-6 inhibitors. Here in our patient with help of tissue biopsy we diagnosed CAPA, started treatment early and treated successfully. CONCLUSIONS: CAPA can be difficult to diagnose and needs high index of suspicion in the appropriate clinical scenario when dealing with post COVID respiratory complaints like hemoptysis. Bronchoalveolar lavage alone without tissue biopsy might miss the diagnosis in the context of invasive aspergillosis like the scenario we observed in our case. Doing tissue biopsy through bronchoscopy might add more clinical benefit when Aspergillus infections are suspected. Reference #1: Chih-Cheng Lai, Weng-Liang Yu, COVID-19 associated with pulmonary aspergillosis: A literature review, https://doi.org/10.1016/j.jmii.2020.09.004 DISCLOSURES: No relevant relationships by Haytham Adada No relevant relationships by Mahmoud Amarna No relevant relationships by Rishika Bajaj No relevant relationships by Camelia Chirculescu No relevant relationships by Sonia Dogra No relevant relationships by Azad Patel

UNDERSTANDING THE NEED FOR A BROAD DIFFERENTIAL DIAGNOSIS: A CASE OF PNEUMONIC TULAREMIA

SESSION TITLE: Disseminated Bacterial Infections SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 10:15 am - 11:10 am INTRODUCTION: Tularemia is a rare infectious disease caused by Francisella Tularensis that typically affects the skin, eyes, lymph nodes, and lungs. There are a variety of forms of tularemia with varying rates of contagiousness and mortality. Respiratory tularemia has a high mortality rate if left untreated and presents with non-specific viral like symptoms occurring in conjunction with respiratory symptoms: cough, hemoptysis, and pleuritic chest pain. In this COVID ARDS era, it is important to evaluate a broad differential diagnosis. Therefore, the authors describe a patient presenting with flu-like respiratory symptoms whom was ultimately was diagnosed with acute respiratory distress syndrome (ARDS) due to F. Tulerensis. CASE PRESENTATION: A 44-year-old male presented with a four-day history of night sweats, shortness of breath, a productive cough which progressed to hemoptysis, and oliguria. Prior to admission, his initial symptoms were treated as chronic sinusitis with varied antibiotics. Social history including tobacco abuse and deer hunting 1 month prior to presentation. Vitals were stable except for tachycardia, hypoxia, and tachypnea. Laboratory findings were significant for AKI, lactic acidosis, mild transaminitis, hyperbilirubinemia, and leukocytosis with predominant neutrophilia. Thoracic CTA showed bilateral diffused pulmonary edema without evidence of pulmonary embolism. Due to the patient's worsening respiratory status, he was intubated for support. The patient progressed to Severe ARDS per Berlin Criteria eventually requiring pronation and continuous paralyzing. Bronchoscopy was performed with bronchial lavage. Bacterial, viral, and fungal cultures did not show growth while vasculitic work-up was negative. Empiric antibiotic treatment did not show improvement until the patient was diagnosed with F. Taularensis via serological testing with an IgM of 20 U/mL, and patient was transitioned to gentamycin. Ultimately, the patient was extubated, transitioned to oral doxycycline, and discharged home. DISCUSSION: Approximately 250 cases of tularemia are reported to CDC each year. Respiratory tularemia has a mortality rate up to 30% if not treated. For this reason, F. tularensis is a potential biological weapon and is categorized as a Group A pathogenic agent. Serological testing may be negative early in disease progression;therefore, early inflammatory markers with clinical suspicion are essential to diagnose the disease early in its course. DNA microarray has high specificity and sensitivity for rapid diagnosis of tularemia while being cost effective. After prompt diagnosis, intravenous aminoglycosides;such as gentamycin or streptomycin;must be started. CONCLUSIONS: In the above case, we illustrate the gradual onset and rapid patient deterioration when treatment is delayed;yet, there is rapid recovery once appropriate treatment is used. Reference #1: 1. Ranjbar, Reza, Payam Behzadi, and Caterina Mammina. "Respiratory tularemia: Francisella tularensis and microarray probe designing.” The open microbiology journal 10 (2016): 176. Reference #2: 2. Akhvlediani, N., I. Burjanadze, D. Baliashvili, T. Tushishvili, M. Broladze, A. Navdarashvili, S. Dolbadze et al. "Tularemia transmission to humans: a multifaceted surveillance approach.” Epidemiology & Infection 146, no. 16 (2018): 2139-2145. Reference #3: 3. Tularemia in British Columbia: A case report and review. Issue: BCMJ, vol. 52, No. 6, July August 2010 (Pages 303- 307). Megan Isaac-Renton, BSc, Muhammad Morshed, PhD, SCCM Eleni Galanis, MD, MPH, FRCPC Sunny Mak, MSc Vicente Loyola, MD, FRCPC, Linda M.N. Hoang, MD, MHSc, FRCPC DISCLOSURES: No relevant relationships by Munish Adhikari No relevant relationships by Ashma Ul Husna No relevant relationships by Yan Jiang No relevant relationships by Divya Kharel No relevant relationships by Gregory Polcha

SHEWANELLA SEPTIC SHOCK COMPLICATING COVID-19 SURVIVORSHIP FOLLOWING EXTRACORPOREAL MEMBRANE OXYGENATION (ECMO) RECOVERY

SESSION TITLE: Critical Care in Chest Infections Case Report Posters 2 SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Shewanella are gram-negative bacteria that inhabit salt and brackish watery environments, rarely causing skin and soft tissue infections. We report a case of septic shock, bacteremia, and empyema due to Shewanella in a COVID-ARDS survivor who previously received ECMO. CASE PRESENTATION: A 67-year-old man with a medical history of hypertension, diabetes, recent COVID-ARDS illness complicated with STEMI, leading to a VT/VF arrest requiring 21-days of VV-ECMO support presented three weeks after discharge due to worsening oxygen needs. The patient was hypotensive, febrile, tachycardic, tachypneic, with SatO2 92% on HFNC> 50%FIO2. Labs showed leukocytosis, lactic acidosis, and acute kidney injury. Chest x-ray showed a loculated left pleural effusion. Broad spectrum antibiotics were started. Blood cultures grew Shewanella species in aerobic and anaerobic bottles. A CT of the chest is shown (Figure 1). Thoracentesis was performed with findings consistent with empyema (Table 1). The empyema was managed with pigtail catheters and TPAse-DNAse. Pleural fluid cultures had no growth. The patient improved and was discharged on 6-week course of IV ceftazidime. DISCUSSION: Shewanella is a rare cause of skin and soft tissue infections, following traumatic injuries in association with exposure to salt or brackish water. It has also been associated with pneumonia, in the setting of near drownings, in both fresh and saltwater. Individuals with underlying liver disease and immunocompromising conditions are at the highest risk of contracting the pathogen and manifesting illness. Shewanella algae and putrefaciens may manifest as deep ulcers with hemorrhagic bullae, bacteremia, endocarditis, and meningitis (1). In addition, biliary tract infections and peritonitis can occur (2). Our patient had no epidemiologic risk factors for Shewanella infection. Although nosocomial transmission is possible, we are not aware of any previous reports of such exposure in association with this infection. Given negative pleural fluid culture with positive blood culture, we hypothesize our patient's empyema is due to Shewanella given no other apparent infectious etiology. Studies have shown that approximately 40% of pleural infection are culture negative. It is possible that antibiotic therapy started before fluid collection lowered the diagnostic yield of thoracentesis. The prevalence of bloodstream infections during ECMO ranges from 3 to 18%, with coagulase-negative staphylococcus as the most frequent cause, followed by Candida spp., Pseudomonas aeruginosa, Enterobacteriaceae, Staphylococcus aureus and Enterococcus spp. (3) with no known reports of Shewanella per the ELSO registry. CONCLUSIONS: This case may confer possible healthcare-related acquirement of Shewanella. Our case adds awareness to clinicians about potential routes of inoculation, predisposing factors, and the wide clinical manifestations of Shewanellosis. Reference #1: Weiss TJ, Barranco-Trabi JJ, Brown A, Oommen TT, Mank V, Ryan C. Case Report: Shewanella Algae Pneumonia and Bacteremia in an Elderly Male Living at a Long-Term Care Facility. Am J Trop Med Hyg. 2021;106(1):60-61. Published 2021 Nov 15. doi:10.4269/ajtmh.21-0614 Reference #2: Savini V, Marrollo R, Nigro R, Fazii P. Chapter 6-Skin and Soft Tissue Infections Following Marine Injuries. In: The Microbiology of Skin, Soft Tissue, Bone and Joint Infections. Vol 2.;2017:93-103. Reference #3: S. Biffi et al. / International Journal of Antimicrobial Agents 50 (2017) 9–16 DISCLOSURES: No relevant relationships by Akram Alkrekshi No relevant relationships by Robert Kalayjian No relevant relationships by Ismini Kourouni No relevant relationships by Srinivasa Potla No relevant relationships by Zahra Zia

PERICARDITIS EVOLVING INTO CARDIAC TAMPONADE IN A 76-YEAR-OLD PATIENT WITH COVID-19

SESSION TITLE: Cardiovascular Complications in Patients with COVID-19 SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Cardiac tamponade is a medical emergency that requires rapid diagnosis and intervention to prevent hemodynamic collapse. Although COVID-19 typically manifests with pulmonary symptoms, cardiac involvement is becoming better studied through increasingly frequently reported cases [1]. We present a case of COVID-19 cardiac involvement presenting as a rapidly progressive pericardial effusion turning into tamponade. This highlights the importance of a high index of suspicion for patients who develop sudden and atypical respiratory compromise with hypotension in the setting of COVID-19 infection. CASE PRESENTATION: A 76-year-old male with a history of ESRD presented with fatigue after missing hemodialysis. Laboratory investigations revealed a mild troponin elevation and positive SARS-CoV-2 PCR. Initial TTE demonstrated an EF of 60-65% with a small pericardial effusion and thickened calcified pericardium. After a few days, the patient was noted to be encephalopathic and hypotensive. Labs revealed leukocytosis, lactic acidosis as well as an elevated troponin and D-dimer. Chest CTA was significant for a large pericardial effusion with reduced size of the right ventricle, concerning for cardiac tamponade. Repeat TTE had a moderate pericardial effusion and right atrial collapse, consistent with tamponade. Given significantly elevated INR in the setting of anticoagulation, pericardiocentesis was deferred while the patient was transfused FFP. The patient subsequently suffered PEA arrest and expired despite attempted hemodynamic stabilization. DISCUSSION: Cardiac tamponade is a result of accumulating pericardial fluid culminating in decreased cardiac output and shock. Clinicians should be prompted by characteristic findings, including Beck’s triad (JVD, hypotension, and muffled heart sounds) and Kussmaul’s sign of paradoxically elevated JVP with inspiration [2]. However, the diagnosis of tamponade based solely on clinical finding is difficult and may lead to unnecessary intervention [3]. Ultimately, a diagnosis of tamponade requires both hemodynamic instability and pericardial effusion. Echocardiography, including TTE and POCUS, plays a central role in the identification of cardiac tamponade. While it is essential to note the presence of a pericardial effusion, it is important to be familiar with core echocardiographic signs of tamponade: systolic RA collapse (earliest sign), diastolic RV collapse, IVC with minimal respiratory variation, and exaggerated respiratory cycle changes in MV and TV in-flow velocities (a surrogate for pulsus paradoxus) [3]. CONCLUSIONS: Despite the classic association between COVID-19 and pulmonary manifestation, pericardial involvement has been noted in 20% of COVID-19 patients. It is therefore imperative to maintain a high index of suspicion and familiarity of characteristic echocardiogram findings of tamponade to prompt intervention and curtail cardiac hemodynamic collapse. Reference #1: Lala A, Johnson KW, Januzzi JL, et al. Prevalence and Impact of Myocardial Injury in Patients Hospitalized With COVID-19 Infection. J Am Coll Cardiol. 2020;76(5):533-546. doi:10.1016/j.jacc.2020.06.007 Reference #2: Stashko E, Meer JM. Cardiac Tamponade. [Updated 2021 Dec 21]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing;2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK431090/ Reference #3: Alerhand S, Carter JM. What echocardiographic findings suggest a pericardial effusion is causing tamponade?. Am J Emerg Med. 2019;37(2):321-326. doi:10.1016/j.ajem.2018.11.004 DISCLOSURES: No relevant relationships by Christopher Allahverdian No relevant relationships by John Javien No relevant relationships by Vishal Patel No relevant relationships by Sarah Youkhana

Metformin-associated Lactic Acidosis with Hypoglycemia during the COVID-19 Pandemic.

Metformin-associated lactic acidosis (MALA) is an extremely rare but life-threatening adverse effect of metformin treatment. The lifestyle changes associated with the coronavirus disease 2019 (COVID-19) pandemic may increase the potential risk of MALA development in patients with diabetes. We herein report a 64-year-old Japanese man taking a small dose of metformin who presented with MALA accompanied by hypoglycemia secondary to increased alcohol consumption triggered by lifestyle changes during the pandemic. Physicians should prescribe metformin judiciously to prevent MALA development and pay close attention to lifestyle changes in patients at risk for MALA during the COVID-19 pandemic.

Undifferentiated Shock: A Case of Idiopathic Capillary Leak Syndrome

Systemic capillary leak syndrome (SCLS or Clarkson's disease) is a rare condition characterized by episodes of vascular hyperpermeability. The extravasation of plasma to the interstitial space results in hemoconcentration, hypoalbuminemia, hypovolemia and compartment syndrome of the extremities. The disease can be idiopathic or secondary to causes including viral infections or chemotherapeutic toxicity. We present a fatal case of idiopathic SCLS which rapidly deteriorated to multiple organ failure despite initial improvement with methylene blue. A 57-year-old male presented for worsening back pain over one month. He described a flulike illness 2 weeks prior. Testing for respiratory viruses including SARS-CoV-2 was negative. He received intravenous crystalloid fluids acutely developed respiratory distress and hypotension requiring emergent intubation and initiation of norepinephrine infusion. CT angiography of the chest demonstrated pulmonary edema. Early during his hospitalization urine output ceased and body weight increased by 10 kg, developing tense anasarca. Hematocrit concentrated from 42.7 to 54.4%. Serum albumin dropped from 4.6 to 2.5 g/dL. C1 esterase inhibitor level and IgM were normal. Ferritin was elevated at 2515 ng/ml. He received cefepime and vancomycin, though infectious workup returned unremarkable. Continuous renal replacement therapy and stress dose steroids were initiated. Vasopressor requirement worsened until he was on three vasopressors at one point. Given the constellation of hemoconcentration, hypoalbuminemia, and shock a diagnosis was made of idiopathic SCLS. Treatment was started with methylene blue, montelukast, and the β-adrenergic agonist terbutaline. Blood pressure improved and patient came off pressors and lactate improved from 13 to 4. However, he later developed rising creatine kinase continued to climb to >40,000 U/L. He developed rhabdomyolysis with concern for compartment syndrome of the extremities due to third spacing of fluids. Orthopedic surgery was consulted;but did not believe a fasciotomy was indicated due to rapid decline. Lactic acidosis rose to 18 mmol/L. His family decided to transition to comfort measures. He passed with family at bedside on Day 4 of hospitalization. There are fewer than 500 cases of SCLS reported since initial discovery in 1960. Given the overlap in presentation with common causes of plasma leakage such as sepsis, it is likely that many cases are unrecognized. Patients are often mismanaged;development of severe hypovolemia despite fluids and compartment syndrome is overlooked. This case builds on our evolving recognition of this disease, and the potential for the use of methylene blue to help acute exacerbations of the disease.

Uncovering Cocaine Induced Eosinophilic Pneumonia

Cocaine use has a significant public health impact, causing over 1.2 million ER visits annually. Cocaine can cause a wide range of pulmonary pathology, including diffuse alveolar hemorrhage (“Crack Lung”), barotrauma, bronchiectasis, granulomatous disease, and pulmonary vascular disease. Acute eosinophilic pneumonia (AEP) is a rare and potentially life-threatening complication of cocaine use that can be successfully treated if identified. We describe a case of persistent fevers, hypoxemia, and air space opacities due to AEP related to cocaine use.A 34-year-old male with a history of polysubstance abuse was found unresponsive, apneic, and surrounded by vomitus at a party, where he had smoked marijuana and cocaine and injected heroin. Upon hospital arrival, he was hypotensive and severely hypoxic and was intubated. He had severe rhabdomyolysis, lactic acidosis, acute kidney injury, and acute liver injury. His chest radiograph demonstrated diffuse bilateral alveolar infiltrates. COVID-19 was ruled out. Sputum cultures grew Klebsiella and E. Coli;Streptococcus Pneumoniae urine antigen was positive. He received IV fluids, vasopressors, and broad spectrum antibiotics for septic shock and aspiration pneumonia in the setting of drug overdose. His septic shock and hypoxemia improved, allowing tracheostomy and gastrostomy to be performed. Despite prolonged courses of antibiotics, he had persistent fevers, worsening infiltrates on chest radiograph, and persistent hypoxemia. CT imaging demonstrated diffuse, bilateral ground glass opacities and consolidations, with reticulation and interlobular septal thickening. Viral, bacterial, and fungal cultures collected via bronchoscopy were negative, however, cell count revealed 315 WBC / mm3, with 27% eosinophils. He was started on methylprednisolone 80mg IV every eight hours and had resolution of fevers and improvement in oxygenation and infiltrates. 1 month after discharge, he was decannulated and did not require supplemental oxygen. DiscussionThis case highlights an important aspect of assessing fever in the ICU despite broad spectrum antibiotics in patient with drug overdose. In the above , bronchoscopy unmasked an eosinophilic pneumonia allowing a rapid transition to trach collar and prevention of progression to pulmonary fibrosis. (Figure Presented).

A Case of Hydroxyurea-Induced Interstitial Pneumonitis

Introduction: First synthesized in 1869, Hydroxyurea is known for its efficacy in treating myeloproliferative disorders, cervical cancer, and sickle cell disease. Usually well-tolerated, Hydroxyurea has numerous documented adverse effects, including bone marrow suppression, fevers, gastrointestinal upset, anorexia, and maculopapular rash. In addition, one rare side effect is interstitial pneumonitis, a potentially devastating complication if overlooked. We present one such case of Hydroxyurea-induced interstitial pneumonitis. Case Description: A 65-year-old man with a six-month diagnosis of Chronic Granulocytic Leukemia (CGL) on Hydroxyurea developed acute hypoxemic respiratory failure saturating 80% on room air with HR 102, RR 24, and increasing oxygen requirements (10 Lpm) after being admitted with complaints of worsening dyspnea, fatigue, and productive cough with yellow/green sputum. Physical examination was notable for cachexia, ill appearance, generalized weakness, hoarse voice, tachycardia, tachypnea, diffusely diminished breath sounds, and scattered rales on auscultation of lung fields. Initial imaging was notable for bilateral airspace disease and pulmonary opacities on chest radiography and bilateral pneumonia (concerning for COVID-19 pneumonia), mediastinal adenopathy, and splenomegaly on chest computed tomography. Initial laboratory results were notable for leukocytosis 62.5 th/uL, lactic acidosis 2.5 mmol/L, procalcitonin level 4.95 ng/mL, and negative COVID-19 PCR test. Prompt initiation of Vancomycin/Cefepime therapy ensued upon collection of blood cultures in light of possible sepsis. Flagyl, Valacyclovir, and Posaconazole were added to antimicrobial coverage, along with steroid therapy, due to minimal clinical improvement. Tachycardia with significant oxygen requirements alternating between BiPAP and heated high flow nasal cannula with FiO2 ranging from 70-85% persisted. Daily imaging also showed worsening airspace disease. Negative viral, bacterial, and fungal cultures led to subsequent discontinuation of Hydroxyurea therapy due to suspicion of medicationinduced pneumonitis. Three days after cessation of Hydroxyurea, the patient's oxygen requirements began to decrease and imaging revealed interval resolution of pneumonitic changes in the absence of antimicrobial therapy. The patient was later transitioned to Ruxolitinib for his underlying CGL prior to his discharge home without the need for home oxygen therapy. Discussion: Thought to be caused by hypersensitivity pneumonitis, pulmonary toxicity from Hydroxyurea can easily be misdiagnosed. Unfortunately, while much is known about the pancytopenic, gastrointestinal, and cutaneous side effects of Hydroxyurea, few cases in the literature highlight the potentially fatal interstitial pneumopathy caused by Hydroxyurea, first reported in 1999. Thus, this case serves as an additional contribution to the minutiae of literature detailing Hydroxyurea's adverse pulmonary side effect profile. (Figure Presented).