Session Types Research Articles

SUBOPTIMAL UPTAKE OF OUTPATIENT PULMONARY REHABILITATION FOLLOWING DISCHARGE FOR A COPD EXACERBATION: ONE HOSPITAL'S EXPERIENCE

SESSION TITLE: Practice Management Beyond Coding and StaffingSESSION TYPE: Rapid Fire Original InvPRESENTED ON: 10/17/2022 12:15 pm - 1:15 pmPURPOSE: Despite reduced health care utilization and mortality for COPD patients participating in pulmonary rehabilitation (PR) after hospitalization, few enroll in this intervention. Reasons were explored in a post-discharge survey to inform new ways to market or restructure PR.METHODS: IRB-approved, telephone survey and record review of patients with COPD discharged from one hospital over 1-year period. Inclusion criteria for analysis: 1) Principal diagnosis of COPD or respiratory failure; 2) Discharge home; 3) PR indicated or not contraindicated. Inclusion criteria for survey: 1) Telephone consent; 2) Fluency in English.RESULTS: 191 were studied. Of these, 51 (27%) were not in a home setting (26 died, 25 not discharged home), 32 (16%) had no indication for PR (11 had an incorrect diagnosis, 21 not medically indicated). Of the remaining, 62 could not be surveyed (38 not reachable, 8 language barrier, 16 refused consent), leaving 46 (24% of total group) surveyed at 132 ± 89 days following discharge. Of those surveyed, 89% had a primary care provider, 72% had a pulmonologist, 43% had heard of PR, but only 24% ever participated in this intervention. 28% were ever referred to PR. Pulmonologists were the most common referrers. Desirable outcomes and factors that might influence the patient’s decision to participate in PR are in the Table.Table. Survey Results, n = 46Mean rankings of Importance to Patients: 1 = least important, 5= most importantPotential Outcomes of Importance to PatientReduced Hospitalization Risk 4.80Improvement in Dyspnea 4.54Learn More About Lung Disease 4.34Increase in Ability to do Things 4.26Fewer Flare-ups of Lung Disease 4.26Decrease in Tiredness or Fatigue 4.09Reduced anxiety or nervousness 3.94Opportunity to Interact with Others 3.49Factors that Might Positively Influence Decision for PRLikelihood of Beneficial Outcome 4.34Low Cost 4.23Short Travel Distance to PR 4.00Less Concern over Excessive Dyspnea during Exercise 3.54Convenient Transportation to PR 3.37Fewer Weather-Related Issues 2.89Not Having to Get Up in the AM to Go to PR 2.66No Family Responsibility Conflicts in Attending PR 1.97Not Too Soon After Hospitalization 1.60No Employment Conflicts in Attending PR 1.37CONCLUSIONS: Despite reasonably good access to medical care, uptake of PR was poor. Important factors in under-utilization include non-indication or contraindication or non-referral to PR.CLINICAL IMPLICATIONS: A major limitation of this survey is that it was conducted during the COVID-19 pandemic when PR facilities were closed. Those never participating in PR nevertheless listed desirability of outcomes typically attributed to PR. Although repeating the survey post-pandemic may yield more accurate results, current data indicates the need for improved patient education and referral to PR. This is a potential target for future interventions to increase PR usage.DISCLOSURES: No relevant relationships by Osama ElsankaryNo relevant relationships by Antarpreet KaurNo relevant relationships by Hnin Hnin OoNo relevant relationships by Jane ReardonNo relevant relationships by Ryan TalbertNo relevant relationships by Richard ZuWallack SESSION TITLE: Practice Management Beyond Coding and Staffing SESSION TYPE: Rapid Fire Original Inv PRESENTED ON: 10/17/2022 12:15 pm - 1:15 pm PURPOSE: Despite reduced health care utilization and mortality for COPD patients participating in pulmonary rehabilitation (PR) after hospitalization, few enroll in this intervention. Reasons were explored in a post-discharge survey to inform new ways to market or restructure PR. METHODS: IRB-approved, telephone survey and record review of patients with COPD discharged from one hospital over 1-year period. Inclusion criteria for analysis: 1) Principal diagnosis of COPD or respiratory failure; 2) Discharge home; 3) PR indicated or not contraindicated. Inclusion criteria for survey: 1) Telephone consent; 2) Fluency in English. RESULTS: 191 were studied. Of these, 51 (27%) were not in a home setting (26 died, 25 not discharged home), 32 (16%) had no indication for PR (11 had an incorrect diagnosis, 21 not medically indicated). Of the remaining, 62 could not be surveyed (38 not reachable, 8 language barrier, 16 refused consent), leaving 46 (24% of total group) surveyed at 132 ± 89 days following discharge. Of those surveyed, 89% had a primary care provider, 72% had a pulmonologist, 43% had heard of PR, but only 24% ever participated in this intervention. 28% were ever referred to PR. Pulmonologists were the most common referrers. Desirable outcomes and factors that might influence the patient’s decision to participate in PR are in the Table. Table. Survey Results, n = 46 Mean rankings of Importance to Patients: 1 = least important, 5= most important Potential Outcomes of Importance to Patient Reduced Hospitalization Risk 4.80 Improvement in Dyspnea 4.54 Learn More About Lung Disease 4.34 Increase in Ability to do Things 4.26 Fewer Flare-ups of Lung Disease 4.26 Decrease in Tiredness or Fatigue 4.09 Reduced anxiety or nervousness 3.94 Opportunity to Interact with Others 3.49 Factors that Might Positively Influence Decision for PR Likelihood of Beneficial Outcome 4.34 Low Cost 4.23 Short Travel Distance to PR 4.00 Less Concern over Excessive Dyspnea during Exercise 3.54 Convenient Transportation to PR 3.37 Fewer Weather-Related Issues 2.89 Not Having to Get Up in the AM to Go to PR 2.66 No Family Responsibility Conflicts in Attending PR 1.97 Not Too Soon After Hospitalization 1.60 No Employment Conflicts in Attending PR 1.37 CONCLUSIONS: Despite reasonably good access to medical care, uptake of PR was poor. Important factors in under-utilization include non-indication or contraindication or non-referral to PR. CLINICAL IMPLICATIONS: A major limitation of this survey is that it was conducted during the COVID-19 pandemic when PR facilities were closed. Those never participating in PR nevertheless listed desirability of outcomes typically attributed to PR. Although repeating the survey post-pandemic may yield more accurate results, current data indicates the need for improved patient education and referral to PR. This is a potential target for future interventions to increase PR usage. DISCLOSURES: No relevant relationships by Osama Elsankary No relevant relationships by Antarpreet Kaur No relevant relationships by Hnin Hnin Oo No relevant relationships by Jane Reardon No relevant relationships by Ryan Talbert No relevant relationships by Richard ZuWallack

BILATERAL PULMONARY EMBOLISM MASQUERADING AS MEDIASTINAL LYMPHADENOPATHY DIAGNOSED WITH ENDOBRONCHIAL ULTRASOUND

SESSION TITLE: Variety in Risk Factors and Treatment of VTESESSION TYPE: Rapid Fire Case ReportsPRESENTED ON: 10/19/2022 12:45 pm - 1:45 pmINTRODUCTION: Pulmonary embolism is a life-threatening respiratory condition. It is often a diagnosis that is investigated for in patients presenting with acute onset dyspnea, hypoxemia and/or hypotension. Mediastinal lymphadenopathy begets a separate differential diagnosis in dyspneic patients. Lymphadenopathy can be evaluated and biopsied by endobronchial ultrasound. Here we present a case of a young female with weakness who was felt to have mediastinal lymphadenopathy on chest imaging and on EBUS was found to have pulmonary embolism.CASE PRESENTATION: A 38-year-old female with a history of iron deficiency anemia presented for acute right lower extremity weakness. MRI of the L spine was done with findings of abnormal signal of the conus medullaris. Further MRI of the brain and spine demonstrated diffuse enhancing lesions. Given the cranial nerve involvement and homogenous lesions, the diagnosis was felt to be neurosarcoid. Lumbar puncture was done to evaluate for multiple sclerosis and infection. CT chest without contrast demonstrating bilateral mediastinal lymphadenopathy. EBUS was pursued for tissue sampling. On EBUS, mediastinal lymph nodes appeared normal in size with a normal architecture. Incidentally, EBUS demonstrated large intraluminal floating homogenous material within the left and right pulmonary arteries concerning for pulmonary embolism. CT chest with contrast post procedure showed that the initial mediastinal lymphadenopathy was now revealed as bilateral central pulmonary emboli. Lower extremity dopplers revealed right peroneal vein thrombosis. Echocardiogram did not show RV dysfunction and the patient remained hemodynamically stable. The patient was started on therapeutic anticoagulation as further neurological work up was pursued for alternative diagnoses of acute right lower extremity weakness. The patient was treated with a course of steroids of presumed acute disseminated encephalomyelitis and discharged to acute rehab on anticoagulation.DISCUSSION: CT chest without contrast suspicious for mediastinal lymphadenopathy can be misleading. In this case, mediastinal lymphadenopathy was first reported due to an inherent bias of neurosarcoid being the presumptive diagnosis. Currently, the evaluation of pulmonary embolism involves CT angiography of the chest as the gold standard. While less cost efficient than a CT scan, EBUS can be a safe and reliable tool in the diagnosis of pulmonary embolism in the right patient population in whom a CT is unable to be obtained or is contraindicated. Further studies evaluating the procedural risk in patients unable to get CT imaging is warranted.CONCLUSIONS: It is important to be aware of the limitations of CT imaging without contrast in formulation of a differential diagnosis. The diagnosis of pulmonary embolism can be made from EBUS and may have a role in an appropriate subset of the patient population.Reference #1: Aumiller J, Herth FJ, Krasnik M, Eberhardt R. Endobronchial ultrasound for detecting central pulmonary emboli: a pilot study. Respiration. 2009;77(3):298-302. doi: 10.1159/000183197. Epub 2008 Dec 9. PMID: 19065053.DISCLOSURES: No relevant relationships by Vincent ChanNo relevant relationships by Prarthna KulandaisamyNo relevant relationships by Lindsey Morris SESSION TITLE: Variety in Risk Factors and Treatment of VTE SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Pulmonary embolism is a life-threatening respiratory condition. It is often a diagnosis that is investigated for in patients presenting with acute onset dyspnea, hypoxemia and/or hypotension. Mediastinal lymphadenopathy begets a separate differential diagnosis in dyspneic patients. Lymphadenopathy can be evaluated and biopsied by endobronchial ultrasound. Here we present a case of a young female with weakness who was felt to have mediastinal lymphadenopathy on chest imaging and on EBUS was found to have pulmonary embolism. CASE PRESENTATION: A 38-year-old female with a history of iron deficiency anemia presented for acute right lower extremity weakness. MRI of the L spine was done with findings of abnormal signal of the conus medullaris. Further MRI of the brain and spine demonstrated diffuse enhancing lesions. Given the cranial nerve involvement and homogenous lesions, the diagnosis was felt to be neurosarcoid. Lumbar puncture was done to evaluate for multiple sclerosis and infection. CT chest without contrast demonstrating bilateral mediastinal lymphadenopathy. EBUS was pursued for tissue sampling. On EBUS, mediastinal lymph nodes appeared normal in size with a normal architecture. Incidentally, EBUS demonstrated large intraluminal floating homogenous material within the left and right pulmonary arteries concerning for pulmonary embolism. CT chest with contrast post procedure showed that the initial mediastinal lymphadenopathy was now revealed as bilateral central pulmonary emboli. Lower extremity dopplers revealed right peroneal vein thrombosis. Echocardiogram did not show RV dysfunction and the patient remained hemodynamically stable. The patient was started on therapeutic anticoagulation as further neurological work up was pursued for alternative diagnoses of acute right lower extremity weakness. The patient was treated with a course of steroids of presumed acute disseminated encephalomyelitis and discharged to acute rehab on anticoagulation. DISCUSSION: CT chest without contrast suspicious for mediastinal lymphadenopathy can be misleading. In this case, mediastinal lymphadenopathy was first reported due to an inherent bias of neurosarcoid being the presumptive diagnosis. Currently, the evaluation of pulmonary embolism involves CT angiography of the chest as the gold standard. While less cost efficient than a CT scan, EBUS can be a safe and reliable tool in the diagnosis of pulmonary embolism in the right patient population in whom a CT is unable to be obtained or is contraindicated. Further studies evaluating the procedural risk in patients unable to get CT imaging is warranted. CONCLUSIONS: It is important to be aware of the limitations of CT imaging without contrast in formulation of a differential diagnosis. The diagnosis of pulmonary embolism can be made from EBUS and may have a role in an appropriate subset of the patient population. Reference #1: Aumiller J, Herth FJ, Krasnik M, Eberhardt R. Endobronchial ultrasound for detecting central pulmonary emboli: a pilot study. Respiration. 2009;77(3):298-302. doi: 10.1159/000183197. Epub 2008 Dec 9. PMID: 19065053. DISCLOSURES: No relevant relationships by Vincent Chan No relevant relationships by Prarthna Kulandaisamy No relevant relationships by Lindsey Morris

PSYCHOSIS OR ENCEPHALITIS? HAVE A LOW INDEX OF SUSPICION FOR ANTI-N-METHYL-D-ASPARTATE (NMDA) RECEPTOR ENCEPHALITIS

SESSION TITLE: Neurological Crises in Critical CareSESSION TYPE: Rapid Fire Case ReportsPRESENTED ON: 10/18/2022 01:35 pm - 02:35 pmINTRODUCTION: Anti-N-methyl-d-aspartate receptor(NMDAR) encephalitis is an autoimmune disorder first described in 2007 in women with teratomas. Presenting psychiatric symptoms include psychosis, anxiety, insomnia, mania and catatonia. For patients with anti-NMDAR encephalitis, initial miss-classification as a psychiatric disease results in delayed diagnosis and worse outcome.CASE PRESENTATION: A 37-year-old woman presented to an urgent care center with hallucinations, dizziness and headaches, which was treated as acute otitis media. Her symptoms progressively worsened to agitation and she was admitted to a psychiatric unit for acute psychosis. Antipsychotics did not improve her condition, became catatonic and was transferred to the ICU for further management. Infectious work-up was negative and thyroid function tests were normal. EEG showed generalized rhythmic delta activity. CSF analysis was positive for oligoclonal bands and 98% lymphocytes. She was treated empirically with high-dose steroids(250mg Q6 hours) for 6 days and IV immune globulin 140g over 5 days for high suspicion of autoimmune encephalitis. Her NMDAR antibodies were reported positive in serum and CSF 10 and 31 days after collection with a CSF titer of 1:64. Abdominal US revealed a dermoid cyst which was surgically removed. Rituximab therapy was considered but not initiated due to concern for sepsis. Clinical course was complicated by status epilepticus requiring intubation, symptomatic bradycardia, cardiogenic shock, renal failure, atrial fibrillation and central hypoventilation. Repeat CT revealed anoxic brain injury. She passed a few days later.DISCUSSION: The most common presenting features of anti-NMDAR encephalitis are psychiatric symptoms, like mood alteration(anxiety or depression), aggression, mania, delusion, schizoaffective episodes, hallucinations; and seizures. Lymphocytic pleocytosis or oligoclonal bands in CSF, slow, epileptic activity or delta brush pattern on EEG, and mesiotemporal hyperintensities or atrophy pattern on MRI have been described with anti-NMDAR encephalitis. Patients presenting with high antibody titer groups(>1:32 in CSF), such as observed in our patient, more likely present teratoma and result in poor patient outcome. Although improved outcomes are associated with timely initiation of treatment, residual psychiatric symptoms have been noted in a significant portion of patients. First line immunotherapy includes corticosteroids, immunoglobulins or plasma exchange; and second line escalations like rituximab and cyclophosphamide may be added.CONCLUSIONS: Anti-NMDAR encephalitis may be misdiagnosed as a primary psychotic disorder. Confirmatory diagnostic testing are often delayed leading to worse outcomes. Hence, in a patient presenting with new onset psychosis, high index of suspicion for anti-NMDAR encephalitis and early initiation of therapy should be considered prior to confirmatory diagnostic testing.Reference #1: Ford B, McDonald A, Srinivasan S. Anti-NMDA receptor encephalitis: a case study and illness overview. Drugs Context. 2019;8:212589. Published 2019 Aug 30. doi:10.7573/dic.212589Reference #2: Wang W, Zhang L et al. Psychiatric symptoms of patients with anti-nmda receptor encephalitis. Front. Neurol., 24 January 2020. https://doi.org/10.3389/fneur.2019.01330Reference #3: Dalmau J, Armangué T, et al. An update on anti-NMDA receptor encephalitis for neurologists and psychiatrists: mechanisms and models. The Lancet Neurology, Volume 18, Issue 11, 2019, Pages 1045-1057.DISCLOSURES: No relevant relationships by Aditi DesaiNo relevant relationships by Daniel Fein SESSION TITLE: Neurological Crises in Critical Care SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 01:35 pm - 02:35 pm INTRODUCTION: Anti-N-methyl-d-aspartate receptor(NMDAR) encephalitis is an autoimmune disorder first described in 2007 in women with teratomas. Presenting psychiatric symptoms include psychosis, anxiety, insomnia, mania and catatonia. For patients with anti-NMDAR encephalitis, initial miss-classification as a psychiatric disease results in delayed diagnosis and worse outcome. CASE PRESENTATION: A 37-year-old woman presented to an urgent care center with hallucinations, dizziness and headaches, which was treated as acute otitis media. Her symptoms progressively worsened to agitation and she was admitted to a psychiatric unit for acute psychosis. Antipsychotics did not improve her condition, became catatonic and was transferred to the ICU for further management. Infectious work-up was negative and thyroid function tests were normal. EEG showed generalized rhythmic delta activity. CSF analysis was positive for oligoclonal bands and 98% lymphocytes. She was treated empirically with high-dose steroids(250mg Q6 hours) for 6 days and IV immune globulin 140g over 5 days for high suspicion of autoimmune encephalitis. Her NMDAR antibodies were reported positive in serum and CSF 10 and 31 days after collection with a CSF titer of 1:64. Abdominal US revealed a dermoid cyst which was surgically removed. Rituximab therapy was considered but not initiated due to concern for sepsis. Clinical course was complicated by status epilepticus requiring intubation, symptomatic bradycardia, cardiogenic shock, renal failure, atrial fibrillation and central hypoventilation. Repeat CT revealed anoxic brain injury. She passed a few days later. DISCUSSION: The most common presenting features of anti-NMDAR encephalitis are psychiatric symptoms, like mood alteration(anxiety or depression), aggression, mania, delusion, schizoaffective episodes, hallucinations; and seizures. Lymphocytic pleocytosis or oligoclonal bands in CSF, slow, epileptic activity or delta brush pattern on EEG, and mesiotemporal hyperintensities or atrophy pattern on MRI have been described with anti-NMDAR encephalitis. Patients presenting with high antibody titer groups(>1:32 in CSF), such as observed in our patient, more likely present teratoma and result in poor patient outcome. Although improved outcomes are associated with timely initiation of treatment, residual psychiatric symptoms have been noted in a significant portion of patients. First line immunotherapy includes corticosteroids, immunoglobulins or plasma exchange; and second line escalations like rituximab and cyclophosphamide may be added. CONCLUSIONS: Anti-NMDAR encephalitis may be misdiagnosed as a primary psychotic disorder. Confirmatory diagnostic testing are often delayed leading to worse outcomes. Hence, in a patient presenting with new onset psychosis, high index of suspicion for anti-NMDAR encephalitis and early initiation of therapy should be considered prior to confirmatory diagnostic testing. Reference #1: Ford B, McDonald A, Srinivasan S. Anti-NMDA receptor encephalitis: a case study and illness overview. Drugs Context. 2019;8:212589. Published 2019 Aug 30. doi:10.7573/dic.212589 Reference #2: Wang W, Zhang L et al. Psychiatric symptoms of patients with anti-nmda receptor encephalitis. Front. Neurol., 24 January 2020. https://doi.org/10.3389/fneur.2019.01330 Reference #3: Dalmau J, Armangué T, et al. An update on anti-NMDA receptor encephalitis for neurologists and psychiatrists: mechanisms and models. The Lancet Neurology, Volume 18, Issue 11, 2019, Pages 1045-1057. DISCLOSURES: No relevant relationships by Aditi Desai No relevant relationships by Daniel Fein

DELAYED CEREBRAL VENOUS SINUS THROMBOSIS (CSVT) AFTER AN INVASIVE MENINGIOMA RESECTION: AN UNCOMMON PRESENTATION OF A COMMON COMPLICATION

SESSION TITLE: Remarkable Critical Care CasesSESSION TYPE: Rapid Fire Case ReportsPRESENTED ON: 10/18/2022 12:25 pm - 01:25 pmINTRODUCTION: Postoperative monitoring in the intensive care unit after an elective supratentorial craniotomy is routine in many hospitals. However, the guidelines on when these patients can be safely discharged remain unclear.CASE PRESENTATION: The patient is a 66-year-old male who was admitted to the intensive care unit for postoperative monitoring of an elective supratentorial craniotomy and resection of an invasive meningioma. The postoperative course was uneventful, and the patient was discharged from the hospital to a rehabilitation facility on postoperative day 3. When the patient was discharged, his neurological examination showed only a mild weakness of the right lower extremity. Within 24 hours of discharge, the patient was readmitted with complaints of new-onset left-sided weakness, and aphasia. On neurological exam, the patient's power was noted to be 0/5 in the left upper and lower extremity, along with new-onset expressive aphasia. Shortly afterward, the patient's mentation worsened, and he was noted to have decerebrate posturing. The patient was subsequently intubated and admitted to the ICU. MRI of the brain revealed global diffusion restriction, and accentuation of the grey-white differentiation, consistent with diffuse cerebral ischemia. MRA and MRV of the brain demonstrated little to no flow in the intracranial arterial and venous structures. Due to a lack of improvement and overall poor prognosis, the family decided to withdraw care and the patient passed away on hospital day three. The autopsy revealed venous sinus thrombosis involving the sagittal sinus and resultant diffuse hypoxic neuronal injury.DISCUSSION: Cerebral sinus venous thrombosis (CSVT) is a well-described complication of craniotomy, especially for those surgeries near major dural venous sinuses. These are largely asymptomatic and can be conservatively managed in most patients (1). However, in extremely rare instances, these can lead to large-scale thrombosis, disruption of blood flow to the brain, and diffuse irreversible ischemia (2). In our patient, the relation of the meningioma with that of the sagittal sinus is probably predisposed to the development of this thrombus. However, the patient remained asymptomatic in the immediate post-operative period, with a rapid deterioration on postoperative day three, which makes this presentation highly unusual. There currently exist no recommendations for post-operative prophylactic anticoagulation or cerebral blood flow monitoring in patients undergoing high-risk craniotomy. We suggest that at least in a certain subgroup of patients, there may be a role to prolonged in-hospital monitoring after a high-risk craniotomy near the venous sinuses.CONCLUSIONS: CSVT is an extremely rare fatal complication in patients undergoing high-risk craniotomy, especially in areas that require manipulation of the dural venous sinuses.Reference #1: Benjamin CG, Sen RD, Golfinos JG, Sen C, Roland JT, McMenomey S, et al. Postoperative cerebral venous sinus thrombosis in the setting of surgery adjacent to the major dural venous sinuses. J Neurosurg. 2018 Oct 26;131(4):1317–23.Reference #2: Straight sinus thrombosis during neurosurgical operation [Internet]. Surgical Neurology International. [cited 2022 Apr 4]. Available from: https://surgicalneurologyint.com/surgicalint-articles/straight-sinus-thrombosis-during-neurosurgical-operation/DISCLOSURES: no disclosure submitted for Boning Li;No relevant relationships by Rana Prathap PadappayilNo relevant relationships by Raghu Tiperneni SESSION TITLE: Remarkable Critical Care Cases SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: Postoperative monitoring in the intensive care unit after an elective supratentorial craniotomy is routine in many hospitals. However, the guidelines on when these patients can be safely discharged remain unclear. CASE PRESENTATION: The patient is a 66-year-old male who was admitted to the intensive care unit for postoperative monitoring of an elective supratentorial craniotomy and resection of an invasive meningioma. The postoperative course was uneventful, and the patient was discharged from the hospital to a rehabilitation facility on postoperative day 3. When the patient was discharged, his neurological examination showed only a mild weakness of the right lower extremity. Within 24 hours of discharge, the patient was readmitted with complaints of new-onset left-sided weakness, and aphasia. On neurological exam, the patient's power was noted to be 0/5 in the left upper and lower extremity, along with new-onset expressive aphasia. Shortly afterward, the patient's mentation worsened, and he was noted to have decerebrate posturing. The patient was subsequently intubated and admitted to the ICU. MRI of the brain revealed global diffusion restriction, and accentuation of the grey-white differentiation, consistent with diffuse cerebral ischemia. MRA and MRV of the brain demonstrated little to no flow in the intracranial arterial and venous structures. Due to a lack of improvement and overall poor prognosis, the family decided to withdraw care and the patient passed away on hospital day three. The autopsy revealed venous sinus thrombosis involving the sagittal sinus and resultant diffuse hypoxic neuronal injury. DISCUSSION: Cerebral sinus venous thrombosis (CSVT) is a well-described complication of craniotomy, especially for those surgeries near major dural venous sinuses. These are largely asymptomatic and can be conservatively managed in most patients (1). However, in extremely rare instances, these can lead to large-scale thrombosis, disruption of blood flow to the brain, and diffuse irreversible ischemia (2). In our patient, the relation of the meningioma with that of the sagittal sinus is probably predisposed to the development of this thrombus. However, the patient remained asymptomatic in the immediate post-operative period, with a rapid deterioration on postoperative day three, which makes this presentation highly unusual. There currently exist no recommendations for post-operative prophylactic anticoagulation or cerebral blood flow monitoring in patients undergoing high-risk craniotomy. We suggest that at least in a certain subgroup of patients, there may be a role to prolonged in-hospital monitoring after a high-risk craniotomy near the venous sinuses. CONCLUSIONS: CSVT is an extremely rare fatal complication in patients undergoing high-risk craniotomy, especially in areas that require manipulation of the dural venous sinuses. Reference #1: Benjamin CG, Sen RD, Golfinos JG, Sen C, Roland JT, McMenomey S, et al. Postoperative cerebral venous sinus thrombosis in the setting of surgery adjacent to the major dural venous sinuses. J Neurosurg. 2018 Oct 26;131(4):1317–23. Reference #2: Straight sinus thrombosis during neurosurgical operation [Internet]. Surgical Neurology International. [cited 2022 Apr 4]. Available from: https://surgicalneurologyint.com/surgicalint-articles/straight-sinus-thrombosis-during-neurosurgical-operation/ DISCLOSURES: no disclosure submitted for Boning Li; No relevant relationships by Rana Prathap Padappayil No relevant relationships by Raghu Tiperneni

SECONDARY HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS IN A PATIENT WITH COVID-19 AND HERPES SIMPLEX VIRUS (HSV): A CASE REPORT

SESSION TITLE: Unique Inflammatory and Autoimmune Complications of COVID-19 InfectionsSESSION TYPE: Rapid Fire Case ReportsPRESENTED ON: 10/19/2022 12:45 pm - 1:45 pmINTRODUCTION: Hemophagocytic Lymphohistiocytosis (HLH) is a rare, life-threatening hyperinflammatory syndrome caused by severe, dysregulated hypercytokinemia. This can be associated with genetic defects or immunologic triggers such as infection, malignancy or autoimmune disorder. The clinical picture consists of multi-organ failure including fever, hepatosplenomegaly, cytopenia,hypertriglyceridemia, hemophagocytosis, high ferritin and IL-2 levels, neurological and liver dysfunction. We present a case of a patient with HLH in the setting of Herpes Simplex Virus (HSV) and SARS-CoV-2 co-infection.CASE PRESENTATION: A 39-year-old male presented to the ER with dyspnea and was found to have COVID-19 pneumonia. He had worsening hypoxemia and was admitted to ICU. He rapidly developed multi-system organ failure (MSOF)including severe hepatitis with AST 13,950 U/L and ALT 10,000 U/L, pancytopenia (Hb 12.9 g/dL, WBC 1.7 K/uL, platelet 15,000 K/uL), acute kidney injury (Cr 6.61 mg/dL), and severe ARDS requiring mechanical ventilation. Abdominal ultrasonography showed splenomegaly. Blood HSV1 DNA PCR was positive with liver biopsy revealing viral inclusions consistent with HSV hepatitis. He had elevated ferritin > 100,000 ug/L and LDH > 2500 U/L. Bone marrow biopsy demonstrated hemophagocytosis and trilineage hematopoiesis. He met 6 of 8 diagnostic criteria for HLH per the HLH-2004 protocol. He received dexamethasone. Risks and benefits of HLH-specific therapy were considered in the setting of liver dysfunction and the decision was made to withhold etoposide and administer anakinra. He died of refractory septic shock and disseminated intravascular coagulopathy.DISCUSSION: Diagnosis of HLH can be challenging due to its rarity and the clinical picture may be initially attributed to sepsis in the presence of infection, as in our patient who had COVID-19 infection and HSV hepatitis. However, a ferritin level >10,000 ng/mL is 90% sensitive and 96 % specific for HLH, with very minimal overlap with sepsis, infections, and liver failure. Additionally, infection is a known trigger of HLH. Despite high mortality without therapy, survival can be significantly increased with HLH-specific therapy, such as etoposide. Treatment with etoposide in the setting of severe liver disease can raise concern because it is metabolized by the liver but it is an essential component of optimal therapy and can be considered in patients with hepatic dysfunction with dose reduction.CONCLUSIONS: Our case highlights the importance of maintaining a high index of suspicion for HLH in critically ill patients with MSOF and liver failure, despite an apparent infectious etiology. This may allow timely diagnosis, early referral to a specialist center and consideration of HLH-specific therapy such as etoposide despite liver dysfunction, to prevent high morbidity and mortality in this potentially fatal disease.Reference #1: Filipovich AH. Hemophagocytic lymphohistiocytosis (HLH) and related disorders. Hematology Am Soc Hematol Educ Program 2009; :127.DISCLOSURES: No relevant relationships by Abdul KhanNo relevant relationships by Nehan SherNo relevant relationships by yuttiwat vorakunthada 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: Hemophagocytic Lymphohistiocytosis (HLH) is a rare, life-threatening hyperinflammatory syndrome caused by severe, dysregulated hypercytokinemia. This can be associated with genetic defects or immunologic triggers such as infection, malignancy or autoimmune disorder. The clinical picture consists of multi-organ failure including fever, hepatosplenomegaly, cytopenia,hypertriglyceridemia, hemophagocytosis, high ferritin and IL-2 levels, neurological and liver dysfunction. We present a case of a patient with HLH in the setting of Herpes Simplex Virus (HSV) and SARS-CoV-2 co-infection. CASE PRESENTATION: A 39-year-old male presented to the ER with dyspnea and was found to have COVID-19 pneumonia. He had worsening hypoxemia and was admitted to ICU. He rapidly developed multi-system organ failure (MSOF)including severe hepatitis with AST 13,950 U/L and ALT 10,000 U/L, pancytopenia (Hb 12.9 g/dL, WBC 1.7 K/uL, platelet 15,000 K/uL), acute kidney injury (Cr 6.61 mg/dL), and severe ARDS requiring mechanical ventilation. Abdominal ultrasonography showed splenomegaly. Blood HSV1 DNA PCR was positive with liver biopsy revealing viral inclusions consistent with HSV hepatitis. He had elevated ferritin > 100,000 ug/L and LDH > 2500 U/L. Bone marrow biopsy demonstrated hemophagocytosis and trilineage hematopoiesis. He met 6 of 8 diagnostic criteria for HLH per the HLH-2004 protocol. He received dexamethasone. Risks and benefits of HLH-specific therapy were considered in the setting of liver dysfunction and the decision was made to withhold etoposide and administer anakinra. He died of refractory septic shock and disseminated intravascular coagulopathy. DISCUSSION: Diagnosis of HLH can be challenging due to its rarity and the clinical picture may be initially attributed to sepsis in the presence of infection, as in our patient who had COVID-19 infection and HSV hepatitis. However, a ferritin level >10,000 ng/mL is 90% sensitive and 96 % specific for HLH, with very minimal overlap with sepsis, infections, and liver failure. Additionally, infection is a known trigger of HLH. Despite high mortality without therapy, survival can be significantly increased with HLH-specific therapy, such as etoposide. Treatment with etoposide in the setting of severe liver disease can raise concern because it is metabolized by the liver but it is an essential component of optimal therapy and can be considered in patients with hepatic dysfunction with dose reduction. CONCLUSIONS: Our case highlights the importance of maintaining a high index of suspicion for HLH in critically ill patients with MSOF and liver failure, despite an apparent infectious etiology. This may allow timely diagnosis, early referral to a specialist center and consideration of HLH-specific therapy such as etoposide despite liver dysfunction, to prevent high morbidity and mortality in this potentially fatal disease. Reference #1: Filipovich AH. Hemophagocytic lymphohistiocytosis (HLH) and related disorders. Hematology Am Soc Hematol Educ Program 2009; :127. DISCLOSURES: No relevant relationships by Abdul Khan No relevant relationships by Nehan Sher No relevant relationships by yuttiwat vorakunthada

CRYPTOGENIC ORGANIZING PNEUMONIA: A DIAGNOSTIC DILEMMA IN A WORLD DOMINATED BY COVID-19 PNEUMONIA

SESSION TITLE: Pulmonary Involvement in Critical Care Case PostersSESSION TYPE: Case Report PostersPRESENTED ON: 10/17/2022 12:15 pm - 01:15 pmINTRODUCTION: Cryptogenic organizing pneumonia (COP), also known as bronchiolitis obliterans organizing pneumonia (BOOP), is one of the idiopathic interstitial lung diseases that affects the alveolar epithelium and surrounding interstitium. Its diagnosis is usually delayed due to similar clinical presentation as other illnesses (e.g. pneumonia) [1].CASE PRESENTATION: A 65-year-old male presented with rapidly progressive respiratory failure. Computed tomography (CT) of chest showed multifocal ground glass opacities. He had suboptimal response to antibiotics and had to be intubated on day 9 due to worsening respiratory failure. Bronchoscopy with bronchoalveolar lavage was performed, cytology of which revealed severe acute inflammation and mononuclear infiltration. Decision was made to perform open lung biopsy which showed polypoid plugs of organizing fibroblasts and myofibroblasts in the distal airways and alveoli with focal hyaline membrane and alveolar damage, consistent with acute onset fulminant COP. As expected, the patient responded fairly well to high-dose corticosteroids and was extubated on day 9 of intubation.DISCUSSION: Even though it is very rare, COP should be kept in differentials especially when initial interventions fail (as in our patient). There is no single laboratory study or intervention to diagnose this condition. Hence it is imperative to rule out other causes of similar presentation like pneumonia (using cultures, urine antigen testing, and viral polymerase chain reaction tests). The clinical picture is combined with supportive evidence like elevated erythrocyte sedimentation rate, leukocytosis, imaging findings, and bronchoscopic and histopathology evaluation [2]. Once diagnosed, it is important to rule out any associated CTD, for it can change management and prevent additional complications. The majority of patients with COP exhibit rapid response to glucocorticoid treatment. For fulminant disease, intravenous glucocorticoids (e.g. methylprednisolone 125-250 mg every six hours) should be initiated based on the clinical experience and case reports [3].CONCLUSIONS: Diagnoses of interstitial lung diseases should be pursued in a systemic fashion from more common to less common. However, anchoring to common diagnoses should be avoided to negate delay in diagnoses and allow timely management. If initial workup is unrevealing, bronchoscopy and open lung biopsies should be performed while the patient is stable enough to undergo the interventions to avoid antibiotic resistance, morbidity and mortality associated with rapidly progressive noninfectious illnesses like fulminant COP.Reference #1: Drakopanagiotakis F, Polychronopoulos V, Judson MA. Organizing pneumonia. The American journal of the medical sciences. 2008 Jan 1;335(1):34-9.Reference #2: Cordier JF. Cryptogenic organising pneumonia. European Respiratory Journal. 2006 Aug 1;28(2):422-46.Reference #3: Nizami IY, Kissner DG, Visscher DW, Dubaybo BA. Idiopathic bronchiolitis obliterans with organizing pneumonia: an acute and life-threatening syndrome. Chest. 1995 Jul 1;108(1):271-7DISCLOSURES: No relevant relationships by Fareeha AbidNo relevant relationships by Vipin GargNo relevant relationships by Qirat JawedNo relevant relationships by Asnia LatifNo relevant relationships by Ahmed MowafyNo relevant relationships by Muniba NaqiNo relevant relationships by Muhammad Atif Masood NooriNo relevant relationships by Hasham Saeed SESSION TITLE: Pulmonary Involvement in Critical Care Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Cryptogenic organizing pneumonia (COP), also known as bronchiolitis obliterans organizing pneumonia (BOOP), is one of the idiopathic interstitial lung diseases that affects the alveolar epithelium and surrounding interstitium. Its diagnosis is usually delayed due to similar clinical presentation as other illnesses (e.g. pneumonia) [1]. CASE PRESENTATION: A 65-year-old male presented with rapidly progressive respiratory failure. Computed tomography (CT) of chest showed multifocal ground glass opacities. He had suboptimal response to antibiotics and had to be intubated on day 9 due to worsening respiratory failure. Bronchoscopy with bronchoalveolar lavage was performed, cytology of which revealed severe acute inflammation and mononuclear infiltration. Decision was made to perform open lung biopsy which showed polypoid plugs of organizing fibroblasts and myofibroblasts in the distal airways and alveoli with focal hyaline membrane and alveolar damage, consistent with acute onset fulminant COP. As expected, the patient responded fairly well to high-dose corticosteroids and was extubated on day 9 of intubation. DISCUSSION: Even though it is very rare, COP should be kept in differentials especially when initial interventions fail (as in our patient). There is no single laboratory study or intervention to diagnose this condition. Hence it is imperative to rule out other causes of similar presentation like pneumonia (using cultures, urine antigen testing, and viral polymerase chain reaction tests). The clinical picture is combined with supportive evidence like elevated erythrocyte sedimentation rate, leukocytosis, imaging findings, and bronchoscopic and histopathology evaluation [2]. Once diagnosed, it is important to rule out any associated CTD, for it can change management and prevent additional complications. The majority of patients with COP exhibit rapid response to glucocorticoid treatment. For fulminant disease, intravenous glucocorticoids (e.g. methylprednisolone 125-250 mg every six hours) should be initiated based on the clinical experience and case reports [3]. CONCLUSIONS: Diagnoses of interstitial lung diseases should be pursued in a systemic fashion from more common to less common. However, anchoring to common diagnoses should be avoided to negate delay in diagnoses and allow timely management. If initial workup is unrevealing, bronchoscopy and open lung biopsies should be performed while the patient is stable enough to undergo the interventions to avoid antibiotic resistance, morbidity and mortality associated with rapidly progressive noninfectious illnesses like fulminant COP. Reference #1: Drakopanagiotakis F, Polychronopoulos V, Judson MA. Organizing pneumonia. The American journal of the medical sciences. 2008 Jan 1;335(1):34-9. Reference #2: Cordier JF. Cryptogenic organising pneumonia. European Respiratory Journal. 2006 Aug 1;28(2):422-46. Reference #3: Nizami IY, Kissner DG, Visscher DW, Dubaybo BA. Idiopathic bronchiolitis obliterans with organizing pneumonia: an acute and life-threatening syndrome. Chest. 1995 Jul 1;108(1):271-7 DISCLOSURES: No relevant relationships by Fareeha Abid No relevant relationships by Vipin Garg No relevant relationships by Qirat Jawed No relevant relationships by Asnia Latif No relevant relationships by Ahmed Mowafy No relevant relationships by Muniba Naqi No relevant relationships by Muhammad Atif Masood Noori No relevant relationships by Hasham Saeed

AN UNUSUAL PRESENTATION OF CNS CANDIDIASIS

SESSION TITLE: Cases of Overdose, OTC, and Illegal Drug Critical Cases PostersSESSION TYPE: Case Report PostersPRESENTED ON: 10/17/2022 12:15 pm - 01:15 pmINTRODUCTION: Central nervous system (CNS) candidiasis is uncommon and associated with neonates with low birth weights, neurosurgical patients, and immunocompromised hosts. However, incidence is rising due to increase in intravenous drug abuse (IVDA) and use of corticosteroids, and broad-spectrum antibiotics. We describe a case of CNS candidiasis with fungal endophthalmitis.CASE PRESENTATION: A 29-year-old male with a medical history notable for bilateral posterior uveitis with right eye blindness, IVDA with heroin, and migraines presented with altered mental status, urinary incontinence, and a 6-month duration of progressive blurred vision associated with abnormal gait. His vision was managed by ophthalmology with steroid eye drops for presumed autoimmune uveitis. Vital signs were notable for elevated temperature of 101.2 °F, heart rate of 111 beats per minute, and blood pressure of 185/123 mmHg. He had sluggish left eye pupil constriction and fixed right pupil. Toxicology work-up and ammonia were unremarkable. Non-contrasted brain computed tomography showed acute hydrocephalus and right vitreous hemorrhage. A ventriculostomy catheter was placed with intracranial pressure elevated at 28 mmHg. Serial cerebrospinal fluid (CSF) analysis showed neutrophilic pleocytosis with low glucose of 40 mg/dL, elevated protein of 75 mg/dL, 405 nucleated cells, and 315 red blood cells. CSF meningitis-encephalitis panel and cultures were negative. Blood cultures and serum testing for tuberculosis, human immunodeficiency virus, cytomegalovirus, Bartonella, syphilis, and toxoplasma were negative. 1-3 B-D- glucan in CSF (>500 pg/mL) and serum (137 pg/mL) were elevated. Brain magnetic resonance imaging (MRI) showed basal meningitis and ventriculitis. B- scan ultrasonography showed fungal endophthalmitis. He underwent vitrectomy and enucleation of the right eye and completed a 6-week induction course of liposomal amphotericin B (L-AmB) 5 mg/kg daily and flucytosine 25 mg/kg Q6H with plans for at least 1 year of oral fluconazole 800 mg daily.DISCUSSION: CNS candidiasis has an incidence rate of 7.6% and mortality rate of 30%. The most common causative fungal organism is Candida albicans. Clinical manifestations are hydrocephalus, basal meningitis, and brainstem infarction. CSF analysis may show low glucose, elevated protein, and neutrophilic or lymphocytic pleocytosis. Our case exemplifies the difficulty in diagnosing CNS candidiasis complicated by hydrocephalus and fungal endophthalmitis, as it was initially missed. Treatment of CNS candidiasis requires induction therapy with L-AmB and flucytosine followed by oral fluconazole. Duration is determined by resolution of symptoms and CSF and radiological abnormalities.CONCLUSIONS: In people who inject drugs presenting with neurological symptoms, CNS candidiasis should be considered. Assessment of risk factors is crucial as failure to diagnose fungal meningitis can lead to death.Reference #1: Charalambous LT, Premji A, Tybout C, et al. Prevalence, healthcare resource utilization and overall burden of fungal meningitis in the United States. J Med Microbiol. 2018;67(2):215-227. doi:10.1099/jmm.0.000656Reference #2: Peter G. Pappas, Carol A. Kauffman, David R. Andes, Cornelius J. Clancy, Kieren A. Marr, Luis Ostrosky-Zeichner, Annette C. Reboli, Mindy G. Schuster, Jose A. Vazquez, Thomas J. Walsh, Theoklis E. Zaoutis, Jack D. Sobel, Clinical Practice Guideline for the Management of Candidiasis: 2016 Update by the Infectious Diseases Society of America, Clinical Infectious Diseases, Volume 62, Issue 4, 15 February 2016, Pages e1–e50, https://doi.org/10.1093/cid/civ933Reference #3: Góralska K, Blaszkowska J, Dzikowiec M. Neuroinfections caused by fungi. Infection. 2018;46(4):443-459. doi:10.1007/s15010-018-1152-2DISCLOSURES: No relevant relationships by Shu Xian LeeNo relevant relationships by Kurt SuterNo relevant relationships by Daphne-Dominique VillanuevaNo relevant relationships by Benita Wu SESSION TITLE: Cases of Overdose, OTC, and Illegal Drug Critical Cases Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Central nervous system (CNS) candidiasis is uncommon and associated with neonates with low birth weights, neurosurgical patients, and immunocompromised hosts. However, incidence is rising due to increase in intravenous drug abuse (IVDA) and use of corticosteroids, and broad-spectrum antibiotics. We describe a case of CNS candidiasis with fungal endophthalmitis. CASE PRESENTATION: A 29-year-old male with a medical history notable for bilateral posterior uveitis with right eye blindness, IVDA with heroin, and migraines presented with altered mental status, urinary incontinence, and a 6-month duration of progressive blurred vision associated with abnormal gait. His vision was managed by ophthalmology with steroid eye drops for presumed autoimmune uveitis. Vital signs were notable for elevated temperature of 101.2 °F, heart rate of 111 beats per minute, and blood pressure of 185/123 mmHg. He had sluggish left eye pupil constriction and fixed right pupil. Toxicology work-up and ammonia were unremarkable. Non-contrasted brain computed tomography showed acute hydrocephalus and right vitreous hemorrhage. A ventriculostomy catheter was placed with intracranial pressure elevated at 28 mmHg. Serial cerebrospinal fluid (CSF) analysis showed neutrophilic pleocytosis with low glucose of 40 mg/dL, elevated protein of 75 mg/dL, 405 nucleated cells, and 315 red blood cells. CSF meningitis-encephalitis panel and cultures were negative. Blood cultures and serum testing for tuberculosis, human immunodeficiency virus, cytomegalovirus, Bartonella, syphilis, and toxoplasma were negative. 1-3 B-D- glucan in CSF (>500 pg/mL) and serum (137 pg/mL) were elevated. Brain magnetic resonance imaging (MRI) showed basal meningitis and ventriculitis. B- scan ultrasonography showed fungal endophthalmitis. He underwent vitrectomy and enucleation of the right eye and completed a 6-week induction course of liposomal amphotericin B (L-AmB) 5 mg/kg daily and flucytosine 25 mg/kg Q6H with plans for at least 1 year of oral fluconazole 800 mg daily. DISCUSSION: CNS candidiasis has an incidence rate of 7.6% and mortality rate of 30%. The most common causative fungal organism is Candida albicans. Clinical manifestations are hydrocephalus, basal meningitis, and brainstem infarction. CSF analysis may show low glucose, elevated protein, and neutrophilic or lymphocytic pleocytosis. Our case exemplifies the difficulty in diagnosing CNS candidiasis complicated by hydrocephalus and fungal endophthalmitis, as it was initially missed. Treatment of CNS candidiasis requires induction therapy with L-AmB and flucytosine followed by oral fluconazole. Duration is determined by resolution of symptoms and CSF and radiological abnormalities. CONCLUSIONS: In people who inject drugs presenting with neurological symptoms, CNS candidiasis should be considered. Assessment of risk factors is crucial as failure to diagnose fungal meningitis can lead to death. Reference #1: Charalambous LT, Premji A, Tybout C, et al. Prevalence, healthcare resource utilization and overall burden of fungal meningitis in the United States. J Med Microbiol. 2018;67(2):215-227. doi:10.1099/jmm.0.000656 Reference #2: Peter G. Pappas, Carol A. Kauffman, David R. Andes, Cornelius J. Clancy, Kieren A. Marr, Luis Ostrosky-Zeichner, Annette C. Reboli, Mindy G. Schuster, Jose A. Vazquez, Thomas J. Walsh, Theoklis E. Zaoutis, Jack D. Sobel, Clinical Practice Guideline for the Management of Candidiasis: 2016 Update by the Infectious Diseases Society of America, Clinical Infectious Diseases, Volume 62, Issue 4, 15 February 2016, Pages e1–e50, https://doi.org/10.1093/cid/civ933 Reference #3: Góralska K, Blaszkowska J, Dzikowiec M. Neuroinfections caused by fungi. Infection. 2018;46(4):443-459. doi:10.1007/s15010-018-1152-2 DISCLOSURES: No relevant relationships by Shu Xian Lee No relevant relationships by Kurt Suter No relevant relationships by Daphne-Dominique Villanueva No relevant relationships by Benita Wu

MISLEADING FEVERS: A CASE OF MULTISYSTEM INFLAMMATORY SYNDROME IN ADULTS DUE TO COVID-19

SESSION TITLE: Management of COVID-19-Induced ComplicationsSESSION TYPE: Rapid Fire Case ReportsPRESENTED ON: 10/19/2022 12:45 pm - 1:45 pmINTRODUCTION: Multisystem inflammatory syndrome in children (MIS-C) is a systemic condition that causes multi-organ dysfunction accompanied by fever and extremely elevated inflammatory markers. This syndrome been primarily identified in children or adolescents similar to Kawasaki disease. The hallmark of this illness includes life-threatening complications such as shock and cardiac dysfunction. As the cases of COVID-19 continue to increase worldwide, a form of MIS-C can present in adults known as multisystem inflammatory syndrome in adults (MIS-A). We describe a case of MIS-A after exposure to COVID-19.CASE PRESENTATION: A 28-year-old Hispanic male with no medical history presented with 3 days of persistent fever, diarrhea, and fatigue. He was unvaccinated for COVID-19 but had mild disease three months prior, which did not require hospitalization. Vitals were remarkable for tachycardia and constant fever of up to 103.5 F. Labs were notable for leukocytosis of 26.0 k/uL, CRP of 43 mg/dL, and procalcitonin of 90 ng/mL. Computed tomography with intravenous contrast of his chest revealed multifocal nodular and consolidative airspace disease of the right upper and middle lobes with mediastinal and hilar lymphadenopathy. Echocardiogram revealed ejection fraction (EF) of 29% without wall-motion abnormalities. PCR test for COVID-19 was negative and his infectious work-up was unrevealing. His course was further complicated by shock requiring pressors, intubation, and renal replacement therapy. Despite antibiotics, he did not improve. He was started on pulse dose steroids and intravenous immunoglobulin (IVIG), which decreased his CRP to 34 mg/dL and procalcitonin to 51 ng/mL. He was weaned off the ventilator and pressor support with EF recovery to 51%. He was eventually discharged home without further needs.DISCUSSION: While limited data exists, adult patients of all ages with prior SARS-CoV-2 infection can develop MIS-A. Preliminary reports suggest increased incidence among African American, Hispanic, and Asian ethnic groups. Diagnosis includes one primary and two secondary clinical criteria with two supporting laboratory evidence. Primary criteria includes cardiac dysfunction or rash with conjunctivitis. Secondary criteria includes neurological signs, shock, gastrointestinal disease, or thrombocytopenia. Lab markers include elevated CRP, ferritin, IL-6, ESR, or procalcitonin with a positive SARS-Cov-2 PCR, serology, or antigen detection. Treatment consists of steroids, IVIG, and supportive care based on case reports. There are no current evidence-based guidelines. The best preventative measures include COVID-19 vaccinationCONCLUSIONS: MIS-A is a rare complication of unvaccinated COVID-19 cases. Diagnostic criteria include one primary and two secondary clinical signs with supporting lab data. Treatment includes steroids, IVIG, and supportive care.Reference #1: Riphagen S, Gomez X, Gonzalez-Martinez C, Wilkinson N, Theocharis P. Hyperinflammatory shock in children during COVID-19 pandemic. The Lancet. 2020;395(10237):1607-1608. doi:10.1016/s0140-6736(20)31094-1Reference #2: Kunal S, Ish P, Sakthivel P, Malhotra N, Gupta K. The emerging threat of multisystem inflammatory syndrome in adults (mis-A) in COVID-19: A systematic review. Heart & Lung. 2022;54:7-18. doi:10.1016/j.hrtlng.2022.03.007Reference #3: Morris SB, Schwartz NG, Patel P, et al. Case series of multisystem inflammatory syndrome in adults associated with SARS-COV-2 infection — United Kingdom and United States, March–August 2020. MMWR Morbidity and Mortality Weekly Report. 2020;69(40):1450-1456. doi:10.15585/mmwr.mm6940e1DISCLOSURES: No relevant relationships by Sadaf AfrazNo relevant relationships by Christine GirardNo relevant relationships by Jose RiveraNo relevant relationships by Ivan Romero-LegroNo relevant relationships by Amy Van SESSION TITLE: Management of COVID-19-Induced Complications SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Multisystem inflammatory syndrome in children (MIS-C) is a systemic condition that causes multi-organ dysfunction accompanied by fever and extremely elevated inflammatory markers. This syndrome been primarily identified in children or adolescents similar to Kawasaki disease. The hallmark of this illness includes life-threatening complications such as shock and cardiac dysfunction. As the cases of COVID-19 continue to increase worldwide, a form of MIS-C can present in adults known as multisystem inflammatory syndrome in adults (MIS-A). We describe a case of MIS-A after exposure to COVID-19. CASE PRESENTATION: A 28-year-old Hispanic male with no medical history presented with 3 days of persistent fever, diarrhea, and fatigue. He was unvaccinated for COVID-19 but had mild disease three months prior, which did not require hospitalization. Vitals were remarkable for tachycardia and constant fever of up to 103.5 F. Labs were notable for leukocytosis of 26.0 k/uL, CRP of 43 mg/dL, and procalcitonin of 90 ng/mL. Computed tomography with intravenous contrast of his chest revealed multifocal nodular and consolidative airspace disease of the right upper and middle lobes with mediastinal and hilar lymphadenopathy. Echocardiogram revealed ejection fraction (EF) of 29% without wall-motion abnormalities. PCR test for COVID-19 was negative and his infectious work-up was unrevealing. His course was further complicated by shock requiring pressors, intubation, and renal replacement therapy. Despite antibiotics, he did not improve. He was started on pulse dose steroids and intravenous immunoglobulin (IVIG), which decreased his CRP to 34 mg/dL and procalcitonin to 51 ng/mL. He was weaned off the ventilator and pressor support with EF recovery to 51%. He was eventually discharged home without further needs. DISCUSSION: While limited data exists, adult patients of all ages with prior SARS-CoV-2 infection can develop MIS-A. Preliminary reports suggest increased incidence among African American, Hispanic, and Asian ethnic groups. Diagnosis includes one primary and two secondary clinical criteria with two supporting laboratory evidence. Primary criteria includes cardiac dysfunction or rash with conjunctivitis. Secondary criteria includes neurological signs, shock, gastrointestinal disease, or thrombocytopenia. Lab markers include elevated CRP, ferritin, IL-6, ESR, or procalcitonin with a positive SARS-Cov-2 PCR, serology, or antigen detection. Treatment consists of steroids, IVIG, and supportive care based on case reports. There are no current evidence-based guidelines. The best preventative measures include COVID-19 vaccination CONCLUSIONS: MIS-A is a rare complication of unvaccinated COVID-19 cases. Diagnostic criteria include one primary and two secondary clinical signs with supporting lab data. Treatment includes steroids, IVIG, and supportive care. Reference #1: Riphagen S, Gomez X, Gonzalez-Martinez C, Wilkinson N, Theocharis P. Hyperinflammatory shock in children during COVID-19 pandemic. The Lancet. 2020;395(10237):1607-1608. doi:10.1016/s0140-6736(20)31094-1 Reference #2: Kunal S, Ish P, Sakthivel P, Malhotra N, Gupta K. The emerging threat of multisystem inflammatory syndrome in adults (mis-A) in COVID-19: A systematic review. Heart & Lung. 2022;54:7-18. doi:10.1016/j.hrtlng.2022.03.007 Reference #3: Morris SB, Schwartz NG, Patel P, et al. Case series of multisystem inflammatory syndrome in adults associated with SARS-COV-2 infection — United Kingdom and United States, March–August 2020. MMWR Morbidity and Mortality Weekly Report. 2020;69(40):1450-1456. doi:10.15585/mmwr.mm6940e1 DISCLOSURES: No relevant relationships by Sadaf Afraz No relevant relationships by Christine Girard No relevant relationships by Jose Rivera No relevant relationships by Ivan Romero-Legro No relevant relationships by Amy Van

INTERMITTENT OBSTRUCTION: A CASE OF ENCAPSULATED ENDOBRONCHIAL HAMARTOMA EXHIBITING A CUP-IN-BALL EFFECT

SESSION TITLE: Diagnosis of Lung Disease through Pathology Case PostersSESSION TYPE: Case Report PostersPRESENTED ON: 10/19/2022 12:45 pm - 01:45 pmINTRODUCTION: Pulmonary hamartomas are among the most common pulmonary tumors and generally are composed of a combination of cartilaginous and fatty soft tissue. Treatment, when needed, is directed at relieving obstruction and preventing mass associated tissue damage. Rarely, these tumors are endobronchial.CASE PRESENTATION: A sixty-nine year male with a relevant history of chronic obstructive pulmonary disease [COPD] and tobacco abuse presented with a chief complaint of progressively worsening dyspnea associated with intermittent wheezing and productive cough. The patient reported using his albuterol rescue inhaler 15-20 times daily with minimal improvement. He reported no travel or chemical exposures at work and had no personal or family history of malignancy. He denied any fevers, chills, or infectious complaints. A computed tomography scan of the chest was obtained and showed evidence of diffuse emphysema with a left upper lobe obstruction and a low density pedunculated lesion that extended into the left mainstem bronchus. Initial bronchoscopic intervention revealed an endobronchial lesion with a thickened fibrous capsule that was unable to be sampled via endobronchial ultrasound [EBUS] guided fine needle aspiration [FNA], Wang needle FNA or biopsy forceps due to inability to penetrate the capsule. Patient was referred to a specialty center for further evaluation. Repeat bronchoscopy with endobronchial ultrasound visualized a pedunculated mass with thick yellow-tan capsule which was noted to be echogenic without significant vasculature. Tumor debulking was performed with electrocautery snare and cryotherapy probe. Pathology report was diagnostic for benign adipose tissue and cartilage consistent with a hamartoma. Patient tolerated the procedure well without complications and noted improved dyspnea immediately following the intervention.DISCUSSION: Endobronchial hamartoma itself is a rare presentation of pulmonary hamartomas and due to the unique pedunculated stalk of this patient's tumor, he was noted to have intermittent obstruction with a reported "ball-in-cup” behavior of the tumor. Thus, he exhibited periods of improvement and worsening determined by the position of the tumor.CONCLUSIONS: Because of the coarse impenetrable capsule noted on this patient's hamartoma, pathology diagnosis could not be obtained with standard FNA and forceps biopsy approaches; electrocautery snare was required to resect the lesion and establish tissue diagnosis. Endobronchial and atypically presenting lesions may thus pose a diagnostic challenge that mandates advanced approaches to both tissue diagnosis and therapeutic resection.Reference #1: Abdel Hady SM, Elbastawisy SE, Hassaballa AS, Elsayed HH. Is surgical resection superior to bronchoscopic resection in patients with symptomatic endobronchial hamartoma?. Interact Cardiovasc Thorac Surg. 2017;24(5):778-782. doi:10.1093/icvts/ivw443Reference #2: Guo W, Zhao YP, Jiang YG. et al. Surgical treatment and outcome of pulmonary hamartoma: a retrospective study of 20-year experience. J Exp Clin Cancer Res 27, 8 (2008). doi:10.1186/1756-9966-27-8.Reference #3: Saoud M, Patil M, Dhillon SS, et al. Rare airway tumors: an update on current diagnostic and management strategies. J Thorac Dis. 2016;8(8):1922-1934. doi:10.21037/jtd.2016.07.40DISCLOSURES: No relevant relationships by Lydia MeeceNo relevant relationships by joseph moranNo relevant relationships by Shrey Velani SESSION TITLE: Diagnosis of Lung Disease through Pathology Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Pulmonary hamartomas are among the most common pulmonary tumors and generally are composed of a combination of cartilaginous and fatty soft tissue. Treatment, when needed, is directed at relieving obstruction and preventing mass associated tissue damage. Rarely, these tumors are endobronchial. CASE PRESENTATION: A sixty-nine year male with a relevant history of chronic obstructive pulmonary disease [COPD] and tobacco abuse presented with a chief complaint of progressively worsening dyspnea associated with intermittent wheezing and productive cough. The patient reported using his albuterol rescue inhaler 15-20 times daily with minimal improvement. He reported no travel or chemical exposures at work and had no personal or family history of malignancy. He denied any fevers, chills, or infectious complaints. A computed tomography scan of the chest was obtained and showed evidence of diffuse emphysema with a left upper lobe obstruction and a low density pedunculated lesion that extended into the left mainstem bronchus. Initial bronchoscopic intervention revealed an endobronchial lesion with a thickened fibrous capsule that was unable to be sampled via endobronchial ultrasound [EBUS] guided fine needle aspiration [FNA], Wang needle FNA or biopsy forceps due to inability to penetrate the capsule. Patient was referred to a specialty center for further evaluation. Repeat bronchoscopy with endobronchial ultrasound visualized a pedunculated mass with thick yellow-tan capsule which was noted to be echogenic without significant vasculature. Tumor debulking was performed with electrocautery snare and cryotherapy probe. Pathology report was diagnostic for benign adipose tissue and cartilage consistent with a hamartoma. Patient tolerated the procedure well without complications and noted improved dyspnea immediately following the intervention. DISCUSSION: Endobronchial hamartoma itself is a rare presentation of pulmonary hamartomas and due to the unique pedunculated stalk of this patient's tumor, he was noted to have intermittent obstruction with a reported "ball-in-cup” behavior of the tumor. Thus, he exhibited periods of improvement and worsening determined by the position of the tumor. CONCLUSIONS: Because of the coarse impenetrable capsule noted on this patient's hamartoma, pathology diagnosis could not be obtained with standard FNA and forceps biopsy approaches; electrocautery snare was required to resect the lesion and establish tissue diagnosis. Endobronchial and atypically presenting lesions may thus pose a diagnostic challenge that mandates advanced approaches to both tissue diagnosis and therapeutic resection. Reference #1: Abdel Hady SM, Elbastawisy SE, Hassaballa AS, Elsayed HH. Is surgical resection superior to bronchoscopic resection in patients with symptomatic endobronchial hamartoma?. Interact Cardiovasc Thorac Surg. 2017;24(5):778-782. doi:10.1093/icvts/ivw443 Reference #2: Guo W, Zhao YP, Jiang YG. et al. Surgical treatment and outcome of pulmonary hamartoma: a retrospective study of 20-year experience. J Exp Clin Cancer Res 27, 8 (2008). doi:10.1186/1756-9966-27-8. Reference #3: Saoud M, Patil M, Dhillon SS, et al. Rare airway tumors: an update on current diagnostic and management strategies. J Thorac Dis. 2016;8(8):1922-1934. doi:10.21037/jtd.2016.07.40 DISCLOSURES: No relevant relationships by Lydia Meece No relevant relationships by joseph moran No relevant relationships by Shrey Velani

CLINICAL OUTCOMES FOLLOWING INTRODUCTION OF A MULTIDISCIPLINARY PULMONARY EMBOLISM RESPONSE TEAM AT AN ACADEMIC TERTIARY CARE MEDICAL CENTER

SESSION TITLE: Embolism and CTEPH Abstract PostersSESSION TYPE: Original Investigation PostersPRESENTED ON: 10/18/2022 01:30 pm - 02:30 pmPURPOSE: Pulmonary embolism response teams (PERTs) have been introduced throughout healthcare centers globally to expedite patient access to multidisciplinary specialist teams who can promptly enact multimodality interventions to optimize pulmonary embolism (PE) care. The purpose of our investigation was to analyze the patient characteristics, clinical outcomes, and therapies utilized following the introduction of a PERT at our institution.METHODS: A PERT was introduced at our 617 bed tertiary care hospital in Hartford, Connecticut and the observation period for this analysis was from June 1, 2021 until February 28, 2022. Data was collected via electronic medical record review and included patient age, medical history, ethnicity, home medications, and medical admission unit. Total in-hospital length of stay (LOS) and intensive care unit (ICU) LOS, PE classification by European Society of Cardiology (ESC) guidelines, Pulmonary Embolism Severity Index (PESI) score, Bova score, time to PERT activation, modality of clinical intervention, and in-hospital all cause-mortality were evaluated. Descriptive statistics were undertaken using GraphPad.RESULTS: A total of 43 PERT activations were observed of which 48.8% were male and 51.2% were female; mean ages of the male and female patients were 59.3 and 64.4 years respectively. Of these patients, 81.4% were caucasian, 9.3% were African-American, and 9.3% were hispanic. 20.9% of patients had chronic pulmonary disease, 23.3% had previously diagnosed deep vein thrombosis or PE, 16.3% had previously diagnosed malignancy, and 23.3% were previously on either anticoagulation or antiplatelet therapy. 18.6% of patients were admitted to the general medicine floor, 39.5% to medical step down, and 53.5% to the medical intensive care unit. 9.3% of these cases were low risk (LR), 20.9% were intermediate-low risk (ILR), 60.5% were intermediate-high risk (IHR), and 9.3% were high risk (HR). Mean PESI and Bova scores by risk class were 113.7 and 3.62 for IHR, 97.8 and 1 for ILR, 147.3 and 3.4 for HR, and 70.9 and 0.66 for LR. The mean time to PERT activation was 7.58 hours, mean in-hospital LOS was 5.8 days, and mean ICU LOS was 40.8 hours. 65.1% of patients received heparin only, 16.3% received systemic thrombolysis, 7.0% received mechanical thrombectomy, and 11.6% received catheter-directed thrombolysis. In-hospital all-cause mortality was 7.0%.CONCLUSIONS: Following its introduction, our PERT provided multi-disciplinary care for 43 patients and facilitated prompt advanced endovascular intervention or systemic thrombolysis in 34.9% of patients.CLINICAL IMPLICATIONS: PERTs expedite access to multidisciplinary care to patients presenting with acute PE. Following their introduction, continued surveillance of patient demographics, clinical courses, and outcomes are needed to further optimize their application.DISCLOSURES: No relevant relationships by Evan NadlerNo relevant relationships by Mari-Elena PinoNo relevant relationships by Stephen Simeone SESSION TITLE: Embolism and CTEPH Abstract Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/18/2022 01:30 pm - 02:30 pm PURPOSE: Pulmonary embolism response teams (PERTs) have been introduced throughout healthcare centers globally to expedite patient access to multidisciplinary specialist teams who can promptly enact multimodality interventions to optimize pulmonary embolism (PE) care. The purpose of our investigation was to analyze the patient characteristics, clinical outcomes, and therapies utilized following the introduction of a PERT at our institution. METHODS: A PERT was introduced at our 617 bed tertiary care hospital in Hartford, Connecticut and the observation period for this analysis was from June 1, 2021 until February 28, 2022. Data was collected via electronic medical record review and included patient age, medical history, ethnicity, home medications, and medical admission unit. Total in-hospital length of stay (LOS) and intensive care unit (ICU) LOS, PE classification by European Society of Cardiology (ESC) guidelines, Pulmonary Embolism Severity Index (PESI) score, Bova score, time to PERT activation, modality of clinical intervention, and in-hospital all cause-mortality were evaluated. Descriptive statistics were undertaken using GraphPad. RESULTS: A total of 43 PERT activations were observed of which 48.8% were male and 51.2% were female; mean ages of the male and female patients were 59.3 and 64.4 years respectively. Of these patients, 81.4% were caucasian, 9.3% were African-American, and 9.3% were hispanic. 20.9% of patients had chronic pulmonary disease, 23.3% had previously diagnosed deep vein thrombosis or PE, 16.3% had previously diagnosed malignancy, and 23.3% were previously on either anticoagulation or antiplatelet therapy. 18.6% of patients were admitted to the general medicine floor, 39.5% to medical step down, and 53.5% to the medical intensive care unit. 9.3% of these cases were low risk (LR), 20.9% were intermediate-low risk (ILR), 60.5% were intermediate-high risk (IHR), and 9.3% were high risk (HR). Mean PESI and Bova scores by risk class were 113.7 and 3.62 for IHR, 97.8 and 1 for ILR, 147.3 and 3.4 for HR, and 70.9 and 0.66 for LR. The mean time to PERT activation was 7.58 hours, mean in-hospital LOS was 5.8 days, and mean ICU LOS was 40.8 hours. 65.1% of patients received heparin only, 16.3% received systemic thrombolysis, 7.0% received mechanical thrombectomy, and 11.6% received catheter-directed thrombolysis. In-hospital all-cause mortality was 7.0%. CONCLUSIONS: Following its introduction, our PERT provided multi-disciplinary care for 43 patients and facilitated prompt advanced endovascular intervention or systemic thrombolysis in 34.9% of patients. CLINICAL IMPLICATIONS: PERTs expedite access to multidisciplinary care to patients presenting with acute PE. Following their introduction, continued surveillance of patient demographics, clinical courses, and outcomes are needed to further optimize their application. DISCLOSURES: No relevant relationships by Evan Nadler No relevant relationships by Mari-Elena Pino No relevant relationships by Stephen Simeone

A CASE OF PULMONARY TUMOR THROMBOEMBOLIC MICROANGIOPATHY FROM PROSTATE CARCINOMA

SESSION TITLE: Interesting Pulmonary Vascular AbnormalitiesSESSION TYPE: Case ReportsPRESENTED ON: 10/19/2022 11:15 am - 12:15 pmINTRODUCTION: Pulmonary hypertension as a complication of malignancy can come in many forms. An often underestimated form includes pulmonary tumor microvascular disease, comprising both pulmonary tumor microembolism (PTE) and pulmonary tumor thrombotic microangiopathy (PTTM). Here we report a case of pre-capillary pulmonary hypertension from prostate cancer microemboli.CASE PRESENTATION: Our patient is an 80-year-old man with a history of rectal adenocarcinoma treated with resection and chemotherapy, who presented to the hospital with back pain and was found to have metastatic prostate adenocarcinoma with metastatic disease spread to the bone. He was also found to have hypoxic respiratory failure requiring 3-4 liters of oxygen. During his workup, an echocardiogram revealed pulmonary hypertension, with an estimated right ventricular systolic pressure of 78 mmHg (Figure 1). A ventilation/perfusion scan revealed diffuse decreased perfusion along the bilateral periphery of both lungs. Next, a right heart catheterization was performed, which confirmed pre-capillary pulmonary hypertension (right atrial pressure 2 mmHg, pulmonary artery systolic pressure of 61 mmHg, pulmonary artery diastolic pressure 14 mmHg, mean pulmonary artery pressure 27 mmHg, pulmonary capillary wedge pressure 5 mmHg, cardiac index 2.48 L/min/m2 by Fick and thermodilution, and pulmonary vascular resistance 3.8 Wood units). Pulmonary wedge aspiration cytology was performed which revealed tumor cells that stained positive for prostate-specific antigen (Figure 2, 3). The peripheral blood smear was negative for tumor cells. Overall, this suggests pre-capillary pulmonary hypertension due to tumor microthrombi. The patient was started on sildenafil 20mg three times per day and had subjective improvement in his exercise capacity at this time. His prostate cancer is being treated with leuprolide and abiraterone.DISCUSSION: Pulmonary Tumor Thrombotic Microangiopathy (PTTM), first identified in 1990 is thought to arise from mechanical obstruction, fibrocellular intimal proliferation, and remodeling of the pulmonary vasculature.Gastric malignancies account for >50% of cases with prostate cancer reported as the cause in <5 cases. Definitive diagnosis is by postmortem demonstration of tumor cells and architectural changes in the vasculature. The same can be seen on lung biopsy be it CT-guided, surgical, or transbronchial approaches. Cytological identification of malignant cells in aspirated blood in wedge position during right heart catheterization has been used to diagnose PTTM in some cases as demonstrated in this case.PTTM has a poor prognosis. There has been promising but limited data regarding the use of Imatinib and Bevacizumab for treatment.CONCLUSIONS: PTTM requires a high clinical suspicion for diagnosis with promising therapies using PDGF and VEGF inhibitors that require further clinical trials.Reference #1: Godbole, R. H., Saggar, R., & Kamangar, N. (2019). Pulmonary tumor thrombotic microangiopathy: a systematic review. Pulmonary Circulation, 9(2), 1–13. https://doi.org/10.1177/2045894019851000Reference #2: Katayama, D., Kuriyama, K., Kinoshita, T., Nagai, K., Hongyo, H., Kishimoto, K., Inoue, A., Takamura, M., & Choi, S. (2016). Pulmonary tumor thrombotic microangiopathy caused by prostate carcinoma. Acta Radiologica Open, 5(8), 205846011666230. https://doi.org/10.1177/2058460116662300Reference #3: Godbole, R., Saggar, R., Zider, A., Betancourt, J., Wallace, W. D., Suh, R. D., & Kamangar, N. (2017). Insights on pulmonary tumor thrombotic microangiopathy: a seven-patient case series. Pulmonary Circulation, 7(4), 813–820. https://doi.org/10.1177/2045893217728072DISCLOSURES: No relevant relationships by Angela GibbsNo relevant relationships by Sooraj KumarNo relevant relationships by Muna Omar SESSION TITLE: Interesting Pulmonary Vascular Abnormalities SESSION TYPE: Case Reports PRESENTED ON: 10/19/2022 11:15 am - 12:15 pm INTRODUCTION: Pulmonary hypertension as a complication of malignancy can come in many forms. An often underestimated form includes pulmonary tumor microvascular disease, comprising both pulmonary tumor microembolism (PTE) and pulmonary tumor thrombotic microangiopathy (PTTM). Here we report a case of pre-capillary pulmonary hypertension from prostate cancer microemboli. CASE PRESENTATION: Our patient is an 80-year-old man with a history of rectal adenocarcinoma treated with resection and chemotherapy, who presented to the hospital with back pain and was found to have metastatic prostate adenocarcinoma with metastatic disease spread to the bone. He was also found to have hypoxic respiratory failure requiring 3-4 liters of oxygen. During his workup, an echocardiogram revealed pulmonary hypertension, with an estimated right ventricular systolic pressure of 78 mmHg (Figure 1). A ventilation/perfusion scan revealed diffuse decreased perfusion along the bilateral periphery of both lungs. Next, a right heart catheterization was performed, which confirmed pre-capillary pulmonary hypertension (right atrial pressure 2 mmHg, pulmonary artery systolic pressure of 61 mmHg, pulmonary artery diastolic pressure 14 mmHg, mean pulmonary artery pressure 27 mmHg, pulmonary capillary wedge pressure 5 mmHg, cardiac index 2.48 L/min/m2 by Fick and thermodilution, and pulmonary vascular resistance 3.8 Wood units). Pulmonary wedge aspiration cytology was performed which revealed tumor cells that stained positive for prostate-specific antigen (Figure 2, 3). The peripheral blood smear was negative for tumor cells. Overall, this suggests pre-capillary pulmonary hypertension due to tumor microthrombi. The patient was started on sildenafil 20mg three times per day and had subjective improvement in his exercise capacity at this time. His prostate cancer is being treated with leuprolide and abiraterone. DISCUSSION: Pulmonary Tumor Thrombotic Microangiopathy (PTTM), first identified in 1990 is thought to arise from mechanical obstruction, fibrocellular intimal proliferation, and remodeling of the pulmonary vasculature. Gastric malignancies account for >50% of cases with prostate cancer reported as the cause in <5 cases. Definitive diagnosis is by postmortem demonstration of tumor cells and architectural changes in the vasculature. The same can be seen on lung biopsy be it CT-guided, surgical, or transbronchial approaches. Cytological identification of malignant cells in aspirated blood in wedge position during right heart catheterization has been used to diagnose PTTM in some cases as demonstrated in this case. PTTM has a poor prognosis. There has been promising but limited data regarding the use of Imatinib and Bevacizumab for treatment. CONCLUSIONS: PTTM requires a high clinical suspicion for diagnosis with promising therapies using PDGF and VEGF inhibitors that require further clinical trials. Reference #1: Godbole, R. H., Saggar, R., & Kamangar, N. (2019). Pulmonary tumor thrombotic microangiopathy: a systematic review. Pulmonary Circulation, 9(2), 1–13. https://doi.org/10.1177/2045894019851000 Reference #2: Katayama, D., Kuriyama, K., Kinoshita, T., Nagai, K., Hongyo, H., Kishimoto, K., Inoue, A., Takamura, M., & Choi, S. (2016). Pulmonary tumor thrombotic microangiopathy caused by prostate carcinoma. Acta Radiologica Open, 5(8), 205846011666230. https://doi.org/10.1177/2058460116662300 Reference #3: Godbole, R., Saggar, R., Zider, A., Betancourt, J., Wallace, W. D., Suh, R. D., & Kamangar, N. (2017). Insights on pulmonary tumor thrombotic microangiopathy: a seven-patient case series. Pulmonary Circulation, 7(4), 813–820. https://doi.org/10.1177/2045893217728072 DISCLOSURES: No relevant relationships by Angela Gibbs No relevant relationships by Sooraj Kumar No relevant relationships by Muna Omar

IBRUTINIB-INDUCED SINUS NODE DYSFUNCTION: A RARE CLINICAL ENTITY

SESSION TITLE: Cardiovascular Disease Case Report PostersSESSION TYPE: Case Report PostersPRESENTED ON: 10/19/2022 12:45 pm - 01:45 pmINTRODUCTION: Ibrutinib is a novel bruton tyrosine kinase (BTK) inhibitor used to treat B-cell malignancies. Ibrutinib has cardiotoxic potential, often resulting in new onset atrial fibrillation in its recipients, but bradycardia, sinus pause or arrest are rarely reported.CASE PRESENTATION: A 69-year-old male patient with medical history significant for chronic lymphocytic leukemia (CLL) on chemotherapy with ibrutinib for 1 year, and hypertension controlled on amlodipine presented with complaints of worsening fatigue and tiredness and lightheadedness not associated with any prodrome. The patient denied any chest pain, dyspnea, palpitations, nystagmus, vertigo, seizures, or stroke-like symptoms. Social history was significant for smoking but denied any alcohol or illicit drug use. Physical exam was remarkable for bradycardia. EKG done at that time showed sinus bradycardia with irregular premature atrial complexes. Previous EKGs prior to starting chemotherapy showed baseline regular sinus bradycardia of 55 beats per minute, with stable PR interval. Patient was placed on a Holter monitor for further evaluation. Patient was called into the hospital, 2 weeks later, after noticing a 4-second sinus pause. On further review of Holter monitor, patient was noted to have sinus bradycardia of 40 beats per minute with ventricular ectopy and intermittent episodes of atrial fibrillation with rapid ventricular response. Bloodwork was significant for elevated WBC count of 82,000 / uL consistent with his diagnosis of CLL, but otherwise remaining labs were unremarkable. Echocardiogram revealed normal ventricular function with ejection fraction of 55-60%, without any significant structural abnormalities. CT coronary study was significant for dense calcifications of proximal LAD with 50% stenosis and a total coronary calcium score of 133. Thus, a diagnosis of ibrutinib induced sinus node dysfunction was made and the patient received a dual-chamber permanent pacemaker placement in the electrophysiology lab. EKG done post-procedure showed regular paced rhythm and patient reported significant improvement in energy levels. He was discharged as he remained asymptomatic and hemodynamically stable. He remained symptom-free on follow-up visits.DISCUSSION: Our case is only the third reported instance of ibrutinib induced bradycardia, although the exact mechanism of this adverse effect has not yet been established. In vivo studies on mice sinoatrial node (SAN) myocytes demonstrate that SAN dysfunction and arrhythmogenesis was more profound with ibrutinib compared to more selective BTK inhibitor like acalabrutinib, thus indicating an off-target mechanism playing a role in cardiotoxic effects of the drug.CONCLUSIONS: Through our case, we emphasize the possibility of SAN dysfunction secondary to ibrutinib use and call for further human research to determine the mechanism of cardiotoxic effects of ibrutinib and other BTK inhibitors.Reference #1: Tuomi JM, Bohne LJ, Dorey TW, Jansen HJ, Liu Y, Jones DL, Rose RA. Distinct Effects of Ibrutinib and Acalabrutinib on Mouse Atrial and Sinoatrial Node Electrophysiology and Arrhythmogenesis. J Am Heart Assoc. 2021 Nov 16;10(22):e022369. doi: 10.1161/JAHA.121.022369. Epub 2021 Nov 2. PMID: 34726066; PMCID: PMC8751944.Reference #2: Xu L, Dong Q, Zhang N, Lu K, Tang X. Severe Sinus Bradycardia Associated with Ibrutinib: One Rare Case from China. Am J Med Sci. 2021 Jun;361(6):803-805. doi: 10.1016/j.amjms.2020.11.029. Epub 2020 Nov 26. PMID: 33947585.Reference #3: Mathur K, Saini A, Ellenbogen KA, Shepard RK. Profound Sinoatrial Arrest Associated with Ibrutinib. Case Rep Oncol Med. 2017;2017:7304021. doi: 10.1155/2017/7304021. Epub 2017 Dec 10. PMID: 29375920; PMCID: PMC5742500.DISCLOSURES: No relevant relationships by Tharun BandarupalliNo relevant relationships by Bhavesh GajjarNo relevant relationships by supriya peshinNo relevant relationships by Koushik Sanku SESSION TITLE: Cardiovascular Disease Case Report Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Ibrutinib is a novel bruton tyrosine kinase (BTK) inhibitor used to treat B-cell malignancies. Ibrutinib has cardiotoxic potential, often resulting in new onset atrial fibrillation in its recipients, but bradycardia, sinus pause or arrest are rarely reported. CASE PRESENTATION: A 69-year-old male patient with medical history significant for chronic lymphocytic leukemia (CLL) on chemotherapy with ibrutinib for 1 year, and hypertension controlled on amlodipine presented with complaints of worsening fatigue and tiredness and lightheadedness not associated with any prodrome. The patient denied any chest pain, dyspnea, palpitations, nystagmus, vertigo, seizures, or stroke-like symptoms. Social history was significant for smoking but denied any alcohol or illicit drug use. Physical exam was remarkable for bradycardia. EKG done at that time showed sinus bradycardia with irregular premature atrial complexes. Previous EKGs prior to starting chemotherapy showed baseline regular sinus bradycardia of 55 beats per minute, with stable PR interval. Patient was placed on a Holter monitor for further evaluation. Patient was called into the hospital, 2 weeks later, after noticing a 4-second sinus pause. On further review of Holter monitor, patient was noted to have sinus bradycardia of 40 beats per minute with ventricular ectopy and intermittent episodes of atrial fibrillation with rapid ventricular response. Bloodwork was significant for elevated WBC count of 82,000 / uL consistent with his diagnosis of CLL, but otherwise remaining labs were unremarkable. Echocardiogram revealed normal ventricular function with ejection fraction of 55-60%, without any significant structural abnormalities. CT coronary study was significant for dense calcifications of proximal LAD with 50% stenosis and a total coronary calcium score of 133. Thus, a diagnosis of ibrutinib induced sinus node dysfunction was made and the patient received a dual-chamber permanent pacemaker placement in the electrophysiology lab. EKG done post-procedure showed regular paced rhythm and patient reported significant improvement in energy levels. He was discharged as he remained asymptomatic and hemodynamically stable. He remained symptom-free on follow-up visits. DISCUSSION: Our case is only the third reported instance of ibrutinib induced bradycardia, although the exact mechanism of this adverse effect has not yet been established. In vivo studies on mice sinoatrial node (SAN) myocytes demonstrate that SAN dysfunction and arrhythmogenesis was more profound with ibrutinib compared to more selective BTK inhibitor like acalabrutinib, thus indicating an off-target mechanism playing a role in cardiotoxic effects of the drug. CONCLUSIONS: Through our case, we emphasize the possibility of SAN dysfunction secondary to ibrutinib use and call for further human research to determine the mechanism of cardiotoxic effects of ibrutinib and other BTK inhibitors. Reference #1: Tuomi JM, Bohne LJ, Dorey TW, Jansen HJ, Liu Y, Jones DL, Rose RA. Distinct Effects of Ibrutinib and Acalabrutinib on Mouse Atrial and Sinoatrial Node Electrophysiology and Arrhythmogenesis. J Am Heart Assoc. 2021 Nov 16;10(22):e022369. doi: 10.1161/JAHA.121.022369. Epub 2021 Nov 2. PMID: 34726066; PMCID: PMC8751944. Reference #2: Xu L, Dong Q, Zhang N, Lu K, Tang X. Severe Sinus Bradycardia Associated with Ibrutinib: One Rare Case from China. Am J Med Sci. 2021 Jun;361(6):803-805. doi: 10.1016/j.amjms.2020.11.029. Epub 2020 Nov 26. PMID: 33947585. Reference #3: Mathur K, Saini A, Ellenbogen KA, Shepard RK. Profound Sinoatrial Arrest Associated with Ibrutinib. Case Rep Oncol Med. 2017;2017:7304021. doi: 10.1155/2017/7304021. Epub 2017 Dec 10. PMID: 29375920; PMCID: PMC5742500. DISCLOSURES: No relevant relationships by Tharun Bandarupalli No relevant relationships by Bhavesh Gajjar No relevant relationships by supriya peshin No relevant relationships by Koushik Sanku

CARDIAC TAMPONADE SECONDARY TO COVID-19 INFECTION

SESSION TITLE: Infections In and Around the Heart Case PostersSESSION TYPE: Case Report PostersPRESENTED ON: 10/17/2022 12:15 pm - 01:15 pmINTRODUCTION: Due to the novelty of COVID-19 virus, complications of this severe respiratory infection are continually emerging. The inflammatory response to the virus carries a high mortality rate and can lead to a variety of cardiothoracic complications such as acute coronary syndrome, thromboembolism, and heart failure [1]. Here, we present a case of a young female who suffered cardiac tamponade (CT) from a pericardial effusion (PEEF) attributed to COVID-19 infection, which has only been described a handful of times in the literature.CASE PRESENTATION: A 33-year-old female with a history of Down syndrome and morbid obesity presented with worsening dyspnea and fever for one week. Her initial oxygen saturation was 50% on room air, and bilevel noninvasive ventilatory support was initiated. Her viral PCR was positive for COVID-19. A computed tomography angiogram of the chest revealed small bilateral pulmonary emboli, diffuse ground-glass consolidations, and small bilateral pleural effusions. Her respiratory status continued to decompensate and she was placed on mechanical ventilation. She became hypotensive requiring vasopressor support. The following morning, an echocardiogram (TTE) revealed an ejection fraction of 40-45% and a new PEEF with early right ventricular diastolic collapse consistent with CT physiology. She underwent emergent pericardiocentesis, and 220 mL of bloody fluid was drained. PEEF studies revealed a glucose level of 186 mg/dL, LDH of 1380 U/L, and protein of 3.0 g/dL. Total nucleated count was 16,545/uL with 68% neutrophils. Gram stain showed a few white blood cells without organisms, and final bacterial, fungal, and acid-fast cultures were negative. A pericardial drain was left in place, but the procedure was complicated by a pneumothorax and a chest tube was placed. A follow-up TTE the next day revealed improvement of the PEEF without signs of CT. A repeat chest x-ray showed resolution of the pneumothorax. Unfortunately, the patient’s oxygenation and hemodynamic status continued to worsen. She eventually suffered cardiac arrest with pulseless electrical activity and succumbed to her illness.DISCUSSION: New knowledge regarding complications of COVID-19 infection is continually emerging. According to a February 2022 systematic review, only 30 cases of severe PEEFs with CT secondary to COVID-19 have been recorded. The mechanism by which PEEFs form is unclear. It is proposed that the entry of the virus into inflammatory cells causes a release of cytokines such as TNF-alpha, IL-1, IL-6, and IL-8. This resulting cytokine storm allows rapid inflammation and infiltration of fluid into the pericardial sac [1].CONCLUSIONS: In a decompensated patient with COVID-19, a stat TTE should be obtained to rule out PEEF. Physicians must be cognizant of this uncommon yet highly fatal complication in unstable COVID-19 patients, as cardiac tamponade is a potentially reversible cause of cardiac arrest.Reference #1: Kermani-Alghoraishi, M., Pouramini, A., Kafi, F., & Khosravi, A. (2022). Coronavirus Disease 2019 (COVID-19) and Severe Pericardial Effusion: From Pathogenesis to Management: A Case Report Based Systematic Review. Current problems in cardiology, 47(2), 100933. https://doi.org/10.1016/j.cpcardiol.2021.100933DISCLOSURES: No relevant relationships by Amanda CecchiniNo relevant relationships by Arthur CecchiniNo relevant relationships by Kevin CornwellNo relevant relationships by Krupa Solanki SESSION TITLE: Infections In and Around the Heart Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Due to the novelty of COVID-19 virus, complications of this severe respiratory infection are continually emerging. The inflammatory response to the virus carries a high mortality rate and can lead to a variety of cardiothoracic complications such as acute coronary syndrome, thromboembolism, and heart failure [1]. Here, we present a case of a young female who suffered cardiac tamponade (CT) from a pericardial effusion (PEEF) attributed to COVID-19 infection, which has only been described a handful of times in the literature. CASE PRESENTATION: A 33-year-old female with a history of Down syndrome and morbid obesity presented with worsening dyspnea and fever for one week. Her initial oxygen saturation was 50% on room air, and bilevel noninvasive ventilatory support was initiated. Her viral PCR was positive for COVID-19. A computed tomography angiogram of the chest revealed small bilateral pulmonary emboli, diffuse ground-glass consolidations, and small bilateral pleural effusions. Her respiratory status continued to decompensate and she was placed on mechanical ventilation. She became hypotensive requiring vasopressor support. The following morning, an echocardiogram (TTE) revealed an ejection fraction of 40-45% and a new PEEF with early right ventricular diastolic collapse consistent with CT physiology. She underwent emergent pericardiocentesis, and 220 mL of bloody fluid was drained. PEEF studies revealed a glucose level of 186 mg/dL, LDH of 1380 U/L, and protein of 3.0 g/dL. Total nucleated count was 16,545/uL with 68% neutrophils. Gram stain showed a few white blood cells without organisms, and final bacterial, fungal, and acid-fast cultures were negative. A pericardial drain was left in place, but the procedure was complicated by a pneumothorax and a chest tube was placed. A follow-up TTE the next day revealed improvement of the PEEF without signs of CT. A repeat chest x-ray showed resolution of the pneumothorax. Unfortunately, the patient’s oxygenation and hemodynamic status continued to worsen. She eventually suffered cardiac arrest with pulseless electrical activity and succumbed to her illness. DISCUSSION: New knowledge regarding complications of COVID-19 infection is continually emerging. According to a February 2022 systematic review, only 30 cases of severe PEEFs with CT secondary to COVID-19 have been recorded. The mechanism by which PEEFs form is unclear. It is proposed that the entry of the virus into inflammatory cells causes a release of cytokines such as TNF-alpha, IL-1, IL-6, and IL-8. This resulting cytokine storm allows rapid inflammation and infiltration of fluid into the pericardial sac [1]. CONCLUSIONS: In a decompensated patient with COVID-19, a stat TTE should be obtained to rule out PEEF. Physicians must be cognizant of this uncommon yet highly fatal complication in unstable COVID-19 patients, as cardiac tamponade is a potentially reversible cause of cardiac arrest. Reference #1: Kermani-Alghoraishi, M., Pouramini, A., Kafi, F., & Khosravi, A. (2022). Coronavirus Disease 2019 (COVID-19) and Severe Pericardial Effusion: From Pathogenesis to Management: A Case Report Based Systematic Review. Current problems in cardiology, 47(2), 100933. https://doi.org/10.1016/j.cpcardiol.2021.100933 DISCLOSURES: No relevant relationships by Amanda Cecchini No relevant relationships by Arthur Cecchini No relevant relationships by Kevin Cornwell No relevant relationships by Krupa Solanki

A RARE CASE OF DISSEMINATED MYCOBACTERIUM AS THE CAUSE OF RECURRENT PNEUMOTHORAX

SESSION TITLE: Chest Infections with Pleural Involvement Case PostersSESSION TYPE: Case Report PostersPRESENTED ON: 10/19/2022 12:45 pm - 01:45 pmINTRODUCTION: Mycobacterium avium-intracellulare complex (MAC) is an opportunistic infection that is caused by mycobacterium avium and mycobacterium intracellulare. This infection can cause pulmonary disease or lead to systemic disease and lymphadenitis in immunosuppressed individuals. This case follows a patient who developed a recurrent pneumothorax (PTX) due to disseminated MAC.CASE PRESENTATION: A cachectic 41-year-old male with a past medical history of HIV/AIDS (most recent CD4 count 46, viral load 50,000), esophageal candidiasis, disseminated Mycobacterium avium-intracellulare complex (MAC), anemia, and history of noncompliance presented with sudden onset shortness of breath. Of note, the patient was recently hospitalized for spontaneous PTX and bilateral pneumonia, requiring chest tube placement. He was discharged two days prior to presentation after complete resolution of PTX. In the emergency department he was found to have tachycardia of 166, tachypnea of 22, SPO2 91% on room air. Chest x-ray demonstrated large left-sided PTX, complete collapse of the left lung medially and inferiorly with tracheal deviation to the right. Chest tube was emergently placed, however, CT chest continued to demonstrate persistent large left PTX. In conjunction with antibiotic treatment for MAC, patient underwent video assisted thoracoscopy (VATS) with bleb resection and pleurodesis. Anaerobic, fungal, AFB, aerobic cultures were without growth. Tissue was taken which resulted negative. Due to non-resolving PTX, bronchoscopy was performed and brush biopsy with washings were obtained. Special stain for Pneumocystis species (PJP) was negative. Patient underwent repeat VATS with pleurodesis using blood patch technique and doxycycline. After the resolution of PTX he was discharged with home health services.DISCUSSION: Spontaneous PTX is a potentially fatal infection in HIV-infected patients which occurs 450 times more frequently in individuals with AIDS compared to the general public (1). HIV-infected individuals who are found to have PTX have a mortality rate of up to 30-60% (1). While more commonly isolated organisms including PJP and pulmonary tuberculosis (TB) typically cause PTX, pulmonary MAC infections are a rare but potential microbial etiology as well (2). In addition, although MAC may be treated, the bronchiectasis and additional lung complications continue to persist leading to chronic damage and a susceptibility to future infections (3). As likely seen in our patient, the onset of PTX can be caused by bullae rupture leading to a lung nodule vanishing (3). Therefore, given the high mortality rate patients with AIDS should be closely monitored for possible development of PTX.CONCLUSIONS: Although rare, disseminated MAC can be a fatal culprit leading to PTX in HIV patients. Due to the high mortality, the prompt diagnosis leading to appropriate treatment is necessary for improved patient outcome.Reference #1: Terzi, E., Zarogoulidis, K., Kougioumtzi, I., Dryllis, G., Kioumis, I., Pitsiou, G., Machairiotis, N., Katsikogiannis, N., Tsiouda, T., Madesis, A., Karaiskos, T., & Zarogoulidis, P. (2014). Human immunodeficiency virus infection and pneumothorax. Journal of thoracic disease, 6(Suppl 4), S377–S382. https://doi.org/10.3978/j.issn.2072-1439.2014.08.03Reference #2: Asai, K., & Urabe, N. (2011). Acute empyema with intractable pneumothorax associated with ruptured lung abscess caused by Mycobacterium avium. General thoracic and cardiovascular surgery, 59(6), 443–446. https://doi.org/10.1007/s11748-010-0687-7Reference #3: Kobashi, Y., Fukuda, M., Yoshida, K., Miyashita, N., & Oka, M. (2006). Pulmonary Mycobacterium intracellulare disease with a solitary pulmonary nodule detected at the onset of pneumothorax. Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy, 12(4), 203–206. https://doi.org/10.1007/s10156-006-0451-1DISCLOSURES: No relevant relationships by Jessica LeeNo relevant relationships by Cameron RoweNo relevant relationships by Denis Trinnel SESSION TITLE: Chest Infections with Pleural Involvement Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Mycobacterium avium-intracellulare complex (MAC) is an opportunistic infection that is caused by mycobacterium avium and mycobacterium intracellulare. This infection can cause pulmonary disease or lead to systemic disease and lymphadenitis in immunosuppressed individuals. This case follows a patient who developed a recurrent pneumothorax (PTX) due to disseminated MAC. CASE PRESENTATION: A cachectic 41-year-old male with a past medical history of HIV/AIDS (most recent CD4 count 46, viral load 50,000), esophageal candidiasis, disseminated Mycobacterium avium-intracellulare complex (MAC), anemia, and history of noncompliance presented with sudden onset shortness of breath. Of note, the patient was recently hospitalized for spontaneous PTX and bilateral pneumonia, requiring chest tube placement. He was discharged two days prior to presentation after complete resolution of PTX. In the emergency department he was found to have tachycardia of 166, tachypnea of 22, SPO2 91% on room air. Chest x-ray demonstrated large left-sided PTX, complete collapse of the left lung medially and inferiorly with tracheal deviation to the right. Chest tube was emergently placed, however, CT chest continued to demonstrate persistent large left PTX. In conjunction with antibiotic treatment for MAC, patient underwent video assisted thoracoscopy (VATS) with bleb resection and pleurodesis. Anaerobic, fungal, AFB, aerobic cultures were without growth. Tissue was taken which resulted negative. Due to non-resolving PTX, bronchoscopy was performed and brush biopsy with washings were obtained. Special stain for Pneumocystis species (PJP) was negative. Patient underwent repeat VATS with pleurodesis using blood patch technique and doxycycline. After the resolution of PTX he was discharged with home health services. DISCUSSION: Spontaneous PTX is a potentially fatal infection in HIV-infected patients which occurs 450 times more frequently in individuals with AIDS compared to the general public (1). HIV-infected individuals who are found to have PTX have a mortality rate of up to 30-60% (1). While more commonly isolated organisms including PJP and pulmonary tuberculosis (TB) typically cause PTX, pulmonary MAC infections are a rare but potential microbial etiology as well (2). In addition, although MAC may be treated, the bronchiectasis and additional lung complications continue to persist leading to chronic damage and a susceptibility to future infections (3). As likely seen in our patient, the onset of PTX can be caused by bullae rupture leading to a lung nodule vanishing (3). Therefore, given the high mortality rate patients with AIDS should be closely monitored for possible development of PTX. CONCLUSIONS: Although rare, disseminated MAC can be a fatal culprit leading to PTX in HIV patients. Due to the high mortality, the prompt diagnosis leading to appropriate treatment is necessary for improved patient outcome. Reference #1: Terzi, E., Zarogoulidis, K., Kougioumtzi, I., Dryllis, G., Kioumis, I., Pitsiou, G., Machairiotis, N., Katsikogiannis, N., Tsiouda, T., Madesis, A., Karaiskos, T., & Zarogoulidis, P. (2014). Human immunodeficiency virus infection and pneumothorax. Journal of thoracic disease, 6(Suppl 4), S377–S382. https://doi.org/10.3978/j.issn.2072-1439.2014.08.03 Reference #2: Asai, K., & Urabe, N. (2011). Acute empyema with intractable pneumothorax associated with ruptured lung abscess caused by Mycobacterium avium. General thoracic and cardiovascular surgery, 59(6), 443–446. https://doi.org/10.1007/s11748-010-0687-7 Reference #3: Kobashi, Y., Fukuda, M., Yoshida, K., Miyashita, N., & Oka, M. (2006). Pulmonary Mycobacterium intracellulare disease with a solitary pulmonary nodule detected at the onset of pneumothorax. Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy, 12(4), 203–206. https://doi.org/10.1007/s10156-006-0451-1 DISCLOSURES: No relevant relationships by Jessica Lee No relevant relationships by Cameron Rowe No relevant relationships by Denis Trinnel

WITHDRAWN

SESSION TITLE: PAH with Complications SESSION TYPE: Rapid Fire Original Inv PRESENTED ON: 10/17/2022 12:15 pm - 1:15 pm PURPOSE: Congenital heart disease (CHD) serves as the second most commonly associated form of primary pulmonary arterial hypertension (PAH). The prognosis of PAH related to congenital heart disease differ from other types of PAH due to factors such as defect types and sizes. The aim of the study is to compare the outcomes of PAH secondary to CHD (PAH-CHD) and PAH due to other causes. METHODS: We extracted the data from the National Inpatient Sample (NIS) database for the years 2016 to 2019 and analyzed all hospital admissions for PAH-CHD versus primary PAH due to causes other than CHD (Other PAH). We selected CHDs commonly known to be associated with primary pulmonary hypertension: atrial septal defect (ASD), ventricular septal defect (VSD), aortopulmonary window, atrioventricular septal defect, tetralogy of Fallot, patent ductus arteriosus (PDA), truncus arteriosus, double inlet left ventricle and double outlet right ventricle. We compared baseline characteristics, outcomes, and healthcare utilization between the two groups. RESULTS: Of 37,739 patients admitted with PAH, 1,355 patients had concomitant CHD and were compared with 36,384 adult PAH patients without CHD. In the PAH-CHD group, ASD was the most common associated CHD (1,195, 88%) followed by VSD (125, 9.2%) and PDA (39,2, 9%). The PAH-CHD patients were relatively younger (mean age of 53.15 vs 65.7 years), less likely to be of white race (62.36% vs 66%) and had a lower proportion of comorbid coronary artery disease (14.3% vs 28.86%), obesity (15.13% vs 22.66%), dyslipidemia (44% vs 51%), diabetes (18.08% vs 34.48%) and chronic kidney disease (19.93% vs 33.15%) [all p<0.05*]. A total of 115 (8.5%) PAH-CHD patients and 1,844 (5.07%) other PAH patients died during hospitalization. PAH-CHD patients had a higher in-hospital mortality (aOR=1.73 ;95%CI 1.08-2.76, p=0.02*). The PAH-CHD group had higher odds of having chronic respiratory failure (aOR=1.13;95%CI 1.04-1.22, p=0.003*), right ventricular failure (aOR=1.72 ;95%CI 1.12-2.6, p<0.013*), cardiogenic shock (aOR=2.1;95%CI 1.15-3.84, p=0.015*) and acute ischemic stroke (aOR=25.18;95%CI 6.78-93.46, p<0.0001*). compared to the other PAH group. PAH-CHD patients also had longer length of stay (10.6 vs 7.10 days, p=0.0009*) and higher hospitalization costs per admission ($209,507 vs $90,599, p=0.007*). CONCLUSIONS: The PAH-CHD group had higher in-hospital mortality and healthcare resource utilization than the other PAH group. PAH-CHD group were more likely to have chronic respiratory failure, right ventricular failure, cardiogenic shock and ischemic stroke. CLINICAL IMPLICATIONS: PAH-CHD seem to have higher mortality and worse PAH related in-patient complications. The difference between two groups highlights the need for further research and trials to understand the unique natural history and appropriate management of PAH-CHD patients. DISCLOSURES: No relevant relationships by Cyra-Yoonsun Kang No relevant relationships by Sandhya shri Kannayiram No relevant relationships by parnia khamooshi No relevant relationships by Viviana Reyes Pinzon No relevant relationships by Sujitha Velagapudi

IMPACT OF ENHANCED DISCHARGE EDUCATION ABOUT SEPSIS ON 30-DAY SEPSIS READMISSIONS: QUALITY IMPROVEMENT PILOT PROGRAM AT A LARGE TERTIARY CARE CENTER

SESSION TITLE: Sepsis: Beyond 30cc/kg and AntibioticsSESSION TYPE: Rapid Fire Original InvPRESENTED ON: 10/19/2022 11:15 am - 12:15 pmPURPOSE: Sepsis is the leading cause of hospitalization and mortality in the United States. In addition, sepsis is, by volume, the leading cause of 30 day readmissions across all payer mix in the United States. The risk factors for 30 day readmissions are multifactorial and often portends poor outcomes and increase hospitalization costs. We trialed a pilot program of enhanced sepsis discharge education which consisted of direct patient education prior to discharge, providing a Sepsis Education brochure with tips on self management at home as well as a QR code to direct patients to institutional website in case they needed further assistance, and finally a disposable thermometer to maintain an accurate temperature log to aid in monitoring for signs and symptoms of sepsis. Our primary goal was educate patients about their diagnosis and reduce sepsis readmissions in all non-medicare patients being discharged home.METHODS: The pilot was implemented at on one med/surg unit in our 550-bed tertiary, academic medical center starting in March 2021 and progressively expanded hospital wide over the next six months. The sepsis administrative coordinator screens new in-patient admissions for sepsis (non-Medicare) patients daily and informs medical/surgical unit coordinators of potential candidates. Med/surg coordinators will confirm if patients meet criteria for follow-up (non-Medicare, being discharged to home), provide discharge education and enter the patient in a log for continued surveillance. Subsequently, the administrative coordinator then follows up with a phone call 7-10 days after discharge during which, they assess the patient for worrisome symptoms, confirms follow up appointments, medication compliance and review of temperature log. If the patient needs clinical assistance, they will refer to the patient to the hospital sepsis clinical coordinator or patient’s outpatient physicians.RESULTS: We compared sepsis discharges and 30day readmissions (all excluding COVID-19 cases) from March 1, 2019 – Dec 31, 2019 to March 1, 2021 – Dec 31, 2021. Readmissions amongst Medicare patients discharged home was 15.9 % (110 / 962) in 2019 vs 11.9% (83 / 696) in 2021. For non-medicare patients, the rate was 13.2% (41/311) in 2019 vs 13.1% (51/390) in 2021. In our pilot program, the readmission rate in medicare patients was 17.2% (28/163) versus 5.6% (5/90) in non-medicare patients.CONCLUSIONS: This program captures a patient population which may have been lost to follow-up. Implementation of the enhanced Sepsis Discharge Education led to at least a 30 patient reduction in readmissions yielding an approximate cost savings of $594,000.CLINICAL IMPLICATIONS: Providing educational support, instructions, and follow up calls upon discharge improves medication adherence, compliance, and maintains patient follow up thus reducing readmissions and improving hospital resource utilization and overall cost.DISCLOSURES: No relevant relationships by Laura FreireNo relevant relationships by Nirav MistryNo relevant relationships by Caitlin Tauro SESSION TITLE: Sepsis: Beyond 30cc/kg and Antibiotics SESSION TYPE: Rapid Fire Original Inv PRESENTED ON: 10/19/2022 11:15 am - 12:15 pm PURPOSE: Sepsis is the leading cause of hospitalization and mortality in the United States. In addition, sepsis is, by volume, the leading cause of 30 day readmissions across all payer mix in the United States. The risk factors for 30 day readmissions are multifactorial and often portends poor outcomes and increase hospitalization costs. We trialed a pilot program of enhanced sepsis discharge education which consisted of direct patient education prior to discharge, providing a Sepsis Education brochure with tips on self management at home as well as a QR code to direct patients to institutional website in case they needed further assistance, and finally a disposable thermometer to maintain an accurate temperature log to aid in monitoring for signs and symptoms of sepsis. Our primary goal was educate patients about their diagnosis and reduce sepsis readmissions in all non-medicare patients being discharged home. METHODS: The pilot was implemented at on one med/surg unit in our 550-bed tertiary, academic medical center starting in March 2021 and progressively expanded hospital wide over the next six months. The sepsis administrative coordinator screens new in-patient admissions for sepsis (non-Medicare) patients daily and informs medical/surgical unit coordinators of potential candidates. Med/surg coordinators will confirm if patients meet criteria for follow-up (non-Medicare, being discharged to home), provide discharge education and enter the patient in a log for continued surveillance. Subsequently, the administrative coordinator then follows up with a phone call 7-10 days after discharge during which, they assess the patient for worrisome symptoms, confirms follow up appointments, medication compliance and review of temperature log. If the patient needs clinical assistance, they will refer to the patient to the hospital sepsis clinical coordinator or patient’s outpatient physicians. RESULTS: We compared sepsis discharges and 30day readmissions (all excluding COVID-19 cases) from March 1, 2019 – Dec 31, 2019 to March 1, 2021 – Dec 31, 2021. Readmissions amongst Medicare patients discharged home was 15.9 % (110 / 962) in 2019 vs 11.9% (83 / 696) in 2021. For non-medicare patients, the rate was 13.2% (41/311) in 2019 vs 13.1% (51/390) in 2021. In our pilot program, the readmission rate in medicare patients was 17.2% (28/163) versus 5.6% (5/90) in non-medicare patients. CONCLUSIONS: This program captures a patient population which may have been lost to follow-up. Implementation of the enhanced Sepsis Discharge Education led to at least a 30 patient reduction in readmissions yielding an approximate cost savings of $594,000. CLINICAL IMPLICATIONS: Providing educational support, instructions, and follow up calls upon discharge improves medication adherence, compliance, and maintains patient follow up thus reducing readmissions and improving hospital resource utilization and overall cost. DISCLOSURES: No relevant relationships by Laura Freire No relevant relationships by Nirav Mistry No relevant relationships by Caitlin Tauro

DEALING WITH DOUBLE TROUBLE: EMERGENT CARDIAC CATHETERIZATION COMPLICATED BY PERIPROCEDURAL ISCHEMIC STROKE

SESSION TITLE: Cardiovascular Disease Case Report PostersSESSION TYPE: Case Report PostersPRESENTED ON: 10/19/2022 12:45 pm - 01:45 pmINTRODUCTION: Peri-procedural stroke is a rare but catastrophic complication of cardiac catheterization or percutaneous coronary intervention (PCI). If not recognized immediately it can lead to significant mortality and morbidity. Here we report an emergent cardiac catheterization complicated by an ischemic stroke.CASE PRESENTATION: A 72-year-old woman with a past medical history of hypertension presented with chest pain. Her EKG showed ST elevation in aVR and ST depression in the precordial leads. Emergent cardiac catheterization revealed almost complete occlusion of the LAD with a thrombus. During balloon angioplasty the SBP dropped to the 70s requiring an IABP placement. The decision was made to proceed with manual thrombectomy. Post thrombo-suction the patient developed facial droop, slurred speech, and left-sided weakness. A code stroke was called immediately and her initial NIHSS was 11 per stroke team evaluation. Meanwhile, PCI was completed with successful balloon angioplasty, but a stent was not placed as the use of dual antiplatelet therapy (DAPT) may worsen the possible hemorrhagic stroke. Post-procedure, a stat CT head showed no acute intracranial process. CTA head showed stenosis of right M1. CT perfusion showed watershed ischemia in the right MCA region with no core infarct, suggesting an embolic source that confirming a peri-procedural stroke. At this point tPA was contraindicated as the patient required a heparin drip with the IABP. She received IV fluids to support intracranial pressure. Repeat CTs showed no hemorrhagic transformation. IABP was removed and heparin was discontinued after 48 hours. On discharge to rehab, her NIHSS was 2 with minimal left-sided weakness. She returned a month later for stent placement to LAD and was discharged on DAPT.DISCUSSION: The management of peri-procedural stroke remains controversial; the approach is case and provider dependent. It is important for cardiologists to recognize this complication and act rapidly to provide the best management. In this case, as the patient required IV heparin drip for the IABP in place, thrombolysis was not done and she was managed conservatively. Heparin was stopped as soon as possible to prevent hemorrhagic transformation and serial imaging was done meanwhile to monitor the patient. IV fluids were used to support cerebral blood flow as ischemic stroke could also be caused by decreased blood flow during the cardiac catheterization. Stent placement was also delayed to prevent hemorrhagic transformation with DAPT.CONCLUSIONS: A protocol for peri-procedural stroke should be planned beforehand at any institution with cardiac catheterization services. A neurologist, radiologist and neuro-interventionalist should be involved early and work as a team for best outcomes. Further randomized controlled trials are needed for the safest and most efficacious treatment guidelines for peri-procedural stroke.Reference #1: Khatri P, Kasner SE. Ischemic Strokes After Cardiac Catheterization: Opportune Thrombolysis Candidates? Arch Neurol. 2006;63(6):817–821. doi:10.1001/archneur.63.6.817Reference #2: Hamon M, Baron JC, Viader F, Hamon M. Periprocedural stroke and cardiac catheterization. Circulation. 2008 Aug 5;118(6):678-83. doi: 10.1161/CIRCULATIONAHA.108.784504. PMID: 18678784.DISCLOSURES: No relevant relationships by Kevser AkyuzNo relevant relationships by Ranim ChamseddinNo relevant relationships by verisha khanamNo relevant relationships by Zain KulairiNo relevant relationships by Abdullah Yesilyaprak SESSION TITLE: Cardiovascular Disease Case Report Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Peri-procedural stroke is a rare but catastrophic complication of cardiac catheterization or percutaneous coronary intervention (PCI). If not recognized immediately it can lead to significant mortality and morbidity. Here we report an emergent cardiac catheterization complicated by an ischemic stroke. CASE PRESENTATION: A 72-year-old woman with a past medical history of hypertension presented with chest pain. Her EKG showed ST elevation in aVR and ST depression in the precordial leads. Emergent cardiac catheterization revealed almost complete occlusion of the LAD with a thrombus. During balloon angioplasty the SBP dropped to the 70s requiring an IABP placement. The decision was made to proceed with manual thrombectomy. Post thrombo-suction the patient developed facial droop, slurred speech, and left-sided weakness. A code stroke was called immediately and her initial NIHSS was 11 per stroke team evaluation. Meanwhile, PCI was completed with successful balloon angioplasty, but a stent was not placed as the use of dual antiplatelet therapy (DAPT) may worsen the possible hemorrhagic stroke. Post-procedure, a stat CT head showed no acute intracranial process. CTA head showed stenosis of right M1. CT perfusion showed watershed ischemia in the right MCA region with no core infarct, suggesting an embolic source that confirming a peri-procedural stroke. At this point tPA was contraindicated as the patient required a heparin drip with the IABP. She received IV fluids to support intracranial pressure. Repeat CTs showed no hemorrhagic transformation. IABP was removed and heparin was discontinued after 48 hours. On discharge to rehab, her NIHSS was 2 with minimal left-sided weakness. She returned a month later for stent placement to LAD and was discharged on DAPT. DISCUSSION: The management of peri-procedural stroke remains controversial; the approach is case and provider dependent. It is important for cardiologists to recognize this complication and act rapidly to provide the best management. In this case, as the patient required IV heparin drip for the IABP in place, thrombolysis was not done and she was managed conservatively. Heparin was stopped as soon as possible to prevent hemorrhagic transformation and serial imaging was done meanwhile to monitor the patient. IV fluids were used to support cerebral blood flow as ischemic stroke could also be caused by decreased blood flow during the cardiac catheterization. Stent placement was also delayed to prevent hemorrhagic transformation with DAPT. CONCLUSIONS: A protocol for peri-procedural stroke should be planned beforehand at any institution with cardiac catheterization services. A neurologist, radiologist and neuro-interventionalist should be involved early and work as a team for best outcomes. Further randomized controlled trials are needed for the safest and most efficacious treatment guidelines for peri-procedural stroke. Reference #1: Khatri P, Kasner SE. Ischemic Strokes After Cardiac Catheterization: Opportune Thrombolysis Candidates? Arch Neurol. 2006;63(6):817–821. doi:10.1001/archneur.63.6.817 Reference #2: Hamon M, Baron JC, Viader F, Hamon M. Periprocedural stroke and cardiac catheterization. Circulation. 2008 Aug 5;118(6):678-83. doi: 10.1161/CIRCULATIONAHA.108.784504. PMID: 18678784. DISCLOSURES: No relevant relationships by Kevser Akyuz No relevant relationships by Ranim Chamseddin No relevant relationships by verisha khanam No relevant relationships by Zain Kulairi No relevant relationships by Abdullah Yesilyaprak

UNIQUE CASE OF ISOLATED CONGESTIVE SPLENOMEGALY DUE TO ALCOHOLIC CARDIOMYOPATHY RESULTING IN PANCYTOPENIA

SESSION TITLE: Cardiomyopathy Case PostersSESSION TYPE: Case Report PostersPRESENTED ON: 10/19/2022 12:45 pm - 01:45 pmINTRODUCTION: Isolated splenomegaly has a prevalence of 2% in USA. Etiologies include congestive, infiltrative, immune, and neoplastic. Congestive splenomegaly occurs due to portal hypertension (PHTN) or thrombosis. Alcohol causes a dose-dependent dilated cardiomyopathy, hematopoietic, and granulopoietic stem cell suppression.CASE PRESENTATION: A 49 year-old male with a history of alcoholic cardiomyopathy (ACM) and HCV presented with shortness of breath and anasarca. Vitals demonstrated tachycardia. Physical exam was significant for pitting edema to the upper chest wall with a palpable, non-tender, mobile spleen tip. Platelets were 124 B/L with unremarkable LFTs and INR. Echocardiogram demonstrated an EF of 15%. A bumetanide infusion was required for diuresis. He developed pancytopenia with nadirs of HGB 10.6 g/dL, PLT 77 B/L and WBC 1.5 B/L. US doppler of the abdomen showed ascites and splenomegaly with hepatic vein dilation of 1.2 cm. CT abdomen with contrast redemonstrated US abdomen findings, without cirrhosis, vascular abnormalities or lymphadenopathy. A negative infectious workup included blood cultures, serologies for EBV, CMV, HIV, and parasite smear. Hematologic workup showed iron-deficiency anemia (IDA) with normal reticulocyte count, B12, folate, haptoglobin, and LDH. Blood smear was negative for morphology suggesting myelodysplastic syndrome, hematologic malignancy, or immune thrombocytopenia. Outpatient elastography was negative for cirrhosis. The patient was diagnosed with pancytopenia secondary to congestive splenomegaly from severe ACM and alcoholic myelosuppression.DISCUSSION: Splenomegaly is diagnosed by a palpable spleen or by imaging. Initial workup should include a CBC to evaluate for abnormal WBCs to rule out myeloproliferative disorders. Biopsy of bone marrow, lymph nodes, or a flow cytometry can reveal malignancy. Infectious workup should test for EBV, CMV, parasitemia, HIV, blood cultures, and other serologies if appropriate. US venous doppler and MRA assist in diagnosing vascular or primary splenic lesions. Splenectomy and pathologic evaluation remain gold-standard for diagnosis of isolated splenomegaly. Evaluation of pancytopenia includes blood smear, iron studies, ESR, CRP, LFTs, reticulocyte count, LDH, direct Coombs test, and evaluation for drug interactions. The spleen can swell eight to ten times its size, resulting in platelet sequestration and WBC phagocytosis. Alcohol causes dose-dependent myelosuppression, concurrently impairing leukocyte development, and chemotaxis.CONCLUSIONS: In the absence of positive infectious, immune, neoplastic and hepatic pathology, this patient’s splenomegaly is likely the result of his severe ACM. While congestive splenomegaly is typically associated with portal hypertension, this rarely occurs without concurrent cirrhosis. Splenomegaly typically affects platelets and WBC but alcoholic myelosuppression and concurrent IDA caused his anemia.Reference #1: Chapman J, Bansal P, Goyal A, Azevedo AM. Splenomegaly. In: StatPearls. StatPearls Publishing, Treasure Island (FL); 2021. PMID: 28613657.Reference #2: Ballard HS. The hematological complications of alcoholism. Alcohol health and research world. 1997;21(1):42-52. https://www.ncbi.nlm.nih.gov/pubmed/15706762.Reference #3: Manappallil RG. Acute onset pancytopenia following alcohol heavy drinking. Asian Journal of Bio-Medical Research. Apr-Jun. 2016;2(2).DISCLOSURES: No relevant relationships by Sameer AkhtarNo relevant relationships by Sean CoulsonNo relevant relationships by Brian ThomasNo relevant relationships by Rohan UmraniNo relevant relationships by Yvette Wang SESSION TITLE: Cardiomyopathy Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Isolated splenomegaly has a prevalence of 2% in USA. Etiologies include congestive, infiltrative, immune, and neoplastic. Congestive splenomegaly occurs due to portal hypertension (PHTN) or thrombosis. Alcohol causes a dose-dependent dilated cardiomyopathy, hematopoietic, and granulopoietic stem cell suppression. CASE PRESENTATION: A 49 year-old male with a history of alcoholic cardiomyopathy (ACM) and HCV presented with shortness of breath and anasarca. Vitals demonstrated tachycardia. Physical exam was significant for pitting edema to the upper chest wall with a palpable, non-tender, mobile spleen tip. Platelets were 124 B/L with unremarkable LFTs and INR. Echocardiogram demonstrated an EF of 15%. A bumetanide infusion was required for diuresis. He developed pancytopenia with nadirs of HGB 10.6 g/dL, PLT 77 B/L and WBC 1.5 B/L. US doppler of the abdomen showed ascites and splenomegaly with hepatic vein dilation of 1.2 cm. CT abdomen with contrast redemonstrated US abdomen findings, without cirrhosis, vascular abnormalities or lymphadenopathy. A negative infectious workup included blood cultures, serologies for EBV, CMV, HIV, and parasite smear. Hematologic workup showed iron-deficiency anemia (IDA) with normal reticulocyte count, B12, folate, haptoglobin, and LDH. Blood smear was negative for morphology suggesting myelodysplastic syndrome, hematologic malignancy, or immune thrombocytopenia. Outpatient elastography was negative for cirrhosis. The patient was diagnosed with pancytopenia secondary to congestive splenomegaly from severe ACM and alcoholic myelosuppression. DISCUSSION: Splenomegaly is diagnosed by a palpable spleen or by imaging. Initial workup should include a CBC to evaluate for abnormal WBCs to rule out myeloproliferative disorders. Biopsy of bone marrow, lymph nodes, or a flow cytometry can reveal malignancy. Infectious workup should test for EBV, CMV, parasitemia, HIV, blood cultures, and other serologies if appropriate. US venous doppler and MRA assist in diagnosing vascular or primary splenic lesions. Splenectomy and pathologic evaluation remain gold-standard for diagnosis of isolated splenomegaly. Evaluation of pancytopenia includes blood smear, iron studies, ESR, CRP, LFTs, reticulocyte count, LDH, direct Coombs test, and evaluation for drug interactions. The spleen can swell eight to ten times its size, resulting in platelet sequestration and WBC phagocytosis. Alcohol causes dose-dependent myelosuppression, concurrently impairing leukocyte development, and chemotaxis. CONCLUSIONS: In the absence of positive infectious, immune, neoplastic and hepatic pathology, this patient’s splenomegaly is likely the result of his severe ACM. While congestive splenomegaly is typically associated with portal hypertension, this rarely occurs without concurrent cirrhosis. Splenomegaly typically affects platelets and WBC but alcoholic myelosuppression and concurrent IDA caused his anemia. Reference #1: Chapman J, Bansal P, Goyal A, Azevedo AM. Splenomegaly. In: StatPearls. StatPearls Publishing, Treasure Island (FL); 2021. PMID: 28613657. Reference #2: Ballard HS. The hematological complications of alcoholism. Alcohol health and research world. 1997;21(1):42-52. https://www.ncbi.nlm.nih.gov/pubmed/15706762. Reference #3: Manappallil RG. Acute onset pancytopenia following alcohol heavy drinking. Asian Journal of Bio-Medical Research. Apr-Jun. 2016;2(2). DISCLOSURES: No relevant relationships by Sameer Akhtar No relevant relationships by Sean Coulson No relevant relationships by Brian Thomas No relevant relationships by Rohan Umrani No relevant relationships by Yvette Wang

GEOGRAPHIC DISPARITIES IN OUTCOMES OF OSA HOSPITALIZATIONS: A NATIONWIDE VIEWPOINT

SESSION TITLE: Sleep and Sleep Apnea in Hospitalized PatientsSESSION TYPE: Original InvestigationsPRESENTED ON: 10/17/2022 1:30 pm - 2:30 pmPURPOSE: Obstructive Sleep apnea (OSA) is being recognized more widely and its association with outcomes in various diseases. Geographic disparities in diagnosis, demographics, comorbidities, and outcomes need further assessment to improve the mortality and morbidity of OSA hospitalizations.METHODS: The National Inpatient Sample (NIS), the largest inpatient database in the United States, was queried (2018) to identify OSA hospitalizations using relevant ICD-10 CM diagnostic codes. Using a weighted dataset, we determined the demographics, comorbidities, and outcomes of rural OSA vs urban OSA hospitalizations. The primary outcomes included all-cause mortality, dysrhythmia, and stroke. Secondary outcomes included patient disposition, length of stay, and hospital cost.RESULTS: Of 2,169,730 OSA hospitalizations, 2,003,620 (92.3%, median 65 years) were urban and 166,110 (7.7%, median 67 years) were rural OSA hospitalizations. OSA hospitalizations more often consisted of males, white, Medicare enrollees with the rural OSA cohort showing more patients from lower-income households compared to the urban OSA cohort. CVD risk factors/pre-existing comorbidities such as hyperlipidemia (56% vs. 52.9%), obesity (48.4% vs. 47.8%), PVD (7.1% vs. 6.4%), CKD (26.0% vs. 25.4%), prior history of TIA/stroke (8.6% vs. 8.2%), VTE (8.5% vs. 7.8%) and cancer (11.7% vs. 10.4%) were higher in the urban OSA cohort whereas hypertension (66.3% vs 66%), DM (50.6% vs 48%), smoking (44.8% vs 42.9%), CHF (24.4% vs. 21.3%), COPD (42.3% vs 36.8%) were higer in the rural OSA cohort. Interestingly, nearly 20% of OSA patients had comorbid depression, slightly higher in the rural OSA cohort. Despite being relatively younger, the urban OSA cohort demonstrated higher odds of all-cause mortality [OR 1.21 (CI 1.08-1.35)], dysrhythmia [OR 1.09 (CI 1.05-1.13)], and stroke [OR 1.53 (CI 1.35-1.73)] vs. rural OSA cohort even after adjusting for potential sociodemographics and comorbidities. Nearly 57% of patients were discharged routinely in both groups with higher transfer rates in the rural OSA cohort, with a comparable hospital stay but a higher cost in the urban OSA cohort compared to the rural OSA cohort.CONCLUSIONS: In this nationwide analysis, the odds of all-cause mortality (21% higher), dysrhythmia (9% higher), and stroke (53% higher) were significantly higher in the urban OSA cohort as compared to the rural OSA cohort despite being relatively younger. Comorbid risk factors in the OSA population warrant vigilant screening at primary care level to curtail further complications.CLINICAL IMPLICATIONS: Education and awareness about OSA is on the rise, however, the outcomes of OSA hospitalizations are dependent on the geographic location with potentially worse outcomes in urban settings possibly due underlying complexities. Further prospective studies evaluating the disparities and barriers to healthcare access are needed to improve outcomes.DISCLOSURES: No relevant relationships by Rupak DesaiNo relevant relationships by Zainab GandhiNo relevant relationships by Vibhor GargNo relevant relationships by Akhil JainNo relevant relationships by Sreelatha NaikNo relevant relationships by Ankit Vyas SESSION TITLE: Sleep and Sleep Apnea in Hospitalized Patients SESSION TYPE: Original Investigations PRESENTED ON: 10/17/2022 1:30 pm - 2:30 pm PURPOSE: Obstructive Sleep apnea (OSA) is being recognized more widely and its association with outcomes in various diseases. Geographic disparities in diagnosis, demographics, comorbidities, and outcomes need further assessment to improve the mortality and morbidity of OSA hospitalizations. METHODS: The National Inpatient Sample (NIS), the largest inpatient database in the United States, was queried (2018) to identify OSA hospitalizations using relevant ICD-10 CM diagnostic codes. Using a weighted dataset, we determined the demographics, comorbidities, and outcomes of rural OSA vs urban OSA hospitalizations. The primary outcomes included all-cause mortality, dysrhythmia, and stroke. Secondary outcomes included patient disposition, length of stay, and hospital cost. RESULTS: Of 2,169,730 OSA hospitalizations, 2,003,620 (92.3%, median 65 years) were urban and 166,110 (7.7%, median 67 years) were rural OSA hospitalizations. OSA hospitalizations more often consisted of males, white, Medicare enrollees with the rural OSA cohort showing more patients from lower-income households compared to the urban OSA cohort. CVD risk factors/pre-existing comorbidities such as hyperlipidemia (56% vs. 52.9%), obesity (48.4% vs. 47.8%), PVD (7.1% vs. 6.4%), CKD (26.0% vs. 25.4%), prior history of TIA/stroke (8.6% vs. 8.2%), VTE (8.5% vs. 7.8%) and cancer (11.7% vs. 10.4%) were higher in the urban OSA cohort whereas hypertension (66.3% vs 66%), DM (50.6% vs 48%), smoking (44.8% vs 42.9%), CHF (24.4% vs. 21.3%), COPD (42.3% vs 36.8%) were higer in the rural OSA cohort. Interestingly, nearly 20% of OSA patients had comorbid depression, slightly higher in the rural OSA cohort. Despite being relatively younger, the urban OSA cohort demonstrated higher odds of all-cause mortality [OR 1.21 (CI 1.08-1.35)], dysrhythmia [OR 1.09 (CI 1.05-1.13)], and stroke [OR 1.53 (CI 1.35-1.73)] vs. rural OSA cohort even after adjusting for potential sociodemographics and comorbidities. Nearly 57% of patients were discharged routinely in both groups with higher transfer rates in the rural OSA cohort, with a comparable hospital stay but a higher cost in the urban OSA cohort compared to the rural OSA cohort. CONCLUSIONS: In this nationwide analysis, the odds of all-cause mortality (21% higher), dysrhythmia (9% higher), and stroke (53% higher) were significantly higher in the urban OSA cohort as compared to the rural OSA cohort despite being relatively younger. Comorbid risk factors in the OSA population warrant vigilant screening at primary care level to curtail further complications. CLINICAL IMPLICATIONS: Education and awareness about OSA is on the rise, however, the outcomes of OSA hospitalizations are dependent on the geographic location with potentially worse outcomes in urban settings possibly due underlying complexities. Further prospective studies evaluating the disparities and barriers to healthcare access are needed to improve outcomes. DISCLOSURES: No relevant relationships by Rupak Desai No relevant relationships by Zainab Gandhi No relevant relationships by Vibhor Garg No relevant relationships by Akhil Jain No relevant relationships by Sreelatha Naik No relevant relationships by Ankit Vyas

POSITIVE END-EXPIRATORY PRESSURE (PEEP) INDEX: A NOVEL, BETTER DISCRIMINATION MARKER THAN PAO2/FIO2 FOR RESCUE MEASURES IN COVID-RELATED ARDS

SESSION TITLE: ECMO and ARDS in COVID-19 InfectionsSESSION TYPE: Rapid Fire Original InvPRESENTED ON: 10/17/2022 12:15 pm - 1:15 pmPURPOSE: COVID-related acute respiratory distress syndrome (ARDS) is associated with significant morbidity and mortality. PaO2/Fio2 (PFR) is a prognostic and severity marker for ARDS. Other markers have been posited for ARDS. PEEP Index (PIx) [PEEP/PFR] or [(PEEP*Fio2)/PaO2] could serve as a new discriminatory marker to assess rescue therapies such as proning or ECMO referral.METHODS: Retrospective cohort study of all intubated COVID-19 patients with ARDS hospitalized at our institution between February 5th – May 11th, 2020. ARDS were calculated within first 24 hours of worst PaO2/FIO2 and their associated PEEP with bilateral infiltrates on Chest X-ray manually confirmed within 24hours of intubation fulfilling 2012 Berlin criteria. Outcomes of interest were all-cause in-hospital mortality, need for pronation and paralysis use. Binomial logistic regression with ROC curve were performed for univariate association for outcomes of interest. Cox proportional hazard regression modeling was performed and adjusted for potential confounders. PFR was transformed into a denominator of itself to reflect a direct proportional relationship.RESULTS: Data was analyzed from 113 hospitalized COVID-19 patients with identified ARDS. Mean age was 56.4 (STD 14.4); 24% (27/113) were female. Median BMI was 30.3 [IQR 48.5,65.5]. Mean Tidal Volume (Vt) was 430 (STD 54). 64% (72/113) were compliant with low Vt (=<6mL/kg based on IBW). Median PFR 125 [IQR 99,192]. Mortality was 66% (74/113). 44% (50/113) were proned. 62% (70/113) required paralysis. PEEP Index outperformed PFR for discrimination for proning use: AUC 0.73 [95%CI 0.63,0.82], p< 0.005; vs AUC 0.674 [95%CI 0.58,0.77], p= 0.02. PEEP Index performed mildy better than PFR for discrimination of requiring paralytic use in ARDS with AUC 0.68 [95% 0.57,0.78], p< 0.05; vs AUC 0.62 [95%CI 0.51,0.73], p<0.05. APACHE2 score showed poor discrimination for both proning and paralytic use (AUC= 0.46 [95%CI 0.35,0.56]; p=0.43 and respectively, AUC=0.45 [95%CI 0.34,0.56]; p=0.36). After adjusting for confounders, PEEP Index nor PFR didn’t for predict for mortality (p>0.05); however, our sample was not powered.CONCLUSIONS: PEEP Index (PIx) is a novel tool that can serve as a better discriminatory function to evaluate patients with ARDS in the ICU who will require proning in comparison to traditional used PFR.CLINICAL IMPLICATIONS: PEEP Index (PIx) can serve as an easy alternative calculation to Oxygenation Index (OI) [(FiO2 x PAW) / PaO2] to identify patients that would benefit from early proning and other rescue therapies. Further studies are required to compare and validate PIx and OI prospectively as well as benefit cut-off points between proning and ECMO.DISCLOSURES: No relevant relationships by Perminder GulaniNo relevant relationships by Manuel Hache Marliereno disclosure on file for Adarsh Katamreddy;No relevant relationships by Hyomin LimNo relevant relationships by Marzio NapolitanoNo relevant relationships by Leonidas PalaiodimosNo relevant relationships by Anika Sasidharan NairNo relevant relationships by Jee Young You SESSION TITLE: ECMO and ARDS in COVID-19 Infections SESSION TYPE: Rapid Fire Original Inv PRESENTED ON: 10/17/2022 12:15 pm - 1:15 pm PURPOSE: COVID-related acute respiratory distress syndrome (ARDS) is associated with significant morbidity and mortality. PaO2/Fio2 (PFR) is a prognostic and severity marker for ARDS. Other markers have been posited for ARDS. PEEP Index (PIx) [PEEP/PFR] or [(PEEP*Fio2)/PaO2] could serve as a new discriminatory marker to assess rescue therapies such as proning or ECMO referral. METHODS: Retrospective cohort study of all intubated COVID-19 patients with ARDS hospitalized at our institution between February 5th – May 11th, 2020. ARDS were calculated within first 24 hours of worst PaO2/FIO2 and their associated PEEP with bilateral infiltrates on Chest X-ray manually confirmed within 24hours of intubation fulfilling 2012 Berlin criteria. Outcomes of interest were all-cause in-hospital mortality, need for pronation and paralysis use. Binomial logistic regression with ROC curve were performed for univariate association for outcomes of interest. Cox proportional hazard regression modeling was performed and adjusted for potential confounders. PFR was transformed into a denominator of itself to reflect a direct proportional relationship. RESULTS: Data was analyzed from 113 hospitalized COVID-19 patients with identified ARDS. Mean age was 56.4 (STD 14.4); 24% (27/113) were female. Median BMI was 30.3 [IQR 48.5,65.5]. Mean Tidal Volume (Vt) was 430 (STD 54). 64% (72/113) were compliant with low Vt (=<6mL/kg based on IBW). Median PFR 125 [IQR 99,192]. Mortality was 66% (74/113). 44% (50/113) were proned. 62% (70/113) required paralysis. PEEP Index outperformed PFR for discrimination for proning use: AUC 0.73 [95%CI 0.63,0.82], p< 0.005; vs AUC 0.674 [95%CI 0.58,0.77], p= 0.02. PEEP Index performed mildy better than PFR for discrimination of requiring paralytic use in ARDS with AUC 0.68 [95% 0.57,0.78], p< 0.05; vs AUC 0.62 [95%CI 0.51,0.73], p<0.05. APACHE2 score showed poor discrimination for both proning and paralytic use (AUC= 0.46 [95%CI 0.35,0.56]; p=0.43 and respectively, AUC=0.45 [95%CI 0.34,0.56]; p=0.36). After adjusting for confounders, PEEP Index nor PFR didn’t for predict for mortality (p>0.05); however, our sample was not powered. CONCLUSIONS: PEEP Index (PIx) is a novel tool that can serve as a better discriminatory function to evaluate patients with ARDS in the ICU who will require proning in comparison to traditional used PFR. CLINICAL IMPLICATIONS: PEEP Index (PIx) can serve as an easy alternative calculation to Oxygenation Index (OI) [(FiO2 x PAW) / PaO2] to identify patients that would benefit from early proning and other rescue therapies. Further studies are required to compare and validate PIx and OI prospectively as well as benefit cut-off points between proning and ECMO. DISCLOSURES: No relevant relationships by Perminder Gulani No relevant relationships by Manuel Hache Marliere no disclosure on file for Adarsh Katamreddy; No relevant relationships by Hyomin Lim No relevant relationships by Marzio Napolitano No relevant relationships by Leonidas Palaiodimos No relevant relationships by Anika Sasidharan Nair No relevant relationships by Jee Young You