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1.
Front Med (Lausanne) ; 9: 1027586, 2022.
Article in English | MEDLINE | ID: covidwho-2109790

ABSTRACT

Background: Coronavirus disease 2019 (COVID-19) has resulted in high hospitalization rates worldwide. Acute kidney injury (AKI) in patients hospitalized for COVID-19 is frequent and associated with disease severity and poor outcome. The aim of this study was to investigate the incidence of kidney replacement therapy (KRT) in critically ill patients with COVID-19 and its implication on outcome. Methods: We retrospectively analyzed all COVID-19 patients admitted to the Department of Intensive Care Medicine at the University Medical Center Hamburg-Eppendorf (Germany) between 1 March 2020 and 31 July 2021. Demographics, clinical parameters, type of organ support, length of intensive care unit (ICU) stay, mortality and severity scores were assessed. Results: Three-hundred critically ill patients with COVID-19 were included. The median age of the study population was 61 (IQR 51-71) years and 66% (n = 198) were male. 73% (n = 219) of patients required invasive mechanical ventilation. Overall, 68% (n = 204) of patients suffered from acute respiratory distress syndrome and 30% (n = 91) required extracorporeal membrane oxygenation (ECMO). We found that 46% (n = 139) of patients required KRT. Septic shock (OR 11.818, 95% CI: 5.941-23.506, p < 0.001), higher simplified acute physiology scores (SAPS II) (OR 1.048, 95% CI: 1.014-1.084, p = 0.006) and vasopressor therapy (OR 5.475, 95% CI: 1.127-26.589, p = 0.035) were independently associated with the initiation of KRT. 61% (n = 85) of patients with and 18% (n = 29) without KRT died in the ICU (p < 0.001). Cox regression found that KRT was independently associated with mortality (HR 2.075, 95% CI: 1.342-3.208, p = 0.001) after adjusting for confounders. Conclusion: Critically ill patients with COVID-19 are at high risk of acute kidney injury with about half of patients requiring KRT. The initiation of KRT was associated with high mortality.

2.
Int Immunopharmacol ; 113(Pt B): 109428, 2022 Nov 07.
Article in English | MEDLINE | ID: covidwho-2095518

ABSTRACT

Coronavirus disease 2019 (COVID-19) outbreak has become a global public health emergency and has led to devastating results. Mounting evidence proposes that the disease causes severe pulmonary involvement and influences different organs, leading to a critical situation named multi-organ failure. It is yet to be fully clarified how the disease becomes so deadly in some patients. However, it is proven that a condition called "cytokine storm" is involved in the deterioration of COVID-19. Although beneficial, sustained production of cytokines and overabundance of inflammatory mediators causing cytokine storm can lead to collateral vital organ damages. Furthermore, cytokine storm can cause post-COVID-19 syndrome (PCS), an important cause of morbidity after the acute phase of COVID-19. Herein, we aim to explain the possible pathophysiology mechanisms involved in COVID-19-related cytokine storm and its association with multi-organ failure and PCS. We also discuss the latest advances in finding the potential therapeutic targets to control cytokine storm wishing to answer unmet clinical demands for treatment of COVID-19.

3.
American Journal of Transplantation ; 22(Supplement 3):948, 2022.
Article in English | EMBASE | ID: covidwho-2063503

ABSTRACT

Purpose: Currently there are no UNOS guidelines regarding the selection criteria required for simultaneous heart-kidney transplant recipients (SHKT). As of 2018 our center has begun performing these dual transplants for appropriate candidates. We report on the criteria devised to guide SHKT candidate selection at our institution and the subsequent clinical outcomes. Method(s): This is a single center, retrospective study of 26 patients who received SHKT at our institution from Dec 2018 to Oct 2021. A multidisciplinary team composed of heart and kidney transplant medical and surgical members determined appropriate recipient-donor SHKT candidate pairs. Selection criteria for SHKT was established by our kidney transplant group and included an evaluation for chronic kidney disease (CKD) or evidence of acute kidney injury (AKI) with a prolonged course or requiring renal replacement therapy (RRT). The surgery was conducted according to our institution's standardized protocols. The majority of patients received IL2-RA and methylprednisolone induction therapy, and all patients received triple immunosuppression therapy with prednisone, mycophenolate mofetil and tacrolimus. Adjustments in long term therapy were made in collaboration between the heart and kidney transplant teams. Result(s): From Dec 2018 to Oct 2021, 26 patients underwent SHKT at our institution. 24 patients (92%) carried a diagnosis of chronic kidney disease (CKD) as defined as an eGFR <60 ml/min/1.73m2 for at least 90 days on at least two separate tests. Clinical risk factors for CKD, the presence of proteinuria, and renal imaging data were also taken into consideration when determining a diagnosis of CKD. Two patients (8%) carried a diagnosis of stage III AKI for at least 4 weeks and required renal replacement therapy during their hospital course. Of our 26 patients, one patient received a DCD donor and 12 patients (46%) received hepatitis C donors. 25 patients (96%) received induction therapy with IL2-RA. During the first 3 months post-transplant, the only patient who received ATG had 7 severe infections;11 patients (44%) and 13 patients (52%) who received IL2 -RA had no infections and <= 4 mild infections, respectively. One patient died due to COVID 19 pneumonia complicated by multisystem organ failure. For a median follow up period of 410 (187-707) days, 8% patients in the IL2-RA induction cohort experienced a 2R/3A heart rejection, 8% patients remained on HD due to primary kidney graft nonfunction, and the survival rate was 96%. Conclusion(s): UNOS guidelines regarding selection criteria for SHKT are an important next step in the care of heart transplant candidates with kidney disease, particularly as the number of SHKT performed yearly increase. Compared to the literature, our data supports the use of standardized criteria for SHKT selection and the use of IL2- RA as an induction strategy with excellent patient survival.

4.
Cardiology in the Young ; 32(Supplement 2):S268, 2022.
Article in English | EMBASE | ID: covidwho-2062093

ABSTRACT

Background and Aim: Kawasaki-like (multisystem inflammatory) syndrome associated with SARS-CoV-2 infection is characterized by acute severe systemic vasculitis, often with multi-organ dys-function and cardiac involvement. Although most patients recover, long-term outcomes are poorly studied [Gema de Lama Caro-Paton et al., 2021;Guimaraes D. et et al., 2021;Sharma C. et al., 2021]. Method(s): We analyzed the results of laboratory, clinical, radiologi-cal, ECG and EchoCG data in the dynamic observation of 15 patients (M 9, 1.5-16 yo, m = 7) in 3 months after the suffered MIS-C. Result(s): At the disease onset high refractory fever was observed in all cases, symptoms of Kawasaki disease in 12 (80%) of them, shock with multi-organ dysfunction-in 8 (53.3%), including symptoms of acute heart failure-in 5 (33%), concomitant in two cases with severe left ventricular dilatation with low LV EF. Myocardial damage was seen in 11 patients (73%), pericarditis in 12 (80%), coronary dilatation in two (13%);troponin level increased in 5 (33%), CK-MB-in 5 (33%), BNP-in 3 (25%). After 3 months, there were no signs of myocardial dysfunction and/or cardiomegaly in any patient, troponin and BNP levels normalized in all patients, a moderate increase of CK-MB was seen in 8 (53%), and coronary dilatation persisted in one patient. Arrhythmias were documented at onset in 9 (60%) patients, 3 (20%) after 3 months (p = 0.028). Conclusion(s): preliminary results of follow-up of children after MIS-C demonstrate favorable course in the majority of patients by clinical, laboratory, ECG and echocardiographic data. Further observations are needed to determine the long-term prognosis.

5.
Chest ; 162(4):A2300, 2022.
Article in English | EMBASE | ID: covidwho-2060934

ABSTRACT

SESSION TITLE: Rare Cases of Nervous System and Thrombotic Complication Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Covid 19 virus has impacted nearly 450 million people across the globe;ranging from an asymptomatic carrier state to respiratory symptoms, cardiovascular symptoms, hematologic manifestations and multiorgan failure to death. Thrombotic events are one of its devastating complications. CASE PRESENTATION: A 66 year old man with a history of diabetes mellitus, hypertension and 30 pack years smoking history presented to the emergency room with hypoxia and altered mental status. On exam, his GCS was 8/15 and oxygen saturation was 85% on room air. He was subsequently intubated. CTA chest demonstrated bilateral diffuse ground glass opacities and left pulmonary embolism (PE). CT abdomen and pelvis showed multifocal infarcts in the right kidney with findings suggestive of renal artery thrombosis. Initial platelet count was 80,000/ul with creatinine of 3.9 mg/dl and creatine kinase (CK) of 3977 u/l. His INR was 1.4. Patient was not a candidate for thrombolysis given his thrombocytopenia. He was started on intravenous (IV) heparin and given IV hydration. On day 3 of his admission, he developed dry gangrene of the toes. Ankle brachial index of the right lower extremity (LE) was 1.16 and left LE was 0. Duplex ultrasonography of left LE showed mid to distal popliteal artery thrombus occluding below knee popliteal and tibial arteries. Echocardiogram showed ejection fraction of 55% and bubble study was negative for any intra atrial or pulmonary shunting. On day 4 of his admission, he developed oliguria and his gangrene got worse. His platelet counts decreased to 36,000/ul. Other pertinent labs showed INR 1.2, PT 15.3, PTT 34, D dimer 14.82, fibrinogen 498, CK 6434 mg/dl, hemoglobin 13.2 g/dl, haptoglobin 243 mg/dl and LDH 1041 U/l. Given his poor prognosis in the setting of ventilator dependent respiratory failure, multiple thrombosis and kidney failure requiring hemodialysis, the family decided to withdraw care. DISCUSSION: There are multiple hypotheses of thrombus formation in Covid 19 infection such as interleukin 6 and other cytokines induced endothelial injury, angiogenesis and elevated prothrombotic factors such as factor VIII and fibrinogen. Our patient had PE, renal artery thrombosis and popliteal artery thrombosis. Despite being on full dose anticoagulation, he developed gangrene of the toes. His lab results were not consistent with disseminated intravascular coagulation, thrombotic thrombocytopenic purpura and he was not known to have any baseline hypercoagulable disorder. He did not have any intra cardiac shunts. Hence, it is most likely Covid 19 induced multiple arterial and venous thrombosis. CONCLUSIONS: The treatment of Covid 19 related thrombosis has become very challenging especially in the setting of multiple clots. It is crucial to have large multicenter studies to investigate vascular complications of Covid-19 and to formulate management strategies to ensure good patient outcomes. Reference #1: https://www.nejm.org/doi/full/10.1056/nejmoa2015432 Reference #2: https://journal.chestnet.org/article/S0012-3692(21)01126-0/fulltext DISCLOSURES: No relevant relationships by Devashish Desai No relevant relationships by Swe Swe Hlaing no disclosure on file for Jean Marie Koka;No relevant relationships by Hui Chong Lau No relevant relationships by Subha Saeed No relevant relationships by Anupam Sharma No relevant relationships by Muhammad Moiz Tahir

6.
Chest ; 162(4):A1100, 2022.
Article in English | EMBASE | ID: covidwho-2060768

ABSTRACT

SESSION TITLE: Studies on COVID-19 Infections Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/18/2022 01:30 pm - 02:30 pm PURPOSE: COVID-19 infection has a wide spectrum of clinical presentation ranging from asymptomatic carriers to severe critical illness associated with high morbidity and mortality. Although severe COVID-19 disease is associated primarily with pulmonary dysfunction and hypoxemia, many patients with lung disease can be supported by invasive mechanical ventilation allowing for other causes or complications to be the primary factor leading to death. The contribution of pulmonary dysfunction to the primary cause of death is not well-described. METHODS: We performed a retrospective cohort study of adult patients (age ≥ 18 years) admitted to the MICU at Los Angeles County + University of Southern California (LAC + USC) hospital from April 2020 to December 2020 with a primary diagnosis of COVID-19 pneumonia associated with documented in-hospital death. Data including baseline patient characteristics, primary cause of death and/or circumstance prior to withdrawal of care, and disease course were collected. The primary organ system responsible for death was defined as the organ dysfunction that most directly resulted in the patient’s death or impacted the decision for withdrawal of life support with details adapted from Ketcham, et al (Crit Care, 2020). RESULTS: We identified 86 patients who were admitted to the ICU that met inclusion criteria for review, of which 75% were male and 93% were Latino/Hispanic. Mean age on admission was 64 years. Of the 86 patients, 47 (54%) died from a primary pulmonary cause, 28 (32%) died from sepsis, 5 (6%) died from neurologic causes, and 4 (5%) died from either renal or hemorrhagic causes. Of the 47 patients who died primarily from pulmonary causes, 34 (72%) died from hypoxemic respiratory failure, 8 (17%) died from hypercapnic respiratory failure, and 5 (11%) died from combined respiratory failure. Of the 28 patients who died primarily from sepsis, 13 (46%) died from pneumonia, 7 (25%) died from fungemia, and 3 (11%) died from bacteremia with an identified source. Overall, 58 (67%) patients had multi-organ failure at time of death. Mean time from symptom onset to death was 27 days. Of the 69 patients who were intubated, mean times from admission to intubation and intubation to death was 4 and 19 days respectively. Only 1 patient who died underwent tracheostomy. CONCLUSIONS: We found that pulmonary dysfunction was the primary cause of death in the first year of the pandemic in our patient population at our single center MICU. Future studies are needed to further evaluate the primary cause of death in COVID-19 infection throughout the pandemic as medical management evolved and virus variant changed with time. CLINICAL IMPLICATIONS: Our study confirmed that a majority of patients with severe COVID-19 pneumonia died from hypoxemic respiratory failure. Further studies regarding COVID-19 interventions should focus on therapies to improve oxygenation. DISCLOSURES: No relevant relationships by Christopher Do No relevant relationships by Luis Huerta No relevant relationships by Janice Liebler

7.
Chest ; 162(4):A1035, 2022.
Article in English | EMBASE | ID: covidwho-2060758

ABSTRACT

SESSION TITLE: Challenging Cases of Hemophagocytic Lymphohistiocytosis SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Hemophagocytic lymphohistiocytosis (HLH) is a rare syndrome involving pathologic immune activation that is often fatal. The link between the cytokine storm related to COVID-19 and development of HLH has been reported since the onset of the pandemic, but little is known about clinical manifestations of HLH, thereby delaying treatment. CASE PRESENTATION: A 50 year-old male presented with a several day history of progressive weakness in the setting of missed dialysis session. Medical history was significant for ESRD on dialysis and diastolic heart failure (EF 35%). Initial vitals were unremarkable. Physical exam was notable for peripheral edema bilaterally. Laboratory studies were consistent with hyperkalemia, elevated ferritin (28,383) and elevated liver function tests. COVID-19 PCR was positive upon admission. Chest x-ray, CTA chest and a right upper quadrant ultrasound were unremarkable. He was admitted to the medical ICU for emergent dialysis. Soon after arrival to the ICU, he became lethargic and confused with increasing oxygen requirements and a subsequent a code blue was called. Cardiopulmonary resuscitation was immediately initiated, with a first rhythm consistent with ventricular fibrillation. He was shocked and placed on an amiodarone infusion with return of spontaneous circulation. TTE revealed a severely reduced EF <10%. Despite initiation of advanced COVID-19 therapies with Solu-Medrol and tocilizumab he remained ventilator dependent. Due to hemodynamic instability and persistent metabolic acidosis, he was transitioned to continuous renal replacement. Further blood work showed worsening inflammatory markers (ferritin 33,500, LDH 6981). Because of the significantly elevated ferritin, there were concerns for possible HLH. Triglycerides and IL-2 receptor were 395 mg/dL and 9300 pg/mL respectively. Total NK cells were decreased to 1.2%. He remained persistently unstable despite aggressive measures. He suffered a second cardiopulmonary arrest, which was unable to achieve return of spontaneous circulation and he ultimately passed away. DISCUSSION: HLH is characterized by uncontrolled activation and proliferation of benign macrophages in reticuloendothelial organs. This results in histiocytic hemophagocytosis, worsening peripheral blood cytopenia(s), cytokine storm, and cytokine mediated biochemical alteration ultimately culminating in multiorgan dysfunction and disseminated intravascular coagulation. Although a distinctive constellation of features has been described for HLH, diagnosis remains challenging as patients have diverse presentations associated with a variety of triggers. CONCLUSIONS: As HLH is a medical emergency with poor prognosis, prompt recognition and early treatment is crucial for improving clinical outcomes. We hope this case will create increased awareness and timely diagnosis of cytokine storm syndromes in patients with severe COVID-19 infection. Reference #1: Meazza Prina M, Martini F, Bracchi F, Di Mauro D, Fargnoli A, Motta M, Giussani C, Gobbin G, Taverna M, D'Alessio A. Hemophagocytic syndrome secondary to SARS-Cov-2 infection: a case report. BMC Infect Dis. 2021 Aug 13;21(1):811. doi: 10.1186/s12879-021-06532-7. PMID: 34388982;PMCID: PMC8361241. Reference #2: Schnaubelt, Sebastian MDa,*;Tihanyi, Daniel MDb;Strassl, Robert MDc;Schmidt, Ralf MDc;Anders, Sonja MDb;Laggner, Anton N. MDa;Agis, Hermine MDd;Domanovits, Hans MDa Hemophagocytic lymphohistiocytosis in COVID-19, Medicine: March 26, 2021 - Volume 100 - Issue 12 - p e25170 doi: 10.1097/MD.0000000000025170 DISCLOSURES: No relevant relationships by Garrett Fiscus No relevant relationships by Niala Moallem No relevant relationships by Resham Pawar

8.
Chest ; 162(4):A951, 2022.
Article in English | EMBASE | ID: covidwho-2060739

ABSTRACT

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

9.
Chest ; 162(4):A950, 2022.
Article in English | EMBASE | ID: covidwho-2060738

ABSTRACT

SESSION TITLE: Extraordinary Cardiovascular Reports SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 01:35 pm - 02:35 pm INTRODUCTION: The COVID-19 pandemic has resulted in millions of deaths worldwide. Many cases involved a primary pulmonary process, yet myocarditis associated with COVID-19 has been observed.1 We present a novel case of rapidly progressive fulminant peri-myocarditis with minimal lung involvement in acute COVID-19 infection. CASE PRESENTATION: A 39-year-old female with no medical history presented with chest pain and dyspnea with an acute COVID-19 infection. She had a brief cardiac arrest with rapid ROSC and no intubation. Chest CT angiogram showed essentially normal pulmonary parenchyma and moderate pericardial effusion. EKG showed sinus tachycardia with global ST segment elevation. An echocardiogram showed an ejection fraction (EF) of 25% with a moderate sized pericardial effusion and right ventricle collapse. She was transferred for emergent drainage of the effusion to our institution. Her circulatory shock initially improved following pericardial drainage, yet she declined warranting increasing vasopressor and inotropic support. An emergent echo showed an EF of less than 10% and no re-accumulation of pericardial fluid. It was clear that the patient required mechanical circulatory support (MCS) and was transferred to the catheterization lab. While in the lab, the patient suffered cardiac arrest and an Impella device was placed during prolonged ACLS without achieving ROSC. Venoarterial ECMO cannulation was then performed. She was transferred to a cardiac transplant center where she later developed multi-organ failure leading to death. DISCUSSION: While COVID-19 has been shown to affect multiple organs apart from the lungs, this case was notable due to minimal pulmonary involvement. The patient's manifestation of her infection was almost entirely cardiac in nature. MCS was discussed in the catheterization lab at the time of pericardial drain insertion. The decision was made to not pursue MCS as the patient's shock had improved. Additionally, the patient did not undergo pulmonary arterial catheter (PAC) placement. Prompt placement of a PAC has been associated with early access to MCS and reduced in-hospital mortality.2 Perhaps we would have obtained MCS earlier if PAC data supported this intervention before the patient deteriorated. It will be important to consider primary cardiac manifestations of COVID-19 infection and early consideration of invasive hemodynamic monitoring to identify a need for timely MCS. CONCLUSIONS: We present the first reported case of fulminant peri-myocarditis in the absence of acute hypoxemic respiratory failure or radiographic pulmonary parenchymal lung abnormality. Isolated rapidly progressive cardiogenic shock secondary to COVID-19 associated peri-myocarditis is a phenomenon important for critical care clinicians to be aware of during this pandemic. One should have a low threshold to establish invasive hemodynamic monitoring and consideration for early MCS in these cases. Reference #1: Siripanthong B, Nazarian S, Muser D, et al. Recognizing COVID-19-related myocarditis: The possible pathophysiology and proposed guideline for diagnosis and management. doi:10.1016/j.hrthm.2020.05.001 Reference #2: Osman M, Syed M, Patel B, et al. Invasive Hemodynamic Monitoring in Cardiogenic Shock Is Associated With Lower In-Hospital Mortality. Journal of the American Heart Association J Am Heart Assoc. 2021;10:21808. doi:10.1161/JAHA.121.021808 DISCLOSURES: No relevant relationships by Samuel Bullick No relevant relationships by Jonathan Greenberg No relevant relationships by Scott Slusarenko

10.
Chest ; 162(4):A918, 2022.
Article in English | EMBASE | ID: covidwho-2060728

ABSTRACT

SESSION TITLE: Critical Renal and Endocrine Disorders Case Report Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: About 7% of acute pancreatitis (AP) cases are caused by hypertriglyceridemia (HTG). In such cases bowel rest, IV fluids, symptomatic therapy, and triglyceride (TG) lowering interventions are initiated. Plasmapheresis is one of the treatment options, but it has specific indications. We present a case of severe hypertriglyceridemia-induced pancreatitis that required plasmapheresis. CASE PRESENTATION: A 30 y/o man with type 2 diabetes, hyperlipidemia, multiple previous admissions for HTG-AP, presented with severe abdominal pain, nausea, and vomiting x 1 day. On admission, he was tachycardic, hypotensive, afebrile, SpO2 > 96% on RA. Labs: Glu 491 mg/dL, TG > 1000 mg/dL, Cholesterol 509 mg/dL, Lipase 987 U/L, Cr/BUN 2.4 mg/dL /20 mg/dL, VBG pH 7.25/PCO2 36.2 mmHg/PO2 19.4 mmHg/Ca 0.8/lactate 5.6;WBC 13.07 K/cm;COVID PCR positive. CXR: diffuse patchy opacities. CTAP with contrast was deferred because of AKI. He was admitted to the ICU and started on insulin drip with no improvement over 24hrs. He was still acidotic, Ca persistently low, TG still >1000, and kidney function worsened. Plasmapheresis was initiated. After one session his TG lowered to 700. He was restarted on insulin drip and in the next 24hr TG decreased to < 500 and metabolic acidosis resolved. Once AKI resolved, CT abdomen/pelvis with contrast confirmed acute pancreatitis, with focal hypodensities within the uncinate process and the proximal body, concerning infarcts as well as large phlegmon surrounding the pancreas, but no evidence of necrotizing or hemorrhagic pancreatitis. His hospital course was complicated with sepsis and DVT, which resolved with therapy. He was discharged home with TG lowering agents, Apixaban, and his previous T2DM regimen. DISCUSSION: Plasmapheresis is indicated in patients with severe HTG (>1000- 2000 mg/dl), severe HTG-AP, and when standard treatment options are inadequate. It lowers the lipid levels and removes proinflammatory markers and cytokines stopping further inflammation and damage to the pancreas and other organs faster compared to conservative therapy. Most patients need only one session which lowers TG level by 50-80%, as seen in our patient. CONCLUSIONS: Plasmapheresis should be considered in cases of HTGP with worrisome features such as lactic acidosis, hypocalcemia, worsening inflammation, and multi organ failure. Reference #1: Rajat Garg, Tarun Rustagi, "Management of Hypertriglyceridemia Induced Acute Pancreatitis", BioMed Research International, vol. 2018, Article ID 4721357, 12 pages, 2018. https://doi.org/10.1155/2018/4721357 Reference #2: Pothoulakis I, Paragomi P, Tuft M, Lahooti A, Archibugi L, Capurso G, Papachristou GI. Association of Serum Triglyceride Levels with Severity in Acute Pancreatitis: Results from an International, Multicenter Cohort Study. Digestion. 2021;102(5):809-813. doi: 10.1159/000512682. Epub 2021 Jan 21. PMID: 33477149. Reference #3: Gavva C, Sarode R, Agrawal D, Burner J. Therapeutic plasma exchange for hypertriglyceridemia induced pancreatitis: A rapid and practical approach. Transfus Apher Sci. 2016 Feb;54(1):99-102. doi: 10.1016/j.transci.2016.02.001. Epub 2016 Feb 20. PMID: 26947356. DISCLOSURES: No relevant relationships by Adam Adam No relevant relationships by Moses Bachan No relevant relationships by Chen Chao No relevant relationships by Vaishali Geedigunta No relevant relationships by Zinobia Khan No relevant relationships by Jelena Stojsavljevic

11.
Chest ; 162(4):A875, 2022.
Article in English | EMBASE | ID: covidwho-2060715

ABSTRACT

SESSION TITLE: Unusual Critical Care SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 10:15 am - 11:10 am INTRODUCTION: Babesiosis can have a clinical spectrum ranging from mild illness in most cases to more severe manifestations in immunosuppressed individuals or in those with high-grade parasitemia. This patient had severe babesiosis resulting in ARDS and shock in spite of being immunocompetent and having low-grade parasitemia, making it a rare presentation. CASE PRESENTATION: A 49-year-old, previously healthy woman, was admitted with high-grade fevers. Physical exam findings were normal, except for fever (103 F). Initial lab results were significant for hemolytic anemia and thrombocytopenia. Chest radiography was normal. Other microbiology studies, including COVID-19, were negative. Empiric antibiotic therapy with piperacillin-tazobactam and doxycycline was started. Peripheral smear identified rare, minute intracellular ring forms, suspicious for babesia. IV azithromycin and oral atovaquone were started. PCR was done to confirm the diagnosis and Babesia microti DNA was detected. As peripheral smear showed parasitemia of only 1% (percentage of red blood cells infected), exchange transfusion was not considered as a treatment option. Two days after admission, worsening hemodynamic and respiratory status was noted with increasing oxygen requirements. CT chest now revealed diffuse interstitial infiltrates. ARDS ensued and the patient was intubated and started on mechanical ventilation with vasopressor support. Immunodeficiency workup was normal. In view of clinical deterioration, the antimicrobials were switched from atovaquone and azithromycin to IV clindamycin and quinidine for 14 days. After a protracted ICU stay, the patient showed gradual clinical improvement, parasitemia resolved, and she was eventually discharged to a rehabilitation facility. DISCUSSION: Babesiosis is a tick-borne infectious disease endemic to the North-East and Midwest United States. Majority of the infections are self-limited. However, in immunocompromised individuals and in those with high-grade parasitemia (>10%), it manifests as a severe illness with ARDS, severe hemolysis, or shock. Diagnosis is made by identifying parasites on thin peripheral blood smears with Giemsa/Wright stains. PCR can be used for species identification and for confirming the diagnosis in cases with low-grade parasitemia (<4%). IV azithromycin plus oral atovaquone is the preferred initial regimen and IV clindamycin plus quinidine is an alternative combination that can be used in severe infection. Red blood cell exchange transfusion can be considered in patients with high-grade parasitemia or organ failure. CONCLUSIONS: Babesiosis can very rarely cause ARDS and shock in immunocompetent patients with low-grade parasitemia. Prompt diagnosis and escalation of antimicrobial regimens to clindamycin and quinidine in such cases can lead to improved clinical outcomes. Exchange transfusion can serve as a treatment option in patients with high-grade parasitemia. Reference #1: Ord RL, Lobo CA. Human babesiosis: Pathogens, prevalence, diagnosis, and treatment. Current clinical microbiology reports. 2015 Dec;2(4):173-81. Reference #2: Ripoll JG, Rizvi MS, King RL, Daniels CE. Severe Babesia microti infection presenting as multiorgan failure in an immunocompetent host. Case Reports. 2018 May 30;2018:bcr-2018. Reference #3: Sanchez E, Vannier E, Wormser GP, Hu LT. Diagnosis, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: a review. Jama. 2016 Apr 26;315(16):1767-77. DISCLOSURES: No relevant relationships by Shankar Chhetri No relevant relationships by Vasudev Malik Daliparty No relevant relationships by Preethi Dendi No relevant relationships by samer talib

12.
Chest ; 162(4):A786, 2022.
Article in English | EMBASE | ID: covidwho-2060688

ABSTRACT

SESSION TITLE: Rare Cases of Nervous System and Thrombotic Complication Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Rivaroxaban is a dose-dependent inhibitor of factor Xa. It is approved by the FDA to help reduce the risk of blood clots. Although bioavailability is not significantly affected at lower doses (80-100%), bioavailability at higher doses (≥15 mg) is as low as 66% when given without food [1] [3]. Here, we present a patient with poor oral intake who developed deep vein thrombosis (DVT) while on high dose Xarelto. CASE PRESENTATION: Our patient was a 48-year-old male with a history of pulmonary embolism diagnosed two months prior to admission (on 20 mg rivaroxaban daily at home) and morbid obesity who presented with dyspnea, fever, and decreased appetite. His viral PCR was positive for COVID-19, and CT angiogram showed multifocal ground glass opacities but was negative for pulmonary embolism. He was severely hypoxic on room air and required noninvasive ventilatory support in the intensive care unit. He was treated with remdesivir, dexamethasone, and baricitinib. His food intake was extremely poor due to near continuous use of noninvasive ventilation and decreased appetite. A nasogastric (NG) tube was offered, but the patient declined and elected to continue diminished oral feedings. He was able to take all of his home medications including rivaroxaban during this time. On day four, clinical nutrition was consulted because he had 3% loss of body weight. On day seven, the patient developed a fever of 101.6° F. Ultrasound of his lower extremities revealed acute DVTs in his left popliteal vein, posterior tibial vein, and peroneal vein. His anticoagulation was switched to full-dose enoxaparin and a NG tube was placed. On day ten, he was intubated due to worsening hypoxia. Unfortunately, the patient deteriorated into multiorgan failure and died on day seventeen. DISCUSSION: The latest expert guidelines suggest that direct oral anticoagulants (DOAC) should be used over vitamin K antagonists (VKA) in patients with acute venous thromboembolism (VTE) due to lower rates of major bleeding and recurrent VTE as well as convenience. Although VKAs are preferred in situations with extreme weight and renal impairment, DOACs have been proven to be effective for the large majority of patients [2]. Unlike rivaroxaban, the bioavailabilities of other DOACs like apixaban, edoxaban, and dabigatran are all unaffected by food and should be preferred in patients with tenuous oral intake [3]. It is well known that COVID-19 can produce a hypercoagulable state. This factor, combined with our patient's predisposition to blood clots and poor appetite, ended up precipitating new onset VTEs in his left leg despite rivaroxaban therapy. CONCLUSIONS: In patients with decreased oral intake, DOACs other than rivaroxaban should be considered. Patients should be briefed on the importance of taking high dose rivaroxaban with food. Our goal is to bring awareness to providers about this significant pharmacodynamic property of rivaroxaban. Reference #1: Mueck W, Stampfuss J, Kubitza D, Becka M. Clinical pharmacokinetic and pharmacodynamic profile of rivaroxaban. Clin Pharmacokinet. 2014 Jan;53(1):1-16. doi: 10.1007/s40262-013-0100-7. PMID: 23999929;PMCID: PMC3889701. Reference #2: Stevens SM, Woller SC, Baumann Kreuziger L, Bounameaux H, Doerschug K, Geersing GJ, Huisman MV, Kearon C, King CS, Knighton AJ, Lake E, Murin S, Vintch JRE, Wells PS, Moores LK. Executive Summary: Antithrombotic Therapy for VTE Disease: Second Update of the CHEST Guideline and Expert Panel Report. Chest. 2021 Dec;160(6):2247-2259. doi: 10.1016/j.chest.2021.07.056. Epub 2021 Aug 2. PMID: 34352279. Reference #3: Lexicomp Online. Copyright © 1978-2022 Lexicomp, Inc. DISCLOSURES: No relevant relationships by Rishika Bajaj No relevant relationships by Ann Hylton No relevant relationships by Roger McSharry No relevant relationships by Krupa Solanki

13.
Chest ; 162(4):A755, 2022.
Article in English | EMBASE | ID: covidwho-2060683

ABSTRACT

SESSION TITLE: COVID-19 Co-Infections SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Human cytomegalovirus (CMV) is a herpesvirus with a high prevalence that causes latent disease in immunocompetent hosts. It is an important opportunistic infection with a variety of clinical manifestations, including pneumonia, in immunocompromised patients.[1] CASE PRESENTATION: A 45-year-old man with no past medical history presented with fever and dyspnea and was positive for coronavirus disease 2019 (COVID-19). He developed acute respiratory distress syndrome (ARDS) and was intubated 13 days after presentation, but developed refractory hypoxemia requiring veno-venous extracorporeal membrane oxygenation (ECMO) (cannulated 16 days after presentation). He received a 5-day course of remdesivir and 10 days of dexamethasone 6 mg daily. His course was complicated by acute renal failure requiring continuous renal replacement therapy, septic shock due to a pseudomonal ventilator-associated pneumonia, right ventricular failure, heparin induced thrombocytopenia, and right pneumothorax requiring chest tube thoracostomy. After 4 weeks of ECMO there was lung recovery with ECMO sweep gases <1L/minute, improved radiographic appearance and tidal volumes, and decannulation was anticipated. However, he subsequently developed profound shock of unknown etiology with a rapid worsening of his lung function requiring increased ECMO support. Care was withdrawn at ECMO day 46 due to multiorgan failure. Pathology of his lungs at autopsy showed prominent intranuclear viral inclusions and positive immunohistochemistry in alveolar macrophages consistent with a diagnosis of CMV pneumonia. DISCUSSION: While CMV typically causes latent disease it can reactivate in the setting of immunosuppression and/or critical illness.[1] Patients with severe COVID-19 frequently are treated with immunosuppressive therapies, such as corticosteroids, anti-interluekin-6 therapies, and JAK inhibitors. Due to this immunosuppression, opportunistic infections have been reported in these patients.[2] It can be difficult to differentiate COVID-19 pneumonia from other respiratory infections based on imaging and lab studies alone, especially in patients with prolonged mechanical ventilation and with severe parenchymal disease requiring ECMO support. Little is known about the incidence of CMV and COVID-19 coinfection. There are several cases of biopsy-proven CMV pneumonia in immunocompromised critically ill patients with COVID-19, but this is the first reported case in an immunocompetent patient. CONCLUSIONS: This case highlights the need to maintain a high degree of suspicion for CMV pneumonia in patients with severe COVID-19 pneumonia who receive immunosuppressive therapies. While the diagnosis was made at autopsy in this case, it may be possible to arrive at an earlier diagnosis with CMV polymerase chain reaction (PCR) assays sent from the serum and bronchoalveolar lavage (as lung biopsies are usually impractical in ARDS). Reference #1: de la Hoz RE, Stephens G, Sherlock C. Diagnosis and treatment approaches of CMV infections in adult patients. J Clin Virol. 2002 Aug;25 Suppl 2:S1-12. doi: 10.1016/s1386-6532(02)00091-4. PMID: 12361752. Reference #2: Abdoli A, Falahi S, Kenarkoohi A. COVID-19-associated opportunistic infections: a snapshot on the current reports [published online ahead of print, 2021 Aug 23]. Clin Exp Med. 2021;1-20. doi:10.1007/s10238-021-00751-7 DISCLOSURES: No relevant relationships by Nancy Law No relevant relationships by Mazen Odish No relevant relationships by Robert Owens No relevant relationships by Travis Pollema No relevant relationships by Alyssa Self No relevant relationships by Cassia yi

14.
Chest ; 162(4):A664, 2022.
Article in English | EMBASE | ID: covidwho-2060663

ABSTRACT

SESSION TITLE: A Look Into Poisoning and Drug Overdoses SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: We present a case of a 64-year-old woman with severe obesity (BMI 53) who presented with shock after beta-blocker (BB) and calcium channel-blocker (CCB) overdose. CASE PRESENTATION: The patient presented after an intentional suicide attempt, taking multiple antihypertensive medications, including tablets of nifedipine 90mg, carvedilol 25mg, and losartan 100mg. She had also been experiencing shortness of breath and lower extremity pain for several days. Upon arrival, she was lethargic and minimally responsive, and was found to be in shock with a heart rate 63. She was intubated for airway protection and started on multiple vasopressors including norepinephrine, phenylephrine, vasopressin, dopamine and epinephrine for circulatory support. She was also found to be positive for SARS-CoV-2. She was given activated charcoal, received gastric lavage, and whole bowel irrigation. She received a bolus of regular insulin at 1U/kg, and subsequently started on a high-dose insulin infusion titrated to 11U/kg/h along with dextrose infusion and calcium gluconate. By day four of admission, vasopressor requirements had been reduced to only norepinephrine and the insulin infusion had been successfully discontinued. However, her hospital course was further complicated MRSA and Pseudomonas pneumonia, and renal failure requiring hemodialysis. She continued to develop refractory shock, and remained over 50 liters net positive. Her condition progressively deteriorated and her gross volume overload was difficult to manage, and ultimately expired on day ten of admission. DISCUSSION: The management of CCB and BB overdose has been studied, with hyperinsulinemic euglycemic therapy (HIET)1,2 as our choice. Our patient's decline was likely secondary to the high volumes of dextrose infusion required after HIET. With underlying renal failure, insulin clearance proved to be a significant challenge. Such severe obesity with a weight-based regimen resulted in over 1500U insulin/hr at any given point with our patient. Renal clearance is governed by a proportion of t/V, where t denotes length of a dialysis session and V the volume of fluid in the patient's body.3 Patients with significant volume would require extensive dialysis sessions and fluid balances would be challenging. Continuous renal replacement therapy (CRRT) was attempted later in her hospital course. However, the patient was not able to tolerate it as she had progressed to multiorgan failure. CONCLUSIONS: HIET has shown to be a successful management strategy for CCB and BB overdose. However, weight-based dosing can prove to be a challenge in patients with severe obesity. CRRT should be considered early in severely obese patients that undergo HIET, given the rapid accumulation of fluid secondary to the large-volume insulin and dextrose infusions. Further investigations should look into identifying maximal safe dosages of HIET, especially in severely obese patients. Reference #1: Cole JB, Arens AM, Laes JR, Klein LR, Bangh SA, Olives TD. High dose insulin for beta-blocker and calcium channel-blocker poisoning. Am J Emerg Med. 2018 Oct;36(10):1817-1824. doi: 10.1016/j.ajem.2018.02.004 Reference #2: Krenz JR, Kaakeh Y. An Overview of Hyperinsulinemic-Euglycemic Therapy in Calcium Channel Blocker and β-blocker Overdose. Pharmacotherapy. 2018 Nov;38(11):1130-1142. doi: 10.1002/phar.2177 Reference #3: Turgut F, Abdel-Rahman E, M: Challenges Associated with Managing End-Stage Renal Disease in Extremely Morbid Obese Patients: Case Series and Literature Review. Nephron 2017;137:172-177. doi: 10.1159/000479118 DISCLOSURES: No relevant relationships by Alejandro Garcia No relevant relationships by Vishad Sheth no disclosure on file for Andre Sotelo;

15.
Chest ; 162(4):A663, 2022.
Article in English | EMBASE | ID: covidwho-2060662

ABSTRACT

SESSION TITLE: Challenging Cases of Hemophagocytic Lymphohistiocytosis SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Worsening respiratory disease is the most common complication of severe COVID-19. However, when patients develop multi-organ dysfunction, clinicians must have a high index of suspicion for rare syndromes such as hemophagocytic lymphohistiocytosis (HLH). CASE PRESENTATION: A 39-year-old male smoker presented with 1 week of shortness of breath and malaise. Initial physical examination revealed T 37.3 C, pulse 85 min-1, respiratory rate 18 breaths min-1, SPO2 96% and clear breath sounds without labored respirations. Chest X-ray showed bilateral patchy airspace opacities in the mid and lower lung fields. A SARS-COV2 PCR test was positive. The patient was prescribed antibiotics and discharged home. Subsequently, the patient's symptoms worsened and he presented 1 week later with SPO2 90% (O2 10 L/min via nasal cannula). He was admitted to the hospital with COVID-19 pneumonia and began remdesivir, barcitinib, systemic steroids, albuterol and IV antibiotics. On admission his complete blood count and complete metabolic panel were unremarkable. After 3 weeks of hospitalization, he developed multi-organ failure with acute liver injury, acute kidney injury, shock, pancytopenia and worsening hypoxemia leading to endotracheal intubation and mechanical ventilation. CT chest imaging showed bilateral ground glass opacities in the lungs with superimposed consolidation (figure 1). Blood cultures remained sterile, HIV, hepatitis B and C viral serologies were negative. Serum viral polymerase chain reaction detected Herpes Simplex Virus-1 (HSV-1) and Epstein Barr Virus (EBV) infections. Trans-jugular liver biopsy confirmed HSV-1 hepatitis and showed sub-massive hemorrhagic necrosis of the liver (figure 2). Bone marrow biopsy demonstrated phagocytic histiocytes engulfing red blood cells and platelets consistent with HLH (figure 3). The patient began HLH targeted therapy with anakinra and high dose steroids. Despite this, the patient continued to deteriorate, developed refractory shock and subsequently expired. DISCUSSION: HLH is a rare disease of the immune system in which a genetic or infectious trigger causes uncontrolled T cell activation. T cell activation triggers macrophage activation, cytokine storm and macrophage phagocytosis of erythrocytes, leukocytes, platelets and precursors in the bone marrow and other tissues. If the syndrome is unrecognized, it can quickly lead to multi-organ failure and death. EBV is the most common infectious trigger of HLH;however, infection with HSV-1 and SARS-COV-2 viruses have been identified as rare and independent causes. CONCLUSIONS: This case illustrates the high index of suspicion providers should have for HLH in patients with severe COVID-19 who develop multi-organ injuries. Once HLH is suspected, prompt initiation of HLH-94 protocol with etoposide and dexamethasone may be lifesaving. For those patients with liver failure, other agents (e.g. anakinra) may be provided. Reference #1: Ramos-Casals M, Brito-Zerón P, López-Guillermo A, et al.: Adult haemophagocytic syndrome. Lancet 2014;383:1503–1516 Reference #2: Risma K, Jordan MB: Hemophagocytic lymphohistiocytosis: updates and evolving concepts. Curr Opin Pediatr 2012;24:9–15 Reference #3: Trottestam H, Horne A, Aricò M, et al.: Chemoimmunotherapy for hemophagocytic lymphohistiocytosis: long-term results of the HLH-94 treatment protocol. Blood 2011;118:4577–4584 DISCLOSURES: No relevant relationships by Erin Biringen No relevant relationships by Christine Brennan No relevant relationships by Joann Hutto No relevant relationships by Daniel Puebla Neira

16.
Chest ; 162(4):A421, 2022.
Article in English | EMBASE | ID: covidwho-2060592

ABSTRACT

SESSION TITLE: Severe and Unusual Blastomycosis Infections SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: This is a case of a patient 74-year-old immunosuppressed woman presenting with a one-week history of skin lesions. CASE PRESENTATION: A 74-year-old woman with Crohn's disease (on weekly adalimumab);pulmonary hypertension (RVSP 76 mmHg);OHS/OSA, on home BPAP 17/7 cmH2O;and morbid obesity presented with a one-week history of skin lesions. She was seen by her primary care physician two days prior with skin lesions, shortness of breath, and decreased vision. She was hypoxic during the visit and given doxycycline for empiric treatment of pneumonia. She denied recent travel or exposure to animals. On admission, she was afebrile (36.9C) and saturating 98% on 2 L nasal cannula. She appeared chronically ill with mouth ulcers and an eroded nodule with overlying hemorrhagic crusting and peripheral pustular area above her right eyebrow (figure 1). Throughout her skin, she had multiple erythematous papules, some with overlying vesicles/pustules. Labs were significant for a leukocytosis of 19.3 with left shift, lactate of 3.5, serum creatinine of 1.9 (likely higher than patient's previous baseline of 1.7 with previous history of recurrent AKIs on CKD), elevated inflammatory markers, and normal ALT/AST. Influenza and COVID were negative. A CT chest showed consolidations and numerous pulmonary nodules highly suspicious for an infectious or inflammatory process (figure 2). She was treated empirically with vancomycin, piperacillin-tazobactam, valacyclovir, and amphotericin B, the latter given the concern of blastomycosis. During her hospitalization, she had further respiratory failure requiring intubation and multiorgan failure. Disseminated blastomycosis was confirmed via a skin biopsy which demonstrated pyogranulomatous inflammation with numerous broad-based budding yeasts (figure 3) and supported with a bronchoalveolar lavage (BAL) culture growing the same. Given her continued decline, her medical decision maker decided to transition the patient to hospice care. DISCUSSION: Blastomycosis is a systemic pyogranulomatous infection that is caused from the inhalation of the conidia form of the dimorphic fungus. It can manifest as asymptomatic infection, acute or chronic pneumonia, or extrapulmonary disease. BAL yields a positive diagnosis in 92% of patients and definitive diagnosis requires growth of the organism from a clinical specimen. Without appropriate treatment of amphotericin B or one of the azole antifungals, the disease had a 90% mortality rate. CONCLUSIONS: Prompt recognition of multiorgan failure secondary to blastomycosis is important for early treatment and improved survival in immunocompromised patients Reference #1: 1)Chapman, S W et al. "Endemic blastomycosis in Mississippi: epidemiological and clinical studies.” Seminars in respiratory infections vol. 12,3 (1997): 219-28. Reference #2: 2)Saccente, Michael, and Gail L Woods. "Clinical and laboratory update on blastomycosis.” Clinical microbiology reviews vol. 23,2 (2010): 367-81. doi:10.1128/CMR.00056-09 Reference #3: 3)Chapman, Stanley W et al. "Clinical practice guidelines for the management of blastomycosis: 2008 update by the Infectious Diseases Society of America.” Clinical infectious diseases : an official publication of the Infectious Diseases Society of America vol. 46,12 (2008): 1801-12. doi:10.1086/588300 DISCLOSURES: No relevant relationships by Jennifer Duke No relevant relationships by Ashley Egan

17.
Chest ; 162(4):A292, 2022.
Article in English | EMBASE | ID: covidwho-2060553

ABSTRACT

SESSION TITLE: Severe and Unusual Blastomycosis Infections SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: Severe pulmonary blastomycosis (PB) usually affects immunocompromised patients, with very high mortality rate of up to 40%. PB can mimic pneumonia caused by other organisms (1), which can delay diagnosis and treatment initiation. We present a case of severe PB that was initially thought to be COVID-19 pneumonia, to our knowledge this is 2nd case of concomitant PB and COVID-19 infection in literature. (2) CASE PRESENTATION: Patient is 52 year old female with past medical history of atrial fibrillation, asthma, bariatric surgery, that presents with shortness of breath for 2 weeks. Despite receiving only 1 dose of COVID-19 vaccine (Moderna) 5 months ago, patient tested positive for COVID-19 on PCR test at the urgent care 4 days prior. Her symptoms progressed despite initial outpatient treatment with steroids and antibiotics. Initial emergency department chest computed tomography (CT) revealed dense bilateral consolidations, with hypoxic respiratory failure, patient was admitted for treatment of presumed COVID-19 pneumonia, and guideline directed treatment was initiated. Despite maximal medical management, that included steroids, broad spectrum antibiotics, remedisivir, patient failed to improve, with repeat CT chest revealing worsening consolidations. Bronchoscopy was performed 12 days into the admission revealed thick white secretions, with cultures growing blastomyces dermatitidis. At this point patient development of septic shock with multiorgan failure. Patient was subsequently intubated, and due to significant renal failure, initiated on hemodialysis (HD). Anti-fungal treatment was initiated with amphotericin B, and transitioned to itraconazole afterwards. Patient required several HD sessions, after which her renal function fully recovered. Patient was successfully extubated 7 days later, but required additional 22 days of medical care and physical therapy before being ready for discharge to rehabilitation facility. On the outpatient follow up 6 weeks after discharge, patient continues to slowly recover. Repeat CT chest still with significant bilateral consolidations. Patient will require at least 12 months of itraconazole therapy. DISCUSSION: PB can mimic bacterial and viral pneumonia symptoms. (1) In the widespread COVID-19 pandemic, clinicians can be misled by COVID-19 positive test in patient with bilateral pneumonia, and initiate guideline directed therapy. Immunosuppression agents can lead to adverse outcomes in patients with underlying PB. Questionable is the significance of COVID positive PCR test in semi-vaccinated individual. Potentially even mild COVID-19 infection could predispose patient for PB. Early diagnosis of PB is important, as delay in treatment and medical immunosuppression can lead to worse outcomes. CONCLUSIONS: PB should be suspected even in patients presenting with positive COVID-19 PCR test. Guideline directed therapy for COVID-19 can worsen underlying PB. Reference #1: https://www.cdc.gov/fungal/covid-fungal.html Reference #2: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8503152/ DISCLOSURES: No relevant relationships by Dovile Baniulis No relevant relationships by Dovile Cerkauskaite No relevant relationships by Igor Dumic No relevant relationships by Momcilo Durdevic No relevant relationships by Dragana Durdevic No relevant relationships by Ashutossh Naaraayan No relevant relationships by Ankita Subedi

18.
Chest ; 162(4):A121-A122, 2022.
Article in English | EMBASE | ID: covidwho-2060540

ABSTRACT

SESSION TITLE: Cardiovascular Complications in Patients with COVID-19 SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Multisystem inflammatory syndrome in adults (MIS-A) is a hyperinflammatory condition characterized by fever, elevated inflammatory markers, and multi-organ dysfunction, including severe cardiac illness, neurological and gastrointestinal symptoms, mucocutaneous involvement, and thrombocytopenia usually 2-5 weeks after COVID-19 infection (1). There are currently no guidelines for the management of this novel syndrome. CASE PRESENTATION: A 20-year-old obese male presented for 3 days of fatigue, fever, dyspnea, diarrhea, and worsening encephalopathy. He tested positive for COVID-19 3 weeks prior and experienced 4 days of mild symptoms. He had received 2 doses of Moderna mRNA vaccine 9 months prior. On presentation, he had a GCS of 3. He was febrile, hypotensive, tachycardic, not hypoxic, and found to have non-purulent conjunctivitis but no rash. He was intubated for airway protection and started on norepinephrine (NE) shortly after arrival. Labs revealed positive COVID-19 PCR, lactate of 5.6 mmol/L, elevated hs-troponin which peaked at 11,300 ng/L, D-Dimer 12,574 ng/ml, ferritin >16,500 ng/ml, CRP 224 mg/L, platelet count 18 x109/L. EKG showed sinus tachycardia without ST changes. CT chest/abdomen/pelvis was unremarkable. The patient was given broad-spectrum antibiotics and admitted to ICU. An echocardiogram (echo) showed global hypokinesis with an ejection fraction of 10-15%. Right heart catheterization found a wedge pressure of 23 mmHg, and a cardiac index of 1.4 L/min/m2. NE was weaned, and dobutamine and bumetanide drips were started. Infectious disease was consulted and diagnosed the patient with MIS-A. Treatment was started with methylprednisolone 2mg/kg/day and IVIG (2 g/kg x2 days). 48 hours later, dobutamine was able to be discontinued and follow-up echo showed normalization of biventricular systolic function. Steroids were continued for 7 days before tapering off. The patient’s presenting symptoms, platelets, and inflammatory markers rapidly improved, and he was ultimately able to be discharged home. DISCUSSION: MIS-A is a rare but serious extrapulmonary sequela of COVID-19 which can cause critical illness including cardiogenic shock. The long-term consequences of MIS-A are not known, but fortunately, as demonstrated by our case, severe cardiac dysfunction can be effectively reversed with timely diagnosis and initiation of immunosuppressive treatment. This recovery was achieved without immunomodulators (eg tocilizumab) which have been used in other MIS-A cases (2). MIS-A should be considered in patients with severe cardiac dysfunction and evidence of systemic inflammation even with no known history of COVID as this can develop after mild or even asymptomatic COVID-19 infections. CONCLUSIONS: Immunosuppressive therapies can rapidly reverse severe multiorgan dysfunction in MIS-A. Still, further study is needed to identify at-risk patients and create definitive treatment guidelines. Reference #1: Vogel TP, Top KA, Karatzios C, et al. Multisystem inflammatory syndrome in children and adults (MIS-C/A): Case definition & guidelines for data collection, analysis, and presentation of immunization safety data. Vaccine. 2021;39(22):3037-3049. doi:10.1016/j.vaccine.2021.01.054 Reference #2: Patel P, DeCuir J, Abrams J, Campbell AP, Godfred-Cato S, Belay ED. Clinical Characteristics of Multisystem Inflammatory Syndrome in Adults: A Systematic Review. JAMA Netw Open. 2021;4(9):e2126456. doi:10.1001/jamanetworkopen.2021.26456 DISCLOSURES: No relevant relationships by Christopher Allison no disclosure on file for Sandeep Arepally;No relevant relationships by Amad Chohan No relevant relationships by Albert Manudhane No relevant relationships by Griffin Reed

19.
African Journal of Respiratory Medicine ; 15(2), 2020.
Article in English | EMBASE | ID: covidwho-2058658

ABSTRACT

Objective: Severe acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) seen in SARs-CoV-2 infection has been attributed to the disruption of the immune response in COVID-19 patients. Neutrophilia and marked lymphocyte reductions are associated with disease severity and seem predictive of disease outcome in moderate and severe COVID-19 patients. Herein, we aim to decipher possible mechanisms involved in extensive tissue injury observed in COVID-19 patients, accompanied by vasculopathy, coagulopathy, and a high incidence of thrombotic complications in severe patients. Method(s): We searched PubMED for keywords including COVID-19 pathogenesis, thrombosis, and vasculities. Result(s): Neutrophils can undergo a specialized form of apoptosis to yield thread-like extracellular structures termed neutrophil extracellular traps (NETs), termed NETosis, which form web-like scaffolds of DNA, histones, and toxic protein granules and enzymes, whose primary function is to trap and eliminate microbes. However, uncontrolled NET production can lead to ALI and ARDS, coagulopathy, multiple organ failure, and autoimmune disease. Dysregulation of NETs promotes production of anti-neutrophil cytoplasmic antibodies (ANCA) which affects small vessels through ANCA-associated vasculitis (AAV). Furthermore, NETs can also induce thrombosis via formation of scaffolds that trap platelets, RBCs, fibronectin, and other proteins, which can also induce coagulation. Conclusion(s): We suggest that NET production is central during SARS-CoV-2 infection and COVID-19 pathogenesis, associated with alveolar damage accumulation of edema, endothelial injury and coagulopathy, elevated platelet activation and thrombogenesis forming a NET production feed-forward loop, causing diffuse small vessel vasculitis in the lungs and other organs. Copyright © 2020 FSG Communications Ltd. All rights reserved.

20.
Acute Med Surg ; 9(1): e793, 2022.
Article in English | MEDLINE | ID: covidwho-2059279

ABSTRACT

Background: The new coronavirus disease (COVID-19) causes gastrointestinal symptoms as well as respiratory symptoms. Case Presentation: A 60-year-old man was transferred with respiratory difficulty. He was diagnosed as having COVID-19 and was intubated and placed on mechanical ventilation. He suffered from diarrhea from day 12 and produced a maximum of approximately 6,384 mL/day of watery diarrhea on day 21. He required massive transfusion. Adsorbents and pectin-containing oligomeric formulas were administered, which decreased the amount of diarrhea. Fecal metagenomic analysis showed the proportions of the genera Enterococcus and Staphylococcus were the most dominate at the genus level. The proportion of Bacteroidetes was <1%. Thereafter, his diarrhea decreased to several times, and he was transferred to another ward on day 104. Conclusion: Therapy for intestinal complications as well as that for pneumonia might be important in treating COVID-19.

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