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COVID-19 is a highly transmissible disease with severe course especially in patients with nephrogenic hypertensive disease and chronic kidney disease due to a higher incidence of all-type infections than in the general population. The aim of the study is to describe a clinical case of SARS-CoV-2 infection complicated by nephrogenic pulmonary edema and COVID-associated pneumonitis, alveolitis. Description of the case. Patient K.S., born in 1975, was hospitalized 24 hours after symptom onset at emergency hospital due to complaints of increased blood pressure up to 180-200/110-120 mm Hg, temperature up to 38.7degreeC, dry cough, feeling of heaviness in the chest, change in urine color. PCR smear for SARS-CoV-2 was positive. Computed tomography revealed a pattern of bilateral COVID-associated pneumonitis, alveolitis, with 75% involvement. The electrocardiogram revealed signs of left ventricular myocardial hypertrophy. Ultrasound examination showed numerous cysts in the kidneys. Urinalysis at admission: leukocytes - 499, erythrocytes - 386. Glomerular filtration rate (CKD-EPI: 29 ml/min/1.73 m2) and corresponds to stage IV of chronic kidney disease. Coagulogram: fibrinogen: 32.3 (1.6-4.0) g/l, D-dimer: 663 (0-250). Despite the treatment, the patient's condition worsened, the phenomena of cardiopulmonary and renal insufficiency increased, which led to a fatal outcome. During a virological study of sectional material: SARS-CoV-2 coronavirus RNA was found in the lung and kidneys. Signs of bilateral COVID-associated pneumonitis, alveolitis with diffuse cellular infiltrates in combination with changes in the alveolar apparatus, signs of pulmonary edema were revealed. Heart-related signs - swelling of the interstitium, fragmented muscle fibers, some of them hypertrophied, a wave-like deformation of cardiomyocytes, blurring of the transverse striation. Arteries with thickened sclerosed walls. In the kidneys - diffuse damage to the proximal tubules of the nephron with areas of cortical and proximal necronephrosis, areas of fibrinoid swelling. Conclusion. The cause of death of a 45-year-old patient was a severe course of bilateral COVID-associated pneumonitis, alveolitis, which contributed to the development of renal medullary hypoxia and type 1 cardiorenal syndrome, which led to early nephrogenic pulmonary edema.Copyright © 2023 Saint Petersburg Pasteur Institute. All rights reserved.
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Chronic respiratory diseases affect both the upper and lower airways. The main components of the respiratory system are the rib cage, airways, and the pulmonary interstitium. The airway originates in the trachea, a structure located in the mediastinum, which splits into two parts to form the main bronchus (right and left bronchi). The bronchi gradually divide into secondary bronchi, bronchioles, alveolar ducts, and alveoli. Acute or chronic respiratory diseases are present in all age groups, with many different forms of clinical presentation. In general, the most common diseases are asthma, chronic obstructive pulmonary disease, respiratory allergies, occupational lung diseases, pulmonary hypertension, sinusitis, pharyngitis, bronchitis, tuberculosis, cold, and influenza (flu). Among the acute illnesses, infections of the upper respiratory tract, flu, and pneumonia are particularly prominent, and since 2019, we could include in this group the COVID-19 with the beginning of the pandemic of this disease. For chronic diseases, diseases of the lower respiratory tract are the most common, such as bronchitis, emphysema, and asthma. © 2023 Elsevier B.V.
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SESSION TITLE: Drug-Induced and Associated Critical Care Cases Posters 1 SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Interstitial pneumonitis (ILD) is inflammation of lung interstitium leading to scarring and pulmonary fibrosis. Various etiologies include idiopathic, connective tissue disorders, sarcoidosis and drug induced1. Many chemotherapy agents have been implicated in drug related ILD such as bleomycin, taxanes. However, newer chemotherapeutic drugs such as molecular agents such as anti-VEGF, anti-EGFR (panitumumab) could be causative of drug induced ILD. CASE PRESENTATION: A 75-year-old female with stage IV sigmoid colon cancer treated with surgery, adjuvant FOLFOX chemotherapy and Panitumumab. She presented to the emergency department with shortness of breath and hypoxia after known COVID-19 exposure. Initial imaging with chest radiography showed bilateral ground glass opacities. A chest CT pulmonary embolism protocol was negative for pulmonary embolism but showed bilateral ground glass opacities (GGOs) and some interstitial thickening (L>R) not typical of COVID-19 infection. She was treated with remdesivir and dexamethasone, however her oxygen requirements continued to rapidly escalate. A repeat CT chest without contrast showed bilateral asymmetric interstitial thickening and GGOs. Given persistence of CT chest abnormalities, workup for interstitial lung disease was initiated. The results include ANA titer 1:80, otherwise negative ANCA profile, rheumatoid factor, anti-CCP, Scl-70, Sjogren antibodies. Given clinical history and imaging findings, diagnosis of ILD was suspected, and she was started on solumedrol 1 mg/kg. Her oxygen requirements decreased significantly over the next 2 days, and she was discharged home on oral steroid taper and pneumocystis pneumonia prophylaxis. DISCUSSION: Panitumumab is a fully humanized monoclonal antibody against EGFR. Approved by the US Food and Drug Administration in 2006 for advanced or recurrent colorectal cancer exhibiting wild-type KRAS mutation.2 ILD is rarely reported with panitumumab monotherapy, but higher incidence when used as a combination treatment such as with FOLFOX or FOLFIRI. A Japanese post-marketing surveillance study from 2010-2015 showed an ILD incidence of 1.3% but mortality rates of 51.3%.2 EGFR is expressed on basal cells and non-cilia cells of the bronchioles and type II cells of the alveolus. EGFR mediated mechanisms are important in tissue repair.3 Therefore inhibition of this pathway has been postulated to play a role in development of ILD. Another mechanism was decreased surfactant production by type II cells in pre-clinical study.4,5 ILD secondary to Panitumumab can occur at any point during therapy and up to 1 year after administration of drug.6 The role of infectious processes, in this case, COVID-19 pneumonia, could synergistically worsen ILD presentation. CONCLUSIONS: Although the incidence of ILD is low, the mortality rate is high, therefore early recognition and treatment is associated with improved clinical outcomes. Reference #1: Mudawi D, Heyes K, Hastings R, Rivera-Ortega P, Chaudhuri N. An update on interstitial lung disease. Br J Hosp Med (Lond). Jul 2 2021;82(7):1-14. Reference #2: Osawa M, Kudoh S, Sakai F, et al. Clinical features and risk factors of panitumumab-induced interstitial lung disease: a postmarketing all-case surveillance study. Int J Clin Oncol. Dec 2015;20(6):1063-1071. Reference #3: The FASEB Journal - 2000 - Puddicombe - Involvement of the epidermal growth factor receptor in epithelial repair in asthma.pdf. DISCLOSURES: No relevant relationships by Navitha Ramesh No relevant relationships by Uba Udeh
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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
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SESSION TITLE: Post-COVID-19 Infection Complications SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: COVID-19 has affected over 200 million people worldwide. Clinicians continue to observe unusual manifestations of this disease. In an attempt to improve our understanding of COVID-19 pneumonia, we present the details of one patient who developed large bilateral pulmonary cysts. CASE PRESENTATION: A 40-year-old woman with no known medical problems presented with the chief complaint of fever, nausea, vomiting, generalized weakness followed by difficulty breathing that developed over a few days. Her vital signs on admission included temperature 98.4° F, heart rate 104 beats/minute, respiratory rate 48 breaths/minute, O2 saturation 88 percent on 15 liters of oxygen through a non-rebreather mask, and Body Mass Index 42 kg/m2. The patient tested positive for COVID-19. Computed tomography (CT) of the chest to rule out a pulmonary embolism showed bilateral extensive ground-glass opacities and reticular and nodular opacities. She was intubated for acute hypoxic respiratory failure. Twenty days into the hospital admission, she was noted to have a bulla in the right lower lobe. A repeat CT chest on day 45 revealed an increase in the number and size of cysts bilaterally. Patient was discharged to rehab and later readmitted for worsening respiratory status. This time she tested positive for human metapneumovirus. A CT chest showed increase in the size of the right sided lung cysts;the left sided lung cysts had resolved. DISCUSSION: The first COVID-19 related pulmonary cystic lesions were reported in May 2020(1). Since then, several reports have now established a relationship between an infection and cyst formation. The most common distribution is peripheral in the lower lobes. The pathogenesis remains uncertain, but several mechanisms have been proposed. Microthrombi in the pulmonary circulation could lead to ischemia and subsequent remodeling of interstitial matrix and bronchial obstruction with distal hyperinflation due to check valve mechanism. (1,2). Hamad et al. propose that pneumatoceles are formed by air leaked in to the interstitium which causes stripping and separation of a thin layer of lung parenchyma with further injury to the small blood vessels and bronchioles. The rate of barotrauma in non-COVID-19 related ARDS is 0.5%;the rate in COVID-19 ARDS is 15% (3). This suggests a close relation between COVID-19 pneumonia and subsequent development of pulmonary cysts. Our patient had no preexisting pulmonary disease and was noted to have pulmonary cysts after being on mechanical ventilation for almost 2 weeks. The patient later contracted the human metapneumovirus infection and CT showed that the right-sided lung cysts had become bigger in size. However, the left-sided cysts which had a maximum diameter of 4.8 cm had resolved. CONCLUSIONS: We need to follow patients with COVID 19 induced lung cysts clinically and radiologically to understand the clinical course and best management strategies. Reference #1: Kefu Liu et al. COVID 19 with cystic features on Computed tomography;Medicine (Baltimore) 2020May;99(18): e20175. PMCID: PMC7486878 Reference #2: Galindo J, Jimenez L, Lutz J et al. Spontaneous pneumothorax with or without pulmonary cysts, in patients with COVID 19 Pneumonia. Journal of infections in developing countries 2021;15(10);1404-1407 Reference #3: McGuinness G, Zhan C, Rosenberg N, Azour L, Wickstrom M, Mason DM, Thomas KM, Moore WH. Increased incidence of barotrauma in patients with COVID-19 on invasive mechanical ventilation. Radiology. 2020;297(2): E252–E262. doi: 10.1148/radiol.2020202352 DISCLOSURES: No relevant relationships by Arunee Motes No relevant relationships by Kenneth Nugent No relevant relationships by Tushi Singh No relevant relationships by Myrian Vinan Vega
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SESSION TITLE: The Cardiac Intensivist 2 SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: Hydroxychloroquine and chloroquine are medications derived from aminoquinoline. They are disease-modifying antirheumatic drugs used in the treatment of systemic lupus erythematosus (SLE). Although well tolerated, they do have side effects such as retinopathy, vacuolar myopathy, neuropathy, and as seen in our patient, cardiotoxicity. CASE PRESENTATION: Patient is a 48 year old female with a past medical history significant for chronic kidney disease secondary to autosomal dominant polycystic kidney disease, SLE on hydroxychloroquine who presented to the emergency department complaining of weakness. On arrival the patient was found to be in cardiogenic shock. Her transthoracic echocardiogram revealed a reduced ejection fraction of 37% and a large pericardial effusion concerning for tamponade physiology. Her COVID-19 PCR test was positive. She was taken for emergent pericardiocentesis which revealed 300cc of exudative fluid. Patient’s right heart catheterization revealed mean pulmonary capillary wedge pressure of 23 mmHg, pulmonary artery pressures of 44 mmHg/24 mmHg, mean 31mmHg, cardiac index 1.1L/min/m² by thermodilution, 1.7 L/min/m² by Fick. Following right heart catheterization and intra aortic balloon pump placement, the patient was admitted to the medical intensive care unit (MICU) and placed on intravenous inotropic and vasopressor support. Shortly after arrival to the MICU, patient had an increase in vasopressor requirements. Bedside ultrasound revealed cardiac tamponade. Patient had approximately 400cc of bloody pericardial fluid removed from her pericardial drain. The decision was made for emergent venoarterial extracorporeal membrane oxygenation (ECMO) to be initiated. Endomyocardial biopsy was performed which revealed vacuolization in the cytoplasm of several myocytes as well as lymphocytes in the interstitium of the endocardium. The vacuoles found in the cardiac myocytes were PAS positive. These biopsy results are consistent with hydroxychloroquine cardiotoxicity. The patient’s hydroxychloroquine was discontinued. In addition to hemodynamic support, she also received intravenous immunoglobuluin and systemic steroids. After a prolonged hospitalization she was successfully discharged. DISCUSSION: Cardiotoxicity is a rare adverse reaction seen with hydroxychloroquine. A 2018 systematic review revealed 127 cases of cardiac toxicity associated with the use of hydroxychloroquine or chloroquine. Most patients had been treated with the medication for a prolonged period of time and the toxicity is dose dependent. The mechanism behind hydroxychloroquine and chloroquine induced cardiomyopathy is believed to be secondary to lysosomal dysfunction as a result of toxic phospholipid accumulation in cardiomyocytes. CONCLUSIONS: In patients with new onset cardiomyopathy, a detailed medication reconciliation should be conducted to evaluate for toxins such as hydroxychloroquine and chloroquine. Reference #1: Della Porta, A., Bornstein, K., Coye, A., Montrief, T., Long, B., & Parris, M. A. (2020). Acute chloroquine and hydroxychloroquine toxicity: A review for emergency clinicians. The American Journal of Emergency Medicine. Reference #2: Abbi, B., Patel, S., Kumthekar, A., Schwartz, D., & Blanco, I. (2020). A Case of Cardiomyopathy With Long-term Hydroxychloroquine Use. JCR: Journal of Clinical Rheumatology, 26(8), e300. Reference #3: Chatre, C., Roubille, F., Vernhet, H., Jorgensen, C., & Pers, Y. M. (2018). Cardiac complications attributed to chloroquine and hydroxychloroquine: a systematic review of the literature. Drug safety, 41(10), 919-931. DISCLOSURES: no disclosure on file for Joseph Adams;no disclosure on file for Suliman Alradawi;No relevant relationships by George Kalapurakal No relevant relationships by Mohammed Siddiqui
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Introduction: Acute Interstitial Nephritis (AIN) is an important cause of Acute Kidney Injury (AKI), and infections are the second most common etiology, after the drugs. However, AIN following fungal infections is rare. We describe two cases of AIN, which on the investigation turn out to be candidemia following fungal infective endocarditis. Methods: CASE 1: A 65-year-old man with hypertension and diabetes without diabetic or hypertensive retinopathy and prior normal renal function, presented to us with vague abdominal pain with steadily creeping creatinine to 2mg/dl within 2 weeks, and urine showed no albuminuria and sediments. There was no history of any specific drug intake. His hematological and other parameters were normal. Blood and urine cultures were sterile. He underwent a renal biopsy which revealed acute interstitial nephritis (Figure 1). He was started on prednisolone at 1mg/kg/day for 1-week following which he had a rapidly worsening azotemia requiring hemodialysis. Steroids were stopped. Repeat blood cultures were sent which grew candida albicans resistant to flucytosine. Re-evaluation of the fundus revealed macular infarct in the right eye with vitreoretinitis in the left eye suggestive of endophthalmitis. PET CT showed increased FDG uptake in both kidneys suggestive of pyelonephritis. Trans-esophageal echocardiography (TEE) showed aortic valve vegetations. He was treated with antifungals for 3 months. He was dialysis-dependent for 2 weeks. He gradually regained normal renal function 3 weeks after starting anti-fungal agents. CASE 2: A 57-years-old man with diabetic, hypertensive, and no diabetic retinopathy had severe covid pneumonia in June 2021 requiring oxygen and tocilizumab 80 mg for 4 days, recovered with normal renal function. He presented to us 1 month later with unexplained non-oliguric severe AKI requiring dialysis, with bland urine sediments. Renal biopsy showed lymphocytic infiltrates in the interstitium suggestive of AIN (Figure 2). Blood cultures were sterile, but serum beta-D-glucan was elevated at 333 pg/ml. He was Initiated on 1mg/kg of prednisolone, on the presumption of drug-induced AIN. Simultaneously workup for systemic infection revealed mitral anterior leaflet endocarditis. He was initiated on anti-fungal therapy on the advice of an infectious disease specialist and the steroid was stopped. He continued to be dialysis-dependent after 6 weeks, despite anti-fungal agents. Results: [Formula presented] Conclusions: AIN contributes a significant proportion of cases in unexplained AKI. Prompt evaluation with a renal biopsy is warranted. Acute interstitial nephritis particularly due to candidemia can be oligosymptomatic as seen in our two cases. Since steroids have a significant role in treating early AIN, a dedicated search for underlying silent endocarditis and candidemia is advisable before initiating steroid therapy. Ophthalmic fundus evaluation, TEE, and repeat blood culture may be necessary to identify hidden candidemia. We recommend an evaluation to exclude fungal endocarditis in patients with AIN who present with minimal or no symptoms and no definitive cause for AIN is present. No conflict of interest