The spectrum of COVID-19-associated chorioretinal vasculopathy.

Purpose: Although conjunctivitis represents the most common ocular manifestation of COVID-19 infection, sight-threatening retinal involvement has been reported. Herein, we report and characterize with multimodal retinal imaging 5 cases of acute vision loss secondary to presumed chorioretinal vasculopathy temporally associated with COVID-19 infection with varying severity, visual morbidity, and treatment response, and review the available literature on the association between COVID-19 infection and retinal microvascular changes. Design: Observational case series and literature review. Methods: Multicenter case series of 5 patients who presented to academic centers and private offices with acute vision loss temporally associated with COVID-19 infection. A review of the literature was conducted using online databases. Results: 10 eyes of 5 patients, 3 men and 2 women, with a mean age of 30.8 years (median 33, range 16-44) were described. All patients had a recently preceding episode of COVID-19, with symptomatology ranging from mild infection to life-threatening encephalopathy. Treatment for their retinal disease included topical, oral, intravitreal, and intravenous steroids, steroid-sparing immunosuppression, retinal photocoagulation, antivirals, and antiplatelet and anticoagulant agents. Treatment response and visual recovery ranged from complete recovery of baseline acuity to permanent vision loss and need for chronic immunosuppression. Conclusions and Importance: Clinicians should be mindful of the potential for vision-threatening retinal involvement after COVID-19 infection. If found, treatment with both anti-inflammatory therapy and anticoagulation should be considered, in addition to close monitoring, as some patients with this spectrum of disease may require chronic immune suppression and/or anti-VEGF therapy.

Multivessel Epicardial Coronary Artery Thrombosis after Heart Transplantation

Introduction: Although cardiac allograft vasculopathy (CAV) remains one of the leading causes of graft failure after heart transplantation (HTx), simultaneous thrombosis of multiple epicardial coronary arteries (CA) is an uncommon finding. Case Report: A 43-year-old male patient with non-ischemic dilated cardiomyopathy underwent successful HTx in 2019. The first two years after HTx were uneventful, surveillance endomyocardial biopsies (EMB) did not reveal any rejection episodes, coronary CTA revealed only minimal non-calcified CA plaques. The patient was admitted to hospital due to fever and chest pain in 2021. Immunosuppressive therapy consisted of tacrolimus, mycophenolate-mofetil and methylprednisolone. ECG verified sinus rhythm. Laboratory test revealed elevated hsTroponin T, NT-proBNP and CRP levels. Cytomegalovirus, SARS-CoV-2-virus and hemoculture testing was negative. Several high-titre donor-specific HLA class I and II antibodies (DSAs;including complement-binding DQ7) could have been detected since 2020. Echocardiography confirmed mildly decreased left ventricular systolic function and apical hypokinesis. EMB verified mild cellular and antibody-mediated rejection (ABMR) according to ISHLT grading criteria. Cardiac MRI revealed inferobasal and apical myocardial infarction (MI);thus, an urgent coronary angiography was performed. This confirmed thrombotic occlusions in all three main epicardial CAs and in first diagonal CA. As revascularization was not feasible, antithrombotic therapy with acetylsalicylic acid, clopidogrel and enoxaparin was started for secondary prevention. Tests for immune system disorders, thrombophilia and cancer were negative. Patient suddenly died ten days after admission. Necropsy revealed intimal proliferation in all three main epicardial CAs, endothelitis, thrombosis, chronic pericoronary fat inflammation, fat necrosis, and subacute MI. CA vasculitis owing to persistent high-titre DSAs, chronic ABMR and acute cellular and antibody-mediated rejection led to multivessel CA thrombosis and acute multiple MI. ABMR after HTx may be underdiagnosed with traditional pathological methods. Pathologies affecting coronary vasculature of HTx patients with DSAs, unique manifestations of CAV lesions and occlusive thrombosis of non-stenotic, non-atherosclerotic lesions should be emphasized.Copyright © 2023

The Impact Of Years Since Transplant On The Clinical Course After SARS-CoV-2 Infection In Heart Transplant Recipients

Introduction: The risk of Severe Acute Respiratory Syndrome - Coronavirus-2 (SARS-CoV-2) infection and mortality is higher in heart transplant (HT) recipients compared to immunocompetent individuals. The impact of years since transplant on clinical course risk is unknown. We evaluated the differences in clinical phenotypes and outcomes according to years since transplant in HT recipients with active SARS-CoV-2 infection. Method(s): Consecutive HT recipients from our National Transplant Centre with confirmed SARS-CoV-2 between April 2020 and March 2022 were enrolled in this retrospective observational study. Patients were stratified into 2 groups: <5 years after HT (Group A) and >/= 5 years after HT (Group B). Result(s): A total of 63 HT recipients were enrolled [median age 56 (41,66) years, 32% female] with 33% of patients (n=21) assigned to Group A, and 67% (n=42) to Group B. In Group B patients, the prevalence of diabetes mellitus and cardiac allograft vasculopathy was significantly higher compared to those in Group A. Meanwhile, Group A patients were more likely to have a history of neutropenia prior to SARS-CoV-2 infection and were more frequently taking maintenance steroids and antimetabolite immunosuppressants (Table 1). Those recipients less than 5 years since HT were also significantly more likely than those >5 years out to develop the infection despite a 3rd dose of COVID vaccine (60% vs 31%, p 0.03).During the active infection, Group A recipients more frequently developed neutropenia (73% vs 27%, p 0.01), and trended towards higher rates of hospitalizations (57% vs 32%, p 0.06). Notably, none of the patients in Group A required mechanical ventilation compared to just under 10 % (n=4) of those in Group B. Further, no Group A patients died during the active infection hospitalization compared to 14% (n=6) of those in Group B. Conclusion(s): In HT recipients, years since transplant is a simple, clinically useful parameter stratifying outcomes after SARS-CoV-2 infection. While patients with less than 5 years since transplant are more likely to develop infection despite booster vaccination and require hospitalization, greater number of years since transplant was associated with more severe consequences during hospitalization.Copyright © 2022

Abnormal thrombosis and neutrophil activation increase hospital-acquired sacral pressure injuries and morbidity in COVID-19 patients.

Hospitalized patients have an increased risk of developing hospital-acquired sacral pressure injury (HASPI). However, it is unknown whether SARS-CoV-2 infection affects HASPI development. To explore the role of SARS-CoV-2 infection in HASPI development, we conducted a single institution, multi-hospital, retrospective study of all patients hospitalized for ≥5 days from March 1, 2020 to December 31, 2020. Patient demographics, hospitalization information, ulcer characteristics, and 30-day-related morbidity were collected for all patients with HASPIs, and intact skin was collected from HASPI borders in a patient subset. We determined the incidence, disease course, and short-term morbidity of HASPIs in COVID-19(+) patients, and characterized the skin histopathology and tissue gene signatures associated with HASPIs in COVID-19 disease. COVID-19(+) patients had a 63% increased HASPI incidence rate, HASPIs of more severe ulcer stage (OR 2.0, p<0.001), and HASPIs more likely to require debridement (OR 3.1, p=0.04) compared to COVID-19(-) patients. Furthermore, COVID-19(+) patients with HASPIs had 2.2x increased odds of a more severe hospitalization course compared to COVID-19(+) patients without HASPIs. HASPI skin histology from COVID-19(+) patients predominantly showed thrombotic vasculopathy, with the number of thrombosed vessels being significantly greater than HASPIs from COVID-19(-) patients. Transcriptional signatures of a COVID-19(+) sample subset were enriched for innate immune responses, thrombosis, and neutrophil activation genes. Overall, our results suggest that immunologic dysregulation secondary to SARS-CoV-2 infection, including neutrophil dysfunction and abnormal thrombosis, may play a pathogenic role in development of HASPIs in patients with severe COVID-19.

First reported case of parvovirus triggering painful widespread livedoid vasculopathy: another virus causing hypercoagulability?

Livedoid vasculopathy (LV) is a noninflammatory thrombotic disease caused by occlusion of dermal small vessels associated with systemic autoimmune disorders and coagulopathies. However, LV is often reported as being 'idiopathic', despite extensive investigation. We report a case of severe LV in an otherwise healthy 27-year-old woman, associated with parvovirus infection. The patient presented with a short history of a livedoid rash initially covering her torso, which spread to acral sites. Burning pains in the lower limb caused reduced mobility;systemically, she remained well and stable throughout. Examination revealed generalized acral skin pallor, livedoid patches of violet erythema and purpura with deep serpiginous ulcerations over extensor aspects of upper and lower limbs with a more broken/racemosa nonulcerated livedoid appearance on the trunk. On admission a transaminitisareas continued to ulcerate. Codeine was present with a creatine kinase of 1569 U L.1, but other blood test results were unremarkable including erythrocyte sedimentation rate, complement, cryoglobulins, antinuclear antibodies, antineutrophil cytoplasmic antibodies, extractable nuclear antigen, rheumatoid factor, myositis screen, antiphospholipid screen and thrombophilia screen. Parvovirus IgG and IgM were both positive and tested for, as the patient's young daughter had recently been diagnosed with 'slapped cheek disease'. Magnetic resonance imaging of the thighs showed a diffuse mild myositis;electromyography, nerve-conduction studies, barium swallow and computed tomography of the chest, abdomen and pelvis were all normal. An incisional skin biopsy was performed, which revealed a blood vessel with organizing (Solimani F, Mansour Y, Didona D et al. Development of severe pemphigus vulgaris following SARS-CoV-2 vaccination with BNT162b2. J Eur Acad Dermatol Venereol 2021;35: e649- 51) have been reported. The main proposed mechanisms for AstraZeneca vaccine-induced pemphigus could be a hyperimmune reaction in genetically predisposed individuals, with eventual formation of anti-desmoglein antibodies. An alternative hypothesis is that vaccine components could act as foreign antigens resulting in a cross-reaction with pemphigus antigens. The close association of COVID-19 vaccination with the acute onset of pemphigus in our patient, as well as exacerbations after subsequent vaccine administration, is more than coincidental. Considering the recent pandemic with COVID-19 and the widespread administration of the COVID-19 vaccine, continued observation and documentation of true adverse events is essential.

Defibrotide mitigates endothelial cell injury induced by plasmas from patients with COVID-19 and related vasculopathies.

BACKGROUND AND OBJECTIVES: COVID-19 progression is characterized by systemic small vessel arterial and venous thrombosis. Microvascular endothelial cell (MVEC) activation and injury, platelet activation, and histopathologic features characteristic of acute COVID-19 also describe certain thrombotic microangiopathies, including atypical hemolytic-uremic syndrome (aHUS), thrombotic thrombocytopenic purpura (TTP), and hematopoietic stem cell transplant (HSCT)-associated veno-occlusive disease (VOD). We explored the effect of clinically relevant doses of defibrotide, approved for HSCT-associated VOD, on MVEC activation/injury. METHODS: Human dermal MVEC were exposed to plasmas from patients with acute TMAs or acute COVID-19 in the presence and absence of defibrotide (5µg/ml) and caspase 8, a marker of EC activation and apoptosis, was assessed. RNAseq was used to explore potential mechanisms of defibrotide activity. RESULTS: Defibrotide suppressed TMA plasma-induced caspase 8 activation in MVEC (mean 60.2 % inhibition for COVID-19; p = 0.0008). RNAseq identified six major cellular pathways associated with defibrotide's alteration of COVID-19-associated MVEC changes: TNF-α signaling; IL-17 signaling; extracellular matrix (ECM)-EC receptor and platelet receptor interactions; ECM formation; endothelin activity; and fibrosis. Communications across these pathways were revealed by STRING analyses. Forty transcripts showing the greatest changes induced by defibrotide in COVID-19 plasma/MVEC cultures included: claudin 14 and F11R (JAM), important in maintaining EC tight junctions; SOCS3 and TNFRSF18, involved in suppression of inflammation; RAMP3 and transgelin, which promote angiogenesis; and RGS5, which regulates caspase activation and apoptosis. CONCLUSION: Our data, in the context of a recent clinical trial in severe COVID-19, suggest benefits to further exploration of defibrotide and these pathways in COVID-19 and related endotheliopathies.

Chronic skin ulcers in hemodialysis patient: A fatal case of calciphylaxis.

Calciphylaxis is a rare and deadly vascular disease with poorly understood pathophysiology and without definitive treatment. Early presentations include skin ulcers with risk factors including end stage renal disease on hemodialysis, hypertension, hyperlipidemia, and diabetes mellitus. In our case, we present an 80-year-old female with multiple risk factors including hemodialysis and clinical features of necrotic and gangrenous skin lesions diagnostic of calciphylaxis who became hemodynamically unstable and ultimately expired secondary to toxic sequelae. We illustrate this case to explore early clinical presentation, limitations of current disease management and treatments, and the role for further studies to improve diagnosis and reduce mortality.

COVID-19 Associated Vasculitis Confirmed by the Tissues RT-PCR: A Case Series Report.

BACKGROUND: Several cases of skin and central nervous system vasculopathy associated with COVID-19 in children have been published, but the information is rather limited. Our study aimed to describe these cases of vasculitis associated with COVID-19 in children. METHODS: In the retrospective-prospective case series study we included information regarding four children with COVID-19-associated vasculitis. In every case, we had a morphological description and the etiology was confirmed via real-time polymerase chain reaction during a tissue biopsy. RESULTS: The most involved systems were skin (4/4), respiratory (3/4), cardiovascular (2/4), nervous (1/4), eye (1/4), kidney (1/4), and inner year (1/4). All patients had increased inflammatory markers and thrombotic parameters (D-dimer). No patient met the criteria for multisystem inflammatory syndrome in children. Two patients met polyarteritis nodosa criteria, one met Henoch-Schonlein purpura criteria, and one met unclassified vasculitis criteria. All patients were treated with systemic glucocorticosteroids (two-pulse therapy). Non-biologic DMARDs were prescribed in all cases; 1/4 patients (25%) was treated with intravenous immunoglobuline, and 3/4 (75%) were treated with biologics (etanercept, tocilizumab, and adalimumab). CONCLUSIONS: Vasculitis associated with COVID-19 could be a life-threatening condition; SARS-CoV-2 might be a new trigger or etiological agent for vasculitis and other immune-mediated diseases. Further research and collection of similar cases are required.

Pathways of Coagulopathy and Inflammatory Response in SARS-CoV-2 Infection among Type 2 Diabetic Patients.

Chronic inflammation and endothelium dysfunction are present in diabetic patients. COVID-19 has a high mortality rate in association with diabetes, partially due to the development of thromboembolic events in the context of coronavirus infection. The purpose of this review is to present the most important underlying pathomechanisms in the development of COVID-19-related coagulopathy in diabetic patients. The methodology consisted of data collection and synthesis from the recent scientific literature by accessing different databases (Cochrane, PubMed, Embase). The main results are the comprehensive and detailed presentation of the very complex interrelations between different factors and pathways involved in the development of arteriopathy and thrombosis in COVID-19-infected diabetic patients. Several genetic and metabolic factors influence the course of COVID-19 within the background of diabetes mellitus. Extensive knowledge of the underlying pathomechanisms of SARS-CoV-2-related vasculopathy and coagulopathy in diabetic subjects contributes to a better understanding of the manifestations in this highly vulnerable group of patients; thus, they can benefit from a modern, more efficient approach regarding diagnostic and therapeutic management.

Livedoid vasculopathy - A diagnostic and therapeutic challenge.

Livedoid vasculopathy is a rare, chronic-recurrent occlusive disorder in the microcirculation of dermal vessels. The clinical appearance is characterized by Livedo racemosa, painful ulceration, located in the distal parts of the lower extremities, followed by healing as porcelain-white, atrophic scars, the so-called Atrophie blanche. Different conditions that can promote a hypercoagulable state, such as inherited and acquired thrombophilias, autoimmune connective-tissue diseases and neoplasms, can be associated with livedoid vasculopathy. Therefore, livedoid vasculopathy is currently considered to be a coagulation disorder, clearly distinguished from inflammatory vasculitis. Although there are hints to hypercoaguability and secondary inflammation, pathophysiology is not completely understood. Diagnosis is made by synopsis of history, clinical and histopathological findings. Early and adequate therapy is essential to maintain life quality and avoid irreversible complications. Better understanding of molecular mechanisms is required to establish appropriate therapy regimens. This article presents the current state of knowledge about livedoid vasculopathy and proposes an algorithmic approach for diagnosis and therapy.

Noninvasive Physiologic Assessment of Cardiac Allograft Vasculopathy Is Prognostic for Post-Transplant Events.

BACKGROUND: Cardiac allograft vasculopathy (CAV) causes impaired blood flow in both epicardial coronary arteries and the microvasculature. A leading cause of post-transplant mortality, CAV affects 50% of heart transplant recipients within 10 years of heart transplant. OBJECTIVES: This analysis examined the outcomes of heart transplant recipients with reduced myocardial blood flow reserve (MBFR) and microvascular CAV detected by 13N-ammonia positron emission tomography (PET) myocardial perfusion imaging. METHODS: A total of 181 heart transplant recipients who underwent PET to assess for CAV were included with a median follow-up of 4.7 years. Patients were classified into 2 groups according to the total MBFR: >2.0 and ≤2.0. Microvascular CAV was defined as no epicardial CAV detected by PET and/or coronary angiography, but with an MBFR ≤2.0 by PET. RESULTS: In total, 71 (39%) patients had an MBFR ≤2.0. Patients with an MBFR ≤2.0 experienced an increased risk for all outcomes: 7-fold increase in death or retransplantation (HR: 7.05; 95% CI: 3.2-15.6; P < 0.0001), 12-fold increase in cardiovascular death (HR: 12.0; 95% CI: 2.64-54.12; P = 0.001), and 10-fold increase in cardiovascular hospitalization (HR: 10.1; 95% CI: 3.43-29.9; P < 0.0001). The 5-year mean survival was 302 days less than those with an MBFR >2.0 (95% CI: 260.2-345.4 days; P < 0.0001). Microvascular CAV (adjusted HR: 3.86; 95% CI: 1.58-9.40; P = 0.003) was independently associated with an increased risk of death or retransplantation. CONCLUSIONS: Abnormal myocardial blood flow reserve, even in the absence of epicardial CAV, identifies patients at a high risk of death or retransplantation. Measures of myocardial blood flow provide prognostic information in addition to traditional CAV assessment.

Acute testicular infarction in the setting of SARS-CoV-2 infection and diabetic vasculopathy.

Acute testicular pain with no arterial flow on Doppler ultrasonography is highly consistent with testicular torsion. In adults, there are rare etiologies of testicular infarction other than torsion, including infection, vasculitis, and trauma. We describe a 41-year-old man with type 2 diabetes complicated by severe vasculopathy and positive SARS-CoV-2 status presenting with acute right testicular pain. Surgical exploration and pathology were concerning for arteriosclerosis and vasculitis. These observations suggest that medically complex patients presenting with acute testicular pain in the setting of COVID-19 infection could be at risk for ischemia; causes of testicular pain beyond torsion should be considered.

Imaging of COVID-19 vasculopathy from head to toe: Egyptian collective experience after 2 years of the pandemic

Background: COVID-19 vasculopathy is a critical condition that impacts the disease prognosis including vasculitis and thromboembolic complications. This study aimed to provide the Egyptian experience about the COVID-19 vasculopathy during the past two years of the pandemic and to collectively include the different modalities and imaging techniques for the diagnosis of cerebrovascular, pulmonary, gastrointestinal, and peripheral arterial vascular complications. Result(s): This is a multi-center retrospective analysis of 3500 PCR-proved COVID-19 infection between March 2020 and December 2021. A cohort of 282 consecutive patients with COVID-19 vasculopathy was considered for inclusion. They included 204 males and 78 females (72:28%). The mean age was 68 years, and age ranged from 48 to 90 years. Five radiologists evaluated the different imaging examinations in consensus including computed tomography (CT), CT-angiography (CTA), CT-perfusion (CTP), magnetic resonance imaging (MRI), MR-arteriography (MRA), and MR-venography (MRV). 244/282 (86.5%) patients suffered from non-hemorrhagic cerebral ischemic infarctions. 13/282 (4.6%) patients suffered from hemorrhagic cerebral infarctions. 5/282 (1.8%) patients suffered from cerebral vasculitis. Pulmonary vascular angiopathy was detected in 10/282 (3.5%) patients, including pulmonary embolism in 10/10 patients, pulmonary infarctions in 8/10 patients, pulmonary vascular enlargement in 5/10 patients, and vascular "tree-in-bud" sign in 2/10 patients. Intestinal ischemia and small bowel obstruction were detected in 3/282 patients (1%) while GIT bleeding was encountered in 4/282 patients (1.4%). Lower limb arterial ischemia was found in 3/282 patients (1%). Additionally;39/282 (13.8%) patients developed peripheral deep venous thrombosis (DVT) due to prolonged ICU recumbence while 28/282 (10%) patients developed jugular vein thrombosis sequel to prolonged catheterization. A p value (0.002) and (r) = 0.8 statistically proved strong significant relation between COVID-19 vasculopathy and D-dimer levels. Conclusion(s): Multi-system vasculopathy was a serious complication of COVID-19 which impacted the patients' morbidity and mortality. An Egyptian experience about the COVID-19 vasculopathy during the past two years of the pandemic was provided. It encountered the different modalities and imaging techniques for the diagnosis of cerebrovascular, pulmonary, gastrointestinal, and peripheral arterial COVID-19 vascular complications. Copyright © 2022, The Author(s).

Dabbing Lung Injury Managed by Vv Ecmo

INTRODUCTION: E-cigarette or vaping-associated lung injury (EVALI) is an uncommon complication of e-cigarettes or vaping. Most cases are associated with tetrahydrocannabinol (THC) containing products. "Dabbing" refers to the process of ingesting high concentrations of THC-containing oils or waxes with butane solvents to vaporize cannabinoids for inhalation. Another distinction is the presence of impurities and unpurged butane in the vapors inhaled by the users. DESCRIPTION: A 29-year-old male presented with cough, dyspnea, and fever seven days prior to admission. He reported smoking marijuana but denied vaping. Initial chest radiograph demonstrated multifocal pneumonia. PCR for SARS-CoV-2 was negative. He required four liters of supplemental oxygen. Physical exam was remarkable for diffuse pulmonary crackles. Broad spectrum antibiotics for pneumonia were initiated. Oxygen requirements rapidly increased, prompting intubation 48 hours from presentation. Ventilator settings escalated to a positive end-expiratory pressure of 18 cm H2O with 100% FiO2. Computed tomography angiography ruled out pulmonary embolism, however showed diffuse patchy nodular and confluent opacities. Respiratory cultures grew commensal flora and blood cultures were negative. Comprehensive laboratory investigations for an infectious etiology and autoimmune vasculitis were negative. In further discussion with the patient's wife, he has been "dabbing" for the past six months. High dose intravenous steroids were initiated. The patient continued to have refractory hypoxemic and hypercapnic respiratory failure with ARDS requiring prone positioning. The patient ultimately required transition to veno-venous extracorporeal membrane oxygenation (VV-ECMO). The patient received 12 days of VV-ECMO and was eventually liberated after 19 days of ventilator support. At discharge he was asymptomatic, at his baseline level of function, and required no supplemental oxygen. He was discharged on daily steroids with a taper and outpatient follow-up. DISCUSSION: The necessity of VV-ECMO utilization in "dabbing" associated acute lung injury represents a rare severe presentation. Dabbing is emerging as a trend among young adults and represents an under-investigated cause of severe inhalational lung injury.

A RARE CASE OF ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES (ANCA)-ASSOCIATED VASCULITIS IN THE SETTING OF COVID-19 INFECTION

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: Anti-neutrophil cytoplasmic antibody-associated vasculitis (ANCA-AV) is an autoimmune mediated inflammation of small and medium sized vessel walls. The occurrence of this autoimmune vasculitis is typically associated with underlying infection, medications, and genetic predisposition.(1) The objective of this case report is to describe a rare presentation of ANCA-AV in the setting of COVID-19 infection. CASE PRESENTATION: A 67-year-old male presented to the hospital with a three-week history of cough productive of brown sputum, epistaxis, fatigue, decreased appetite, and unintentional weight loss. During the previous week, he experienced worsening dyspnea and bilateral lower extremity swelling. On physical examination, he was hypoxic requiring 4L of supplemental oxygen to maintain saturations greater than 90%. Diffuse and bilateral wheezes were heard on auscultation of his lungs. A tender petechial rash was dispersed over his limbs, trunk, oropharynx, and nasopharynx. A basic metabolic panel revealed a mild, acute renal impairment. Urinalysis showed new onset proteinuria and hemoglobinuria. Nasopharyngeal swab was positive for SARS-COV-2. Contrast-enhanced computed tomography of the chest revealed diffuse, bilateral ground glass opacities and interstitial changes. Therapy with piperacillin-tazobactam was started for presumed superimposed bacterial community acquired pneumonia in the setting of COVID-19 infection. On day three of hospitalization, the petechial rash progressed to hemorrhagic blisters. His oral petechiae were now ulcerated. A punch biopsy of the affected skin showed leukocytoclastic vasculitis. Anti-Proteinase 3 (PR3) antibodies were positive. Subsequent renal biopsy showed pauci-immune focal necrotizing crescentic glomerulonephritis consistent with ANCA-AV. Therapy with intravenous pulse dose corticosteroids led to improvement in his rash and body aches, and he was discharged home on oral steroids ten days after admission. DISCUSSION: This report describes a rare case of ANCA-AV in the setting of recent COVID-19 infection. Differentiation of ANCA-AV, bacterial and COVID-19 pneumonia can be challenging on chest imaging alone.(1) New onset renal impairment, hematuria, proteinuria and the presence of the petechial rash were suspicious for co-existing ANCA-AV in this patient. COVID-19- associated cytokine storm and formation of neutrophil extracellular traps (NETs) is postulated to be the underlying cause.(1-3) NETs present myeloperoxidase (MPO) and PR3 antigens to the immune system. Formation of auto-antibodies to MPO and PR3 lead to the development of ANCA-AV. The findings of NETs on kidney biopsy specimens in patients with ANCA-AV supports this hypothesis.(1,2) CONCLUSIONS: To avoid the misdiagnosis of COVID-19-induced vasculitis, a low threshold to investigate co-existing vasculitis in patients with COVID-19 and associated clinical findings is highly recommended. Reference #1: Izci Duran T, Turkmen E, Dilek M, Sayarlioglu H, Arik N. ANCA-associated vasculitis after COVID-19. Rheumatol Int. 2021;41(8):1523-1529. Reference #2: Uppal NN, Kello N, Shah HH, et al. De Novo ANCA-Associated Vasculitis With Glomerulonephritis in COVID-19. Kidney Int Rep. 2020;5(11):2079-2083. Reference #3: Cobilinschi C, Cobilinschi C, Constantinescu A, Draniceanu I, Ionescu R. New-Onset ANCA-Associated Vasculitis in a Patient with SARS-COV2. Balkan Med J. 2021;38(5):318-320. DISCLOSURES: No relevant relationships by Andrei Hastings No relevant relationships by Jason Lane No relevant relationships by Tanya Marshall No relevant relationships by Palak Rath No relevant relationships by Sterling Shriber No relevant relationships by inderprit Singh No relevant relationships by Samuel Wiles

Bilateral persistent placoid maculopathy following COVID-19 Vaccines: real or co-incidence?

Purpose : COVID-19 vaccination has been accompanied by reports of inflammatory events. We aim to report the first case of bilateral persistent placoid maculopathy (PPM) following COVID-19 vaccination. Methods : Case report Results : A 58-year-old man presented with bilateral sudden painless decrease in vision approximately two weeks after the second dose of AstraZenaca® COVID-19 vaccine. Visual acuity (VA) at presentation was 1.00 LogMAR in the right eye (RE) and hand movement in the left eye (LE). He had no known medical or ophthalmic history, up until after his first AstraZenaca® COVID-19 vaccine dose, he was diagnosed with palmoplantar pustular psoriasis and was started on 60mg of oral Prednisolone. Fundus examination revealed bilateral well-delineated whitish plaque-like macular lesions involving the fovea, sparing the peripapillary region in the RE (Figure 1a & e). Multimodal imaging including fluorescein angiography, indocyanine-green angiography, fundus autofluorescence and optical coherence tomography were consistent with PPM (Figure 1 & 2). Infective and auto-immune screen were all negative apart from a positive MPO-ANCA, prompting a rheumatology review which subsequently excluded any systemic vasculitis. Patient was monitored closely and his VA improved and stabilised with tapering regime of oral Prednisolone. To prevent relapse of PPM, patient was commenced on Mycophenolate Mofetil as a long-term steroid sparing immunosuppression. Conclusions : Our case demonstrated a likely inflammatory or autoimmune response affecting choriocapillaris driven by the COVID-19 vaccine and there may be a correlation between the two. The patient in our case portrayed features classical of PPM, which is a selective autoimmune vasculitis causing microinfarcts on choriocapillaris, resulting in focal choroidal hypoperfusion after the COVID-19 vaccine. (Figure Presented).

Vasculopathy and Increased Vascular Congestion in Fatal COVID-19 and Acute Respiratory Distress Syndrome.

Rationale: The leading cause of death in coronavirus disease 2019 (COVID-19) is severe pneumonia, with many patients developing acute respiratory distress syndrome (ARDS) and diffuse alveolar damage (DAD). Whether DAD in fatal COVID-19 is distinct from other causes of DAD remains unknown. Objective: To compare lung parenchymal and vascular alterations between patients with fatal COVID-19 pneumonia and other DAD-causing etiologies using a multidimensional approach. Methods: This autopsy cohort consisted of consecutive patients with COVID-19 pneumonia (n = 20) and with respiratory failure and histologic DAD (n = 21; non-COVID-19 viral and nonviral etiologies). Premortem chest computed tomography (CT) scans were evaluated for vascular changes. Postmortem lung tissues were compared using histopathological and computational analyses. Machine-learning-derived morphometric analysis of the microvasculature was performed, with a random forest classifier quantifying vascular congestion (CVasc) in different microscopic compartments. Respiratory mechanics and gas-exchange parameters were evaluated longitudinally in patients with ARDS. Measurements and Main Results: In premortem CT, patients with COVID-19 showed more dilated vasculature when all lung segments were evaluated (P = 0.001) compared with controls with DAD. Histopathology revealed vasculopathic changes, including hemangiomatosis-like changes (P = 0.043), thromboemboli (P = 0.0038), pulmonary infarcts (P = 0.047), and perivascular inflammation (P < 0.001). Generalized estimating equations revealed significant regional differences in the lung microarchitecture among all DAD-causing entities. COVID-19 showed a larger overall CVasc range (P = 0.002). Alveolar-septal congestion was associated with a significantly shorter time to death from symptom onset (P = 0.03), length of hospital stay (P = 0.02), and increased ventilatory ratio [an estimate for pulmonary dead space fraction (Vd); p = 0.043] in all cases of ARDS. Conclusions: Severe COVID-19 pneumonia is characterized by significant vasculopathy and aberrant alveolar-septal congestion. Our findings also highlight the role that vascular alterations may play in Vd and clinical outcomes in ARDS in general.