Bilateral Diffuse Ground-glass Opacities Research Articles

Radioclinical Profile of Eosinophilic Lung: A Case Series.

In this study, we present findings from an analysis of 17 patients diagnosed with eosinophilic lung disease, with a majority (64.70%) being male. The average age of the patients was 54±13.22 years. A history of uncontrolled asthma was noted in nine cases. The clinical picture was characterized by persistent dyspnea and cough. Blood hypereosinophilia was present in all cases, with a median of 1770 cells/ul. Two patients had a pulmonary eosinophilia greater than 25%.Radiological findings were consistent with diffuse bilateral ground-glass opacities or areas of consolidation in the majority of cases. The main etiologies identified were chronic eosinophilic pneumonia (12 cases), followed by eosinophilic granulomatosis with polyangiitis(3 cases), idiopathic hypereosinophilic syndrome (1 case) and drug-induced hypereosinophilia (1 case). All patients were treated with systemic corticosteroids, with the addition of immunosuppressive therapy necessary in three cases. Notably, five relapses were recorded after corticosteroid therapy was stopped.

Pneumocystis jirovecii pneumonia: a case report

Introduction and importancePneumocystis jirovecii (PJP) pneumonia is a serious life-threatening condition in immunocompromised individuals and is often associated with human immunodeficiency virus (HIV) + patients. We describe a case of PJP pneumonia which provided a diagnostic challenge in a patient who presented with no known risk factors leading to a delay in initiation of appropriate antibiotic therapy.Case presentationA 71-year-old previously healthy white/Caucasian male presented with subacute hypoxic respiratory failure due to multifocal pneumonia with diffuse bilateral ground glass opacities with consolidations despite prior treatment with antibiotics and steroids. He was admitted and started on intravenous broad-spectrum antibiotics but continued to deteriorate, eventually requiring intubation and transfer to the ICU. Bronchoscopy revealed PJP and treatment was initiated, but the patient developed refractory shock and multiorgan failure, and ultimately died. It was later discovered that he was HIV-1 positive.Clinical discussionPJP, as a potential cause of his presentation, was not considered given that our patient lacked any overt risk factors for PJP pneumonia. He continued to worsen despite broad spectrum antibiotic therapy and hence bronchoscopy was pursued. His clinical profile, in hindsight, was suspicious for PJP pneumonia and early PJP-directed antibiotic therapy may have prevented a fatal outcome, as in this case. There was an element of cognitive bias across multiple providers which may have contributed to the delay in treatment despite his rapid clinical decline while on conventional pneumonia treatment protocol. His diagnosis was later evident when his BAL-DFA grew PJP in addition to his low levels of CD4 and CD8 cells. He was found to be HIV-1 positive five days after his death; there was a delay in this diagnosis since all positive HIV tests from the hospital are reported as ‘pending’ until the presumptive positive sample goes to the Connecticut Department of Public Health State laboratory for the confirmatory test. PJP-targeted therapies were initiated later in our patient’s hospital course when the infection had progressed to refractory septic shock with multiorgan failure and eventual death.ConclusionPJP pneumonia is a fatal disease if not recognized early in the course of illness, and the patient usually undergoes multiple antibiotic regimens before they are diagnosed and receive appropriate clinical care. The gold standard of diagnostic testing for PJP is by obtaining bronchial washings through a flexible bronchoscopy and the turnaround time for such results may take a few days to result. A significant proportion of patients may not have any overt risk factors of immunosuppression and early empiric treatment for PJP may be clinically appropriate as the delay in diagnosis may be associated with significant morbidity and mortality risk.

A NSCLC patient with novel ALK fusion responded to crizotinib therapy after alectinib-induced interstitial lung disease.

A 54-year-old, non-smoking woman was diagnosed as stage ⅣB adenocarcinoma with widespread bone metastasis (cT4N2M1c) in our hospital. Immunohistochemistry (Ventana D5F3 antibody) result showed the presence of ALK rearrangement; and next-generation sequencing assay (NGS) indicated EML4-ALK fusion (E6:A20) with concurrent CCDC148-ALK (C1:A20), PKDCC-ALK (Pintergenic:A20)and VIT-ALK (V15:A20) fusions. After 32 weeks of alectinib treatment, the patient complained cough and exertional chest distress but had no sign of infection. Computed tomography (CT) showed bilateral diffuse ground glass opacities, suggesting a diagnosis of alectinib-related interstitial lung disease (ILD). Following corticosteroid treatment and discontinuation of alectinib, clinical presentations and CT scan gradually improved, but the primary lung lesions enlarged in the regular follow-up. The administration of a first-generation ALK inhibitor crizotinib was then initiated and the disease was stable for 25 months without recurrence of ILD.

Severe Presentation of Acute Eosinophilic Pneumonia Possibly Secondary to Recent E-Cigarette Use

A 52-year-old man with type 2 diabetes mellitus presented with fever and hypoxemic respiratory failure requiring intubation. He had no history of pulmonary disease but recently started smoking nicotine-containing electronic cigarettes (e-cigarettes) after 10 years of tobacco abstinence. He had diffuse bilateral ground-glass opacities on chest imaging, 11% peripheral eosinophilia (absolute eosinophil count 1300/µL), and 50% eosinophilia in the bronchoalveolar lavage fluid without evidence of bacterial, viral, fungal, or parasitic infection. Hypoxia and pulmonary infiltrates rapidly resolved after initiation of high-dose corticosteroids after bronchoscopy. A diagnosis of acute eosinophilic pneumonia was made, possibly secondary to recent e-cigarette use.

Diffuse Alveolar Hemorrhage: A Rare Underlying Disease in a Child with Chronic Respiratory Symptoms

Background: Diffuse lung disease (DLD), conventionally known as interstitial lung disease (ILD), encompasses a spectrum of diseases involving the pulmonary parenchyma with impairment of gaseous exchange. Most of the diseases under DLD have similar presentations, but appropriate investigations can delineate the exact disease. Diffuse alveolar hemorrhage (DAH) is one of the diseases under this umbrella group of DLD. Clinical Description: A 3-year-old girl suffering from persistent breathlessness and intermittent hypoxic exacerbations over 1 year, presented to us with acute respiratory worsening. She was underweight with stunting and had severe pallor. She had received blood transfusions in previous hospitalizations. Chest-X-ray shows reticular opacities, with High Resolution Computed Tomography (HRCT) chest showing bilateral diffuse ground glass opacities involving all lobes with the prominent pulmonary artery. The broncho-alveolar lavage showed hemosiderin-laden macrophages, thereby confirming alveolar hemorrhage. Antinuclear antibody was positive, though double-stranded DNA and Anti-neutrophil cytoplasmic antibody were negative. The child was thus diagnosed with a case of DAH, probably, immune mediated. Management: The child was treated with supportive care, including oxygen, intravenous fluids, antibiotics, and packed red cell transfusion. Even after improvement in hemoglobin, oxygen dependency persisted. The child was then administered Intravenous Immunoglobulin and prednisolone, to which the child showed a response with gradual weaning off oxygen. Conclusions: In any child presenting with persistent respiratory symptoms, especially exercise intolerance, over a prolonged period with intermittent hypoxic exacerbations, a pediatrician should consider diagnoses beyond infections and multitrigger wheezing. Such manifestations, particularly if associated with failure to thrive, may be due to DLD. DAH, a rare form of DLD, may be a possibility in such children.

ATYPICAL PRESENTATION OF FAT EMBOLISM SYNDROME IN AN IMMUNOCOMPROMISED PATIENT

ATYPICAL PRESENTATION OF FAT EMBOLISM SYNDROME IN AN IMMUNOCOMPROMISED PATIENT

INVASIVE PULMONARY FUSARIOSIS WITH SUPERIMPOSED HISTOPLASMOSIS IN AN IMMUNOCOMPETENT HOST

INVASIVE PULMONARY FUSARIOSIS WITH SUPERIMPOSED HISTOPLASMOSIS IN AN IMMUNOCOMPETENT HOST

A CASE REPORT OF COMPLICATIONS IN A SURVIVOR OF SEVERE COVID-19: PULMONARY FIBROSIS AND LONG-TERM SUPPLEMENTAL OXYGEN REQUIREMENT

TYPE: Case Report TOPIC: Diffuse Lung Disease INTRODUCTION: COVID 19 has caused about 4.5 million deaths worldwide and still counting. More than 50% of survivors develop post covid respiratory symptoms. we are presenting a case report of severe COVID 19 survivor with diffuse pulmonary fibrosis after longterm follow up. CASE PRESENTATION: 75 year old male with BMI 38, history of hypertension, CAD, CKD, diabetes presented with shortness of breath. Further testing came back COVID 19 and influenza B positive, CT chest showing bilateral diffuse ground glass opacities and infiltrates consistent with COVID 19 pneumonia. He was given empiric antibiotics, IV steroids, plasma therapy and supportive care with NIV, weaned down to vapotherm 40 L, 100%fio2. He didn’t undergo mechanical ventilation, has been in hospital for 50 days and was discharged on 5L oxygen. After 8 months, he was readmitted to hospital for pneumonia requiring 7 L supplemental oxygen, followup CT chest showing diffuse bilateral pulmonary fibrosis which was not present on initial CT. Upon discharge he continued to require 5l supplemental oxygen with no significant symptoms after 1 month follow up. DISCUSSION: In our case obesity, obstructive sleep apnea, uncontrolled hypertension, coexisting infection with influenza are likely risk factors for prolonged oxygen requirement and pulmonary fibrosis. Cytokine storm in severe covid could be a triggering factor. Chronic post covid 19 symptoms beyond 12 weeks should get further evaluation by pulmonary function tests, high resolution CT to asses severity. CONCLUSIONS: Close followup and early intervention can decrease mortality. The role of antifibrotic drugs, long-term steroid therapy, chest physical therapy need to be evaluated. DISCLOSURE: Nothing to declare. KEYWORD: post covid, pulmonary fibrosis, long term oxygen

A CASE OF INTERMITTENT HEMOPTYSIS: THE SPECTRUM OF ANTIPHOSPHOLIPID ANTIBODY SYNDROME

TYPE: Late Breaking Case Report TOPIC: Pulmonary Manifestations of Systemic Disease INTRODUCTION: A 46 year old WM presented with several years of intermittent hemoptysis. Symptoms resolve spontaneously, improve with diuresis or required antibiotics/steroids. Evaluation for infection was negative and was maintained on daily prednisone with benefit. Malaise, hypoxemia, edema with hemoptysis but no other associated symptoms. CASE PRESENTATION: Past medical history includes CVA at age 24 related to antiphospholipid antibody syndrome and treated with anticoagulation. No other organ involvement reported. Medical history: CKD, HTN, non-ischemic cardiomyopathy. Remote 15PY tobacco history, no other exposures. On exam, room air O2 saturation 92%, desaturation to 70s with exertion. Oropharynx class III Mallampati score, lungs clear, CV RRR, no murmurs, gallops, extremities with lower extremity edema, no clubbing, rashes, ecchymosis, petechiae. Evaluation: negative ANA, DS-DNA, ENA, ANCA, anti-GBM, anti-CCP Ab. Normal immunoglobulins, complements and positive lupus anticoagulant. Chemistries: elevated creatinine, WBC 13.1, Hemoglobin 10.5, platelets 89. BNP 659, normal urinalysis. PFTs: restriction and reduced DLCO. Cardiac echo: moderately dilated LV, LVEF 40%, normal right ventricular size and function. CT chest showed diffuse bilateral pulmonary ground glass opacities. DISCUSSION: Clinical course included empiric antibiotics, bronchoscopy, heart failure management, high-dose steroids, and cyclophosphamide initiation for diffuse alveolar hemorrhage. He had clinical improvement but required readmission with progressive pulmonary symptoms, acute renal failure, and an acute ischemic stroke despite adequate anticoagulation. This met criteria for Catastrophic Antiphospholipid Antibody Syndrome. He was treated with plasma exchange, steroids/cyclophosphamide and rituximab. CONCLUSIONS: This case represents the spectrum of disorders seen in antiphospholipid antibody syndrome. Antiphospholipid antibody syndrome can have a broad range of presentation in the lungs. DISCLOSURE: Nothing to declare. KEYWORD: ANTIPHOSPHOLIPID ANTIBODY SYNDROME

A Nonimmune Hydrops Case.

A Nonimmune Hydrops Case.

Progressive lymphocytosis in familial hemophagocytic lymphohistiocytosis with lymphocytic interstitial pneumonia: a case report

Familial hemophagocytic lymphohistiocytosis (FHL) is a genetically heterogeneous disorder which is less typical in adults than pediatric patients. In this study, we reported a rare case of adult-onset FHL3 with progressive lymphocytosis and lymphocytic interstitial pneumonia (LIP). A 20-year old female was admitted to our institution for persistent cough with fever. A chest high-resolution computed tomography (HRCT) scan showed diffuse bilateral ground glass opacities (GGO). A lung biopsy revealed infiltration of lymphocyte in the pulmonary interstitium. The patient was treated with corticosteroids and immunosuppressants, followed by significant clinical improvement although lymphocytosis still persisted. The definitive diagnosis of FHL was based on whole genome sequencing by which heterozygous mutations in UNC13D gene were identified. Lymphocytosis may be a remarkable feature of some patients with FHL. Performing gene sequencing is important to improve the recognition of FHL to avoid misdiagnosis.

Diffuse Alveolar Hemorrhage as a Life-Threatening Feature of Juvenile Onset Systemic Lupus Erythematosus: A Case-Based Review

Diffuse alveolar hemorrhage is an uncommon but serious complication of systemic lupus erythematosus (SLE). We reported a 17-year-old boy with idiopathic thrombocytopenic purpura, who admitted with pallor and petechiae. He had Coombs positive hemolytic anemia and thrombocytopenia (hemoglobin 6.2g/dL, platelets 10,000/mm3 and lactate dehydrogenase 1024U/L), cough, tachypnea, and desaturation in the room air. Chest radiograph revealed bilateral diffuse alveolar opacities and computed tomography showed bilateral diffuse alveolar infiltrates and ground-glass opacity consistent with pulmonary hemorrhage. Anti-nuclear antibody (ANA) was 1:640 with positive Ro and anti-phospholipid antibodies, low C3 and C4, but negative anti-double-stranded DNA. He was treated with pulse methylprednisolone followed by tapering doses of steroids and with 6 doses of intravenous cyclophosphamide once every two weeks followed by mycophenolate mofetil. He had no relapse in the following 3 years. The case was reported to emphasise this life-threatening complication of juvenile-onset SLE and we reviewed the literature.

Drug-induced hypersensitivity syndrome caused by minodronic acid hydrate

BackgroundDrug-induced hypersensitivity syndrome (DIHS)/drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is an important adverse reaction caused by a few drugs. Reactivation of human herpesvirus 6 (HHV-6) is known to be associated with its pathogenesis. DIHS occasionally manifests as pulmonary lesions with a variety of imaging findings.Case presentationAn 83-year-old woman started taking minodronic acid hydrate 5 years before admission. She noticed a generalized skin rash 44 days before admission and started oral betamethasone-d-chlorpheniramine maleate combination tablets for allergic dermatitis. She developed a fever and cough in addition to the rash, and was referred to our hospital. Laboratory data showed a high level of eosinophils and liver and biliary enzymes. Computed tomography (CT) studies revealed bilateral diffuse ground-glass opacities with ill-defined centrilobular nodules from the central to peripheral regions of the lungs. Transbronchial lung cryobiopsy specimens showed that lymphocyte infiltration was observed in the alveolar walls and fibrinous exudates and floating macrophages in the alveolar lumina. Immunohistochemistry of biopsy specimens showed more CD4+ lymphocytes than CD8+ lymphocytes, while few Foxp3+ lymphocytes were recognized. The serum anti-HHV-6 immunoglobulin G titer increased at 3 weeks after the first test. Based on these findings, we diagnosed her with DIHS. We continued care without using corticosteroids since there was no worsening of breathing or skin condition. Eventually, her clinical symptoms chest CT had improved. Minodronic acid hydrate was identified as the culprit drug based on the positive results of the patch test and drug-induced lymphocyte stimulation test.ConclusionsWe described the first case of DIHS caused by minodronic acid hydrate. Lung lesions in DIHS can present with bilateral diffuse ground-glass opacities and ill-defined centrilobular nodules on a CT scan during the recovery phase. Clinicians should be aware of DIHS, even if patients are not involved with typical DIHS/DRESS-causing drugs.

A RAPIDLY PROGRESSIVE AND RARE ILLNESS: AUTOANTIBODIES AGAINST MELANOMA DIFFERENTIATION-ASSOCIATED PROTEIN 5 (ANTI-MDA5): AMYOPATHIC DERMATOMYOSITIS WITH PROGRESSIVE INTERSTITIAL LUNG DISEASE THAT DEVELOPED AFTER COVID-19 VACCINE

TOPIC: Critical Care TYPE: Global Case Reports INTRODUCTION: Anti-MDA5 dermatomyositis is a subtype of dermatomyositis characterized by a high risk of rapidly progressive interstitial lung disease. It is characterized by fever, progressive shortness of breath, joint swelling and skin ulcerations. (1) There is invariable hyper-ferritinemia and radiographically there is a pattern of diffuse bilateral ground glass opacities. Complications with spontaneous pneumothorax and pneumomediastinum are not uncommon. Diagnosis is confirmed by biopsy as well as serum antibodies against MDA5. A known trigger is viral infection. (2) CASE PRESENTATION: We present the case of a 58-year-old man who was admitted to the Intensive Care Unit on account of respiratory failure and shock. He had a progressive Illness that started 4 days after receiving a novel mRNA COVID-19 Vaccine. He developed bilateral extremities edema, oral sores, worsening fatigue and dyspnea on exertion. He failed outpatient treatment for empiric pneumonia as well as prednisone for vaccine reaction. He presented to the hospital with fever, progressive dyspnea and fatigue. On physical exam he had oral blisters, digital tip ischemia and ulceration. His vital signs were pertinent for a SpO2 of 90% on ventilator support. A chest CT revealed diffuse and sub-pleural ground-glass opacities.There was an extensive negative infectious work up from serum, urine and BAL samples. These included negative SARS COV2 Antigen and SARS-Cov2 IgG. His inflammatory markers were pertinent for a positive ANA with titer of 1:320, Ferritin of 2,143 mcg/L, LDH of 1,105 U/L and CRP of 2.7mg/dL. Based on this information the differential for amyopathic dermatomyositis with progressive interstitial lung disease was considered. A skin biopsy of his index finger confirmed the diagnosis. His therapeutic interventions through his hospitalization included a trial of stress dose steroids, cyclophosphamide, IVIG, colchicine and tacrolimus. His ICU course was complicated by pneumomediastinum, pneumothorax and pericardial effusion. These were managed by placing a chest tube thoracotomy and pericardial drain respectively. His plan of care was changed to comfort measures after he had a drastic and prolonged desaturation episode without recovery. DISCUSSION: For conditions that lead to cytokine storm with subsequent development of ARDS or multi-organ dysfunction;there is a progressive clinical deterioration and high risk of death. We had insufficient evidence to definitively demonstrate a direct correlation between the vaccination and the patient's illness. CONCLUSIONS: In conditions that lead to Cytokine storm with multi-organ dysfunction targeting timely control of this inflammatory cascade via immunomodulation, cytokine antagonist and reduction of inflammatory cell infiltration in particular early in the process could lead to a reduction in mortality. REFERENCE #1: Fiorentino D, Chung L, Zwerner J, Rosen A, Casciola-Rosen L. The mucocutaneous and systemic phenotype of dermatomyositis patients with antibodies to MDA5 (CADM-140): a retrospective study. J Am Acad Dermatol. 2011;65(1):25-34. doi:10.1016/j.jaad.2010.09.016 REFERENCE #2: Sakamoto N., Ishimoto H., Nakashima S. Clinical features of anti-MDA5 antibody-positive rapidly progressive interstitial lung disease without signs of dermatomyositis. Intern Med. 2019;58(6):837–841. doi: 10.2169/internalmedicine. 1516-18. REFERENCE #3: Margherita Giannini,1 Mickael Ohana,2 Benoit Nespola,3 Giovanni Zanframundo,4,5 Bernard Geny,1,6 and Alain Meyer1,6,7 Similarities between COVID-19 and anti-MDA5 syndrome: what can we learn for better care? Eur Respir J. 2020 Sep;56(3): 2001618. Published online 2020 Sep DISCLOSURES: No relevant relationships by Ashlie Arthur, source=Web Response No relevant relationships by Leonel Carrasco, source=Web Response no disclosure on file for Chad Case;No relevant relationships by Juan Gaitan Rueda, source=Web Response

TOLUENE-INDUCED ACUTE LUNG INJURY: CASE REPORT

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Toluene is an aromatic hydrocarbon widely used as a solvent in industrial and commercial products including paints, adhesives, ink, and rubber. It is occasionally used as an inhalant drug for its intoxicating properties. While mostly known for producing neurologic effects, here we report a case of toluene induced acute lung injury. CASE PRESENTATION: A 61-year-old female with a medical history of alcohol abuse, depression, congestive heart failure with preserved ejection fraction presented with one week of weakness and shortness of breath. She had been seen twice in the week prior having tested negative for SARS-COV2. In the emergency department, O2 saturation was 70% with respiratory distress on room air requiring high flow nasal cannula support. Labs were notable for a potassium of 2.7 mmol/L, acute kidney injury, elevated transaminases, lactate of 2.8 mmol/L and leukocyte count of 9800/nL. CT showed diffuse bilateral ground glass opacities involving the lung parenchyma concerning for atypical including viral pneumonia. Upon admission to the ICU she developed worsening hypoxia and respiratory failure requiring intubation.A discussion with the patient's husband revealed she had a history of glue sniffing. She had recently been decreasing her alcohol intake and substituting this with an increased frequency of sniffing both permanent markers and modeling glue. This raised suspicion for chemical pneumonitis secondary to toluene induced acute lung injury. DISCUSSION: Toluene is a highly lipophilic molecule readily inhaled via the lungs and distributed widely throughout the body producing side effects like ethanol intoxication via interfering mainly with GABA receptors. Neurologic manifestations range from euphoria and hallucinations to cognitive dysfunction and ataxia with chronic use. It specifically causes renal tubular acidosis typically manifesting as a normal anion gap hyperchloremic acidosis with hypokalemia. It can also cause hepatic injury and cardiac automaticity and conduction abnormalities.Acute lung injury secondary to toluene has been described but less frequently reported. Toxicity can result in Reactive Airway Dysfunction Syndrome (RADS) from acute or chronic exposure to various chemical irritants. All hydrocarbons, including toluene, can cause chemical pneumonitis by direct contact with the pulmonary parenchyma and destroying alveolar and capillary membranes resulting in vascular permeability and edema. Symptoms may include cough, wheezing, respiratory distress, and hypoxia. Bilateral interstitial infiltrates may be delayed for several hours after the development of pneumonitis. There is no specific antidote for toluene toxicity. CONCLUSIONS: Treatment for toluene and many chemical induced pneumonitides consists of supportive care, supplemental oxygen, bronchodilators, inhaled and systemic glucocorticoids and may require intubation and admission to an ICU in severe cases. REFERENCE #1: Camara-Lemarroy CR, Rodríguez-Gutiérrez R, Monreal-Robles R, González-González JG. Acute toluene intoxication--clinical presentation, management and prognosis: a prospective observational study. BMC Emerg Med. 2015;15:19. Published 2015 Aug 18. doi:10.1186/s12873-015-0039-0 REFERENCE #2: Alberts WM, do Pico GA. Reactive airways dysfunction syndrome. Chest. 1996;109(6):1618-1626. doi:10.1378/chest.109.6.1618 REFERENCE #3: Tormoehlen LM, Tekulve KJ, Nañagas KA. Hydrocarbon toxicity: A review. Clin Toxicol (Phila). 2014;52(5):479-489. doi:10.3109/15563650.2014.923904 DISCLOSURES: No relevant relationships by Ryan Lee, source=Web Response No relevant relationships by Dominic Valentino, source=Web Response

MYCOPLASMA GORDONAE: A RARE CAUSE OF ARDS IN THE IMMUNOCOMPROMISED

TOPIC: Chest Infections TYPE: Fellow Case Reports INTRODUCTION: Mycobacterium gordonae, a commonly found species of mycobacteria. While frequently encountered in the environment and clinical laboratories it is almost always considered nonpathogenic. Despite being a non-virulent organism, there are many cases of clinically significant disease. Occasionally, it has been known to cause severe infections, especially in patients with an underlying predisposition or immunosuppression such as AIDS. CASE PRESENTATION: A 39-year-old male with no known PMH presents to the hospital with complaint of worsening dyspnea, fever, and nonproductive cough. He was in his usual state of health until 3 weeks prior when he began to experience body aches, sore throat, fever and shortness of breath. Continued symptoms prompted visit to the hospital at which time he discharged from the emergency department. The patient continued to have progressive worsening of dyspnea with fever prompting return to the hospital and subsequent admission for acute hypoxic respiratory failure. He lives at home with his wife and 4 children who do not have similar symptoms. He has lived in the US for 17 years and denies recent travel, sick contacts, history of autoimmune diseases, smoking history, vaping history, drug use, skin rash, joint pain. On admission vital signs and physical exam showed tachycardia and tachypnea with fever and inspiratory rales. Laboratory data including comprehensive metabolic panel and complete blood count with differential was unrevealing. Chest imaging showed diffuse bilateral dense ground glass opacities. Inflammatory markers including D-dimer, Ferritin, LDH, CRP were elevated. Influenza, COVID-19, mycoplasma, legionella antigen resulted negative. Testing for HIV returned positive with a CD4 count of 8. Given the clinical picture the patient was started on steroids, Bactrim, and Highly active antiretroviral therapy (HAART). Bronchoscopy with BAL was performed showing negative cytology, negative GMS-silver stain. However, AFB testing showed positive M. gordonae with fungal culture showing Candida albicans. Prednisone was discontinued and the patient was continued on HAART therapy along with Bactrim and sent for further treatment with Infectious Disease specialists. DISCUSSION: While there are reports of M. gordonae infections involving many organ systems, pulmonary infection is the most common site of symptomatic disease. Common symptoms include cough, weight loss, dyspnea, hemoptysis and fever. In addition to clinical symptoms and radiographic abnormalities, positive cultures from sputum, bronchial wash, transbronchial or lung biopsy are necessary for diagnosis. CONCLUSIONS: M.gordonae is capable of causing significant infections in both immunocompromised and immunocompetent hosts. Although the likelihood of this being a contamination is significant, its isolation should prompt further evaluation especially in those patients who are immunocompromised. REFERENCE #1: Weinberger M, Berg SL, Feurstein IM, Pizzo PA, Witebsky FG. Disseminated infection with Mycobacterium gordonae: Report of a case and critical review of the literature. Clin Infect Dis. 1992;14:1229–1239. REFERENCE #2: Asija A, Prasad A, Eskridge E. Disseminated Mycobacterium gordonae infection in an immunocompetent host. Am J Ther. 2011 May. REFERENCE #3: Brener ZZ, Zhuravenko I, Bergman M. Acute kidney injury in a patient with nontuberculous mycobacterial infections: a case report. Cases J. 2009 Jan 23. DISCLOSURES: No relevant relationships by mohammed halabiya, source=Web Response No relevant relationships by Richard Miller, source=Web Response No relevant relationships by Shawn Pate, source=Web Response

OCCUPATIONAL-HYPERSENSITIVITY PNEUMONITIS: A DIAGNOSIS NOT TO BE MISSED BY PROPER HISTORY TAKING

TOPIC: Occupational and Environmental Lung Diseases TYPE: Medical Student/Resident Case Reports INTRODUCTION: Hypersensitivity Pneumonitis (HP) is an inflammatory and/or fibrotic disease affecting the lung parenchyma. Radiographic or histopathological findings help to categorize HP as either fibrotic (mixed inflammatory plus fibrotic or purely fibrotic) or non-fibrotic (purely inflammatory), being the primary determinant of prognosis. Rarely acute respiratory decline can be the first manifestation of chronic HP that may develop within a wide timeframe from weeks to years of exposure. CASE PRESENTATION: A 38-year-old male with no comorbidities or smoking history, presented with one week of progressive shortness of breath. Further questions revealed that since childhood he was working in a car painting shop without using protective equipment. Vital signs: Temperature 36.9, pulse 98 beats/min, respiratory rate 22 breaths/min, blood pressure 116/96 mmHg, and oxygen saturation 37% on room air, improved to 98% via a non-rebreather mask. He was not in respiratory distress. Findings included diffuse bilateral crackles over the lung fields. CXR showed diffuse patchy bilateral alveolar opacities. WBC count and serum procalcitonin were within normal limits. SARS-CoV-2 PCR performed was negative. Chest CT showed extensive diffuse bilateral lung consolidations, ground-glass opacities, honeycombing, and prominent mediastinal lymph nodes. Given the patient symptoms, high-risk exposure to isocyanate which exists in paints, radiologic findings, and by ruling out infectious etiologies, the suspected diagnosis of HP was made and treatment with IV Methylprednisone 60mg twice daily initiated. After 2 days, clinical status improved and oxygen requirements decreased to 8 LPM via Nasal Cannula. Bronchoscopy showed erythema throughout the tracheobronchial tree. Bronchoalveolar lavage (BAL) was performed and cytology showed: Reactive bronchial cells (24% Lymphocytes, 31% macrophages, 44% neutrophils). Consequently, a diagnosis of chronic, non-fibrotic HP was confirmed. Finally, after completing 7 days of IV steroid treatment, he was discharged home with 2 LPM supplemental oxygen. Instructions regarding oral corticosteroid tapering over a 3 week-period were provided. DISCUSSION: Diagnosis of chronic HP is predominantly based on exposure identification, CT scan pattern, and bronchoscopic/histopathological findings. BAL in the majority of the patients with non-fibrotic chronic HP shows elevated cell count with greater than 20% lymphocytes and this group responds to steroid therapy significantly. CONCLUSIONS: We would like to emphasize the high value of taking detailed patient history to detect causative agent exposure. Unprotected exposure to isocyanate was the key leading to further investigation including performing BAL in our patient. We also recommend health care providers educate their patients regarding proper safety equipment use, in case of occupational exposure to HP inducers. Prevention is always better than cure! REFERENCE #1: Raghu G, Remy-Jardin M, Ryerson CJ, Myers JL, Kreuter M, Vasakova M, et. al. Diagnosis of hypersensitivity pneumonitis in adults. An official ATS/JRS/ALAT clinical practice guideline. Am J Respir Crit Care Med 2020; 202(3):e36–e69. REFERENCE #2: Koster MA, Thomson CC, Collins BF, Jenkins AR, Ruminjo JK and Raghu G. Diagnosis of hypersensitivity pneumonitis in adults, 2020 clinical practice guideline: summary for clinicians. Ann Am Thorac Soc 2020. DISCLOSURES: no disclosure on file for Manish Gugnani; No relevant relationships by Irina Gutierrez Puentes, source=Web Response No relevant relationships by Julio Piedra Butina, source=Web Response No relevant relationships by Asieh TakallooBakhtiari, source=Web Response

RECURRENT DIFFUSE ALVEOLAR HEMORRHAGE IN SYSTEMIC SCLEROSIS AS COMPLICATION OF COVID-19

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Diffuse alveolar hemorrhage (DAH) is a rare but severe life-threatening condition characterized by widespread bleeding of the pulmonary vasculature into the alveolar space. DAH have a myriad of underlying etiologies. Rheumatic diseases have shown association with DAH. The Coronavirus disease 2019 (COVID-19) pandemic has increased the complexity associated with diagnosing DAH. Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infects the endothelium using the angiotensin-converting enzyme 2 receptor causing a lymphocytic endotheliitis. The increased inflammatory state secondary to COVID-19 has been associated with development of vasculitis syndromes. Although systemic sclerosis (SSc) has been linked to recurrent DAH, there is scarce evidence associating COVID-19 and SSc with DAH. CASE PRESENTATION: A 61-year-old female with a past medical history of SSc, interstitial lung disease (ILD) and DAH presented with worsening shortness of breath of 2 days duration. She was found to have acute hypoxic respiratory failure. Computed tomography (CT) of thorax showed diffuse bilateral ground-glass opacities. SARS-Cov-2 polymerase chain reaction was positive. She was started on broad spectrum antibiotics, dexamethasone and received two units of COVID-19 convalescent plasma. Due to respiratory distress, she was intubated. A decline in her hemoglobin prompted a diagnostic bronchoscopy that showed increasing frank blood in the bronchoalveolar lavage. Antinuclear antibody with centromere pattern and rheumatoid factor were positive with low complement C3 and C4. Steroids were switched to high-dose IV methylprednisolone. Three cycles of plasmapheresis were given with no clinical improvement. DISCUSSION: COVID-19 pandemic has changed the traditional approach to dyspnea. This change in the paradigm, as a result of limited resources and increased occupational risk, may hinder the diagnosis of complex disorders like SSc-ILD and DAH. It's of paramount importance to test rapidly for SARS-CoV-2 infection. ILD is a common complication of SSc. The high-resolution CT similarities between the 2 diseases make it difficult to distinguish COVID-19-ILD superinfection from worsening of SSc-ILD. Bronchoscopy and surgical lung biopsy should always be weighed against their possible complications, occupational exposure and prognosis. CONCLUSIONS: COVID-19 may overlap and complicate the diagnosis of SSc-ILD. COVID-19 associated acute respiratory distress syndrome is attributed to cytokines release (cytokine storm). This likely worsens the underlying inflammatory process in SSc-ILD and could explain the development of DAH. Although there is limited evidence to guide specific treatment, steroid therapy has proven to have mortality benefit in severe COVID-19. The role of steroids, plasmapheresis, immunomodulators and antifibrotic therapy in COVID-19 with SSc-ILD complicated with DAH is unknown. REFERENCE #1: Colby TV, Fukuoka J, Ewaskow SP, Helmers R, Leslie KO. Pathologic approach to pulmonary hemorrhage. Annals of Diagnostic Pathology. 2001;5(5):309-19. REFERENCE #2: Varga Z, Flammer AJ, Steiger P, Haberecker M, Andermatt R, Zinkernagel AS, et al. Endothelial cell infection and endotheliitis in COVID-19. The Lancet. 2020;395(10234):1417-8. REFERENCE #3: Wong AW, Fidler L, Marcoux V, Johannson KA, Assayag D, Fisher JH, et al. Practical Considerations for the Diagnosis and Treatment of Fibrotic Interstitial Lung Disease During the Coronavirus Disease 2019 Pandemic. Chest. 2020;158(3):1069-78. DISCLOSURES: No relevant relationships by Vedesh Babu, source=Web Response No relevant relationships by Alejandra Garcia Fernandez, source=Web Response No relevant relationships by ahmad hamdan, source=Web Response No relevant relationships by Carlos Matute Martinez, source=Web Response

Spontaneous Pneumothorax Complicating COVID-19 Pneumonia: AMulticenter Analysis

Background: Spontaneous pneumothorax is a rare complication seen in patients of COVID-19 pneumonia. The risk factors associated with this complication and its incidence remain unknown largely. We herein, review and present the incidence, clinical characteristics and outcomes of spontaneous pneumothorax in 1767 patients admitted in three COVID treatment tertiary care centers in Lahore. Study Design: Retrospective study Place and Duration of Study: Services Institute of Medical Sciences Lahore and Bahria International Hospital Lahore from 15thApril 2020 to 15thMay 2021. Methodology: One thousandseven hundred and sixty-seven patients who were diagnosed with a spontaneous pneumothorax were enrolled. Clinical characteristics of these cases were also reviewed and recorded. Results: One thousand and five hundred patients had positive RT PCR from nasopharyngeal swab. Eleven (.62%) cases of COVID-19 patients who developed spontaneous pneumothorax were identified. The initial HRCT imaging showed typical and diffuse bilateral ground-glass opacities and consolidations, mainly in their peripheral, posterior and basal lung regions. Three patients had pneumothorax late in the course of disease after they were discharged home. We had only one mortality among those (11) cases and that was also not related to the pneumothorax directly but to development of sepsis and multi-organ failure. Conclusion: Spontaneous pneumothorax is a rare complication seen in COVID-19 pneumonia. Keywords: Pneumothorax, COVID-19, Spontaneous pneumothorax, Lung injury, Barotrauma, Pneumomediastinum

A Case Series of Electronic or Vaping Induced Lung Injury

Introduction: Since their introduction, electronic cigarette use has increased and was even proposed as an alternative to traditional tobacco use. Recently, a series of patients with acute respiratory failure due electronic cigarette, or vaping, associated lung injury (EVALI) in 2019 has been described which has largely been attributed to tetrahydrocannabinol (THC) containing vaporizer itself, as well as vitamin E acetate. Several case series have been published regarding the acute presentation, diagnosis and management. In addition to diagnosis and management of EVALI, we sought to describe potential long-term effects of lung parenchyma in these patients. Methods: A retrospective review was performed on 16 patients with clinically diagnosed EVALI at OSF St Francis Medical Center between August 01 2019 and February 1 2020. Relevant demographic and clinical data were collected in patients diagnosed with EVALI. Results: Of the 16 patients in the study the median age (IQR) age was 25.25 (20-29) and 94% were male. The predominant presenting symptoms were dyspnea (94%), cough (56%), nausea 63%), vomiting (63%), abdominal pain (50%), diarrhea (50%), and fever (63%). 2 (13%) patients required endotracheal intubation. Common features of computerized tomography (CT) scan were bilateral diffuse ground glass opacity (93%), septal thickening (53%), and subpleural sparing (47%). Bronchoalveolar lavage (BAL) was obtained in 3 patients and all demonstrated neutrophil predominance of 69% (56-90). One BAL was significant for hemosiderin laden macrophages. Post hospital follow up pulmonary function tests were obtained in 3 and 2 of these were significant for obstructive lung disease. Conclusions: In this case series of patients diagnosed with vaping associated lung injury, obstructive lung disease may be seen on pulmonary function testing and surveillance of these patients should occur regardless of duration.