Diffuse Pulmonary Infiltrates Research Articles

Successful Use of Therapeutic Plasma Exchange Following Red Blood Cell Exchange for Severe Acute Chest Syndrome: A Single Institution Experience

Introduction: Severe acute chest syndrome (ACS) is a potentially fatal complication of sickle cell disease (SCD) that can progress to multiorgan failure. Treatment includes red blood cell (RBC) exchange to improve oxygenation and reduce vaso-occlusion by decreasing the proportion of hemoglobin (Hb) S. Patients with poor response to RBC exchange are at high risk for mortality. Therapeutic plasma exchange (TPE) may be beneficial in cases of severe organ dysfunction refractory to RBC exchange. TPE is postulated to remove pro-inflammatory cytokines, reduce circulating free hemoglobin, and decrease complement products that contributes to vaso-occlusion and inflammation. The use of TPE for severe ACS and multiorgan failure has been rarely described in adult patients and is even less commonly described for pediatric patients. Aim: To describe use of TPE for the management of severe ACS with multiorgan failure in two pediatric patients and one young-adult patient who did not respond to standard medical management with RBC exchange transfusion. Methods: Case reports Case 1: A six-year-old male with homozygous SCD (HbSS) and moderate persistent asthma was admitted for ACS. His course was complicated by hypoxemia requiring intubation, oliguria, and hypotension. On hospital day 3, he underwent RBC exchange with four units of RBCs. Despite decrease of Hb S to 15%, he remained hypoxic on high ventilatory support and developed acute respiratory distress syndrome. After multidisciplinary discussion, TPE was trialed in hopes of improving oxygenation and reversing multiorgan dysfunction. He underwent 3 TPEs, each with 1.5 total plasma volume (TPV) using 5% albumin (days 4, 5 and 7). After a single session of TPE, his oxygenation saturations improved to the 90s, and his ventilator support was weaned. He was extubated on day 8 and was discharged on day 13 in stable condition. Case 2: A sixteen-year-old male with HbSS, recurrent hyper-hemolytic syndrome, and sickle cell hepatopathy was admitted for medical optimization before scheduled cholecystectomy. His Hb was raised pre-operatively with erythropoietin, in lieu of RBC transfusion, due to history of severe refractory hyper-hemolysis with transfusions. He underwent uncomplicated cholecystectomy on hospital day 2. On day 3, he developed ACS, septic shock, and an exacerbation of known hepatopathy. He was intubated and underwent RBC exchange with 8 units of RBCs. His Hb S decreased to 20% but he had no improvement in clinical status. High-dose steroids and TPE were then trialed. The use of TPE was dual purposed to reduce inflammatory cytokines contributing to systemic dysfunction and to prevent hyper-hemolysis following exchange transfusion. He underwent 3 TPEs each with 1.5 TPV using 5% albumin for three days (days 5, 6, and 7). Throughout his course of TPE, he was extubated (day 6), weaned off pressor support (day 6), and his liver dysfunction began to improve (day 7). He was discharged home on day 16. Case 3: A thirty-five-year-old female with HbSS without chronic complications was transferred from an outside hospital where she presented 3 days prior with ACS and progressive neurologic deterioration with minimal responsiveness. Imaging revealed diffuse pulmonary infiltrates and extensive cerebral micro emboli consistent with fat embolism syndrome. She underwent RBC exchange on the day of arrival to our facility (hospital day 4) with 5 units of RBCs. Her Hb S decreased to 20% but she had no improvement in neurologic function. After multidisciplinary evaluation, TPE was trialed alongside high-dose steroids. She underwent 5 TPEs each with 1.0 TPV using 5% albumin (days 5, 6, 8, 9, and 12). Shortly after initiating TPE, she began recovering neurologically with eye-opening, response to noxious stimuli, and tracking (day 6). After 3 days of TPE, CRP fell from 21 to 5 and ESR from 49 to 23 (day 8). She followed commands on day 10 and was taken off oxygen on day 15. She was discharged to a rehabilitation facility on day 30 with significant improvements in mental status, cognition, and functional abilities. Conclusions: TPE for three to five days should be considered in patients with severe ACS and multiorgan failure with high risk of mortality when standard management fails. The early initiation of TPE likely contributed to the successful recoveries of these three cases. Further studies are needed to delineate the role of TPE in the management of acute complications of SCD.

A Rare Case of Pulmonary Veno-Occlusive Disease, Pulmonary Capillary Hemangiomatosis

A 40-year-old male with past medical history of chronic pain on methadone for a few years, hypertension, and obesity presented with worsening dyspnea and was found to have significant hypoxemia. A CT-angiogram of the chest showed extensive diffuse bilateral pulmonary infiltrates with bilateral hilar and mediastinal lymphadenopathy.

Case Report: Whole lung lavage therapy for pulmonary alveolar proteinosis: a double-edged sword

Pulmonary alveolar proteinosis (PAP) is an uncommon disease characterized by the excessive accumulation of lipoprotein material in the alveoli. No uniform treatment existed. However, whole lung lavage (WLL) remains the main treatment. We report the case of a 33-year-old non-smoking man, with no reported history of medical problems, who complained of dyspnea on exertion and cough for over 5 years. A CT scan revealed diffuse pulmonary interstitial infiltrates. Bronchoalveolar lavage was milky. WLL was planned, and the procedure was repeated 70 times and a total of 3,5 liters of saline serum was instilled and 2,8 liters of milky liquid was removed. The operation procedure was interrupted because of acute pulmonary edema. The patient was transferred to the intensive care unit for acute respiratory distress syndrome. He received 3 days of noninvasive ventilation and regression of supplemental oxygen.  Faced with the seriousness of the complication it was decided not to perform a third wash and to monitor the patient functionally and radiologically. Currently, after one year of the lung wash the patient is stable functionally and radiologically. We presented a rare complication of a WLL in a patient with PAP. Physicians should evaluate the patient carefully before suggesting WLL, which is an invasive procedure requiring general anesthesia for a pathology that may evolve spontaneously favorably.

Major Histocompatibility Complex (MHC) Class II Deficiency- A Case of Primary Immunodeficiency Disorder.

Major Histocompatibility Complex (MHC) Class II deficiency is a rare autosomal recessive primary immunodeficiency caused by mutations in regulatory genes of MHC Class II proteins. Clinical manifestations include respiratory/gastrointestinal infections, failure-to-thrive, septicemia and early death. A 9-mo-old-girl presented with repeated episodes of pneumonia requiring hospitalization and ventilator support since the last 5 mo. Examination revealed absent tonsils, sparse scalp-hair, seborrhea and firm hepato-splenomegaly. Radiograph showed absence of thymic shadow with diffuse pulmonary infiltrates. CT scan showed multiple bilateral ground glass pulmonary opacities with patchy consolidation. Primary immunodeficiency disorder was suspected in view of repeated pulmonary infections, failure to thrive and suggestive family history. Lymphocyte subset assay revealed lymphocytopenia and HLA typing showed absence of HLA-DR expression on B cells suggestive of MHC Class II deficiency. Targeted gene panel detected a homozygous mutation in the RFX-5 gene (RFX5: c.848_849del:p.R283Tfs*6;Homozygous). Though this patient succumbed, parents have been counseled regarding need for prenatal diagnosis.

Exploring m6A-RNA methylation as a potential therapeutic strategy for acute lung injury and acute respiratory distress syndrome.

N6-methyladenosine (m6A) is the most common methylation modification in mammalian messenger RNA (mRNA) and noncoding RNAs. m6A modification plays a role in the regulation of gene expression and deregulation of m6A methylation has been implicated in many human diseases. Recent publications suggest that exploitation of this methylation process may possess utility against acute lung injury (ALI). ALI and its more severe form, acute respiratory distress syndrome (ARDS) are acute, inflammatory clinical syndromes characterized by poor oxygenation and diffuse pulmonary infiltrates. This syndrome is associated with microvascular endothelial dysfunction, subsequent pulmonary hypertension and may ultimately lead to mortality without rigorous and acute clinical intervention. Over the years, many attempts have been made to detect novel therapeutic avenues for research without much success. The urgency for the discovery of novel therapeutic agents has become more pronounced recently given the current pandemic infection of coronavirus disease 2019 (COVID-2019), still ongoing at the time that this review is being written. We review the current landscape of literature regarding ALI and ARDS etiology, pathophysiology, and therapeutics and present a potential role of m6A methylation. Additionally, we will establish the axiomatic principles of m6A methylation to provide a framework. In conclusion, METTL3, or methyltransferase-like 3, the selective RNA methyltransferase for m6A, is a hub of proinflammatory gene expression regulation in ALI, and using a modern drug discovery strategy will identify new and effective ALI drug candidates targeting METTTL3.

A case report Case Report of Idiopathic Pulmonary Haemosiderosis in a Child with recurrent chest infections

Idiopathic Pulmonary Hemosiderosis (IPH) is a rare condition, usually occurring in children and teenagers.  The classic presentation is of haemoptysis, iron deficiency anaemia and diffuse pulmonary infiltrates. We report a case of IPH in an 8 year old boy, who presented with recurrent episodes of fever, cough and respiratory infections without any trigger since childhood.

A narrative review of minimally invasive fundoplication for gastroesophageal reflux disease and interstitial lung disease

: Interstitial lung disease (ILD) encompasses a heterogeneous group of acute and chronic disorders characterized by diffuse pulmonary infiltrates with histologic features of pulmonary inflammation, dyspnea, and restrictive lung patterns. Gastroesophageal reflux disease (GERD) and ILD are two pathological conditions often strictly related, even if a clear relationship of causality has not been demonstrated. The mechanisms leading to ILD are not completely understood, although it is recognized that different factors are involved. In recent years, it has been suggested that acid gastroesophageal reflux is an important cause of both systemic sclerosis (SSc)-ILD and idiopathic pulmonary fibrosis (IPF). It has been hypothesized that micro aspiration of gastric material may play a fundamental role in the fibrotic transformation of pulmonary parenchyma. According to that, some studies have described antireflux procedures for patients affected by ILD and GERD. However, although some studies reported good results in terms of improvement of lung function, the role of antireflux surgery remains uncertain as well as not univocal. An extensive literature search was performed from January 1970 to 31 December 2020 in PubMed and the Cochrane Central Register of Controlled Trials. The research was limited to English-language studies. The aim of the present study was to summarize the effect of antireflux surgery for the treatment of abnormal acid GER on the natural history of this disease.

Diffuse Pulmonary Meningotheliomatosis: A Case Report

Abstract Introduction/Objective Diffuse pulmonary meningotheliomatosis (DPM) is a pulmonary disease characterized by the presence of widespread bilateral minute pulmonary meningothelial-like nodules (MPMNs). It is exceedingly rare and predominantly seen in females. The nodules are typically asymptomatic and detected incidentally on imaging. Methods/Case Report We present a case of a 57-year-old woman with a history of chronic cough and CT imaging findings of bilateral multiple ground-glass nodules. Wedge resections from the right upper and right lower lobes were obtained, which revealed gross changes suggestive of interstitial lung disease. Histologic evaluation of the wedges showed similar morphology, consisting of discrete areas with variable interstitial expansion of the stroma with ovoid/spindle cells, collagen, elastosis, and mild chronic inflammatory cells, in a somewhat perivascular pattern. Some areas were also cystic. This appeared in a background of emphysematous change and focal foreign body giant cell reaction to non-polarizable material. Immunohistochemical stains were diffusely positive for vimentin, EMA , and PR, and CD163 highlighted increased cells that were S100 and CD1a negative. Additionally, the ovoid/spindle cells were negative for desmin, SMM, HMB-45, HHV8, pan-CK, chromogranin, and multiplex SOX10-MART1. Results (if a Case Study enter NA) NA Conclusion Diffuse pulmonary meningotheliomatosis is a rare entity that requires sufficient histological evaluation to identify the ovoid/spindle cell component histologically and immunohistochemically. This disease should be considered in the differential for cases of diffuse interstitial pulmonary infiltrates. Few cases have been reported in the literature, requiring further research to understand the mechanisms of this disease and its clinical significance.

Calcified Granulomatous Pneumocystis Jirovecii Pneumonia in a Toddler with Severe Combined Immunodeficiency—A Case Report

Pneumocysis jirovecii pneumonia (PJP) is a type of pneumonia originating from the fungus Pneumocystis jiroveci and is a major cause of serious pneumonia in immunocompromised conditions. PJP typically appears as bilateral diffuse pulmonary infiltrates. Granulomatous PJP is an uncommon form of pneumocystis infection, occurring in only 3% to 5% of patients. Calcification is exceptional. We present a 9-month-old boy affected by Severe Combined Immunodeficiency (SCID) that has been diagnosed at the age of 7 months following a lung Pneumocystis jirovecii infection. He underwent a routine total-body magnetic resonance imaging (MRI) prior to an allogeneic hematopoietic stem cell transplantation (HSCT). The MRI showed significant alterations of the pulmonary parenchyma; hence, a computer tomography of the lung was performed showing the presence of 11 calcified granulomatous nodules. We report a unique case of calcified granulomatous PJP in a toddler affected by SCID. Awareness of this rare yet possible presentation in patients with SCID is important given the potential clinical implications when managing a patient undergoing HSCT and it further enhances the importance of advanced radiologic imaging prior to HSCT.

A RARE MANIFESTATION OF SYSTEMIC LUPUS ERYTHEMATOSUS (SLE): DIFFUSE ALVEOLAR HEMORRHAGE

SESSION TITLE: Autoimmune Diseases Gone Wild: Rare Cases of Pulmonary ManifestationsSESSION TYPE: Rapid Fire Case ReportsPRESENTED ON: 10/18/2022 01:35 pm - 02:35 pmINTRODUCTION: Systemic lupus erythematosus (SLE) is an autoimmune multisystemic disease that can involve the lungs in up to 50-70% of cases, which include pleuritis, obliterative bronchiolitis, acute or chronic lupus pneumonitis, interstitial lung disease, diffuse alveolar hemorrhage (DAH), and other infrequent manifestations. Here we report a case of DAH associated with SLE.CASE PRESENTATION: A 39 -year-old female with Multiple Sclerosis and epilepsy presented a persistent fever of 105.1°F. Physical examination was significant for diffuse alopecia and inspiratory crackles in the lower lungs. Chest Xray revealed new bilateral patchy opacities and CT Angiogram of the chest revealed bilateral patchy ground-glass opacities. She was progressively hypoxemic and required intubation due to hypoxic and hypercapnic respiratory failure; endotracheal aspirates were blood tinged. Labs revealed a WBC of 3.9, Hb of 8.2 (from 10.0), platelets of 91, ANA 1:2560 with speckled pattern, Anti-RNP positive, and low complement levels. Due concerns for DAH in newly diagnosed SLE, a bronchoscopy was performed revealing bleeding without a definable source, persistent bloody sequential lavage and negative microbiology consistent with DAH. The patient was started on a 3-day course of IV 1 g methylprednisolone and Rituximab (RTX). She was weaned off of vasopressors, steroids were tapered, and she was extubated after nine days. Lung infiltrates resolved after 2 weeks of treatment.DISCUSSION: DAH is a rare, but devastating manifestation of SLE. Suggested pathophysiology is immune-mediated damage of the small blood vessels and alveolar spaces with histopathological findings of immune complex deposition that results in alveolar-capillary damage. The clinical picture of DAH is characterized by hemoptysis, an acute drop in hemoglobin, hypoxemic respiratory failure and diffuse pulmonary infiltrates. As seen with our patient, these nonspecific findings prove a diagnostic challenge and make it necessary to rule out infections, drug toxicity, pulmonary embolism and heart failure. A combination of careful history, physical examination, chest imaging, and bronchoscopy will provide a diagnosis of DAH. High-dose steroids and immunosuppression including cyclophosphamide, RTX, plasmapheresis, mycophenolate, azathioprine, and IVIG are current treatment options. Infections can trigger DAH therefore broad-spectrum antibiotics should be also considered if an infection is suspected.CONCLUSIONS: DAH should be included in the differential diagnosis for patients with lung parenchymal involvements. The mortality of DAH associated with SLE is high despite available treatments, therefore early diagnosis and prompt treatment are crucial. The mainstay of treatment is early administration of high-dose steroid, corticosteroid-sparing agents and supportive care.Reference #1: Aguilera-Pickens, G., Abud-Mendoza, C. Pulmonary manifestations in systemic lupus erythematosus: pleural involvement, acute pneumonitis, chronic interstitial lung disease and diffuse alveolar hemorrhage. Reumatologia Clinica (Engl Ed), (2018). 14(5):294-300. Doi:10.1016/j.reumae.201Reference #2: Virdi, R.P.S., Bashir, A., Shahzad, G., et al. Diffuse alveolar hemorrhage: a rare life-threatening condition in systemic lupus erythematosus. Case Reports in Pulmonology, (2012). 2012:836017-4. doi:10.1155/2012/836017.Reference #3: Al-Adhoubi, N. K., Bystrom, J. Systemic lupus erythematosus and diffuse alveolar hemorrhage, etiology and novel treatment strategies. Lupus, (2020). 29(4):355-363. Doi:10.1177/09612033209DISCLOSURES: No relevant relationships by Jonathan Ariyaratnamno disclosure on file for Carlos gonzalez;No relevant relationships by Ricardo LopezNo relevant relationships by Jasmine Sandhuno disclosure on file for Bahtiyar Toz; SESSION TITLE: Autoimmune Diseases Gone Wild: Rare Cases of Pulmonary Manifestations SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 01:35 pm - 02:35 pm INTRODUCTION: Systemic lupus erythematosus (SLE) is an autoimmune multisystemic disease that can involve the lungs in up to 50-70% of cases, which include pleuritis, obliterative bronchiolitis, acute or chronic lupus pneumonitis, interstitial lung disease, diffuse alveolar hemorrhage (DAH), and other infrequent manifestations. Here we report a case of DAH associated with SLE. CASE PRESENTATION: A 39 -year-old female with Multiple Sclerosis and epilepsy presented a persistent fever of 105.1°F. Physical examination was significant for diffuse alopecia and inspiratory crackles in the lower lungs. Chest Xray revealed new bilateral patchy opacities and CT Angiogram of the chest revealed bilateral patchy ground-glass opacities. She was progressively hypoxemic and required intubation due to hypoxic and hypercapnic respiratory failure; endotracheal aspirates were blood tinged. Labs revealed a WBC of 3.9, Hb of 8.2 (from 10.0), platelets of 91, ANA 1:2560 with speckled pattern, Anti-RNP positive, and low complement levels. Due concerns for DAH in newly diagnosed SLE, a bronchoscopy was performed revealing bleeding without a definable source, persistent bloody sequential lavage and negative microbiology consistent with DAH. The patient was started on a 3-day course of IV 1 g methylprednisolone and Rituximab (RTX). She was weaned off of vasopressors, steroids were tapered, and she was extubated after nine days. Lung infiltrates resolved after 2 weeks of treatment. DISCUSSION: DAH is a rare, but devastating manifestation of SLE. Suggested pathophysiology is immune-mediated damage of the small blood vessels and alveolar spaces with histopathological findings of immune complex deposition that results in alveolar-capillary damage. The clinical picture of DAH is characterized by hemoptysis, an acute drop in hemoglobin, hypoxemic respiratory failure and diffuse pulmonary infiltrates. As seen with our patient, these nonspecific findings prove a diagnostic challenge and make it necessary to rule out infections, drug toxicity, pulmonary embolism and heart failure. A combination of careful history, physical examination, chest imaging, and bronchoscopy will provide a diagnosis of DAH. High-dose steroids and immunosuppression including cyclophosphamide, RTX, plasmapheresis, mycophenolate, azathioprine, and IVIG are current treatment options. Infections can trigger DAH therefore broad-spectrum antibiotics should be also considered if an infection is suspected. CONCLUSIONS: DAH should be included in the differential diagnosis for patients with lung parenchymal involvements. The mortality of DAH associated with SLE is high despite available treatments, therefore early diagnosis and prompt treatment are crucial. The mainstay of treatment is early administration of high-dose steroid, corticosteroid-sparing agents and supportive care. Reference #1: Aguilera-Pickens, G., Abud-Mendoza, C. Pulmonary manifestations in systemic lupus erythematosus: pleural involvement, acute pneumonitis, chronic interstitial lung disease and diffuse alveolar hemorrhage. Reumatologia Clinica (Engl Ed), (2018). 14(5):294-300. Doi:10.1016/j.reumae.201 Reference #2: Virdi, R.P.S., Bashir, A., Shahzad, G., et al. Diffuse alveolar hemorrhage: a rare life-threatening condition in systemic lupus erythematosus. Case Reports in Pulmonology, (2012). 2012:836017-4. doi:10.1155/2012/836017. Reference #3: Al-Adhoubi, N. K., Bystrom, J. Systemic lupus erythematosus and diffuse alveolar hemorrhage, etiology and novel treatment strategies. Lupus, (2020). 29(4):355-363. Doi:10.1177/09612033209 DISCLOSURES: No relevant relationships by Jonathan Ariyaratnam no disclosure on file for Carlos gonzalez; No relevant relationships by Ricardo Lopez No relevant relationships by Jasmine Sandhu no disclosure on file for Bahtiyar Toz;

Thoracic Computed Tomography to Assess ARDS and COVID-19 Lungs.

This review was designed to discuss the role of thoracic-computed tomography (CT) in the evaluation and treatment of patients with ARDS and COVID-19 lung disease. Non-aerated lungs characterize the ARDS lungs, compared to normal lungs in the lowermost lung regions, compressive atelectasis. Heterogenous ARDS lungs have a tomographic vertical gradient characterized by progressively more aerated lung tissues from the gravity-dependent to gravity-independent lungs levels. The application of positive pressure ventilation to these heterogeneous ARDS lungs provides some areas of high shear stress, others of tidal hyperdistension or tidal recruitment that increases the chances of appearance and perpetuation of ventilator-induced lung injury. Other than helping to the correct diagnosis of ARDS, thoracic-computed tomography can help to the adjustments of PEEP, ideal tidal volume, and a better choice of patient position during invasive mechanical ventilation. Thoracic tomography can also help detect possible intra-thoracic complications and in the follow-up of the ARDS patients’ evolution during their hospital stay. In COVID-19 patients, thoracic-computed tomography was the most sensitive imaging technique for diagnosing pulmonary involvement. The most common finding is diffuse pulmonary infiltrates, ranging from ground-glass opacities to parenchymal consolidations, especially in the lower portions of the lungs’ periphery. Tomographic lung volume loss was associated with an increased risk for oxygenation support and patient intubation and the use of invasive mechanical ventilation. Pulmonary dual-energy angio-tomography in COVID-19 patients showed a significant number of pulmonary ischemic areas even in the absence of visible pulmonary arterial thrombosis, which may reflect micro-thrombosis associated with COVID-19 pneumonia. A greater thoracic tomography severity score in ARDS was independently related to poor outcomes.

P108 PLEURAL EFFUSION AND THE POSTERIOR THORACIC WINDOW: ONE MORE CHANCE TO IMAGE THE AORTIC VALVE

Abstract   A 85–year–old woman was admitted to our institution with acute respiratory distress. Clinical examination revealed a 5/6 systo–diastolic murmur radiating to both carotid arteries and bilateral lung crackles. Laboratory workup was notable for a N–terminal pro–brain natriuretic peptide (NT–proBNP) of 15.000 ng/L (normal range: < 300 ng/L) and a moderate high–sensitive troponin T elevation of 245 ng/L (normal range: < 14 ng/L) with no increase on serial testing. The hemoglobin and renal function was normal. Evaluation by chest X–ray showed bilateral diffuse pulmonary infiltrates consistent with pulmonary edema and bilateral pleural effusion. The patient was admitted in CCU. A transthoracic echocardiogram was performed bedside, but it was extremely difficult to obtain good quality images from standard view given the ortopnoic decubitus of the patient. However, the aortic valve was heavily calcified and severe aortic stenosis was documented with a mean gradient of 42 mmHg from apical 5 chambers view; 35 mmHg from right parasternal view, with an functional aortic valve area ≈0.6 cm2 (figure, upper panel). Left ventricle shows eccentric hypertrophy and a moderate diffuse reduction of ejection fraction (EF 35–40%). Then, the patient was positioned sitting upright, because the left pleural effusion offered an additional acoustic window—the posterior thoracic window (PTW)—that allowed better alignment of the ultrasound beam with the aortic jet. Mean gradient was recorded definitely higher than from standard view at 50 mm Hg. Moreover, aortic regurgitation that appeared mild from standard view was documented as significant from PTW. In fact, a proper alignment of the aortic regurgitation jet was feasible from this view with a quantification of severity with multiparameter criteria as suggested from the guidelines (PHT 166 ms, Vena contracta 8 mm; Rvol 60 ml). (Figure, lower panel) Conclusion Obtaining adequate echocardiographic images in critically ill patients is important for better diagnosis and treatment. For several reasons, this group of patients remains among the most challenging with regard to quality of echocardiographic images. In presence of pleural effusion and technically difficult echo exams, the PTW should be considered in the assessment of cardiac structures including aortic valve as a potentially useful option to provide further diagnostic information.

Etiology, diagnosis, and management of pneumonia in immunosuppressed patients

Patients with a compromised immune system suffer a wide variety of insults. Pulmonary complications remain a major cause of both morbidity and mortality in immunocom-promised patients. When such individuals present with radio-graphic infiltrates, the clinician faces a diagnostic challenge. The differential diagnosis in this setting is broad and includes both infectious and non-infectious conditions. Evaluation of the immunocompromised host with diffuse pulmonary infiltrates can be difficult, frustrating, and time-consuming. This common and serious problem results in significant morbidity and mortality, approaching 90%. Infections are the most common causes of both acute and chronic lung diseases leading to respiratory failure. Non-invasive diagnostic methods for evaluation are often of little value, and an invasive procedure (such as bronchoalveolar lavage, transbronchial biopsy or even open lung biopsy) is therefore performed to obtain a microbiologic and histologic diagnosis. Bronchoscopy allows certain identification of some aetiologies, and often allows the exclusion of infectious agents. Early use of computed tomography scanning is able to demonstrate lesions missed by conventional chest X-ray. However, even when a specific diagnosis is made, it might not impact patient’s overall survival and outcomes.

A novel differential diagnosis for diffuse cavitating nodules: primary pulmonary plasmacytoma

BackgroundExtramedullary plasmacytoma is a rare monoclonal plasma cell neoplasm that originates from tissues other than the bone marrow and constitutes only 3%–5% of all plasma cell neoplasms. Most cases involve the upper respiratory tract. Extramedullary plasmacytoma involving the lung is extremely rare. Primary pulmonary plasmacytoma is a rare type of extramedullary plasmacytoma, usually presenting with a nodule or mass in hilar region. Literature search has shown very few cases of immunohistochemically confirmed cases of pulmonary plasmacytoma. Diffuse pulmonary infiltration is an unusual presentation.Case presentationWe report the case of a 56 year old lady with history of cough and breathlessness since one month. Computed Tomography revealed diffusely scattered multiple cavitating nodules and consolidation in both lungs. Computed Tomography guided biopsy of one of the lung nodules was done. Histopathologic examination and immunohistochemistry showed features of pulmonary plasmacytoma .This is an unique case of primary pulmonary plasmacytoma with the rare presentation as diffusely scattered multiple cavitating nodules and consolidation. According to our literature search, primary pulmonary plasmacytoma manifesting as cavitating nodules is being reported for the first time.ConclusionsPrimary pulmonary plasmacytoma should be also be considered in the differential diagnosis of multiple diffusely scattered cavitating lung nodules.

ACUTE EOSINOPHILIC PNEUMONIA: COMPLICATIONS OF SMOKE EXPOSURE AND VAPING-ASSOCIATED LUNG INJURY

TOPIC: Occupational and Environmental Lung Diseases TYPE: Medical Student/Resident Case Reports INTRODUCTION: E-cigarette or vaping product use-associated lung injury (EVALI) encompass a host of pulmonary complications including diffuse alveolar hemorrhage, lipoid pneumonia, hypersensitivity pneumonitis, and rarely, acute eosinophilic pneumonia (AEP) [1]. AEP presents as an acute febrile illness with hypoxemia, diffuse pulmonary infiltrates, and eosinophilia on bronchoalveolar lavage (BAL) without evidence of prior infection or atopic illness [2]. Presented is a young adult patient with a history of continuous vaping and extended exposure to kitchen smoke who developed acute hypoxemic respiratory failure later diagnosed as AEP. CASE PRESENTATION: An 18-year-old male with no significant past medical history presented to the emergency department with acute onset malaise, fever, non-productive cough, and shortness of breath over 12 hours. Social history revealed 3-week workplace exposure to smoke as a barbeque cook and a 5-year history of daily vaping with reported cessation 3 weeks prior. Vitals were notable for hypoxemia which was corrected with administration of 8L of oxygen via nasal cannula. Quickly after admission, he had worsening respiratory status: tachypnea, increased oxygen requirement, use of accessory muscles, and bilaterally diminished breath sounds. He was transferred to the medical intensive care unit for emergent endotracheal intubation. Laboratory testing revealed a neutrophil predominant leukocytosis of 19.3x109/L. COVID-19, rapid influenza A and B, and urine antigens for streptococcus and legionella were negative as were autoimmune serologies. A computed tomography (CT) scan of the chest revealed diffuse bilateral consolidative opacities [Figure 1] with worsening over the next 24 hours [Figure 2]. Further investigation was undertaken with bronchoscopy. A BAL was obtained, and cell count and cultures were sent. BAL cell count was remarkable for 33% eosinophilia. The diagnosis of AEP was made, and the patient was started on systemic glucocorticoids, with significant improvement within 24 hours. DISCUSSION: The modified Philit criteria is used to make the diagnosis of AEP, which the patient satisfied [3]. Although a 5-year vaping history was present, no previous significant respiratory symptoms were reported. Prior studies have demonstrated a relationship between workplace smoke exposure and AEP [3]. Based on the modified Philit criteria, we suspect that the patient had acute respiratory failure from AEP as a result of chronic EVALI acutely exacerbated by workplace smoke exposure. The treatment of AEP treatment involves high-dose intravenous glucocorticoids followed by a prolonged oral steroid taper. CONCLUSIONS: Obtaining occupation history as well as smoke exposure is as important as obtaining vaping history in an otherwise healthy young patient who presents with acute hypoxemic respiratory failure with bilateral diffuse opacities on imaging. REFERENCE #1: Winnicka L, Shenoy MA. EVALI and the Pulmonary Toxicity of Electronic Cigarettes: A Review. J Gen Intern Med. 2020;35(7):2130-2135. doi:10.1007/s11606-020-05813-2 REFERENCE #2: Allen JN, Pacht ER, Gadek JE, Davis WB. Acute Eosinophilic Pneumonia as a Reversible Cause of Noninfectious Respiratory Failure. N Engl J Med. 1989;321(9):569-574. doi:10.1056/nejm198908313210903 REFERENCE #3: Philit F, Etienne-Mastroïanni B, Parrot A, Guérin C, Robert D, Cordier JF. Idiopathic acute eosinophilic pneumonia: A study of 22 patients. Am J Respir Crit Care Med. 2002;166(9):1235-1239. doi:10.1164/rccm.2112056 DISCLOSURES: No relevant relationships by Nurjahan Khatun, source=Web Response No relevant relationships by Parth Patel, source=Web Response No relevant relationships by Naleen Patel, source=Web Response No relevant relationships by Tarang Patel, source=Web Response No relevant relationships by SACHIN PATIL, source=Web Response No relevant relationships by Shyam Shankar, source=Web Response No relevant relationships by Rodger Wilhite, source=Web Response

A CRACK LUNG WITH CRACK COCAINE

TOPIC: Lung Pathology TYPE: Medical Student/Resident Case Reports INTRODUCTION: Crack lung is an acute pulmonary syndrome with a spectrum of clinical and histopathologic findings occurring within 48 hours of smoking crack cocaine.1 Patients may present with clinical features of pneumonia. As such, it is important to differentiate the two clinical entities as the management approach differs. Here we present a case of acute pulmonary cocaine toxicity mimicking possible pneumonia. CASE PRESENTATION: A 40 year old man with a history of depression was brought in by paramedics after being found unconscious.He was given naloxone en route with improved consciousness but was tachypneic and hypoxic, requiring oxygen. On arrival to the Emergency Department, he admitted to having smoked crack cocaine which was impure.He reported having hemoptysis and rhinorrhea but denied any chest pain, fever or any gastrointestinal symptoms.There was no personal or family history of lung or autoimmune disease. On presentation he was afebrile, tachycardic, tachypneic and persistently hypoxic requiring high flow nasal cannula (HFNC). Pertinent findings were diminished breath sounds with diffuse rales, with an otherwise unremarkable exam. Laboratory results were notable for cocaine on urine toxicology, leukocytosis with neutrophilia, elevated procalcitonin with normal CRP, BNP, serial troponins, lactic acid, COVID-19 test and HIV. Initial CXR showed bilateral extensive nodular interstitial lung pattern. He was admitted for acute hypoxic respiratory failure (AHRF) secondary to crack lung syndrome with superimposed pneumonia on HFNC and started on empiric antibiotics as well as methylprednisolone. Unfortunately, he remained persistently tachypneic and required non-invasive ventilation (NIV) and transfer to the intensive care unit. On day 2, his respiratory status markedly improved and he was weaned from NIV to room air. Final blood cultures and mycoplasma antibody were negative and the rest of his hospital stay was uneventful. DISCUSSION: In 2018, approximately 5.5 million persons aged ≥ 12 years reported cocaine use within the past year of which 757,000 used crack cocaine.2,3 With likely underreported usage, the deleterious pulmonary complications related to cocaine use including pulmonary edema, alveolar hemorrhage, eosinophilic pneumonia, pneumothorax, thromboembolic disease and AHRF,4 are clinically relevant. However, the diagnosis of cocaine-induced pulmonary diseases remains challenging for clinicians given that the clinical features and chest images are non specific and can mimic several other processes e.g. pneumonia.5 This distinction is important as mortality for pneumonia requiring ICU admission approaches 30%,6 while acute eosinophilic pneumonia portends an excellent prognosis with rapid clinical recovery. CONCLUSIONS: This case highlights that "Crack Lung" should be considered as a differential diagnosis in patients with AHRF and diffuse bilateral pulmonary infiltrates. REFERENCE #1: Forrester, J. M., Steele, A. W., Waldron, J. A., & Parsons, P. E. (1990). Crack lung: an acute pulmonary syndrome with a spectrum of clinical and histopathologic findings. The American review of respiratory disease, 142(2), 462–467. https://doi.org/10.1164/ajrccm/142.2.462 REFERENCE #2: National Institute on Drug Abuse.(2020) What is the scope of cocaine use in the United States? Available from:https://www.drugabuse.gov/publications/research-reports/cocaine/what-scope-cocaine-use-in-united-states REFERENCE #3: 3.Center for Disease Control and Prevention. (2019). Annual surveillance report of drug-related risks and outcome. Available from:https://www.cdc.gov/drugoverdose/pdf/pubs/2019-cdc-drug-surveillance-report.pdf DISCLOSURES: No relevant relationships by Sahai Donaldson, source=Web Response No relevant relationships by Lorenzo Leys, source=Web Response No relevant relationships by Alicia Thomas, source=Web Response No relevant relationships by Felix Wireko, source=Web Response

COVID-19-ASSOCIATED THROMBOTIC THROMBOCYTOPENIC PURPURA: A FATAL NIGHTMARE

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: COVID-19 virus has been reported to be associated with many unusual conditions and coagulopathies including thrombotic microangiopathies, DVTs, and PEs. However, cases of COVID 19 associated TTP are very rare. We discuss a patient with confirmed COVID-19 pneumonia who then developed acquired autoimmune TTP. CASE PRESENTATION: A 68-year-old female with no significant past medical history presented to the hospital with generalized weakness, shortness of breath, and cough. The onset of symptoms was about 7 days. Initial labs were significant for positive COVID-19 on PCR, WBC 10.4 k/ul, Lactic 1.3, D-dimer 3109 ng/ml. Chest x-ray revealed diffuse bilateral pulmonary infiltrates. She was placed on high flow oxygen with saturation between 80 - 89%. Remdesivir, Dexamethasone & one unit of COVID Convalescent Plasma were started for COVID-19 pneumonia. On day 2, she was switched to BIPAP due to worsening respiratory distress. On day 3, she was intubated due to rapidly progressive ARDS. Blood cultures were negative. She developed neutrophil predominant leukocytosis and anemia. On day 5, she developed thrombocytopenia. On day 8, her platelet counts declined to 17,000. Peripheral smears showed minor areas of clumping while platelet still significantly decreased. Redraw with citrate tube showed no major difference in platelet count. Testing showed evidence of hemolysis with undetectable haptoglobin, rising bilirubin level, and markedly elevated LDH with worsening renal functions. Directs Coombs test was IgG positive with abundant schistocytes on smear. PLASMIC SCORE 7 indicating a high risk for ADAMTS 13 deficiency. The patient was started on high dose IV steroids and needed a total of 2 units of packed red blood cell, 7 units of platelets, and 27 units of fresh frozen plasma. Her condition continued to deteriorate, and she was transferred to a tertiary care center that has plasmapheresis capability. Unfortunately, the patient died a few days later despite treatment. DISCUSSION: There have been only few cases in the literature discussing TTP involvement with COVID-19 infection. A case series and a four patient mini-review of this association were published in January 2021. COVID-19 seems to be the primary trigger. Autoimmunity and endothelial damage could be important factors in these manifestations. Plasmapheresis seem to improve this condition. However, due to the low population of patients, more cases are needed to draw a conclusion and better understand the presentation of COVID-associated coagulopathy. CONCLUSIONS: This case highlights the importance of evaluating and recognizing the hematological complication associated with COVID-19. Therapeutic plasma exchange and IV steroids should be started early. Rapid progression if not treated promptly. Further studies are needed to understand pathogenesis, clinical course, and proper management. REFERENCE #1: George JN, Nester CM. Syndromes of thrombotic microangiopathy. N Engl J Med. 2014 Nov 6;371(19):1847-8. doi: 10.1056/NEJMc1410951. PMID: 25372103. REFERENCE #2: I ba, T., Levy, J.H., Connors, J.M. et al. The unique characteristics of COVID-19 coagulopathy. Crit Care 24, 360 (2020). https://doi.org/10.1186/s13054-020-03077-0 REFERENCE #3: Tehrani HA, Darnahal M, Vaezi M, Haghighi S. COVID-19 associated thrombotic thrombocytopenic purpura (TTP) ; A case series and mini-review. Int Immunopharmacol. 2021 Apr;93:107397. doi: 10.1016/j.intimp.2021.107397. Epub 2021 Jan 22. PMID: 33524803; PMCID: PMC7825972. DISCLOSURES: No relevant relationships by Musa Abu-Jubara, source=Web Response No relevant relationships by Dania Abu-Jubara, source=Web Response No relevant relationships by Adebayo Fasanya, source=Web Response

DIFFUSE ALVEOLAR HEMORRHAGE: A RARE COMPLICATION OF ACUTE MYELOID LEUKEMIA

TOPIC: Pulmonary Manifestations of Systemic Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Diffuse alveolar hemorrhage (DAH) is a life-threatening pulmonary syndrome affecting individuals with hematologic malignancies with increased incidence post bone marrow transplant. We present a rare case of DAH presumably related to pulmonary leukemic infiltration (PLI) in a newly diagnosed Acute Myelogenous Leukemia (AML) patient. CASE PRESENTATION: A 55-year-old female, previously healthy, presented to the emergency room with a 1-week history of dyspnea, cough, and epistaxis. Laboratory data were relevant for leukocytosis (WBC 150,000/mm3) with 84% blasts, thrombocytopenia (platelets 15,000/mm3), and anemia (Hb 8.9 g/dL). CT angiography of the chest was negative for pulmonary embolism but showed scattered bilateral ground-glass opacities (GGO). Peripheral blood flow cytometry revealed AML. She underwent leukapheresis with an appropriate response. On day 5 of admission, she was transferred to the intensive care unit for increased oxygen requirement and required endotracheal intubation the day after. Chest CT showed significant worsening in bilateral GGO and septal thickening. WBC 27,000/mm3, Hb 7.7 g/dL, and platelets 50,000/mm3. Bronchoscopy with serial bronchoalveolar lavages (BAL) showed an increasingly bloody return. BAL cell differential was significant for 75% blasts. She was treated with platelet transfusion, nebulized tranexamic acid, high dose corticosteroids, and empiric antibiotic therapy. Emergent induction chemotherapy (daunorubicin + cytarabine) was started. Repeat bronchoscopy in 48h showed resolution of DAH and undetectable blasts in BAL. She was extubated on day 7 post-intubation, and her respiratory status improved back to baseline. DISCUSSION: Pulmonary opacities in leukemia may be the result of an infectious process, pulmonary edema, drug toxicity, diffuse alveolar hemorrhage, intravascular leukostasis, or pulmonary leukemic infiltrates. Though the timing of pulmonary complications, clinical presentation, and chest CT findings may help identify the etiology, diagnosis is frequently challenging, and early BAL may be of benefit. In this patient, worsening respiratory status and pulmonary infiltrates despite leukapheresis excluded leukostasis and suggested PLI. Hemoptysis is absent in more than one-third of patients with DAH. She had no hemoptysis, and DAH was subsequently diagnosed with bronchoscopy. We believe that early diagnosis of PLI, excellent response to induction chemotherapy, along with other supportive measures led to a favorable outcome. CONCLUSIONS: Early recognition of acute respiratory failure etiology in patients with leukemia and pulmonary infiltrates is essential. Albeit rare, DAH should always be on the differential as early identification and treatment can likely improve outcomes. REFERENCE #1: Nanjappa S, Jeong DK, Muddaraju M, Jeong K, Hill ED, Greene JN. Diffuse Alveolar Hemorrhage in Acute Myeloid Leukemia. Cancer Control. 2016 Jul;23(3):272-7 REFERENCE #2: Nucci M, Nouér SA, Anaissie E. Distinguishing the Causes of Pulmonary Infiltrates in Patients with Acute Leukemia. Clin Lymphoma Myeloma Leuk. 2015 Jun;15 Suppl: S98-103. DISCLOSURES: No relevant relationships by Tony Abdo, source=Web Response No relevant relationships by Samiksha Gupta, source=Web Response No relevant relationships by SYED HUSSAIN, source=Web Response No relevant relationships by Miloni Parmar, source=Web Response

Cerebral tuberculosis - a diagnostic challenge

Abstract Background: Central nervous system (CNS) tuberculosis (TB) accounts for 1% of all cases of TB and is a major cause of mortality and morbidity. Cerebral tuberculomas represent 30% of CNS TB and is a diagnostic challenge. Case presentation: A 42-year-old male patient, known with alcoholic cirrhosis, performs a cerebral computer tomography (CT) after a lipothymic episode accompanied by right hemiparesis, which showed multiple parenchymal ring-lesions (inflammatory-infectious substrate/secondary tumours). Subsequently, the thoracic-abdominal-pelvic-CT-scan reveals micronodular diffuse pulmonary infiltrate and right pleural effusion. Cerebral Magnetic resonance imaging (MRI) describes bilateral infra/supratentorial lesions, raising the suspicion of tuberculomas. HIV serology was negative, cerebrospinal fluid showed no pleocytosis, but high protein level, pleural lymphocytosis in the pleural effusion and positive GeneXpert test in bronchial aspirate. The diagnosis of military TB with cerebral tuberculomas was established. The outcome was favourable under antituberculous treatment initially associated with corticosteroids. At two months the patient had a significant improvement in pulmonary lesions, but while some cerebral lesions decreased in size other lesions increased (paradoxical reaction). At the 14-month end-of-treatment re-evaluation there was an important regression in number and size of the brain lesions. Conclusions: The diagnosis of cerebral tuberculoma remains a challenge for the clinician due to non-specific clinical and radiological findings. The survival rate is over 80% with early diagnosis and correct treatment.

Rat model of smoke inhalation-induced acute lung injury

BackgroundAcute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a lethal disease with limited therapeutic options and an unacceptably high mortality rate. Understanding the complex pathophysiological processes involved in the...