Diffuse Bilateral Infiltrates Research Articles

Inhibition of cIAP1/2 reduces RIPK1 phosphorylation in pulmonary endothelial cells and alleviate sepsis-induced lung injury and inflammatory response.

Acute respiratory distress syndrome (ARDS)/acute lung injury (ALI) is a severe complication of sepsis characterized by acute respiratory distress, hypoxemia, and diffuse bilateral pulmonary infiltrates. The regulation of RIPK1 is an important part of the inflammatory response, and cIAP1/2 serves as the E3 ubiquitin ligase for RIPK1. In this study, we investigated the effect and mechanism of cIAP1/2 inhibition on sepsis-induced lung injury. Our results showed that cIAP1/2 inhibition can alleviate sepsis-induced lung injury and reduce the inflammatory response, which is accompanied by downregulation of RIPK1 phosphorylation and ubiquitination. Additionally, cIAP1/2 inhibition led to the up-regulation of programmed cell death, including apoptosis, necroptosis, and pyroptosis, and inhibiting these three cell death pathways can further reduce the inflammatory response, which is similar to the recently discovered programmed cell death pathway PANoptosis. Our findings suggest that cIAP1/2 and PANoptosis inhibition may be a new strategy for treating sepsis-induced lung injury and provide important references for further exploring the mechanism of sepsis-induced lung injury and identifying new therapeutic targets.

Itaconate to treat acute lung injury: recent advances and insights from preclinical models.

Acute lung injury (ALI) is defined as the acute onset of diffuse bilateral pulmonary infiltration, leading to PaO2/FiO2 ≤ 300 mmHg without clinical evidence of left atrial hypertension. Acute respiratory distress syndrome (ARDS) involves more severe hypoxemia (PaO2/FiO2 ≤ 200 mmHg). Treatment of ALI and ARDS has received renewed attention as the incidence of ALI caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has increased. Itaconate and its derivatives have shown therapeutic potential against ALI. This review provides an in-depth summary of the mechanistic research of itaconate in the field of acute lung injury, including inducing autophagy, preventing ferroptosis and pyroptosis, shifting macrophage polarization to an anti-inflammatory M2 phenotype, inhibiting neutrophil activation, regulating epigenetic modifications, and repressing aerobic glycolysis. These compounds merit further consideration in clinical trials. We anticipate that the clinical translation of itaconate-based drugs can be accelerated.

HLH Secondary to Influenza

Introduction Hemophagocytic lymphohistiocytosis (HLH) is a pathological condition characterized by excessive inflammation and tissue damage resulting from an aberrant immune system response. HLH can be classified into two distinct categories: primary HLH and secondary HLH. Secondary hemophagocytic lymphohistiocytosis (HLH) is an acquired condition that can be precipitated by various infections, malignancies, or rheumatological disorders. Herein, we present a rare case of HLH secondary to influenza B infection. Case Presentation A 37-year-old who routinely vapes and smokes cannabis presented to the emergency department with subjective fevers, body pains, fatigue, productive cough, shortness of breath, nausea, non-bloody, non-bilious vomiting, and watery diarrhea for one week. He was tachypneic, tachycardic, and febrile (101.1 F). He had loud bibasilar crackles on auscultation. Hb 14.8, total WBC 2.2, platelets 170, AKI with serum creatinine 1.9, and transaminitis with AST/ALT/ALP 130/56/122 U/L were the patient's initial lab results. Rapid influenza, strep, and COVID-19 antigen tests were negative. He exhibits hypoxemia with pH 7.46, pCO2 32.5, pO2 52.1, HCO3 22.9, and FIO2 40%. Urinalysis showed nonsignificant. CRP was 8.3 mg/dL. Negative procalcitonin. chest x-ray and ct showed bilateral diffuse patchy airspace infiltration, suggesting infectious process with mild pleaural effusion. In the critical care unit, he received Antibiotics and inhaled therapy for acute hypoxic respiratory failure with severe ARDS. After deteriorating, he was intubated. The respiratory pathogen panel detected Influenza B. Blood cultures and remaining pneumonia workup were negative. The lab results suggested HLH (table 1). Autoimmune tests were negative. Oseltamivir was given for 5 days. Repeat chest x-rays showed stable pulmonary infiltrates in the right middle and lower lobes, but the patient decompensated clinically with increasing ventilator requirements and dyssynchrony despite heavy sedation, paralytics, and proning and was transferred to a different hospital for ECMO evaluation on day 12. Discussion Primary and secondary HLH: Secondary HLH is caused by infections, malignancies, or rheumatological illnesses, while primary HLH is hereditary. The mortality outcome of HLH is extremely dependent on early detection and treatment 1. Due to the rarity of this disease entity, difficult diagnostic criteria, and concern for alternate diagnoses, internists may be less aware of it. Further complicating the diagnosis is the fact that the first bone marrow biopsy may not always show hemophagocytosis 2. This is why it is important to be cognizant of this diagnosis and it's diagnostic criteria. Our patient was suspected of HLH based on HScore for reactive hemophagocytic syndrome and the newest updated HLH diagnostic criteria (5 of 8 criteria should be met) 6. EBV is the most common viral infection which can cause HLH. CMV, Parvo, HSV, and H1N1 are other infections. HLH-Influenza B connection is poorly documented 7 Only one case of HLH induced by influenza B in a healthy patient was found in literature. To our knowledge, Our 38-year-old patient is the second known case of secondary HLH secondary to Influenza B in a healthy patient. Influenza B seldom causes HLH. This connection in adulthood is poorly researched. Patients with influenza virus infections have significant intestinal apoptosis and reactive hemophagocytic activity in bone marrow, lungs, and liver3. Influenza variants reduce CD8+ T cell cytotoxicity and perforin expression, likely causing HLH syndrome 4. A study suggests that virus-associated hemophagocytic syndrome (VAHS) is a common consequence of severe 2009 influenza A (H1N1) infection and contributes to multiorgan failure and mortality. 9 (36%) of 25 severely ill patients with confirmed 2009 influenza A (H1N1) infection developed VAHS, and 8 (89%) died 5. Conclusion: We present this case to raise awareness among physicians regarding the potential occurrence of hemophagocytic lymphohistiocytosis (HLH) as a complication in adult patients who present with influenza B virus infection accompanied by fever and pancytopenia. The aim is to emphasize the importance of considering HLH as a differential diagnosis in order to facilitate timely identification and initiation of appropriate treatment for this condition.

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.

Joint classification and segmentation for an interpretable diagnosis of acute respiratory distress syndrome from chest x-rays.

Acute respiratory distress syndrome (ARDS) is a life-threatening condition that can cause a dramatic drop in blood oxygen levels due to widespread lung inflammation. Chest radiography is widely used as a primary modality to detect ARDS due to its crucial role in diagnosing the syndrome, and the x-ray images can be obtained promptly. However, despite the extensive literature on chest x-ray (CXR) image analysis, there is limited research on ARDS diagnosis due to the scarcity of ARDS-labeled datasets. Additionally, many machine learning-based approaches result in high performance in pulmonary disease diagnosis, but their decisions are often not easily interpretable, which can hinder their clinical acceptance. This work aims to develop a method for detecting signs of ARDS in CXR images that can be clinically interpretable. To achieve this goal, an ARDS-labeled dataset of chest radiography images is gathered and annotated for training and evaluation of the proposed approach. The proposed deep classification-segmentation model, Dense-Ynet, provides an interpretable framework for automatically diagnosing ARDS in CXR images. The model takes advantage of lung segmentation in diagnosing ARDS. By definition, ARDS causes bilateral diffuse infiltrates throughout the lungs. To consider the local involvement of lung areas, each lung is divided into upper and lower halves, and our model classifies the resulting lung quadrants. The quadrant-based classification strategy yields the area under the receiver operating characteristic curve of 95.1% (95% CI 93.5 to 96.1), which allows for providing a reference for the model's predictions. In terms of segmentation, the model accurately identifies lung regions in CXR images even when lung boundaries are unclear in abnormal images. This study provides an interpretable decision system for diagnosing ARDS, by following the definition used by clinicians for the diagnosis of ARDS from CXR images.

Fat embolism syndrome after humerus and pelvis fracture complicated by acute kidney injury requiring blood purification: a case report and literature review

BackgroundFat embolism syndrome (FES) is a rare syndrome that typically occurs 12–72 h after long bone or pelvic fractures with a classic triad of respiratory distress, neurologic changes, and petechial rash. Although Gurd’s criteria for FES include anuria or oliguria, the mechanism of acute kidney injury (AKI) remain unknown. Here, we present a case of FES complicated by AKI that required blood purification.Case presentationA 79-year-old woman was admitted to our hospital because of a right humerus and pelvic fracture caused by a traffic accident. On the second day of hospitalization, she developed impaired consciousness, respiratory failure, and disseminated intravascular coagulation (DIC). Chest radiography revealed bilateral diffuse alveolar infiltration. Brain magnetic resonance imaging revealed diffuse high signal intensity on diffusion-weighted imaging and diffuse low signal intensity on susceptibility-weighted imaging in the cerebral and cerebellar regions. The diagnosis of FES was confirmed and the patient was treated with methylprednisolone (40 mg/day) and ulinastatin. On the third day of hospitalization, she was admitted to our department because of AKI with oliguria. Although echocardiography showed an elevated right ventricular artery systolic pressure suggestive of pulmonary hypertension (PH), pulmonary congestion was initially considered on chest imaging, and hemodialysis and rapid ultrafiltration were initiated. However, she developed hypovolemic shock and treatment was switched to continuous hemodiafiltration and slow ultrafiltration. Thereafter, her consciousness, hypoxemia, DIC and PH completely improved. She was weaned from blood purification therapy on the 29th day of hospitalization. She had hemolytic anemia that might have been caused by thrombotic microangiopathy (TMA), but it resolved without plasmapheresis. On the 51st day of hospitalization, the patient was transferred to another hospital for rehabilitation.ConclusionsFES can be complicated by AKI. In this case, DIC, which was difficult to differentiate from TMA, and/or renal congestion were considered to be a cause of AKI. Chest radiographs of FES may be indistinguishable from pulmonary congestion. In our case, chest radiography showed bilateral diffuse alveolar infiltrates which was not indicative of pulmonary congestion but pulmonary involvement of FES. FES is associated with PH, which may lead to right heart failure. Therefore, the patient could have developed hypovolemic shock due to hemodialysis and rapid ultrafiltration. Clinicians should pay attention to the hemodynamics when blood purification for FES is performed.

Exploring Diverse Presentations of Cryptogenic Organizing Pneumonia: A Case Series

Cryptogenic Organizing Pneumonia (COP), the idiopathic form of Organizing Pneumonia (OP) previously known as “bronchiolitis obliterans organizing pneumonia,” is a well-documented medical condition with distinct clinicoradiological features and diagnostic criteria. COP can exhibit a diverse range of radiological presentations, including multiple patchy alveolar opacities (typical pattern), a solitary focal lesion, or diffuse bilateral infiltration. Corticosteroid therapy is typically effective in achieving rapid clinical and imaging improvement, but caution must be exercised in cases of active infections where corticosteroids are contraindicated, posing a challenge for OP diagnosis. This case series emphasizes the need for healthcare providers to be knowledgeable about the various atypical clinical manifestations of COP, recognize the diverse and uncommon radiological presentations that may mimic other pulmonary pathologies, and consider COP in the differential diagnosis to ensure appropriate management and enhance patient outcomes.

Colonic oxygen microbubbles augment systemic oxygenation and CO2 removal in a porcine smoke inhalation model of severe hypoxia

Inhalation injury can lead to pulmonary complications resulting in the development of respiratory distress and severe hypoxia. Respiratory distress is one of the major causes of death in critically ill patients with a reported mortality rate of up to 45%. The present study focuses on the effect of oxygen microbubble (OMB) infusion via the colon in a porcine model of smoke inhalation-induced lung injury. Juvenile female Duroc pigs (n = 6 colonic OMB, n = 6 no treatment) ranging from 39 to 51 kg in weight were exposed to smoke under general anesthesia for 2 h. Animals developed severe hypoxia 48 h after smoke inhalation as reflected by reduction in SpO2 to 66.3 ± 13.1% and PaO2 to 45.3 ± 7.6 mmHg, as well as bilateral diffuse infiltrates demonstrated on chest X-ray. Colonic OMB infusion (75–100 mL/kg dose) resulted in significant improvements in systemic oxygenation as demonstrated by an increase in PaO2 of 13.2 ± 4.7 mmHg and SpO2 of 15.2 ± 10.0% out to 2.5 h, compared to no-treatment control animals that experienced a decline in PaO2 of 8.2 ± 7.9 mmHg and SpO2 of 12.9 ± 18.7% over the same timeframe. Likewise, colonic OMB decreased PaCO2 and PmvCO2 by 19.7 ± 7.6 mmHg and 7.6 ± 6.7 mmHg, respectively, compared to controls that experienced increases in PaCO2 and PmvCO2 of 17.9 ± 11.7 mmHg and 18.3 ± 11.2 mmHg. We conclude that colonic delivery of OMB therapy has potential to treat patients experiencing severe hypoxemic respiratory failure.

How is ischemic stroke linked to a COVID-19-infected patient different from other cardiovascular risk factors? a case report.

On 19 September 2022, 3h after the commencement of the right-sided weakness, a 61-year-old black African male farmer was sent to transported to the emergency room. When an radiography of the chest was performed, it showed diffuse bilateral infiltrates, coarse, slightly bilateral crepitation, and scattered reticulations. Cardiovascular testing of the patient turned up nothing unexpected. The eye-opening reaction was 1/4 (no eye opening) on the Glasgow Coma Scale, the motor response was 3/6 (abnormal flexion), and the verbal response was 3/5 (inappropriate words). When his breathing became difficult, he needed five intranasal doses of oxygen every minute to maintain saturation. He started taking low-dose aspirin daily for a month at 81mg. He took consumed 75mg of clopidogrel once a day for a month. Stroke was associated with in-hospital death among hospitalized patients with the COVID-19 infection. In patients who have risk factors for stroke, such as high blood pressure, obesity, and diabetes, COVID-19 increases the risk of stroke. The risk of stroke was highest in older people within the first few days after receiving a COVID-19 diagnosis. Patients with COVID-19 are more likely to get an ischemic stroke from large infarctions, mostly as a result of major artery thrombosis. From the start of COVID-19 signs, neurological problems can appear anywhere between 3 and 14 days later. Due to severe inflammation, immobility, hypoxia, and diffuse intravascular coagulation, SARS-CoV-2 also possesses neurological invasive capabilities and may migrate from the respiratory system to the central nervous system.

Internal Jugular Vein Cannulation in Prone Position.

Since 1970, prone decubitus (PD) has been used as adjuvant therapy to treat severe hypoxia in patients with acute respiratory distress syndrome (ARDS), and now with the COVID-19 pandemic, its use has become widespread in ICUs. ARDS is characterized by diffuse bilateral radiographic infiltrates, decreased respiratory compliance, small lung volumes, and severe hypoxemia. The placement of vascular access in PD seems to be feasible and safe, since, as has been described, the number of complications such as pneumothorax, bleeding, and arterial punctures are almost nil, especially when performed under ultrasound guidance. The patients who could benefit most from this procedure seem to be those with obesity, mainly with a body mass index greater than 30 kg/m2, in whom the return to the supine position may represent a risk of respiratory or hemodynamic deterioration.

Fat Embolization Syndrome Secondary to Steroid Treatment for Intractable Migraine

Sickle vaso-occlusive crises secondary to steroid therapy are well reported in the medical literature. Fat embolization syndrome (FES) is an uncommon yet serious complication that occurs due to bone marrow necrosis and is usually associated with increased mortality or damaging neurologic sequelae to the surviving patient. We report a case of FES secondary to steroid therapy administered for an unrelated condition. Our patient was initially admitted for intractable migraine. The initial work up for other intracranial emergencies was negative and she was administered steroids for intractable migraine. Within 24 hours of initiating steroid therapy, she developed pain in her neck and shoulders progressing to her chest and lower extremities. The initial signs of FES following steroid therapy in this patient included altered mental status and hypoxic respiratory failure. Cerebral imaging showed diffuse bilateral cerebral/cerebellar and brainstem micro-hemorrhages. Lung imaging showed bilateral diffuse lung infiltrates confirming acute chest syndrome. The patient was transferred to the intensive care unit for further management of her hypoxic respiratory failure secondary to acute chest syndrome (ACS). In addition to ACS, she had acute kidney and hepatocellular injury in keeping with multi-organ failure. Steroid therapy was discontinued and she was treated with red cell exchange transfusion for multi-organ failure. The patient had an almost complete resolution of multiple organ damage except for hypoesthesia of her lower jaw and lower lip- the "numb chin syndrome". This case report highlights the importance of recognizing potentially fatal multi-organ failure secondary to steroid therapy and for hematologists to consider concurrent red cell transfusions to attenuate the risk of such complications from steroid therapy.

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.

IGG4-RELATED DISEASE PRESENTING AS A PULMONARY INFLAMMATORY PSEUDOTUMOR

IGG4-RELATED DISEASE PRESENTING AS A PULMONARY INFLAMMATORY PSEUDOTUMOR

ARDS IN THE SETTING OF SEROTONIN SYNDROME

ARDS IN THE SETTING OF SEROTONIN SYNDROME

P231 The first case of neonatal fungemia caused by Aureobasidium melanogenum

Poster session 2, September 22, 2022, 12:30 PM - 1:30 PM Background Aureobasidium melanogenum is a ubiquitous, saprophytic, dematiaceous fungus commonly isolated from environmental sources. It has the highest virulence potential among all Aureobasidium species and is implicated in catheter-related infections, particularly in immunocompromised hosts.Case ReportA 6-day-old female child was admitted to the neonatal intensive care unit (NICU), AIIMS, Jodhpur with respiratory distress, hypotension, bradycardia, and sepsis. The baby was preterm with a very low birth weight (1140 g) and was born to a 34-year-old G3P1A2 mother at 30 weeks gestation by elective caesarian section at a private hospital. The mother had a primary ovarian failure and had a history of spontaneous abortions for two consecutive times following in vitro fertilization. She also had a history of gestational diabetes mellitus and pregnancy-induced hypertension, for which she was on medication. At birth, the baby had respiratory distress (Apgar scores were 6 and 7 at 1 and 5 minutes of life, respectively), for which she was shifted to NICU and intubated. On day 2, she developed hypotension, bradycardia, hypocalcemia, and sepsis with deranged coagulation profile, for which she received inotropes, broad-spectrum antibiotics, fluconazole, and fresh frozen plasma. On day 3, the baby developed chest retractions and seizure-like episodes with intermittent myoclonic jerks and was started on anti-epileptics. She had persistently raised serum urea, creatinine, and C-reactive protein from day 3 of life. Due to clinical deterioration, she was shifted to AIIMS NICU for further management where she was continued on inotropes, broad-spectrum antibiotics, and fluconazole. After 46 h of admission at AIIMS NICU, the baby developed hypotension with cold extremities, feeble pulses, and increased ventilatory requirements. Chest X-ray showed bilateral diffuse infiltrates suggestive of acute respiratory distress syndrome. Culture of tracheal aspirate yielded Klebsiella pneumoniae, sensitive to piperacillin/tazobactam, amikacin, and carbapenems. The patient was started on intravenous meropenem and colistin. Blood culture showed growth of Gram-positive budding yeast cells after 48 h of incubation (Fig. 1). Subculture on Sabouraud dextrose agar revealed yeast-like colonies, initially cream-colored, becoming dark-brown with an olive-green feathery margin (Fig. 2a). Microscopically, the isolate had septate pigmented hyphae with ellipsoidal hyaline conidia (Fig. 2b). The morphologic features were consistent with Aureobasidium species. Sequencing the internal transcribed spacer region of rDNA confirmed the identity of the isolate as A. melanogenum. Antifungal susceptibility testing revealed the following MICs: amphotericin B, 0.5 μg/ml, itraconazole, 0.25 μg/ml, voriconazole, 0.125 μg/ml, fluconazole, 16 μg/ml, and caspofungin, 0.25 μg/ml. Despite maximum inotropic and ventilatory support, the baby had persistent desaturations and hypoxia and developed multiple organ dysfunction syndrome, following which she succumbed to death on day 3 of admission to AIIMS.ConclusionThis is the first documented case of neonatal fungemia caused by the emerging yeast A. melanogenum. The patient had multiple arterial and intravenous catheters and this could be the portal of entry of the pathogen. Accurate identification is crucial for initiating appropriate antifungal therapy. Physicians should be mindful of possible A. melanogenum infection in patients with risk factors, and provide appropriate antifungal therapy with the removal of indwelling catheters whenever possible.

Clinical Characteristic, Diagnosis and Treatment of Acute Lymphoblastic Leukemia Combined with Pneumocystis Carinii Pneumonia in Children

To investigate the clinical characteristics and treatment of pneumocystis carinii pneumonia (PCP) in children with acute lymphoblastic leukemia (ALL), in order to improve the early diagnosis and effective treatment. Clinical data of five children with ALL developing PCP in the post-chemotherapy granulocyte deficiency phase were analyzed retrospectively. The clinical manifestations, laboratory tests, imaging findings, treatment methods and effect were summarized. The male-to-female ratio of the five children was 1∶4, and the median age was 5.5 (2.9-8) years old. All patients developed PCP during granulocyte deficiency phase after induction remission chemotherapy. The clinical manifestations were generally non-specific, including high fever, tachypnea, dyspnea, non-severe cough, and rare rales in two lungs (wet rales in two patients). Laboratory tests showed elevated C-reactive protein (CRP), serum procalcitonin (PCT), (1,3)-β-D-glucan (BDG), lactate dehydrogenase (LDH) and inflammatory factors including IL-2R, IL-6 and IL-8. Chest CT showed diffuse bilateral infiltrates with patchy hyperdense shadows. Pneumocystis carinii(PC) was detected in bronchoalveolar lavage fluid (BALF) or induced sputum by high-throughput sequencing in all patients. When PCP was suspected, chemotherapy was discontinued immediately, treatment of trimethoprim-sulfame thoxazole (TMP-SMX) combined with caspofungin against PC was started, and adjunctive methylprednisolone was used. Meanwhile, granulocyte-stimulating factor and gammaglobulin were given as the supportive treatment. All patients were transferred to PICU receiving mechanical ventilation due to respiratory distress during treatment. Four children were cured and one died. PCP should be highly suspected in ALL children with high fever, dyspnea, increased LDH and BDG, and diffuse patchy hyperdense shadow or solid changes in lung CT. The pathogen detection of respiratory specimens should be improved as soon as possible. TMP/SMZ is the first-line drug against PCP, and the combination of Caspofungin and TMP/SMZ treatment for NH-PCP may have a better efficacy. Patients with moderate and severe NH-PCP may benefit from glucocorticoid.

PH Grand Rounds: COVID-19 Infection Causing Delayed Pulmonary Arterial Hypertension

PH Grand Rounds: COVID-19 Infection Causing Delayed Pulmonary Arterial Hypertension

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

Respiratory Bronchiolitis-Interstitial Lung Disease in Chronic Kidney Disease Mimicking Uremic Lung: A Case Report

Introduction: Uremic lung is a frequent complication of chronic kidney disease (CKD), while interstitial lung is an inflammation of the parenchyma which impairs its capacity. These two conditions manifest similar radiological features with bilateral diffuse infiltrates. Therefore, their clinical appearance and radiological lesions are often mistaken. Case: This study reported a case of a 55-year-old male patient with shortness of breath for 1 month and worsening 1 week before hospitalization. The patient had a smoking history for 30 years with severe Brinkman index, hypertension (HT), and diabetes mellitus (DM). Auscultation examination showed crackles in both lungs, while laboratory results showed anemia, leukocytosis, increased urea and creatinine levels, and radiological features of bilateral infiltrate suggesting a uremic lung. Furthermore, the ultrasonography showed bilateral chronic pyelonephritis and was diagnosed with CKD, uremic lung, pneumonia, anemia, hypoalbuminemia, mild hypokalemia, DM, and HT. The patient was treated with regular hemodialysis three times a week, and the serial chest X-ray after hemodialysis showed persistent bilateral infiltrates. An MSCT examination was also performed, and the results showed respiratory bronchiolitis-interstitial lung disease (RB-ILD). The patient was treated with antibiotic therapy, inhaled salbutamol, systemic steroids, and mucolytics. The patient was discharged from the hospital after the respiratory complaint were improved. Conclusion: In uremia patients with bilateral infiltrates resembling uremic lung and unresponsive to hemodialysis or other therapies, interstitial illness should be explored. To improve patient management, risk factors for suspected interstitial lung disease should always be examined.

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.