Intra-alveolar Hemorrhage Research Articles

Epidemiological Aspects, Clinicopathology, Hemato-biochemistry and Therapeutic Management of Viperine Snake Envenomation in Buffaloes (Bubalus bubalis)

Background: Poisonous snakebite is a neglected tropical disease, frequently reported in animals including buffaloes. Snakebites are responsible for considerable morbidity and mortality in animals causing economic losses to dairy farmers. Methods: To establish the baseline data of epidemiology, clinical syndrome, hemato-biochemistry and diagnosis of viper snakebites and to standardize the treatment of viper snakebite in buffaloes. Result: The highest incidence of viper envenomation was observed during the monsoon and post-monsoon season in female buffaloes above 4 years of age. The clinical signs such as tachycardia, increased respiration rate, ascending swelling of affected limbs, asymmetrical swelling with dyspnea in case of bite over face and bleeding at the site of bite were observed in envenomed buffaloes. Hemato-biochemical analysis revealed neutrophilic leukocytosis, thrombocytopenia, prolonged capillary blood clotting time, elevated values of blood urea nitrogen (BUN) and creatinine. Post-mortem examination showed hemorrhages and blood-stained serous fluid in subcutaneous tissue and skeletal muscles of the affected limbs. The histopathological changes such as extensive myonecrosis and hemorrhages with marked edema in skeletal muscles, widespread interstitial and intra-alveolar hemorrhages and fibrinous microthrombi in pulmonary vasculature, multifocal to coalescing areas of massive hemorrhages and coagulative necrosis within hepatic parenchyma and marked degeneration of renal tubular epithelium were evident. Therapeutic regimen consisting of polyvalent anti-snake venom, with antibiotics, diuretics, vitamin B complex, styptics, fluids and corticosteroids in non-pregnant while non-steroidal anti-inflammatory drugs in pregnant buffaloes was used. The present treatment strategy showed subsidence of clinical signs, restoration of platelet count, blood clotting time, urea nitrogen and creatinine values depicting clinical recovery with 88.15% survival rate in treated buffaloes.

Histopathological changes in the human tissues in various types of poisoning: A cross-sectional autopsy study

BackgroundPoisoning is a critical health issue caused by exposure to harmful substances, leading to a range of biological effects from mild irritation to severe organ damage and death. Acute poisoning is particularly prevalent in developing countries reliant on agriculture, where agricultural poisons such as organophosphates, carbamates, pyrethroids, and aluminum/zinc phosphide are common. This study aims to analyze the histopathological changes in various organs in autopsy of poisoning cases to understand the extent and nature of organ damage. MethodsAutopsies were performed on cases with an established or suspected history of poison ingestion. Tissue samples from the stomach, intestine, liver, spleen, kidneys, brain, and lungs were examined for histopathological changes. ResultsOut of 52 cases analyzed, aluminum phosphide was the predominant poison, accounting for 76.92 % of cases. Histopathological findings in poisoning cases included significant pulmonary edema (55.77 %), intra-alveolar hemorrhage (48.08 %), liver ballooning degeneration (48.08 %), acute tubular necrosis (51.92 %) in kidney, and universal brain and spleen congestion (100 %). Stomach findings showed partial loss of rugosity (80.77 %), congestion (51.92 %), necrosis of the mucosa (30.77 %), congestion (71.15 %), denudation of the epithelium (48.08 %), and mucosal inflammation (48.08 %) as predominant findings. Aluminum phosphide caused severe histopathological changes across all examined organs. ConclusionThe study highlights the critical role of histopathological examination in diagnosing and understanding organ damage in poisoning cases. Forensic pathologists can use these histopathological patterns as reference points to differentiate poisoning from other causes of death, aiding in accurate diagnosis and targeted treatment.

Severe Coagulopathy and Intra-Alveolar Haemorrhage Due to Fat Malabsorption in Celiac Disease.

Celiac disease can cause severe coagulopathy due to fat malabsorption and vitamin K deficiency.High suspicion is required for atypical presentations of celiac disease.A gluten-free diet is essential for managing celiac disease and normalising coagulation profiles.

3-methyladenine ameliorates acute lung injury by inhibiting oxidative damage and apoptosis

BackgroundAcute lung injury (ALI) is a condition characterized by inflammation and oxidative damage. 3-methyladenine (3-MA) has great potential for regulating apoptosis, but its regulatory role in ALI is unknown. MethodsLipopolysaccharide (LPS)-treated mice and tert-butyl hydroperoxide (TBHP)-treated bronchial epithelial cells were used to simulate in vivo and in vitro ALI models, respectively. In vivo, lung injury was assessed by histopathological analysis and lung injury scoring. The total cell count, protein content, and inflammatory factors in bronchoalveolar lavage fluid (BALF) were examined. The level of apoptosis in lung tissue was assessed through TUNEL staining. In the vitro ALI model, cell viability and levels of reactive oxygen species and apoptosis were assessed. Results3-MA pretreatment ameliorated lung injury, including intra-alveolar hemorrhage and inflammatory cell accumulation, both in vitro and in vivo. 3-MA pretreatment also decreased inflammatory factor levels in the BALF. 3-MA pretreatment alleviated oxidative damage, decreased reactive oxygen species levels, and attenuated morphological changes. TUNEL and Annexin V-FITC/PI staining revealed that pretreatment with 3-MA reduced the level of apoptosis. 3-MA pretreatment significantly decreased the expression of caspase-3 and Bax but increased the expression of Bcl-2 in ALI. Mechanistically, 3-MA pretreatment also affected the PKCα/NOX4 and Nrf2 pathways, which decreased the level of apoptosis in ALI. Conclusions3-MA pretreatment inhibited inflammation and oxidative damage in ALI and inhibited apoptosis to mitigate ALI in part by inhibiting the PKCα/NOX4 pathway and activating the Nrf2 pathway. Based on these results, 3-MA might be a viable medication to treat with ALI.

COVID-induced pulmonary renal syndrome with severe intra-alveolar hemorrhage

Since the initial surge of COVID-19, there has been an increased number of connective tissue diseases and vasculitis associated with this diagnosis. These cases include systemic lupus erythematosus, lupus nephritis, antineutrophil cytoplasmic antibody (ANCA) associated vasculitis, polymyalgia, and giant cell arteritis. There are a number of presumed mechanisms behind that including the deregulation of the angiotensin-converting enzyme 2 as well as interferon related genes, leading to increased release of inflammation markers including cytokines as well as interleukin-6, complement activation and B cell proliferation and production of autoantibodies.

Pulmonary embolism versus pulmonary vasculitis in Hughes-Stovin syndrome: Characteristic computed tomography pulmonary angiographic findings and diagnostic and therapeutic implications. HSS International Study Group

Background and aimHughes-Stovin syndrome (HSS) is a rare systemic vasculitis with widespread venous/arterial thrombosis and pulmonary vasculitis. Distinguishing between pulmonary embolism (PE) and in-situ thrombosis in the early stages of HSS is challenging. The aim of the study is to compare clinical, laboratory, and computed tomography pulmonary angiography (CTPA) characteristics in patients diagnosed with PE versus those with HSS. MethodsThis retrospective study included 40 HSS patients with complete CTPA studies available, previously published by the HSS study group, and 50 patients diagnosed with PE from a single center. Demographics, clinical and laboratory findings, vascular thrombotic events, were compared between both groups. The CTPA findings were reviewed, with emphasis on the distribution, adherence to the mural wall, pulmonary infarction, ground glass opacification, and intra-alveolar hemorrhage. Pulmonary artery aneurysms (PAAs) in HSS were assessed and classified. ResultsThe mean age of HSS patients was 35 ± 12.3 years, in PE 58.4 ± 17 (p < 0.0001). Among PE 39(78 %) had co-morbidities, among HSS none. In contrast to PE, in HSS both major venous and arterial thrombotic events are seen.. Various patterns of PAAs were observed in the HSS group, which were entirely absent in PE. Parenchymal hemorrhage was also more frequent in HSS compared to PE (P < 0.001). ConclusionMajor vascular thrombosis with arterial aneurysms formation are characteristic of HSS. PE typically appear loosely-adherent and mobile whereas “in-situ thrombosis” seen in HSS is tightly-adherent to the mural wall. Mural wall enhancement and PAAs are distinctive pulmonary findings in HSS. The latter findings have significant therapeutic ramifications.

Development of rabbit models of ventilator-associated bacterial pneumonia produced by carbapenem-resistant Pseudomonas aeruginosa.

Ventilator-associated bacterial pneumonia (VABP) is among the most intractable of carbapenem-resistant Gram-negative bacterial infections. New antimicrobial agents are critically needed for the treatment of VABP. However, current conventionally used animal model systems are inadequate to meet this challenge. We, therefore, developed rabbit models of VABP caused by carbapenem-resistant Pseudomonas aeruginosa. Persistently neutropenic New Zealand White rabbits were used throughout the study. The early-phase intubated model (0-24 h) received mechanical ventilation, while the late-phase intubated model (72-96 h) was ambulatory. The following outcome parameters were studied: survival, residual tissue bacterial burden (CFU/g), residual BAL bacterial burden (CFU/mL), lung weights, pulmonary lesion score, histology, O2 saturation, radiographic imaging, and histology. Each anesthetized rabbit received a predetermined endotracheal bacterial inoculum, and ventilators were set to FiO2 = 40% and PEEP = 8 mmHg. Within the first 12 h post-inoculation, mean bacterial burdens in lung tissue and BAL fluid, respectively, were established at approximately 107 CFU/g and 106 CFU/mL, persisted through 24 h in the early-phase model and increased in the late-phase model to approximately 108 CFU/g and 107 CFU/mL. Mean max SpO2 was ≥98 mmHg, and mean nadir SpO2 was ≥68 mmHg. Serial thoracic radiographs demonstrated progressive multilobar pneumonic infiltrates. Lung histology revealed progressive focal bronchopneumonia, coagulative necrosis, intra-alveolar hemorrhage, alveolar epithelial cell necrosis, and bacterial microcolonies. The new rabbit model of VABP produced by carbapenem-resistant Pseudomonas aeruginosa recapitulates the pathophysiological, microbiological, diagnostic imaging, and histological patterns of human disease by which to assess critically needed new antimicrobial agents against this lethal infection.

Advanced Diagnostic Tools in Hypothermia-Related Fatalities-A Pathological Perspective.

Although classical gross features are known in hypothermia victims, they lack specific diagnosis features. The aim of our study was to reveal specific brain and lung pathological features in a group of hypothermia-related fatalities. The study group comprised 107 cases from our files associated with hypothermia. Routine hematoxylin-eosin (H&E) staining and postmortem immunohistochemistry were performed. The microscopic cerebral exam revealed diffuse perineuronal and perivascular edema, gliosis, mononuclear cell infiltration, acute brain injuries, focal neuronal ischemia, lacunar infarction, and variable hemorrhages. Variable alveolar edema, pulmonary emphysema, intra-alveolar and/or pleural hemorrhage, and bronchopneumonia, as well as other pre-existing lesions, were identified in lung tissue samples. Glial cells displayed S100β expression, while neurons showed moderate Hsp70 immunopositivity. Alveolar basal membranes exhibited diffuse ICAM-1 positive expression, while ICAM-1 and AQP-1 positivity was observed in the alveolar septum vascular endothelium. Statistical analysis revealed a significant correlation between S100β and Hps70 immunoexpression and cerebral pathological features, between ICAM-1 immunoexpression and alveolar edema and pulmonary emphysema, and between AQP-1 immunoexpression and pulmonary emphysema. Our results add supplementary data to brain and lung pathological findings in hypothermia-related fatalities, with potential therapeutic value in hypothermia patients.

Sea Cucumber and Blueberry Extracts Suppress Inflammation and Reduce Acute Lung Injury through the Regulation of NF-κB/MAPK/JNK Signaling Pathway in Lipopolysaccharide-Treated C57BL/6 Mice.

Acute lung injury (ALI) represents a life-threatening condition with high morbidity and mortality despite modern mechanical ventilators and multiple pharmacological strategies. Therefore, there is a need to develop efficacious interventions with minimal side effects. The anti-inflammatory activities of sea cucumber (Cucumaria frondosa) and wild blueberry (Vaccinium angustifolium) extracts have been reported recently. However, their anti-inflammatory activities and the mechanism of action against ALI are not fully elucidated. Thus, the present study aims to understand the mechanism of the anti-inflammatory activity of sea cucumber and wild blueberry extracts in the context of ALI. Experimental ALI was induced via intranasal lipopolysaccharide (LPS) instillation in C57BL/6 mice and the anti-inflammatory properties were determined by cytokine analysis, histological examination, western blot, and qRT-PCR. The results showed that oral supplementation of sea cucumber extracts repressed nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways, thereby downregulating the expression of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF) in the lung tissue and in the plasma. Wild blueberry extracts also suppressed the expression of IL-4. Furthermore, the combination of sea cucumber and wild blueberry extracts restrained MAPK signaling pathways by prominent attenuation of phosphorylation of NF-κB, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK) while the levels of pro-inflammatory cytokines were significantly suppressed. Moreover, there was a significant and synergistic reduction in varying degrees of ALI lesions such as distorted parenchyma, increased alveoli thickness, lymphocyte and neutrophil infiltrations, fibrin deposition, pulmonary emphysema, pneumonia, intra-alveolar hemorrhage, and edema. The anti-inflammatory effect of the combination of sea cucumber and wild blueberry extracts is associated with suppressing MAPK and NF-κB signaling pathways, thereby significantly reducing cytokine storm in LPS-induced experimental ALI.

Intra-Alveolar Hemorrhage of Unusual Etiology

Cannabis use is steadily increasing worldwide and is an emerging public health problem. This consumption is responsible for harmful respiratory effects, including intra-alveolar hemorrhage. We report the case of a 26-year-old man admitted with exertional dyspnea and profuse hemoptysis. Investigations revealed intra-alveolar hemorrhage. Immunological and tuberculosis tests were negative. When the case history was taken again, it was noted that the patient had been a regular cannabis user for several years, and the blood and urine tests for toxic substances revealed the presence of tetra-hydro-cannabinoids. This case illustrates the seriousness of respiratory complications caused by cannabis, and highlights the need to emphasize the importance of weaning and educating young people.

Plasma Exchanges: Observational Study at the Mohammed V Rabat Military Training Hospital Blood Transfusion Center from January 2016 to December 2019

Since their initial indications as the ultimate treatment for certain serious pathologies, plasma exchanges (PE) have been utilized as frontline therapies up to lifesaving interventions. In this observational study conducted at the Mohammed V Military Training Hospital Blood Transfusion Center from January 2016 to December 2019, we aimed to elucidate the practical modalities and therapeutic indications of plasma exchanges. Our findings revealed that among the patients treated, the majority suffered from neurological pathologies (37%), followed by autoimmune pathologies such as thrombotic thrombocytopenic purpura and thrombotic microangiopathy (25%), and finally haematological and nephrological pathologies, each representing 19%. These results align with existing literature, emphasizing the prevalence of neurological indications for plasma exchanges.&#x0D; Moreover, the study showcased the effectiveness of plasma exchanges in various neurological conditions, with notable sessions for myasthenia, multiple sclerosis, neuromyelitis, polyradiculoneuritis, and meningoencephalitis. For nephrological pathologies, the sessions were primarily conducted for patients with ANCA+ intra-alveolar haemorrhage and Wegener's disease. Additionally, plasma exchanges demonstrated significant clinical improvements in patients with haematological pathologies, such as Waldenstrom's disease and hemolytic anaemia, and autoimmune diseases like thrombotic thrombocytopenic purpura and thrombotic microangiopathy.&#x0D; Ultimately, this study underscores the importance of collaboration between the transfusion centre and clinical and biological services for optimal patient management. The insights gained contribute to the broader understanding of plasma exchange applications in various pathologies, emphasizing its role as a crucial therapeutic intervention.

Pulmonary Haemosiderosis Secondary to Mitral Valve Stenosis-Known Association of Uncommon Entity: A Case Report

Pulmonary haemosiderosis is a rare lung disease characterised by haemosiderin deposition in the lungs due to recurrent intra-alveolar bleeding. It can be idiopathic or secondary due to mitral stenosis. Affected patients will have symptoms of cough, haemoptysis, and shortness of breath. Radiologically, it is characterised by widespread tiny alveolar nodular opacities with or without septal thickening. Therefore, in the case of mitral valve stenosis, this imaging pattern on High-resolution Computed Tomography (HRCT) should prompt suspicion of secondary pulmonary haemosiderosis. Here, the authors present the case of a 27-year-old male patient with mitral stenosis who presented with progressive shortness of breath, mild atypical chest pain for two months, and a cough with occasional haemoptysis in the last 10 days before the hospital visit, along with typical radiological findings of widespread tiny ground glass alveolar nodules on HRCT. The radiological knowledge of this rare entity is very important for confidently making the diagnosis in the proper clinical context, to avoid unnecessary investigations and treatment.

A 16-year-old man with leptospirosis and atypical disseminated intravascular coagulation: a case report

BackgroundLeptospirosis is known for its pulmonary form characterized by intra-alveolar hemorrhage, exhibiting a high mortality rate. Management by venous–venous extracorporeal membrane oxygenation has been reported in a small number of cases.Case presentationWe report herein the case of a 16-year-old Caucasian male who was admitted with rapidly deteriorating respiratory and digestive complaints. He developed severe acute respiratory distress syndrome secondary to disseminated intravascular coagulation and intra-alveolar hemorrhage, requiring initiation of venous–venous extracorporeal membrane oxygenation. Initial infectious and immunological assessments were inconclusive, but repeat serology on the tenth day of admission confirmed a diagnosis of leptospirosis. The patient received multiple transfusions, and upon favorable response to treatment with corticosteroids and antibiotics, he was successfully weaned off venous–venous extracorporeal membrane oxygenation, which was discontinued after 12 days.ConclusionLeptospirosis is a rare cause of severe acute respiratory failure following pulmonary hemorrhage. It is typically diagnosed by serology, with detectable IgM antibodies 5–7 days after the onset of symptoms. We report that early support with respiratory extracorporeal membrane oxygenation favors timely clearance of endobronchial clotting, parenchymal recovery, and prevention of ventilator-induced lung injury. Major hypofibrinogenemia, which did not seem to worsen during extracorporeal membrane oxygenation application, was managed by repeated transfusions. Further studies investigating the pathogenesis of this coagulopathy are required to further optimize the management of this rare and severe complication.

2557. Development of Rabbit Models of Ventilator-Associated Carbapenem-Resistant Acinetobacter baumannii Pneumonia

Abstract Background Carbapenem-resistant (CR) Gram-negative bacteria are emerging worldwide as global public health threats. Mortality rates from these pathogens are especially high in immunocompromised patients. Ventilator-associated bacterial pneumonia (VABP) is among the most intractable of CR Gram-negative bacterial infections. We therefore aimed to develop rabbit animal models of VABP caused by CR strains of Acinetobacter baumannii. Methods Persistently neutropenic NZW rabbits were used throughout the study. A novel endotracheal tracheostomy system was developed for intubation. The early-phase intubated model (0-24h) received mechanical ventilation, while the late-phase intubated model (72-96h) was ambulatory. Ventilators were set to FiO2=40% and PEEP=8mmHg. The following outcome variables were assessed: survival, residual tissue bacterial burden (log CFU/g), residual BAL bacterial burden (log CFU/mL), lung weights, pulmonary lesion score, histology, pulse O2 saturation, radiographic imaging, pro-inflammatory cytokines, quantitative tissue and BAL PCR, and histology. Results Within the first 12h post-inoculation, mean bacterial burdens in lung tissue and BAL fluid, respectively, which were established at approximately 106 CFU/g and 105 CFU/mL, persisted through 24h in the early-phase model and were increased in the late-phase model (72-96h) to approximately 107 CFU/g, and 106 CFU/mL. Mean Max SpO2 was ≥99 mmHg and mean nadir SpO2 was ≥74 mmHg. Serial thoracic radiographs over the course of 12-96h demonstrated progressive multilobar pneumonic infiltrates, while lung histology revealed progressive development of focal bronchopneumonia, intra-alveolar hemorrhage, alveolar epithelial cell necrosis, macrophage activation, monocytic infiltration, alveolar septal disruption, and microcolonies of bacteria. Conclusion The new rabbit model of VABP produced by CR A. baumannii recapitulates the pathophysiological, microbiological, diagnostic imaging, and histological patterns of human disease by which to assess critically needed new antimicrobial agents against this lethal infection. Disclosures All Authors: No reported disclosures

Intrinsic pulmonary sealing, its mechanisms and impact on validity and translational value of lung sealant studies: a pooled analysis of animal studies.

No validated and standardized animal models of pulmonary air leakage (PAL) exist for testing aerostatic efficacy of lung sealants. Lack of negative control groups in published studies and intrinsic sealing mechanisms of healthy animal lungs might contribute to a translational gap, leading to poor clinical results. This study aims to address the impact of intrinsic sealing mechanisms on the validity of PAL models, and investigate the conditions required for an ovine model of PAL for lung sealant testing. An ovine acute aerostasis model was developed, consisting of a bilateral thoracotomy with lesion creation, chest tube insertion and monitoring of air leaks using digital drains (≥80 minutes), under spontaneous respiration. Healthy mixed-breed adult female sheep were used and all in vivo procedures were performed under terminal anesthesia. Superficial parenchymal lesions were tested post-mortem and in vivo, extended lesions including bronchioles (deep bowl-shaped and sequential lung amputation lesions) were tested in vivo. Experiment outcomes include air leakage (AL), minimal leaking pressure (MLP) and histology. Two post-mortem (N=4 superficial parenchymal lesions) and 10 in vivo experiments (N=5 superficial parenchymal and N=16 lesions involving bronchioles) were performed. In contrast to the post-mortem model, superficial parenchymal lesions in vivo showed less air leak [mean flow ± standard deviation (SD): 760±693 vs. 42±33 mL/min, P=0.055]. All superficial parenchymal lesions in vivo sealed intrinsically within a median time of 20 minutes [interquartile range (IQR), 10-75 minutes]. Histology of the intrinsic sealing layer revealed an extended area of alveolar collapse below the incision with intra-alveolar hemorrhage. Compared to superficial parenchymal lesions in vivo, lesions involving bronchioles induced significantly higher air leak post-operatively (normalized mean flow ± SD: 459±221 mL/min, P=0.003). At termination, 5/9 (55.6%) were still leaking (median drain time: 273 minutes, IQR, 207-435 minutes), and intrinsic sealing for the remaining lungs occurred within a median of 115 minutes (IQR, 52-245 minutes). Lung parenchyma of healthy sheep shows a strong intrinsic sealing mechanism, explained pathologically by an extended area of alveolar collapse, which may contribute to a translational gap in lung sealant research. A meaningful ovine model has to consist of deep lesions involving bronchioles of >⌀1.5 mm. Further research is needed to develop a standardized PAL model, to improve clinical effectiveness of lung sealants.

The Polyanionic Drug Suramin Neutralizes Histones and Prevents Endotheliopathy.

Drugs are needed to protect against the neutrophil-derived histones responsible for endothelial injury in acute inflammatory conditions such as trauma and sepsis. Heparin and other polyanions can neutralize histones but challenges with dosing or side effects such as bleeding limit clinical application. In this study, we demonstrate that suramin, a widely available polyanionic drug, completely neutralizes the toxic effects of individual histones, but not citrullinated histones from neutrophil extracellular traps. The sulfate groups on suramin form stable electrostatic interactions with hydrogen bonds in the histone octamer with a dissociation constant of 250 nM. In cultured endothelial cells (Ea.Hy926), histone-induced thrombin generation was significantly decreased by suramin. In isolated murine blood vessels, suramin abolished aberrant endothelial cell calcium signals and rescued impaired endothelial-dependent vasodilation caused by histones. Suramin significantly decreased pulmonary endothelial cell ICAM-1 expression and neutrophil recruitment caused by infusion of sublethal doses of histones invivo. Suramin also prevented histone-induced lung endothelial cell cytotoxicity invitro and lung edema, intra-alveolar hemorrhage, and mortality in mice receiving a lethal dose of histones. Protection of vascular endothelial function from histone-induced damage is a novel mechanism of action for suramin with therapeutic implications for conditions characterized by elevated histone levels.

#5034 ANCA ASSOCIATED VASCULITIS AFTER COVID-19

Abstract Background and Aims ANCA associated vasculitis (AAV) is a group of systemic autoimmune diseases characterized by inflammation of small and medium sized vessels. The three main types of AAV are granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA) and eosinophilic granulomatosis with polyangiitis (EGPA). Similar pathways are involved mechanisms of disease involving COVID-19 and ANCA-associated vasculitis. For instance, neutrophil extracellular traps (NETs) are induced in both entities. Method We describe 3 cases reports of patients with ANCA associated vasculitis after COVID19. Results Case 1: A 46-year-old female patient was hospitalized in intensive care unit for COVID19 pneumonia. She has fever, cough and dyspnea. A few days before, the SARS-CoV-2 polymerase chain reaction(PCR) was positive on nasopharyngeal swab. She received high flu nasal canula. She presented a pneumo-renal syndrome with intra-alveolar hemorrhage and acute kidney injury. Chest scanner shows lesions on bilateral lung parenchyma, and an acute kidney injury (AKI) on admission. Urinalysis revealed an active sediment with dysmorphic erythrocytes and signifcant proteinuria. Renal function gradually deteriorated. So intermittent hemodialysis treatment was initiated. Serological evaluation showed negative antinuclear antibody, and anti-dsDNA, normal serum complements, and an elevated MPO. In kidney biopsy, pauci-immune necrotizing GN with cellular crescents was detected. The patient received pulse dose corticosteroids and subsequently, she was transitioned to oral prednisone. She underwent 2 sessions of plasmapheresis, which were stopped in the absence of confirmation of pulmonary involvement. She received cyclophosphamide during the hospitalization. While hematuria and proteinuria were persistant in the most recent urinalysis, the sCr level decreased to 159 µmol/L. In addition, she developed adrenal insufficiency after stopping corticosteroid therapy, requiring her to be put on Cortef. Case 2: A 63-year-old female patient with past medical history of hypertension, was hospitalized in intensive care unit for dyspnea and hemoptysis. A few months before, the SARS-CoV-2 polymerase chain reaction(PCR) was positive on nasopharyngeal swab. She received high flu nasal canula (HFNC). At this moment, she had acute kidney injury with a sCr level of 165µmol/L that was not explored. Currently she presented a pneumo-renal syndrome with a rapidly progressive glomerulonephritis and intra-alveolar hemorrhage. Renal function gradually deteriorated and peak sCr level of 308µmol/L. Chest scanner shows ground glass lesions of bilateral lung parenchyma, and hemoglobin at 4.9 g/dL. Urinalysis revealed an active sediment with dysmorphic erythrocytes and signifcant proteinuria. So intermittent hemodialysis treatment was initiated. The patient received pulse dose corticosteroids and subsequently, she was transitioned to oral prednisone. She received cyclophosphamide during the hospitalization. Serological evaluation showed negative antinuclear antibody, and anti-dsDNA, normal serum complements, and an elevated MPO. She underwent 6 sessions of plasmapheresis, for intra-alveolar hemorrhage. There was an improvement in respiratory and renal function Case 3: 57 years old, with a history of functional colopathy, covid infection 1 month before her hospitalization in nephrology department for kidney injury. Currently she presented a pneumo-renal syndrome with a rapidly progressive glomerulonephritis and intra-alveolar hemorrhage. Urinalysis revealed an active sediment with dysmorphic erythrocytes and signifcant proteinuria. Serological evaluation showed negative antinuclear antibody, and anti-dsDNA, normal serum complements, an elevated MPO and positive anti GBM. She was treated with plasmapheresis and cyclophosphamide. Conclusion SARS-CoV-2 infection can be a 'trigger factor' for vasculitis. ANCA-associated vasculitis should be kept in mind in patients who develop acute kidney injury after COVID-19.

Radiofrequency ablation of lung metastases of colorectal cancer: could early radiomics analysis of the ablation zone help detect local tumor progression?

To determine whether radiomics data can predict local tumor progression (LTP) following radiofrequency ablation (RFA) of colorectal cancer (CRC) lung metastases on the first revaluation chest CT. This case-control single-center retrospective study included 95 distinct lung metastases treated by RFA (in 39 patients, median age: 63.1 years) with a contrast-enhanced CT-scan performed 3 months after RFA. Forty-eight radiomics features (RFs) were extracted from the 3D-segmentation of the ablation zone. Several supervised machine-learning algorithms were trained in 10-fold cross-validation on reproducible RFs to predict LTP, with/without denoising CT-scans. An unsupervised classification based on reproducible RFs was built with k-means algorithm. There were 20/95 (26.7%) relapses within a median delay of 10 months. The best model was a stepwise logistic regression on raw CT-scans. Its cross-validated performances were: AUROC = 0.72 (0.58-0.86), area under the Precision-Recall curve (AUPRC) = 0.44. Cross-validated balanced-accuracy, sensitivity and specificity were 0.59, 0.25 and 0.93, respectively, using p = 0.5 to dichotomize the model predicted probabilities (vs 0.71, 0.70 and 0.72, respectively using p = 0.188 according to Youden index). The unsupervised approach identified two clusters, which were not associated with LTP (p = 0.8211) but with the occurrence of per-RFA intra-alveolar hemorrhage, post-RFA cavitations and fistulizations (p = 0.0150). Predictive models using RFs from the post-RFA ablation zone on the first revaluation CT-scan of CRC lung metastases seemed moderately informative regarding the occurrence of LTP. Radiomics approach on interventional radiology data is feasible. However, patterns of heterogeneity detected with RFs on early re-evaluation CT-scans seem biased by different healing processes following benign RFA complications.

Mikrorüptüre Kist Hidatik Kaynaklı Pulmoner Parazitik Embolizasyon: Bir Otopsi Olgusu

Echinococcosis generally remains asymptomatic for many years, but it can also be fatal if complications like cyst rupture or superinfection occur. It is highly uncommon for a macroscopically non-ruptured cyst to cause death, and its exact mechanism is unknown. In the literature, there are several cases with identical characteristics diagnosed by autopsy. This autopsy case has illustrated the death due to a micro ruptured hydatid cyst. The deceased's lung underwent microscopic inspection, and it revealed broad intraalveolar hemorrhage, edema, severe hyperemia, neutrophil stasis in the interstitial capillary lumens, and a large number of parasites in the capillary lumen. Anaphylaxis against cyst contents that leaked into the bloodstream from liver cysts and non-thrombotic pulmonary embolization were shown to be the causes of mortality. In countries where echinococcosis is endemic, echinococcosis should be considered in all cases of anaphylaxis and sudden death.

Neuropathies périphériques au cours des maladies de système : partie II (vascularites)

Primary systemic vasculitides, mainly of the small and medium-sized vessels, are frequently associated with peripheral neuropathies. When the disease is already known, the appearance of a neuropathy should suggest a specific injury, especially when associated with other systemic manifestations. Conversely, when neuropathy is inaugural, close collaboration between neurologists and internists is necessary to reach a diagnosis. A standardized electro-clinical investigation specifying the topography, the evolution and the mechanism of the nerve damage enables the positive diagnosis of the neuropathy. Several elements orient the etiological diagnosis and allow to eliminate the main differential diagnosis: non systemic vasculitic neuropathy. The existence of associated systemic manifestations (glomerular or vascular nephropathy, interstitial lung disease, intra-alveolar hemorrhage, ENT involvement…), biological markers (ANCA, cryoglobulinemia, rheumatoid factor), and invasive examinations allowing histological analysis (neuromuscular biopsy) are all useful tools for.