Scrub typhus is a common cause of an acute, unexplained febrile illness. Without proper treatment, it can lead to life-threatening complications and even death. We present the case of a 16-year-old girl who presented with complaints of fever with reddish spots all over her body for 10 days and breathing difficulty for three days. She had an episode of gum bleeding just prior to admission and two episodes of hemoptysis after admission. She had severe thrombocytopenia, a low serum fibrinogen level, raised D-dimer levels, a raised activated partial thromboplastin time as well as a raised prothrombin time, and an international normalized ratio. Her chest radiograph showed diffuse bilateral interstitial infiltrates. A diagnosis of disseminated intravascular coagulation and diffuse alveolar hemorrhage secondary to possible hematological malignancy or vector-borne infectious disease was made. She was treated with intravenous doxycycline and broad-spectrum antibiotics, along with other supportive measures. Bone marrow aspiration and biopsy showed normal trilineage differentiation, normal erythropoiesis, myelopoiesis, and megakaryopoiesis. Finally, a positive immunoglobulin M (IgM) antibody for scrub typhus clinched the diagnosis. Her condition improved over the next week, and she was discharged with the advice to continue oral doxycycline for a week. This case highlights one of the rare complications of scrub typhus, disseminated intravascular coagulation, and the importance of timely initiation of treatment in such patients.

Diffuse alveolar hemorrhage (DAH) is described as the collection of blood in alveolar spaces caused by damaged pulmonary vasculature. It often presents as a life-threatening medical emergency that requires urgent medical intervention along with timely diagnosis and management of the underlying cause. We hereby report a 19-year-old female who presented with clinical and radiological characteristics consistent with DAH. Laboratory workup studies revealed a diagnosis of systemic lupus erythematosus (SLE) as well as Mycobacterium tuberculosis (MTB) infection. This report describes an extremely unusual case of undiagnosed SLE and coexistent tuberculosis presenting as DAH. This leads to an interesting possibility of risks in patients with immune-mediated vasculitis towards developing severe pulmonary disease in the setting of pulmonary mycobacterial infection.

In recent decades, the potential of PRF has been extensively studied. The number of studies about PRF has increased three times since the year 2012, but the full spectrum of its fundamental properties, such as antimicrobial and anti-inflammatory activity, is not clearly described. In oral and maxillofacial surgery, PRF is described in alveolar ridge preservation, orthognathic surgery, cleft lip and palate surgery, maxillary sinus augmentation, and dental implant placement as demonstrating favorable results and its clinical advantages. The structural complexity, inhomogeneous nature, and clotting ability of PRF make its antimicrobial effect evaluation complicated. Nevertheless, most of the used antimicrobial testing methods are based on antibacterial agent diffusion ability in culture media. Because the oral and maxillofacial region is the most frequent area of PRF application, its antimicrobial activity evaluation also prevails in the oral microbiome. PRF's biological potential is highly dependent on the specific preparation protocol and methodology used; it should be carefully prepared and kept under proper conditions to keep cellular content alive. PRF's influence on living cells demonstrates a stimulating effect on bone regeneration, and an angiogenetic effect, and it provides anti-inflammatory activity. According to analyzed studies, PRF demonstrated success in oral and maxillofacial surgery in various methods of application. Antibacterial and anti-inflammatory properties were proven by antibacterial activity against different bacterial species, sustained growth factor, sustained release, and cell activity on the material application. Accurately and correctly prepared PRF can ensure antibacterial and anti-inflammatory properties, and it can be a beneficial clinical tool in oral and maxillofacial surgery.

Pulmonary-renal syndrome (PRS) is defined as a combination of diffuse alveolar haemorrhage and glomerulonephritis. An 18-year-old woman visited our hospital with a 2-day history of fever, dyspnoea, and leg edema. Laboratory investigations revealed an elevated inflammatory reaction, increased serum creatinine levels, and normocytic anaemia. Additionally, the anti-streptolysin-O titre was positive, and complement component-3 levels were decreased. Urinalysis revealed proteinuria and hematuria. Bronchoalveolar lavage aliquots were progressively more hemorrhagic. These findings supported a diagnosis of PRS secondary to streptococcal infection. The patient was treated with high-dose methylprednisolone and antibiotics. After 4 days of treatment, her respiratory symptoms and serum creatinine levels improved. Steroid tapering was performed over 15 days. The findings in this case indicate that streptococcal infection is a potential cause of PRS, and that short-term steroid therapy is an effective treatment.

Objective Treatment-refractory antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a life-threatening condition without evidence-based treatment options. One emerging treatment option for several antibody-mediated autoimmune diseases is the anti-CD38 antibody daratumumab, which depletes autoantibody-secreting plasma cells.Methods We treated two patients with severe life-threatening AAV with renal and pulmonary manifestation despite induction therapy with rituximab and cyclophosphamide with four to eight doses of 1800 mg daratumumab. We followed clinical and immunological responses.Results The first patient with myeloperoxidase-ANCA-positive microscopic polyangiitis had resolution of pneumonitis and pleuritis and stabilisation of kidney function after daratumumab. The second patient with proteinase 3-ANCA-positive granulomatosis with polyangiitis, diffuse alveolar haemorrhage necessitating extracorporeal membrane oxygenation (ECMO) and acute kidney failure, requiring kidney replacement therapy, was weaned off ECMO, mechanical ventilation and dialysis and discharged home after daratumumab. Clinical improvement was paralleled by a strong reduction in serum ANCA levels as well as total IgG, indicating depletion of plasma cells. Apart from the depletion of CD38+ natural killer cells, blood leucocyte levels were not notably influenced by daratumumab. Only mild adverse events, such as hypogammaglobulinaemia and an upper respiratory tract infection occurred.Conclusion Daratumumab was safe and effective in inducing remission in two patients with severe treatment-refractory AAV, warranting prospective clinical trials to establish safety and efficacy.

Pulmonary renal syndrome (PRS) is a rare and life-threatening syndrome. Interstitial lung disease (ILD) has been recently considered another phenotype of lung dysfunction in patients with PRS, but there are very limited data. The characteristics of fifty PRS patients were retrospectively reviewed after a 3-year follow-up, and the differences between PRS patients whose lung dysfunction presented as diffuse alveolar hemorrhage (DAH group) and those with interstitial lung disease (ILD group) were also analyzed. The median age at diagnosis of PRS patients was 50.78 ± 17.88 years, and the main symptoms at disease onset were proteinuria (94.00%), hemoptysis (68.00%), dyspnea (32.00%) and fever (12.00%). DAH patients were younger and had significantly lower hemoglobin levels, a higher incidence of hemoptysis, and higher serum creatinine levels at onset than ILD patients. Univariate analyses of PRS patients showed that respiratory failure and the initiation of mechanical ventilation predicted patient death and that the initiation of hemodialysis and higher serum creatinine levels at onset predicted ESRD. Multivariate analyses showed that respiratory failure and anti-GBM antibody positivity could independently predict patient death. Survival analyses showed that 1- and 3-year patient survival rates and ESRD-free survival rate were not significantly different between the two groups. ILD was another important phenotype of lung dysfunction in patients with PRS. Poor outcomes were observed in PRS patients with ILD and in PRS patients with DAH.

We describe acute mitral valve regurgitation in a young, previously healthy male patient presenting with diffuse alveolar hemorrhage. The patient initially presented with acute respiratory failure with refractory arterial hypoxemia despite mechanical ventilation. Bronchoscopy showed diffuse alveolar hemorrhage. The patient quickly developed cardiogenic shock, which required vasopressor infusion. Echocardiography showed severe mitral regurgitation and myxomatous mitral valve with anterior leaflet prolapse along with chordal rupture involving the anterior leaflet, which was flail. An Impella device was emergently placed, and the patient underwent mitral valve replacement with subsequent quick resolution of all symptoms.

COVID-19 (Coronavirus disease 2019) in children is usually mild. However, multiple organ disorders associated with SARS-CoV-2 (severe acute respiratory syndrome-related coronavirus 2) have been detected with poor respiratory symptoms. Cardiac changes are noted in 17% to 75% of cases, which are associated with diagnostic difficulties in high-risk groups for the development of complications that are associated with myocardial damage by the SARS-CoV-2 virus. The objective of this review is to identify the most significant symptoms of cardiac involvement affected by COVID-19, which require in-depth examination. The authors analyzed publications from December 2019 to the October 2022, which were published in accessible local and international databases. According to the analysis data, the main sign of myocardial involvement was increasing as cardiomarkers in the patient's blood, in particular troponin I or troponin T. Many authors noted that the increased level of CRP (C-reactive protein) and NT-proBNP, which are accompanied by changes in the ECG (electrocardiogram) and EchoCG (echocardiography), as a rule, were nonspecific. However, the identified cardiac functional dysfunctions affected by SARS-CoV-2, required an cardiac MRI. The lack of timely diagnosis of myocardial involvements, especially in children at high risk for the development of complications associated with SARS-CoV-2 myocardial injury, can lead to death. The direct damage of the structural elements of myocardial blood vessels in patients with severe hypoxic changes resulted from respiratory failure caused by SARS-CoV-2 lung damage, with the development of severe acute diffuse alveolar damage and cell-mediated immune response and myocardial involvement affected by SARS-CoV-2 damage. In this article, the authors introduce a clinical case of a child who dead from inflammatory myocardities with COVID-19 in a background of congenital heart disease and T-cell immunodeficiency.

A 15-year-old female patient was initially transferred due to symptomatic anemia following months of menorrhagia, fatigue, dyspnea, and weight loss. Early during her hospital course, pulmonary complications occurred with the development of respiratory failure secondary to bilateral pleural effusions. She was managed with bi-level pressure support ventilation alternating with a high-flow nasal cannula. An extensive workup resulted in a diagnosis of systemic lupus erythematosus: C3 level was 9 mg/dl (81-157 mg/dl) and her C4 level was 2 mg/dl (12-39 mg/dl); ANA titer was 1:5120 in a homogenous pattern. Scl-70 was qualitatively positive, quantitative anti-dsDNA level was 1044 IU/ml (<150 IU/ml), hemoglobin at presentation was 6.3 g/dl (11.8-15.7 g/dl), and her albumin level was 2.8 g/dl (3.5-5.0 g/dl). The patient was started on prednisone 60 mg daily and then transitioned to cyclophosphamide. Her symptoms improved initially; however, several days into admission she developed acute respiratory decompensation with blood-tinged sputum. Her hemoglobin levels, which had stabilized, began decreasing from 9.5 to 7.4 g/dl. Chest radiography showed new bilateral hazy infiltrates, and computerized tomography of the chest showed bilateral pleural effusions and parenchymal disease. A bronchoscopy confirmed a diagnosis of diffuse alveolar hemorrhage. The patient was treated with plasma exchange therapy and her corticosteroids were restarted. She completed a course of steroids and at initial pulmonology follow-up and showed stable pulmonary status with an improvement of her symptoms.

129Xe MRI red blood cell to alveolar tissue plasma ratio (RBC:TP) abnormalities have been observed in ever-hospitalised and never-hospitalised people with postacute COVID-19 syndrome (PACS). But, it is not known if such abnormalities resolve when symptoms and quality-of-life scores improve. We evaluated 21 participants with PACS, 7±4 months (baseline) and 14±4 months (follow-up) postinfection. Significantly improved diffusing capacity of the lung for carbon monoxide (DLCO, Δ=14%pred ;95%CI 7 to 21, p<0.001), postexertional dyspnoea (Δ=-0.7; 95%CI=-0.2 to -1.2, p=0.019), St George's Respiratory Questionnaire-score (SGRQ Δ=-6; 95% CI=-1 to -11, p=0.044) but not RBC:TP (Δ=0.03; 95% CI=0.01 to 0.05, p=0.051) were observed at 14 months. DLCO correlated with RBC:TP (r=0.60, 95% CI=0.22 to 0.82, p=0.004) at 7 months. While DLCO and SGRQ measurements improved, these values did not normalise 14 months post-infection. ClinicalTrials.gov NCT04584671.

Immunoglobulin A (IgA) nephropathy is the most common cause of primary glomerulonephritis worldwide. IgA vasculitis (formerly known as Henoch-Schonlein purpura) typically presents with IgA nephropathy on renal biopsy in addition to extrarenal symptoms like purpura, abdominal pain, and arthritis. Diffuse alveolar hemorrhage (DAH) is the most common pulmonary complication, but this is rarely seen. In this case report, we describe a 35-year-old male with chronic untreated hepatitis B infection who presented with pulmonary-renal syndrome. He was found to have clinical findings of DAH and concomitant IgA nephropathy on renal biopsy, without having any other typical manifestations of IgA vasculitis. This shows that IgA nephropathy should be considered in the differential diagnosis of DAH and emphasizes the importance of a renal biopsy in patients presenting with pulmonary-renal syndrome.

Haemophagocytic syndrome, diffuse alveolar haemorrhage, catastrophic antiphospholipid syndrome and various types of thrombotic microangiopathies are rare conditions with significant morbidity and mortality. A common feature is late diagnosis, which can affect the success of treatment. The aim of this review article is to summarize the basic diagnostic and therapeutic steps of the present subpopulation of critically ill patients.

Diffuse alveolar hemorrhage is known to be a devastating clinical condition with myriad etiologies. The immediate post-transplant period is plagued by immunosuppression, surgical complications, and nosocomial sources of infection. Diffuse alveolar hemorrhage in this setting is usually attributed to infection. In this case report, an unusual cause of diffuse alveolar hemorrhage due to anti-thymocyte globulin used as an induction agent is described, and an approach to DAH in the immediate post-transplant setting is discussed.

Amiodarone hydrochloride is an antiarrhythmic drug, with proven efficacy in prevention and treatment of numerous arrhythmias, atrial fibrillation especially, or ventricular arrhythmias, with a long half-life (55-60 days). The increased risk of developing amiodarone-induced pulmonary fibrosis is directly related to the dose and the duration of the intake. Amiodarone-induced pulmonary toxicity is conditioned by dose, patient's age, and pre-existent pulmonary pathologies. The pattern for drug-induced lung injury may vary in many forms, but the amiodarone can cause polymorphous injuries such as diffuse alveolar damage, chronical interstitial pneumonia, organizing pneumonia, pulmonary hemorrhage, lung nodules or pleural disease. The pathological mechanism of pulmonary injury induced by amiodarone consists of the accumulation of phospholipid complexes in histocytes and type II pneumocytes. Differential diagnosis of pulmonary fibrosis induced by amiodarone is made mainly with idiopathic pulmonary fibrosis, left ventricular failure or infectious disease. Before starting treatment with amiodarone, patients should be informed of potential adverse effects and any new respiratory symptoms should promptly be reported to their family physician or attending physician. The assessment carried out at the initiation of amiodarone treatment should include at least chest X-ray and respiratory function tests and extrapulmonary evaluation.

This report describes a highly unusual and refractory case of PR3-positive ANCA-associated vasculitis, which was associated with marked eosinophilia and only achieved remission after interleukin-5 blockade was added to maximal induction therapy. The patient was a healthy 18-year-old woman who presented with scleritis, otitis, constitutional symptoms, skin and mucosal lesions, and diffuse alveolar hemorrhage, found to have refractory eosinophilia of unclear etiology. The case did not meet classification criteria for a diagnosis of granulomatosis with polyangiitis or eosinophilic granulomatosis with polyangiitis. Despite induction therapy with glucocorticoids, cyclophosphamide, and rituximab, she did not achieve remission or normalization of eosinophilia until the addition of mepolizumab, which corresponded with suppression of peripheral blood eosinophils and clinical remission. This case highlights the limitations of classification criteria and success of interleukin-5 in a multimodal treatment of severe vasculitis with eosinophilia.

Diffuse alveolar hemorrhage (DAH) is an uncommon but life-threatening condition. Although DAH must be distinguished from other lung diseases, no specific computed tomography (CT) signs of DAH have been reported. This study aimed to evaluate the diagnostic value of "hyperdense consolidation" CT sign. We retrospectively evaluated non-contrast CT findings of 25 DAH patients and age- (≤ 2 years) and sex-matched controls with symptoms of dyspnea and hypoxemia. Two radiologists compared the two groups for the presence of hyperdense consolidation signs in lung parenchyma, defined as consolidation that visually contains areas with higher density than the aorta in the specific narrow window setting (window level = 35 Hounsfield units [HU], width = 80 HU) with a mediastinal filter. The sensitivity, specificity, positive- and negative-predictive values of the hyperdense consolidation sign for detection of DAH were 32.0%, 100%, 100%, and 59.5% with perfect interobserver agreement (к = 1.00). The hyperdense consolidation sign was found to be a highly specific sign for DAH.

The coronavirus disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), evolved into a global pandemic. As ACE2 on the surface of alveolar cells of the lung epithelium is one of the potential target receptors for SARS-CoV-2, the respiratory symptoms are the most common presentation of COVID-19. The aim of our study was to investigate the morphological findings in lung tissue after being infected by SARS-CoV-2 and compare histopathologic changes in patients with COVID-19 infection history who died to those who survived. We analyzed lung tissue samples from 9 patients who died from COVID-19 and from 35 patients with COVID-19 infection history who survived and had undergone lung surgery for different reasons. Most of histopathological changes in autopsy and survivors' cases overlapped; however, they occurred with different frequency. The predominant histologic finding both in the case of the deceased and the survivors was patchy distribution of foamy macrophages in the alveolar spaces. In comparison with autopsy cases viral cytopathic-like changes in hyperplastic pneumocytes were rarely observed in the survivors' lung tissue. Pulmonary edema, fibrin deposition within alveoli, bronchopneumonia, small vessel thrombosis and type II pneumocyte hyperplasia were also more often observed within autopsy cases. Life-threatening complications such as hyaline membrane formations and diffuse alveolar damage were present only within the deceased, whereas changes requiring enough time to progress to the fibrotic phase, such as organizing pneumonia, bronchiolization of the alveoli, and interstitial fibrosis were observed in the lung parenchyma only in survivors. Additionally, 14 cases of pulmonary pneumo-hematocele in patients with COVID-19 infection history who survived were observed. It is a newly observed entity in the form of a cystic lesion formed by large accumulation of blood and fibrin between the collapsed and rejected lung parenchyma and/or present with air-fluid levels. The thin wall of pneumo-hematocele is formed by the inter lobar interstitial fibroconnective tissue and has no epithelial lining or bronchial wall elements. As the COVID-19 pandemic continues, new complications following SARS-CoV-2 infection are identified. Newly observed entity in patients with COVID-19 infection history who survived is pulmonary pneumo-hematocele. The appearance of these lesion has become increasingly frequent.

Human T-cell leukemia virus type 1 (HTLV-I) associated bronchioloalveolar disorder (HABA) is a chronic and progressive bronchiolar/alveolar disorder related to HTLV-1 infection. Clinical knowledge and guidance are lacking for the diagnosis and management of this condition.

Systemic lupus erythematosus (SLE) is a complex autoimmune disease with multiorgan manifestations, including pleuropulmonary involvement (20-90%). The precise mechanism of pleuropulmonary involvement in SLE is not well-understood; however, systemic type 1 interferons, circulating immune complexes, and neutrophils seem to play essential roles. There are eight types of pleuropulmonary involvement: lupus pleuritis, pleural effusion, acute lupus pneumonitis, shrinking lung syndrome, interstitial lung disease, diffuse alveolar hemorrhage (DAH), pulmonary arterial hypertension, and pulmonary embolism. DAH has a high mortality rate (68-75%). The diagnostic tools for pleuropulmonary involvement in SLE include chest X-ray (CXR), computed tomography (CT), pulmonary function tests (PFT), bronchoalveolar lavage, biopsy, technetium-99m hexamethylprophylene amine oxime perfusion scan, and (18)F-fluorodeoxyglucose positron emission tomography. An approach for detecting pleuropulmonary involvement in SLE includes high-resolution CT, CXR, and PFT. Little is known about specific therapies for pleuropulmonary involvement in SLE. However, immunosuppressive therapies such as corticosteroids and cyclophosphamide are generally used. Rituximab has also been successfully used in three of the eight pleuropulmonary involvement forms: lupus pleuritis, acute lupus pneumonitis, and shrinking lung syndrome. Pleuropulmonary manifestations are part of the clinical criteria for SLE diagnosis. However, no review article has focused on the involvement of pleuropulmonary disease in SLE. Therefore, this article summarizes the literature on the epidemiology, pathogenesis, diagnosis, and management of pleuropulmonary involvement in SLE.

We present the autopsy procedure and findings of severe coronavirus disease 2019 (COVID-19) pneumonia in an 85-year-old man. The patient required intubation immediately after admission for severe COVID-19 pneumonia. He had severe hypoxia that did not improve despite treatment with remdesivir, corticosteroids, and appropriate mechanical ventilation. On day 13, the patient developed sudden hypercapnia. His renal dysfunction subsequently worsened and became associated with hyperkalemia, and he passed away on day 15. An autopsy was performed to clarify the cause of the hypercapnic hypoxia. None of the medical personnel involved in the autopsy developed symptoms of COVID-19. Histologic examination showed various stages of diffuse alveolar damage throughout the lungs, with intra-alveolar hemorrhage in the upper zones. Microscopic examination of the kidneys revealed acute tubular necrosis. There was no significant systemic thrombosis. The autopsy findings were consistent with those typical of COVID-19.