Clarification on Pleural Effusions in COVID-19.

The purpose of this study was to investigate the relationship between pleural temperature and pneumothorax or pleural effusion after radiofrequency (RF) ablation of lung tumors. The pleural temperature was measured immediately outside the lung surface nearest to the tumor with a fiber-type thermocouple during 25 ablation procedures for 34 tumors in 22 patients. The procedures were divided into two groups depending on the highest pleural temperature: P-group I and P-group II, with highest pleural temperatures of <40 degrees C and >/=40 degrees C, respectively. The incidence of pneumothorax or pleural effusion was compared between the groups. Multiple variables were compared between the groups to determine the factors that affect the pleural temperature. The overall incidence of pneumothorax and pleural effusion was 56% (14/25) and 20% (5/25), respectively. Temperature data in five ablation procedures were excluded from the analyses because these were affected by the pneumothorax. P-group I and P-group II comprised 10 procedures and 10 procedures, respectively. The incidence of pleural effusion was significantly higher in P-group II (4/10) than in P-group I (0/10) (p = 0.043). However, the incidence of pneumothorax did not differ significantly (p = 0.50) between P-group I (4/10) and P-group II (5/10). Factors significantly affecting the pleural temperature were distance between the electrode and the pleura (p < 0.001) and length of the lung parenchyma between the electrode and the pleura (p < 0.001). We conclude that higher pleural temperature appeared to be associated with the occurrence of pleural effusion and not with that of pneumothorax.

Comparison of temporal evolution of computed tomography imaging features in COVID-19 and influenza infections in a multicenter cohort study

Background: Although Epicutaneo cava catheters (ECCs) are being routinely used for intravenous access for long-term parenteral nutrition and prolonged medication administration in neonates, ECC use can be associated with rare but acute life-threatening events such as pleural effusion (PE). It is important to identify and maintain the ECC tip in a central location for preventing complications. Recently, intracavitary electrocardiogram (IC-ECG) has been developed for the real-time monitoring and verification of ECC tip position.Objective: To investigate the causes and preventive measures of ECC-related PE in neonates.Methods: This prospective cohort study was conducted between January 2013 and December 2017. We observed and analyzed the clinical characteristics and causes of ECC-related PE. From January to December 2017, all ECCs were guided by IC-ECG. The incidence of ECC-related PE and first-attempt success rates were analyzed before and after the introduction of IC-ECG. Additionally, the sensitivity and specificity of IC-ECG were evaluated.Results: ECC-related PE was identified in 14 infants. Catheters were malpositioned in three cases; in the other 11 cases, catheters were located centrally on insertion but had migrated to non-central locations at the time of PE. After the introduction of IC-ECG, the incidence of PE was zero (P < 0.05). The incidence of ECC-related PE was lower when veins of the lower extremities were selected as the insertion site (P < 0.05). The first-attempt success rate was significantly higher in the group with IC-ECG-guided ECC placement than in the group without (P < 0.05). The sensitivity and specificity of IC-ECG were 97.9 and 84.6%, respectively.Conclusion: ECC-related PE can be associated with either primary malposition or migration of the catheter tip. IC-ECG can help detect malposition and migration of catheter tips and improve the first-attempt success rate. Choosing a lower extremity insertion site may help decrease the rate of ECC-related PE. In neonates, IC-ECG is a reliable positioning method for ECCs with superior sensitivity and specificity.

HomeHypertensionVol. 76, No. 5Plasma Angiotensin Peptide Profiling and ACE (Angiotensin-Converting Enzyme)-2 Activity in COVID-19 Patients Treated With Pharmacological Blockers of the Renin-Angiotensin System Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBPlasma Angiotensin Peptide Profiling and ACE (Angiotensin-Converting Enzyme)-2 Activity in COVID-19 Patients Treated With Pharmacological Blockers of the Renin-Angiotensin System Ulrich Kintscher, Anna Slagman, Oliver Domenig, Robert Röhle, Frank Konietschke, Marko Poglitsch and Martin Möckel Ulrich KintscherUlrich Kintscher Correspondence to Ulrich Kintscher, Charité–Universitätsmedizin Berlin, Institute of Pharmacology, Center for Cardiovascular Research, Hessische Strasse 3-4, 10115 Berlin, Germany. Email E-mail Address: [email protected] https://orcid.org/0000-0001-7386-0990 From the Charité–Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Germany (U.K., A.S., M.M., R.R., F.K.) Institute of Pharmacology, Center for Cardiovascular Research, Germany (U.K.) DZHK (German Centre for Cardiovascular Research), Partner Site Berlin (U.K.) , Anna SlagmanAnna Slagman From the Charité–Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Germany (U.K., A.S., M.M., R.R., F.K.) Department of Emergency and Acute Medicine, Campus Mitte and Campus Virchow Clinic (A.S., M.M.) , Oliver DomenigOliver Domenig Attoquant Diagnostics, Vienna, Austria (O.D., M.P.). , Robert RöhleRobert Röhle https://orcid.org/0000-0002-8130-6524 From the Charité–Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Germany (U.K., A.S., M.M., R.R., F.K.) Institute of Biometry and Clinical Epidemiology, Coordinating Center for Clinical Studies (R.R.) Berlin Institute of Health, Germany (R.R., F.K.) , Frank KonietschkeFrank Konietschke From the Charité–Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Germany (U.K., A.S., M.M., R.R., F.K.) Institute of Biometry and Clinical Epidemiology (F.K.) Berlin Institute of Health, Germany (R.R., F.K.) , Marko PoglitschMarko Poglitsch Attoquant Diagnostics, Vienna, Austria (O.D., M.P.). and Martin MöckelMartin Möckel https://orcid.org/0000-0002-7691-3709 From the Charité–Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Germany (U.K., A.S., M.M., R.R., F.K.) Department of Emergency and Acute Medicine, Campus Mitte and Campus Virchow Clinic (A.S., M.M.) Originally published27 Aug 2020https://doi.org/10.1161/HYPERTENSIONAHA.120.15841Hypertension. 2020;76:e34–e36Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: August 27, 2020: Ahead of Print Pharmacological blockade of the renin-angiotensin system (RAS) with ACE (angiotensin-converting enzyme) inhibitors or angiotensin type 1 receptor blockers (ARB) reduces morbidity and mortality in various cardiovascular diseases. One of the key RAS-modulating enzymes, ACE2, has recently gained increasing attention because it converts not only angiotensin (Ang) II to the alternative RAS metabolite Ang-(1–7) but also functions as the cellular entry receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2.1 At the beginning of the SARS-CoV-2 pandemic, some investigators suggested that because ACE inhibitor or ARB may lead to upregulation of ACE2 expression/activity, use of these agents in coronavirus disease 2019 (COVID-19) patients might be associated with worsened outcomes.1 Meanwhile, several observational studies have shown that neither the risk of COVID-19 nor its severity is negatively affected by ACE inhibitor or ARB.2,3 However, it remains unclear how RAS activity, particularly ACE2, is regulated in COVID-19 and how this is altered by ACE inhibitor/ARB therapy. In this study, we analyzed distinct RAS components in plasma from patients with COVID-19 ±ACE inhibitor/ARB therapy using liquid chromatography-mass spectrometry/mass spectrometry.The study was approved by the Charité-Universitäts-medizin, Berlin, Germany, Institutional Ethics Committee (EA2/204/19, Amendment 1) and registered in the German Registry for Clinical Studies (DRKS00019207). Surplus plasma samples were collected at the time of admission to the emergency room from 6 different patient groups (total, n=58 [women, 21]): SARS-CoV-2 negative control group (control, n=9 [4]), SARS-CoV-2 negative with ACE inhibitor (control-ACE inhibitor, n=10 [2]), SARS-CoV-2 negative with ARBs (control-ARB, n=8 [5]), COVID-19 without ACE inhibitor/ARB (COVID, n=12 [5]), COVID-19 with ACE inhibitor (COVID-ACE inhibitor, n=10 [2]), and COVID-19 with ARBs (COVID-ARB, n=9 [3]). Equilibrium levels of Ang-peptides (Ang I, Ang II, Ang-[1–7], and Ang-[1–5]) were measured using liquid chromatography-mass spectrometry/mass spectrometry technology (Attoquant Diagnostics).4 Ang-based markers for ACE (Ang II/Ang I) and plasma renin activity (Ang I+Ang II) were calculated from Ang-peptide levels. ACE2 activity was assayed by a classical kinetic approach applying its natural substrate (ex vivo spiked Ang II) and measuring the turnover to Ang-(1–7)±ACE2 inhibitor MLN-4760. The inhibitor-sensitive ACE2-specific turnover was converted to an ACE2 concentration using a calibration curve of recombinant human ACE2. Ang-peptide concentrations/ratios, ACE2 activity, and age between groups were compared using the Kruskal-Wallis test. In case of a significant result, the Dunn-Test for pairwise comparisons using Bonferroni correction was applied. A P of <0.05 was considered statistically significant, although results have to be considered exploratory.Patient CharacteristicsAge (years, mean±SD): control, 44.8±19.7; control-ACE inhibitor, 63.6±17.8; control-ARB, 73.1±11.4 (P=0.02 versus control); COVID, 50±15.1; COVID-ACE inhibitor, 61.4±20.9; COVID-ARB, 74.2±10.1 (P=0.02 versus COVID); COVID severity (n/group), as defined previously,3 severe (intensive care unit admission, mechanical ventilation, and death): COVID (2), COVID-ACE inhibitor (1), COVID-ARB (1); acute renal failure ([n/group] control-ARB [2], COVID [1], COVID-ARB [1]); diuretic use (n/group): control (0), control-ACE inhibitor (4), control-ARB (6), COVID (0), COVID-ACE inhibitor (1), and COVID-ARB (3). Coexisting conditions are outlined in the Figure (A).ResultsAng-peptide equilibrium concentrations did not significantly differ between the control and COVID groups without ACE inhibitor/ARB treatment (Figure [B], left). More importantly, Ang I+II, Ang II/Ang I, and ACE2 activity were not significantly different between both groups (Figure [C]). These data suggest that patients with COVID-19 are not those with increased RAS activity levels and that particularly COVID-19–induced alternative RAS activation, potentially mediated through circulating ACE2, is not a typical feature in our patient cohort.Download figureDownload PowerPointFigure. Patient characteristics, Ang (angiotensin) peptide profiles, and ACE (angiotensin-converting enzyme)-2 levels. A, The presence of cardiovascular disease (hypertension, coronary artery disease, and chronic heart failure) and type 2 diabetes mellitus depicted as percentage of patients in each group. B, Plasma Ang-peptide concentrations and renin-angiotensin system (RAS) enzymatic cascade are depicted as RAS Fingerprints. The concentration of indicated Ang metabolites is reflected by the size of the corresponding sphere. Blue arrows indicate enzymes that are known to carry out metabolic conversions between connected Ang metabolites. Numbers represent median concentrations (pmol/L) and interquartile ranges in parentheses. C, Ang-based markers for plasma renin activity: Ang I+Ang II and ACE: Ang II/Ang I were calculated from Ang-peptide levels. ACE2 activity was measured as described above. Data are shown as dot plots and median. Significant P values within each group (control and coronavirus disease 2019 [COVID]) are indicated. control: severe acute respiratory syndrome coronavirus 2 negative control group without ACE inhibitor/angiotensin type 1 receptor blocker (ARB) therapy; control+ACE inhibitor: severe acute respiratory syndrome coronavirus 2 negative control group with ACE inhibitor therapy; control+ARB: severe acute respiratory syndrome coronavirus 2 negative control group with ARB therapy; COVID: patients with COVID-19 without ACE inhibitor/ARB; COVID+ACE inhibitor: patients with COVID-19 with ACE inhibitor therapy; COVID+ARB: patients with COVID-19 with ARB therapy. ACEi indicates ACE inhibitor; and CTRL, control.Comparison of all groups, including ACE inhibitor/ARB treatment groups, revealed no significant differences of Ang I+II levels between the groups (Figure [C], upper left). Ang I+II is a reliable marker for plasma renin activity and did not change significantly, despite the use of ACE inhibitor/ARB, while median values were clearly increased in patients on ACE inhibitor/ARB. This is consistent with previous observations demonstrating a broad spectrum of intensity in compensatory renin secretion in patients treated with ACE inhibitor or ARB.4 As expected, patients in the control-ACE inhibitor and COVID-ACE inhibitor group showed increased Ang I and markedly suppressed Ang II levels (Figure [B]), resulting in a significant reduction of the Ang II/Ang I ratio (Figure [C], lower left). Ang-(1–5) levels did not significantly differ between groups, whereas Ang-(1–7) was significantly increased in the COVID-ACE inhibitor group versus COVID without ACE inhibitor/ARB (P=0.01) and versus COVID-ARB (P=0.045). ACE2 activity was significantly higher in patients with COVID-19 treated with ACE inhibitor compared with patients with COVID-19 without ACE inhibitor/ARB (Figure [C], right). ACE2 activity was also increased in the control-ACE inhibitor and control-ARB group but did not reach statistical significance (Figure [C], right). ARB treatment in COVID-19 did not significantly affect ACE2 activity (Figure [C], right).The main findings of this study are as follows: (1) patients with COVID-19 are not characterized by major changes in RAS activity in plasma including ACE2 activity, (2) ACE inhibitor therapy significantly suppressed Ang II/Ang I ratios, the Ang-based marker for ACE, in COVID-19 and in non–patients with COVID-19, and (3) plasma ACE2 activity is increased in patients with COVID-19 treated with ACE inhibitor. These data are consistent with previously published results in SARS-CoV-2–negative patients treated with ACE inhibitor or ARB demonstrating an Ang II/Ang I suppression and a more profound increase of Ang-(1–7) under ACE inhibitor compared with ARBs.4 The data published so far on plasma ACE2 activity and Ang-(1–7) levels in patients without COVID treated with ACE inhibitor or ARBs are controversial.1 Some studies showed an increase in circulating ACE2 activity and Ang-(1–7) levels that cannot be proven by other studies.1 In addition, increased ACE2 activity has been identified in multiple cardiovascular diseases such as hypertension, coronary artery disease, and chronic heart failure, which are usually treated with ACE inhibitor.1 Whether the ACE inhibitor treatment in our study plays a role in ACE2 upregulation or whether these changes are mediated by the increased presence of cardiovascular disease in this group requires further investigation. Furthermore, the clinical significance of the elevated ACE2 activity in patients with COVID-19 treated with ACE inhibitor is currently not completely understood. Whether plasma ACE2 level may be a reliable marker of the full-length membrane bound form1 and whether ACE2 serves as a marker for disease severity or endothelial regeneration in the lung5 need to be clarified in future studies. Some of the major limitations of this study include small sample sizes, lack of a power analysis, lack of any data on blood pressure when the plasma samples were obtained, and lack of any data on duration of illness. Finally, it should be emphasized that the majority of the study patients were not experiencing severe COVID-19. However, we provide for the first time a snapshot of distinct systemic RAS components in patients with COVID-19 under ACE inhibitor/ARB therapy that helps to understand the clinical data on a molecular pharmacological level.AcknowledgmentsWe thank Fabian Holert, Jana Eberst, and Beata Hoeft for the support with sample preparation/handling and clinical data collection.Sources of FundingThis study was supported by institutional funding from the Charité–Universitätsmedizin Berlin, Germany. U. Kintscher is supported by the DZHK (German Centre for Cardiovascular Research) and by the BMBF (German Ministry of Education and Research); BER 5.4 PR, the Deutsche Forschungsgemeinschaft (KI 712/10-1), the BMBF/BfR1328-564 m, and the Einstein Foundation/Foundation Charité (EVF-BIH-2018-440).DisclosuresO. Domenig and M. Poglitsch are employees of Attoquant Diagnostics, Vienna, Austria. U. Kintscher received research grants/speaker honoraria from Bayer. U. Kintscher received speaker honoraria from Berlin Chemie, Boehringer Ingelheim, Daiichi Sankyo, Novartis, Sanofi, and Servier and participated in advisory boards of Berlin Chemie, Boehringer Ingelheim, Novartis, and Sanofi. M. Möckel received research grants/speaker honoraria from Roche Diagnostics and BRAHMS ThermoFisher; M. Möckel received speaker honoraria from Boehringer Ingelheim, Daiichi Sankyo, Novartis, and Bristol Myers Squibb and participated in advisory boards of Daiichi Sankyo and Boehringer Ingelheim. The other authors report no conflicts.FootnotesCorrespondence to Ulrich Kintscher, Charité–Universitätsmedizin Berlin, Institute of Pharmacology, Center for Cardiovascular Research, Hessische Strasse 3-4, 10115 Berlin, Germany. Email ulrich.kintscher@charite.de

In December 2019, a novel coronavirus was identified in Wuhan City, Hubei Province, China and later the disease was named coronavirus disease 2019 (COVID-19). On March 11, 2020, the World Health Organization (WHO) officially announced that COVID-19 had reached global pandemic status. This article summarized the understanding of the etiology, pathogenesis, epidemiology, clinical characteristics, diagnosis, treatment, rehabilitation, and prevention and control measures of COVID-19 based on the available data and anti-epidemic experience in China.

Épanchements pleuraux en réanimation

Oxalate Nephropathy Caused by Excessive Vitamin C Administration in 2 Patients With COVID-19

Pleural Effusions in Hospitalized Patients Receiving Long-term Hemodialysis

Pleural effusions are rarely observed in patients with acute myelogenous leukemia (AML), acute lymphocytic leukemia (ALL) and myelodysplastic syndrome (MDS)/myeloproliferative neoplasm (MPN). Therefore the underlying etiology of pleural effusions and the efficacy and safety of pleural procedures in this population has not been well studied. In a retrospective review of cases from 1997 to 2007, we identified 111 patients with acute leukemia or MDS/MPN who underwent pleural procedures. Clinical characteristics were reviewed, and survival outcomes were estimated by Kaplan–Meier methods. A total of 270 pleural procedures were performed in 111 patients (69 AML, 27 ALL, 15 MDS/MPN). The main indications for pleural procedures were possible infection (49%) and respiratory symptoms (48%), and concomitant clinical symptoms included fever (34%), dyspnea (74%), chest pain (24%) and cough (37%). Most patients had active disease (61%). The most frequent etiology of pleural effusions was infection (47%), followed by malignancy (36%). Severe thrombocytopenia (platelet count < 20 × 103/µL) was present in 43% of the procedures, yet the procedural complication rate was only 1.9%. Multivariate analysis revealed that older age, AML, MDS/MPN and active disease status were associated with a shorter median overall survival. Infection and malignant involvement are the most common causes of pleural effusion in patients with acute leukemia or MDS. After optimizing platelet count and coagulopathy, thoracentesis may be performed safely and with high diagnostic yield in this population. Survival in these patients is determined by the response to treatment of the hematologic malignancy.

Introduction: Urinothorax is a rare cause of pleural effusion, characterized by urine within the pleural cavity, typically caused by urinary tract obstruction or trauma. Its diagnosis is challenging due to its uncommon occurrence and nonspecific symptoms, which may easily mimic other frequent etiologies of transudative pleural effusion. This case illustrates a delayed presentation of urinothorax following a traumatic bladder injury. Description: A 61-year-old female with a history of complicated rectosigmoid adenocarcinoma, pelvic metastasis, and multiple abdomino-pelvic surgeries including cystostomy repair for micro-perforation of the bladder two years ago, presented with worsening shortness of breath, chest discomfort and decreased urine output. On examination she was tachypneic with decreased right-sided breath sounds, and required oxygen. Laboratory findings showed acute kidney injury and metabolic acidosis with unremarkable results for troponin, BNP, albumin, urinalysis and COVID-19. CT imaging revealed a large right pleural effusion with compressive atelectasis, and intraperitoneal free fluid. Pulmonology was consulted and a chest tube was placed, draining 3.3L of transudative effusion. Given her urinary symptoms and prior extensive surgical history, the pleural fluid-to-serum creatinine ratio was obtained, which was greater than 2.2, consistent with the diagnosis of urinothorax. Further imaging, including a CT scan and Renal scintigraphy showed no obstructive uropathy or extravasation. Patient was discharged after symptomatic improvement, but was later readmitted for recurrent urinothorax. Urology recommended a cystogram which revealed intraperitoneal leakage from the dome of the urinary bladder, suggesting a potential cause of the ascites and the pleural effusion, likely secondary to microscopic trans-diaphragmatic pores. A Foley catheter was placed and the patient underwent an elective bladder patch repair. She improved significantly and remained asymptomatic on subsequent follow-up. Discussion: Urinothorax is an uncommon cause of transudative pleural effusion caused by extravasation of urine into the pleural space either directly through diaphragmatic defects or indirectly through retroperitoneal lymphatic drainage. This patient's presentation of dyspnea, right-sided pleural effusion, and decreased urine output, were initially challenging to diagnose, especially when typical findings such as hydronephrosis or extravasation were absent on initial imaging, including a nuclear scan. The diagnosis was confirmed through thoracentesis, which revealed pleural fluid-to-serum creatinine ratio greater than 2. Additionally, cystogram showed an intraperitoneal bladder leak, which indicated that the pleural effusion was likely due to trans-diaphragmatic defects. This case highlights the importance of keeping urinothorax in the differential diagnosis in patients with a prior history of urological procedures, even if initial imaging results are inconclusive.

Background: Pleural effusion is an abnormal accumulation of fluid in the pleural cavity which present with spectrum of clinico-aetiological manifestations often requiring multidisciplinary approach.&#x0D; Objectives: This study set out to determine the prevalence, aetiology, clinical presentation, treatment modalities and outcome of pleural effusion in children.&#x0D; Materials and Methods: This was a retrospective study where records of children with diagnosis of pleural effusion admitted at UDUTH, Sokoto were obtained between January 2017 and December 2022 and reviewed. Diagnosis was based on clinical presentation and radiological confirmation of pleural effusion. Data was analyzed with SPSS version 20.0.&#x0D; Results: A total of 49 cases were retrieved. The prevalence of pleural effusion was 0.54% (9,056). It was more prevalent in males with ratio of 2.5:1 (χ² = 9.833, P = 0.007). The median age was 9 years (IQR 7). The most common cause of pleural effusion was pneumonia 26 (53.1%) followed by tuberculosis 16 (32.6%), malignancy 3 (6.1%), cardiac and renal causes accounted for 2 (4.1%) each. Cough (100.0%), difficulty in breathing (100.0%), tachypnea (100.0%), respiratory distress (100.0%), and desaturation (98.0%) were the common presentations. Most (77.5%) of them presented with right sided pleural effusion. The majority (93.9%) had closed thoracostomy tube drainage. The outcome showed majority (83.7%) of the cases been discharged, with a median duration of hospital stay of 22days (IQR 17). However, mortality rate for the malignant causes was 100.0%.&#x0D; Conclusion: Infections were the major cause of paediatric pleural effusion with relatively good outcome. Surgical intervention and multidisciplinary team approach are needed to reduce the morbidity and mortality in patients with pleural effusion especially for the malignant causes.

Lung cancer management challenges amidst COVID-19 pandemic: hope lives here.

Dear Editor, The pandemic coronavirus disease 2019 (COVID-19) infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), especially B.1.617.2 (delta variant), has catastrophic impact over the world started from December 2019.1-3 Cancer patients are immunosuppressed and have high severity and mortality rate of COVID-19 infection4; therefore, we present a successful case of an 82-year-old man who was infected with COVID-19 delta variant and severe concomitant complications. An 82-year-old male presented to the emergency department who had fallen at home. In the preceding 3 days, the patient had progressive confusion, obtundation, slurred speech and difficulty with word finding. The past medical history includes stage IV prostate cancer with brain metastasis for 6 years, pulmonary emphysema, hypertension and coronary atherosclerotic heart disease with coronary stenting for 1 month. The patient was under active therapy for late-stage brain metastasis of prostate cancer. He daily took abiraterone 1000 mg, rosuvastatin 5 mg, bayaspirin enteric-coated 100 mg, clopidogrel 75 mg and felodipine 10 mg. He took betaloc 25 mh twice a day. The patient was real time-PCR (RT-PCR) confirmed positive for the COIVD-19 delta variant. He had a history of public gathering and a potential contacting people tested positive for COVID-19. Physical examination was unremarkable. His vitals were as follows: heart rate 88 beats/min, blood pressure 105/79 mm Hg, respiration rate 19 breaths/min and oxygen saturation 95%. Initial head computed tomography (CT) showed that several solid masses were seen in temporal horn of the right lateral ventricle, largest as 32 mm × 25 mm with calcified deposit. Intracerebral haematoma within the right lateral ventricle was seen with surrounding edema. Extra-axial fluid collection without midline shift was also observed. The size of solid masses was consistent with previous head CT scan with diagnosis of prostate cancer brain metastasis. No new lesions and enlargement of the tumour was found. The chest CT scan showed multiple, bilateral ground-glass opacities in the lower lobes consistent with COVID-19 viral pneumonia. Pulmonary emphysema can also be seen on the chest CT (Figure 1). A mild pericardial effusion and a pleural effusion were observed on chest CT. The laboratory is summarized in Table 1. Chemistry panel showed hypokalaemia (2.62 mmol/L), high C-reaction protein (93.6 mg/L) and high creatine kinase (2026 U/L). He was hospitalized in the Intensive Care Unit (ICU) ward for COVID-19 treatment and intracranial haemorrhage, following protocol from infectious disease for COVID-19 positive patient. He was started on treatment with neutralizing anti-COVID 19 antibody 2000 mg once on day 2, and supplementary oxygen was 4 L/min. He was on potassium supplement for correcting hypokalaemia. Osmotic mannitol was administered to reduce swelling of the brain. On day 3, the patient had small amount of black tarry fluid from the nasogastric tube and proton pump inhibitor omeprazole 40 mg daily was prescribed to the treatment of a stress ulcer. There was no black tarry fluid from nasogastric tube found from day 5. The patient's neurological condition has been improved from day 5. From day 9, COVID 19 testing was consecutively negative for 3 days. On day 16, a repeat chest CT scan showed a significant resolution of the bilateral pulmonary opacities (Figure 1). The patient was then discharged from ICU and transferred to an in-patient ward for further supporting treatment. According to the studies on COVID-19 alpha strain, people with certain conditions can get severe illness, including older adults cancer, chronic lung disease, neurological conditions, diabetes, coronary artery disease, HIV infection, liver disease, overweight, liver disease and smoking.1 Our patient had various high-risk factors: elderly patient; concomitant late-stage active prostate cancer; long-term of anti-cancer treatment; neurological condition of brain metastasis from prostate cancer; pre-existing underline disease of the lung and heart; 1-month post-surgical condition of coronary stenting and intracerebral haemorrhage. All these risk factors indicated severe disease and higher mortality rate in patient with COVID-19 delta variant infection. Intracerebral haemorrhagic stroke is a common and lethal complication of COVID-19 infection with reported incidence of 7.2% in a UK surveillance study.5 Angiotensin-converting enzyme 2, a major target in SARS-CoV-2 infections, is highly expressed on vascular endothelial cells and the heart. COVID-19 virus can attack the vascular system and cause bleeding.6 Neurologic complications were also commonly seen in patients with COVID-19.7 Critical patients seem to have higher incidents of neurological involvement than patients who have mild disease.8 Since pre-existing brain metastasis, our patient showed no new lesions. Haemorrhage on the head CT scan made COVID-19 the most likely cause of neurologic dysfunction. Patient neurological condition was improved from day 5. On the day 9, COVID 19 RT-PCR was converted into negative. There were not many reported successful cases of the patient who was infected with COVID-19 delta variant with various risk factors. Management is challenging because experience is limited from a few cases. The severe complication of COVID-19 disease in the patient was well controlled by early initiation of non-competitive SARS-CoV-2 neutralizing antibody cocktail against receptor-binding domain domain of SARS-CoV-2. This treatment can block entry of the virus, decrease the viral load, and therefore minimize the chance of causing the disease severity and improving recovery.9 Our patient was given a single infusion of neutralizing antibody cocktail BRII-196 and BRII-198 2000 mg on the second day after admitted, which was fall in the efficient timeline for the neutralizing antibody to reduce the viral loading. We believed this is one of the key factors which successfully rescued the patient from severe COVID conditions. Another main reason for successful treatment was enhanced supportive care in this patient. Supplemental oxygen was given to the patient at 4 L/min on the second day of hospitalization. Adequate hydration and nutrition (1500 kcal/day) with nasogastric tube insertion were also administrated to the patient. Finally, patient was put on a prone ventilation position, which was recommended by other experts.10 This position would reduce the lung compression, improve oxygenation and improve the lung perfusion. Active late-stage prostate cancer patient populations with pre-existing various high risks are required a thoughtful treatment approach to the COVID infection. To the best of our knowledge, this is the first reported successful case of a patient presented with infection of COVID-19 delta variant and severe concomitant complications. We would like to thank all the frontline healthcare workers who have been fighting in the COVID-19 pandemic. None. The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.

Evaluation of a pleural effusion has historically focused on establishing a single etiology. Pleural fluid may accumulate through multiple pathophysiological processes. The prevalence of multiple causes for pleural effusions has not been established. The identification of contributing processes may improve clinical outcomes. The objective of this prospectively collected case series was to establish the prevalence and nature of multiple etiologies for a unilateral pleural effusion. Consecutive patients presenting with an undiagnosed unilateral pleural effusion were recruited at a tertiary pleural center. Patients underwent a comprehensive structured diagnostic clinical evaluation and were followed up for a minimum of 12 months, after which one or more diagnoses were recorded independently by two experienced clinicians. One hundred thirty patients were recruited to the study over a 24-month period, and 126 patients completed follow up. Altogether, 88 patients (70%) had a single cause for their pleural effusion, and 38 (30%) had multiple causes. Serum N-terminal pro-brain natriuretic peptide (NT-pro BNP) greater than or equal to 1,500 pg/ml was predictive of multiple etiologies. NT-pro BNP had a sensitivity and specificity of 79 and 88%, respectively, for establishing heart failure as a primary or contributory cause. Thirteen patients with a malignant pleural effusion also had an NT-pro BNP greater than or equal to 1,500 pg/ml. This study is the first to estimate the prevalence of more than one identifiable cause for a unilateral pleural effusion. Out of 130 study subjects, 38 (30%) had multiple causes for an effusion. The identification of multiple pathologies underlying an accumulation of fluid in the pleural space may be important in determining optimum treatment and improving patients' symptoms.

Introduction: Pleuroperitoneal leak is the translocation of dialysate from the abdominal to pleural cavities in patients receiving peritoneal dialysis (PD). It represents a rare cause of transudative pleural effusion. Case: A 60-year-old female with history of end stage renal disease on PD for six months presented with dyspnea for one day. She had no apparent inciting factors. Exam was significant for increased work of breathing and decreased breath sounds to the right lung fields. Chest x-ray showed a large right sided pleural effusion. Thoracentesis removed 1.3 L serous fluid with subsequent improvement to the patient's symptoms. Pleural fluid studies were significant for protein 0.3 g/dL, LDH 12 U/L, and glucose 418 mg/dL. Serum values were protein 7.2 g/dL, LDH 182 mg/dL, and glucose 402 mg/dL. Pleural fluid cholesterol was &amp;lt; 5 mg/dL, triglycerides 10 mg/dL, amylase 6 U/L, and cytology and bacterial culture were negative. A contrast enhanced chest x-ray series was performed however the results were non-diagnostic. The patient's symptoms recurred after a routine PD session in which the net fluid balance was even despite an expected net negative 2 L. Repeat chest x-ray showed rapid reaccumulation of the right sided pleural effusion. Given the constellation of findings, the diagnosis of pleuroperitoneal leak was made. Repeat thoracentesis was done, and PD was transitioned to hemodialysis (HD). The patient's pleural effusion has since resolved. Discussion: Pleuroperitoneal leak is a rare cause of pleural effusion that occurs in approximately 1.6% of PD patients. Most cases are related to congenital diaphragmatic defects and present as dyspnea within the first year of PD. It less frequently occurs via acquired defects and present later. Diagnosis can be made by obtaining evidence of dialysate in the pleural space or by special imaging techniques. Treatment is discontinuation of PD and, if desired, video-assisted thoracic surgery to identify and repair the anatomic defect. This case highlights the importance of considering pleuroperitoneal leak in PD patients who have pleural effusion without evidence of generalized volume overload in a context of inadequate PD ultrafiltration.