Correlación fisiopatológica, diagnóstica y terapéutica en el derrame pleural paraneumónico / Pathophysiological, diagnostic and therapeutic correlation in parapneumonic pleural effusion

Introducción: La inflamación de la pleura desencadenada por bacterias y mediada por citocinas, aumenta la permeabilidad vascular y produce vasodilatación, lo cual genera desequilibrio entre la producción de líquido pleural y su capacidad de reabsorción por eficientes mecanismos fisiológicos. La condición anterior conduce al desarrollo de derrame pleural paraneumónico. Objetivo: Exponer la importancia de la correlación fisiopatológica y diagnóstica con los pilares fundamentales de actuación terapéutica en el derrame pleural paraneumónico. Métodos: Revisión en PubMed y Google Scholar de artículos publicados hasta abril de 2021 que abordaran el derrame pleural paraneumónico, su fisiopatología, elementos diagnósticos, tanto clínicos como resultados del estudio del líquido pleural, pruebas de imágenes, y estrategias terapéuticas. Análisis y síntesis de la información: El progreso de una infección pulmonar y la producción de una invasión de gérmenes al espacio pleural favorece la activación de mecanismos que conllevan al acúmulo de fluido, depósito de fibrina y formación de septos. Este proceso patológico se traduce en manifestaciones clínicas, cambios en los valores citoquímicos y resultados microbiológicos en el líquido pleural, que acompañados de signos radiológicos y ecográficos en el tórax, guían la aplicación oportuna de los pilares de tratamiento del derrame pleural paraneumónico. Conclusiones: Ante un derrame pleural paraneumónico, con tabiques o partículas en suspensión en la ecografía de tórax, hallazgo de fibrina, líquido turbio o pus en el proceder de colocación del drenaje de tórax, resulta necesario iniciar fibrinólisis intrapleural. Cuando el tratamiento con fibrinolíticos intrapleurales falla, la cirugía video-toracoscópica es el procedimiento quirúrgico de elección(AU)

Introduction: The inflammation of the pleura triggered by bacteria and mediated by cytokines, increases vascular permeability and produces vasodilation, which generates imbalance between the production of pleural fluid and its resorption capacity by efficient physiological mechanisms. The above condition leads to the development of parapneumonic pleural effusion. Objective: To expose the importance of the pathophysiological and diagnostic correlation with the fundamental pillars of therapeutic action in parapneumonic pleural effusion. Methods: Review in PubMed and Google Scholar of articles published until April 2021 that addressed parapneumonic pleural effusion, its pathophysiology, diagnostic elements, both clinical and results of the pleural fluid study, imaging tests, and therapeutic strategies. Analysis and synthesis of information: The progress of a lung infection and the production of an invasion of germs into the pleural space favors the activation of mechanisms that lead to the accumulation of fluid, fibrin deposition and formation of septa. This pathological process results in clinical manifestations, changes in cytochemical values and microbiological results in the pleural fluid, which accompanied by radiological and ultrasound signs in the chest, guide the timely application of the pillars of treatment of parapneumonic pleural effusion. Conclusions: In the event of a parapneumonic pleural effusion, with septums or particles in suspension on chest ultrasound, finding fibrin, turbid fluid or pus in the procedure of placement of the chest drain, it is necessary to initiate intrapleural fibrinolytic. When treatment with intrapleural fibrinolytics fails, video-thoracoscopic surgery is the surgical procedure of choice(AU)

A 49-Year-Old Woman With Persistent Bilateral Pleural Effusions.

CASE PRESENTATION: A 49-year-old woman presented to the ED with sudden onset abdominal pain, nausea, and vomiting. Her medical history included an uncomplicated gastric lap band surgery 9 years ago and subsequent removal of lap band after 6 years. She had a Roux-en-Y gastric bypass and cholecystectomy 5 months prior to the current presentation. The patient had been diagnosed with asthma and was prescribed an inhaled corticosteroid that she used only as needed. The patient denied smoking and heavy alcohol consumption. She was currently employed as a scrub technician in a local surgical center.

Diagnostic accuracy of interleukin-33 for tuberculous pleural effusion: A systematic review and meta-analysis.

BACKGROUND: The detection of interleukin 33 (IL-33) in pleural effusion may be more sensitive in diagnosing tuberculous pleural effusion (TPE). The present study aimed to assess the accuracy of pleural IL-33 for the diagnosis of TPE by means of meta-analysis and systematic review of relevant studies. METHOD: After retrieving the published studies, the sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, diagnostic odds ratio, and a summary receiver operating characteristic curve were assessed to estimate the usefulness of pleural IL-33 in diagnosing TPE using meta-analysis with a random-effects model. We also performed meta-regression and subgroup analysis. RESULTS: A total of 639 patients from 6 studies were analyzed. The pooled sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, and diagnostic odds ratio were 0.87 (95% confidence interval [CI], 0.82-0.91), 0.76 (95% CI, 0.72-0.80), 6.54 (95% CI, 2.65-16.15), 0.17 (95% CI, 0.10-1.27), and 45.40 (95% CI, 12.83-160.70) respectively. The area under the curve was 0.94. The composition of the included population was the main cause of heterogeneity and subgroup analysis showed that pleural IL-33 had a higher specificity (0.93, 95% CI 0.87-0.96) when used for differential diagnosis between TPE and malignant pleural effusion. CONCLUSION: The detection of IL-33 alone in pleural effusion seems to not be an efficient diagnostic marker for TPE but may serve as a novel biomarker to differentiate between TPE and malignant pleural effusion.

Clinical and pathophysiological characteristics of valproate-induced pleural effusion.

INTRODUCTION: Valproic acid is a carboxylic acid derivative commonly prescribed for several types of seizure disorders or for acute manic episodes in patients with bipolar disorder. Several cases of valproate-induced pleural effusion have been reported, although the precise pathophysiological mechanism remains unknown. OBJECTIVE: To describe the presentation of pleural effusion associated with valproate use and to categorize published case reports according to clinical, immunological, and pleural effusion cell type. METHODS: PubMed/MEDLINE and Embase databases were systematically searched from January 1970 until November 2020 using the following search terms: "valproic acid" OR "valproate" OR "pleural fluid" OR "exudative effusion" OR "transudative effusion" OR "valproic lung adverse events". These searches yielded 171 references of which 135 articles were considered irrelevant, leaving 36 potentially relevant references which were carefully scrutinized. Twenty-eight cases of valproate-induced pleural effusion were identified after excluding two articles reporting five patients with lung parenchymal adverse reactions to treatment with valproic acid; two articles reporting three patients in whom the pleural effusion could not be attributed to valproic acid alone; one case discussing valproate therapy and fungal pleural effusion; and one describing a patient who suffered from severe cardiac failure. There were also two cases, in an abstract form, with pericardial and pleural effusion, but without any further informative details, and, thus, they were also excluded from this survey. EXUDATIVE EOSINOPHILIC PLEURAL EFFUSION: This was the most common type of valproate-induced pleural effusion reported in 17 out of 28 cases (60.7%), with concurrent peripheral eosinophilia in ten. Acute hypersensitivity reaction, inflammation of the pleural cavity induced by the drug, drug toxicity, and damage to mesothelial cells due to oxidants, comprise the possible pivotal mechanisms. EXUDATIVE LYMPHOCYTIC PLEURAL EFFUSION: This was reported in two cases, with concurrent pericardial effusion in one. Discontinuation of valproate led to resolution of the effusion, although the underlying pathophysiological mechanisms remain abstruse. Interestingly, a patient presented with recurrent pleural effusion characterized by transition from eosinophilic to lymphocytic predominance after readministration of valproate. TRANSUDATIVE PLEURAL EFFUSION: Three out of 28 cases (10.7%) were characterized by neutrophilic transudative pleural effusion after long-term therapy with valproate, while concurrent pericardial effusion was also noted in two. VALPROATE-INDUCED LUPUS ERYTHEMATOSUS WITH PLEURAL EFFUSION: Five patients receiving valproate therapy (17.9% out of the 28 cases) developed drug-induced lupus erythematosus with concurrent pleural effusion that was eosinophilic in three. All patients had positive antinuclear antibodies; anti-histone antibodies were positive in two. CONCLUSIONS: Valproate-induced pleural effusion is rare, but patients receiving treatment with valproic acid who develop respiratory symptoms should be examined for valproate-induced pleural effusion.

The Relationship of Pleural and Pericardial Effusion With Pulmonary Hemodynamics in Patients With Pulmonary Hypertension.

BACKGROUND: The relationship between the presence of pleural and pericardial effusion in reference to hemodynamic parameters remains unclear in ambulatory patients with pulmonary hypertension (PH). METHODS: Consecutive patients who underwent right catheterization (RHC) for the evaluation of pulmonary hypertension were enrolled. Point-of- care ultrasound was performed prior to the RHC to determine the presence of pleural effusion and pericardial effusion. We conducted a cross-sectional study to determine the association between presence of pericardial and pleural effusion with pulmonary hemodynamic variables. RESULTS: Twenty-five (78.1%) of 32 patients had evidence of PH by RHC. Mean pulmonary artery pressure of the population was 40.6 mmHg, and 68% (17/25) had WHO group I PH. Six (24.0%) of 25 PH patients had pleural effusions identified, of which 4 out of 6 (66.7%) had a pulmonary artery wedge pressure >15 mmHg. Eleven (44.0%) of the 25 PH patients were also found to have pericardial effusions, and most of those patients 10/11(90.9%) had an elevated right atrial pressure >10 mmHg. The presence of a pleural effusion was associated with a pulmonary artery wedge pressure >15 mmHg (p = 0.032) and the presence of a pericardial effusion was associated with a right atrial pressure >10 mmHg (p = 0.004). Detection of pleural effusion had a poor positive predictive value (67%) for the presence of pulmonary venous hypertension, whereas presence of a pericardial effusion was highly predictive (89%) of the presence of systemic venous hypertension. CONCLUSIONS: Systemic venous hypertension was associated with the presence of pericardial effusions, while pulmonary venous hypertension is associated with pleural effusion development in ambulatory patients with pulmonary hypertension.

Pleural Effusion Is Associated with Severe Renal Dysfunction in Patients with Acute Pancreatitis.

BACKGROUND Renal dysfunction is a leading cause of death in patients with acute pancreatitis (AP) and often occurs later than respiratory complications. Whether respiratory complications can predict renal impairment remains unclear. The aim of this study was to investigate the association between pleural effusion and renal dysfunction in AP. MATERIAL AND METHODS Medical records were reviewed from individuals who were hospitalized with AP from January 1, 2015 to December 31, 2019. The patients were divided into 2 groups, based on the presence or absence of pleural effusion on admission. Disease severity, renal function parameters, and outcomes were compared between the 2 groups. RESULTS A total of 222 patients were enrolled, 25 of whom had pleural effusion on admission and 197 who did not. Patients with AP who had pleural effusion had more serious illness (higher incidences of pancreatic inflammation, pancreatic fluid collection, and moderate-to-severe AP; worse Bedside Index for Severity in Acute Pancreatitis score; and a higher modified computed tomography severity index [all P<0.05]) plus worse outcomes (higher incidences of ventilation and vasopressor use [both P<0.05]). Moreover, patients with pleural effusion had a higher level of blood urea nitrogen and lower estimated glomerular filtration rate (both P<0.05). After adjustment for potential confounders, pleural effusion was a risk factor for renal failure in patients with AP (odds ratio 6.32, 95% confidence interval 1.08-36.78, P=0.040). CONCLUSIONS Pleural effusion is associated with severe renal dysfunction in AP. Therefore, efforts should be made to improve early recognition and timely treatment of renal failure by closely monitoring renal function in patients with AP and pleural effusion on admission.

Endothelial Cell Protein C Receptor Deficiency Attenuates Streptococcus pneumoniae-induced Pleural Fibrosis.

Streptococcus pneumoniae is the leading cause of hospital community-acquired pneumonia. Patients with pneumococcal pneumonia may develop complicated parapneumonic effusions or empyema that can lead to pleural organization and subsequent fibrosis. The pathogenesis of pleural organization and scarification involves complex interactions between the components of the immune system, coagulation, and fibrinolysis. EPCR (endothelial protein C receptor) is a critical component of the protein C anticoagulant pathway. The present study was performed to evaluate the role of EPCR in the pathogenesis of S. pneumoniae infection-induced pleural thickening and fibrosis. Our studies show that the pleural mesothelium expresses EPCR. Intrapleural instillation of S. pneumoniae impairs lung compliance and lung volume in wild-type and EPCR-overexpressing mice but not in EPCR-deficient mice. Intrapleural S. pneumoniae infection induces pleural thickening in wild-type mice. Pleural thickening is more pronounced in EPCR-overexpressing mice, whereas it is reduced in EPCR-deficient mice. Markers of mesomesenchymal transition are increased in the visceral pleura of S. pneumoniae-infected wild-type and EPCR-overexpressing mice but not in EPCR-deficient mice. The lungs of wild-type and EPCR-overexpressing mice administered intrapleural S. pneumoniae showed increased infiltration of macrophages and neutrophils, which was significantly reduced in EPCR-deficient mice. An analysis of bacterial burden in the pleural lavage, the lungs, and blood revealed a significantly lower bacterial burden in EPCR-deficient mice compared with wild-type and EPCR-overexpressing mice. Overall, our data provide strong evidence that EPCR deficiency protects against S. pneumoniae infection-induced impairment of lung function and pleural remodeling.

Clinical characteristics of COVID-19 complicated with pleural effusion.

BACKGROUND: Epidemiological and clinical features of patients with corona virus disease 2019 (COVID-19) were well delineated. However, no researches described the patients complicated with pleural effusion (PE). In the present study, we aimed to clinically characterize the COVID-19 patients complicated with PE and to create a predictive model on the basis of PE and other clinical features to identify COVID-19 patients who may progress to critical condition. METHODS: This retrospective study examined 476 COVID-19 inpatients, involving 153 patients with PE and 323 without PE. The data on patients' past history, clinical features, physical checkup findings, laboratory results and chest computed tomography (CT) findings were collected and analyzed. LASSO regression analysis was employed to identify risk factors associated with the severity of COVID-19. RESULTS: Laboratory findings showed that patients with PE had higher levels of white blood cells, neutrophils, lactic dehydrogenase, C-reactive protein and D-dimer, and lower levels of lymphocytes, platelets, hemoglobin, partial pressure of oxygen and oxygen saturation. Meanwhile, patients with PE had higher incidence of severe or critical illness and mortality rate, and longer hospital stay time compared to their counterparts without pleural effusion. Moreover, LASSO regression analysis exhibited that pleural effusion, lactic dehydrogenase (LDH), D-dimer and total bilirubin (TBIL) might be risk factors for critical COVID-19. CONCLUSIONS: Pleural effusion could serve as an indicator for severe inflammation and poor clinical outcomes, and might be a complementary risk factor for critical type of COVID-19.

Hypo-attenuated leaflet thickening and reduced leaflet motion after the implantation of the Perceval S sutureless bioprosthesis.

Hypo-attenuated leaflet thickening (HALT) is gaining attention as a relatively common issue after surgical or transcatheter aortic valve replacement (AVR). However, only a few reports have described HALT in sutureless bioprosthesis, which has emerged as a promising tool with excellent hemodynamics and enhanced implantability. We herein report a 75-year-old woman who underwent quintuple coronary artery bypass grafting and sutureless AVR with a Perceval S bioprosthesis (LivaNova PLC, London, UK). Despite an uneventful perioperative course, her recovery was slow with persistent pleural effusion. Echocardiography revealed an increased transvalvular pressure gradient, and HALT was confirmed by computed tomography. The patient received aggressive anticoagulation therapy with resolution of the HALT and made an uneventful recovery. Current guidelines provide no specific recommendations for peri-procedural antithrombotic therapy for sutureless AVR. However, HALT is not rare after sutureless AVR and can lead to significant clinical consequences. In this case, aggressive anticoagulation therapy with systemic heparinization was effective as HALT treatment following early post-sutureless AVR. Further investigation is required to determine the optimal antithrombotic strategy for sutureless AVR.

A 28-Year-Old Pregnant Woman With a Lung Abscess and Complicated Pleural Effusion.

CASE PRESENTATION: A 28-year-old woman G1P0 at 22 weeks of gestation and with no significant medical history presented to the ED complaining of worsening dyspnea and right-sided pleuritic chest pain. Symptoms started 2 weeks before presentation, with minimal productive cough and dyspnea on exertion. One week after the initial symptoms, the patient started noticing right-sided chest and shoulder pain along with subjective fevers and night sweats. She denied hemoptysis, weight loss, abdominal pain, diarrhea, nausea, vomiting, arthralgia, or rash. Her pregnancy had so far been uncomplicated. The patient did not use tobacco, alcohol, or recreational drugs. She worked at a daycare center but denied any particular sick contacts. She moved to the United States 7 years ago from Sudan and denied any recent travel.

Pancreaticopleural fistula: an uncommon cause of amylase-rich pleural effusion.

Pancreaticopleural fistula (PPF) causing pleural effusion as a complication of chronic pancreatitis is a rare finding. We present this finding in a 52-year-old man with a medical history significant for alcohol abuse, acute on chronic pancreatitis and severe chronic obstructive pulmonary disease, who presented with worsening dyspnoea for 3 days. CT scan of the chest showed a new large right-sided pleural effusion. Thoracentesis was performed and pleural fluid analysis showed an amylase-rich, exudative pleural effusion. The effusion reaccumulated within 3 days necessitating repeat thoracentesis. Endoscopic retrograde chloangiopancreatography showed contrast leak through a single disruption in the dorsal pancreatic duct, suspicious for an underlying PPF. The patient underwent stenting of the pancreatic duct with subsequent resolution of right-sided pleural effusion.

Nephrotic syndrome due to preeclampsia before 20 weeks of gestation: a case report.

BACKGROUND: Preeclampsia (PE) refers to the development of hypertension and new-onset proteinuria or progressive organ damage (especially kidney) in a previously normotensive pregnant women after 20 weeks of gestation. Thus, new-onset nephrotic syndrome due to PE before 20 weeks of gestation seems to be rare, making its diagnosis difficult in this time period. CASE PRESENTATION: A 28-year-old woman presented with a new-onset nephrotic syndrome at 16 weeks of gestation. A high dose of oral glucocorticoids (prednisolone, 40 mg) was initiated for presumed glomerulonephritis since she presented with severe nephrotic syndrome before 20 weeks of gestation, however, the treatment was not effective. At 21 weeks of gestation, we confirmed that the soluble fms-like tyrosine kinase-1 (sFlt-1)/placental growth factor (PlGF) ratio was very high (sFlt-1, 13,400 pg/mL; PlGF, 21.9 pg/mL; serum sFlt-1/PlGF ratio 611.9). Therefore, we diagnosed nephrotic syndrome due to PE, and oral glucocorticoids were discontinued. After she underwent a cesarean section at 24 weeks & 3 days, we performed a kidney biopsy. Focal segmental sclerotic lesions with epithelial cell hyperplasia and foam cells in the tubular poles were seen on light microscopy. On immunofluorescence tests, C4d staining showed linear peripheral patterns in the glomeruli. Electron microscopy revealed diffuse subendothelial edema with focal foot process effacement. The histological diagnosis was severe glomerular endotheliosis with focal segmental glomerulosclerosis. Furthermore, the histology of placenta was consistent with PE. Eight months after delivery, her proteinuria disappeared completely. CONCLUSIONS: We not only confirmed an abnormal serum sFlt-1/PlGF ratio but also presented the histology compatible with pure PE in the kidney and placenta in a case of nephrotic syndrome before 20 weeks of gestation. The serum sFlt-1/PlGF ratio may be useful in determining the treatment strategy for atypical cases of pregnant women with nephrotic syndrome, particularly before 20 weeks of gestation.

Lung pulse visualized through pleural effusion as a diagnostic sign of complete obstructive atelectasis of the left lung in a critical patient with respiratory failure. / Pulso pulmonar visualizado a través de derrame pleural como signo diagnóstico de atelectasia obstructiva completa del pulmón izquierdo en paciente crítico con insuficiencia respiratoria.

Complete obstructive atelectasis occurs when mucous or a foreign body obstruct one of the main bronchi. Several lung ultrasound signs have been associated with this entity. We describe the case of a patient admitted to the surgical critical care unit in whom lung ultrasound led to a diagnosis of complete obstructive atelectasis, and the presence of pleural effusion provided direct visualization of lung pulse, a sign that has only previously been described by interpreting ultrasound artifacts.

Premature infant with sudden respiratory distress.

Here we describe a case of a premature neonate who showed initial improvement after being on invasive ventilation. She was gradually weaned to room air and was started on a feeding protocol for preterm infants together with total parenteral nutrition through a peripherally inserted central catheter (PICC) when she suddenly deteriorated and developed respiratory distress associated with signs of shock, requiring support from a high-setting mechanical ventilation as well as an inotropic support. A full sepsis work-up was ordered and she was started on antibiotics. The diagnosis was confirmed on chest X-ray and ultrasound, which showed automigration and displacement of the PICC line from its initial site on the left side to the right lung base, causing significant right-side pleural effusion which affected her haemodynamics. The PICC line was removed, and 30 hours later the pleural effusion completely resolved and the patient improved. She was discharged from hospital without any concerns with regard to growth and development during her regular follow-up.

Tobacco smoking as a risk factor for tuberculous pleural effusion: a case-control study.

This study assessed the tobacco smoking-associated risk for tuberculous pleural effusion (TPE) in India. Ninety-two patients with TPE and 184 controls were randomly selected and assessed regarding their tobacco-smoking status and type, quantity and duration of tobacco used. Odds ratios (ORs) for the association of smoking cigarette, beedi and cigarette or beedi with TPE were 19.22 (p < 0.0001), 2.89 (p = 0.0006) and 4.57 (p < 0.0001) respectively. ORs for developing TPE increased with an increase in beedi/cigarette consumption, duration and pack years of smoking (p < 0.001 each). TPE was significantly associated with confounding risk factors viz., regular alcohol use (OR = 1.89, p = 0.019), history of contact with tuberculosis (TB) patient (OR = 8.07, p < 0.0001), past history of TB (OR = 22.31, p < 0.0001), family history of TB (OR = 9.05, p = 0.0002) and underweight (OR = 3.73, p = 0.0009). Smoking (OR = 3.07, p < 0.001), regular alcohol use (OR = 2.10, p = 0.018), history of contact with TB patient (OR = 4.01, p = 0.040), family history of TB (OR = 10.80, p = 0.001) and underweight (OR = 5.04, p < 0.001) were independently associated with TPE. Thus, both cigarette- and beedi-smoking have a significant association with TPE. The risk for TPE in tobacco smokers is dose- and duration-dependent.

Immune reconstitution inflammatory syndrome in non-HIV patients with tuberculosis. A case series.

Tuberculosis associated Immune reconstitution inflammatory syndrome (IRIS) in a HIV negative patient can present with a multitude of clinic-radiological presentations that are often confused with drug resistance/treatment failure. Being a diagnosis of exclusion, this clinical entity is often prone to under-diagnosis. We present a series of 5 patients who presented with varied but uncommon IRIS manifestations. High index of suspicion coupled with clinical reasoning and judicious use of phenotypic and genotypic culture methods helped in their timely detection and successful treatment.