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Romero S, Lim AK, Singh G, Kodikara C, Shingaki-Wells R, Chen L, Hui S, Robertson M. Natural history and outcomes of patients with liver cirrhosis complicated by hepatic hydrothorax. World J Gastroenterol 2022; 28(35): 5175-5187 [PMID: 36188717 DOI: 10.3748/wjg.v28.i35.5175]
Sarah Romero, FRACP, MBBS, Doctor, Department of Gastroenterology, Monash Health, 246 Clayton Road, Clayton 3168, Victoria, Australia. s.romero.md@gmail.com
Retrospective Cohort Study
Natural history and outcomes of patients with liver cirrhosis complicated by hepatic hydrothorax
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Retrospective Cohort Study Open Access
Sarah Romero, Andy KH Lim, Gurpreet Singh, Chamani Kodikara, Rachel Shingaki-Wells, Lynna Chen, Samuel Hui, Marcus Robertson
Sarah Romero, Chamani Kodikara, Rachel Shingaki-Wells, Samuel Hui, Marcus Robertson, Department of Gastroenterology, Monash Health, Clayton 3168, Victoria, Australia
Andy KH Lim, Marcus Robertson, Department of General Medicine, School of Clinical Sciences, Monash University, Clayton 3168, Victoria, Australia
Gurpreet Singh, Lynna Chen, Gastroenterology and Liver Transplant Unit, Austin Health, Heidelberg 3084, Victoria, Australia
ORCID number: Sarah Romero (0000-0003-2707-6390); Andy KH Lim (0000-0001-7816-4724); Gurpreet Singh (0000-0001-6760-566X); Chamani Kodikara (0000-0002-2381-2875); Rachel Shingaki-Wells (0000-0002-8714-591X); Lynna Chen (0000-0002-7093-2036); Samuel Hui (0000-0002-2839-6209); Marcus Robertson (0000-0002-8848-1771).
Author contributions: Romero S, Lim AK and Robertson M performed literature review, data analysis and interpretation and manuscript composition and critical revision; Lim AK, Robertson M and Hui S conducted statistical analysis; Romero S, Singh G, Kodikara C, Shangaki-Wells R and Chen L performed data acquisition; Robertson M was responsible for study concept and design; and all authors have read and approved the final manuscript.
Institutional review board statement: The Human Research Ethics Committee at Monash Health and Austin Health approved the study as a quality assurance activity and the committee provided a waiver for informed consent (RES-19-0000-343Q).
Informed consent statement: The informed consent was waived by the Human Research Ethics Committee.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: Technical appendix, statistical code, and dataset available from the corresponding author at s.romero.md@gmail.com. Patient consent was not obtained for this study, however study data has been anonymised.
STROBE statement: That authors have read the STROBE statement-checklist, and the manuscript was prepared and revised according to the STROBE statement-checklist of items.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Sarah Romero, FRACP, MBBS, Doctor, Department of Gastroenterology, Monash Health, 246 Clayton Road, Clayton 3168, Victoria, Australia. s.romero.md@gmail.com
Received: January 24, 2022
Peer-review started: January 24, 2022
First decision: April 10, 2022
Revised: April 28, 2022
Accepted: July 25, 2022
Article in press: July 25, 2022
Hepatic hydrothorax (HH) is an uncommon and difficult-to-manage complication of cirrhosis with limited treatment options.
To define the clinical outcomes of patients presenting with HH managed with current standards-of-care and to identify factors associated with mortality.
Cirrhotic patients with HH presenting to 3 tertiary centres from 2010 to 2018 were retrospectively identified. HH was defined as pleural effusion in the absence of cardiopulmonary disease. The primary outcomes were overall and transplant-free survival at 12-mo after the index admission. Cox proportional hazards analysis was used to determine factors associated with the primary outcomes.
Overall, 84 patients were included (mean age, 58 years) with a mean model for end-stage liver disease score of 29. Management with diuretics alone achieved long-term resolution of HH in only 12% patients. At least one thoracocentesis was performed in 73.8% patients, transjugular intrahepatic portosystemic shunt insertion in 11.9% patients and 33% patients received liver transplantation within 12-mo of index admission. Overall patient survival and transplant-free survival at 12 mo were 68% and 41% respectively. At multivariable analysis, current smoking [hazard ratio (HR) = 8.65, 95% confidence interval (CI): 3.43-21.9, P < 0.001) and acute kidney injury (AKI) (HR = 2.91, 95%CI: 1.21-6.97, P = 0.017) were associated with a significantly increased risk of mortality.
Cirrhotic patients with HH are a challenging population with a poor 12-mo survival despite current treatments. Current smoking and episodes of AKI are potential modifiable factors affecting survival. HH is often refractory of diuretic therapy and transplant assessment should be considered in all cases.
Key Words: Cirrhosis, Portal hypertension, Hepatic hydrothorax, Ascites, Liver transplantation
Core Tip: The development of hepatic hydrothorax (HH) in cirrhotic patients continues to be associated with a very poor prognosis despite current standards-of-care. In one of the largest series to investigate the natural history of patients with hepatic hydrothoraces, a 45-d overall survival rate of 80% and 12-mo transplant-free survival of 41% was observed after index hospitalisation with HH. At multivariate analysis, current smoking and development of acute kidney injury were both independently associated with mortality, and represent important modifiable risk factors.
Citation: Romero S, Lim AK, Singh G, Kodikara C, Shingaki-Wells R, Chen L, Hui S, Robertson M. Natural history and outcomes of patients with liver cirrhosis complicated by hepatic hydrothorax. World J Gastroenterol 2022; 28(35): 5175-5187
Hepatic hydrothorax (HH) is an uncommon but serious complication occurring in patients with decompensated cirrhosis. HH is defined as the accumulation of more than 500 mL of transudative pleural fluid in a patient with cirrhosis and portal hypertension, where primary cardiopulmonary or malignant aetiologies have been excluded[1]. HH has been reported to occur in 5% to 11% of patients with cirrhosis, with more than 90% of cases occurring in Child-Pugh B or C disease[1,2]. HH is thought to arise from direct passage of fluid from the peritoneal cavity to the pleural cavity through diaphragmatic fenestrations[1]. Nuclear medicine studies, using labelled albumin have confirmed unidirectional passage of fluid from the abdominal to the pleural cavity[3], thus supporting a diaphragmatic defect process.
Clinically significant HH develops when accumulation of ascites in the pleural cavity exceeds the absorptive capacity of the pleura and patients typically present with shortness of breath, cough, hypoxia or chest discomfort[1,3]. Most cases occur in patients with appreciable ascites, however ascites may not be a prominent finding in up to 42%[1]. HH is most often unilateral and right-sided (59%-80%), however, there are increasing reports of left-sided (12%-17%) or bilateral (8%-24%) involvement[1,4]. Similar to the development of spontaneous bacterial peritonitis (SBP) in patients with ascites, patients with HH may develop spontaneous infections within the pleural fluid, which are termed spontaneous bacterial empyema (SBEM)[3].
The clinical management of HH remains complex and challenging. Treatment priorities in cirrhotic patients presenting with a pleural effusion include confirming a diagnosis of HH and excluding alternative pathology, relieving symptoms, preventing pulmonary complications and managing the underlying ascites. Diagnostic or therapeutic thoracocentesis is typically performed to confirm the presence of transudative fluid and to exclude SBEM or alternative pathology[5]. Recently developed American Association for the Study of Liver Disease (AASLD) guidelines state that first-line management should include sodium restriction and diuresis[6]. It is recognised, however, that 20%-30% of patients with cirrhosis and HH will develop persistent or recurrent pleural effusion despite these measures[6]. Refractory HH represents a particularly challenging management issue and patients are often considered for repeat therapeutic thoracocentesis and transjugular intrahepatic portosystemic shunt (TIPS) placement. Liver transplantation (LT) is the definitive treatment for HH, and post-transplant outcomes are comparable to outcomes for alternative indications[6].
Currently, there remains a paucity of literature examining the natural history and prognostic significance of HH. No randomised controlled trials have been performed in this population and clinical guidelines were only published for the first time in 2020[6]. Previous small studies have indicated the development of HH is associated with significant morbidity and extremely poor survival in the absence of LT[2,7,8]. The aims of this study were to: (1) Evaluate the probability of survival in a cohort of patients with liver cirrhosis presenting with HH and to examine factors associated with mortality; and (2) Provide a descriptive analysis of the treatments and complications associated with HH treatment during hospitalisation.
Study design and setting
We conducted a multi-centre retrospective cohort study of patients with cirrhosis and HH presenting to three Australian metropolitan tertiary hospitals, one of which was a liver transplant centre, over a 9-year period from 2010 to 2018. Across all study sites, patients with decompensated cirrhosis were admitted under a specialist gastroenterology or liver transplant unit. Individual patient management was at the discretion of the attending gastroenterologist.
The Human Research Ethics Committee at Monash Health and Austin Health approved the study as a quality assurance activity and the committee provided a waiver for informed consent (RES-19-0000-343Q).
International Classification of Diseases (10th revision) codes for cirrhosis and chronic liver disease (K74, K74.6), HH (J 94.8) and pleural effusion (J90, J91) were used to retrospectively identify eligible patients with cirrhosis and HH[9]. The study eligibility criteria were: (1) Adult patients ≥ 18 years; (2) A confirmed diagnosis of cirrhosis, either biopsy-proven or based on clinical complications of cirrhosis; (3) Confirmed diagnosis of pleural effusion, based on imaging (plain X-ray or computed tomography); (4) Evidence of portal hypertension, as established by the presence of oesophageal varices, ascites and/or thrombocytopenia; and (5) Exclusion of cardiopulmonary or malignant pathology as a cause for the pleural fluid collection. Eligible patients were excluded if they had previously undergone LT. Included patients were followed for 12-mo from the date of the index admission.
The primary outcomes were 12-mo overall and transplant-free patient survival following index hospital admission with HH. Patients were followed-up from the date of first hospital admission with HH to an endpoint of death, LT or end of the study period. We report the 12-mo overall survival using the endpoint of death, censored for LT; and the 12-mo transplant-free survival using a composite endpoint of death and LT. The secondary outcomes included the incidence of specific treatments of HH and associated complications and to determine patient-specific prognostic factors associated with mortality.
HH definition and treatment protocols
HH was defined as the presence of a pleural effusion occurring in a patient with liver cirrhosis where no alternative aetiology was identified. Each patient was reviewed by a specialist hepatologist to ensure that the aetiology of pleural effusion was secondary to HH. Patients were excluded if the pleural effusion was felt to be due to primary infection, cardiopulmonary or malignant pathology.
Paracentesis was performed following radiological marking and thoracocentesis was performed by an interventional radiologist or the unit treating doctor with ultrasound guidance. In all cases, baseline observations were recorded, and the procedure was performed using sterile technique. Intravenous albumin (100 mL of 20% concentrated human albumin) was administered after every 2 liters of ascites or pleural fluid drained as per institutional protocol. Clinical observations were performed every 30 min for the duration of the procedure. Pleural and ascitic fluid was sent for analysis at the discretion of the physician performing the procedure according to indication and specimen viability. Where available, serum-pleural ascites gradient (SPAG) or serum-ascites albumin gradient values were obtained. SPAG greater than 11 g/L is consistent with a transudate[2], and was used to confirm portal hypertensive pathophysiology. SBEM was defined as pleural fluid with polymorphonuclear count of > 500 cells/mm3 or > 250 cells/mm3 with a positive culture, where parapneumonic effusion had been excluded[3]. Thoracocentesis without significant fluid drainage (diagnostic aspiration) was not considered in this analysis. TIPS insertion was available at all study centres and was performed by interventional radiology.
Treatment modalities pertaining to HH were categorized as: (1) Medical therapy with diuretics, and/or thoracocentesis; (2) TIPS; and (3) LT. All patients were risk stratified using the model for end-stage liver disease (MELD) score which was calculated at the time of presentation for each admission. An in-hospital complication was defined as the occurrence of one or more of the following: Infection, procedural complication (hematoma, pneumothorax, death), acute kidney injury (AKI, defined as at least 1.5-1.9 times baseline or ≥ 26.5 mmol/L increase from baseline[10]), and new-onset acute hepatic encephalopathy which was not present on admission.
For each patient, baseline demographic data, aetiology of liver disease, comorbidities, medication use, radiology results and laboratory results were extracted from electronic medical records. For patients with recurrent hospital admissions due to HH during the study period, data was collected for each presentation. Death was determined through hospital medical records and confirmed with a patient's Local Medical Officer if required.
mean ± SD was used to describe normally distributed continuous data, and median and interquartile range (IQR) for data that was significantly skewed. χ2 analysis was used to examine the association between categorical variables. For the primary outcome, we used the Cox proportional hazards regression survival model to analyze the time of onset of HH to death. The time at risk begins at the first admission for HH (the index admission, t0) and patients were censored at the time of LT or study conclusion (365 d after t0). For transplant-free survival analysis, we omitted censoring LT and treated the transplant date as an outcome event. For each readmission, further clinical data was collected for analysis. The model incorporates enduring baseline variables (age, sex, comorbidities, smoking, alcohol intake, aetiology of cirrhosis) as well as a number of time-varying covariates (MELD score, AKI, encephalopathy, treatment-related complications, functional status, and TIPS).
From the univariable analyses, we included variables with a P < 0.20 into the multivariable model. Through backward elimination steps, we retained covariates with a P < 0.05 and checked the general model fit using partial Cox-Snell residuals. We used fractional polynomials to assist parameterization of continuous variables. The proportional hazards assumption was tested by examining the Schoenfeld residuals. The DFBETA estimates were used to detect influential observations. To validate our findings, we conducted bootstrapping of the Cox regression analysis with 1000 replications to generate bootstrapped confidence intervals (CIs). All analyses were conducted with STATA 16.1 (StataCorp, TX, United States), and a P < 0.05 was considered statistically significant.
A total of 246 patients with cirrhosis presenting to hospital with a pleural effusion were identified during the study period, of which 162 were excluded as the pleural effusion did not meet the criteria for HH. The final analysis included 84 patients who had a total of 167 hospital admissions over the study period. The baseline characteristics of the patients are summarized in Table 1. The mean age was 58.3 years, with only 11% patients over the age of 70, and there was a slight predominance of males. All patients had established liver cirrhosis and clinical evidence of portal hypertension. The median MELD score at time of hospital admission was 29 (IQR: 25-33). A diagnosis of hepatocellular carcinoma was present in 27.4% patients.
Table 1 Baseline characteristics of patients with cirrhosis during the index hospital admission for hepatic hydrothorax (n = 84).
Age, mean ± SD, yr 58.3 ± 11.5
Male, n (%) 46 (54.8)
Diabetes mellitus, n (%) 23 (27.4)
Ischaemic heart disease, n (%) 7 (8.3)
Heart failure, n (%) 4 (4.8)
Chronic obstructive lung disease, n (%) 5 (6.0)
Hepatocellular carcinoma, n (%) 23 (27.4)
Other cancer, n (%) 3 (3.6)
Chronic kidney disease, n (%) 11 (13.1)
Current smoker, n (%) 12 (14.3)
Current alcohol drinker, n (%) 9 (10.7)
Aetiology of liver disease1, n (%)
Hepatitis C virus 25 (29.8)
Non-alcoholic fatty liver 17 (20.2)
Alcoholic liver disease 13 (15.5)
Hepatitis B virus 9 (10.7)
Primary biliary cirrhosis/sclerosing cholangitis 7 (8.3)
Cryptogenic 7 (8.3)
Autoimmune hepatitis 6 (7.1)
Budd-Chiari syndrome 3 (3.6)
Metabolic/others2 7 (8.3)
MELD score, mean ± SD 26.8 ± 7.1
Platelet count, median (IQR), per nL 103 (65-132)
Platelet count < 50/nL, n (%) 9 (10.7)
Anticoagulation, n (%) 6 (7.1)
Previous ascitic taps, n (%) 69 (82.1)
Beta-blockers, n (%) 11 (13.1)
Lactulose, n (%) 34 (40.5)
Rifaximin, n (%) 14 (16.7)
SBP prophylaxis, n (%) 32 (38.1)
1Categories are not mutually exclusive as > 1 aetiology may be attributed to each patient.
2Hemochromatosis, α1-antitrypsin deficiency, sarcoidosis.
MELD: Model for end-stage liver disease; SBP: Spontaneous bacterial peritonitis; IQR: Interquartile range.
Across all hospital admissions, 59% of patients were treated with lactulose (13% variation within patients between admissions), 27% of patients were treated with rifaximin (average 12% variation within patients between admissions), and 56% of patients were receiving prophylaxis for SBP (average 12% variation within patients between admissions). Prior to hospital presentation with HH, 93% patients were prescribed diuretic therapy, with median furosemide and spironolactone doses of 40 mg and 100 mg per day respectively and 70% of these patients were receiving dual diuretic treatment.
HH clinical features and management
The clinical features and management of HH are summarized in Table 2. The majority of the hydrothoraces were unilateral on the right side. Of the 167 episodes of HH, 20 (12.0%) were managed solely with increased diuretics. Concurrent treatment with diuretics and ascitic fluid drainage was commonly performed, with abdominal paracentesis performed during 47 (28.1%) presentations, where the median volume of fluid drained was 5 litres. The proportion of patients requiring thoracocentesis, abdominal paracentesis and the complications rates were similar for readmissions compared to the index admission. However, the dose of diuretics used was higher on readmissions than during the index admission.
Table 2 Clinical features of hepatic hydrothorax, management, and complications.
Index admission (n = 84)
Readmissions (n = 83)
NYHA severity of dyspnoea, n (%)
Class I 13 (15.5) 4 (4.3)
Class II 23 (27.4) 37 (39.4)
Class III 28 (33.3) 22 (23.4)
Class IV 20 (23.8) 31 (33.0)
Distribution of hydrothorax, n (%)
Unilateral, left 13 (15.5) 10 (12.1)
Unilateral, right 68 (81.0) 72 (86.8)
Bilateral 3 (3.6) 1 (1.2)
Admission hepatic encephalopathy, n (%) 12 (14.3) 14 (16.9)
De novo hepatic encephalopathy, n (%) 11 (13.1) 10 (12.0)
Thoracocentesis performed, n (%) 53 (63.1) 62 (74.7)
Pneumothorax, n (% of procedures) 6 (11.3) 11 (17.7)
Haematoma, n (% of procedures) 2 (3.8) 1 (1.6)
Pre-procedure platelet infusion, n (%) 11 (13.3) 6 (7.2)
Pre-procedure blood products1, n (%) 18 (21.7) 12 (14.5)
Pleural fluid drained, mean ± SD, litres 2.8 ± 1.7 3.0 ± 1.5
Indwelling intercostal catheter, n (%) 10 (11.9) 8 (9.6)
Infection, n (%) 17 (20.2) 14 (16.9)
Acute kidney injury, n (%) 30 (35.7) 28 (33.7)
Concurrent ascites drainage, n (%) 23 (27.1) 24 (28.9)
Volume drained, mean ± SD, litres 6.0 ± 3.1 5.5 ± 2.1
TIPS performed, n (%) 2 (2.4) 8 (9.6)
Furosemide, n (%)
None 27 (32.1) 9 (10.8)
20 to < 100 mg daily 52 (61.9) 60 (72.3)
100 to 240 mg daily 5 (5.6) 14 (16.9)
Spironolactone, n (%)
None 27 (32.1) 18 (21.7)
100 to 300 mg daily 42 (50.0) 43 (51.8)
1One or more of fresh frozen plasma, cryoprecipitate, or prothrombin complex concentrate.
NYHA: New York Heart Association; TIPS: Transjugular intrahepatic portosystemic shunt.
Thoracocentesis and complications: In total, 115 thoracocentesis procedures were performed in 62 (73.8%) patients with a median of 3 litres drained per procedure. Thoracocentesis was performed in 53 of 84 (63%) patients during the index admission. A further 62 thoracocentesis procedures were performed in 33 of 43 patients who required one or more readmissions. On average, the probability of receiving another thoracocentesis was 77% during each readmission episode. Sufficient laboratory data to perform pleural/ascitic fluid analysis was available in 31% of procedures. Of these, SBEM was detected in 10 (8.7%) thoracocentesis procedures.
Blood products, including pooled platelets, fresh frozen plasma, cryoprecipitate, were administered in 29% of patients prior to or following thoracocentesis. Sixteen patients received an indwelling intercostal catheter for ongoing drainage rather than simple thoracocentesis in the setting of acute instability (n = 4) or refractory disease (n = 12). A pneumothorax complicated 17 (15%) thoracocentesis procedures, of which 7 were managed conservatively, 9 required an intercostal catheter insertion, and 1 patient died. Bleeding complications from thoracocentesis were uncommon and we could not determine if blood product infusions (platelets, fresh frozen plasma, cryoprecipitate, or prothrombin complex concentrate) reduced procedural complications or affected patient survival.
Other complications: One or more non-pleural complications were recorded in 80 (48%) of HH admissions. The most frequent complications were AKI in 58 (35%) patients, followed by infection in 31 (19%) and new-onset hepatic encephalopathy in 21 (13%). The incidence of these complications was similar for the index admission and readmissions.
TIPS insertion: Ten (12%) patients received a TIPS insertion, with 2 patients receiving TIPS insertion during the index admission, and 8 patients on a readmission. Significantly more females than males received a TIPS (21% vs 4%, P = 0.038), but age and MELD score did not differ between patients who received TIPS and those who did not. No patient who received a TIPS proceeded to LT within 12 mo of the index admission.
LT: Forty-seven patients (56%) were referred for liver transplant assessment and 28 patients (33%) were successfully transplanted in the 12-mo following their index admission. The median time to transplantation from the index admission was 105 d (IQR: 55-200 d). The effect of LT on survival could not be estimated as there were no deaths amongst the transplanted patients within the study period.
Hospital length of stay and readmissions
The median hospital length of stay was 8 d (IQR: 4-17) for the index admission and 6 d (IQR: 4-14) for subsequent hospital readmissions. Within 12-mo of the index admission, 22 (26%) patients had 1 readmission, 9 (11%) had 2 readmissions, and 12 (14%) had ≥ 3 readmissions. In the 43 patients who required readmission, the median time interval between the index admission and the first readmission was 32 d (IQR: 12-74 d). The primary reasons for hospital readmissions were recurrent hydrothorax in 24 (38%) patients and decompensated cirrhosis in 26 (41%). There was strong evidence for an association between the New York Health Association (NYHA) functional class of dyspnoea and total number of readmissions (χ2= 46.2, P < 0.001) but the strength of the association was weak (Kendall's tau-b = 0.11). Intensive care unit (ICU) admission was required in 13 (15%) patients during the index admission, and 10 (12%) of 83 readmission episodes.
There were 23 deaths (27.4% of the cohort) within 12-mo of the index admission. The total time-at-risk was 17850 patient-days with a mortality rate of 1.3 deaths per 1000 patient-days. The Kaplan-Meier survivor functions for overall and transplant-free patient survival are shown in Figure 1. Most deaths occurred early after the index admission, with 30-d overall survival of 87% (95%CI: 78%-93%), 45-d survival of 80% (95%CI: 70%-87%), and 12-mo survival of 68% (95%CI: 56%-78%). For transplant-free survival, the 30-d survival was 85% (95%CI: 75%-91%), 45-d survival of 76% (95%CI: 66%-84%), and 12-mo survival of 41% (95%CI: 30%-51%). Most deaths were due to complications of end-stage liver disease and multiorgan failure (75%) or hepatocellular carcinoma (10%), but a small number were due to cardiovascular events (15%). We noted that the mortality rate for current smokers was 5.58 per 1000 patient-days, compared to non-smokers of 0.86 per 1000 patient-days, giving a mortality rate ratio for current smokers of 6.5 (95%CI: 2.5-16.1, P < 0.001).
Figure 1 Kaplan-Meier survival curves. Kaplan-Meier survival curves showing transplant-free survival at 12 mo, with liver transplantation and death treated as composite endpoints, and overall patient survival at 12 mo, with patients censored at the time of liver transplantation (ticks on survival curve).
Univariable and multivariable Cox regression analysis
The results of univariable analyses are summarised in Table 3. Factors consistently associated with an increased hazard of death were current smoking, episodes of AKI, higher MELD score, and hepatic encephalopathy. In addition, when analysing transplant-free survival, diabetes and TIPS insertion were associated with a lower hazard for death or LT while incident pneumothoraces were associated with greater hazard.
Table 3 Univariable Cox regression on patient survival to 12 mo.
Enduring variables Overall1, 12-mo survival
Transplant-free, 12-mo survival
HR (95%CI)
Age, per 5-yr 1.13 (0.94-1.35) 0.95 (0.85-1.07)
Male sex 2.05 (0.84-4.99) 1.68 (0.94-3.00)
Diabetes 0.56 (0.25-1.50) 0.39 (0.19-0.81)
Ischaemic heart disease 2.00 (0.68-5.92) 0.80 (0.29-2.23)
Heart failure 0.86 (0.12-6.38) 0.35 (0.05-2.55)
Chronic obstructive lung disease NE 1.02 (0.32-3.30)
Chronic kidney disease 1.13 (0.38-3.32) 0.82 (0.37-1.83)
Hepatocellular carcinoma 2.11 (0.92-4.81) 1.55 (0.87-2.76)
Hepatitis B 3.36 (1.32-8.53) 1.68 (0.75-3.74)
Hepatitis C 0.81 (0.32-2.05) 1.28 (0.71-2.28)
Alcoholic liver disease 0.76 (0.22-2.55) 0.94 (0.44-2.01)
Non-alcoholic fatty liver 0.51 (0.15-1.73) 0.43 (0.18-1.02)
Current smoking 5.01 (2.15-11.7) 2.27 (1.13-4.56)
Current alcohol intake 0.68 (0.42-1.13) 0.93 (0.68-1.26)
Time varying variables
MELD score, per 5-points 1.28 (0.93-1.77) 1.82 (1.41-2.34)
NYHA functional class 1.14 (0.74-1.75) 1.09 (0.81-1.46)
TIPS procedure 0.37 (0.05-2.83) 0.13 (0.02-0.96)
Acute kidney injury 2.57 (1.13-5.88) 2.36 (1.35-4.11)
Thoracocentesis 0.51 (0.23-1.16) 1.28 (0.70-2.34)
Pneumothorax 2.37 (0.80-7.00) 2.78 (1.39-5.56)
Intercostal catheter inserted 1.56 (0.53-4.62) 1.85 (0.90-3.82)
Admission hepatic encephalopathy
None 1.00 (reference) 1.00 (reference)
Mild 0.75 (0.17-3.25) 1.21 (0.54-2.70)
Severe 11.4 (3.28-39.6) 7.93 (2.36-26.6)
Encephalopathy during admission2 2.30 (0.84-6.32) 3.20 (1.65-6.24)
Any encephalopathy 2.30 (0.97-5.45) 2.21 (1.22-4.03)
1Censored at time of liver transplantation.
2New-onset during admission not present on admission, all episodes were mild.
HR: Hazard ratio; CI: Confidence interval; MELD: Model for end-stage liver disease; NYHA: New York Heart Association; TIPS: Transjugular intrahepatic portosystemic shunt; NE: Not estimable.
The results of the multivariable analyses are summarised in Table 4. When examining the overall patient survival model, we decided not to include hepatic encephalopathy in the multivariable model as there were only 4 cases of severe encephalopathy on admission which were associated with an increased risk of death. In the transplant-free survival model, age, diabetes, TIPS and incident pneumothoraces were not statistically significant after adjusting for MELD, smoking, AKI, and hepatic encephalopathy. There were no significant statistical interactions between variables in the final models, and the models were a reasonable fit for the data when assessed by partial Cox-Snell residuals.
Table 4 Multivariable Cox regression on patient survival to 12 mo.
Model and variables
AHR (95%CI)
P value
Bootstrap CI
Overall survival1
Age, per 5-yr increase 1.30 (1.01-1.67) 0.043 0.91-1.85 0.15
MELD score, per 5 points 1.53 (1.06-1.67) 0.025 0.89-2.66 0.13
Current smoking 8.65 (3.43-21.9) < 0.001 2.54-29.5 0.001
Acute kidney injury 2.91 (1.21-6.97) 0.017 1.04-8.12 0.042
Transplant-free survival
Hepatic encephalopathy 2.00 (1.08-3.67) 0.030 0.93-4.28 0.078
MELD score, per 5 points 1.78 (1.38-2.29) < 0.001 1.31-2.44 < 0.001
Current smoking 3.11 (1.49-6.52) 0.003 1.16-8.30 0.024
1Censored for liver transplantation.
MELD: Model for end-stage liver disease; AHR: Adjusted hazard ratio; CI: Confidence interval.
Due to the cohort size, we conducted bootstrapped analysis to validate our findings (Table 4). The significance of current smoking and AKI remained robust. In the overall survival model, a current smoker had 8.7 times the hazard of death of a non-smoker or ex-smoker; and one or more episodes of AKI was associated with a 2.9-fold increase in the hazard of death, after allowing for age and MELD score. In the transplant-free survival model, a current smoker had 3.1 times the hazard of death of a non-smoker or ex-smoker; and AKI was associated with a 2.2-fold increase in the hazard of death; after allowing for MELD and hepatic encephalopathy. These findings are represented in Figure 2.
Figure 2 Multivariate survival analysis. A: Multivariable Cox regression of overall patient survival (censored for transplantation), showing survival estimates for patients with hepatic hydrothorax by smoking and acute kidney injury status, with age and model for end-stage liver disease (MELD) scores held at the mean values; B: Bootstrapped pointwise confidence intervals for survival functions by active smoking status, in the absence of acute kidney injury and with age and MELD held at the means, demonstrating a robust association between active smoking and mortality in patients with hepatic hydrothorax. AKI: Acute kidney injury.
Other analysis
To compare with the traditional Cox model, we also performed a competing risks regression analysis (Fine-Gray subdistribution proportional hazards) using the same covariates, with the assumption that all patients were on the active liver transplant waiting list. In this analysis, the effect of smoking and AKI on survival remained significant, and our conclusions remained unchanged. The subhazard ratio (SHR) of smoking on mortality was 6.26 (95%CI: 2.75-14.3), P < 0.001. The SHR of AKI on mortality was 2.60 (95%CI: 1.25-5.36), P = 0.01. The clear effect of smoking can be illustrated by examining the cumulative incidence function for active smokers compared to non-smokers (see Supplementary Figure 1).
HH remains an uncommon but extremely challenging complication in patients with liver cirrhosis. This study represents one of the largest series to analyse the natural history and outcomes of patients with HH and to our knowledge, is the first study to examine factors associated with survival in this population. We demonstrated that development of HH was associated with poor prognosis despite current therapeutic modalities, with a 45-d overall survival of 80% and 12-mo transplant-free survival of 41%. HH is a refractory disease, and the use of diuretics in isolation was rarely effective in this cohort, with 52% of patients experiencing recurrence of HH and rehospitalisation. At multivariable analysis, smoking status and the presence of AKI confer significant additional mortality risk.
Hospitalisation with symptomatic HH is an uncommon presentation, with 84 patients recruited over a 9-year period to 3 metropolitan tertiary hospitals. The majority of patients presented with a right-sided pleural effusion and concurrent ascites, which is consistent with previous series[1,2,4]. The median MELD score of 29 in our cohort highlights that HH typically occurs in patients with advanced cirrhosis who often have other decompensating events such as hepatic encephalopathy. The median MELD score in our study was higher than that reported in other smaller studies[2,4,11], which may reflect use of data from a LT centre.
Patient management in this study aligns with recent AASLD guidelines, which recommend diuresis as the first-line therapy[6]. Most patients in our study were receiving diuretic therapy at the time of hospital presentation, with 70% receiving 2 diuretic agents, however the median doses of furosemide and spironolactone was well below the recommended maximum doses of 160 mg and 400 mg daily respectively[1]. Nonetheless, only 12% patients achieved long-term resolution of HH with diuretic therapy alone. An important limiting factor in relation to diuretic therapy is the propensity for AKI in patients with advanced cirrhosis. AKI was recorded in nearly one-third of presentations, and this was associated with a significantly higher risk of mortality. This suggests that diuretic therapy should be titrated cautiously in patients with HH with close monitoring of renal function.
There remains no consensus on universal diagnostic thoracocentesis in hospitalised patients with HH. In practice, whilst HH may be suspected on the basis of imaging and clinical presentation, thoracocentesis is useful to confirm transudative fluid and exclude other causes of a pleural effusion. We demonstrated that thoracocentesis in the HH population was associated with a significant higher risk of pneumothorax of 15% compared to the standard pneumothorax risk of 6% in non-cirrhotic populations, despite being performed under ultrasound guidance[12]. Shojaee et al[13] reported that repeat thoracocentesis in cirrhotic patients was associated with a higher rate of major complications compared to thoracocentesis for other aetiologies (8% vs 0%). In addition, Xiol et al[5], observed a pneumothorax rate of 25% in cirrhotic patients undergoing serial therapeutic thoracocentesis. Our analysis suggested that pneumothorax complications were associated with lower transplant-free survival [hazard ratio (HR) = 2.78; 95%CI: 1.39-5.56], however this was not significant in multivariable analysis. Other series have also suggested that HH requiring thoracocentesis independently confers significant morbidity and increased mortality[7,14]. Given the greater complications associated with thoracocentesis in cirrhotic patients, it was concerning that 74.7% of patients who were readmitted underwent repeat thoracocentesis. Further study is needed to elucidate the cause of the high complication rate and strategies to mitigate this risk. For example, it remains unclear if abdominal paracentesis effectively prevents HH recurrence[1].
In relation to other treatment modalities, indwelling intercostal catheter drains are thought to carry substantial risk and are not recommended by current guidelines, with some studies observing complication rates of 80%-90%[11,15]. In our cohort, an indwelling intercostal catheter was placed in 19% of patients, most commonly due to respiratory compromise and rapid re-accumulation of pleural fluid. In contrast, consideration of TIPS insertion is recommended by AASLD guidelines, based on evidence of a 70%-80% response rate in patients with refractory HH[3,6,16-18]. The outcomes following TIPS insertion may be comparable to those for management of refractory ascites and although a survival benefit in HH has not been established[19], the study by Badillo and Rockey[2] suggests a trend toward improved survival in patients proceeding to TIPS. Only 10 (17.9%) of the 56 patients in our cohort who were deemed not suitable for LT received TIPS insertion. No overall survival benefit from TIPS insertion was demonstrated, but transplant-free survival was higher (HR = 0.13; 95%CI: 0.02-0.96), as no patient who had TIPS insertion underwent LT.
Multiple studies have demonstrated that development of HH is associated with a poor prognosis[2,20,21], but mortality is difficult to compare due to heterogeneity between studies[2,4,11,15,21,22]. Our 12-mo transplant-free survival of 41%, however, is comparable to the 12-mo mortality of 57% reported by Badillo and Rockey[2]. In multivariable analysis, increasing age and MELD score, hepatic encephalopathy, development of AKI and active smoking were important factors independently associated with mortality. Given that the majority of deaths in our cohort were observed within 45-d of hospital admission and were most frequently due to complications of end-stage liver disease, we would advocate that in all patients presenting with HH, the appropriateness of transplantation should be considered with early referral for suitable candidates. Indeed, no deaths were recorded in patients who received LT, highlighting the successful outcomes of transplantation in patients with HH.
The strong association between smoking and poor outcomes has not previously been reported in patients with HH. Our study echoes a growing body of literature demonstrating an association between cigarette smoking and poorer outcomes in patients with liver disease[23,24]. Current smokers with cirrhosis have up to a 3.6 times higher mortality risk and cigarette smoking has been linked with progression of fibrosis in non-alcoholic fatty liver disease[24], hepatitis C and primary biliary cholangitis and is associated with an increased incidence of hepatocellular carcinoma[23]. Cigarette smoking represents an important modifiable risk factor that should be actively addressed in all patients with cirrhosis but appears critical in the HH population.
Study strengths and limitations
This is one of the largest, multicentre studies to investigate the prognostic significance of HH requiring hospitalisation in cirrhotic patients. Study inclusion criteria were broad and pragmatic, and represent generalisable real-world data. The Victorian Liver Transplant Centre was established in 1988 and currently performs over 100 transplants annually. The cohort had comprehensive assessments by gastroenterology specialists to confirm HH, which also assured treatment consistent with current standard-of-care practice guidelines. We used multivariable analysis to allow for confounders of mortality, and were able to identify smoking as a novel factor associated with significantly lower 12-mo survival in patients with HH. This study was able to elucidate the less well-described challenges in HH patients, such as need for ICU admission, hospital readmissions, and blood product requirement.
This study is limited by its retrospective design, with the inherent risks of missing information or extraction of inaccurate records. Complete pleural fluid analysis was only available in 31% of patients, which limited our ability to detect complications such as SBEM. SBEM has been associated in other studies with high short-term mortality (20% to 38%)[1]. SBEM was detected in 8.7% of thoracocentesis procedures in our study, which is almost certainly an underrepresentation of the true rate and lower than a study by Xiol et al[5], which found SBEM was present in 13% of patients with HH on presentation. Reasons for the low rate of complete pleural fluid analysis included the large number of hospital settings in which thoracocentesis was performed (including the emergency department, ICU, gastroenterology ward, radiology department or other acute hospital wards) with associated heterogeneity in process, incorrect requests for fluid analysis, incorrect tube collection to facilitate fluid analysis, clotting of fluid which precluded analysis, emergency procedures due to patient distress or instability and thoracocentesis performed prior to a diagnosis of HH being made. This reflects the real-world nature of the study and pleural fluid analysis rates were similar across all study sites. As such, we were not able to determine if specific pleural fluid findings were associated with refractory symptoms, rehospitalisation, or poor survival. In addition, factors associated with treatment failure or rehospitalisation such as compliance with diuretics were difficult to discern. The observational nature of the study also limits any causality inferences and eliminates the ability to ensure standardisation, which is particularly relevant to thoracocentesis technique. We could not exclude the possibility that some patients may have been admitted to a non-study hospital, although in practice this would be uncommon, and thus readmissions and complications may be underestimated.
In order to assess if TIPS may have provided clinical benefit apart from survival, we examined the readmissions, thoracocentesis, or ascitic drainage procedures in patients who received TIPS. Four patients had a single readmission post-TIPS, of which 3 occurred < 30 d and one at 6 mo post-TIPS. Thoracocentesis was performed in 3 of 4 of these readmitted patients, and ascitic drainage in 1 of 4 of these readmitted patients. Due to these low frequencies and different timing of TIPS, we cannot provide a meaningful statistical comparison with patients who did not have TIPS.
The development of HH is associated with poor transplant-free survival despite current standards-of-care and should prompt consideration of the appropriateness of LT in all patients. HH is often refractory to both conservative and invasive management and patients frequently require repeat hospitalisations. Active smoking and AKI may be important modifiable risk factors to reduce mortality in cirrhotic patients with HH.
Hepatic hydrothorax (HH) is an important complication of cirrhosis, however management is often challenging and the natural history is poorly understood.
Research motivation
HH is a significant complication of cirrhosis, with a paucity of literature studying natural history and factors affecting survival.
This study sought to: (1) Evaluate factors associated with survival in a cohort of patients hospitalised with HH; and (2) Provide descriptive analysis of treatments, complications and outcomes following HH hospitalisation.
Cirrhotic patients with HH presenting to three tertiary centres from 2010 to 2018 were retrospectively identified. Patients were followed-up from the date of first hospital admission with HH to an endpoint of death, liver transplantation (LT) or end of the study period. The primary outcomes were overall and transplant free survival at 12 mo after the index admission. The secondary outcomes included the incidence of specific treatments of HH and associated complications and to determine patient-specific prognostic factors associated with mortality.
Only 12% of patients achieved long-term resolution of HH with diuretic therapy alone. 74% of patients required thoracocentesis, with 15% of procedures being complicated by pneumothorax. 12-mo transplant free survival was 41%. 45-d overall survival was 80%.
Research conclusions
The development of HH is associated with poor transplant-free survival despite current standards-of-care and should prompt consideration of the appropriateness of LT in all patients. HH is often refractory to both conservative and invasive management and patients frequently require repeat hospitalisations. Active smoking and acute kidney injury may be important modifiable risk factors to reduce mortality in cirrhotic patients with HH.
Research perspectives
This study represents one of the largest series examining survival in persons hospitalised with HH, and importantly has identified modifiable risk factors that may alter the natural history in this challenging patient population.
Provenance and peer review: Unsolicited article; Externally peer reviewed
Peer-review model: Single blind
Specialty type: Gastroenterology and hepatology
Country/Territory of origin: Australia
Peer-review report's scientific quality classification
Grade A (Excellent): 0
Grade B (Very good): B, B, B
Grade C (Good): C
Grade D (Fair): 0
Grade E (Poor): 0
P-Reviewer: Cao HC, China; Gupta T, India; Papadopoulos VP, Greece S-Editor: Wang JJ L-Editor: A P-Editor: Wang JJ
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text:
Fan Recreated Classic Game Duck Hunt For VR And It's Pretty Neat
Published: Feb. 13. 2016 1:22 PM
Computer science student Joseph Delgado worked on a VR Duck Hunt variant for the Global Jam 2016 event. It's an impressive little demo that uses Razer's Hydra, the Oculus Rift DK2 development kit headset, and some neat tricks with Python scripts and the Unreal Engine 4's voxel rendering of sprites.
Jump Radio did a quick write-up on the project by Delgado, who managed to snap some footage of the project when he went to pay visit to his parent's house. You can check out the footage below.
Joseph Delgado, a student at the New Jersey Institute of Technology, used the sprites from the NES version of Duck Hunt and turning them into 3D voxels. This was only applied to some of the assets- mostly the moving ones and the background objects closest to the foreground where the 360 degree view could capture the feeling of a 3D environment, such as the hedges and the trees closest to the player's view.
Joseph Delgado mentions that frame-rate had become an issue and that it's easy to get motion sickness with the Oculus Rift if the FPS drops below 75fps. While there are people who will argue to their death that the human eye can only see 30fps, trust that in a VR environment if you're suffering from some serious frame stutter or dropped frames below 60fps, you will get sick. This is because the human brain is interpreting what your eyes are seeing and assuming that you're actually there, even when you aren't. This is one of the reasons why they tell you not to lean back when wearing VR headgear without tilting your head because your body is making motions that the VR tech may not pick up and it sends mixed signals to your brain, resulting in sickness.
Joseph Delgado ran into this problem a couple of times, as noted on his blog, where he explained that the Razer Hydra and Oculus Rift weren't always synching up on the same frame and the delay from the Hydra was, once again, giving him a bit of motion sickness. He eventually synched up the Rift and Hydra on the same input latency to limit the frame delay.
But as for the game maintaining 75fps – Delgado turned some of the backdrops into "billboards" or little more than one-dimensional cutouts based on a sprite plastered on a single vector face. This is the equivalent of putting a city on a green screen to cut down the costs of actually filming in a city.
From there, Joseph Delgado had a decently running VR simulation of Duck Hunt. He put the remix of the game's theme from Leonardo Zuccarelli on a 3D prop radio he designed – and yes, he did design some of the assets in the demo himself, mostly all the stuff in the starting hub cabin, including beds, desks and a few other props. He mentions that since he was playing Rainbow Six Siege he wanted to make it possible to shoot the radio... so if someone gets tired of the radio they can turn it off by shooting it.
As mentioned on the blog, the game faithfully recreates the inclining challenge present in the NES version of Duck Hunt, with each day offering fewer ammo pellets, more ducks to shoot and faster ducks. One of the things I thought was really awesome was the binaural surround effects that give users an idea of where the ducks are coming from, which causes users to have to listen closely as to where the ducks are in the play area. Very impressive stuff from Delgado.
Experiences like the one above will be available to consumers widely once the Oculus Rift starts shipping on March 28th, next month.
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People's Review > Economy > Why Nobel Laureate Abhijit Banerjee when we've Piyush Goyal and Nirmala Sitharaman?
Youth & Campus
Why Nobel Laureate Abhijit Banerjee when we've Piyush Goyal and Nirmala Sitharaman?
19/10/2019 19/10/2019 Tanmoy Ibrahim Economy
Who needs Nobel Laureate economists like Abhijit Banerjee, Esther Duflo or Amartya Sen, when a chartered accountant like Piyush Goyal is there? Why would Bharatiya Janata Party (BJP) need economists when India faces its severest economic crisis in decades? Finance Minister Nirmala Sitharaman will ignore former prime minister Dr Manmohan Singh's advice. Prime Minister Narendra Modi can mock economists, a practice, which would traverse down the Hindutva fascism's pyramid structure.
Goyal called Banerjee a "left-leaning" economist and claimed that India has rejected Banerjee's economic proposal — the Nyuntam Aay Yojana (NYAY) or the universal basic income (UBI) scheme — by not voting the Congress party. This castigation shows how Modi's cohorts, laced with self-assuring hubris and driven by an ill-gotten sense of entitlement, suffer from insecurity.
This visceral hatred for Banerjee, who is neither "left-leaning" nor an economist seeking Indian people's endorsement for his opinion, comes from the saffron camp's parochialist template. The BJP politicians like Goyal or Sitharaman, who have lived in this eco-system, can't help but despise any idea or theory that contradicts theirs.
Under Modi, India's economy is ruined. It's going to worsen than the financial year (FY) 2011-12 when the GDP growth came down to 5.5%. After the GDP growth fell to 5% for the first quarter (Q1) of FY 2019-20, negativity became epidemic. The Reserve Bank of India (RBI) has projected the Q2 growth of FY 2019-20 to be at 5.3%. The RBI forecast 6.1% GDP growth in FY 2019-20 from its earlier projection of 6.9%.
GDP calculation is done using a new computing methodology adopted by the Modi regime to magnify its economic achievements vis-a-vis the Dr Singh-led years. The Q1 growth could be below 4.5% if computed according to the previous methodology. There has been no other government in India that has forged data like the Modi regime. This pathetic attempt to paint a rosy picture using forged data, when the economy is at tatters, isn't going to help the BJP any more as the demand-side crisis has reached its peak in FY 2019-20 and it will be impossible to evade the issue by adopting supply-side measures.
The present economic crisis isn't a recession, which happens technically when for two consecutive quarters the economy goes into negative growth. Rather, the crisis is a demand-side crisis and is triggered by the disastrous economic blunders like demonetisation of November 2016 and Goods and Services Tax (GST) of July 2017. The unemployment that these two measures created, affected demand severely. On one hand, India's unemployment rate reached 45-years-high in 2019, while on the other hand, the government took no affirmative steps to improve the demand-side economy.
More unemployment led to further fall in demand, as not only the unemployed people lack money to spend, even those who are employed, got conservative about spending the money and became conscious of their choices so that they can save more money for exigencies. This negative feeling about the state of the economy caused a further fall of demand, especially of automobiles, consumer goods, fast-moving consumer goods, textile, real estate, etc. This led to far more lay-offs, adding more people to the number of unemployed and thereby, demand continued to decline.
According to the Centre for Monitoring Indian Economy (CMIE), the unemployment rate in October rose to 8.1%, and both urban and rural unemployment rates are in a pernicious stage. The CMIE data shows that employment opportunities are shrinking fast. From 41.6% in September employment rate fell to 40.7% in the first two weeks of October, which is the same as the average of the preceding three months.
Despite a spike in September due to Kharif sowing season, the employment rate receded in October. Even though few industries will do fairly better than the rest of the year during autumn due to a lot of Hindu festivals, it's expected that they will continue to face the slump in demand from December 2019 onwards, unless the employment situation improves.
This is a classic case of a microeconomic demand issue, which any serious undergraduate student can solve. Sitharaman, being a doctorate in economics, is either clueless, as one can surmise from her actions, or is intentionally aggravating the crisis. The only solution right now to this economic crisis within the current setup is to increase demand by providing people with employment opportunities or a basic income support. It's only the state that can play a pivotal role here and not the private sector, as it will not risk investing in a gloomy market situation.
Rather than playing the pivotal role in providing income opportunity to the people by either taxing the rich or by increasing revenue from the non-traditional sources, like withdrawing tax holidays and exemptions to big corporations, Sitharaman is trying to fix the supply-side of the economy. How can the merger of public sector banks help falling demand? How can tax exemption to corporate houses or withdrawal of wealth tax help in generating demand that's caused due to unavailability of money in the hands of the poor? How can providing more capital to the banks help generate income, when the corporate houses aren't eager to take new credit due to the volatile situation of the market?
She withdrew the wealth taxes, allowed tax cuts to the rich and those who will set up manufacturing units in India in a few years. While there are negative perceptions about the sustainability of existing businesses in the market, as they are unable to sell their goods and services due to falling demand, how can the government lure corporate houses to invest in new projects in such a situation? Even zero-interest loans won't increase setting up of new enterprises or increase employment opportunities. The only resort for the government will be to return back to the realm of data forgery and claim that either the MUDRA scheme has provided self-employment opportunities to millions or that people are not willing to work and, therefore, they are outside the job market.
The Modi regime's initiatives are targeted at enriching the rich, as neither corporate tax exemption nor wealth tax exemption will bring the extra money into the market to create employment opportunities. Rather, viewing a very unstable market situation, the investors will park their money in such bubbles that promise a higher return. So, while stock trading will increase, due to the speculative fetish of capital, domestic and foreign, employment-generating initiatives will continue to experience a free fall. It means rich will become richer, while the poor, the majority of Indian people, including 194m of starving people, will suffer.
Sitharaman claims that the 3.3% fiscal deficit target she had fixed is "non-negotiable". Such ambitious claim sounds outlandish when large-scale tax exemptions to the rich and corporate houses will cause a straight loss of Rs 1.46 trillion to the Indian exchequer, especially, at a time when the GST collection has fallen to the sub-1-trillion zone. It will widen the fiscal deficit by a few percentage points at least, if not by some per cent. How this gap will be filled has not been clarified by the finance minister or her ministry.
In case, without showing generosity to the corporate houses, Sitharaman would have increased the allocation for the Mahatma Gandhi National Rural Employment Guarantee Act from 0.2% of the GDP to 0.6%, it would have provided a better opportunity for the rural poor to earn some money and, thereby, boost demand for goods and services. Increased demand would've boosted the economy by providing more jobs and subsequent disposable income. Rather, the Modi regime thought about investing the money in fuelling the growth of the rich and the richest-of-the-rich.
Goyal has all rights to criticise the economists like Sen or Banerjee; similarly, Sitharaman, who ignored Dr Singh's suggestion that the Modi regime must stop blaming its predecessor in its sixth year and acknowledge that a problem exists to resolve it, can continue to boast that India is one of the "fastest-growing economies" sitting in Washington DC, however, it won't change the fact that the entire government is either deliberately accelerating the economic crisis or it's run by dimwits with no idea about how an economy works.
Banerjee's method of "randomized controlled trials" aren't left-wing economism. However, one of his approach regarding India, the NYAY scheme, had the possibility to reverse the slowdown by demand creation and also enable people to take risks as they would know there is something to fall back to. He even denied that his UBI was exclusively designed for the Congress party, but across the ideological spectrum, he could've shared it with anyone who would've asked for it.
The Congress party asked for it, the BJP didn't. Thus, the Congress was the first to propose the UBI of Rs 72,000 per annum in the 2019 Lok Sabha election taking a cue from Banerjee, however, the BJP's manoeuvre by promoting Modi's Rs 6,000 per farmer family an annum in three instalments stole the show with a promise of mere 1/12th of the NYAY's amount to a smaller group of beneficiaries. The loss of the Congress party doesn't mean that the concept of a UBI, which the state will provide, is actually thumbed down by the very people who are suffering due to the lack of it.
The people of India could have had voted for or against the UBI if there were concrete understanding and experience of the same. The votes that the BJP and its allies got from 250m voters, wasn't over its economic promises but for its mainstreaming of bigotry as a ruling party and its ability to communally polarise the majority Hindu community using xenophobia. The economic policies didn't cut ice in the political battle and that can't be Banerjee's fault.
Yet, driven by their audacity, and hubris, Goyal can fire a salvo at Banerjee or Sitharaman can negate Dr Singh, however, it won't change the fact that their disastrous economic mismanagement has brought the Indian economy to its knees and ruined millions of lives, ended numerous possibilities and continues to prevent millions from living a bare minimum life with a square meal a day. The Congress party's NYAY may have lost the election in 2019, but India has lost the economy and whatever was left of it, under Modi's rule.
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text:
La Punta Reboul Vidal és un cim de 3.007 m d'altitud, amb una prominència de 10 m, que es troba a l'aresta sud del Turó de Néouvielle, al massís de Nhèuvièlha, al departament dels Alts Pirineus (França).

Aquesta punta porta el nom dels primers ascensionistes del Turó de Néouvielle, el primer tresmil del que la seva ascensió està documentada.

Referències

Muntanyes dels Alts Pirineus

redpajama_set_name: RedPajamaWikipedia