Use of the Serum Level of Cholinesterase as a Prognostic Marker of Nonfatal Clinical Outcomes in Patients Hospitalized with Acute Exacerbations of Chronic Obstructive Pulmonary Disease.

Introduction: Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) contributes to a poor prognosis. Reliable biomarkers to predict adverse outcomes during hospitalization are important. Aim: To investigate the relationship between the serum cholinesterase (ChE) level and adverse clinical outcomes, including hypoxemia severity, hypercapnia, duration of hospital stay (DoHS), and noninvasive ventilation (NIV) requirement, in patients with AECOPD. Methods: Patients hospitalized with AECOPD in the Wuhu Hospital of Traditional Chinese Medicine between January 2017 and December 2021 were included. Results: A total of 429 patients were enrolled. The serum ChE level was significantly lower in patients with hypercapnia, who required NIV during hospitalization and who had a DoHS of >10 days, with an oxygenation index < 300. The ChE level was correlated negatively with the C-reactive protein level and neutrophil-to-lymphocyte ratio and correlated positively with the serum albumin level. Multivariate logistic regression analysis indicated that a serum ChE level of ≤4116 U/L (OR = 2.857, 95% CI = 1.46-5.58, p = 0.002) was associated significantly with NIV requirement. Conclusions: The serum ChE level was correlated significantly with complicating severe hypoxemia, hypercapnia, prolonged DoHS, and the need for NIV in patients hospitalized with AECOPD. The serum ChE level is a clinically important risk-stratification biomarker in patients hospitalized with AECOPD.

Inspiratory Muscle Dysfunction Mediates and Predicts a Disease Continuum of Hypercapnic Failure in Chronic Obstructive Pulmonary Disease.

INTRODUCTION: Advanced chronic obstructive pulmonary disease (COPD) is associated with chronic hypercapnic failure. The present work aimed to comprehensively investigate inspiratory muscle function as a potential key determinant of hypercapnic respiratory failure in patients with COPD. METHODS: Prospective patient recruitment encompassed 61 stable subjects with COPD across different stages of respiratory failure, ranging from normocapnia to isolated nighttime hypercapnia and daytime hypercapnia. Arterialized blood gas analyses and overnight transcutaneous capnometry were used for patient stratification. Assessment of respiratory muscle function encompassed body plethysmography, maximum inspiratory pressure (MIP), diaphragm ultrasound, and transdiaphragmatic pressure recordings following cervical magnetic stimulation of the phrenic nerves (twPdi) and a maximum sniff manoeuvre (Sniff Pdi). RESULTS: Twenty patients showed no hypercapnia, 10 had isolated nocturnal hypercapnia, and 31 had daytime hypercapnia. Body plethysmography clearly distinguished patients with and without hypercapnia but did not discriminate patients with isolated nocturnal hypercapnia from those with daytime hypercapnia. In contrast to ultrasound parameters and transdiaphragmatic pressures, only MIP reflected the extent of hypercapnia across all three stages. MIP values below -48 cmH2O predicted nocturnal hypercapnia (area under the curve = 0.733, p = 0.052). CONCLUSION: In COPD, inspiratory muscle dysfunction contributes to progressive hypercapnic failure. In contrast to invasive tests of diaphragm strength only MIP fully reflects the pathophysiological continuum of hypercapnic failure and predicts isolated nocturnal hypercapnia.

Hypercapnia Causes Injury of the Cerebral Cortex and Cognitive Deficits in Newborn Piglets.

In critically ill newborns, exposure to hypercapnia (HC) is common and often accepted in neonatal intensive care units to prevent severe lung injury. However, as a "safe" range of arterial partial pressure of carbon dioxide levels in neonates has not been established, the potential impact of HC on the neurodevelopmental outcomes in these newborns remains a matter of concern. Here, in a newborn Yorkshire piglet model of either sex, we show that acute exposure to HC induced persistent cortical neuronal injury, associated cognitive and learning deficits, and long-term suppression of cortical electroencephalogram frequencies. HC induced a transient energy failure in cortical neurons, a persistent dysregulation of calcium-dependent proapoptotic signaling in the cerebral cortex, and activation of the apoptotic cascade, leading to nuclear deoxyribonucleic acid fragmentation. While neither 1 h of HC nor the rapid normalization of HC was associated with changes in cortical bioenergetics, rapid resuscitation resulted in a delayed onset of synaptosomal membrane lipid peroxidation, suggesting a dissociation between energy failure and the occurrence of synaptosomal lipid peroxidation. Even short durations of HC triggered biochemical responses at the subcellular level of the cortical neurons resulting in altered cortical activity and impaired neurobehavior. The deleterious effects of HC on the developing brain should be carefully considered as crucial elements of clinical decisions in the neonatal intensive care unit.

Hypercapnia in hospitalized children and adolescents with anorexia nervosa as a predictive marker for readmission: a prospective study.

PURPOSE: To determine whether hypercapnia is associated with risk of hospital readmission related to anorexia nervosa (AN) in children and adolescents. METHODS: We performed a prospective study of patients ≤ 18 years old admitted due to AN decompensation from November 2018 to October 2019. Both subtypes of AN, restricting subtype (AN-R) and binge-eating/purging subtype (AN-BP), were included. Study participants were evaluated upon admission, at discharge and six months after discharge. T-tests or Mann-Whitney U tests was used to compare means values. Pearson or Spearman correlations were used to measure the association between two variables. Logistic regression models were developed to evaluate the relationship between scoring methods and readmission. RESULTS: Of the 154 persons admitted during the study period, 131 met the inclusion criteria. Median age was 15.1 years. At admission, 71% of participants were malnourished and 33 (25%) had been previously admitted. We observed a marked decrease in venous pH and stable pCO2 elevation during follow-up period. Hypercapnia at discharge was associated with a twofold increased likelihood of readmission and the odds of readmission increased as discharge pCO2 rose. These findings did not depend on AN subtype or participant sex. Electrolytes persisted within the normal range. CONCLUSION: Hypercapnia and respiratory acidosis are common alterations in children and adolescents hospitalized due to AN decompensation. Hypercapnia persists for at least 6 months after discharge despite clinical improvement and is associated with higher odds of readmission. This is the first study to identify an abnormal laboratory finding as a potential predictor of readmission in AN. LEVEL OF EVIDENCE: IV: Multiple time series without intervention.

Ultrastructural Changes in Hippocampal Region CA1 Neurons After Exposure to Permissive Hypercapnia and/or Normobaric Hypoxia.

Isolated exposure to intermittent hypoxia and permissive hypercapnia activates signaling mechanisms that induce ultrastructural changes in mitochondria and endoplasmic reticulum, accompanied by the development of maximal ischemic tolerance in neurons under the combined influence of these factors. However, there are a lack of data on the combined impact of these factors on the ultrastructure of neuronal organelles. The present study aims to comparatively assess the ultrastructural changes in neurons following isolated and combined exposure to hypoxia and hypercapnia, as well as to correlate these changes with the neuroprotective potential previously observed for these factors. Following a 15-session course of 30-min exposures to permissive hypercapnia (PCO2 ≈ 50 mmHg) and/or normobaric hypoxia (PO2 ≈ 150 mmHg), morphometric assessment was conducted to evaluate the extent of ultrastructural changes in hippocampal neurons (mitochondria, perinuclear space, and granular endoplasmic reticulum). It was found that in hippocampal neurons from the CA1 region, permissive hypercapnia resulted in increased mitochondrial size, expansion of membranous compartments of the granular endoplasmic reticulum, and perinuclear space. Normobaric hypoxia affected only mitochondrial size, while hypercapnic hypoxia specifically widened the perinuclear space. These ultrastructural changes objectively reflect varying degrees of the influence of hypoxia and hypercapnia on organelles responsible for energy metabolism, anti-apoptotic, and synthetic functions of neurons. This confirms the effect of potentiation of their neuroprotective effects under combined exposure and highlights the dominant role of the hypercapnic component in this mechanism.

Home high-flow nasal therapy in a patient with pleuroparenchymal fibroelastosis: A case report.

A 62-year-old man with pleuroparenchymal fibroelastosis (PPFE), who had been under observation for 19 years, was admitted due to headache, fatigue, and dyspnea. Although no acute findings were detected, his symptoms were attributed to hypercapnia and exertional hypoxemia. He had a history of pneumothorax, but chose not to undergo positive airway pressure ventilation. Consequently, home high-flow nasal therapy (HFNT) was initiated, and 4 months later, he observed an improvement in his quality of life, body weight gain, and relief from hypercapnia. These outcomes suggested that home HFNT holds potential for improving the quality of life for patients with PPFE.

Lowering PCO2 With Noninvasive Ventilation Is Associated With Improved Survival in Chronic Hypercapnic Respiratory Failure.

BACKGROUND: Chronic hypercapnic respiratory failure is associated with high mortality. Although previous work has demonstrated a mortality improvement with high-intensity noninvasive ventilation in COPD, it is unclear whether a PCO2 reduction strategy is associated with improved outcomes in other populations of chronic hypercapnia. METHODS: The objective of this study was to investigate the association between PCO2 reduction (by using transcutaneous PCO2 as an estimate for PaCO2 and survival in a broad population of individuals treated with noninvasive ventilation for chronic hypercapnia. We hypothesized that reductions in PCO2 would be associated with improved survival. Therefore, we performed a cohort study of all the subjects evaluated from February 2012 to January 2021 for noninvasive ventilation initiation and/or optimization due to chronic hypercapnia at a home ventilation clinic in an academic center. We used multivariable Cox proportional hazard models with time-varying coefficients and PCO2 as a time-varying covariate to test the association between PCO2 and all-cause mortality and when adjusting for known cofounders. RESULTS: The mean ± SD age of 337 subjects was 57 ± 16 years, 37% women, and 85% white. In a univariate analysis, survival probability increased with reductions in PCO2 to < 50 mm Hg after 90 d, and these remained significant after adjusting for age, sex, race, body mass index, diagnosis, Charlson comorbidity index, and baseline PCO2 . In the multivariable analysis, the subjects who had a PaCO2 < 50 mm Hg had a reduced mortality risk of 94% between 90 and 179 d (hazard ratio [HR] 0.06, 95% CI 0.01-0.50), 69% between 180 and 364 d (HR 0.31, 95% CI 0.12-0.79), and 73% for 365-730 d (HR 0.27, 95% CI 0.13-0.56). CONCLUSIONS: Reduction in PCO2 from baseline for subjects with chronic hypercapnia treated with noninvasive ventilation was associated with improved survival. Management strategies should target the greatest attainable reductions in PCO2 .

Hypercapnic respiratory failure - review.

This review summarizes the issue of acute hypercapnic respiratory failure. Acute respiratory failure is a condition in which the respiratory system is unable to fulfill its basic function, i.e. enriching the blood with oxygen and excreting carbon dioxide. Chronologically, we divide it into acute and chronic, and according to the manifestation into hypoxemic or hypoxemic with hypercapnia. Multiple factors, such as reduced ventilation and increased dead space, contribute to the development of hypoxemic-hypercapnic (global) respiratory failure. Both the patient's clinical presentation and laboratory examination of blood gases and acid-base balance (preferably from arterial blood) are used for diagnosis. In the absence of contraindications, non-invasive ventilation is used to establish normocapnia.

Association between prehospital end-tidal carbon dioxide levels and mortality in patients with suspected severe traumatic brain injury.

PURPOSE: Severe traumatic brain injury is a leading cause of mortality and morbidity, and these patients are frequently intubated in the prehospital setting. Cerebral perfusion and intracranial pressure are influenced by the arterial partial pressure of CO2 and derangements might induce further brain damage. We investigated which lower and upper limits of prehospital end-tidal CO2 levels are associated with increased mortality in patients with severe traumatic brain injury. METHODS: The BRAIN-PROTECT study is an observational multicenter study. Patients with severe traumatic brain injury, treated by Dutch Helicopter Emergency Medical Services between February 2012 and December 2017, were included. Follow-up continued for 1 year after inclusion. End-tidal CO2 levels were measured during prehospital care and their association with 30-day mortality was analyzed with multivariable logistic regression. RESULTS: A total of 1776 patients were eligible for analysis. An L-shaped association between end-tidal CO2 levels and 30-day mortality was observed (p = 0.01), with a sharp increase in mortality with values below 35 mmHg. End-tidal CO2 values between 35 and 45 mmHg were associated with better survival rates compared to < 35 mmHg. No association between hypercapnia and mortality was observed. The odds ratio for the association between hypocapnia (< 35 mmHg) and mortality was 1.89 (95% CI 1.53-2.34, p < 0.001) and for hypercapnia (≥ 45 mmHg) 0.83 (0.62-1.11, p = 0.212). CONCLUSION: A safe zone of 35-45 mmHg for end-tidal CO2 guidance seems reasonable during prehospital care. Particularly, end-tidal partial pressures of less than 35 mmHg were associated with a significantly increased mortality.

Impact of Arterial CO2 Retention in Patients With Moderate or Severe ARDS.

BACKGROUND: Lung-protective ventilation (reduced tidal volume and limited plateau pressure) may lead to CO2 retention. Data about the impact of hypercapnia in patients with ARDS are scarce and conflicting. METHODS: We performed a non-interventional cohort study with subjects with ARDS admitted from 2006 to 2021 and with PaO2 /FIO2 ≤ 150 mm Hg. We examined the association between severe hypercapnia (PaCO2 ≥ 50 mm Hg) on the first 5 days after the diagnosis of ARDS and death in ICU for 930 subjects. All the subjects received lung-protective ventilation. RESULTS: Severe hypercapnia was noted in 552 subjects (59%) on the first day of ARDS (day 1); 323/930 (34.7%) died in the ICU. Severe hypercapnia on day 1 was associated with mortality in the unadjusted (odds ratio 1.54, 95% CI 1.16-1.63; P = .003) and adjusted (odds ratio 1.47, 95% CI 1.08-2.43; P = .004) models. In the Bayesian analysis, the posterior probability that severe hypercapnia was associated with ICU death was > 90% in 4 different priors, including a septic prior for this association. Sustained severe hypercapnia on day 5, defined as severe hypercapnia present from day 1 to day 5, was noted in 93 subjects (12%). After propensity score matching, severe hypercapnia on day 5 remained associated with ICU mortality (odds ratio 1.73, 95% CI 1.02-2.97; P = .047). CONCLUSIONS: Severe hypercapnia was associated with mortality in subjects with ARDS who received lung-protective ventilation. Our results deserve further evaluation of the strategies and treatments that aim to control CO2 retention.

Association between rate of change in PaCO2 and functional outcome for patients with hypercapnia after out-of-hospital cardiac arrest: Secondary analysis of a randomized clinical trial.

BACKGROUND: Normocapnia is suggested for post resuscitation care. For patients with hypercapnia after cardiac arrest, the relationship between rate of change in partial pressure of carbon dioxide (PaCO2) and functional outcome was unknown. METHODS: This was the secondary analysis of Resuscitation Outcomes Consortium (ROC) amiodarone, lidocaine, and placebo (ALPS) trial. Patients with at least 2 PaCO2 recorded and the first indicating hypercapnia (PaCO2 > 45 mmHg) after return of spontaneous circulation (ROSC) were included. The rate of change in PaCO2 was calculated as the ratio of the difference between the second and first PaCO2 to the time interval. The primary outcome was modified Rankin Score (mRS), dichotomized to good (mRS 0-3) and poor (mRS 4-6) outcomes at hospital discharge. The independent relationship between rate of change in PaCO2 and outcome was investigated with multivariable logistic regression model. RESULTS: A total of 746 patients with hypercapnia were included for analysis, of which 264 (35.4%) patients had good functional outcome. The median rate of change in PaCO2 was 4.7 (interquartile range [IQR] 1.7-12) mmHg per hour. After adjusting for confounders, the rate of change in PaCO2 (odds ratio [OR] 0.994, confidence interval [CI] 0.985-1.004, p = 0.230) was not associated the functional outcome. However, rate of change in PaCO2 (OR 1.010, CI 1.001-1.019, p = 0.029) was independently associated with hospital mortality. CONCLUSIONS: For OHCA patients with hypercapnia on admission, the rate of change in PaCO2 was not independently associated with functional outcome; however, there was a significant trend that higher decreased rate was associated with increased hospital mortality.

Chronic psychic stress can cause metabolic syndrome through mild hypercapnia.

The author presents a new psychosomatic stress model. All the elements of the hypothesis are well known but, in this context, are published first. The following are the most critical aspects of the recommended chronic stress model. 1/ Stress contains both sympathetic and parasympathetic elements, but the latter predominate. 2/ The mediator of stress is carbon dioxide, the substance that can turn the psyche into soma. 3/ In humans, chronic stress is mainly social; people cause it to each other. Chronic social stress is created frequently due to deviations in civilisation, education and tolerance. 4/ The freeze response (or freezing behaviour) plays a subordinate role in the animal world; it lasts mainly for a maximum of minutes, while in humans, it dominates and can continue for decades. 5/ The decisive step of freeze is apnea, hypopnea, which occurs due to aversive psychological eff ects. After a more extended existence, mild chronic respiratory acidosis develops and most often appears in the clinical form of obstructive sleep apnea. 6/ Chronic hypercapnia can shape the metabolism into metabolic syndrome. 7/ After that, various cardiovascular and metabolic complications (hypertension, atherosclerosis, type 2 diabetes, depression) may develop - partly due to genetic and lifestyle reasons. (Neuropsychopharmacol Hung 2022; 24(3): 126-133).

A comparison between bronchial blockers and double-lumen tubes for patients undergoing lung resection: A propensity score-matched cohort study.

Objective: The aim of this study is to compare the effect of bronchial blockers (BB) and double-lumen tubes (DLT) on patients' postoperative recovery after lung resection. Method: 4,636 patients undergoing lung resection and receiving either BB or DLT intubation were reviewed and matched using the propensity score matching method. The primary outcome was the surgical duration. The secondary outcomes included diagnostic results of postoperative chest X-ray, postoperative oxygenation index, incidence of hypercapnia, hypoxemia and sore throat, chest tube duration, incidence of ICU admission, length of hospital stay and incidence of the 30-day readmission. Results: After matching, 401 patients receiving BB were matched to 3,439 patients receiving DLT. There was no statistical difference on the surgical duration between the two groups (P>0.05). However, compared with the DLT group, patients in the BB group showed more infiltrate especially at the surgery side (14.96% versus 9.07%, P<0.001) based on the chest X-ray, together with higher incidence of ICU admission (5.23% versus 2.61%, P<0.05). Additionally, no statistical differences were found between the two groups about chest tube duration, oxygenation index, incidence of hypercapnia, hypoxemia and sore throat, duration of surgery, hospital stays and 30-day readmission (P>0.05). Conclusions: Compared with the DLT, patients receiving BB technique tend to have increased pulmonary infiltrate (especially the surgery side) and higher incidence of ICU admission at the early post-operative stage, which may have an influence on the patients' recovery.

Ventilatory neural drive in chronically hypercapnic patients with COPD: effects of sleep and nocturnal noninvasive ventilation.

Sleep brings major challenges for the control of ventilation in humans, particularly the regulation of arterial carbon dioxide pressure (P aCO2 ). In patients with COPD, chronic hypercapnia is associated with increased mortality. Therefore, nocturnal high-level noninvasive positive-pressure ventilation (NIV) is recommended with the intention to reduce P aCO2 down to normocapnia. However, the long-term physiological consequences of P aCO2 "correction" on the mechanics of breathing, gas exchange efficiency and resulting symptoms (i.e. dyspnoea) remain poorly understood. Investigating the influence of sleep on the neural drive to breathe and its translation to the mechanical act of breathing is of foremost relevance to create a solid rationale for the use of nocturnal NIV. In this review, we critically discuss the mechanisms by which sleep influences ventilatory neural drive and mechanical consequences in healthy subjects and hypercapnic patients with advanced COPD. We then discuss the available literature on the effects of nocturnal NIV on ventilatory neural drive and respiratory mechanics, highlighting open avenues for further investigation.

Relationship Between Episodic Nocturnal Hypercapnia and History of Exacerbations in Patients with Advanced Chronic Obstructive Pulmonary Disease.

Purpose: An episodic increase in transcutaneous carbon dioxide pressure (PtcCO2) is often recognized in patients with advanced chronic obstructive pulmonary disease (COPD) by overnight PtcCO2 monitoring. This phenomenon, called episodic nocturnal hypercapnia (eNH), mainly corresponds to rapid eye movement (REM) sleep-related hypoventilation. However, it is unclear whether eNH is associated with the frequency of COPD exacerbation. We aimed to investigate whether a relationship exists between COPD exacerbation and eNH. Patients and Methods: We enrolled consecutive patients with stable, severe, or very severe COPD with a daytime arterial carbon dioxide pressure (PaCO2) <55.0 mmHg who underwent overnight PtcCO2 monitoring from April 2013 to January 2017. We retrospectively analyzed the prevalence of eNH and sleep-associated hypoventilation (SH) as defined by the American Academy of Sleep Medicine. Moreover, we compared the relationship between the frequency of COPD exacerbations in the previous year and eNH or SH. Results: Twenty-four patients were included in this study. The study patients had a mean daytime PaCO2 and nocturnal PtcCO2 of 43.3 ± 6.8 mmHg and 42.9 ± 9.6 mmHg, respectively. Six (25.0%) and 11 (45.9%) of the 24 patients met the SH and eNH criteria, respectively. The odds ratios of SH and eNH for at least one annual exacerbation were 1.0 [95% confidence interval (CI): 0.16-6.00] and 11.1 [95% CI: 1.39-87.7], respectively. The odds ratios of SH and eNH for at least two annual exacerbations were 0.3 [95% CI: 0.04-2.64] and 6.6 [95% CI: 1.06-39.4], respectively. Conclusion: In patients with advanced COPD and a daytime PaCO2 <55.0 mmHg, eNH may be associated with a history of more frequent exacerbations than SH. Further studies are required to validate these findings.

Leptin-mediated neural targets in obesity hypoventilation syndrome.

Obesity hypoventilation syndrome (OHS) is defined as daytime hypercapnia in obese individuals in the absence of other underlying causes. In the United States, OHS is present in 10%-20% of obese patients with obstructive sleep apnea and is linked to hypoventilation during sleep. OHS leads to high cardiorespiratory morbidity and mortality, and there is no effective pharmacotherapy. The depressed hypercapnic ventilatory response plays a key role in OHS. The pathogenesis of OHS has been linked to resistance to an adipocyte-produced hormone, leptin, a major regulator of metabolism and control of breathing. Mechanisms by which leptin modulates the control of breathing are potential targets for novel therapeutic strategies in OHS. Recent advances shed light on the molecular pathways related to the central chemoreceptor function in health and disease. Leptin signaling in the nucleus of the solitary tract, retrotrapezoid nucleus, hypoglossal nucleus, and dorsomedial hypothalamus, and anatomical projections from these nuclei to the respiratory control centers, may contribute to OHS. In this review, we describe current views on leptin-mediated mechanisms that regulate breathing and CO2 homeostasis with a focus on potential therapeutics for the treatment of OHS.

A Study of Cardiac Troponin T Levels in Acute Exacerbation of Copd and its Correlation with Severity.

Chronic obstructive pulmonary disease (COPD) is a significant health burden and is one of the leading causes of death having rising mortality rate in developed and developing countries. Cardiac troponin t (cTnT) is an established myocardial injury marker and not only increases in flow- limiting coronary artery stenosis or occlusion of coronary arteries but also in pulmonary embolism, septic shock, heart failure and stroke. The positive association between elevation of cTnT and neutrophils due to exaggerated inflammatory response leading to myocardial injury and increased cTnT can have prognostic value in acute exacerbation of COPD. Material: The present study was conducted with the aim of predicting the severity of COPD exacerbation based on level of cardiac TnT. 85 patients with a diagnosis of COPD age more than 20 years admitted in general medicine wards in SMS medical college during 2020 were enrolled in this study. Spirometry and Chest Xray were used in diagnosing COPD. Troponin T level was measured within 1 hour of admission. Severity of the exacerbation was estimated by PaO2 & PaCO2 levels and need for assisted ventilation. Observation: Here, in our study 43.53% cases has troponin-T elevated. And amongst those with Trop T elevated 82.4% needed assisted ventilation compared to 24.6 % patients with normal Trop T needing assisted ventilation indicating significant positive correlation of Trop t level with need for assisted ventilation in acute exacerbation of COPD. Amongst those with elevated Trop T, mean oxygen saturation was77.97 % and mean pco2 was 73%. Whilst those with normal troponin T level they had mean oxygen saturation of 86% and mean co2 level of 42% indicating that those with elevated cardiac Trop T has more severe hypoxia and more severe hypercapnia compared to those with normal cardiac Trop T level implying significant positive association of elevated Trop T level with severity of COPD exacerbation Conclusion: This observation implies there is a positive correlation of elevated trop T level and severity of acute exacerbation of COPD in terms of need for assisted ventilation, severity of hypoxia and hypercapnia .So assessment of Trop T level in acute exacerbation of COPD will be having prognostic benefit and can be used for assessing course of the disease along with better management of the patients.

Baseline Level and Reduction in PaCO2 are Associated with the Treatment Effect of Long-Term Home Noninvasive Positive Pressure Ventilation in Stable Hypercapnic Patients with COPD: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

Purpose: The evidence of long-term home noninvasive positive pressure ventilation (LTHNIPPV) in patients with stable hypercapnic chronic obstructive pulmonary disease (COPD) is controversial. In this meta-analysis study, we sought to establish whether a baseline level and reduction in partial pressure of arterial carbon dioxide (PaCO2) were associated with the treatment effect of LTHNIPPV in these patients. Patients and Methods: Six electronic databases were comprehensively searched from January 1980 until June 2020. Randomized clinical trials (RCTs) comparing LTHNIPPV with control treatment were included. Two authors independently extracted data, assessed the study quality, and used the GRADE approach to evaluate evidence quality. The main outcome was mortality. Results: Nineteen studies involving 1482 patients (LTHNIPPV, n = 730; control, n = 752) were included. LTHNIPPV significantly reduced mortality (relative risk [RR] = 0.76; 95% confidence interval [CI]: 0.61-0.95; p = 0.02; I2 = 14%), the frequency of hospital admissions, PaCO2, and improved partial pressure of oxygen (PaO2) compared to control treatment. LTHNIPPV also relieved dyspnea and improved exercise capacity and health-related quality of life (HRQL) but showed no significant benefit for improving the forced expiratory volume in one second in predicted (FEV1% pred). Subgroup analysis revealed that the baseline level and reduction in PaCO2 were associated with decreased mortality (baseline PaCO2 ≥ 55 mmHg RR = 0.69, P = 0.02; vs baseline PaCO2 < 55 mmHg RR = 0.87, P = 0.32; and higher dPaCO2 RR = 0.42, P < 0.0001; vs lower dPaCO2 RR = 0.91, P = 0.38). Conclusion: LTHNIPPV significantly reduced mortality. The baseline level and reduction in PaCO2 were associated with the treatment effect of LTHNIPPV in patients with stable hypercapnic COPD. Large-scale, multicenter RCTs are needed to confirm our results.

The difference in clinical features and prognosis of severe adenoviral pneumonia in children of different ages.

This study aims to analyze the difference in clinical features and prognosis of severe adenovirus pneumonia (SAP) in children of different ages and analyze the risk factors for poor prognosis in children with SAP. A retrospective observational study was performed to describe the clinical features and analyze the risk factors for death and postinfectious bronchiolitis obliterans (PIBO) in 303 children hospitalized with SAP from January 2015 through to January 2020. The participants were divided into four age groups: <6 months (n = 25, 8.3%); 6-12 months (n = 98, 32.3%); 12-36 months (n = 118, 38.9%); and >36 months (n = 62, 20.5%). Fever rate, peak, and duration were the lowest in the <6 months group, while no significant difference was found among other age groups. Serum levels of lactate dehydrogenase and a load of adenovirus were the lowest in the <6 months group, and the highest in the 6-12 and 12-36 months groups, respectively. A total of 80.9% of patients recovered, 3.3% of patients died, and 15.8% of patients were diagnosed with PIBO. The mortality rate showed no significance between age groups. The >36 months group had the highest recovery rate and the lowest incidence of PIBO, while the 6-12 months group had the lowest recovery rate and the highest incidence of PIBO. Independent risk factors for PIBO among all participants from the four groups were invasive mechanical ventilation, administration of intravenous steroids, duration of fever, and male gender. Independent risk factors for death among all participants from the four groups were hypercapnia, low albumin levels, and invasive mechanical ventilation. Risk factor analysis of different ages was not possible due to the limited sample size. The morbidity, clinical features, and prognosis of SAP are affected by children's ages. Pediatric patients with a longer duration of fever, hypercapnia, low serum albumin levels, invasive mechanical ventilation, and intravenous steroids use are more likely to develop a poor prognosis in SAP, especially if the patient is male.