Obesity and Acute Lung Injury
Section snippets
Pulmonary physiology in obesity and implications for patients with acute lung injury
The most significant change in pulmonary mechanics seen in obesity is a decrease in pulmonary compliance,6 which has been attributed to one of several factors: fatty infiltration of the chest wall, increased pulmonary blood volume, and extrinsic compression of the thoracic cage by weight from excess soft tissue.6, 7, 8, 9 As a result, obese subjects exhibit an increased work of breathing6, 10 and may note a subjective increase in dyspnea.11 In addition, respiratory resistance has been shown to
Pathophysiology of acute lung injury and the possible role of obesity
A full description of the pathophysiology of ALI/ARDS is beyond the scope of the current review and the reader is directed to recent reviews for further details.2, 39 In brief, in ALI/ARDS imbalances occur between pro- and anti-inflammatory cytokines, oxidants and antioxidants, and coagulation factors. Alterations in neutrophil activation, recruitment, and clearance and release of proteases also are important. The net result of these changes is alveolar filling with proteinaceous fluid,
Adipocytokines and acute lung injury/acute respiratory distress syndrome
In addition to classic cytokines, adipose tissue releases adipocytokines that act as mediators of subsequent proinflammatory and anti-inflammatory pathways.54 Although there are a number of known adipocytokines, of primary importance are leptin and adiponectin.54 Leptin is a polypeptide hormone secreted by adipocytes that is elevated in states of obesity and functions as a mediator of energy balance.61 It is secreted mainly by adipose tissue and meant to signal adequate stores of energy and
Obesity and outcomes from acute lung injury
Although a number of studies explore the association between obesity and outcome for critically ill adults (see article in this issue by Honiden and McArdle), few articles have focused specifically on patients with ALI/ARDS (Table 2). The first such study77 reported a secondary analysis of patients enrolled in the National Heart, Lung and Blood Institute's (NHLBI) multicenter, randomized trials of the Acute Respiratory Distress Syndrome Network.80, 81, 82 These studies included comparisons of
Obesity as a risk factor for acute lung injury and multiorgan failure in at-risk patients
Because of changes in physiology and inflammation associated with excess weight, it is conceivable that obese patients might be at greater risk for ALI/ARDS when suffering a predisposing acute event, such as sepsis or trauma. One of the earliest studies exploring an association between obesity and outcome among the critically ill reviewed data from 184 patients admitted to a trauma service over 6 months.84 In this study, mortality was significantly higher in patients with a BMI greater than 31
Measures of Excess Weight and the Heterogeneity of Obesity
Existing studies of excess weight and ALI have examined BMI as the only measure of excess weight. Although this measure is highly reliable and associated with adult body fat in ambulatory patients,87 BMI might not be the best representation of risk (or benefit) for critically ill patients. For example, the distribution of excess weight may have particular relevance for mechanically ventilated patients kept in a supine or semi-supine position.88 In selected epidemiologic studies, waist
Summary
ALI/ARDS is a common cause of acute respiratory failure with a high mortality rate. Although current data are premature, obesity and ALI/ARDS appear to share alterations in inflammation, endothelial dysfunction, and oxidative stress. This raises the possibility that obese patients may be at higher risk of developing ALI/ARDS and have poorer outcomes from ALI/ARDS. However, data supporting such an association are inconclusive. Additionally, obese ALI/ARDS patients may receive different care than
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Correlation between levels of adipokines and inflammatory mediators with spirometric parameters in individuals with obesity and symptoms of asthma: Cross-sectional study
2022, PulmonologyCitation Excerpt :In addition to inflammatory alterations, inflammatory cytokines act on the lung which causes lung function impairment. Such changes are evidenced in the literature by the reduction of Forced Expiratory Volume in the First Second (FEV1), Functional Residual Capacity (FRC), Forced Expiratory Flow in 25–75% (FEF25–75%) and increase in FEV1/FVC (Forced Vital Capacity) ratio.5,13,14 Thus, the aim of the present study was to correlate adipokines levels and inflammatory mediators with lung function in individuals with obesity and bronchial asthma symptoms.
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2022, Pharmacological ResearchCitation Excerpt :Additionally, increased inflammation and disordered metabolism in obese patients always increase ALI risk [59]. The adipose tissues explosively spread surrounding the pulmonary artery increases the susceptibility to pulmonary arterial hypertension, which is the critical pathological stage in chronic obstructive pulmonary disease [85]. Moreover, obesity changes the airway geometry, especially decreasing expiratory reserve volume and facilitating the progress of asthma [14].
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