Aspiration pneumonias: under-diagnosed and under-treated

Afshar, Kamyar

doi:10.1097/mcp.0b013e3280f629f0

Cited by 39 publications

(18 citation statements)

References 63 publications

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“…16 Decreased salivary clearance and poor oral hygiene likely contribute to this development. 9 Impaired cough reflex and immune defense, not uncommon in the elderly, are additional factors that promote the development of pneumonia aft er aspiration of pathologic microbes.…”

Section: Pathophysiologymentioning

confidence: 99%

“…Videofl uoroscopic swallow study (performed by a speech therapist or radiologist) is generally considered to be the procedure of choice and should assess oral, pharyngeal, and esophageal phases. 9,12,17 Other methods of evaluation include fi ber-optic nasoendoscopy, motility testing, and upper GI endoscopy. Endoscopy with biopsy and ambulatory pH monitoring are useful in confi rming GERD.…”

Section: Diagnostic Evaluationmentioning

confidence: 99%

“…3,4 Although aspiration generally triggers coughing, it can be silent, causing diffi culties in recognizing aspiration as the cause of undiagnosed respiratory diseases. [5][6][7][8][9][10] For example, aspiration was suspected clinically in only 9% of 59 patients in whom aspiration was confi rmed on lung biopsy. 11 Aspiration syndromes, such as airway obstruction from an inhaled foreign body, aspiration pneumonitis, and aspiration pneumonia, are well recognized.…”

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confidence: 98%

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Aspiration-Related Pulmonary Syndromes

Lee

Pianosi

et al. 2015

Chest

130

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Section: Pathophysiologymentioning

confidence: 99%

Section: Diagnostic Evaluationmentioning

confidence: 99%

mentioning

confidence: 98%

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Aspiration-Related Pulmonary Syndromes

Lee

Pianosi

et al. 2015

Chest

130

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“…A lcohol abuse is associated with a variety of health problems (e.g., liver diseases and cancer), and alcoholics have an increased risk for serious infectious complications, such as pulmonary and gut bacteria-associated infections (1)(2)(3)(4)(5). The majority of the causative pathogens in these infections in alcoholics are microbes normally found in the upper respiratory tracts (staphylococci, Klebsiella) and the upper and lower intestine (enterococci, Clostridium, Pseudomonas) (3-6).…”

Section: Cd14mentioning

confidence: 99%

M2b Monocytes Provoke Bacterial Pneumonia and Gut Bacteria–Associated Sepsis in Alcoholics

Tsuchimoto

Asai

Tsuda

et al. 2015

The Journal of Immunology

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Chronic alcohol consumption markedly impairs host antibacterial defense against opportunistic infections. γ-irradiated NOD-SCID IL-2Rγnull mice inoculated with nonalcoholic PBMCs (control PBMC chimeras) resisted Klebsiella pneumonia and gut bacteria-associated sepsis, whereas the chimeras created with alcoholic PBMCs (alcoholic PBMC chimeras) were very susceptible to these infections. M1 monocytes (IL-12+IL-10−CD163−CD14+ cells), major effector cells in antibacterial innate immunity, were not induced by a bacterial Ag in alcoholic PBMC cultures, and M2b monocytes (CCL1+CD163+CD14+ cells), which predominated in alcoholic PBMCs, were shown to be inhibitor cells on the Ag-stimulated monocyte conversion from quiescent monocytes to M1 monocytes. CCL1, which functions to maintain M2b macrophage properties, was produced by M2b monocytes isolated from alcoholic PBMCs. These M2b monocytes reverted to quiescent monocytes (IL-12−IL-10−CCL1−CD163−CD14+ cells) in cultures supplemented with CCL1 antisense oligodeoxynucleotide, and the subsequent quiescent monocytes easily converted to M1 monocytes under bacterial Ag stimulation. Alcoholic PBMC chimeras treated with CCL1 antisense oligodeoxynucleotide were resistant against pulmonary infection by K. pneumoniae and sepsis stemming from enterococcal translocation. These results indicate that a majority of monocytes polarize to an M2b phenotype in association with alcohol abuse, and this polarization contributes to the increased susceptibility of alcoholics to gut and lung infections. Bacterial pneumonia and gut bacteria-associated sepsis, frequently seen in alcoholics, can be controlled through the polarization of macrophage phenotypes.

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“…Large aspirations cause severe lung inflammation, leading to acute lung injury (ALI) that associates with high mortality and morbidity (21). Mild aspirations prime the lung for secondary pneumonitis (30,34). No specific treatment is available for acid-induced ALI.…”

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confidence: 99%

Acid contact in the rodent pulmonary alveolus causes proinflammatory signaling by membrane pore formation

Westphalen

Monma

Islam

et al. 2012

American Journal of Physiology-Lung Cellular and Molecular Phys

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Westphalen K, Monma E, Islam MN, Bhattacharya J. Acid contact in the rodent pulmonary alveolus causes proinflammatory signaling by membrane pore formation. Am J Physiol Lung Cell Mol Physiol 303: L107-L116, 2012. First published May 4, 2012 doi:10.1152/ajplung.00206.2011Although gastric acid aspiration causes rapid lung inflammation and acute lung injury, the initiating mechanisms are not known. To determine alveolar epithelial responses to acid, we viewed live alveoli of the isolated lung by fluorescence microscopy, then we microinjected the alveoli with HCl at pH of 1.5. The microinjection caused an immediate but transient formation of molecule-scale pores in the apical alveolar membrane, resulting in loss of cytosolic dye. However, the membrane rapidly resealed. There was no cell damage and no further dye loss despite continuous HCl injection. Concomitantly, reactive oxygen species (ROS) increased in the adjacent perialveolar microvascular endothelium in a Ca 2ϩ -dependent manner. By contrast, ROS did not increase in wild-type mice in which we gave intraalveolar injections of polyethylene glycol (PEG)-catalase, in mice overexpressing alveolar catalase, or in mice lacking functional NADPH oxidase (Nox2). Together, our findings indicate the presence of an unusual proinflammatory mechanism in which alveolar contact with acid caused membrane pore formation. The effect, although transient, was nevertheless sufficient to induce Ca 2ϩ entry and Nox2-dependent H2O2 release from the alveolar epithelium. These responses identify alveolar H2O2 release as the signaling mechanism responsible for lung inflammation induced by acid and suggest that intra-alveolar PEG-catalase might be therapeutic in acid-induced lung injury.calcium; hydrogen peroxide; nitric oxide synthase 2; nitric oxide; reactive oxygen species; catalase; flash photolysis; resealing; clodronate THE GASTRIC AND THE PULMONARY epithelial surfaces are potentially exposed to highly concentrated HCl. The gastric epithelium secretes the acid at pH 1-2; the pulmonary epithelium encounters the acid following aspiration of gastric contents. Although a 200-m-thick mucus layer protects the gastric epithelium from acid injury (4), the much thinner layer of surfactant (6) is likely to provide relatively little protection to alveoli. Large aspirations cause severe lung inflammation, leading to acute lung injury (ALI) that associates with high mortality and morbidity (21). Mild aspirations prime the lung for secondary pneumonitis (30,34). No specific treatment is available for acid-induced ALI.An unsolved problem in the understanding of acid-induced ALI relates to the question of how the injury initiates following the first contact of acid with the alveolar membrane. Particularly lacking is the absence of studies defining the immediate alveolar response to the acid contact. Although animal studies confirm that airway instillation of highly concentrated acid (pH Ͻ2) causes ALI, these studies have largely focused on lung responses occurring well after the injury has alread...

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Aspiration pneumonias: under-diagnosed and under-treated

Cited by 39 publications

References 63 publications

Aspiration-Related Pulmonary Syndromes

Aspiration-Related Pulmonary Syndromes

M2b Monocytes Provoke Bacterial Pneumonia and Gut Bacteria–Associated Sepsis in Alcoholics

Acid contact in the rodent pulmonary alveolus causes proinflammatory signaling by membrane pore formation

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