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Aspiration Syndrome (aspiration + syndrome)

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Medical Sciences	100%

Selected Abstracts

Aspiration syndromes: 10 clinical pearls every physician should know

INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 5 2007
H. S. Paintal
Summary Aspiration syndromes are clinically and pathologically classified into three sets of disorders: (i) large airway mechanical obstruction caused by foreign bodies; (ii) aspiration pneumonitis; and (iii) aspiration pneumonia. In this article, we discuss the common clinical presentations, risk factors, radiographic features and methods of management of these disorders. We highlight recent recommendations and controversies surrounding the prevention of aspiration pneumonia in the critically ill patient. Finally, we review ethical dilemmas surrounding feeding and aspiration risk concerns in debilitated and demented patients. [source]

Meconium aspiration syndrome: a role for phospholipase A2 in the pathogenesis?

ACTA PAEDIATRICA, Issue 4 2001
P KääpäArticle first published online: 2 JAN 200
The pathophysiology of neonatal meconium aspiration syndrome (MAS), often resulting in severe respiratory failure, is complex and still largely unclear. Factors involved in the propagation of acute lung injury after perinatal aspiration of meconium include obstruction of the airways, ventilation/perfusion mismatch, increase of the pulmonary vascular resistance and a rapidly developing parenchymal and alveolar inflammatory reaction with associated surfactant dysfunction. Conclusion: Although the early pulmonary inflammatory response is believed to play a central pathogenetic role in the meconium-induced acute lung damage, its initiating mechanisms are still poorly defined. However, increasing evidence indicates a direct toxic effect of meconium. [source]

Phospholipase A2 is present in meconium and inhibits the activity of pulmonary surfactant: an in vitro study

ACTA PAEDIATRICA, Issue 4 2001
AJJ Schrama
Atelectasis, a major contributor to pulmonary dysfunction in meconium aspiration syndrome (MAS), is produced by bronchiolar obstruction and surfactant inactivation. It has been shown that substances in meconium, e.g. fatty acids, inhibit surfactant activity. However, the role of the enzyme phospholipase A2 (PLA2), which hydrolyses surfactant in adult respiratory distress syndrome (ARDS), has not yet been studied. Our objective was to investigate whether PLA2 is present in meconium and inhibits pulmonary surfactant activity in vitro. Therefore, the presence of PLA2 activity in meconium, collected from 10 newborns, was measured by the formation of lysophosphatidylcholine after incubation of meconium with radioactively labelled dipalmitoylphosphati-dylcholine. Meconium was fractionated by Sephadex G-100 column chromatography and the fractions were assayed for PLA2 activity. Also, their effect on the surface tension of surfactant (Curosurf) was measured using a pulsating bubble surfactometer (PBS). PLA2 activity was present in all meconium samples. Addition of meconium to surfactant significantly increased surface tension (mean ± SD: 17 ± 1.6 mN/m to 24.3 ± 6.7 mN/m, p= 0.0001) and only the addition of the PLA2 containing fraction from meconium to surfactant also significantly increased surface tension (mean 1.7 ± 1.6mN/m to 19.0 ± 3.58 mN/m, p < 0.0001). Conclusion: PLA2 is present in meconium and inhibits the activity of pulmonary surfactant in vitro. Therefore, PLA2 in meconium may contribute to surfactant inactivation and alveolar ateectasis in MAS. [source]

Overcoming surfactant inhibition with polymers

ACTA PAEDIATRICA, Issue 12 2000
PA Dargaville
Inhibition of the function of pulmonary surfactant in the alveolar space is an important element of the pathophysiology of many lung diseases, including meconium aspiration syndrome, pneumonia and acute respiratory distress syndrome. The known mechanisms by which surfactant dysfunction occurs are (a) competitive inhibition of phospholipid entry into the surface monolayer (e.g. by plasma proteins), and (b) infiltration and destabilization of the surface film by extraneous lipids (e.g. meconium-derived free fatty acids). Recent data suggest that addition of non-ionic polymers such as dextrano and polyethylene glycol to surfactant mixtures may significantly improve resistance to inhibition. Polymers have been found to neutralize the effects of several different inhibitors, and can produce near-complete restoration of surfactant function. The anti-inhibitory properties of polymers, and their possible role as an adjunct to surfactant therapy, deserve further exploration. [source]

Corticosteroid treatment in meconium aspiration syndrome: a solution for better outcome?

ACTA PAEDIATRICA, Issue 1 2004
P KääpäArticle first published online: 2 JAN 200
Corticosteroid treatment in severe meconium aspiration syndrome may afford, especially if started early, some improvement in oxygenation, lung function and pulmonary haemodynamics during the acute phase of the disorder. Still, the effects of corticosteroids on lung tissue perturbations and outcome of diseased infants remain unclear. Conclusion: Further research is needed to determine the clinical significance and optimal timing and dosing of corticosteroid treatment in severe meconium aspiration syndrome. [source]

Efficacy of three treatment schedules in severe meconium aspiration syndrome

ACTA PAEDIATRICA, Issue 1 2004
MD Salvia-Roigés
Aim: To compare three different schedules in severe meconium aspiration syndrome (MAS) treatment: standard, bronchoalveolar lavage (BAL) with diluted surfactant, and diluted surfactant BAL plus a single early dexamethasone dose. Methods: Twenty-four full-term newborns with severe MAS (needing mechanical ventilation and with oxygenation index ± 15) were divided into three groups: group I (historical control group; n= 6) treated with standard therapy; group II (n= 7) treated in the first hours of life with one BAL using diluted surfactant (beractant 5 mg/mL) in a volume of 15 mL/kg in four aliquots; and group III (n = 11) treated with one diluted surfactant BAL and a previous single dose of intravenous dexamethasone (0.5 mg/kg) Results: At 12h, groups II and III showed a significant improvement in oxygenation index (OI) compared with group I (14.7% and 27.0% vs , 19.6% respectively; p= 0.012). Group III also showed a significantly lower OI than group I at 24 h (63.6% vs , 27.9%) and at 48 h (87.1% vs 49.6%). Group III, in comparison to group I, showed a lower FiO2 requirement at 12 h (0.66 vs 1), at 24 h (0.4 vs 0.87) and at 48 h (0.35 vs 0.67), and a decrease in the number of days of inhaled nitric oxide administration, mechanical ventilation, oxygen therapy and hospitalisation period. All patients from groups II and III survived and none developed pneumothorax or respiratory infections. Conclusion: Diluted surfactant BAL in the first hours of life combined with an intravenous single dose of dexamethasone may be an effective treatment for severe MAS. [source]