Sequential Effects of Acute Meconium Obstruction on Pulmonary Function

Abstract

SummaryThe relationship between pulmonary function and the migration of meconium to distal airways was determined in 10 rabbits (mean weight 2.6 kg) after insumation of a meconium-saline mixture (1-2 ml/kg). Animals were anesthetized, cannulated, intubated, and mechanically ventilated with 100% oxygen. Lung mechanical dysfunction was most severe during the early phase of meconium migration, 15 min postinsumation. Substantial increases in inspiratory lung resistance (RI) and expiratory lung resistance (RE) suggest that the site of obstruction at 15 min was the large airways. A decrease in dynamic lung compliance with unchanged static compliance characterizes the obstruction as partial. At 15 min and thro&hout the migration process, RE was greater than RI, demonstrating a check-valve effect. This phenomenon was substantiated by an increased functional residual capacity (FRC) in all rabbits, presumably due to gas trapping. Secondary to these changes, marked hypoxemia, hypercapnea, and acidosis developed in spite of assisted ventilation with 100% oxygen. At 60 and 120 min postinsufflation, both RI and RE decreased as compared to 15 min. This suggests that the predominant site of obstruction shifted to medium and small airways concomitant with the migration of meconium. Widespread and uneven distribution of meconium still produced significant frequency dependence of lung compliance. Static compliance remained unchanged, indicating that meconium !nnsylvania, USA ing the pathologic process of meconium aspiration have been conducted (I, 10, 11, 19, 21,22). Results have shown that whereas the irritating action of meconium on the pulmonary parenchyma might initiate a chemical or bacterial pneumonitis (4, 21), the importance of inflammation with regard to severe respiratory dysfunction may not be great (1 1). Rather, mechanical airway obstruction by particles of meconium has been shown to play the most important role in the early pathophysiology of MAS (21).Evidence for obstruction and migration of meconium has been supported by roentgenographic methods, where Gooding et a/.(10) demonstrated that tantalum-labeled meconium was cleared from the trachea and mainstem bronchi within 1 hr and migrated progressively into the lung periphery with breathing. Whereas physiologic effects of obstruction on lung function have been studied (2,8,12,15,24), little data are available on pulmonary mechanics in animals or infants with acute meconium obstruction. Because of the migration properties of meconium, the physiologic resnonse of obstructive ~henomena in general cannot be extrapo l i e d to the pathophysi~logy of p u l m o~r y function in meconium aspiration. The purpose of this study is to determine the sequential physiologic efficts bf acute meconium obstruction on pulmonary function as they vary with the migration of meconium to the distal airways. Such data will provide further insight into the pathophysiology and respiratory management of infants with MAS.does not affect surface-active or tissue propries of the lung within 120 ...

Surfactant inhibition in experimental meconium aspiration

“…Tran et al (1 1) instilled large amounts of meconium into the airways of adult rabbits and noticed decreased dynamic compliance during artificial ventilation, but static compliance (determined from pressure-volume recordings) was not influenced. Our results, as well as recent data from in-vitro experiments reported by others (1 5), indicate that the establishment of very low alveolar surface tension at end-expiration-a prerequisite for successful neonatal lung adaptation-might be disturbed by aspiration of meconium at birth. We found that meconium inhibited surfactant function in a concentration-dependent manner both in the pulsatingbubble and in the Wilhelmy-balance system, as indicated by delayed film adsorption and elevated values for minimum and maximum surface tension during cyclic film compression.…”

“…Meconium aspiration syndrome occurs mainly in term and post-term newborn infants, usually as a consequence of intrauterine asphyxia triggering both passage of meconium into the amniotic cavity and fetal gasping (1). Despite recent improvements in immediate postpartum care, including suctioning of the airways and assisted ventilation, intrauterine aspiration of large amounts of meconium remains associated with high mortality (2-4).…”

Tidal Volume Requirement in Mechanically Ventilated Infants with Meconium Aspiration Syndrome

“…The heterogeneous aeration and increased functional residual capacity (FRC) seen in MAS may lead to increased alveolar dead space. [2][3][4][5][6] Optimal ventilatory strategy for MAS would avoid/treat pulmonary hypertension and at the same time avoid overventilation of lungs already at risk for overdistention and air leak. It has been demonstrated that volume, rather than pressure, is the important determinant of lung injury 7 and volume targeted ventilation is being increasingly used to ventilate newborn infants.…”

Meconium aspiration induces ARDS-like pulmonary response in lungs of ten-week-old pigs

“…The acute detrimental effects of meconium aspiration on lung function have been well described in many animal models, including the pig, but experimental hemodynamic studies are sparse. [3][4][5][13][14][15][16] Meconium aspiration has been shown to induce pulmonary hypertension in rabbits. 3 Despite a tendency toward increased right ven-tricular systolic pressures, it did not produce significant pulmonary hypertension in prematurely born baboons.…”

“…The fatal outcome is frequently associated with persistent pulmonary hypertension, which further contributes to the hemodynamic and respiratory dysfunction. 2 The pathophysiology of the lung injury is still unclear, although hypoxemia, 3,4 pulmonary inflammation, 3,5 surfactant dysfunction, 6 and imbalance in pulmonary vasoregulation 7 have been considered as contributing factors.…”