Meconium aspiration syndrome (MAS) is a commonly encountered problem in neonates. Meconium is the viscous green material found in the fetal gastrointestinal tract from approximately the tenth week of gestation. Meconium is composed of a mixture of bile, bile acids, mucous, pancreatic secretions and cellular debris (Wiswell 1993). Approximately 10 ‐ 15% of pregnancies are complicated by the passage of meconium around the time of delivery (Wiswell 1993). An adverse intrauterine environment compromising fetal well being can lead to meconium stained amniotic fluid (MSAF) (Ahanya 2005). "Meconium aspiration syndrome" is defined as respiratory distress with compatible chest roentgenographic findings in an infant born through MSAF, whose symptoms cannot be otherwise explained (Wiswell 1990). Despite current interventions such as intubation with tracheal suction, it is estimated that 5 ‐ 12% of infants born through MSAF develop MAS (Wiswell 2000). An estimated 25,000 to 30,000 cases and 1,000 deaths related to MAS occur annually in the United States (Gelfand 2004).

The clinical features of MAS include tachypnea, retractions, grunting and/or cyanosis with or without the radiological features of aspiration pneumonia. The radiological features of MAS consist of areas of atelectasis and consolidation, along with regions of hyperexpansion. Histologically, a significant inflammatory reaction with a diffuse pulmonary infiltrate of polymorphonuclear leukocytes has been observed (Burgess 1996). Although initially sterile, meconium can get secondarily colonized with bacteria following rupture of membranes in utero (Florman 1969) or during neonatal interventions like endotracheal intubation.

Some of the proposed explanations for the widespread use of antibiotics in patients with MAS are the difficulty in radiological differentiation between aspiration pneumonia and bacterial pneumonia (Lee 2004), the possibility of meconium induced inhibition of phagocytic activity and respiratory burst response by alveolar macrophages rendering infants with MAS susceptible to pulmonary infections (Craig 2005), in vitro enhancement of bacterial growth in the presence of meconium in amniotic fluid (Lembet 2003, Florman 1969), the combination of meconium and bacteria aggravating in vivo inflammatory response (Speer 1998), the likelihood of fetal bacterial infection in the causation of in utero meconium passage (Bortolucci 1990; Blot 1983) and apprehension about complications associated with untreated bacterial pneumonia (Wiswell 1992). Several authors have reported increased rates of chorioamnionitis associated with MSAF (Romero 1991; Mazor 1995; Usta 1995; Rao 2001), although it is unclear whether chorioamnionitis is a cause or secondary effect of meconium passage. In a retrospective study of 215 well term babies born through MSAF (of whom 88 patients required tracheal meconium aspiration at birth), no significant difference in the incidence of culture positive sepsis [1 (1.1%) vs 2 (1.6%), p > 0.05] was reported when compared with 127 control infants not requiring tracheal suctioning of meconium passage (Krishnan 1995). The administration of intravenous Ampicillin‐ Sulbactam therapy or cefazolin infusion into the amniotic cavity during amnioinfusion in mothers with MSAF has not shown to be of any benefit in reducing neonatal sepsis (Adair 1996; Edwards 1999). The widespread use of antibiotics in neonates is of some concern (CDC 2004). Excessive use of antibiotics in the neonatal units can lead to emergence of resistant bacterial strains (Tom‐Revzon 2004). Nephrotoxicity has been reported even after brief periods of antibacterial treatment in newborns (Fanos 1999). Ototoxicity has been reported in neonates following aminoglycoside treatment (McCracken 1986). The role of antibiotics in infants born through MSAF has not been systematically evaluated.