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PubMed1996

Amniotic fluid meconium: a fetal environmental hazard.

OBJECTIVE: To investigate the hypothesis that meconium aspiration syndrome, the major hazard of meconium during labor, may be associated with superimposed fetal acute acidemia. METHODS: Umbilical artery blood gases were measured in 7816 term pregnancies with meconium in the amniotic fluid (AF) and the results were correlated with intrapartum and neonatal outcomes. RESULTS: Sixty-nine (1%) infants developed meconium aspiration syndrome and 31 (45%) of these were in association with fetal acidemia at birth. Moreover, umbilical blood gas analysis and intrapartum events suggested that the fetal acidemia linked to meconium aspiration was an acute event rather than a long-duration process, which might be expected if meconium was itself a marker of an antecedent fetal asphyxial event. CONCLUSION: Meconium in the AF may be a fetal environmental hazard when acidemia supervenes rather than solely a marker of preexisting fetal compromise leading to the release of meconium.

Acid-Base Imbalance↗

PubMed1994

Amnioinfusion during labor complicated by particulate meconium-stained amniotic fluid decreases neonatal morbidity.

OBJECTIVE: Our purpose was to evaluate the efficacy of prophylactic amnioinfusion in decreasing neonatal morbidity associated with labor complicated by particulate meconium-stained amniotic fluid and to assess potential complications of this procedure. STUDY DESIGN: One hundred five laboring pregnant women with particulate (moderate or thick) meconium by subjective clinical analysis were randomly assigned to receive amnioinfusion or to receive standard obstetric care without amnioinfusion. Patients with any antepartum complications, other than the presence of meconium, were excluded from the study. Statistical analyses consisted of the two-tailed and paired Student t tests, Pearson chi 2 test, and Wilcoxon nonparametric test. Significance was set at p < 0.05. RESULTS: The study included 47 patients in the study group and 58 patients in the control group. A significantly greater proportion of study patients demonstrated decreased meconium concentration between rupture of membranes and delivery (46 of 46 vs 15 of 58, p < 0.001). The relative dilution of meconium consistency by objective analysis was significantly different between the study group and the control group (77.1% decrease vs 9.3% increase, p < 0.001). The proportion of neonates with meconium below the vocal cords was reduced in the study group (two of 47 vs 36 of 58, p < 0.001). Umbilical artery pH was increased in the study group neonates (7.29 +/- 0.01 vs 7.25 +/- 0.009, p < 0.05). The rate of neonatal acidemia was reduced in the study group (4 of 45 vs 12 of 50, p < 0.05). The rate of meconium aspiration syndrome was reduced in the study group (1 of 47 vs 8 of 58, p < 0.05). Maternal and neonatal morbidity rates were similar. CONCLUSION: Prophylactic amnioinfusion should be considered a possible addition to the intrapartum management of patients with particulate meconium-stained amniotic fluid.

Acidosis↗

PubMed2001

Meconium aspiration syndrome in term neonates with normal acid-base status at delivery: is it different?

OBJECTIVE: Our aim was to compare the clinical characteristics of meconium aspiration syndrome in cases with pH > or =7.20 and in those with pH <7.20. STUDY DESIGN: Medical records of diagnostic codes from the International Classification of Diseases, Ninth Revision, were used to identify neonates with severe meconium aspiration syndrome who had been delivered at our institution from 1994 through 1998. Severe meconium aspiration syndrome was defined as a mechanical ventilator requirement of >48 hours. Clinical data including neonatal outcomes of cases of meconium aspiration syndrome associated with umbilical pH > or =7.20 at delivery were compared with data on outcomes of cases with pH <7.20. RESULTS: During this 4-year study period, 4985 singleton term neonates were delivered through meconium-stained amniotic fluid. Forty-eight cases met all study criteria, and pH values at delivery were as follows: pH > or =7.20, n = 29, and pH <7.20, n = 19. There were no differences between groups in the incidence of clinical chorioamnionitis, in the presence of meconium below the vocal cords, or in birth weight. Neonates with meconium aspiration syndrome and umbilical pH > or =7.20 at delivery developed seizures as often as those with pH <7.20 (20.1% vs 21.1%; P = 1.0). CONCLUSION: Normal acid-base status at delivery is present in many cases of severe meconium aspiration syndrome, which suggests that either a preexisting injury or a nonhypoxic mechanism is often involved.

Acid-Base Equilibrium↗

PubMed2005

Meconium passage in utero: mechanisms, consequences, and management.

Meconium passage in newborn infants is a developmentally programmed event normally occurring within the first 24 to 48 hours after birth. Intrauterine meconium passage in near-term or term fetuses has been associated with fetomaternal stress factors and/or infection, whereas meconium passage in postterm pregnancies has been attributed to gastrointestinal maturation. Despite these clinical impressions, little information is available on the mechanism(s) underlying the normal meconium passage that occurs immediately after birth or during the intrauterine period of fetal development. Birth itself is a stressful process and it is possible that fetal stress-mediated biochemical events may regulate the meconium passage occurring either during labor or after birth. Aspiration of meconium during intrauterine life may result in or contribute to meconium aspiration syndrome (MAS), representing a continued leading cause of perinatal death. This article reviews aspects of meconium passage in utero, its consequences, and management.

Adult↗

PubMed1998

The Collaborative Randomised Amnioinfusion for Meconium Project (CRAMP): 1. South Africa.

OBJECTIVE: To evaluate transcervical amnioinfusion for meconium stained amniotic fluid during labout. DESIGN: Multicentre randomised controlled trial. SETTING: Four urban academic hospitals in South Africa. Obstetric surveillance included the use of electronic fetal heart rate monitoring in most cases. PARTICIPANTS: Women in labour at term with moderate or thick meconium staining of the amniotic fluid. INTERVENTIONS: Transcervical amnioinfusion of 800 mL saline at 15 mL per minute, followed by a maintenance infusion at 3 mL per minute. The control group received routine care. Blinding of the intervention was not possible. MAIN OUTCOME MEASURES: Caesarean section, meconium aspiration syndrome and perinatal mortality. RESULTS: Caesarean section rates were similar (amnioinfusion group 70/167 vs control group 68/159; RR 0.98, 95% CI 0.76-1.26). The incidence of meconium aspiration syndrome was lower than expected on the basis of previous studies (4/162 vs 6/163; RR 0.67, 95% CI 0.19-2.33). There were no perinatal deaths. There were no significant differences between any of the subsidiary outcomes. CONCLUSIONS: This study concurred with three previous trials which found no effect of amnioinfusion for meconium-stained amniotic fluid on caesarean section rate, though the pooled data from all identified trials to date show a significant reduction. The findings with respect to meconium aspiration syndrome were inconclusive in this study alone because of the small number of babies affected, but the point estimate of the relative risk was consistent with the finding of a significant reduction in previous studies and with the Zimbabwe arm (CRAMP 2) of this study. Pooled data clearly support the use of amnioinfusion for meconium stained amniotic fluid to reduce the incidence of meconium aspiration syndrome.

Amnion↗

PubMed2003

Comparison of pulmonary and inflammatory effects of lipid- and water-soluble components in meconium in newborn piglets.

To understand the pathogenesis of meconium aspiration syndrome, we compared the pulmonary and inflammatory effects of the water and lipid extracts of human meconium instilled into the lungs of newborn piglets. The piglets were artificially ventilated, made hypoxemic, and randomized into three groups. At start of reoxygenation, 3 ml/kg of one of the following mixtures was instilled intratracheally: (1) meconium (n = 12); (2) water extract of meconium (n = 12), and (3) lipid extract of meconium (n = 12). During 8 h of reoxygenation, hemodynamics, pulmonary gas exchange, lung mechanics, and interleukin-8 concentrations in tracheobronchial aspirates were monitored. Oxygenation index (p = 0.04) and mean airway pressure (p = 0.04) increased more in the lipid extract group than in the water extract group. Dynamic compliance and mean arterial blood pressure decreased (p < 0.05) in the meconium and lipid extract groups, but not in the water extract group. At 8 h of reoxygenation, the interleukin-8 concentration in the tracheobronchial aspirates was three times higher in the lipid extract group as compared with the water extract group (110 +/- 102 vs. 37 +/- 27 pg/ml; p = 0.02). In conclusion, pulmonary dysfunction in meconium aspiration syndrome is caused by both the water- and lipid-soluble fractions of meconium, with stronger inflammatory and more detrimental effects promoted by the lipid extract than the water extract.

Animals↗

PubMed1988

[Prevention of meconium aspiration].

The aim of the study was to determine the risk of meconium aspiration by perinatal and obstetric characteristics and to give directions for prophylactic management. 67 infants with meconium-stained amniotic fluid received intrapartum pharyngeal suctioning and postpartum direct laryngoscopy and suctioning of the trachea. The risk for the presence of meconium in airways is increased if meconium is visible at the vocal cords (p less than 0.01), amniotic fluid showing thick meconium staining (p less than 0.001) Fischer-score being below 7 points (p less than 0.05) or Apgar-score being below 8 points(p less than 0.05). Immediately after delivery inspection of the vocal cords is necessary by direct laryngoscopy. Suctioning of the trachea under direct vision after delivery should be done if meconium is visualized at the vocal cords. Meticulous care of the fetus exposed to a meconium containing amniotic fluid environment and the avoidance of acute fetal stress may decrease the incidence of meconium aspiration.

Amniotic Fluid↗

PubMed1994

Meconium: a 1990s perspective on an old obstetric hazard.

OBJECTIVE: To quantify the current perinatal consequences associated with intrapartum detection of meconium in the amniotic fluid (AF). METHODS: We compared retrospectively the outcomes in 8136 term singleton cephalic pregnancies with meconium and 34,573 similar pregnancies with clear AF. RESULTS: Virtually all measures of adverse fetal-neonatal outcomes were significantly increased with meconium. For example, perinatal mortality increased from 0.3 per 1000 births with clear AF to 1.5 deaths per 1000 with meconium (P < .001). Most of these deaths resulted from meconium aspiration. Other unwanted outcomes also increased; eg, severe fetal acidemia at birth (umbilical artery blood pH 7.00 or less) increased from three per 1000 to seven per 1000 when meconium was diagnosed (P < .001). Delivery by cesarean also increased with meconium, from 7 to 14% (P < .001). CONCLUSION: Meconium in the AF is an obstetric hazard with small but significantly increased risks of adverse fetal-neonatal outcomes.

Adolescent↗

PubMedDate not supplied

Meconium does not guarantee fetal lung maturity.

OBJECTIVE: In utero passage of meconium may represent a response to hypoxic stress or a normal maturational event. When found during the third trimester, one may be tempted to use its presence as prima facie evidence of fetal lung maturity. The purpose of our study was to determine the frequency of meconium-stained fluid in the third trimester and the incidence of biochemical and physiologic lung immaturity in these fetuses. METHODS: Amniotic fluid specimens obtained at our institution from 1991 through 1993 (n = 2,377) were analyzed for maturity and visually inspected for meconium. Perinatal outcome was obtained for intramural deliveries occurring within 3 days of amniotic fluid collection (n = 905). Gestational age was defined as the best obstetric estimate based on menstrual dates, clinical examination, and ultrasound results. RESULTS: Meconium staining was present in 2.7% (n = 64) of specimens. Although meconium-stained specimens were more likely to have mature lecithin-sphingomyelin (L:S) ratios (OR 2.1, 95% confidence interval [CI] = 1.2-3.6) and phosphatidylglycerol (PG) concentrations (OR 3.8, CI 2.2-6.7), 17.2% were immature for both L:S and PG (n = 11, CI = 9.9-28.2%). When analysis was limited to fetuses delivering intramurally within 3 days of amniotic fluid collection, respiratory distress syndrome occurred in 3.0% (CI = 0.5-15%) with meconium-stained fluid. CONCLUSIONS: The presence of meconium in amniotic fluid does not guarantee lung maturity. The same consideration of the risks of prematurity must be given to the fetus with meconium-stained fluid as given to the fetus with clear fluid.

Amniotic Fluid↗

PubMed2005

Effects of meconium aspiration in isolated perfused rat lungs.

Our objective was to study meconium-induced lung injury in isolated perfused rat lungs exposed to anoxia. Our working hypothesis was that meconium-induced lung injury is independent of preexisting hypoxia, and that hypoxia will increase severity of lung injury observed after meconium aspiration. We compared five different groups of animals (n = 5) for pulmonary arterial pressure (PAP), weight lung changes, and TNFalpha expression. Group I had lungs instilled with 4 ml of normal saline. Group II had lungs exposed to 5 min of anoxia. Group III had lungs instilled with 4 ml of 30% filtered human meconium. Group IV had lungs exposed to 5 min of anoxia and then instilled with 4 ml of 30% filtered human meconium. Group V had lungs instilled with 4 ml of 30% unfiltered human meconium. Our subjects were adult Sprague-Dawley rats. The isolated rat lung model was prepared according to Levey and Gast (J Appl Physiol 1966;21:313-316). Lungs were ventilated with room air. Anoxia was caused by the use of N(2). The pulmonary artery was cannulated, and pulmonary arterial pressure and lung weight were measured. Lung weight and pulmonary arterial pressure were monitored for 120 min, and TNFalpha levels were measured in effluent at 15, 30, 60, and 120 min. Experiments were done at the Michael Reese Hospital (Chicago, IL). At the end of the experiment, PAP reached its highest values in group V (10.0 +/- 1.7 mmHg). Final PAPs in groups I-IV were: 4.85 +/- 0.3, 4.99 +/- 0.4, 5.93 +/- 0.3, and 7.25 +/- 0.51 mmHg, respectively). Lung wet weight increased significantly only in groups IV and V vs. group I; at 120 min, they were: 0.96 +/- 0.3 g, P < 0.01, and 1.5 g +/- 0.2 g, P < 0.01, respectively. TNFalpha levels did not change significantly over time in group I. TNFalpha is a marker as well as proprietor of pulmonary inflammatory response. TNFalpha reached its highest levels in groups IV and V: 595 and 753 pg/ml at 120 min, respectively. In conclusion, a short episode of anoxia prior to meconium aspiration may increase lung sensitivity to meconium-induced lung injury. This effect may be moderated by the TNFalpha present in the pulmonary circulation.

Animals↗

PubMed1985

Fatal meconium aspiration syndrome occurring despite airway management considered appropriate.

A combined obstetric-pediatric approach to tracheal toilet is said to prevent serious cases of the potentially fatal meconium aspiration syndrome. After delivery of the head a DeLee trap is used to suction the oropharynx and nasopharynx. Immediately following delivery, endotracheal suction is performed in an effort to remove any remaining meconium-stained amniotic fluid. Although routinely using this approach, we continue to have occasional cases of fatal meconium aspiration syndrome. Therefore, we reviewed the outcome of infants born through meconium-stained fluid. During a 5-year period, 1420 (15%) of 9299 live-born infants had meconium-stained fluid. Thirty (2.1%) of these 1420 developed meconium aspiration syndrome and 12 (40%) died; eight received a postmortem examination. Four had unequivocal evidence of meconium aspiration, two had large numbers of intra-alveolar squamous cells, and two had no evidence of aspiration. We conclude that aggressive airway management during and immediately after delivery does not always prevent fatal meconium aspiration syndrome.

Amniotic Fluid↗

PubMed1995

Markers of acute and chronic asphyxia in infants with meconium-stained amniotic fluid.

OBJECTIVE: Cord blood pH, lactate, hypoxanthine, and erythropoietin levels have all been used as markers of either acute or chronic asphyxia. We sought to determine whether these index values were significantly different in infants with or without meconium-stained amniotic fluid. STUDY DESIGN: Fifty-six pregnant women in spontaneous labor at term were divided into two groups on the basis of the presence or absence of meconium-stained amniotic fluid. All meconium-stained fluid was centrifuged, and the volume percentage of particulate matter (i.e., meconium) was recorded. Umbilical artery blood and mixed arterial and venous cord blood were obtained at each delivery. Lactate, hypoxanthine, and erythropoietin levels were measured. Statistical analysis included Student t test and rank sum statistics where appropriate. Normal and Spearman correlation coefficients were also used. RESULTS: There were no significant differences in mean umbilical artery pH (7.26 +/- 0.06 vs 7.25 +/- 0.10), lactate levels (32.8 +/- 10 mg/dl vs 30.4 +/- 14.2 mg/dl), and hypoxanthine levels (13.4 +/- 6.7 mumol/L vs 14.0 +/- 6.0 mumol/L) in newborns with meconium (n = 28) compared with controls (n = 28). Erythropoietin levels were significantly greater in newborns with meconium (median 39.5 mIU/ml vs 26.8 mIU/ml, p = 0.039). There was no correlation between the amount of particulate matter and any marker of asphyxia. CONCLUSIONS: There was no correlation between markers of acute asphyxia (i.e., umbilical artery blood pH, lactate, or hypoxanthine) and meconium. However, erythropoietin levels were significantly elevated in newborns with meconium-stained amniotic fluid. This latter marker may better correlate with chronic asphyxia.

Acute Disease↗

PubMed1976

Maternal and postnatal hypermagnesemia and the meconium plug syndrome.

Thirty dated pregnant Srague-Dawley rats received IM MgSO4 (750 mg/kg/ X 5 days) until birth. Fifteen untreated pregnant Sprague-Dawley rats of similar gestation served as controls. A total of 453 rats were born. Ninety neonates (two from each of 45 liters) were randomly removed before suckling, sacrificed, and the water content of the meconium and serum magnesium determined. The remaining 363 bewborn rats were observed for delayed passage of meconium or abdominal distention. Hypermagnesemic (6.3 +/- 0.5 mg/100 ml) neonates had neither abdominal distention nor delayed passage of meconium. The water content of meconium in hypermagnesemic rats (84.7 +/- 4.2% and in untreated controls (85.5 +/- 3.8%) were statistically similar. Dated pregnant mongrel dogs were given magnesium sulfate by continuous intravenous infusion and by bolus intravenous injection. The water content of meconium, transit time, and basic electrical rhythm (BER) of treated neonates were similar to untreated neonatal controls. The water content of meconium, transit time, and BER of neonatal dogs made hypermagnesemic (12.0 +/- 1.2 mg/100 ml) in the postnatal period were similar tp untreated neonatal controls. In adult and newborn pupies, receiving a continuous intravenous magnesium sulfate infusion, deep tendon reflexes ceased at serum magnesium levels of 9.0-10.0 mg/100 ml, spontaneous respiration at 14.0-15.0 mg/100 ml, and BER was suppressed (transiently) at 20.0-25.0 mg/10 ml. These data suggest that high (sublethal) doses of MgSO4 in pregnant and newborn animals have little effect on BER, meconium transit time or water content of the neonates. No correlation between MgSO4 treatment and the meconium plug syndrome was observed in the experiments.

Animals↗

PubMed1994

Meconium-induced lung injury mediated by activation of alveolar macrophages.

To clarify the mechanism of meconium-induced cellular injury, we examined the effect of meconium on the alveolar macrophages (AM) and bronchial epithelial cells (AK-D). Meconium obtained from healthy newborns was added to culture medium of AM and/or AK-D, which were cultured for 1 hour. Superoxide anion production of AM and the expression of intercellular adhesion molecule-1 (ICAM-1) on AK-D stimulated by meconium or oxygen radicals were determined. As a result, superoxide anion production of AM significantly increased when AM was cultured with meconium. Expression of ICAM-1 on AK-D appeared when AK-D was stimulated by hydroxyl radical but did not when AK-D was cultured with meconium. These results suggest that meconium-induced lung injury may occur through an activation of alveolar macrophages and the macrophage-epithelial cell axis may be important for the pathogenesis of meconium aspiration syndrome.

Animals↗

PubMed2005

Meconium aspiration induces oxidative injury in the hippocampus of newborn piglets.

BACKGROUND: Meconium aspiration-induced hypertensive lung injury has been associated with neuronal damage in the newborn, but the mechanisms of the injury are poorly known. AIMS: The aim of the study was to determine the contribution of oxidative stress to the brain damage after pulmonary meconium contamination. STUDY DESIGN: Sixteen anesthetized and ventilated newborn piglets were studied for 6 h. Eight piglets were instilled with a bolus of human meconium intratracheally and eight piglets with saline instillation served as controls. Brain tissue lipid peroxidation products (TBARS), reduced glutathione (GSH), myeloperoxidase activity and oxidized DNA were analyzed as indicators of oxidative stress. RESULTS: Meconium aspiration did not change the systemic or carotid hemodynamics, but caused a well-established pulmonary hypertensive response. Sustained increase in additional oxygen demand was also observed after meconium insult, but no actual hypoxemia or hypercarbia was evident during the whole study period. Myeloperoxidase activity was elevated in the cerebellum after pulmonary meconium instillation, whereas concentrations of peroxidation products and glutathione were similar in the cortical, cerebellar and hippocampal regions of the two groups. Still, the amount of oxidized DNA was increased in the hippocampus of the meconium-aspirated piglets when compared to controls. CONCLUSIONS: Our data thus suggest that oxidative injury associated with pulmonary, but not systemic, hemodynamic disturbances may contribute to hippocampal damage after meconium aspiration in newborns.

Analysis of Variance↗

PubMed2006

Infrared spectrophotometry of intraluminal meconium calculi in a neonate with imperforate anus and rectourethral fistula.

BACKGROUND/PURPOSE: Intraluminal meconium calculi are a rare cause of neonatal abdominal calcifications in patients with anorectal malformations. To investigate their pathogenesis, we performed infrared spectroscopic analysis of meconium-calcified lesions. METHODS: Meconium calculi were collected from the colostomy in a newborn patient with imperforate anus and rectourethral fistula. The potassium bromide method was employed to obtain the infrared absorption spectrum of the meconium calculi. RESULTS: The wavelength pattern of the meconium calculi exhibited 4 specific peaks at 1570, 1390, 1105, and 1005 cm(-1) between 22% and 45% transmittance values. The unique absorption spectrum exclusively indicated ammonium hydrogen urate (C(5)N(5)O(3)H(7)), having the combined constituents of ammonium and uric acid. CONCLUSIONS: These results suggest that the intraluminal meconium calculi were originally derived from meconium and fetal urine. The stasis of meconium passage and fetal urine mixing through the rectourethral fistula in a low-pH condition was deduced to be the main cause of this rare stone formation.

Anus, Imperforate↗

PubMed1994

Failure of acute perinatal asphyxia or meconium aspiration to produce persistent pulmonary hypertension in a neonatal baboon model.

OBJECTIVE: Our purpose was to determine whether perinatal asphyxia or meconium aspiration, or both, can produce the physiologic and histologic pulmonary vascular changes associated with the meconium aspiration syndrome. STUDY DESIGN: Twenty neonatal baboons were studied in four groups: 1, control; 2, meconium aspiration; 3, asphyxia (intermittent cord compression); and 4, asphyxia with meconium aspiration. Animals were ventilated for 24 hours under ketamine, diazepam, and pancuronium. Data were analyzed by means of mixed model analysis of measures. RESULTS: Meconium significantly impaired oxygenation (p < 0.001), whereas concurrent asphyxia moderated this effect (p < 0.034). Meconium also increased the need for ventilatory support (p < 0.002). No animal had persistent pulmonary hypertension; neither systemic nor pulmonary systolic pressures differed statistically between the groups. No animal showed evidence of abnormal pulmonary arteriolar muscularization. CONCLUSION: Sublethal perinatal asphyxia or meconium aspiration were insufficient to produce either the physiologic or histologic changes of severe meconium aspiration syndrome. It is unlikely that intrapartum fetal distress alone can produce this syndrome in human neonates.

Acute Disease↗

PubMed1982

The spectrum of meconium disease in infancy.

Meconium diseases in infancy cannot be neatly separated into discrete categories of meconium plug syndrome, meconium ileus, and meconium peritonitis; nor can the therapy of each condition. A patient with any of the three may or may not have cystic fibrosis. All babies with any form of meconium obstruction or atresia must have a sweat chloride test to confirm or rule out this diagnosis. Repeated gastrografin enemas can decrease the need for operative intervention in all babies with meconium plug syndrome and in selected babies with meconium ileus. Babies with meconium diseases can now be managed with a low perinatal mortality.

Barium Sulfate↗