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PubMed1995

Meconium inhibits the contraction of umbilical vessels induced by the thromboxane A2 analog U46619.

OBJECTIVE: Our objective was to study the direct effects of meconium on isolated umbilical artery and vein in vitro. STUDY DESIGN: Intact umbilical artery and vein rings were suspended in 5 ml organ baths containing kreb's solution (pH 7.2, 37 degrees C; bubbled with 2.5% oxygen and 8.07% carbon dioxide, balance nitrogen) for isometric tension recording. Meconium alone (final bath concentration 1%), centrifuged and filtered meconium, and meconium with the lipid fraction removed (separated into < 30,000 kd and > 30,000 kd) were added to the baths. Some vessels were also incubated in 1% meconium for 30 minutes, after which the meconium was washed out. Concentration-response curves to U46619 were obtained. The negative log of the concentration that evokes 50% of the maximal contraction was determined. RESULTS: Umbilical artery and vein had no sustained response to meconium. Tension that developed by rings exposed to meconium was significantly less than control at all concentrations of U46619. There was some loss of the efficacy of meconium after centrifugation-filtration and washing out. Meconium without the lipid fraction had less inhibitory effect than did native meconium. CONCLUSIONS: Meconium does not cause sustained contraction of umbilical artery and vein in vitro. It does, however, inhibit the contractile effect of U46619 in both umbilical artery and vein smooth muscle. The inhibitory activity of meconium appears to be concentrated in the lipid fraction.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMedDate not supplied

Meconium analysis for cocaine: a validation study and comparison with paired urine analysis.

We established the validity of a drug-screening method to detect the presence of cocaine or benzoylecgonine or both in meconium and then undertook an analysis of results from urine and meconium specimens obtained concurrently from neonates within 3 days of birth. Meconium specimens from 82 consecutive newborns were analyzed using fluorescence polarization immunoassay (FPIA), Kinetic Interaction of Microparticles in Solution (KIMS), and gas chromatography-mass spectrometry (GC-MS). Each meconium specimen was analyzed by all three methods. Fifty-four paired urine and meconium specimens were obtained over a 13-month period from a neonatal intensive care unit. Urine drug testing was performed by immunoassay (enzyme multiplied immunoassay [EMIT] technique), whereas meconium specimens utilized FPIA with GC-MS confirmation on all but one specimen (due to insufficient quantity). Ten true positives were found by GC-MS, 10 positives were found by FPIA, and 70 positives were found by KIMS. Of the 54 paired samples, 39 samples tested negative for cocaine in both urine and meconium; four specimens were positive by both routes; 10 specimens were negative in urine but positive in the meconium; and one specimen tested positive in urine but negative in the meconium. Thus, 9.3% of the urine specimens tested positive, and 25.9% of meconium samples tested positive (p = .011; McNemar's Test). We conclude that screening meconium specimens by FPIA followed by GC-MS confirmation of screened positives yields highly accurate determinations of the presence of cocaine or benzoylecgonine or both in meconium and that testing of meconium for cocaine and its metabolites is more sensitive than testing of urine.

Cocaine↗
PubMed2000

[Meconium and its significance].

OBJECTIVE: A review of meconium patophysiology and its contribution to the incidence of perinatal infection. DESIGN: Review article. SETTING: Department of Gynaecology and Obstetrics, Charles University and Faculty Hospital Plzen, Czech Republic. METHOD: The reported incidence of meconium-stained amniotic fluid varies between 7 and 22%. The patophysiology of the presence of meconium in the amniotic fluid is not sufficiently explained. Meconium in fetal bowels is under hormonal and neurol control. The presence of the meconium-stained amniotic fluid was always considered to be a potential risk for the fetal and neonatal well-being. The review is further divided in to three chapters. (II. Meconium and meconium aspiration syndrome, III. Meconium and postnatal neurological handicap). RESULTS AND CONCLUSION: The first chapter on deals with meconium risk in the development of perinatal infection: intraamniotic infection/chorioamnionitis, postnatal endometritis, infection of the abdominal wound after Caesarean and neonatal infection. The incidence of clinical chorioamnionitis is 15% with the presence of meconium compared to 3% in controls. The incidence of puerperal endometritis is 10% in comparison to 3% under normal conditions. Two main mechanisms of development (or coincidence) of intraamniotic infection in the presence of meconium exist. 1) Infection may be a cause of meconium passage. 2A) Alteration of Zn/P ratio in the amniotic fluid can promote bacterial growth. 2B) Meconium attached to macrophages or absorbed by phagocytosis can impair cellular immune response. The antibiotic prophylaxis is discussed.

Amniotic Fluid↗
PubMed2002

Elevated immunoreactive endothelin-1 levels in newborn rabbit lungs after meconium aspiration.

OBJECTIVE: Our prime objective was to study the production of big endothelin-1 (Big ET-1) and its conversion to ET-1 in the lungs of newborn rabbits exposed to meconium. Our second objective was to study the effect of captopril on endothelin expression. DESIGN: Prospective, comparative study. SETTING: Research laboratory of the Michael Reese Hospital and the University of Illinois, Chicago. SUBJECTS: Two-wk-old rabbit pups. INTERVENTIONS: Rabbit pups were instilled with meconium or saline into the lungs. Another group, pretreated with captopril, was also instilled with either meconium or saline. MEASUREMENTS AND MAIN RESULTS: After meconium or saline instillation, lung lavage was performed. Big ET-1 and ET-1 were measured in lung lavage fluid by using a commercially available enzyme-linked immunosorbent assay kits in all groups. Also, lungs were studied by histochemistry analysis for a morphologic evaluation of meconium-induced damage. In the lavage fluid of saline-instilled pups, ET-1 remained low and no increase in Big ET-1 levels was observed. In meconium-instilled animals, bioactive ET-1 levels were significantly higher, with a peak at 8 hrs after instillation. The conversion ratio of Big ET-1 to ET-1 in the meconium group increased from 2.19 at the initial period to 7.19 at 8 hrs after meconium instillation. CONCLUSIONS: Our conclusion is that aspiration of meconium causes lung injury in the newborn and that this injury is associated with a significant increase in ET peptide production in the lungs. We also showed that ET production is inhibited by pretreatment of rabbits with captopril before meconium-induced injury. ET-1 and its conversion from ET-1 in response to meconium may play important roles in increasing pulmonary vascular resistance and lung cell death, even in the absence of hypoxia. In general, we conclude, that ET-1 levels are significantly elevated in meconium-instilled rabbits compared with saline-instilled ones, and both can be significantly inhibited by pretreatment with captopril. Whether ET-1 contributes directly to the pathophysiology of or is simply a marker of meconium aspiration syndrome remains speculative.

Journal Article↗
PubMed1996

Inflammation of the lungs, umbilical cord and placenta associated with meconium passage in utero. Review of 123 autopsied cases.

It is uncertain how often the passage of meconium in utero is a response to some event causing fetal distress as opposed to being simply the physiologic functioning of a maturing intestinal tract. The extent to which meconium may produce injury or inflammation in pulmonary and placental tissues after intrauterine exposure is also unclear. This study was a retrospective review of 123 cases, 79 stillborn and 44 liveborn less than one month of age, autopsied at The Johns Hopkins Hospital, and showing histologic evidence of intrauterine meconium exposure by aspirated meconium or meconium macrophages in placental tissues. Of 55 cases with pulmonary inflammation, 13 (24%) had fetal pneumonia, 5 (9%) had postnatal bronchopneumonia, and 37 (67%) had inflammation secondary to meconium aspiration. There was inflammation of the umbilical cord in 31 (41%) of the 75 cases with available slides, 11 (15%) had funisitis associated with chorioamnionitis and 18 (58%) were secondary to meconium exposure. There were 19 cases with focal injury of cord vessels from meconium, two of which had cord ulceration. Inflammation of the membranes and chorionic plate was present in 24 (33%) of the 72 cases where it could be assessed, and was due to chorioamnionitis in 11 (46%) and to meconium in 13 (54%). In general, meconium-related inflammations was much less severe in the membranes than in the cord. There were 67 (54%) cases with definite or probable evidence of fetal distress. In 38 (48%) stillborns no cause of fetal death in utero was identified and in 18 (41%) liveborns there was no known prenatal problem. The results support the concept that meconium passage in utero may occur either as a response to fetal distress or as a physiologic process. Inflammation in the lung and placental tissues, and vascular injury in the umbilical cord may arise secondary to in utero exposure to meconium.

Female↗
PubMed1994

Delivery room management of infants born through thin meconium stained liquor.

A total of 3472 deliveries were studied over a year to evaluate (i) the importance of thin meconium stained liquor (MSL) in the causation of meconium aspiration syndrome (MAS), and (ii) the efficacy of intrapartum plus endotracheal suction at birth in the prevention of MAS due to thin meconium. Two hundred and ninety four (8.5%) of deliveries had meconium stained liquor of which thin MSL was present in 101. MAS occurred in 98 babies. Thin MSL was responsible for 19.4% of cases of MAS. Inspite of intrapartum suction, a high proportion (55-78%) of infants had meconium in the trachea, though thin meconium was found in the trachea significantly less often than thick meconium. Combined intrapartum and endotracheal suction reduced the incidence of MAS due to thin meconium from 26% to 16%. MAS due to thin meconium occurred in asphyxiated as well as vigorous babies inspite of combined suction. Thin meconium accounts for a significant proportion of deliveries with MSL and causes a considerable number of cases of MAS. To prevent meconium aspiration syndrome caused by thin meconium, all neonates born through thin MSL, whether they are asphyxiated or not should undergo intrapartum suction followed by immediate endotracheal suction at birth.

Asphyxia Neonatorum↗
PubMedDate not supplied

Contemporary management of meconium ileus.

Meconium ileus was noted as an early manifestation of cystic fibrosis in 60 neonates between 1972 and 1991. There were 20 girls and 40 boys. A family history of cystic fibrosis was present in six children. Twenty-five neonates had uncomplicated meconium ileus due to inspissated meconium within the terminal ileum. Thirty-five neonates presented with 56 complications of meconium ileus, including volvulus (n = 22), atresia (n = 20), perforation (n = 6), and giant cystic meconium peritonitis (n = 8). Clinical presentation included abdominal distension, bilious vomiting, and failure to pass meconium. In two recent cases, prenatal ultrasonography detected a mass with proximal bowel distension indicative of cystic meconium peritonitis. Mechanical bowel obstruction in the other neonates was diagnosed from plain abdominal radiographs and barium enema. Ten patients with uncomplicated meconium ileus were successfully treated with a diatrizoate meglumine (Gastrografin) enema. The remaining 15 patients required a laparotomy, with 9 treated by bowel resection and enterostomy and 6 recent cases managed with enterotomy and irrigation. Complicated cases were managed by bowel resection and anastomosis (n = 15) or enterostomy (n = 20). Survival at 1 year was 92% in patients with uncomplicated meconium ileus and 89% for those with complicated meconium ileus. The therapy of choice for uncomplicated meconium ileus is nonoperative Gastrografin enema, with enterotomy and irrigation reserved for enema failures. Complicated cases require exploration and, in the absence of giant cystic meconium peritonitis, are usually amenable to bowel resection and primary anastomosis.

Anastomosis, Surgical↗
PubMed1996

Meconium increases surfactant secretion in isolated rat alveolar type II cells.

One of the underlying causes of pathophysiology of meconium aspiration syndrome is access of meconium to the alveolar space and inhibition of activity of lung surfactant. This study examines the effects of meconium on type II cell function by following surfactant secretion. Isolated rat alveolar type II cells were labeled with [methyl-3H]choline during the initial 21-22 h of incubation. During the subsequent 150 min of incubation, phosphatidylcholine (PC) secretion in the presence of 1% meconium was increased 250 +/- 11% (mean +/- SE, n = 23) over controls. The secretagogue effect was concentration-dependent and reached a maximum at 0.5% meconium. The meconium effect was not due to cellular toxicity as evaluated by vital dye exclusion, lactate dehydrogenase release, and PC synthesis. The secretagogue effect of meconium was associated with the particulate fraction pelleted by centrifugation of the suspension for 1 h at 100,000 x g. Heat treatment of meconium decreased the effect, suggesting the active component to be a protein. The effect of meconium was additive with that of 0.1 mM terbutaline, or 1 mM ATP, suggesting different pathways of action of each agent. The effect of meconium was reduced in the presence of 0.1 mM 4,4'-diisothiocyanato-2,2'-disulfonic acid, or 100 ng/mL surfactant protein A. These agents were previously shown to inhibit surfactant secretion in a stimulus-independent manner. Our results suggest that meconium at low concentrations is not toxic to type II cells, and a component of meconium, possibly a protein, increases PC secretion.

Animals↗
PubMed2004

[Protective effects and mechanisms of recombinant human superoxide dismutase in acute lung injury of rats following meconium aspiration].

OBJECTIVE: To evaluate the protective effects of recombinant human superoxide dismutase (rhSOD) in acute lung injury (ALI) following meconium aspiration. METHODS: Thirty-two healthy male Sprage-Dawley rats were divided into two groups, 8 were used as control (saline group) by infusing 1 ml/kg saline through endotracheal tube; the other 24 rats were used to establish model of ALI by infusing 1 ml/kg of 20% human newborn meconium suspension through endotracheal tube, and then were randomized to 3 groups (8 each): meconium group with no administration of saline or rhSOD; meconium + saline group by infusing 1 ml/kg saline through endotracheal tube; meconium + rhSOD group by infusing 20 mg/kg rhSOD dissolved in 1 ml/kg saline through endotracheal tube. The rats were killed 24 h after treatment. The measurements included bronchoalveolar lavage fluid (BALF) cell counts, protein, BALF protein/plasma protein (pulmonary permibility index, PPI), lactic dehydrogenase (LDH), pulmonary myeloperoxidase (MPO) and superoxide dismutase (SOD) activity, malonyldialdehyde (MDA) and nitric oxide (NO) level. Lung injury score was also evaluated. RESULTS: Compared with the saline group, the rats in the meconium group had significantly increased BALF cell counts (4.04 +/- 1.01 vs. 0.53 +/- 0.19), protein (2.54 +/- 0.74 vs. 0.67 +/- 0.26), PPI (0.50 +/- 0.18 vs. 0.12 +/- 0.05), LDH (263.50 +/- 97.84 vs. 17.38 +/- 3.58), pulmonary MPO (1.49 +/- 0.22 vs. 0.62 +/- 0.16), MDA (3.30 +/- 0.85 vs. 1.40 +/- 0.35), NO (12.77 +/- 5.00 vs. 4.89 +/- 1.32) and lung injury score (9.88 +/- 2.10 vs. 2.25 +/- 1.04), P < 0.01 for all, whereas pulmonary SOD activity had no statistically significant differences (103.28 +/- 24.53 vs. 94.49 +/- 12.93, P > 0.05). There were no statistically significant differences between meconium + saline group and meconium group (all P > 0.05). Compared with the meconium + saline group, meconium + rhSOD group had decreased BALF cell counts (3.13 +/- 0.77 vs. 4.68 +/- 1.40, P < 0.01), LDH (162.63 +/- 76.90 vs. 273.75 +/- 111.83, P < 0.05), pulmonary MPO activity (1.23 +/- 0.28 vs. 1.54 +/- 0.24, P < 0.05), MDA (2.46 +/- 0.42 vs. 3.50 +/- 0.82, P < 0.01), NO level (9.17 +/- 2.34 vs. 13.04 +/- 4.38, P < 0.05), lung injury score (8.63 +/- 1.30 vs. 10.00 +/- 1.07, P < 0.05) and increased pulmonary SOD activity (134.45 +/- 23.30 vs. 106.79 +/- 17.77, P < 0.05), but there were no statistically significant differences in BALF protein and PPI between these two groups. CONCLUSION: Inflammation and lipid peroxidation might play important roles in the pathogenesis of ALI with meconium aspiration, a single early administration of 20 mg/kg rhSOD intratracheally can reduce lung damage in rats following meconium aspiration.

Acute Lung Injury↗
PubMed2001

Meconium aspiration injury: Uncoupling between the in vivo physiologic and in vitro inflammatory responses.

OBJECTIVE: To correlate the in vivo physiologic changes that occur with meconium aspiration injury to an associated in vitro cellular response to meconium. DESIGN: Experimental, prospective, randomized, controlled study. SETTING: University research laboratory. SUBJECTS: Eighteen adult Sprague-Dawley rats with meconium aspiration injury. INTERVENTIONS: Rats were given 3 mL/kg of a 25% meconium solution and were treated with conventional gas ventilation; nine rats were given exogenous surfactant therapy (Survanta, 4 mL/kg), and nine rats were not treated (control). Bronchoalveolar lavages were collected for total cell counts. Histologic samples also were taken for analysis. In addition, the in vitro effect of meconium on granulocytic elastase release from human neutrophils was determined. MEASUREMENTS AND MAIN RESULTS: Meconium caused significant morbidity in vivo, including poor oxygenation, elevated Paco(2), diminished compliance, and elevated white cell count in the bronchial lavages. Lung white cell count was significantly less in the surfactant group (p <.01). Meconium did not cause elastase release from human neutrophils in vitro. CONCLUSIONS: This study demonstrated uncoupling between in vivo physiologic responses to meconium injury in rats and the in vitro effect of meconium on human neutrophils. Surfactant therapy alleviated some of the perturbations associated with meconium injury, including a reduction in the inflammatory cell count in lung lavages. The absence of direct neutrophil activation by meconium suggests the requirement of an intermediary in the pathogenesis of meconium aspiration injury.

Journal Article↗
PubMed2000

Obstetric and perinatal outcome of pregnancies with term labour and meconium-stained amniotic fluid.

The purpose of this study was to evaluate the meconium staining of amniotic fluid (AF) in term of fetal distress, meconium aspiration syndrome, and perinatal morbidity and mortality. In a prospective study at Princess Badeea Teaching Hospital from April to November 1999, women with a singleton cephalic pregnancy of completed 37-42 weeks and with no pre-defined risk factor were recruited into the study. Study patients comprised 390 (10%) patients with meconium and 400 patients as controls but with clear amniotic fluid. Virtually meconium staining of the amniotic fluid was significantly associated with poor neonatal outcome in all outcomes measures assessed. Perinatal mortality increased from 2 per 1000 births with clear AF to 10 per 1000 with meconium (P<0.001). Other adverse outcomes also increased; e. g., severe fetal acidemia, Apgar score < or = 3 at 1 min and 5 min, and meconium aspiration syndrome. Delivery by cesarean section also increased with meconium from 7-14% (P<0.001). We concluded that meconium in the amniotic fluids associated with an obstetric hazard and significantly increase risks of adverse neonatal outcomes. Women with thin meconium in the presence of normal fetal heart rate can be safely managed at the clinical level. Mod-thick meconium alone should alert the obstetrician to a high risk fetal condition. Continuous fetal heart rate monitoring during labour and reassurance of fetal well-being by acid-base assessment were most significant factors in the reduction of meconium aspiration syndrome.

Adult↗
PubMed2005

Meconium inhibits phagocytosis and stimulates respiratory burst in alveolar macrophages.

The meconium aspiration syndrome is an important cause of respiratory distress in newborn infants. Alveolar macrophages (AMs) provide a first line of defense in the lower respiratory tract against inhaled pathogens and particles such as meconium. In this study, we examined the effect of meconium on two primary macrophage functions: phagocytosis and respiratory burst. Short-term exposure of rat NR8383 AMs to sterile meconium from human or equine neonates (1.2-24 mg/mL) produced a dose-dependent decrease in phagocytosis of fluorescent latex beads. This effect was not due to decreased cell viability or to an elevation of intracellular cAMP. The effect of short-term exposure to meconium on the respiratory burst response in AMs was quantified using flow cytometry to measure oxidation of dichlorofluorescin diacetate. A robust respiratory burst was triggered when AMs were exposed to 12 or 24 mg/mL meconium. This effect was attenuated but not eliminated by filtration of the meconium. However, subsequent to meconium exposure, AMs had a reduced respiratory burst in response to stimulation with phorbol myristate acetate. In addition, AMs that were exposed to meconium for an extended period (24 h) showed DNA fragmentation indicative of apoptosis. Meconium therefore may interfere with AM function by inducing oxidative stress and apoptosis. Tissue injury from release of reactive oxygen species by AMs may be important in the pathophysiology of the meconium aspiration syndrome.

Animals↗
PubMed2002

Effect of meconium on the rate of in vitro subtype conversion of swine pulmonary surfactant.

UNLABELLED: The interactions between pulmonary surfactant and meconium have been previously reported, however, no prior study has paid attention to the effect of meconium on the extracellular surfactant metabolism. We studied the effect of meconium on the rate of surfactant subtype conversion from surface-active large surfactant aggregates to inactive small surfactant aggregates using the in vitro surface area cycling method. Human meconium was added to a suspension of large surfactant aggregates isolated from swine lung lavage fluid and the mixture was cycled in a capped polystyrene tube at 37 degrees C. The conversion rate from large to small surfactant aggregates was dependent upon the amount of meconium added. By sufficiently increasing the surfactant concentration, meconium could not significantly affect the surfactant subtype conversion. The conversion rate was temperature-dependent and was slower at 4 degrees C. Heat treatment of meconium diminished the rate of conversion. The potent effect of meconium on surfactant subtype conversion appears to be related to an enzymatic protein containing a serine active site, since the conversion occurred at 37 degrees C and not at lower temperatures and the conversion was blocked in the presence of diisopropyl fluorophosphate. CONCLUSION: Our study suggests that meconium can accelerate surfactant subtype conversion. We believe that the increased rate of conversion caused by meconium is a new mechanism for surfactant inactivation that could occur with lung injuries associated with meconium aspiration syndrome.

Animals↗
PubMed1989

The pulmonary vasculature in meconium aspiration.

Some studies have suggested that pulmonary hypertension in the newborn with meconium aspiration can be attributed to a primary prenatal increase in pulmonary arterial musculature; but this concept has been controversial. To examine this question, we reviewed 62 infants autopsied at The Johns Hopkins Hospital, 24 of whom demonstrated meconium aspiration, 20 with meconium staining but no aspiration, and 18 with abruptio placentae without meconium aspiration or staining. Clinical and pathologic features were evaluated and cross-sectional arterial medial area was determined at the junction of the conducting and respiratory airways in nondistended lungs. No significant difference in arterial medial area was found between infants with meconium aspiration and those with meconium staining only or abruptio placentae. In addition, circumferentially muscularized intraacinar arteries were present in all infants with meconium aspiration and abruptio placentae, and all but one infant with meconium staining alone. Comparison of lungs with and without arterial injection and fixation in distention showed that injection does not uniformly distend vessels and that formalin distention may remove or mask meconium. The study suggests that meconium aspiration and its complications, not primary structural arterial changes, account for pulmonary hypertension in infants with meconium aspiration.

Arterioles↗
PubMed1993

A method for continuous monitoring of meconium in the amniotic fluid during labour.

In about 10% of pregnancies overall, the fetus discharges meconium (its bowel contents) into the amniotic fluid during labour. In about 10% of cases where meconium is passed, the fetus gasps, inhaling the sticky meconium into the upper respiratory tract. After birth, the meconium blocks the air passages in the lungs, impairing gas exchange--meconium aspiration syndrome (MAS). Up to 20% of infants suffering from MAS die and recently published studies have shown a long-term effect of MAS in causing cough and wheeze. The risk of meconium aspiration is thought to be increased by intrauterine hypoxia. At present, meconium is only noticed at birth or occasionally when amniotic fluid leaks past the presenting part of the fetus. A method has been developed which measures absolute meconium concentration with a 99% prediction interval of +/- 30 g l-1; allows monitoring of the rate of appearance of meconium linearly with a nonlinearity of 5%, and differentiates between meconium and blood. The method uses the ratio of the intensity of back-scattered light from the amniotic fluid at 700 and 415 nm, the latter being near the peak of light absorption by meconium and the former a reference value. The ratio is also affected by the presence of blood. However, blood has specific absorption peaks at 540 and 575 nm from which it can be detected (the presence of blood is also a significant abnormality, and is relatively uncommon). The measurement method could easily be integrated into an optical sensor mounted onto an intrauterine probe.(ABSTRACT TRUNCATED AT 250 WORDS)

Amniotic Fluid↗
PubMed2002

Is meconium passage a risk factor for maternal infection in term pregnancies?

OBJECTIVE: To study the association between meconium and maternal infection. METHODS: This was a retrospective cohort study of 678 pregnant women. All term deliveries during a 31-month period with meconium passage were included. Each meconium delivery was matched with a consecutive delivery without meconium at the same gestational age. RESULTS: The overall infection rate was 16%, with 13% of the infections directly related to the pregnancy, labor, and delivery. The endometritis rate was 5%, with 7.1% and 3% in the meconium and no-meconium group, respectively. The chorioamnionitis rate was 8.3%, with 9.5% in the meconium and 7.1% in the no-meconium group. Factors found to be associated with overall obstetric infections had the following odds ratios (ORs) and 95% confidence intervals (CIs): meconium (OR 1.8, 95% CI 1.1, 2.8), internal monitoring (OR 3.4, 95% CI 1.9, 5.9), amnioinfusion (OR 2.0, 95% CI 1.3, 3.3), number of vaginal exams (OR 4.5, 95% CI 2.8, 7.1), length of labor (OR 2.8, 95% CI 1.8, 4.4), and cesarean (OR 3.1, 95% CI 1.9, 5.1). Logistic regression analyses revealed the following ORs and 95% CIs: 1) for endometritis-cesarean (OR 4.2, 95% CI 1.9, 8.9), internal monitoring (OR 2.5, 95% CI 1.1, 5.9), and meconium (OR 2.5, 95% CI 1.1, 5.5), and 2) for chorioamnionitis-length of labor greater than 10 hours (OR 2.7, 95% CI 1.4, 5.6), number of vaginal exams greater than seven (OR 3.4, 95% CI 1.7, 6.6), and use of internal monitors (OR 2.5, 95% CI 1.2, 5.3). CONCLUSION: Meconium passage increases the risk of postpartum endometritis but not chorioamnionitis. Length of labor, internal monitoring, and number of vaginal exams are risk factors for chorioamnionitis.

Adult↗
PubMed2001

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

UNLABELLED: 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 dipalmitoylphosphatidylcholine. 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: 1.7 +/- 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 +/- 1.6 mN/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 atelectasis in MAS.

Biological Products↗
PubMed1990

Objective assessment of meconium content of amniotic fluid.

The amount of meconium in amniotic fluid is subjectively estimated by visual inspection and classified as thin (light), moderate, or thick (heavy). This estimate may be important for assessing the neonatal risk of perinatal asphyxia and meconium aspiration syndrome. This study reports on the "meconium-crit," a simple, rapid, inexpensive, and reproducible method of quantifying meconium concentration in amniotic fluid. The purpose of the study was to determine the relationship between the meconium-crit and meconium concentration. Specimens were prepared by placing 3.0 g of fresh neonatal meconium into clear amniotic fluid and vortexing for 15 minutes to obtain a stock solution of 15.0 g meconium/100 mL amniotic fluid. Stock solutions were then diluted with clear amniotic fluid to obtain concentrations of 10.0, 7.5, 5.0, 3.0, and 1.5 g/100 mL. One-tenth milliliter of the amniotic fluid/meconium mixture was drawn into a standard hematocrit tube and centrifuged. The meconium-crit was then measured directly as with a hematocrit. Regression analysis indicated that meconium-crit values were linearly related to meconium concentration (r = 0.901-0.995). This method provides a reproducible means of quantifying meconium in amniotic fluid.

Amniotic Fluid↗