Meconium-stained amniotic fluid and meconium aspiration syndrome: a prospective study

BACKGROUND: The incidence of meconium aspiration syndrome (MAS), associated perinatal factors, morbidity and deaths varies widely. This study aimed to assess the perinatal attributes and morbidity associated with MAS. METHODS: Over a 2-year period, all neonates born through meconium-stained amniotic fluid (MSAF) were observed for respiratory distress (RD). Birth details, chest radiograph (CXR) and clinical course were documented. Neonates with consistent CXR findings whose RD could not otherwise be explained were defined as MAS. RESULTS: Of 409 neonates born through MSAF, meconium was thick in 196 (47.9%). Fifty-five (13.4%) had RD and 45 (11.3%) were consistent with MAS. Six (1.5%) neonates died. Mean (SD) birthweight and gestation of MAS infants were 2721.9 (510.2) g and 38.67 (1.09) weeks, respectively. About one-third were of low birthweight and 28 were born by caesarean section. On univariate analysis, caesarean delivery, meconium in the trachea and thick meconium were the significant perinatal factors for the development of MAS. On multiple regression analysis, thick meconium was the only independent factor for MAS (OR 7.08, 95% CI 3.08-16.27, p<0.001). An Apgar score of 相似文献   

Hyaline Membranes in Postmature Infants

Hyaline membranes in 21 of postmature infant autopsies were studied, using 27 term infant autopsies as the control population.

The occurrence of hyaline membranes was much higher in postterm (86%) than term infant autopsies (26%). Seventeen of 21 postmature infants had clinical and microscopic evidence of aspiration, contaminated by meconium in 14, suggesting that meconium and/or amniotic aspiration may be an etiologic factor in postmature hyaline membrane formation. Thirteen infants had severe hyaline membrane formation, microscopically distinguishable from hyaline membrane disease of the premature only by the maturity of the underlying lung.

Besides the pulmonary findings, little difference in organ histology was observed between the two groups. This study showed that hyaline membrane formation resulted in asphyxia and respiratory failure in the majority of the postmature infants who were already troubled with hypoxia and a combined respiratory and metabolic acidosis secondary to meconium aspiration, and eventually led to death.     

Hyaline membranes in postmature infants

Hyaline membranes in 21 of postmature infant autopsies were studied, using 27 term infant autopsies as the control population. The occurrence of hyaline membranes was much higher in postterm (86%) than term infant autopsies (26%). Seventeen of 21 postmature infants had clinical and microscopic evidence of aspiration, contaminated by meconium in 14, suggesting that meconium and/or amniotic aspiration may be an etiologic factor in postmature hyaline membrane formation. Thirteen infants had severe hyaline membrane formation, microscopically distinguishable from hyaline membrane disease of the premature only by the maturity of the underlying lung. Besides the pulmonary findings, little difference in organ histology was observed between the two groups. This study showed that hyaline membrane formation resulted in asphyxia and respiratory failure in the majority of the postmature infants who were already troubled with hypoxia and a combined respiratory and metabolic acidosis secondary to meconium aspiration, and eventually led to death.     

Meconium “aspiration” (or respiratory distress associated with meconium-stained amniotic fluid?)

The designation meconium aspiration syndrome (MAS) reflects a spectrum of disorders in infants born with meconium-stained amniotic fluid, ranging from mild tachypnea to severe respiratory distress and significant mortality. The frequency of MAS is highest among infants with post-term gestation, thick meconium, and birth asphyxia. Pulmonary hypertension is an important component in severe cases. Prenatal hypopharyngeal suctioning and postnatal endotracheal intubation and suctioning of vigorous infants are not effective. Intubation and suctioning of non-breathing infants is controversial and needs more investigation. Oxygen, mechanical ventilation, and inhaled nitric oxide are the mainstays of treatment. Surfactant is often used in infants with severe parenchymal involvement. High-frequency ventilation and extracorporeal membrane oxygenation are usually considered rescue therapies.     

Pathological complications of non-survivors of newborn extracorporeal membrane oxygenation

The pathology was reviewed of the early deaths identified from the first 50 neonates treated with extracorporeal membrane oxygenation (ECMO) during its introduction to the UK. Fifteen neonates died during or shortly after ECMO between August 1989 and June 1992. Data on 12 are presented (three did not have a postmortem examination). The clinical diagnoses at referral for ECMO were as follows: persistent pulmonary hypertension of the newborn (six infants), primary congenital pneumonia (one infant), community acquired pneumonia (two infants), birth asphyxia (one infant), respiratory distress syndrome (one infant), and meconium aspiration syndrome (one infant). In our group, at necropsy, five had significant haemorrhage (three intracranial, one pulmonary, one pericardial and intraventricular). Three of five infants with evidence of haemorrhage also had signs of sepsis. Six infants had evidence at necropsy of systemic sepsis, five showed evidence of severe anoxic brain injury, and four infants had cerebellar haemorrhages. Three infants had evidence of myocardial ischaemia. It is difficult to discriminate between the relative influence of the primary diagnosis, the mode of treatment, and the severity of presentation in the genesis of this pathology. It is likely that the extent and severity of some of the findings represent a pathological progression that would have been interrupted by the death of the patient, had ECMO not been instituted.     

Pathological complications of non-survivors of newborn extracorporeal membrane oxygenation

The pathology was reviewed of the early deaths identified from the first 50 neonates treated with extracorporeal membrane oxygenation (ECMO) during its introduction to the UK. Fifteen neonates died during or shortly after ECMO between August 1989 and June 1992. Data on 12 are presented (three did not have a postmortem examination). The clinical diagnoses at referral for ECMO were as follows: persistent pulmonary hypertension of the newborn (six infants), primary congenital pneumonia (one infant), community acquired pneumonia (two infants), birth asphyxia (one infant), respiratory distress syndrome (one infant), and meconium aspiration syndrome (one infant). In our group, at necropsy, five had significant haemorrhage (three intracranial, one pulmonary, one pericardial and intraventricular). Three of five infants with evidence of haemorrhage also had signs of sepsis. Six infants had evidence at necropsy of systemic sepsis, five showed evidence of severe anoxic brain injury, and four infants had cerebellar haemorrhages. Three infants had evidence of myocardial ischaemia. It is difficult to discriminate between the relative influence of the primary diagnosis, the mode of treatment, and the severity of presentation in the genesis of this pathology. It is likely that the extent and severity of some of the findings represent a pathological progression that would have been interrupted by the death of the patient, had ECMO not been instituted.     

The pros and cons of suctioning at the perineum (intrapartum) and post-delivery with and without meconium

Routine oronasopharyngeal suctioning (ONPS) of the infant at delivery is a common practice in the delivery room. ONPS is performed to remove lung fluid, meconium, or other secretions from the airway, thereby improving oxygenation and/or preventing aspiration. However, there are controversies regarding this practice, as it seems to be associated with complications. In the presence of clear amniotic fluid, routine ONPS in infants born vaginally and by cesarean section is associated with bradycardia, apnea, and delays in achieving normal oxygen saturations, with no benefit. Intrapartum ONPS and post-natal endotracheal suctioning of vigorous infants born through meconium-stained amniotic fluid (MSAF) does not prevent meconium aspiration syndrome (MAS). Although depressed infants born through MSAF are at risk of developing MAS, there is no evidence that endotracheal suctioning of these infants reduces MAS.     

Neonatal acute respiratory failure

Acute respiratory failure is the most common problem seen in the preterm and term infants admitted to neonatal intensive care units. In preterm infants, the most common cause of acute respiratory failure is respiratory distress syndrome caused by surfactant deficiency. Acute respiratory failure in term and near term infants is usually a result of meconium aspiration syndrome, sepsis, pulmonary hypoplasia, and primary pulmonary hypertension of the newborn. The response to various methods of treatment may vary, depending on the severity of respiratory failure and the cause of the acute respiratory failure. We reviewed the evidence for efficacy and current utilization of newer treatment modalities, including exogenous surfactant administration, high frequency ventilation, inhaled nitric oxide therapy, antenatal steroids for the prevention of respiratory distress syndrome, and use of postnatal steroids for the prevention of chronic lung disease.     

TOLAZOLINE AND DOPAMINE THERAPY IN NEONATAL HYPOXIA AND PULMONARY VASOSPASM

Abstract. Hegyi, T. and Hiatt, I. M. (Division of Perinatology, Monmouth Medical Center and Department of Pediatrics, the Hahnemann Medical College, Philadelphia, USA). Tolazoline and dopamine therapy in neonatal hypoxia and pulmonary vasospasm. Acta Paediatr Scand, 69: 101, 1980.—Severe hypoxia unresponsive to maximum ventilatory support occurs both in idiopathic respiratory distress syndrome and meconium aspiration. We recently encountered a 980 g female infant with respiratory distress syndrome and 3300 g female infant with meconium aspiration and persistant fetal circulation whose clinical course necessitated the use of tolazoline and dopamine to reduce pulmonary and to stabilize systemic pressures. The infant with respiratory distress syndrome responded with a P_aO2 increase of 2.7 kPa while the infant with persistant fetal circulation and meconium aspiration showed a 51.6 kPa rise. Combined pharmacologic therapy may have a role in improving oxygenation status in severely hypoxemic infants receiving maximum support     

Expanded use of surfactant replacement therapy

There are a number of respiratory diseases affecting infants in which there is surfactant dysfunction or deficiency. Surfactant is inactivated by cholesterol, free fatty acids and bilirubin in meconium aspiration syndrome, by haemoglobin and red blood cell lipids in pulmonary haemorrhage and plasma proteins are the culprit in conditions associated with increased alveolar capillary permeability. Surfactant production can be adversely affected by damage to the type 2 pneumocytes by viruses and neutrophil derived reactive oxygen metabolites. Not surprisingly, therefore, the efficacy of exogenous surfactant has been tested, usually in animal models and anecdotal series in “non respiratory distress syndrome” respiratory disorders. Improvements in oxygenation have usually been described. Relatively few randomized trials, however, have been performed, but those undertaken have demonstrated longer term benefits. In term infants with severe respiratory failure, surfactant administration significantly shortened the duration of extracorporeal membrane oygenation and, in those in the early phase of severe respiratory failure or with meconium aspiration syndrome, it significantly reduced the need for extracorporeal membrane oygenation. In meconium aspiration syndrome, a smaller number of surfactant treated patients compared to controls developed airleaks. Surfactant administration was also associated with a reduction in the duration of ventilation and intensive care unit stay in patients with meconium aspiration syndrome or bronchiolitis. Those data are very promising and should encourage studies to identify the optimum type of surfactant, dosage regimen and administration method. Conclusion Further randomized trials are required to fully assess the efficacy and cost benefit ratio of surfactant treatment in “non respiratory distress syndrome” respiratory diseases. Received: 24 January 2000 / Accepted: 6 April 2000     

What (not) to do at and after delivery? Prevention and management of meconium aspiration syndrome

Meconium aspiration syndrome (MAS) is a life-threatening disorder in newborn infants. Universal intrapartum suction of infants with meconium stained amniotic fluid (MSAF) and postnatal suction of vigorous infants have been used in an attempt to decrease the incidence and severity of the disease by clearing the airway. Both procedures have been proven fruitless when challenged through randomised control trials (RCTs). Endotracheal intubation and suctioning are currently recommended only for non-vigorous infants. Respiratory failure in infants with MAS is frequently treated initially with conventional or synchronized mechanical ventilation. Surfactant administration and high-frequency ventilation (HFV) are commonly used as rescue therapy for severe cases. Nitric oxide (NO) is added when severe pulmonary hypertension is demonstrated. ECMO is an option when other treatments have failed. In the pathophysiology of severe MAS, asphyxia and pulmonary hypertension are considered to be more important than the obstruction of the airways and/or damage to the lung produced by meconium.     

中国住院新生儿流行病学调查

目的：通过全国范围内城市医院住院新生儿的调查,以了解我国目前住院新生儿的疾病谱及转归。方法：抽取全国22个省和自治区的47个城市中的80所医院,回顾性调查了2005年1月1日至同年12月31日期间出院的住院新生儿 43 289名。结果：①男女性别比为1.73∶1。②早产儿占住院新生儿的26.2%,其中晚期早产儿占住院新生儿的 16.4%,住院早产儿所占比例较2002年（19.7%）有明显增高。③发生率最高的前3位的疾病依次为黄疸、肺炎和缺氧缺血性脑病。④足月儿肺炎、胎粪吸入综合征和胆红素脑病等疾病的发生率高于早产儿;而早产儿窒息、呼吸窘迫综合征和肺出血等疾病的发生率高于足月儿。⑤妊娠高血压综合征母亲所生的新生儿中窒息、小于胎龄儿（SGA）和湿肺等疾病所占比率均高于无妊娠高血压综合征母亲。⑥转归：治愈占63.9%,好转占27.3%,自动出院占7.6%,死亡占1.2%。新生儿死亡发生在入院后24 h内占46.4%。结论：①住院新生儿中早产儿所占比例有增加趋势。②住院新生儿死亡主要发生在入院后24 h内,应加强入院后24 h内的监护工作。［中国当代儿科杂志,2009,11（1）：15-20］     

Neonatal aspiration syndrome due to vernix caseosa

Fetal aspiration of meconium in amniotic fluid is a well-known cause of respiratory distress in newborn infants. It causes an irregular, coarse, nodular pattern on chest radiographs. Less known is that aspiration of vernix caseosa causes a similar syndrome. We present a post-mature infant in whom aspiration of vernix caseosa caused respiratory distress, ventilatory difficulty, and radiographic changes essentially the same as in aspiration of meconium.     

Steroids in full term infants with respiratory failure and pulmonary hypertension due to meconium aspiration syndrome

Persistent pulmonary hypertension of the newborn (PPHN) due to meconium aspiration syndrome (MAS), has a high morbidity and mortality especially in centres with limited access to extra-corporeal membrane oxygenation or nitric oxide therapy. In such a setting, we conducted a pilot study to evaluate the effect of dexamethasone on severe respiratory failure with PPHN due to MAS with a view to exploring possible justification for randomised controlled trials in similar patients. We prospectively managed a consecutive case series of 14 infants over a 3-year period with the above mentioned diagnosis, who were ventilated and with an oxygenation index >25. Dexamethasone was commenced in a dose of 0.5 mg/kg per day and given for up to a maximum of 9 days in a reducing schedule. Differences between time points were analysed using analysis of variance for repeated measures. The mean age of commencing dexamethasone was 79.9 h. There was a rapid, significant improvement (P < 0.05) in the respiratory status in 13 of these infants after commencing dexamethasone, allowing weaning from the ventilator and eventual extubation at a mean age of 8.7 days. One infant died. Two infants had infective episodes. Conclusion Dexamethasone, if started early in infants with respiratory failure and persistent pulmonary hypertension of the newborn due to meconium aspiration syndrome may be effective in improving gas exchange, and possibly avoiding extra-corporeal membrane oxygenation. A randomised controlled trial of using dexamethasone early in similar patients and setting is warranted. Received: 18 May 2000 / Accepted: 13 September 2000     

Handling the meconium-stained infant

Clinicians who care for infants in the delivery room or afterward must frequently manage many born through meconium-stained amniotic fluid (MSAF). Approximately 5% of infants born through MSAF develop meconium aspiration syndrome (MAS). This disorder can be severe in nature, with half or more of the affected children needing mechanical ventilation. It is frequently associated with pulmonary air leaks and the presence of persistent pulmonary hypertension. MAS is the most common disorder for which babies may be treated with extracorporeal life support. Various possibilities for preventing MAS exist during labor, parturition, and the first minutes of life. Proposed antenatal therapies include amnioinfusion; intrapartum maneuvers include oropharyngeal suctioning prior to delivery of the babies shoulders; the postnatal intervention of intubation for intratracheal suctioning should be reserved for the non-vigorous meconium-stained infant.     

High frequency oscillation in newborn infants with respiratory failure

Objective: To report ventilation strategies, survival and complications in 39 outborn infants treated with high frequency oscillatory ventilation (HFOV).
Methodology Data were collected prospectively between 1 May 1992 and 31 December 1993 on all infants treated with HFOV who had severe respiratory failure despite optimal conventional ventilation.
Results Twenty-eight out of 39 (72%) survived. Of the 15 infants with birthweights <1500g, eight survived. Best survival rates were for infants with pulmonary interstitial emphysema with air leak (4/5) and for infants of birthweight >1500g with hyaline membrane disease (8/8), and meconium aspiration syndrome (7/7). Three infants deteriorated while on HFOV and required extracorporeal membrane oxygenation. Complications were: (i) development of pulmonary interstitial emphysema (1); (ii) recurrence of pneumothorax (3); (iii) hypotension (2); and (iv) bronchopulmonary dysplasia (9). One of the eight infants weighing <1500g who received HFOV in the first week of life developed periventricular haemorrhage.
Conclusion The initial results of HFOV for severe respiratory failure were encouraging although a learning curve was encountered with its introduction.     

Therapeutic lung lavage in meconium aspiration syndrome: a preliminary report

AIM: To explore the effects of a large volume lung lavage procedure in ventilated infants with meconium aspiration syndrome. METHODS: Infants with severe meconium aspiration requiring high-frequency ventilation underwent lung lavage using dilute bovine surfactant at a phospholipid concentration of 5 mg/mL. Lavage aliquot volumes were increased through the case series, aiming to deliver two aliquots of 15 mL/kg in rapid sequence. Physiological effects of lavage were documented, and comparison was made with a group of infants with meconium aspiration requiring high-frequency ventilation, in whom lavage was not performed. RESULTS: Nine episodes of lavage were performed in eight infants at a median age of 23 h (range 8-83 h). Three infants underwent a lavage that was defined as potentially therapeutic (total lavage volume of at least 25 mL/kg administered before 24 h of age). Lavage was not associated with bradycardia or hypotension. Recovery of arterial oxygen saturation to above 80% was achieved within 12 min in all but one infant in whom oxygen saturation was below 80% at the outset. Mean airway pressure was significantly lower in the Therapeutic lavage group compared with non-lavaged infants in the first 48 h, with a trend towards improved oxygenation. CONCLUSION: Dilute surfactant lavage with aliquots of up to 15 mL/kg appears to be feasible in haemodynamically stable ventilated infants with meconium aspiration syndrome, and its efficacy deserves further investigation in a randomised controlled trial.     

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

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.     

Birth asphyxia: incidence, clinical course and outcome in a Swedish population

A total of 42 203 live infants were born in Goteborg in 1985-1991, and 292 term infants had Apgar scores < 7 at 5 min. Infants with congenital malformations, infections and opioid-induced respiratory depression were excluded and thus 227 infants were included in the birth asphyxia group, which formed the basis of this retrospective study. Clinical signs of mild, moderate or severe hypoxic-ischemic encephalopathy (HIE) were present in 65 infants, and in another 10 infants, sedated and on controlled ventilation, HIE was assumed but grading was not possible. The incidences of Apgar scores < 7 at 5 min, birth asphyxia and birth asphyxia with HIE were 6.9, 5.4 and 1.8 per 1000 live born infants: 95% of infants resuscitated with bag and mask ventilation only, did well, compared with 1 of 11 in whom resuscitation included adrenaline. Seizures occurred in 27 of 227 infants, beginning in 18 infants within 12 h of birth. Small-for-gestational-age (SGA) infants were overrepresented in the birth asphyxia group but not in the birth asphyxia-HIE group. All infants with severe HIE died or developed neurological damage. Half of the infants with moderate, and all of the infants with mild, HIE were reported to be normal at 18 months of age. A total of 0.3 per 1000 live born infants died and 0.2 per 1000 developed a neurological disability related to birth asphyxia. The disabilities were dyskinetic (4), tetraplegic (2), spastic diplegic (2), cerebral palsy and mild neuromotor dysfunction (1). The relatively low incidences of birth asphyxia and HIE were probably due to effective antenatal care. Asphyxia neonatorum, cerebral palsy, hypoxic-ischemic encephalopathy, incidence, outcome, population, resuscitation, seizures, term infant
E Thornberg, Department of Pediatric Anesthesia and Intensive Care, Östra Hospital, S-416 85 Göteborg, Sweden     

肺泡毛细血管发育不良一例报告并文献复习

目的 报道1例肺泡毛细血管发育不良(alveolar capillary dysplasia,ACD),并复习文献20例.方法 自Medline检索国外报道病例.结果 本例为足月顺产,生后5 h开始出现呼吸窘迫,给予呼吸机辅助呼吸等无效,生后第4天死亡,尸检病理学诊断符合肺泡毛细血管发育不良.21例中,19例足月儿,2例早产儿.19例出生体重正常,男∶女=7∶14.15例出生Apgar评分正常;16例在出生24 h内出现缺氧症状,5例在生后1～19 d内起病;20例出现肺动脉高压,全部患儿出现心脏血液右向左分流.20例给予呼吸机辅助呼吸;7例行高频振荡通气;12例行体外膜肺支持;14例行一氧化氮吸入治疗,4例行肺表面活性物质治疗.6例行肺部活检.胸部X线检查显示,3例表现正常,9例出现气胸,7例出现双肺网状影、颗粒状影以及弥漫性斑片状影、透过度减低等,2例肺血管影减少.全部21例均死亡,其中8例在出生10 d内死亡,7例在出生30 d内死亡,最长存活时间为4个月.14例伴有先天性心血管系统、消化系统、泌尿系统、呼吸系统等畸形,其中1例伴发染色体畸形,2例有家族遗传倾向.结论 目前,本病尚无特效治疗、且预后不良、医疗费用巨大.当新生儿出现呼吸衰竭或者PPHN,常规治疗无效时,应该高度怀疑此病,并行常规开放式肺组织活检,以明确诊断.