#MECONIUM IN AMNIOTIC FLUID SKIN#

The presence of inflammation/infection in maternal history has been associated with MAS. suggested that increased lactate levels in blood gases during the first hour of life may also be a risk factor for the development of MAS in MSAF patients. Fetal distress or non-reassuring/abnormal cardiotocography have been frequently reported in MAS patients (43–67%) as well as umbilical cord metabolic acidosis (21–24%) and a low Apgar score at 5 min (18–60%). Several studies have investigated antenatal and perinatal factors associated with MAS to improve the identification and management of such patients. Understanding the mechanisms underlying the inflammatory cascade in MAS could be useful for addressing new therapeutic strategies. In vivo, it is reasonable to hypothesize that additional triggers for inflammation can be hypoxia due to MAS, baro- and volu-trauma related to ventilation and oxygen therapy. It has been hypothesized that the two main systems of the recognition of innate immunity (the toll-like receptor and the complement system) may recognize meconium as dangerous and activate the inflammatory cascade. As meconium is produced in the intestine and is therefore only minimally exposed to the immune system during fetal life, it may be recognized as “not self”, triggering the activation of innate immunity. However, the cellular mechanism underlying the initiation of the inflammatory cascade in humans remains to be clarified. For decades it has been widely known that meconium is toxic and induces inflammation and apoptosis and can lead to chemical pneumonia in the first 48 h of life with a risk of bacterial over-infection. Despite the repairing role of inflammation, its destructive potential can cause local tissue damage.

Meconium contains substances with a chemotactic action for neutrophils it also activates the complement, has a vasoactive function and is also a source of pro-inflammatory mediators (such as IL-1, IL-6 and IL-8 and TNF). Īctivation of the inflammatory cascade : the alveolar interstitium of patients with MAS shows inflammatory cellular infiltrates characterized by the release of cytokines and complement activation. Risk factors for MAS include thick meconium, a pathological cardiotocographic trace, fetal acidosis, caesarean section, the need for intubation at birth and low Apgar scores. MAS results from the aspiration of MSAF during gasping in intrauterine life or during the first breaths after birth. Risk factors for MSAF include placental insufficiency, maternal hypertension, pre-eclampsia, oligohydramnios with umbilical cord compression during labor, infections and maternal substance abuse (especially nicotine and cocaine). The presence of MSAF is considered to be an indicator of fetal stress due to hypoxia and acidosis causing a vagal response that triggers an increase in peristalsis and anal sphincter release with a resulting meconium passage into the uterine cavity. When found in a preterm infant, biliary discoloration (due to intestinal obstruction) or fetal diarrhea (secondary to sepsis, particularly from Listeria) should also be considered.

While meconium appears in the intestine at around 12 weeks’ gestation, the passage into the amniotic fluid is unlikely in preterm infants because of ineffective peristalsis, good anal sphincter tone and low motilin levels.

However, meconium can sometimes be released early into the amniotic fluid causing the so-called “stained fluid”. Meconium is usually found in the intestine of the fetus and newborn with its first emission occurring within the first day of life. The term meconium is derived from the Greek “mekoni” (poppy juice or opium) because of its black appearance.

#MECONIUM IN AMNIOTIC FLUID SKIN#

Meconium is a black-greenish, sterile, odorless, dense, sticky and viscous material consisting of water, skin and intestinal desquamation cells, gastrointestinal secretions, bile, pancreatic juices, mucus, lanugo, vernix, blood glycoproteins and amniotic fluid.

Meconium in amniotic fluid