2. Etiology and embryology

Though unexplained, a young maternal age and low socioeconomic status are the commonest risk factors for GS [10, 11]. Smoking, drugs, environmental toxins and poor nutrition have also been implicated [12]. A genetic link in the form of homozygous gene polymorphisms has been reported [13] and is substantiated by an increased prevalence among familial cases of birth defects and twins [14].

The embryological origin of GS is still a matter of conjecture. Several theories have been put forward attempting to expound the abdominal wall defect: failed body-wall folding [15]; a vascular insult to the omphalo-mesenteric artery [16] or to the right umbilical vein [17]; a localized disruption of the amniotic membrane [18]

midline and may involve solid organ prolapse. Ultrasound is instrumental in picking up closing GS which is defined as a worsening ratio of intra vs. extra peritoneal bowel dilatation [27]. Further aids to diagnosis of GS are high levels of maternal serum alpha-fetoprotein (MSAFP) [28], intrauterine growth retardation with or without oligo-/an-hydramnios [7, 29, 30]. As GS is usually an isolated anomaly with very few risks to the mother or child, termination of pregnancy is not habitually

A spontaneous onset of labor will typically occur around 36 weeks gestation and the route of delivery is dependent on obstetric indications [33, 34]. There is a lack of high-level evidence to support early induction of labor in uncomplicated GS cases [35, 36] and a similar lack of evidence to support cesarean section [37]. Early

LMICs have an overall high mortality rate in neonates with correctable congenital anomalies [38, 39] and suffer from a lack of medical facilities and personnel [40]. Non-governmental and governmental organizations have been criticized for not doing enough [41, 42] though new partnerships are attempting to redress this

Mortality from GS in low-to-middle-income countries (LMICs) can reach up to 80–100% [45–48] which is in sharp contrast to the <10% in HICs [49]. Sepsis is a major culprit in most cases of neonatal mortality in LMICs [48]. The Gastroschisis International (GiT) network has suggested that poor resuscitation combined with sepsis and abdominal compartment syndrome is directly linked to the poor outcome [50].

Antenatal care may not be well developed [51] or mothers may engage poorly with it [52] which risks births in areas far from the reach of the pediatric surgeon. A delay in transfer of the neonate with GS remains a main concern [47, 53] however a recent study from South Africa has suggested that resuscitation at the initial point of care and throughout transfer may be the key to improving the end result [51].

A GS infant is ideally delivered at or near a facility with pediatric surgical support [25]. Conversely, outborn cases have been shown to have worse outcomes such as longer days on parenteral nutrition and longer duration to achieving full

The accepted approach to managing GS is to cover the gut with a sterile bag (Figure 3), nasogastric decompression and fluid resuscitation. Hypothermia is a major risk due to the exposed gut and significant fluid losses [55]. Premature babies are particularly prone to hypothermia because of their high ratio of skin surface to weight and a lower amount of subcutaneous and brown fat. They may also have respiratory

The authors follow the protocol outlined in Figure 4. At the outset doctors and nurses are reminded that the triad of hypovolemia, hypothermia and sepsis are the major threats to this neonate and that resuscitation is directed to mitigating their

issues which impact on their oxygen consumption and heat production [55].

offered [2, 31, 32].

Management of Gastroschisis

[43, 44].

feeds [54].

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4. Timing and mode of delivery

DOI: http://dx.doi.org/10.5772/intechopen.85510

(emergency) delivery is beneficial in closing GS [26].

5. GS in low to middle income countries (LMICs)

6. Initial management (pre-operative management)

Figure 1. Gastroschisis with prolapsed bowel to the right of the umbilicus.

or teratogen-induced mesenchymal failure [19]. None of the theories are fully satisfactory [20]. The right-sided occurrence of the defect has been linked to the position of the yolk sac [15, 21] without clear reasoning as to why. Left-sided defects have also been described [22].
