9. Fluid management in GS

Publications frequently refer to a "consensus" among doctors on the optimal fluids required for GS. However, there is sparse evidence-based literature to guide the perioperative fluid management [65, 66]. Reports of fluid administration have varied from twice to three-times the normal maintenance volumes for neonates [67, 68] and were based on original research by Phillippart et al. in 1972 [69].

10.2 Sepsis

Box 2.

catheters [50, 51].

Management of Gastroschisis

compartment syndrome.

10.3 Silo complications

10.4 Pneumothorax

Figure 12.

127

Large abdominal wall defect with granulation in long-standing silo.

Sepsis is a common complication in LMICs. Most common sources are intra-abdominal, silo/wound infections, indwelling central lines or urinary

• Gastric/urinary bladder pressure < 200 cm H2O or < 15–

20 mmHg

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

Reference values for safe abdominal closure [78–81].

• End-tidal CO2 < 50 mmHg

• Ventilation <24 cm H2O

• CVP < 4 mmHg or < 5.4 cm H2O

As always, prevention is better than cure. Meticulous antisepsis protocols and timely use of antibiotics are important first tools. Early suspicion of central lineassociated blood stream infection (CLABSI) or urinary tract infection (UTI) should prompt urgent cultures to be sent to the lab. The authors remove the urinary catheter once there is a stable urine output and no further risk of abdominal

Both pre-formed and surgical silos are prone to dislodgement and may cause bowel kinking, ischemia and perforation [58]. It is prudent to keep the silo and its contents visible at all times to allow early detection of any of these complications.

Iatrogenic pneumothorax secondary to barotrauma is an unfortunate complication in ventilated neonates and occurs in around 8.7% of the cases [82]. In GS this may be due to high intra-abdominal pressure after bowel reduction. This is best anticipated in theatre and if pressures exceed 24 cm H2O, a staged reduction should

Fluid overload in the absence of hypovolemia has been proven to be deleterious in neonates [70]. It affects a patent ductus arteriosus, may cause intracranial hemorrhage, bronchopulmonary dysplasia or may even be fatal [71, 72]. Therefore the mere assumption that GS cases need vigorous volume expansion may be harmful. Preterm neonates may also benefit from fluid restriction according to a recent Cochrane review [73]. It has been suggested that the fluid overload will contribute to intestinal edema leading to a longer hospital stay and longer duration of parenteral nutrition through the increase of total body water and salt [65]. It may also play a part in development of NEC [74].

This practice of over transfusion is routinely carried out postoperatively as well [75]. While it may be of value in cases with a silo where there are ongoing losses of fluid from the base, it has no real justification in cases which undergo primary closure.

Few published sources will give an outright volume to go by. They will always be ranges and the clinician must be guided by continuous assessment of the child. Postnatal diuresis can complicate fluid-balance calculations but a useful milestone to assess the cardiovascular status is after administering 40 ml/kg of fluid. Albumin has been advocated as a volume expander in hypovolemic GS cases. It is not particularly useful in hypoalbuminemia associated with sepsis [76, 77]. An additional tool to help restore insensible water loss incurred through breathing is the humidification of incubator air.

### 10. Complications

#### 10.1 Abdominal compartment syndrome (ACS)

A large degree of viscero-peritoneal disproportion and over-zealous reduction runs the risk of increased intra-abdominal pressure. The latter will result in restricting diaphragmatic movement and compression of the inferior vena cava, which will in turn result in respiratory distress, renal, liver and bowel ischemia, respectively. They manifest as metabolic acidosis, oliguria, renal and liver dysfunction [55].

Frequent monitoring of oxygen saturation/ventilation setting, serial blood gases, urine output, serial abdominal examinations, lower limb perfusion are important in early detection of ACS. Oliguria alone is not a sensitive indicator of ACS as it may be due to hypovolemia. Pressure measurements can be taken using sophisticated transducers used with anesthesia machines or by simply connecting the tubing to a CVP water manometer. Reference values are quoted in Box 2 [78–81].

```
• Gastric/urinary bladder pressure < 200 cm H2O or < 15–
  20 mmHg
• End-tidal CO2 < 50 mmHg
• CVP < 4 mmHg or < 5.4 cm H2O
• Ventilation <24 cm H2O
```
### Box 2.

enema should be done to rule out a bowel atresia. An atresia detected at the time of initial closure of by subsequent imaging may be safely repaired after 3–6 weeks. Albeit uncommon in GS, cases with any associated malformations will require

Publications frequently refer to a "consensus" among doctors on the optimal fluids required for GS. However, there is sparse evidence-based literature to guide the perioperative fluid management [65, 66]. Reports of fluid administration have varied from twice to three-times the normal maintenance volumes for neonates [67, 68] and were based on original research by Phillippart et al. in 1972 [69].

Fluid overload in the absence of hypovolemia has been proven to be deleterious in neonates [70]. It affects a patent ductus arteriosus, may cause intracranial hemorrhage, bronchopulmonary dysplasia or may even be fatal [71, 72]. Therefore the mere assumption that GS cases need vigorous volume expansion may be harmful. Preterm neonates may also benefit from fluid restriction according to a recent Cochrane review [73]. It has been suggested that the fluid overload will contribute to intestinal edema leading to a longer hospital stay and longer duration of parenteral nutrition through the increase of total body water and salt [65]. It may also

This practice of over transfusion is routinely carried out postoperatively as well [75]. While it may be of value in cases with a silo where there are ongoing losses of fluid from the base, it has no real justification in cases which undergo primary

Few published sources will give an outright volume to go by. They will always be

A large degree of viscero-peritoneal disproportion and over-zealous reduction

Frequent monitoring of oxygen saturation/ventilation setting, serial blood gases, urine output, serial abdominal examinations, lower limb perfusion are important in early detection of ACS. Oliguria alone is not a sensitive indicator of ACS as it may be due to hypovolemia. Pressure measurements can be taken using sophisticated transducers used with anesthesia machines or by simply connecting the tubing to a

runs the risk of increased intra-abdominal pressure. The latter will result in restricting diaphragmatic movement and compression of the inferior vena cava, which will in turn result in respiratory distress, renal, liver and bowel ischemia, respectively. They manifest as metabolic acidosis, oliguria, renal and liver dysfunc-

CVP water manometer. Reference values are quoted in Box 2 [78–81].

ranges and the clinician must be guided by continuous assessment of the child. Postnatal diuresis can complicate fluid-balance calculations but a useful milestone to assess the cardiovascular status is after administering 40 ml/kg of fluid. Albumin has been advocated as a volume expander in hypovolemic GS cases. It is not particularly useful in hypoalbuminemia associated with sepsis [76, 77]. An additional tool to help restore insensible water loss incurred through breathing is the humidifica-

further investigations and management according to the findings.

9. Fluid management in GS

Pediatric Surgery, Flowcharts and Clinical Algorithms

play a part in development of NEC [74].

10.1 Abdominal compartment syndrome (ACS)

closure.

tion of incubator air.

10. Complications

tion [55].

126

Reference values for safe abdominal closure [78–81].
